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Medicine Medical Science Thread

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Fifty thousands or more Indian die each year from snakebite, that's about half the worlds total snakebite deaths. Mind boggling numbers. WHO estimated 5.4 million people worldwide are bitten by snakes each year and more than 100,000 die. They make the antivenoms in horses same as CSL, but the major antivenom doesn't cover all the common bites.

https://www.bbc.com/news/articles/cy8p27vmyvmo

"Currently, India has antivenom that only protects against the "big four" snakes - the spectacled cobra, common krait, Russell's viper and the saw-scaled viper - which are believed to be responsible for a majority of the bites. The antivenom is produced by injecting venom from these snakes into horses, whose antibodies are then used as treatment for humans, Martin explains

But there are dozens of other poisonous snake species for which India does not have targeted antivenom. These include the green pit viper commonly found in the northern state of Himachal Pradesh, the Malabar pit viper and hump-nosed pit viper found in southern states and many other species in the north-eastern states."
 
A recent study looked at the biochemical changes in aging and noted 2 periods of greatest change, in your 40's and in your early 60's. As a long term user of one of these pesky human bodies I can only say it agrees with my user experience. There is a link to the original Nature paper at the end of the article, which I must confess I haven't read yet, but I will.

 
40% of men loose their Y chromosomes by 60 years of age and by 95 it goes up to 57%. Thought I'd better see if I could find mine, I checked under the bed, down the back of the couch to see if it had slipped down there, even looked in the car where I often leave things. Couldn't find the bloody thing!

Seriously, the article does look at the science behind it and the health implications.

https://theconversation.com/men-los...idnt-matter-but-now-were-learning-more-275823

Devo warned us about this devolutionary trend 50 years ago, including the ultimate fate of the male organ of generation.

 

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Article from the Conversation about the use of psychedelics for mental health problems and the role of the "mystical experience" in improvement (or not). My first "mystical experience" occurred when I was a teenager, no drugs involved, just a girl called Dolly. If I was a New Zealander it would have been a sheep called Dolly.

 
2025 had the highest flu deaths this century, though a tad behind Covid.

Last year, there were about 2,161 deaths involving COVID-19 and 1,701 deaths involving influenza.

There were also about 582 deaths associated with RSV, which was about a hundred more than in 2024.

Epidemiologist Catherine Bennett said the emergence of a new flu variant H3N2, known as Subclade K, has contributed to the higher rates of death.

"We had the highest rates that we'd seen for a long time continuing right through December and into January," Professor Bennett said.
 
Lost in Space is the obvious headline for this one and I'm glad they took it. I reckon it will be a case of life will find a way, I have great confidence the sperm will sort it out. If not breeding chambers, with artificial G from centrifugal force.

 
There is nothing worse than neuro-muscular degenerative diseases, untreatable and many affect kiddies. I always found it heart breaking dealing with families with kiddies who had no future. Fortunately science progresses and therapies are available for a small number of these conditions. The ABC had a heart warming (yes, it really is!) story about infants born with Spinal Muscular Atropy, who previously all died before 12 months.


I asked my silicon chum to list the treatable conditions along with their treatments. There's six now, there were none when I started work. Most, but not all are gene therapies, the result of the biomedical revolution late last century. Most have only become avaiable in the last 20 years. Still it's progress. Most have come out of US NIH funded research, which I remind folks, Mr Trump has decimated. Money for stupid wars but not research.

Unfortunately only a rare form of Amyotrophic Lateral Sclerosis (SOD1‑ALS) has treatment, I've known a few souls who have passed away with ALS. I have pasted the list below as others might be interested. From Copilot:

1. Spinal Muscular Atrophy (SMA)

MedicationTypeMechanismFirst Approval
Nusinersen (Spinraza)Antisense oligonucleotideModifies SMN2 splicing to increase SMN protein2016 (US)
Onasemnogene abeparvovec (Zolgensma)AAV9 gene therapyReplaces missing SMN1 gene2019 (US)
Risdiplam (Evrysdi)Oral small‑molecule splicing modifierIncreases SMN2 full‑length protein2020 (US)

Impact: SMA Type 1—once the leading genetic cause of infant death—now has infants sitting, walking, and surviving into childhood and beyond.

