Dr. Wakefield Sues Brian Deer and BMJ's Fiona Godlee
That’s My Boy!

The Inflammation Highway: aka Autism

  Tummy-ache-abdominal-pain-t13513By Lisa Goes

"The one thing about my husband and I...we laugh...A lot. We find a way. We really do. Poop filled sleepless nights, injuries, missed appointments, clutter everywhere, missing paperwork...sometimes all you can do is laugh. But today, looking at the dark circles we've seen so many times under our children's eyes, seeing the suffering, the real genuine human suffering that we have worked for three years to alleviate...to see it reach these depths...there is no laughing today. There is sadness. Even the fight is gone. I should be sleeping, but I have to read up on one of our new remedies. Maybe this will be the one that touches his immune damage and regulates him? Maybe. Maybe, it will work for him like it has for THOUSANDS of other children. Maybe. I can't sleep when this could be it and I could be calling the next doctor tomorrow and we could have one less day of this. Plus, I already have an appointment to see a doctor tomorrow and I will need him to know that I know what I'm talking about. If there is one thing you learn as an autism parent it is that YOU MUST KNOW WHAT YOU ARE TALKING ABOUT WITH DOCTORS. You must learn to speak their language. If you don't you will get dismissed. Must read, now.



But, before I go, just need to let everyone know the women who work for us are angels from God. They were hurt today. Two of them. In their sweetest voices they kept repeating, "nice hands." And "time to get down monkey" when he climbed on the counter for the 27th time on their shift. He is 50 lbs now. Very fast and very strong. They get him. They see the real Noah in there, fighting like hell. He is mad. In fact, that's what he said in therapy today, "I'm MAD!" His therapists were thrilled. They were so excited to see him emote appropriately. I agree with them, it's encouraging. It's just that, he's mad he's sick. He's mad his head hurts all the time. He's mad his three year old brother can use the toliet and he cannot. He's mad that his body is rebelling against him and everything hurts. He's mad that in addition to not getting to go where everyone else goes and doing all the fun things other 5 year olds do, he also cannot EAT anything they do. It seems cruel doesn't it? It is.

Autism is the cruelest most malicious, devious, conniving, heinous disease. If you fear the chicken pox or diarrhea more you are in big, big trouble. Because I guarantee with the new schedule autism will come a knocking at your door. And it will get in. It finds a way. Sometimes it looks like OCD, sometimes it looks like ADHD, even arthritis. "That's nuts!", you say. Not really. It should all just be called autism. Because any time pharma causes inflammation they don't want you to find out about, they just make up a word for it. Autism. Asthma. ADD. Just made up words for inflammation. Off to read ABOUT AUTISM . It's a good one, you might want to check it out yourself... Much hope for all our beautiful children. xo lj "

Lisa Goes is Contributing Editor to Age of Autism.

Comments

benedetta

Nick; you are one of my favorite people too.

Visitor

There is no ethnic enemy. Man is his own enemy. Alone Again Naturally. Johnny Cash, one of the few I would have trusted to lead as he knows himself better..

https://www.youtube.com/watch?v=8AHCfZTRGiI

Immunoceptive inference: why are psychiatric disorders and immune responses intertwined?

Conclusions
In this paper, we have introduced ‘immunoceptive inference’: active inference from the perspective of the immune system. This is in a similar vein to the notion of ‘interoceptive inference’, which frames emotions as emerging from—or perhaps furnishing—predictions about the causes of visceral sensations. In brief, interoceptive inference claims the brain is continuously updating predictions about, and acting upon, the body it inhabits (Seth 2013). In our formulation, the body itself (in this case, the immune system) is seen as furnishing predictions of—and acting upon—sensory input, informing ‘beliefs’ about whether an antigen belongs to the category of ‘self’ or ‘nonself’.

In so doing, we have highlighted three practical contributions (translation, unification and simulation) of the active inference framework to answering and—crucially—redefining the question, “Why are psychiatric disorders and immune responses intertwined?” We suggested that it is inevitable that two systems within the same Markov blanket influence each other: the brain and the body together make predictions about exteroceptive, interoceptive, and immunoceptive input. To this end, we have proposed an example of a common generative model that the brain and immune system jointly optimise, treating molecular components of the immune system as sensory or active states and the resulting cellular response as message passing at lower levels of a ‘sensory’ hierarchy that interfaces with the brain. Our scheme expresses the classical conditioning of the immune system in terms of inference at an immunological level, that may alter the message passing at a psychological level (or vice versa) through an optimal interface between the two systems.

This surrender of mind–body and brain-body dualisms may be of particular importance to psychiatric practice, where it encourages a holistic treatment of patients. For example, with an embodied perspective on the mind, a patient presenting with psychosis may be treated with reference to the mechanisms leading to this syndromic endpoint, whether that be schizophrenia (treated with antipsychotics), or an alternative (e.g., endocrine) diagnosis such as Cushing’s syndrome, which can be effectively treated by normalising cortisol levels (Tang, O'Sullivan et al. 2013, Wu, Chen et al. 2016)—or indeed autoimmune encephalitis (Symmonds et al. 2018). We also advance the possibility of drawing immunological analogues of concepts defined under active inference for neurological phenomena, such as sensory attenuation. Finally, we introduce the novel concept of neuroimmunological diaschisis and the possibility of a diaschisis of threat-avoidance that may contribute to the overlap between psychiatric disorders and immunological hypersensitivities. This kind of overlap leads to clear empirical predictions; for example, an association between psychopathology and (measurable) immunological responses, much in the same way that clinical tools such as the dexamethasone suppression test leverages the link between neuroendocrine function and stress or depression (Naughton et al. 2014)."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8085803/

I cannot invoke God in these explanations.


"In this paper, we have introduced ‘immunoceptive inference’: active inference from the perspective of the immune system. This is in a similar vein to the notion of ‘interoceptive inference’, which frames emotions as emerging from—or perhaps furnishing—predictions about the causes of visceral sensations. In brief, interoceptive inference claims the brain is continuously updating predictions about, and acting upon, the body it inhabits (Seth 2013). In our formulation, the body itself (in this case, the immune system) is seen as furnishing predictions of—and acting upon—sensory input, informing ‘beliefs’ about whether an antigen belongs to the category of ‘self’ or ‘nonself’.

In so doing, we have highlighted three practical contributions (translation, unification and simulation) of the active inference framework to answering and—crucially—redefining the question, “Why are psychiatric disorders and immune responses intertwined?” We suggested that it is inevitable that two systems within the same Markov blanket influence each other: the brain and the body together make predictions about exteroceptive, interoceptive, and immunoceptive input. To this end, we have proposed an example of a common generative model that the brain and immune system jointly optimise, treating molecular components of the immune system as sensory or active states and the resulting cellular response as message passing at lower levels of a ‘sensory’ hierarchy that interfaces with the brain. Our scheme expresses the classical conditioning of the immune system in terms of inference at an immunological level, that may alter the message passing at a psychological level (or vice versa) through an optimal interface between the two systems.

This surrender of mind–body and brain-body dualisms may be of particular importance to psychiatric practice, where it encourages a holistic treatment of patients. For example, with an embodied perspective on the mind, a patient presenting with psychosis may be treated with reference to the mechanisms leading to this syndromic endpoint, whether that be schizophrenia (treated with antipsychotics), or an alternative (e.g., endocrine) diagnosis such as Cushing’s syndrome, which can be effectively treated by normalising cortisol levels (Tang, O'Sullivan et al. 2013, Wu, Chen et al. 2016)—or indeed autoimmune encephalitis (Symmonds et al. 2018). We also advance the possibility of drawing immunological analogues of concepts defined under active inference for neurological phenomena, such as sensory attenuation. Finally, we introduce the novel concept of neuroimmunological diaschisis and the possibility of a diaschisis of threat-avoidance that may contribute to the overlap between psychiatric disorders and immunological hypersensitivities. This kind of overlap leads to clear empirical predictions; for example, an association between psychopathology and (measurable) immunological responses, much in the same way that clinical tools such as the dexamethasone suppression test leverages the link between neuroendocrine function and stress or depression (Naughton et al. 2014)."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8085803/

https://www.youtube.com/watch?v=NOa5UOHdwnc

Visitor

All is Said...

https://www.youtube.com/watch?v=xywOYUgOKtA

Best To All

https://www.youtube.com/watch?v=Ku07A-FObLY

Visitor

Benedetta have said things while was drunk that were not meant to hurt or offend you. I hold you in verity high esteem. Please overlook my pain outbursts that are actually in general and not at you.. I like Disturbed's performances. Family is an issue for me and you feel like family so you get some of my vent. I love you.

susan welch

https://www.ageofautism.com/2020/05/autism-up-82-in-northern-ireland-schools-in-5-years.html

M2021 Information about rates of autism in Ireland, thanks to Ann Dachel, AoA

benedetta

M2021
South Korea a few years back said for them it was on in 32? Or was that 23? It was high.

Other than that, not much.

Japan had trouble with vasculitis of all small blood vessels, in children called Kawasakis disease way back in the 70s and 80s.

Even in the United States the CDC whose main job is suppose to track health trends; is hiding it as hard as they can.
Example: What William Thompson said the CDC did with their research material for the MMR.
Utah tried to fudge the statistics and got sued by one of the people working on the stats for their criminal behavior.

M2021

Charcoal soap/certain earth clays/spirulina help eliminate aluminum + toxins in general.

And autism is especially pronounced/most known in the Anglo Saxon world, but it’s also striking areas such as Japan, Korea, China, Malaysia, Ireland, Philippines, etc.

What are the current rates 4 all those countries?

benedetta

M2021:

Oh yeah, I got that covered, probably the best of all.

Dr. Exley - Told us that a bunch of research studies on rats are showing that a special type of silica in the volcanic water of Fiji - Fiji water that is high in it, will take out what you are consuming and will eventually take it on out of your brain.

I go to a special spring that runs out of a rock in the middle of Daniel Boone National Forest.
I come home, and use a special recipe that some wonderful, smart, person on this website told me about and I found in this book: Silica Water the Secret of Healthy Blue Zone Longevity in the Aluminum Age
by Dennis N Crouse PhD.

Crouse also has a video on the internet where he makes it as well.

I don't know if the water I am getting from the spring that rolls through a bunch of ancient limestone - rocks already have a lot of this special silica form - but if I treat every gallon with Crouse's recipe; it has a sulfur taste, and no one is going to drink it. So, I only treat one gallon, and put it in the other water in my three gallon water container.

In addition -- the man that wrote the book "Crooked: Man-Made Disease Explained: The incredible story of metal, microbes, and medicine - hidden within our faces."
by Forrest Maready says to use glycine too.

So since glycine is a some what sweet taste, I put it in the water along with a tsp of concentrated lemon juice. All the urine doctors/kidney stone doctors says a teaspoon of lemon in your water will keep the stones as bay.

Sometimes I get the special magnesium/glycine powder and put it in our lemonade.

.

M2021

The elephant in the room is the countless toxins + high aluminum inside ASD brains thanks to vaccines.

The only green in vaccines is the injection site pus.

Now lots of American + Anglo Saxon children (sadly) are prone to violent rages, criminal behaviors, wandering, extreme social delays etc, thanks to aluminum adjuvants.

Focusing only on gut micro biome (while ignoring brain’s aluminum content) is negligent.

Visitor

https://www.youtube.com/watch?v=9UVjjcOUJLE&list=RD7jVmW41LOMM&index=4ost again it will be from the motivation of this.
https://www.youtube.com/watch?v=9UVjjcOUJLE&list=RD7jVmW41LOMM&index=4

Visitor

"It's just as well for all I've seen" I don't think I have more to say.

Visitor

Benedetta,
You are my kind of people.

Visitor

One that keeps me holding on.. I miss my mother.

https://www.youtube.com/watch?v=8THtJ5T4u_E

I said I miss my mother in reference to this song. I said my mother! That means Disturbed need not apply.

Visitor

https://www.bing.com/videos/search?q=sound+of+silence+by+disturbed&ru=%2fsearch%3fq%3dsound%2bof%2bsilence%2bby%2bdisturbed%26cvid%3d7a2ba59e33384553a948726d7aa68c58%26pglt%3d43%26FORM%3dANNTA1%26PC%3dU531&view=detail&mid=2A9F676FD0105B19A1412A9F676FD0105B19A141&rvsmid=44F600D7B15EC73DAAF344F600D7B15EC73DAAF3&FORM=VDQVAP&ajf=60

benedetta

We are all nobodies, and together our voices will make sure they know us nobodies matters. Some day.

Love the Peterson's and thanks for sharing. Nice to find such musical, talented no bodies. Cause I never heard of them.

Visitor

I thought of speaking of gdf15 morning sickness , mitochondrial dysfunction and autism, but remembered I am a nobody.

https://www.genecards.org/cgi-bin/carddisp.pl?gene=GDF15

https://www.youtube.com/watch?v=OeDiK2uy3DU

https://www.youtube.com/watch?v=y2zeudxXjuU

Visitor

My family is musical and this takes my Kentucky home.

https://www.youtube.com/watch?v=Y3hXYININJw

Visitor

Earlier link does not work.

https://www.youtube.com/watch?v=WLLYpKFW43c

Visitor

Brain-immune interactions in neuropsychiatric disorders: lessons from transcriptome studies for molecular targeting

Abstract
Understanding the pathophysiological mechanisms of neuropsychiatric disorders has been a challenging quest for neurobiologists. Recent years have witnessed enormous technological advances in the field of neuroimmunology, blurring boundaries between the central nervous system and the periphery. Consequently, the discipline has expanded to cover interactions between the nervous and immune systems in health and diseases. The complex interplay between the peripheral and central immune pathways in neuropsychiatric disorders has recently been documented in various studies, but the genetic determinants remain elusive. Recent transcriptome studies have identified dysregulated genes involved in peripheral immune cell activation, blood-brain barrier integrity, glial cell activation, and synaptic plasticity in major depressive disorder, bipolar disorder, autism spectrum disorder, and schizophrenia. Herein, the key transcriptomic techniques applied in investigating differentially expressed genes and pathways responsible for altered brain-immune interactions in neuropsychiatric disorders are discussed. The application of transcriptomics that can aid in identifying molecular targets in various neuropsychiatric disorders is highlighted.

