Williams' Syndrome is a genetic disorder caused by the deletion of multiple genes in one region of chromosome 7. In almost all cases, these are spontaneous deletions on one copy; the other copy is functionally normal, while the exceptions are those who are the children of those with Williams' Syndrome. (In other words, the trait is dominant or partially dominant; all cases that I can find have those afflicted be heterozygous for the trait.)
Is there any research on the effects for being homozygous for the deletion?
Why YSK While it is uncommon, people have suffered strokes from hyperextending their neck into the shampoo bowl which puts pressure on arteries. Putting a towel under your neck is one thing you can do to lessen the risk. This article explains it well: https://www.self.com/story/what-is-beauty-parlor-stroke-syndrome/amp
Mania following addition of hydroxytryptophan to monoamine oxidase inhibitor
So I have a very short face: long midface but short/small bottom third. Recently i did a comparison between myself and a friend who has vertical facial growth but a longer-looking face. I asked him to perform this move (my picture) Where the bottom front and top front teeth bite onto each other, I found that I have this large open bite in the back but he has all the teeth roughly aligned. This makes me conclude that I do have SFS caused by resting the back of my tongue between my back teeth. But my question is from a structural perspective what is happening here. I can imagine a downward growth maxilla but not a seemingly upwards grown mandible. especially given that my mandible/bottom jaw has the typical downwards angle.
btw: jutting my bottom jaw out does improve my appearance notably.
tbc: this is not my normal bite, in my normal bite I have an overbite where my 2 front bottom teeth hit the roots of my 2 front top teeth, its actually quite painful and an issue all the time.
Pre-print paper: https://www.researchsquare.com/article/rs-1756189/v1
There is mounting evidence that SARS-CoV-2 targets tissues beyond the respiratory tract. Long-term sequelae after COVID-19 are frequent and of major concern. Prolonged virus detection in the gut has been particularly intriguing. Of note, SARS-CoV-2 infection also disturbs the gut microbiota composition, a finding linked with disease severity in patients with COVID-19. Here, we aimed to characterize the functional role of the gut microbiota in the long-term consequences of COVID-19. To this end, we characterized the gut microbiota from COVID-19 human subjects and followed the effects of human fecal transfer to germ-free mice.
The gut microbiota of post-COVID subjects (up to 4 months from the initial positive test) revealed a remarkable predominance of Enterobacteriaceae strains with multidrug-resistance phenotype compared to healthy controls. After fecal transfer to germ-free mice, animals receiving samples from post-COVID subjects displayed higher lung inflammation and increased susceptibility to pulmonary infection caused by an antimicrobial resistant Klebsiella pneumoniae strain. These mice also showed poorer cognitive performance associated with increased expression of TNF-α, reduced levels of brain-derived neurotrophic factor-BDNF and postsynaptic density protein-PSD-95 in the brain, as well as alterations of several biochemical pathways. These alterations were observed in the absence of SARS-CoV-2, suggesting that alterations in the gut microbiota caused them. Consistent with this hypothesis, brain dysfunctions induced in a mouse model of coronavirus infection were partially prevented by modulation of the microbiota via treatment with the commensal probiotic bacteria Bifidobacterium longum 51A.
Our results show prolonged impact of SARS-CoV-2 infection in the gut microbiota that persists even after the individuals have cleared the virus. Increased Enterobacteriaceae with antimicrobial resistance phenotype were of particular concern. Moreover, microbiota transfer from post-COVID subjects induced loss of brain cognitive functions and impaired lung defense in mice. Altogether, our work emphasizes the importance of microbiota as a target for therapies to help treat post-COVID sequelae.
I am trying to figure out why this is happening and what to do about it.
Some background, I used NA-Selank Amidate for the first time for 5 days; dosing was 200mcg (100mcg each nostril) every 12 hours (morning and night). During this time, I experienced a clear-mindedness unlike any other. I have experienced mania before, and this was not like that. For lack of a better way to explain it, it felt like a limitless pill while being still grounded, happy, and healthy. That being said, the reason I only used the nootropic for 5 days was that I was starting to experience immense insomnia; I was unable to sleep more than 3 hours a night and when lying down, it felt like my mind was going 1000mph with thoughts, “sounds” (like music stuck in my head on repeat), etc. Once again, it felt somewhat similar to taking too much of a stimulant like amphetamine without the physical restlessness and brain fog.
Since this experience ended about a week ago, I am still finding myself experiencing this insomnia, coupled with something known as “exploding-head syndrome” which is usually associated with SSRI withdrawals; it essentially is when attempting to go to sleep, a person will hear a very loud bang/scream/sensation of falling that will jolt them awake.
I have a sensitive gabanergic system after in the past taking Wellbutrin at 150mg. I experienced a period of suicidal ideation (I am doing fine and not experiencing that now) and stopped taking the Wellbutrin. For a period of 3-6 months, my gaba system was thrown way off and healed while experiencing brain zaps, intense anxiety, weird twitching, and exploding-head syndrome. I am currently feeling symptoms similar to these without the brain zaps only to a lesser extent than before.
I am coming to this community wondering mechanistically why this is occurring as well as what I can do about it. When looking at research about Selank, it seems like it is almost somewhat protective to GABAa receptors by not decreasing mRNA levels associated with GABAa receptors. Additionally, most people state that Selank is anxiolytic while I experienced the opposite.
I thank you all for this community! I am looking forward to learning from all of you in the comments! Feel free to ask me any questions and I will do my best to answer them!
Edit: Thank you all for the comments, I am surprised by the amount of people that have picked out and empathized with my experiences with Wellbutrin. While I am happy to have helped some of you, th... keep reading on reddit ➡
Self Improvement causes lone wolf syndrome here is why
When we are improving ourselves our ENTIRE values change drastically, if u keep improving u will start to feel lonely and like a lone wolf. Why ? Because u don't have a real close friend anymore, u don't share the same values you had with your friends, now you have different values. It's like having a filter when you talk, you can't talk about the things u like or the things that really matter because it's value they don't have. Basically you have now another common interests and you eliminated your last interest you shared with your friends.
If u are on self improvement probably if you are consistent enough you will experience this massive "Lone Wolf Syndrome" and a sense of Lonely so fucking big that will even shake your foundations, it will never make your tower fall but it will make it weaker because at this point self improvement is now a big part of you, its a value that can't be changed anymore.
I had been on self improvement for 1 year, got massive changes but now im feeling this "Lone Wolf Syndrome" everybody talks about. Im trying to get friends so if you are from Argentina Buenos Aires dm me