2. Duchenne Muscular Dystrophy (DMD)

(Multiple new treatments, including gene therapy.)
MedicationTypeMechanismFirst Approval
EteplirsenASO (exon 51 skipping)Restores dystrophin reading frame2016
GolodirsenASO (exon 53 skipping)Same mechanism2019
ViltolarsenASO (exon 53 skipping)Same mechanism2020
CasimersenASO (exon 45 skipping)Same mechanism2021
Delandistrogene moxeparvovec (Elevidys)AAV gene therapyDelivers micro‑dystrophin gene2023 (expanded 2024)
VamoroloneNovel steroid‑like anti‑inflammatorySlows muscle degeneration with fewer side effects2023–2024
GivinostatHDAC inhibitorReduces fibrosis and inflammation2024

Impact: These therapies slow progression, improve motor function, and in the case of gene therapy, introduce functional dystrophin.

3. Hereditary Transthyretin Amyloidosis (hATTR / FAP)
(A neuromuscular + systemic degenerative disease affecting peripheral nerves.)
MedicationTypeMechanismFirst Approval
Patisiran (Onpattro)siRNASilences TTR production2018
Inotersen (Tegsedi)ASOReduces TTR protein2018
Vutrisiran (Amvuttra)siRNALong‑acting TTR silencing2022

Impact: These drugs halt or reverse neuropathy progression, something previously impossible.

4. SOD1‑Amyotrophic Lateral Sclerosis (SOD1‑ALS)

(A major breakthrough in 2023.)
MedicationTypeMechanismFirst Approval
TofersenASOReduces toxic SOD1 protein2023 (US)

Impact: First therapy to slow progression in a genetic form of ALS.

5. Myasthenia Gravis (Autoimmune neuromuscular junction disease)

(Not degenerative in the genetic sense, but historically “untreatable” severe cases now have targeted therapies.)
MedicationTypeMechanismFirst Approval
Eculizumab (Soliris)Complement inhibitorBlocks complement‑mediated AChR damage2017
Ravulizumab (Ultomiris)Long‑acting complement inhibitorSame mechanism2022
Efgartigimod (Vyvgart)FcRn inhibitorReduces pathogenic IgG2021

6. Pompe Disease (Glycogen storage disease type II)

(A metabolic neuromuscular degenerative disease.)

MedicationTypeMechanismFirst Approval
Alglucosidase alfa (Myozyme/Lumizyme)Enzyme replacementReplaces acid α‑glucosidase2006
Avalglucosidase alfa (Nexviazyme)Improved ERTBetter uptake into muscle2021
 
It's been thought for a long time that amyloid plaques and tau protein tangle have 'something to do' with Alzheimer's disease. What they actually did and how they did it has been a mystery. We now have unifying theory that relates the 2 and how it might work in the brain. Warning, this study is a test tube experiment (in vitro) so may have nothing to do with what happens in the brain (in vivo). To cut a long story short, the changes the proteins go through end up disrupting the neurons microtubules. Microtubules are very important!

To investigate, Julian and his colleagues conducted a series of protein binding studies, focusing on how amyloid-beta and tau interact around microtubules. Noticing that amyloid-beta peptides resembled, in sequence, the part of tau proteins that attach to microtubules, the team mixed the two proteins together in solution, along with tubulin, the building block of microtubules.

"Our work shows amyloid beta and tau compete for the same binding sites on microtubules, and that [amyloid-beta] can prevent tau from functioning correctly," says Julian. Using fluorescently labeled amyloid-beta, the researchers could see when amyoid-beta peptides 'stole' the binding sites normally used by tau proteins.

The researchers also 'tempted' amyloid-beta with another common protein, myoglobin, and found that amyloid-beta peptides still preferred binding to microtubules – meaning they weren't just binding to any protein in solution.....

.....If amyloid-beta peptides displace tau from its usual binding sites, as these protein studies suggest, then this might explain how tau can knot itself in tangles and microtubules become destablized, disrupting core functions of neurons and ultimately leading to cell death.



Back to microtubules, the Orchestrated Objective Reduction (Orch OR) theory of the origin of consciousness places the humble microtubules centre stage. Developed by Stuart Hameroff (anaesthetist) and Roger Penrose (Nobel prize), the theory suggests that microtubules host quantum computations, functioning as quantum processors that generate moments of conscious experience. There is no evidence for this really, it's just a theory, speculation. However when one of the cleverest men in the world suggests a prime role for the microtubules in the maintenance of consciousness I tend to listen.
 
Scientists have identified some of the genes (SP6 and SP8) responsible for growing back limbs on Salamanders and Axolotls. The same genes are responsible for regrowing tips of digits on mice and I must confess I did not know mice could do that.


There will be difficulties with control, localising and limiting the effect. Many years ago Walt Disney experimented on Snow White with gene promoters with some unfortunate effects.