Keywords: brain-immune interactions; immune cells; neuropsychiatric disorders; transcriptomics.

https://pubmed.ncbi.nlm.nih.gov/33773976/

I sit back and watch. It is true, but it is like slow motion watching the dawning of this reality in the community.

Visitor

This proves nothing, but nothing does. It is as good as anything.
I value Matthew, Mark, Luke, and John as much as anyone. The following show sense and faith do go together as do the 10 utterances and our being. Some might quibble with Einstein being a quasi-deist, but he was too smart imo to not believe.

25 Famous Scientists Who Believed in God

https://www.famousscientists.org/25-famous-scientists-who-believed-in-god/

Thank You Lord Jesus.

Visitor

Benedetta,

In a simple response I say while all sorts of evidence have challenged my faith, and to the point of agnostic response, I can't comprehend it all I trust in God and see so much of His glorious hand in life and creation. My A plus B = C sometimes overtakes me in a moment I will not rust in my own understanding. The Lord sometimes is my adversary, but I would have not other. I confess Jesus is Lord and my Savior. I have made stupid statements and decisions and that is why I love grace. Grace makes life worth living. I believe God is infinitely above man and hiss knowledge. We are a strange kind and to this I say to God be the Glory.

benedetta

At first there is constant, often prayers of pleading.
Which some times in exhausting turns into rage and anger toward God.

Then God asked me a question one day when my son was 18.
You are angry with me, are you angry with Jesus Christ.

It surprised me!

I have had intense Holy Spirit relationship with Jesus since I was 12. Many that did not , i am so very sorry.

But No, Jesus is my friend. A deep love I have for him, He loves me. I don't know how this will work for others? But for me it calmed me down.

Jesus is God in another form. How can I be mad, raging anger at Jesus. I can't.

Then whose fault is all of this.
It is man's fault.
It is my fault for being tricked. I had my warnings. I had that class in infectious diseases and I let the professor with his zeal of a preacher on vaccines persuade me, even when the swine flu shot that very year turned out so horrible, even when the young men teased him in class about it. I had my warning, years later; when my husband said he had heard Kawasaki's disease could be caused by vaccines. I had my warnings as I watched soaring temperatures after vaccines. Passing out and on and on.

But it is not all of my fault either.
It is humans the kind that rises up out of the masses that pretend to care but don't. It is Colleen Boyd, it is Plotkin (even before I saw him on a u tube, I knew his kind existed, It is all my friends and neighbors as well as myself that gave such humans power over us.

God does not stop it because we have free will. how will we learn if he is stopping us from ever bad decision.

It is mankind and we best be aware who we choose to worship -- believe --- trust -- those things are a form of worship.

Visitor

I am a pastor who has not come close to coping with what has come to my door. I remain hopefully anonymous as there is something in the way of life I want to vomit about. I met with a young man today who has had such a horrendous life I wanted to melt away. I did not want to know of it all. My life has been effected in like ways and his questions were my own.. His opine is where is God in the middle of all the suffering. He is seeing things, but the pure light still shines. If all there is to hope on is my insight I want to give up too. The afflicted are the pure.

https://www.youtube.com/watch?v=QVVlyWeaMN4

Visitor

I had planned to post other things, but this new report takes precedence. Early in this thread we discussed the New York girls and the media said it was "conversion Disorder". These new findings sure look familiar. An aspect of the same neuroinflammation, cytokines, and vegF.

Assessment of cytokines, microRNA and patient related outcome measures in conversion disorder/functional neurological disorder (CD/FND): The CANDO clinical feasibility study

"Our study sample showed elevated IL-6, IFNγ, IL17A, IL12 and TNFαscores, normal IL1B scores, and VEGF-a scores significantly lower compared to the normal sample. Another study in acute CD/FND patients found elevated IL-6, TNFαand IL1B scores (Tiyekli, 2013), which is different from our
findings as in our study, IL1B was normal. Dysregulated continual synthesis of IL-6 plays a role in pathologic chronic inflammation and autoimmunity (Tanaka, 2014) so our study supports the idea that IL-6 may play a role in CD/FND of longer duration. IFNγisproduced by CD4þT helper 1 cells (Th1 cells). It plays a key role in B cell maturation, as it works to inhibit migration into lymph nodes while the B cells are still immature (Flaishon, 2000) and inhibits proliferation of T cells (Chu, 2000). Tumour Necrosis Factor Alpha (TNFα) is produced by macrophages/monocytes during inflammation and has widespread cellular effects, although still a great deal is unknown about its function and complex interplay with other cytokines (Zelova, 2013)."

3.8.3. microRNAThere is extensive literature linking several miRNAs to inflammationand neuroinflammation as well as pain (Andersen et al., 2014;Mi et al.,2013). We supplemented our analysis of circulating cytokines in thecohort by measuring levels of 5 miRNAs associated with inflammation(miR-146a, miR-223 (Wang et al., 2010) miR-155 (Alivernini et al.,2018;Singh et al., 2019)) and to angiogenesis and vascular inflammatoryresponses (miR-21 (Liu et al., 2011;Sheedy et al., 2010;Du et al., 2019),miR-132 (Kumarswamy et al., 2014) and miR-155 (Singh et al., 2019))and miR-16, a highly abundant miRNA in circulation.We observed a range of miRNA blood plasm levels within the cohortas shown inFig. 2.We also explored if levels of miRNAs correlated with levels of TNF inthe cohort. We found that this was the case for all tested miRNAs."

https://reader.elsevier.com/reader/sd/pii/S2666354621000314?token=E148248E601850A6DA279FB778C5EA6E128A9EF09E887A047FBFDEB5605C58DBF6DB3E1E390BBCEE34F7142CC42F907C

Visitor

https://www.youtube.com/watch?v=m4oZZhpMXP4

Visitor

Sometimes I forget that while God cares for our bodily ills He died for our souls.

Lamb of God, you take away the sin of the world, have mercy on us.
Lamb of God, you take away the sin of the world, have mercy on us.
Lamb of God, you take away the sin of the world, grant us peace.

O Lamb of God, that takest away the sins of the world, have mercy upon us.
O Lamb of God, that takest away the sins of the world, have mercy upon us.
O Lamb of God, that takest away the sins of the world, grant us thy peace.

Jesus, Lamb of God, have mercy on us.
Jesus, bearer of our sins, have mercy on us.
Jesus, redeemer of the world, grant us peace.

Whatever I am errant about I trust in God's mercy though the Lord Jesus Christ.

https://www.youtube.com/watch?v=iAK2UP9SRWU

God Bless AoA. God Bless you Cia. you are my sister.

Visitor

God Bless You Benedetta.

https://www.youtube.com/watch?v=AiuC_CaObbI

benedetta

Damaging the hypothalamus just a bit, messing up the endocrine system and all that implies from thyroid production, to all of the hormones

Or a fever damaging the nerve running from the brain to the gut (damaging or upsetting the Rhythmic undulating intestine' sweeping out food and lowering the numbers of microbes as well.

Changes the environment.

Change the environment, change the type of microbes that can grow.

SO not much hope?

And yet there are the studies that show after a brain injury that leads to a horrible C Diff: That fecal transplants, the transplanted microbes are holding their own.

Visitor

Infections are involved in many, though many appear to not have these issues or have not realized the nature of some infections.

"Allergies/ Immune System: Many individuals with autism also suffer immune system deficiencies or immune dysregulation. Within the autism spectrum population, there are groups that will experience rashes, allergic sensitivities, gastrointestinal, ear and other infections as a result. Immune deficiencies and/or immune dysregulation make a person with autism more vulnerable to infection, chronic inflammation and autoimmune reactions, most frequently in the brain and gastrointestinal tract (Jepson, 2007)."

https://www.autism-society.org/what-is/diagnosis/related-conditions/

and one on the gut bacteria being understood for its effect...

Microbes may hold the key for treating neurological disorders

"In my wildest dreams, I could have never imagined that microbes in the gut could modulate behavior and brain function. To think now that microbial-based strategies may be a viable way to treat neurological dysfunction, is still wild, but very exciting."

https://www.sciencedaily.com/releases/2021/03/210310122535.htm

Visitor

More from rom a past comment I made on this thread with further thoughts on TBI and Autism.

"I said earlier in this thread; "I maybe should have not called it TBI, but an ongoing process in Autism that has similar effects overall." TBI being Traumatic brain injury and this was in reference to the on going inflammatory issues in Alzheimer's disease, Parkinson's disease, multiple sclerosis and known traumatic brain injury and how this was occurring in much Autism.

Now, a new report is out talking about long term chemical changes in the brain strongly suspected to be related to the inflammation found in TBI. Here a couple of snippets from two reports and then a link to the abstract."

The following report was referre4d to then:

Autism: 'different developmental brain chemistry'

"The study authors also note that the pattern of chemical changes within the autism spectrum disorder group aged 3 to 4 years is comparable to brain chemical changes found in other disorders such as multiple sclerosis, epilepsy and traumatic brain injury, where the N-acetylaspartate level is reduced at the time of onset or injury. This level usually then rises again during periods of remission, after successful treatment or through recovery."

https://www.medicalnewstoday.com/articles/264106#1

Another repost to consider the connections.

miR-155 Regulates claudin1 Expression in Humans With Intestinal Mucosa Dysfunction After Brain Injury.

Abstract

"Patients with craniocerebral trauma often have intestinal mucosal dysfunction, and the claudin1 protein plays an important role in intestinal mucosal function. Our previous work has shown that the expression of microRNA-155 (miR-155) in the peripheral blood of patients with craniocerebral trauma is decreased. Animal experiments also suggest that the expression of miR-155 is increased in the intestinal mucosa of mice with brain injury and the expression of claudin1 is decreased. We recruited 56 samples (35 patients with traumatic brain injury [TBI] and 21 patients without history of head trauma) to detect the expression of miR-155 on claudin1 regulation by quantitative polymerase chain reaction, reverse transcriptase polymerase chain reaction, and so on. We also used the receiver operating characteristic curve (ROC) to further evaluate the diagnostic value of the 2 biomarkers. From the results, we found that the expression level of miR-155 and claudin1 in the case group was lower than that in the control group. Human miR-155 (Hsa-miR-155) may positively regulate intestinal mucosal function by inhibiting the expression of claudin1, leading to intestinal mucosal barrier dysfunction. Combining the ROC curve data, the results further prove that miR-155 and claudin1 might be the new clinical diagnostic markers and treatment targets for the intestinal mucosal barrier dysfunction after TBI."

https://www.ncbi.nlm.nih.gov/pubmed/31810510

another repost

Inhibition of miR-155 Limits Neuroinflammation and Improves Functional Recovery After Experimental Traumatic Brain Injury in Mice.

Abstract

Micro-RNAs (miRs) are short, noncoding RNAs that negatively regulate gene expression at the post-transcriptional level and have been implicated in the pathophysiology of secondary damage after traumatic brain injury (TBI). Among miRs linked to inflammation, miR-155 has been implicated as a pro-inflammatory factor in a variety of organ systems. We examined the expression profile of miR-155, following experimental TBI (controlled cortical impact) in adult male C57Bl/6 mice, as well as the effects of acute or delayed administration of a miR-155 antagomir on post-traumatic neuroinflammatory responses and neurological recovery. Trauma robustly increased miR-155 expression in the injured cortex over 7 days. Similar TBI-induced miR-155 expression changes were also found in microglia/macrophages isolated from the injured cortex at 7 days post-injury. A miR-155 hairpin inhibitor (antagomir; 0.5 nmol), administered intracerebroventricularly (ICV) immediately after injury, attenuated neuroinflammatory markers at both 1 day and 7 days post-injury and reduced impairments in spatial working memory. Delayed ICV infusion of the miR-155 antagomir (0.5 nmol/day), beginning 24 h post-injury and continuing for 6 days, attenuated neuroinflammatory markers at 7 days post-injury and improved motor, but not cognitive, function through 28 days. The latter treatment limited NADPH oxidase 2 expression changes in microglia/macrophages in the injured cortex and reduced cortical lesion volume. In summary, TBI causes a robust and persistent neuroinflammatory response that is associated with increased miR-155 expression in microglia/macrophages, and miR-155 inhibition reduces post-traumatic neuroinflammatory responses and improves neurological recovery. Thus, miR-155 may be a therapeutic target for TBI-related neuroinflammation.


KEYWORDS:

Traumatic brain injury; miR-155; microglial activation; neuroinflammation; neuroprotection

https://www.ncbi.nlm.nih.gov/pubmed/30225790

Pediatric Traumatic Brain Injury and Autism: Elucidating Shared Mechanisms

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5198096/

Halting Excessive Inflammation with New Way to Regulate Lymphocytes

“Mitochondria are important regulators of macrophage polarization. Here, we show that arginase-2 (Arg2) is a microRNA-155 (miR-155) and interleukin-10 (IL-10) regulated protein localized at the mitochondria in inflammatory macrophages, and is critical for IL-10-induced modulation of mitochondrial dynamics and oxidative respiration. Mechanistically, the catalytic activity and presence of Arg2 at the mitochondria is crucial for oxidative phosphorylation,” write the investigators.