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Polycystic Ovarian syndrome (PCOS) has been officially renamed polyendocrine metabolic ovarian syndrome (PMOS) reflecting the modern understanding it's systemic disease not just one that gives you cysts in the ovary.

"PMOS is a common disorder that is characterised by fluctuations in hormones, with impacts on weight, metabolic heath, mental health, skin, and the reproductive system. It affects one in eight women, or 170 million women worldwide.
Researchers say that for too long, its name had reduced a complex and long term hormonal or endocrine disorder to a focus on cysts and the ovaries. Recent research found that women with PMOS did not have a higher rate of abnormal ovarian cysts than women without the
condition."

It was driven by Helena Teade, an endocrinologist from Monash I used to work with a bit. She is a lovely person, a very smart cookie and I am pleased to see her succeed.

 
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Sadly a death from Diphtheria in the NT, the first since 2018. It's a really terrible way to die, suffocating on a gray-colored "pseudomembrane" made of dead mucosa, bacteria, and fibrin. I saw a kiddie die from it in PNG. It's also a terrible tragedy because it's a disease utterly preventable by the vaccine.


"Cases have been recorded in Western Australia, Queensland and South Australia, with a total of 161 testing positive for diphtheria nationwide. He said vaccine hesitancy since COVID-19 could be a contributing factor, alongside lagging vaccination rates in remote areas. While there was a high coverage rate among children, Dr Boffa said teenagers and adults needed to receive booster shots.

"Some late adolescents are getting sick because they haven't had a dose since they were children and they have missed their dose at 12 years old," he said.
 
I noticed some new and somewhat positive work related to improving cognition and potential treatments for dementia and other neurodegenerative disease. The first is a report of the use of D-serine, the D isomer of the amino acid serine, that improved the cognition and memory in older rats. It also appeared to reverse other age related changes. If you are a demented rat this looks good. Unfortunately no human trials yet but I expect some will be done quickly.

'Brain aging is a natural process that involves structural and functional changes that lead to cognitive decline, even in healthy subjects. This detriment has been associated with NMDA receptor (NMDAR) hypofunction because of a reduction in the brain levels of D-serine, the endogenous NMDAR co-agonist. However, it is not clear whether D-serine supplementation could be used as an intervention to reduce or reverse age-related brain alterations. In the present work, we aimed to analyze the D-serine effect on aging-associated alterations in cellular and large-scale brain systems that could support cognitive flexibility in rats. We found that D-serine supplementation reverts the age-related decline in cognitive flexibility, frontal dendritic spine density, and partially restored large-scale functional connectivity without inducing nephrotoxicity; instead, D-serine restored the thickness of the renal epithelial cells that were affected by age."


Checking through the foods that have high levels of D-serine, I was struck by how many of them feature in the diets that are claimed to be good for aging.

The next one is a bit more high tech and looks at therapy with microscopic biological particles called extracellular vesicles (EVs). These tiny structures naturally transport genetic material between cells. In this experiment they were loaded with microRNAs, molecules that help regulate gene and signalling pathways in the brain and delivered by nasal spray and produced pretty amazing results

"MicroRNAs act like master regulators," Narayana said. "They help modulate and regulate many gene and signaling pathways in the brain."


The third paper is another animal study where the mice were given one of 12 hybrid vitamin K homologs and the results compared. Some were linked to retinoic acid, an active metabolite of vitamin A that is known to promote neuronal differentiation. Others included a carboxylic acid moiety or a methyl ester side chain.


"The newly synthesized vitamin K analogues demonstrated approximately threefold greater potency in inducing the differentiation of neural progenitor cells into neurons compared to natural vitamin K. Since neuronal loss is a hallmark of neurodegenerative diseases such as Alzheimer's disease, these analogues may serve as regenerative agents that help replenish lost neurons and restore brain function."

As with all animal studies it doesn't mean this will work in humans and we will have to wait until human experiments are done. It's nice to see some hopeful results, fingers crossed the results are confirmed in human studies.

Added: I looked at the quantities of D-Serine in foods and it's only a few mg's at best, it's a couple orders of magnitude shy of the therapeutic doses which are around 2 grams a day. At these doses there are health risks, mainly with kidney toxicity, which may limit it's utility.

 
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In a world full of bad news, here is some good news. Amivantamab, a monoclonal antibody, is being trialled for a number of cancers and seems promising for head and neck tumours that are recalcitrant to convenetional therapies.


We are seeing increasingly the promise of 'biologicals' in the treatment of cancers.
Hope, nothing better than that.
 

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