“We further show that Arg2 mediates this process by increasing the activity of complex II (succinate dehydrogenase). Moreover, Arg2 is essential for IL-10-mediated downregulation of the inflammatory mediators succinate, hypoxia inducible factor 1α (HIF-1α), and IL-1β in vitro. Accordingly, HIF-1α and IL-1β are highly expressed in an LPS-induced in vivo model of acute inflammation using Arg2−/− mice.

https://www.genengnews.com/news/halting-excessive-inflammation-with-new-way-to-regulate-lymphocytes/
link to study report: https://www.nature.com/articles/s41467-021-21617-2?error=cookies_not_supported&code=b8131469-0694-4bf8-b1a9-7a20befe255b

Further reading in interested.

Inflammation and Neuro-Immune Dysregulations in Autism Spectrum Disorders

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6027314/

Gut microbial dysbiosis after traumatic brain injury modulates the immune response and impairs neurogenesis

https://pubmed.ncbi.nlm.nih.gov/33691793/

Visitor

I made the following comments on this thread in 2012.

"I maybe should have not called it TBI, but an ongoing process in Autism that has similar effects overall."

"Some of you may recognize the benefit of the drug mentioned in the following report for Autism Cytokine control as TBI quick or slow is involved in the biomed Autism pathology."


How much of those with Autism have this as causation or partially so? It is is clear we have dealt with this as a prominent if not central aspect as it is systemic it has to be central. Here are some new reports that basically say in short form what I have said in this thread. The first with Traumatic Brain Injuries, maybe mild to moderate in some with Autism, pointing to pointing to a more permeable GI tract{leaky gut}. The second with dealing with UTI's and the gut microbiome and bacteria from the gut involved with UTI's. My wife had the elements of TBI and UTI's until of a long term regimen of treatment. She almost never has migraines, I can't recall the last, and has not had a UTI hardly at all since 1997. She had numerous from the years prior to that time.

Traumatic Brain Injuries Affect More than the Brain

Key Points: Although traumatic brain injuries involve brain-related symptoms, other organs including the immune system, GI system, lungs, and heart may also be compromised. These injuries can result in changes throughout the body that can increase morbidity and even mortality.

"Traumatic brain injury (TBI) results from a head injury that damages the brain. Symptoms can include loss of consciousness, post-traumatic amnesia, memory loss, disorientation, and confusion. Symptoms occur immediately following the brain trauma and last for a while afterward. Psychiatric symptoms also may occur and include mood fluctuations, depression, anxiety, irritability, and personality changes. Other CNS (central nervous system) symptoms such as dizziness, headache, tinnitus, light sensitivity, and decreased sense of smell can also occur.

In an interesting paper recently published in Trends in Neurosciences, Alan Faden and colleagues discuss the consequences of TBI that involve organ systems other than the brain. They review evidence demonstrating that TBI can lead to significant changes in the immune, gastrointestinal (GI), pulmonary, and cardiovascular systems. These changes have been observed in humans and are being studied in animal models of TBI.

TBI is associated with a high rate of infections. It causes complex changes in the immune system, both systemically and in the brain. The result of these changes is the suppression of immune responses. These changes can persist over time, become chronic, and contribute to increased mortality.

Changes in the GI tract resulting in it being more permeable to substances and, therefore, less able to block the entry of toxins or bacteria into the circulation. The GI system also becomes more susceptible to infections as well as to relapse from ongoing, chronic GI disorders. Changes in the bacteria inhabiting the GI system (the gut microbiome) also occur. As discussed in an earlier post, the gut microbiome system communicates with the brain and influences brain function.

Lung damage is common following TBI. Individuals are susceptible to respiratory infections that can lead to pneumonia. Inflammatory chemicals are released into the lungs. Some of these changes result from TBI-related changes in the immune system.

Levels of certain chemicals in the blood indicate that cardiac damage may occur following TBI. Animal studies also suggest that TBI can lead to diminished cardiac function.

How do traumatic injuries to the brain lead to dysfunction in other organs? The authors review several possibilities. Following TBI, there are changes in the hypothalamic-pituitary-adrenal (HPA) system that lead to alterations in cortisol production. Such changes can interfere with the body’s ability to respond to stressors. TBI also can lead to a surge in activity of the sympathetic nervous system, which involves catecholamines such as norepinephrine. Such a surge can influence the function of various organs. As already mentioned, TBI results in changes in the immune system throughout the body, which can contribute to chronic neuroinflammation and neurodegeneration.

The take-home message is that TBI can result in changes throughout the body that can increase morbidity and even mortality. Increased understanding of these changes will hopefully lead to better treatments to prevent these deleterious consequences of TBI.

This review article by Faden and colleagues reminds all of us of the intimate relationships between brain function and the function of other organs in the body, and that successful treatment of brain diseases can have widespread positive impact on human physiology."

https://www.psychologytoday.com/us/blog/demystifying-psychiatry/202102/traumatic-brain-injuries-affect-more-the-brain

Study: Infectious gut bacteria may predict UTI risk

Urinary tract infections (UTIs) in kidney transplant patients may be caused by bacteria that originate in the digestive tract, according to investigators at Weill Cornell Medicine, Cornell University and NewYork-Presbyterian.

The study, published Dec. 4 in Nature Communications, was led by Dr. John Lee, assistant professor of medicine at Weill Cornell Medicine and a nephrologist at NewYork-Presbyterian/Weill Cornell Medical Center.

Dr. John Lee
Dr. John Lee
The research suggests that the gut microbiota – the unique bacterial population of the digestive system – may be capable of “seeding” the urinary tract with infectious organisms. The research also suggests that new treatments for UTIs may be found in strategies that alter the balance of gut bacteria toward so-called “good” organisms.

The study identifies gut bacterial profiles associated with the risk of developing UTIs. Previous research detected the association at the time of infection, but stopped short of identifying the microbial characteristics believed to precede the UTI.

Lee and his team, including first author Matthew Magruder, a student at Weill Cornell Medical College, investigated the link by collecting fecal and urine samples from 168 kidney transplant recipients over a three-month period, quantifying the specific amount and types of bacteria using state-of-the-art sequencing technology.

Kidney transplant recipients were chosen as study subjects because their anti-rejection medications diminish the activity of the body’s immune system to reduce the likelihood that it will be rejected as a “foreign” organ. The diminished immune response increases the risk for UTIs and other infections.

The researchers discovered that when a disease-causing bacterium, or pathogen, exceeded 1% in these patients’ feces, it significantly increased the chance that they would go on to develop urinary infections caused by the same pathogen.

E. coli accounted for the majority of the UTIs in their subjects.

“While we were excited to see this association between the gut microbiota and development of UTI, we wanted to explore this connection at a deeper level to see whether the origin of the UTI is likely from the gut,” said Lee, who is a named inventor on a patent application focused on detecting cell-free DNA in biological samples.

After further sequencing the bacterial DNA in each transplant patient’s fecal and urine specimens, the investigators found enough similarity to conclude that the gut bacteria were likely the source of infections.

The findings have implications that reach beyond this immunosuppressed population. UTI is one of the world’s most common infections, and accounts for more than 10 million doctor visits each year in the United States alone.

Altering the gut microbiota may someday offer a promising new source of adjunct UTI treatments, particularly for recurrent cases, Lee said. The leading gut-altering techniques today use probiotics (live bacteria introduced via food or supplements) and fecal microbiota transplant (the transfer of gut bacteria from one individual to another) to establish a healthier balance of microorganisms.

The team is now planning follow-up studies to further establish the link between gut microbiota and UTIs.

https://news.cornell.edu/stories/2020/02/study-infectious-gut-bacteria-may-predict-uti-risk


Visitor

Speaking magnesium and migraines I would mention Hyperemesis Gravidarum along with Autism as showing relation to its deficiency. This is mice, but I am guessing it translates a lot.

Dietary magnesium deficiency induces the expression of neuroinflammation-related genes in mouse brain

Abstract
"Aims: Dietary Mg2+ deficiency (MgD) impairs hippocampus-dependent memory in mice; however, the molecular mechanisms underlying MgD-induced memory impairments are unclear. Here, we investigated the molecular signatures in the hippocampus of MgD mice by analyzing the hippocampal transcriptome.

Methods: We performed RNA-sequencing of the hippocampal transcriptome of MgD mice. We used gene ontology analyses and quantitative real-time PCR to validate the RNA-sequencing results.

Results: mRNAs for neuroinflammation-related genes were upregulated in the hippocampus and cortex of MgD mice.

Conclusion: MgD induces neuroinflammation in the mouse brain, including the hippocampus and cortex. Our findings suggest that MgD-induced neuroinflammation triggers the impairments of hippocampus-dependent memory."

INTRODUCTION
"Magnesium (Mg2+) is an essential mineral for maintaining normal cellular functions by functioning as a cofactor in more than 300 enzymatic reactions.1-3 Mg2+ deficiency (MgD) disturbs the homeostasis of numerous biological processes, causing chronic and acute diseases such as metabolic syndrome,4 type 2 diabetes,5 and hypertension.6 Importantly, Mg2+ is required for the voltage‐dependent blockade of N‐methyl‐D‐aspartate‐type glutamate receptors, thereby controlling their opening,7-9 and also contributes to synaptic plasticity such as long‐term potentiation.

Consistently, Mg has been shown to play an important role in learning and memory. Increasing brain Mg2+ concentration improves learning ability, working memory, and short‐ and long‐term memory in rats,10 while MgD impairs fear memory formation.11, 12 We previously investigated the effects of MgD on brain function and found that MgD diet‐fed mice have deficits in hippocampus‐dependent memories such as contextual fear, spatial, and social recognition memories, while they have normal amygdala‐ and insular cortex‐dependent conditioned taste aversion memory, locomotor activity, and emotional behaviors.13 Conversely, MgD mice have normal spine density and morphology of hippocampal neurons. Thus, previous studies have shown that MgD impairs hippocampus‐dependent memory without affecting hippocampal neuron morphology.13 However, the molecular mechanisms underlying the impairments of hippocampus‐dependent memory by MgD remain unclear. In this study, we analyzed the hippocampal transcriptome in MgD mice to identify the molecular signatures of MgD‐induced deficits of hippocampus‐dependent memory performance in mice."

https://onlinelibrary.wiley.com/doi/10.1002/npr2.12167

Visitor

I few posts back when I posted info and the link to "Mimicking a chronic immune response changes the brain" I meant to add the link to the report below as it shows association between Il-17.

The Immunologic Role of IL-17 in Psoriasis and Psoriatic Arthritis Pathogenesis

Abstract
"Psoriasis is a chronic, immune-mediated, inflammatory disease that is pathogenically driven by proinflammatory cytokines. This article reviews the immunologic role of interleukin (IL)-17, the major effector cytokine in the pathogenesis of psoriatic disease, along with the rationale for targeting the IL-17 cytokine family (IL-17A, IL-17F, and IL-17 receptor A) in the treatment of psoriasis and psoriatic arthritis. Emerging evidence indicates that major sources of IL-17A in patients with psoriatic disease are mast cells, γδ T cells, αβ T cells, and innate lymphoid cells in lesional skin and synovial fluid. Within the skin and joints, IL-17A acts on cellular targets, including keratinocytes, neutrophils, endothelial cells, fibroblasts, osteoclasts, chondrocytes, and osteoblasts, to stimulate production of various antimicrobial peptides, chemokines, and proinflammatory and proliferative cytokines, which, in turn, promote tissue inflammation and bone remodeling. The critical importance of the IL-23/IL-17A axis to the pathogenesis of psoriatic disease has resulted in many new biologic treatments targeting these cytokines. These biologics dramatically improve skin and joint symptoms in patients with moderate-to-severe psoriasis and psoriatic arthritis."

https://pubmed.ncbi.nlm.nih.gov/30109481/

Visitor

My wife has Raynaud's, psoriasis, hypothyroidism, some early hair thinning., arthritis. She used to have a lot of migraines until I treated her.

Saw this when it came out. I have waited for them to verify these matters.

Pregnant mother's immunity tied to behavioral, emotional challenges for kids with autism

"The researchers measured the children's autism severity and assessed a set of behavioral and emotional problems such as aggression and anxiety. They also measured the children's development and cognitive functioning.

The study found that around 27% of the mothers had immune conditions during their pregnancy. Of these mothers, 64% reported a history of asthma, the most common immune condition. Other frequent conditions included Hashimoto's thyroiditis (hypothyroidism), Raynaud's disease (blood circulation disease), alopecia (hair loss), psoriasis (skin disease) and rheumatoid arthritis (joint tissue inflammation)."

https://www.sciencedaily.com/releases/2020/08/200814163307.htm

A refrain here.

Developing a Deeper Understanding of Autism: Connecting Knowledge through Literature Mining

"Other immune abnormalities possibly linked to autism are familial autoimmunity, maternal transfer of autoantibodies from the mother to child during pregnancy, production of antibodies against brain tissue in autistic patients, lower levels of normal immunoglobulins, and elevation of some cytokines [5]. Besides immune dysfunctions there are other epigenetic mechanisms potentially linked to autism such as increased level of oxidative stress, mitochondrial dysfunction, and excitotoxicity [2, 3]....

A powerful idea for investigating yet to be explored relationships between biomedical concepts was proposed by Swanson [7]. If there is a relationship between A and B reported in the literature on A, and a relationship between B and C in literature on C, then the concept B, might reveal interesting connections across previously disjoint contexts A and C. Swanson found many relationships, unknown at the time, for example, connecting Raynaud’s syndrome with fish oil, and migraine headaches with magnesium deficiency [7]."

https://www.hindawi.com/journals/aurt/2011/307152/

benedetta

Wow Grace; I had not thought of that.

It could well be mercury fillings.

I hurt a tooth falling down hard on my butt some years back. I think the fall killed that tooth. It has been breaking off pieces ever since. So, I did get a big filling in two years ago, and that filling came out back this past September. The night it came out, I must have really grinded my teeth in my sleep really bad. I woke up the next morning with the most painful muscles in my jaw that morning and was spitting out pieces of my porcelain crown that chipped off. Soon after the tips of my upper, good ear that had no problems begin to form psoriasis.

You might be right!

Grace Green

I often had eczema behind the ears in my teen years. Did this follow the fitting of new mercury fillings? Possibly, but too long ago to make the connection now.
After having several mercury fillings removed by an incompetent dentist who washed the debris down my throat, I had eczema progressively down my body until it disappeared off the end of my hands and feet!
I had numbness of the mouth for years when eating certain foods - completely cured after removal of last mercury fillings.
So many more things. I decided a few days ago that all chronic illnesses are due to poisoning. Then I watched the witness statement of Dr. Robert Young and heard him say the same thing!

benedetta

We they have a lot of things for psoriasis, Ointments, steroids, sunshine, light therapy in the winter.

Some time or another if you have an orange you kept too long in the refrig or out in our garage in a bag, and it gets a lot of blue mold on it, pour some apple cider over it and watch like magic that mold disappear. Better than peroxide, or alcohol or bleach.

Apple cider on and in my ears is working pretty good.

I have been putting it on every night, it is helping.
I think the steroid mask the symptoms. Yes, I got something kind of creme that cost 100 dollars that clears it up for months at a time. Well it did for a while and then that did not work eventually.
Hydrogen peroxide seems to work, but using it night after night can hurt your skin. Apple cider does not.

I think it is Canadensis. Why my immune system is not taking better care of it; I don't know. Better now that I gave up gluten. Better that I do low carb.

I do know that when I upped my thyroid medicine to a higher level ( cause I had some extra pills and it was against the doctor's orders, it went away too) What they consider to low to high on thyroid is a really wide range by the way.

I see that a lot of people are taking apple cider - drinking it with water for yeast infections.

Is it an immune problem of not fighting off fungus, or a endocrine problem of not enough energy to fight off fungus? Maybe just an allergic reaction to a common body fungus?

It cannot be that simple as being a fungus problem though. I mean; we have big phrama, and psoriasis research societies; and if it was a fungus they would have told us.

So much lying and trickery now a days, we are all dazed and confused.

But it can go into arthritis.

Visitor

Benedetta ,
The report I posted that you refer to does point to T cell;s issuing IL-17 from the gut. I have come across, or attempted to determine, why psoriasis may occur in a particular area. My wife has a small amount on her scalp that you haver to look for because her hair covers it. Se also has, and I have mentioned in this thread, Geographic tongue which is thought to be a form of psoriasis. With her food reactivity the food contact with her oral area seems intuitive. Food effects beyond her mouth though.

The book you cite sounds very interesting, be sure to share any valuable things you find. The mouth metal and microbe connection also seems intuitive, also in the gut.

Though beyond well psoriasis IL-17 and mir-155 are inflammatory players though both can have inverse effects under certain conditions. I mentioned psoriasis in previous posts in this thread. Here some of the links I have previously posted.

MiR-155 promotes cell proliferation and inhibits apoptosis by PTEN signaling pathway in the psoriasis.

https://www.ncbi.nlm.nih.gov/pubmed/28402921

Immune Mediated Conditions in Autism Spectrum Disorders

"Psoriasis occurred more than twice as often in cases than in controls "

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4414798/

The codependence of angiogenesis and chronic inflammation.

"Angiogenesis is the growth of new blood vessels from existing ones. It is an important aspect of new tissue development, growth, and tissue repair. It is also a component of many diseases including cancer, blindness, and chronic inflammation such as rheumatoid arthritis (RA) and psoriasis. There is considerable evidence to suggest that angiogenesis and chronic inflammation are codependent; recent studies have begun to reveal the nature of this link, which involves both augmentation of cellular infiltration and proliferation and overlapping roles of regulatory growth factors and cytokines."

http://www.fasebj.org/content/11/6/457

Copper Toxicity

"It causes joint pain and arthritis, digestive problems, irritable bowel, overgrowth of candida albicans, breathing difficulties including asthma, and chronic skin problems which can range from acne to psoriasis."

http://www.tvernonlac.com/copper-toxicity.html

Mycoplasma

A wide spectrum of rheumatic conditions are linked to MP as a co-factor,

"Alzheimer’s disease, Amyotrophic Lateral Sclerosis (ALS), Arthritis Asthma, Arterial sclerosis, Atypical pneumonia, Bronchitis, Cardiovascular diseases, CFS/CFIDS, Crohn’s diseases, COPD, fibromyalgia syndrome (FMS), Interstitial cystitis, Leukemia, Lymphoma, Lupus (SLE), Multiple sclerosis (MS), Pelvic inflammatory disease (PID), Psoriasis, Scleroderma, Solid (&lung) cancers, Sjogren’s syndrome,."

http://www.ra-infection-connection.com/Mpneumoniae.htm

REG3A molecule may lead to new treatments for psoriasis, wound-healing

"An international team of scientists led by principal investigator Richard L. Gallo, MD, PhD, professor of medicine and chief of UC San Diego's Division of Dermatology, analyzed skin biopsies of patients with and without psoriasis, as well as the skin of mice with psoriasis and with wounds on their backs. They discovered that a molecule called regenerating islet-derived protein 3-alpha (REG3A) is highly expressed in skin cells during psoriasis and wound-healing, but not under normal skin conditions.

In tests on mice, researchers found that inhibiting REG3A slowed wound-healing but cleared up psoriasis, which is commonly characterized by patches of inflammation and white, scaly skin.

The scientists also noted that REG3A acts in concert with interleukin-17 (IL-17), an immune system protein involved in the signaling cascade which prompts skin cells to multiply in excess numbers. "IL-17 binds to receptors on skin cells and causes REG3A to be expressed,"

{my note: REG3A is a gut factor in Autism and maybe elsewhere}

http://www.news-medical.net/news/20120622/REG3A-molecule-may-lead-to-new-treatments-for-psoriasis-wound-healing.aspx

benedetta

I see that Psoriasis foods to avoid is like everything.

How come I only got it on my ears?

T cells is going to the gut to make this interleukin 17. Is that a clue happening in the gut before spreading to all the body.

Nick, I have been reading Maready "Crooked"
It kind of circles back around to metals and microbes.

All of the mercury and silver fillings out of my teeth, including lifting the caps as well, well sometimes money is an issue

Visitor

I have failed the Lord in so many ways. He has never failed me once.

Jesus is Lord. Blessed Mary, mother of our Lord.

https://www.youtube.com/watch?v=Yiw6EfrHDhg

Our God never lets go.

https://www.youtube.com/watch?v=C0nM3_lhBWo

May God bless each of the autism family.

Visitor


Mimicking a chronic immune response changes the brain

"Researchers led by Professor Yosuke Takei and Assistant Professor Tetsuya Sasaki at the University of Tsukuba in Japan have been studying an important cytokine called interleukin (IL)-17A. Their recent study shows that chronic increases in the levels of IL-17A circulating in mouse blood can reduce the microglia activity in one part of the brain's hippocampus. This might explain why it's related to several neurological diseases.

The researchers focused on IL-17A because it is known to be involved in neurological autoimmune disorders as well as disorders of the mind. "In addition to being linked to multiple sclerosis," explains Sasaki, "recent reports show that IL-17A is also a factor in Alzheimer's disease, schizophrenia, and autism spectrum disorder." To study how chronically high levels of IL-17A can affect the brain, the team used their knowledge of how IL-17A is made naturally in the body.

The researchers focused on immune cells called helper T-cells. Helper T-cells come in many varieties, each one making its own cytokine, and each one created from a generic helper T-cell. "Our strategy," says Sasaki, "was to induce more generic helper T-cells to become the kind that produce IL-17A." With more of these helper T-cells, called Th17, the mutant mice did indeed produce more IL-17A in the gut, which spread throughout the body in the blood.

IL-17A is known to interact with two kinds of glial cells in the nervous system, astrocytes and microglia. The researchers found that chronically high IL-17A led to reduced activity and density of microglia in one region of the hippocampus, a part of the brain that is needed for learning and forming memories. In contrast, astrocytes in the brain did not differ between the mutant and control mice. Thus, there was reason to believe that chronic IL-17A inflammation would affect cognition, specifically memory. Surprisingly, spatial memory seemed to be just as good in the mutant mice as in the control mice.

"These mutant mice can be used in future studies as a model for chronic IL-17A-related inflammation," says Takei. "Further neuronal and behavioral testing will help us begin to understand IL-17A's role in a range of debilitating neurological disorders."

https://www.sciencedaily.com/releases/2021/02/210217151057.htm

Inflammation and Psoriasis in the two links below.

https://www.healthline.com/health/psoriasis/facts-about-inflammation#systemic-inflammation

https://www.healthline.com/health/psoriasis/food-triggers-for-psoriasis

Visitor

"Scary times; and always has been frustrating time to try to warn." More truth.
"Is anybody listening?

Benedetta

I am so sorry Nick. Scary times; and always has been frustrating time to try to warn.

Now we know how Cassandra was so cursed.

Visitor

For the record my family to this day had dismissed and disparaged everything I told them. They can take this up with God. I was totally abandoned by them. I made the overtures to create a bond and it has been mainly artificial from my end though I had hoped for a real relationship. It I am spitting into the wind, so be it. I have tried to be honest and real. Dirt in my face is all I have received.

Visitor

A diamond necklace played the pawn
Hand in hand some drummed along, oh
To a handsome man and baton
A blind class aristocracy
Back through the opera glass you see
The pit and the pendulum drawn
Columinated ruins domino

Canvass the town and brush the backdrop
Are you sleeping?

Hung velvet overtaken me
Dim chandelier awaken me
To a song dissolved in the dawn
The music hall a costly bow
The music all is lost for now
To a muted trumpeter swan
Columinated ruins domino

Canvass the town and brush the backdrop
Are you sleeping, Brother John?

Dove nested towers the hour was
Strike the street quicksilver moon
Carriage across the fog
Two-Step to lamp lights cellar tune
The laughs come hard in Auld Lang Syne

The glass was raised, the fired rose
The fullness of the wine, the dim last toasting
While at port adieu or die

A choke of grief heart hardened I
Beyond belief a broken man too tough to cry

Surf's up
Aboard a tidal wave
Come about hard and join
The young and often spring you gave
I heard the word
Wonderful thing
A children's song

Child, child, child, child, child
A child is the father of the man
Child, child, child, child, child
A child is the father of the man
A children's song
Have you listened as they played
Their song is love
And the children know the way
That's why the child is the father to the man
Child, child, child, child, child
Child, child, child, child, child
Na na na na na na na na
Child, child, child, child, child
That's why the child is the father to the man
Child, child, child, child, child

Visitor

For me is is intensely sad ...not say. God speed Teresa.

Visitor

For me is is intensely say because Teresa has such a tremendous grasp of the issues. We could have been fiends or at least acquaintances. I hold no animus. Pain and desperation restrain even the most loving. I burn no bridges and cherish grace.

Visitor

I posted the studio elemental version of Dreams in early March of this year. I would almost never simply post as version of a song but this is a nearly complete capture of all the energy of the song. It is jazz in flight. Bravo! I wonder how diverse is her talent.

https://www.youtube.com/watch?v=V1LhC1zGouc

Visitor

I am on a journey too, but know why. I also now mainly understand what directed my sweetheart. It does not change my illusions.

Kentucky is where I began as did my other and this journey. Running to or from. She was nothing like those who have a context. Neurodiversity is awful in concept for my wife and those like her lost in biologicals malice and damage.

I have shared some of my journey in context. My search of looking for something.

Kentucky rain - Barb Jungr

https://www.youtube.com/watch?v=SJxVQVoG_5I

Visitor

So it is fight, flight, or freeze. To a world or away, from a world or away, or frozen in thought or frozen in motion or else in a journey. Flap your hands or rock to escape the unknown. Uncertainty or pain causes these reactions. The glimpses of uninformed effort of knowing. The trip is for the addicted or the lost. The context is moving and shifts as the focus changes. One needs to, or is arrested by change, but has no notion of why. This probably makes no sense to anyone. I believe it to be valid for the effected.

I have long been around cattle. I concur.
The heterogeneity means this is generally the case.

Genetic link between cattle temperament and autism in humans

https://www.sciencedaily.com/releases/2020/08/200827102148.htm

https://www.youtube.com/watch?v=qeMFqkcPYcg&list=RDqeMFqkcPYcg&index=2

Visitor

Gabapentin effective in Hyperemesis Gravidarum in early pregnancy, finds study

https://medicaldialogues.in/obstetrics-gynaecology/news/gabapentin-effective-in-hyperemesis-gravidarum-in-early-pregnancy-finds-study-71163

The following is not new information but relates to the 1st report. It is not a coincidence that the medication has been useful in autism and seizures and now found to be helpful in many cases of hyperemesis-gravidarum. Inthis thread you can find my connecting the conditions.

Study finds altered brain chemistry in people with autism
Neuroscientists link autism to reduced activity of key neurotransmitter in human brain.

https://news.mit.edu/2015/altered-brain-chemistry-autism-1217

Benedetta

Visitor Nick;
I am very sorry for the loss of your mother.

Inflammation Highway in the end looks like it is going to be the way our bodies handles aluminum don't it?

Does it seem that way to you?

Visitor

My mother, the smartest and the best. Went home 2007 , I love you mother.

Visitor

My last post was a bit facetious. the reasons maybe only views accepted by me, but some one followed my presentations of understanding and ignored me. when proclaiming their elements. A virtuoso for me is Pentatonix's performance. I have found I know how to burn bridges. This speaks to me more than "Disturbed's" version. I would have given on God had I not seen worship in my fellow creatures as I do in the members of Pentatonix.

"Yet he has not left himself without testimony: He has shown kindness by giving you rain from heaven and crops in their seasons; he provides you with plenty of food and fills your hearts with joy."

https://www.youtube.com/watch?v=gdVjVtpr55M

One that keeps me holding on.. I miss my mother.

https://www.youtube.com/watch?v=8THtJ5T4u_E

Visitor

Teresa please reconsider your decision. Your contributions ae immerses. For the love of God please reconsider and continue writing for AoA!

Visitor

I do very much like "Disturbed's" version.

I have been in a mental blender for may years and don't find my faith has me on the heavenly side of the sea above creation. I am holding on, but can't really explain the faith I still have as the science challenges severely. Some surely is actually doing the holding.
I come back to that simple blessed place when I go alone in my thoughts to long

Sea of glass brings many visions and states of mind. This song reminds me of home. {only the lambs will appreciate this adoration}

https://www.youtube.com/watch?v=opscb36ltco

Benedetta

Nick;

PENTATONIX: is great in everything that they do. But Disturbed did "Sound of Silence" best:

I have seen people, my best friends that have bound and prayed to the neon God they had made, in the last few years that hurts my heart.


https://www.bing.com/search?q=sound+of+silence+by+disturbed&cvid=7a2ba59e33384553a948726d7aa68c58&pglt=43&FORM=ANNTA1&PC=U531

Benedetta

And speaking of beast, the seven headed beast produced another beast that came out of the earth (like all those metals that medicine and other industries have used on the human body, that is harming people --- like aluminum -- that is causing "Inflammation Highway")

Benedetta

Visitor;
You are one of the Glass Sea, mingled with fire; that stood up against the dark sea that produced the seven headed beast (one head with a mortal wound and yet lived) - that has to represent the medical institutions, for sure. The Glass sea will defeat the beast.

Be of good spirit Visitor, for God delights in you. He gave visions to John that wrote Revelations about you and those like you that loves the truth, and hates lies It is people like you that questions everything and fooled by little. For you are one of the Glass sea mixed with fire!

Visitor

Music has been one of my best teachers. One in four male to female autistic.

https://www.youtube.com/watch?v=gdVjVtpr55M

Visitor

Business Insider was quoted by Cia. in posits on AoA. I am going to give her the benefit of the doubt as to why she vouched for their information.. They have proven to be a lying source of information.

Anti-maskers are the new anti-vaxxers

https://www.businessinsider.com/anti-maskers-are-new-anti-vaxxers-threatening-public-health-coronavirus-2020-7

It is a miniscule amount of people that connect the two notions, but they are aware of who knows the score. They seek to squash any realization of truth. Cia quoted this vile group Business Insider. . Business Insider be cursed. Wake up Cia.

Anti-maskers are the new anti-vaxxers. These peolple arte the defintiojn of evil,

https://www.businessinsider.com/anti-maskers-are-new-anti-vaxxers-threatening-public-health-coronavirus-2020-7
They are only aware of this because of their control agenda. They are evil.

Visitor

I am a very simple man whom God has loved. Please forgive my ignorance and swearing. Love to you Kim and Benedetta. Susan Welch is such a kind spirit.

https://www.youtube.com/watch?v=Ix6Yr9FYFeA

susan welch

Visitor, thanks for the video links. They were both appropriate and enjoyable.

Sorry you appear to be feeling so 'down'. You are right about the powerful, but we have the truth.

Hang in there.

Visitor

from one small voice that has linked to the ":Atlantic", let me me state without qualification the Atlantic is a rag publication that deserves no respect and should be seen as a scumbag piece of journalism. I am ashamed to have ever linked one article of their putrid verbosity.

Visitor

People without autism.

https://www.youtube.com/watch?v=gdVjVtpr55M

Visitor

No money , No status, just truth. It will matter little.

https://www.youtube.com/watch?v=Ilybv2ZKOto

Visitor

II am only one, but I have innocently investigated it all. There is no meaning. Chaos rules. You can find effect continuously. When you seek to the end it all means shit. There is no meaning and I wished there was. The strongest rule. The ,most selfish rule.

Visitor

The ACE2/Angiotensin, Rage TLR's and other aspects including HMGB1. This makes you think about latent viral expression in some with Autism and aspects o vascular effects in vascular constriction and dementia and also in Kawasaki's. Hypoxia diminishes antiviral immune responses. It seems to be a microcosm of how a vaccine may mediate a damaging inflammatory state in those predisposed and Covid may be doing this some with particular states of ACE2, maybe down regulated ACE2. II on't attempt to re-state all that is spoken about in this thread regarding these matters, but it is there.


HMGB1: A Possible Crucial Therapeutic Target for COVID-19?

High mobility group box-1 (HMGB1) is a chromatin-linked, nonhistomic, small protein with cytokine activity that has nuclear, cytosolic, and extracellular actions. It binds to chromosomal DNA but also to Toll-like receptor 3 (TLR3), TLR4, and the receptor for advanced glycation end products (RAGE) that activates nuclear factor (NF)-κB (Fig. 1a), which mediate the upregulation of leukocyte adhesion molecules as well as the production of proinflammatory cytokines and angiogenic factors that promote inflammation. HMGB1 was initially known as alarmin and is a well-recognized damage-associated molecular pattern (DAMP) protein.

Fig. 1.
a HMGB1 shows both intracellular and extracellular effects. By binding to TLR2, TLR4, and RAGE, it activates NF-κB which leads to the production of proinflammatory cytokines that have local and systemic effects. b HMGB1 is increased both locally and in the circulation in conditions like obesity, cystic fibrosis, and polycystic ovary, and, whenever insulin resistance occurs, it is produced by adipose tissue and the immune system. CFTR malfunction causes an increase in HMGB1, besides other changes such as inflammation and increased autophagy.

https://www.karger.com/Article/FullText/508291

In our case my wife had re-occurring bronchial infections which were often viral. These declined progressively with many treatments along with eventually Olmesartan, which does numerous things in cell and immune system.

Doctor offers coronavirus protection advice

"Antihypertensives, a class called ARBs (angiotensin receptor blockers), which are normally used to reduce blood pressure and protect kidney function. ARBs increase ACE-2 activity and have been proposed as a treatment to promote healing of the lung in corona virus pneumonia. A recent study from China demonstrated through indirect measures that ACE-2 function declines with viral load and severity of COVID-19 pneumonia. For people already taking blood pressure medication, the inclusion of an ARB may improve the response to COVID-19 infection. The Federal government is sponsoring a trial of the ARB losartan for amelioration of COVID-19. However, the ARB that most enhances ACE-2 levels in humans is olmesartan (Benicar). Of all the ARBs, olmesartan has the greatest impact on immune function. "

https://www.fox5ny.com/news/doctor-offers-coronavirus-protection-advice

Visitor

On the topic of measles and atopic dermatitis there are conflicting reports, but this one suggests a timing that does associate with the start of measles virus vaccines. Again, many with autism don't show AD, but the terrain of their skin still may reflect aberrant function.

Atopic dermatitis is increased following vaccination for measles, mumps and rubella or measles infection.
"Abstract
The prevalence of atopic dermatitis increased markedly in the period 1960s to the 1990s. Earlier findings indicate that infections acquired in early life enhance or suppress the expression of atopic disease as a result of a change in immune reactivity. Our objectives were to examine the association between measles, mumps and rubella vaccination, measles infection and the risk of atopic dermatitis. A random sample of 9,744 children were followed up from birth to 3-15 years. Their parents responded to a questionnaire including highly structured questions on atopic dermatitis, measles, mumps and rubella vaccination and measles infection. Information on parental educational level was obtained from Statistics Denmark. The cumulative incidence of atopic dermatitis at age 14 was 19.7%. The confounder adjusted incidence ratio of atopic dermatitis among measles, mumps and rubella vaccinated children versus children not subjected to measles, mumps and rubella vaccination and measles infection was 1.86 (95% CI 1.25-2.79); the incidence ratio for measles-infected children was similar. The incidence of atopic dermatitis increased after measles, mumps and rubella vaccination and measles infection, which is surprising in view of the hygiene hypothesis. We suggest further study of the possible short-term and long-term effects of virus and bacteria on the immune responses and expression of atopic disease."

https://www.ncbi.nlm.nih.gov/pubmed/14690341

COVID-19 may be tied to rare syndrome in children, UK doctors warn

Also, I know AoA is aware of this news, but given the detoxification and inflammatory effecting the systems of many with autism and the viral associations it is interesting to read the elements that they describe the condition with. {Toxic shock- Kawasaki's...fits with factors of this thread}

"The alert noted that these cases showed symptoms similar to those found in two rare conditions: toxic shock syndrome and Kawasaki disease. Toxic shock syndrome is a life-threatening condition that's caused by toxins produced by certain types of bacteria; Kawasaki disease is a childhood illness that causes inflammation in blood vessel walls, and in serious cases can cause heart damage."

https://www.livescience.com/covid-19-kids-rare-inflammatory-syndrome.html

Visitor

Not too far back in this thread you will find information on ccr4/ccl17 and findings relating it to autism and showing effects in the brain. I am still working on this and how this could be related to atopic dermatitis which is much higher in those with autism. CCl17 is also related to "Dress Syndrome" and shows hypersensitivity. This possibly could be a trigger after MMR though I have not begun looking as to how this keratinocyte/skin reaction might communicate or effect the same factors in the brain. In the hypersensitive this could conceivably be a trigger and though many more may get atopic dermatitis without having autism there may be a correlation to study as to the age or degree one has the Atopic condition. There are many questions that could prove to abolish this theory, and MMR might only effect a subset in sparking regression or developmental effects or ADHD with or without Atopic Dermatitis. The first masles vaccine did not come till 1963 I have read, but certain flu vaccine among others began in wWorld Wae 2.
The first paragraph might show a timing relationship with Autism.

TARC and CTACK;
Two Pivotal Chemokines in
Atopic Dermatitis
Christian Vestergaard
"The incidence of atopic dermatitis has been rising in the wes
tern countries since World War II (2), a fact which has been
ascribed to better living conditions and the western lifestyle
(3, 4) although it seems to have levelled out during the 90’s
(5). Atopic dermatitis affects between 15% and 20% of all
Danish children (6, 7) however; the number varies with a li
fetime prevalence between 13% and 37% (8). In a Norwegian
study 13% of the population under the age of 20 was affected
by atopic dermatitis, whereas only 2% of the population over
the age of 20 was affected (9). In 60% of the cases the onset of the disease is in the first year of life
and in 85% of the cases before the age 5 years (10)."

"Infections also play a role in the pathogenesis of atopic
dermatitis. In a recent study it was shown that children who
were subjected to the measles, mumbs and rubella vaccination
or measles infectionhad a significantly higher risk of developing atopi dermatitis
ping atopic dermatitis than children who were not vaccinated or had had measles."

https://www.medicaljournals.se/forum/articles/12/Supplement%2014/Suppl14.pdf

Visitor

I t does not matter what i post anymore than the one reading this can be understood by another. I have understood another. That is of note..

Now here I go again, I see the crystal visions
I keep my visions to myself, it's only me
Who wants to wrap around your dreams and,
Have you any dreams you'd like to sell?
Dreams of loneliness,
Like a heartbeat, drives you mad
In the stillness of remembering, what you had,
And what you lost and what you had and what you lost

https://www.youtube.com/watch?v=6ZShvtyeUpk

I keep my visions to myself. I have shared the science the reality would never be believed thoug I have alluded to it.

Visitor

"You have done so very much on all of this, it is staggering piece of work"
After over a hundred thousand studies I am a puddle.
Nihilism. or Faith. I have not fared well in the milieu. over the last 23 years. I have been focused like a laser and am totally taxed in my ability at every turn. The vacillation between the two is a bit unhealthy.{understatement}. I want a n end point, but it just keeps unfolding. What is a post without a song?

https://www.youtube.com/watch?v=Vol9dZ-t93s

Visitor

Isaiah 9:6-7 ESV
For to us a child is born, to us a son is given; and the government shall be upon his shoulder, and his name shall be called Wonderful Counselor, Mighty God, Everlasting Father, Prince of Peace. Of the increase of his government and of peace there will be no end, on the throne of David and over his kingdom, to establish it and to uphold it with justice and with righteousness from this time forth and forevermore. The zeal of the Lord of hosts will do this.

So at his second coming he will be in control of government. No more humans just out for themselves, but instead really working for the good of us all. That is the future of mankind.

It is True - So Be It

Benedetta

Nick;
Your last study you shared toward the end was about intestinal mucosal . After my son's third DPT reaction about a week later -- he filled his diaper with mucous, so I know what that looks like and now I know maybe why. Thanks.

Advent last Sunday and I was looking for a verse to share with my family about "Hope" That is the theme of the first Sunday of December.

Isaiah 9:6-7 ESV
For to us a child is born, to us a son is given; and the government shall be upon his shoulder, and his name shall be called Wonderful Counselor, Mighty God, Everlasting Father, Prince of Peace. Of the increase of his government and of peace there will be no end, on the throne of David and over his kingdom, to establish it and to uphold it with justice and with righteousness from this time forth and forevermore. The zeal of the Lord of hosts will do this.

So at his second coming he will be in control of government. No more humans just out for themselves, but instead really working for the good of us all. That is the future of mankind.

Visitor

Crucial role of NLRP3 inflammasome in a murine model of Kawasaki disease.

Abstract

Kawasaki disease (KD) is a systemic febrile syndrome during childhood that is characterized by coronary arteritis. The etiopathogenesis of KD remains to be elucidated. NLRP3 inflammasome is a large multiprotein complex that plays a key role in IL-1β-driven sterile inflammatory diseases. In the present study, we investigated the role of NLRP3 inflammasome in a murine model of KD induced by Candida albicans water-soluble fraction (CAWS) and found that NLRP3 inflammasome is required for the development of CAWS-induced vasculitis. CAWS administration induced IL-1β production, caspase-1 activation, leukocyte infiltration, and fibrotic changes in the aortic root and coronary arteries, which were significantly inhibited by a deficiency of IL-1β, NLRP3, and ASC. In vitro experiments showed that among cardiac resident cells, macrophages, but not endothelial cells or fibroblasts, expressed Dectin-2, but did not produce IL-1β in response to CAWS. In contrast, CAWS induced caspase-1 activation and IL-1β production in bone marrow-derived dendritic cells (BMDCs), which were inhibited by a specific caspase-1 inhibitor and a deficiency of NLRP3, ASC, and caspase-1. CAWS induced NLRP3 and pro-IL-1β expression through a Dectin-2/Syk/JNK/NF-κB pathway, and caspase-1 activation and cleavage of pro-IL-1β through Dectin-2/Syk/JNK-mediated mitochondrial ROS generation, indicating that CAWS induces the priming and activation of NLRP3 inflammasome in BMDCs. These findings provide new insights into the pathogenesis of KD vasculitis, and suggest that NLRP3 inflammasome may be a potential therapeutic target for KD.

https://www.ncbi.nlm.nih.gov/pubmed/31836541

miR-155 Regulates claudin1 Expression in Humans With Intestinal Mucosa Dysfunction After Brain Injury.

Abstract

Patients with craniocerebral trauma often have intestinal mucosal dysfunction, and the claudin1 protein plays an important role in intestinal mucosal function. Our previous work has shown that the expression of microRNA-155 (miR-155) in the peripheral blood of patients with craniocerebral trauma is decreased. Animal experiments also suggest that the expression of miR-155 is increased in the intestinal mucosa of mice with brain injury and the expression of claudin1 is decreased. We recruited 56 samples (35 patients with traumatic brain injury [TBI] and 21 patients without history of head trauma) to detect the expression of miR-155 on claudin1 regulation by quantitative polymerase chain reaction, reverse transcriptase polymerase chain reaction, and so on. We also used the receiver operating characteristic curve (ROC) to further evaluate the diagnostic value of the 2 biomarkers. From the results, we found that the expression level of miR-155 and claudin1 in the case group was lower than that in the control group. Human miR-155 (Hsa-miR-155) may positively regulate intestinal mucosal function by inhibiting the expression of claudin1, leading to intestinal mucosal barrier dysfunction. Combining the ROC curve data, the results further prove that miR-155 and claudin1 might be the new clinical diagnostic markers and treatment targets for the intestinal mucosal barrier dysfunction after TBI.

https://www.ncbi.nlm.nih.gov/pubmed/31810510

Trying to be cute with the bless you and ___ a couple of post back relating to some want to abuse you from "Sweet Dreams", but I was not in a right frame of mind to make any intelligent remarks at that time. Sorry.

Visitor

Jenny said on June 27, 2015. "I appreciate it, too, Visitor. I'm just not as fast at absorbing and processing it all as you are. " I don't know anyone else who has either and I wish this was not the case. My family ostracized me in these matters early on so I have to eat it all and try to interact with them as though as I am a total ignoramus.

I realize I have been way way ahead of the curve. Do I need to apologize for this? I wish my family had a clue. I don't like conde3scending to others, but in this case I have no choice.


Visitor

Culture is in Control
Creative
https://www.youtube.com/watch?v=Pb9tl8wq3xk

Visitor

If there is a home I want to go there now. I cannot get through to anyone. Let it be over.

Visitor

Sweet Dreams behind a cigarette.

https://www.youtube.com/watch?v=hmLBSCiEoas

And I'm talking to myself at night
Because I can't forget
Back and forth through my mind
Behind a cigarette
And the message coming from my eyes
Says leave it alone

Visitor

The Police video a few posts began with a cigarette. I posted Sweet Dreams right after that. he rei9s on with the lyrics. I am hoping some have some phycological training to understand these posts. I poste sweet dramas right after. The lyric for White Stripe + Sweet dreams.

https://www.youtube.com/watch?v=hmLBSCiEoas

and

https://www.youtube.com/watch?v=0J2QdDbelmY

Visitor

See the cigarette in every in Every Breath You Take posted earlier.

https://www.youtube.com/watch?v=hmLBSCiEoas

Visitor

https://www.youtube.com/watch?v=smX6xCPDbrE

Tring to receive.

Visitor

Benedetta, God is with us. There is only one thing I remain confident in. It is God is good all of the time. I trust His goodness and love. God has taught so much, but I am incredibly slow in understanding , and His patience is endless. Bless the Lord for Jesus, He is our blessed shepherd. Who could give Jesus proper glory? I have tried to love my wife as Christ loved the church. I will have to wait till I cross over to understand. At this point I find great beauty in the liberal mind and equally so in the conservative mind. I lean a bit to the right. That is how God made me. Life would not be worth living without the liberal mind and the same is true for life without the conservative love and life promoting freedom.
At the fringes the mind needs the conservative to preserve being. The liberal is needed to prevent narcissism and the divorce from self.. I find while liberalism teaches the most in this changing world it is the eternal unchanging truth of God that we will glory in through eternity. On the cross our confusion and answer lie. The cross is everything and glory. The Cross is God's one word response to or being. W are all related. Fuck you and bless you. I mean it.

https://www.youtube.com/watch?v=smX6xCPDbrE

https://www.youtube.com/watch?v=3G_UML28Dwg&index=97&list=PLFF3F248AC60CF19E

Benedetta

Nick, sorry. Please ignore the repeat. Too late at night and I did some thing of a copy, paste and mess up!
You have done so very much on all of this, it is staggering piece of work.
The article is a great article too.

Barbara Fisher in her speech on the V.I.E. also continues to beat the drum that it is inflammation, and it is serious stuff.

Benedetta

Thank you Visitor:
I am caring for my 90 and 95 year old parents as well as my family. So I am tired most of the time, and short on time all the time.
It scares me about the Kawasaki's disease. What will it lead to on down the line?

My daughter is working toward a stroke or heart attack. She smokes, on birth control pills (because her hormones do not function correctly since she was 14 years old) She will soon be 39. She was a thin little thing all through college and then gained lots of weight in only one year - 100 pounds or more I think and even developed a buffalo hump. It has to do again with hormones, and the immune system and inflammation.. She has exercised it off, she does walk every day for miles.

I do the gluten free, very little milk except in cooking, I for myself do not eat gluten cause I found for my own self that it hurts my legs and feet. I do not eat peanuts cause it breaks me out, and that is also inflammation. .
Do you know what it takes to just get gluten out of your kitchen, and still cook something?
And getting peanut butter out of my kitchen makes me a food Nazis and apparently is harder than taking bread away from them. They all want their carbs.

We all try to fast. We are suppose to stop eating at six and wait as long as possible in the morning. Fasting I think helps reduce inflammation? Perhaps our bodies have to have so much carbohydrates to make glucose to use as energy to make immune cells? I

One of your links turned up to mention alcoholics -- I never have drank alcohol; I have seen some of my cousins actually die, and other cousins lucky enough to go prison instead of dying because of their addition to alcohol, or drugs,or really both. I don't know if my family history has a lot of alcoholics any more that the rest of the population? But this addiction stuff I think is all associated with pain from inflammation.

My husband was given opioids, lots of them; all nice ahd legal. That caused a crisis in the family as well as coming close to killing him.

Inflammation hurts. It hurts your feet, and legs, everywhere. It can cause people to seek out pain killers that gets us to addition.

A psychologist that treated my daughter six years ago, yeah, she was self medicating with some things that she did not need to be messing with. It was a long episode of events of a lot of health problems following a DPT vaccine (stupid, stupid, stupid), and she got caught right out off the bat when she did that. Anyway this psychologist treats all the unfortunate addicted doctors and nurses, and apparently there are a lot of them ; but he responded to my daughter's complaint that she just hurts all over; that yeah, he too is a recovering addict, and he too hurts all over, but being sober and hurting is better than not. He suggested that she walk and exercise a lot. Which she does.

There are no grand children and there won't be.
There are no significant others for my children and I wept about that this past spring. I am sort of okay with that now. I fear they will be alone in their old age, but then perhaps all of us will be even if we have children.

Inflammation; Aspirin is suppose to help .

A couple of weeks ago my husband is all excited and brings home hemp oil. They are selling it?
I finally looked it up. I know every body says it helps on seizures, but I am not messing with hemp. Well I see that it is not the mind altering stuff, nothing like that at all. It does not contain the THC. It is legal. It fights inflammation. Well, I am so slow on things. So I am just slow Visitor.

Probably Canadensis albicans is in my brain. I think it is in my ear?
We are a mess I think.

There will be no apology or acknowledgment of what has been done to us. Just a quiet changing of things after Del Bigtree, Mark Blaxill, and JF Kennedy Jr, gets done with a bunch of deep state health officials.

I got to go pour some more water over my jars of sauerkraut and then to bed for sweet dreams are Thank you Visitor:
I am caring for my 90 and 95 year old parents as well as my family. So I am tired most of the time, and short on time all the time.
It scares me about the Kawasaki's disease. What will it lead to on down the line?

My daughter is working toward a stroke or heart attack. She smokes, on birth control pills (because her hormones do not function correctly since she was 14 years old) She will soon be 39. She was a thin little thing all through college and then gained lots of weight in only one year - 100 pounds or more I think and even developed a buffalo hump. It has to do again with hormones, and the immune system and inflammation.. She has exercised it off, she does walk every day for miles.

I do the gluten free, very little milk except in cooking, I for myself do not eat gluten cause I found for my own self that it hurts my legs and feet. I do not eat peanuts cause it breaks me out, and that is also inflammation. .
Do you know what it takes to just get gluten out of your kitchen, and still cook something?
And getting peanut butter out of my kitchen makes me a food Nazis and apparently is harder than taking bread away from them. They all want their carbs.

We all try to fast. We are suppose to stop eating at six and wait as long as possible in the morning. Fasting I think helps reduce inflammation? Perhaps our bodies have to have so much carbohydrates to make glucose to use as energy to make immune cells? I

One of your links turned up to mention alcoholics -- I never have drank alcohol; I have seen some of my cousins actually die, and other cousins lucky enough to go prison instead of dying because of their addition to alcohol, or drugs,or really both. I don't know if my family history has a lot of alcoholics any more that the rest of the population? But this addiction stuff I think is all associated with pain from inflammation.

My husband was given opioids, lots of them; all nice ahd legal. That caused a crisis in the family as well as coming close to killing him.

Inflammation hurts. It hurts your feet, and legs, everywhere. It can cause people to seek out pain killers that gets us to addition.

A psychologist that treated my daughter six years ago, yeah, she was self medicating with some things that she did not need to be messing with. It was a long episode of events of a lot of health problems following a DPT vaccine (stupid, stupid, stupid), and she got caught right out off the bat when she did that. Anyway this psychologist treats all the unfortunate addicted doctors and nurses, and apparently there are a lot of them ; but he responded to my daughter's complaint that she just hurts all over; that yeah, he too is a recovering addict, and he too hurts all over, but being sober and hurting is better than not. He suggested that she walk and exercise a lot. Which she does.

There are no grand children and there won't be.
There are no significant others for my children and I wept about that this past spring. I am sort of okay with that now. I fear they will be alone in their old age, but then perhaps all of us will be even if we have children.

Inflammation; Aspirin is suppose to help .

A couple of weeks ago my husband is all excited and brings home hemp oil. They are selling it?
I finally looked it up. I know every body says it helps on seizures, but I am not messing with hemp. Well I see that it is not the mind altering stuff, nothing like that at all. It does not contain the THC. It is legal. It fights inflammation. Well, I am so slow on things. So I am just slow Visitor.

Probably Canadensis albicans is in my brain. I think it is in my ear?
We are a mess I think.

There will be no apology or acknowledgment of what has been done to us. Just a quiet changing of things after Del Bigtree, Mark Blaxill, and JF Kennedy Jr, gets done with a bunch of deep state health officials.

I got to go pour some more water over my jars of sauerkraut and then to bed for sweet dreams are made of these-----

Visitor

Benedetta, I meant respond after your post, but got immersed in thought. I do appreciate your reply: "I will chew on these links a bit." Sweet Dreams to you...

Visitor

A report that I have saved that is current enough and very good.

The Role of CYP2E1 in the Drug Metabolism or Bioactivation in the Brain

https://www.hindawi.com/journals/omcl/2017/4680732/

This one starts with ethanol relation, but the one a couple down o the right on Tuberculosis is another that was of interest for me.

CYP2E1

https://www.sciencedirect.com/topics/medicine-and-dentistry/cyp2e1

Visitor

It is known those with Autism have lot more Atopic Dermatitis.

MicroRNA-155-5p is a key regulator of allergic inflammation, modulating the epithelial barrier by targeting PKIα.

Abstract

"Recent studies have demonstrated that microRNA-155-5p (miR-155-5p) plays an essential role in the regulation of allergen-induced inflammation and is overexpressed in the skin of patients with atopic dermatitis (AD), although the mechanism is unknown. In this study, silencing miR-155-5p attenuated the thickening of the epidermis in AD model and reduced the infiltration of inflammatory cells and the secretion of Th2 cytokines. Protein kinase inhibitor α (PKIα) was identified as a direct target of miR-155-5p and correlated negatively with miR-155-5p in our AD model. Fluorescence in situ hybridization showed that miR-155-5p-expressing cells were predominantly present in the epidermis. When epithelial cells were transfected with an miR-155-5p inhibitor, the expression of PKIα, occludin, and CLDN16 increased and that of TSLP decreased significantly, whereas the overexpression of miR-155-5p resulted in the opposite changes. The increased expression of PKIα and tight junction (TJ) proteins, with reduced TSLP and IL-33, was also detected in miR-155-5p-blocked mice, in both the initial and elicitation stages of AD. The expression of TJ proteins also decreased when cells were transfected with PKIα siRNA. TJ proteins increased and TSLP and IL-33 decreased significantly after the overexpression of PKIα. Our data provide the first evidence that miR-155-5p is critical for the allergic inflammation in a mouse model of AD by directly regulating PKIα and thus epithelial TJ expression. These findings suggest new therapeutic strategies that target miR-155-5p in patients with allergic disorders."

https://www.ncbi.nlm.nih.gov/pubmed/31767859

MiR-155 and other microRNAs downregulate drug metabolizing cytochromes P450 in inflammation.

https://www.ncbi.nlm.nih.gov/pubmed/31758923

A couple on Kawasaki's.

CYP2E1 Gene Polymorphisms Related to the Formation of Coronary Artery Lesions in Kawasaki Disease.

https://www.ncbi.nlm.nih.gov/pubmed/28650933

Regulatory T cell microRNA expression changes in children with acute Kawasaki disease.


Abstract

Kawasaki disease (KD) is a type of systemic vasculitis syndrome related to immune dysfunction. Previous studies have implicated that dysfunctional regulatory T cells (Treg ) may be associated with the immune dysfunction in KD. In the absence of microRNAs (miRNAs), forkhead box protein 3 (FoxP3)(+)  Treg develop but fail to maintain immune homeostasis. This study was designed to investigate the effects of miR-155, miR-21 and miR-31 on Treg in children with KD. The proportions of CD4(+) CD25(+) FoxP3(+) Treg and the mean fluorescence intensity (MFI) of phosphorylated-signal transducer and activator of transcription (pSTAT)-5 and pSTAT-3 protein in CD4(+) CD25(+) Treg were analysed by flow cytometry. The concentration of interleukin (IL)-6 in plasma was measured by cytometric bead array. Real-time polymerase chain reaction was performed to detect the levels of microRNAs and associated factors in CD4(+) CD25(+) Treg . The proportion of Treg and the mRNA levels of the associated factors [FoxP3, glucocorticoid-induced tumour necrosis factor-receptor (GITR), cytotoxic T lymphocyte antigen (CTLA)-4)] were significantly lower in KD patients (P < 0·05). MiR-155 and miR-21 levels were significantly down-regulated and miR-31 expression was higher in KD patients (P < 0·05). Plasma interleukin (IL)-6 concentrations, pSTAT-3 protein levels and suppressors of cytokine signalling (SOCS)-1 mRNA expression were remarkably elevated in acute KD (P < 0·05), while pSTAT-5 protein levels were remarkably decreased in acute KD (P < 0·05). These findings were reversed after intravenous immunoglobulin treatment (P < 0·05). Our results demonstrate that FoxP3 mRNA levels were primarily affected by the miR-155/SOCS1 and the miR-31 signalling pathways. These results suggest that the decrease in FoxP3(+) Treg might be associated with decreased expression of miR-155, leading to aberrant SOCS1/STAT-5 signalling and overexpression of miR-31 in patients with acute KD.

Abstract

BACKGROUND:

Kawasaki disease (KD) is an acute febrile systemic vasculitis that disturbs coronary arteries. Patients' risks of adverse cardiovascular events and subclinical atherosclerosis have been found to significantly increase with polymorphisms of the human cytochrome P450. This current study aims to research the possible relationship between cytochrome P450, family 2, subfamily E and polypeptide 1 (CYP2E1) polymorphisms with KD.

METHODS:

We selected 6 tag single-nucleotide polymorphisms (SNPs) of the CYP2E1 gene for TaqMan allelic discrimination assay in 340 KD patients and performed analysis on the clinical phenotypes and coronary artery lesions (CALs). CAL associations of tag SNPs were adjusted for age and gender in the logistic regression.

RESULTS:

The KD patients with a CC genotype of rs915906 demonstrated a greater proportion of CAL formation (P = 0.009). Furthermore, the GG genotype frequencies of rs2070676 showed a significantly greater risk for CAL formation in KD patients (P = 0.007). However, the SNPs of the CYP2E1 gene did not influence CAL formation in the participating KD patients either with or without high-dose acetylsalicylic acid. Using the expression quantitative trait locus analyses, we found that the SNPs associated with CAL formation in KD also affected CYP2E1 expression in certain cell types.

CONCLUSION:

This study is the first to find that the risk of CAL formation is related to CYP2E1 gene polymorphisms in KD patients.

https://www.ncbi.nlm.nih.gov/pubmed/25039241

Benedetta

Thank you so much Visitor;

I will chew on these links a bit. No, I don't think you are autistic. Something more, I think.
Great love and a desire to have a much time as possible with our love ones, in our little flash of life on this planet.

Don't forget to be kind to yourself though.

Visitor

Benedetta, I won't presume with certainty. But, you referred to DAO in another recent post and as I had recently mentioned this in this thread I thought you may have been prompted to see new associations with it from what I had recently posted. I had mentioned mast cells in the gut bug thread and had seen their involvement forever. I also cited them a few times early in this thread series. I though that most would see their other involvement from those posts and from my post on "brain allergies". Any way in case you are trying to understand these matters here are ac coup[le links that give clarity to matters I had seen many years before these sites were posted. I am not good at understanding at were others may understand a matter.
I may be a bit autistic myself. They say it takes one to know one. I don't think I am, I am the antithesis I think.

https://eatfor.life/histamine-mast-cell-disorder-or-methylation-imbalance/

https://mastcell360.com/autism-and-mast-cell-activation-syndrome/

https://www.youtube.com/watch?v=qeMFqkcPYcg&list=PLmXxqSJJq-yXrCPGIT2gn8b34JjOrl4Xf&index=66


Visitor

Once an English teacher and one of my favorite artist. His Fields of Gold is exquisite.

https://www.youtube.com/watch?v=OMOGaugKpzs&list=PLmXxqSJJq-yXrCPGIT2gn8b34JjOrl4Xf&index=63

Visitor

Susan, thank you for the greeting. I have not forgotten an interchange we had here on AoA. I won't disavow what I am like at times, but I ask you please excuse my manner at times. My apologies for my petulance.

susan welch

Visitor. Happy Thanksgiving from UK and thank you for the beautiful link.

Visitor

Happy Thanksgiving AoA!

https://www.youtube.com/watch?v=mSYq0sNSAkA

Visitor

Knew this for sure by 2002, but always had to believe I was a dumbass because everyone else knew better and you could not learn anything with Google unless you had a medical degree. I loathe this elite dumbass mentality. I knew all of this years before these geniuses declared it to be the fact. The medical establishment is tantamount to a cult In many ways. Their "peer reviewed" holy ones. Barf and gag me. Their arrogance not mine. I just spoke the truth. I have mentioned in this thread for a long time. I saw its relation in 1996. Dumb and Dumber. I am through wallowing on the outside because they are dense.

https://www.sciencedaily.com/releases/2019/10/191003092046.htm

Visitor

Dysbiotic microbiota in autistic children and their mothers: persistence of fungal and bacterial wall-deficient L-form variants in blood

Abstract
Based on our hypothesis for existing microbiota of wall-deficient variants (L-forms) in human blood, we created an innovative methodology, which allowed for the development of L-form populations from blood of all investigated people. In contrast to healthy controls, blood L-forms from autistic children and their mothers converted under appropriate conditions of cultivation into detectable opportunistic bacteria and fungi, а process demonstrated by light and transmission electron microscopy. It can be distinguished into two types of states – “eubiotic” blood microbiota in healthy individuals, and “dysbiotic” in autistic children and their mothers. Remarkably, the unifying finding for autistic children and their mothers was the presence in blood of wall-free variants from life-cycle of filamentous fungi. Increased specific IgG, IgM and IgA, together with typical mold growth were a decisive argument for proven presence of Aspergillus fumigatus in almost all of the autistic children. As it was demonstrated in our previous study, filterable L-forms can be transmitted by vertical pathway from mother to child before birth. Thus, it can be suggested that autistic children may be born already colonized with fungi, while a “silent aspergillosis” could contribute or even be a leading cause for neurodevelopmental disorders in the early childhood.
https://www.nature.com/articles/s41598-019-49768-9#Tab2

Visitor

The jury is out on mir-155 weighing this against the4 last post. It may be in the Goldilocks domain.

Inhibition of miR-155 Limits Neuroinflammation and Improves Functional Recovery After Experimental Traumatic Brain Injury in Mice.

Abstract

Micro-RNAs (miRs) are short, noncoding RNAs that negatively regulate gene expression at the post-transcriptional level and have been implicated in the pathophysiology of secondary damage after traumatic brain injury (TBI). Among miRs linked to inflammation, miR-155 has been implicated as a pro-inflammatory factor in a variety of organ systems. We examined the expression profile of miR-155, following experimental TBI (controlled cortical impact) in adult male C57Bl/6 mice, as well as the effects of acute or delayed administration of a miR-155 antagomir on post-traumatic neuroinflammatory responses and neurological recovery. Trauma robustly increased miR-155 expression in the injured cortex over 7 days. Similar TBI-induced miR-155 expression changes were also found in microglia/macrophages isolated from the injured cortex at 7 days post-injury. A miR-155 hairpin inhibitor (antagomir; 0.5 nmol), administered intracerebroventricularly (ICV) immediately after injury, attenuated neuroinflammatory markers at both 1 day and 7 days post-injury and reduced impairments in spatial working memory. Delayed ICV infusion of the miR-155 antagomir (0.5 nmol/day), beginning 24 h post-injury and continuing for 6 days, attenuated neuroinflammatory markers at 7 days post-injury and improved motor, but not cognitive, function through 28 days. The latter treatment limited NADPH oxidase 2 expression changes in microglia/macrophages in the injured cortex and reduced cortical lesion volume. In summary, TBI causes a robust and persistent neuroinflammatory response that is associated with increased miR-155 expression in microglia/macrophages, and miR-155 inhibition reduces post-traumatic neuroinflammatory responses and improves neurological recovery. Thus, miR-155 may be a therapeutic target for TBI-related neuroinflammation.


KEYWORDS:

Traumatic brain injury; miR-155; microglial activation; neuroinflammation; neuroprotection

https://www.ncbi.nlm.nih.gov/pubmed/30225790


Visitor

I often state things as though possible as in the last post concerning CYP2E1. This is mainly because we have no tests for many of the factors I speak about. The connection of treatment/symptoms and outcomes with many layers of interconnections are very clear about their involvement. Mir-155 is a double-edged sword. The involvement could develop slowly or abruptly. MIR-155 may lead to weight gain and the invoking of Leptin as well as a neuroprotectant may be a part of a good amount of Autism. I posted a link to this MIR found in the Amygdala of those with Autism not many posts back.

Induction of miR-155 after Brain Injury Promotes Type 1 Interferon and has a Neuroprotective Effect

https://www.frontiersin.org/articles/10.3389/fnmol.2017.00228/full

Visitor

One of the very earlier considerations in our case was the effect of Isoniazid on my wife's mother and the persistence of its effect in her system. It is possible issues with CYP2E1 were part of the reason for her susceptibility to TB and mycoplasma. It also may be that Isoniazid disturbed her liver and enzymatic function and microbiome and ultimately her immune system. This would have effected my wife when she was in the womb.If and when a vaccine given to my wife's mother could be involved I have no idea. I do think my wife, although have genetic predisposition, epigenetic effects, very early on dysbiotic gut. and MIA in her gestation already, was further effected by vaccines. The first report abstract was one I found early on and it is more clearly a part as research has elucidated its relationship.

Isoniazid interactions.

Abstract

Isoniazid is an antituberculous drug that is usually administered for nine to 12 months. The potential for clinically important interactions exists because this drug is a potent inhibitor of drug metabolism. Studies and case reports have shown that isoniazid inhibits the metabolism of several drugs, including phenytoin, carbamazepine, anticoagulants, benzodiazepines, and vitamin D. Furthermore, isoniazid inhibits both monoamine oxidase and diamine oxidase (histaminase). Additional study is required to document the clinical significance of other isoniazid interactions. Future investigations will identify new isoniazid interactions.

https://www.ncbi.nlm.nih.gov/pubmed/3890202

Placental DNA methylation levels at CYP2E1 and IRS2 are associated with child outcome in a prospective autism study.

Abstract

DNA methylation acts at the interface of genetic and environmental factors relevant for autism spectrum disorder (ASD). Placenta, normally discarded at birth, is a potentially rich source of DNA methylation patterns predictive of ASD in the child. Here, we performed whole methylome analyses of placentas from a prospective study MARBLES (Markers of Autism Risk in Babies-Learning Early Signs) of high-risk pregnancies. A total of 400 differentially methylated regions (DMRs) discriminated placentas stored from children later diagnosed with ASD compared to typically developing controls. These ASD DMRs were significantly enriched at promoters, mapped to 596 genes functionally enriched in neuronal development, and overlapped genetic ASD risk. ASD DMRs at CYP2E1 and IRS2 reached genome-wide significance, replicated by pyrosequencing and correlated with expression differences in brain. Methylation at CYP2E1 associated with both ASD diagnosis and genotype within the DMR. In contrast, methylation at IRS2 was unaffected by within DMR genotype but modified by preconceptional maternal prenatal vitamin use. This study therefore identified two potentially useful early epigenetic markers for ASD in placenta.

https://www.ncbi.nlm.nih.gov/pubmed/31009952

The landscape of copy number variations in Finnish families with autism spectrum disorders.

Abstract

Rare de novo and inherited copy number variations (CNVs) have been implicated in autism spectrum disorder (ASD) risk. However, the genetic underpinnings of ASD remain unknown in more than 80% of cases. Therefore, identification of novel candidate genes and corroboration of known candidate genes may broaden the horizons of determining genetic risk alleles, and subsequent development of diagnostic testing. Here, using genotyping arrays, we characterized the genetic architecture of rare CNVs (<1% frequency) in a Finnish case-control dataset. Unsurprisingly, ASD cases harbored a significant excess of rare, large (>1 Mb) CNVs and rare, exonic CNVs. The exonic rare de novo CNV rate (∼22.5%) seemed higher compared to previous reports. We identified several CNVs in well-known ASD regions including GSTM1-5, DISC1, FHIT, RBFOX1, CHRNA7, 15q11.2, 15q13.2-q13.3, 17q12, and 22q11.21. Additionally, several novel candidate genes (BDKRB1, BDKRB2, AP2M1, SPTA1, PTH1R, CYP2E1, PLCD3, F2RL1, UQCRC2, LILRB3, RPS9, and COL11A2) were identified through gene prioritization. The majority of these genes belong to neuroactive ligand-receptor interaction pathways, and calcium signaling pathways, thus suggesting that a subset of these novel candidate genes may contribute to ASD risk. Furthermore, several metabolic pathways like caffeine metabolism, drug metabolism, retinol metabolism, and calcium-signaling pathway were found to be affected by the rare exonic ASD CNVs. Additionally, biological processes such as bradykinin receptor activity, endoderm formation and development, and oxidoreductase activity were enriched among the rare exonic ASD CNVs. Overall, our findings may add data about new genes and pathways that contribute to the genetic architecture of ASD.

https://www.ncbi.nlm.nih.gov/pubmed/26052927

In the search for reliable biomarkers for the early diagnosis of autism spectrum disorder: the role of vitamin D.

El-Ansary A1,2,3,4, Cannell JJ5, Bjørklund G6, Bhat RS7, Al Dbass AM7, Alfawaz HA8, Chirumbolo S9, Al-Ayadhi L3,4,10.

Abstract

Autism spectrum disorder (ASD) affects about 1% of the world's population. Vitamin D is thought to be essential for normal brain development and modulation of the immune system. Worldwide about 1 billion people are affected by vitamin D deficiency. High-sensitivity C-reactive protein (hs-CRP), cytochrome P450 2E1 (CYP2E1) and 8-hydroxy-2'-deoxyguanosine (8-OH-dG) are biomarkers related to inflammation and oxidative stress. In the present study, these biomarkers were together with serum 25-hydroxyvitamin D (25(OH)D3) analyzed in 28 (mean age seven years) Saudi male patients with ASD. The study was conducted to determine if there is any relationship between vitamin D levels, the tested biomarkers and the presence and severity of ASD. The hope was to identify if these biomarkers may be useful for early ASD diagnosis. The Childhood Autism Rating Scale (CARS) and the Social Responsiveness Scale (SRS) were used to measure autism severity. The results of the ASD children were compared with 27 age and gender-matched neurotypical controls. The data indicated that Saudi patients with ASD have significantly lower plasma levels of 25(OH)D3 than neurotypical controls (38 ng/ml compared to 56 ng/ml, respectively; [P = 0.001]). Surprisingly, the levels of CYP2E1 were lower in the children with ASD than the neurotypical controls (0.48 ± 0.08 vs. 69 ± 0.07 ng/ml, respectively; P = 0.001). The ASD children also had significantly higher levels of hs-CRP (0.79 ± 0.09 vs. 0.59 ± 0.09 ng/ml, respectively; P = 0.001) and 8-OH-dG (8.17 ± 1.04 vs. 4.13 ± 1.01 ng/ml, respectively; P = 0.001, compared to neurotypical age and gender-matched controls. The values for hs-CRP and 8-OH-dG did not correlate [P < 0.001] with autism severity. There was found a relationship between autism severity on the CARS scale and the levels of 25(OH)D3 and CYP1B1. But this was not found for SRS. All four biomarkers seemed to have good sensitivity and specificity, but the sample size of the present study was too small to determine clinical usefulness. The findings also indicate that inadequate levels of vitamin D play a role in the etiology and severity of autism. Furthermore, the results of the present study suggest the possibility of using 25(OH)D3, CYP1B1, hs-CRP and 8-OH-dG, preferably in combination, as biomarkers for the early diagnosis of ASD. However, further research is needed to evaluate this hypothesis.

https://www.ncbi.nlm.nih.gov/pubmed/29497932


Relationship of anti-tuberculosis drug-induced liver injury and genetic polymorphisms in CYP2E1 and GST.

Abstract

SETTING:

Treatment of tuberculosis (TB) can result in Drug-Induced Liver Injury (DILI) since hepatotoxic metabolites are formed during the biotransformation of isoniazid (INH). DILI can be related to the genetic profile of the patient. Single nucleotide polymorphisms in the CYP2E1 gene and GSTM1 and GSTT1 deletion polymorphisms have been associated with adverse events caused by INH.

OBJECTIVE:

To characterize the genetic polymorphisms of CYP2E1, GSTT1 and GSTM1 in TB carriers.

DESIGN:

This is an observational prospective cohort study of 45 patients undergoing treatment of TB. PCR-RFLP and multiplex-PCR were used.

RESULTS:

The distribution of genotypic frequency in the promoter region (CYP2E1 gene) was: 98% wild genotype and 2% heterozygous. Intronic region: 78% wild genotype; 20% heterozygous and 2% homozygous variant. GST enzyme genes: 24% Null GSTM1 and 22% Null GSTT1. Patients with any variant allele of the CYP2E1 gene were grouped in the statistical analyses.

CONCLUSION:

Patients with the CYP2E1 variant genotype or Null GSTT1 showed higher risk of presenting DILI (p=0.09; OR: 4.57; 95% CI: 0.75-27.6). Individuals with both genotypes had no increased risk compared to individuals with one genotype.

https://www.ncbi.nlm.nih.gov/pubmed/31697922

Mitochondrial CYP2E1 is sufficient to mediate oxidative stress and cytotoxicity induced by ethanol and acetaminophen.

Abstract

Several cytochromes P450 (CYPs) are not only located in the endoplasmic reticulum but also within mitochondria. One such CYP is CYP2E1 which metabolizes numerous substrates and generates significant amount of reactive oxygen species. The presence of CYP2E1 in these organelles raises questions regarding its physiological role but also its possible deleterious effects in the context of drug-induced cytotoxicity. The aim of our study was to investigate the role of mitochondrial CYP2E1 in the toxicity of acetaminophen and ethanol. Hence the effects of these two compounds in cells expressing CYP2E1 in mitochondria only, or in both endoplasmic reticulum and mitochondria, were compared to those observed in mock-transfected cells. Our results indicated that when acetaminophen or ethanol were used as CYP2E1 substrates, the exclusive localization of CYP2E1 within mitochondria was sufficient to induce reactive oxygen species overproduction, depletion of reduced glutathione, increased expression of mitochondrial Hsp70, mitochondrial dysfunction and cytotoxicity. Importantly, these harmful events happened despite lower cellular level and activity of CYP2E1 when compared to cells expressing CYP2E1 in both endoplasmic reticulum and mitochondria, and this was particularly obvious with acetaminophen. Taken together, these data suggest that mitochondrial CYP2E1 could play a major role in drug-induced oxidative stress and cell demise.

https://www.ncbi.nlm.nih.gov/pubmed/21130154

Maternal Gestational Diabetes Mellitus and Newborn DNA Methylation: Findings From the Pregnancy and Childhood Epigenetics Consortium.

Abstract

OBJECTIVE:

Maternal gestational diabetes mellitus (GDM) has been associated with adverse outcomes in the offspring. Growing evidence suggests that the epigenome may play a role, but most previous studies have been small and adjusted for few covariates. The current study meta-analyzed the association between maternal GDM and cord blood DNA methylation in the Pregnancy and Childhood Epigenetics (PACE) consortium.

RESEARCH DESIGN AND METHODS:

Seven pregnancy cohorts (3,677 mother-newborn pairs [317 with GDM]) contributed results from epigenome-wide association studies, using DNA methylation data acquired by the Infinium HumanMethylation450 BeadChip array. Associations between GDM and DNA methylation were examined using robust linear regression, with adjustment for potential confounders. Fixed-effects meta-analyses were performed using METAL. Differentially methylated regions (DMRs) were identified by taking the intersection of results obtained using two regional approaches: comb-p and DMRcate.

RESULTS:

Two DMRs were identified by both comb-p and DMRcate. Both regions were hypomethylated in newborns exposed to GDM in utero compared with control subjects. One DMR (chr 1: 248100345-248100614) was located in the OR2L13 promoter, and the other (chr 10: 135341870-135342620) was located in the gene body of CYP2E1. Individual CpG analyses did not reveal any differentially methylated loci based on a false discovery rate-adjusted P value threshold of 0.05.

CONCLUSIONS:

Maternal GDM was associated with lower cord blood methylation levels within two regions, including the promoter of OR2L13, a gene associated with autism spectrum disorder, and the gene body of CYP2E1, which is upregulated in type 1 and type 2 diabetes. Future studies are needed to understand whether these associations are causal and possible health consequences.

https://www.ncbi.nlm.nih.gov/pubmed/31601636

Tylenol may be involved or a trigger in some cases, or a synergy with a vaccine at times.

The role of oxidative stress, inflammation and acetaminophen exposure from birth to early childhood in the induction of autism.

Author information

Abstract

The wide range of factors associated with the induction of autism is invariably linked with either inflammation or oxidative stress, and sometimes both. The use of acetaminophen in babies and young children may be much more strongly associated with autism than its use during pregnancy, perhaps because of well-known deficiencies in the metabolic breakdown of pharmaceuticals during early development. Thus, one explanation for the increased prevalence of autism is that increased exposure to acetaminophen, exacerbated by inflammation and oxidative stress, is neurotoxic in babies and small children. This view mandates extreme urgency in probing the long-term effects of acetaminophen use in babies and the possibility that many cases of infantile autism may actually be induced by acetaminophen exposure shortly after birth.

https://www.ncbi.nlm.nih.gov/pubmed/28415925

Can autism be triggered by acetaminophen activation of the endocannabinoid system?

Abstract

Acetaminophen use in children has been associated with increased autism risk. Recent evidence suggests that acetaminophen's analgesic actions result from activation of the endocannabinoid system, and activation of this system can have neuromodulatory consequences during development. This investigation was performed to determine if there is evidence to support the hypothesis that acetaminophen use can trigger autism by activation of the endocannabinoid system.

https://www.ncbi.nlm.nih.gov/pubmed/20628445

Visitor

I had tried to post this before the last post as they both speak to collagen and T-Cells and show relation. Maybe I was posting too much of the article.

Surplus of immune cells may mark brains of autistic people

"Blood vessels in the brains of more than half of autistic people have an unusually large number of immune cells called T cells, according to an analysis of postmortem tissue1. This excess may damage cells that form a protective lining for the brain.

The findings jibe with results showing elevated levels of immune molecules, as well as hyperactive immune cells called microglia, in the brains of people with autism2.

“There’s just a chronic inflammatory state,” says the new study’s lead investigator, Matthew Anderson, chief of neuropathology at Beth Israel Deaconess Medical Center in Boston, Massachusetts.

The team found that blood vessels with excess T cells tend to be surrounded by debris from cells that help form part of the blood-brain barrier.

“That’s novel and provocative, and I think it is something that has to be verified and replicated,” says S. Hossein Fatemi, professor of psychiatry at the University of Minnesota, who was not involved in the study. “This is purely a descriptive study.”

Anderson’s team stumbled upon their findings during routine microscopic examinations of tissue from Autism BrainNet, a repository of brain tissue from people with autism. (Anderson is lead neuropathologist for the repository.)

Peering under a microscope, Anderson says, he noticed that samples from autistic people tend to contain numerous round ‘blebs’ — tiny droplets of debris released from cells. These blebs littered the spaces that separate blood vessels from brain tissue.

“I kept seeing little foci of those,” Anderson says. “I’ve never seen that before in any other condition.”

His team then systematically looked for the blebs in samples from 25 people with autism and 30 controls who ranged in age from 1 to 68 years. They first focused on blood vessels and the spaces around them in tissue from the cerebral cortex, the brain’s outer layer.

They suspected, and were able to confirm, that the blebs had been released from nearby astrocytes. These cells surround blood vessels and form part of the blood-brain barrier.

The brains of autistic people have much larger swaths containing blebs than controls do, the team found. The findings appeared 8 October in Annals of Neurology.

Under attack:

Cells often release blebs when attacked by a subset of immune cells called cytotoxic T cells. And the team found that these T cells do often cluster in blood vessels near the blebs.

About 65 percent of the autistic people have more T cells in the cerebral cortex than controls do; they also show excess T cells in seven of eight other brain regions the team examined.

The more T cells a person had, the more astrocyte debris. The space surrounding blood vessels also tends to be enlarged in people with autism, and contains excess collagen, a protein produced in response to tissue damage.

The findings hint that T cells seek out and destroy the astrocytes, Anderson says.

Still, it is unclear why these T cells accumulate in the autism brain or why they might attack this lining. The cells are usually responsible for fighting off viruses and are implicated in autoimmune conditions.

The T cells may be innocent bystanders, attracted to the scene by molecules released after astrocytes are damaged by some other cause.

“Are they damaging those cells, or are they responding to the damage of those cells?” says Judy Van de Water, professor of internal medicine at the University of California, Davis, who was not involved in the study. “You cannot, from this type of study, answer that question.”

Anderson and his team are trying to identify tags on astrocytes that might attract the T cells. They are also exploring whether the damage to the barrier occurs in utero."

https://www.spectrumnews.org/news/surplus-of-immune-cells-may-mark-brains-of-autistic-people/

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