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Comment by Dr. Krishna Kumari Challa on Saturday

Spider Venom Prevents Tissue Damage After Heart Attack and Stroke

Researchers are using peptides isolated from spider venom to develop treatments for a range of neurological and cardiovascular disorders.

 While a handful of spider venoms are deadly to humans, most are not, and many can be incredibly useful.

Biochemists discovered chemical compounds that can be used to treat stroke, cardiovascular disease, epilepsy, pain, and many more diseases over the years. They  began to realize that these venoms were extremely complex, and most of the compounds in them targeted a class of receptors called ion channels.

Ion channels are the second most common target of all currently available drugs, and they play a role in a range of diseases—primarily nervous system disorders. Many ion channels are very hard to target with small molecules. They're very complex, and they don't have a lot of real estate outside of the cell membrane, so they're really hard to target with antibodies.

So they  decided that they should use the gold mine of spider venom peptides that target these receptors to develop human therapeutics. 

Out of  the peptides they tested 's web spider’s venom stood out in initial screens against relevant ion channels. 

They found that when they delivered it two or four hours after a stroke, they could reduce the brain damage by 80 percent.

In an ischemic stroke, the oxygen supply to cells and tissues of the brain is cut off, which results in a more acidic pH within the affected tissues. This lower pH activates the acid-sensing ion channel 1a (ASIC1a), which in turn causes cell death and permanent tissue damage. By blocking ASIC1a, the Hi1a prevents brain damage progression following an ischemic stroke—even up to eight hours after the event.

Then they went on to show that they could reduce the injury after a heart attack using [Hi1a] as well. 

Saez NJ, et al. Spider-venom peptides as therapeutics. Toxins. 2010;2(12):2851-2871.

Jiang Y, et al. Pharmacological inhibition of the voltage-gated sodium channel NaV1.... ACS Pharmacol Transl Sci. 2021;4(4):1362-1378.

Comment by Dr. Krishna Kumari Challa on Saturday

A baby boy from a nearly 31-year-old frozen embryo

A baby boy born last week to a couple developed from an embryo that had been frozen for more than 30 years in what is believed to be the longest storage time before a birth.

In what's known as embryo adoption, Linda and Tim Pierce used a handful of embryos donated in 1994 in pursuit of having a child after fighting infertility for years. Their son was born Saturday from an embryo that had been in storage for 11,148 days, which their  doctor says sets a record.

According to Dr. John David Gordon, the transfer of the nearly 31-year-old embryo marks the longest-frozen embryo to result in a live birth.

Source: News agencies

Comment by Dr. Krishna Kumari Challa on Saturday

Now, researchers have discovered a primate-specific cytokine called IGFL2, produced by a subset of helper T cells known as peripheral helper T (Tph) cells in the joints of patients with RA.

Their findings, published in Science Immunology, suggest that IGFL2 helps regulate inflammation in the synovial tissue of affected joints and could serve as both a marker of disease activity and a promising target for new therapies.
Using gene expression data from single-cell analysis and clinical information, researchers analyzed individual helper T cells from the joint tissue of patients with RA. They identified a distinct subgroup known as Tph cells, which are closely linked to more severe disease.

Notably, these cells produce IGFL2 (Insulin-like Growth Factor-Like Family Member 2), a cytokine found only in primates. IGFL2 was exclusively expressed in helper T cells within synovial tissue, with the highest levels seen in Tph cells.

The researchers then explored how IGFL2 drives inflammation in RA. They found that IGFL2 boosts the production of a protein called CXCL13, which promotes the production of autoantibodies. Additionally, IGFL2 activates immune cells known as monocytes and macrophages, further amplifying inflammation and joint damage. This is supported by the fact that blocking IGFL2 reduces the activation of these cells.

To assess its clinical relevance, the team measured IGFL2 levels in blood samples from patients with RA. IGFL2 levels were much higher in patients compared to healthy individuals, and even higher in those with more severe symptoms. Its ability to distinguish patients with RA from healthy individuals was similar to commonly used diagnostic markers.

Taken together, these findings suggest that IGFL2 is not just a marker of disease activity but may also actively drive inflammation in RA, making it a promising target for new treatments.
Because this gene is unique to primates, this discovery wouldn't have been possible using conventional animal models like mice or rats.

Human CD4+ T cells regulate peripheral immune responses in rheumatoid arthritis via insulin-like growth factor like family member 2, Science Immunology (2025). DOI: 10.1126/sciimmunol.adr3838

Part 2

Comment by Dr. Krishna Kumari Challa on Saturday

When immune commanders misfire: New insights into rheumatoid arthritis inflammation

Rheumatoid arthritis (RA) is a chronic autoimmune disease in which the immune system mistakenly attacks the lining of the joints (the synovium), causing pain, swelling, and progressive damage. Approximately 18 million people worldwide live with RA. Early diagnosis and treatment can relieve symptoms, slow disease progression, and help prevent disability.

Current therapies focus on reducing inflammation and preserving joint function, but up to 30% of patients do not respond well. This underscores the pressing need to better understand its pathology for early diagnosis and the development of more effective therapies.

Helper T cells are a type of white blood cell that act as the "commanders" of the immune system. They play a crucial role by recognizing threats and coordinating immune responses. However, in autoimmune diseases like RA, these commanders become dysregulated and cause the immune system to attack the body's own tissues.

Although helper T cells are known to be major players in RA, the precise molecular mechanisms driving inflammation are still unclear.

Part 1

Comment by Dr. Krishna Kumari Challa on Saturday

This further reduction was a massive effort to take on. The team made over 101,000 codon changes by dividing up the genome into 38 sections and meticulously swapping out redundant codons with synonymous codons—those that perform the same function. Each time a swap was made, the researchers had to determine if the swap would be detrimental to the viability of the bacteria before moving on.

Mapping and fixing at each stage of the synthesis was often crucial to enabling the next step of the synthesis. These experiments provide a paradigm for integrating 'just in time' defect mapping and fixing of initial designs into synthetic schemes, such that local defects are identified and fixed early in the synthesis and longer range, potentially epistatic or synthetic lethal, defects are identified and fixed as they emerge in the assembly process.

In the end, the research team successfully shortened the genetic code to 57 codons by replacing six sense codons and a stop codon with synonymous codons. The resulting bacteria made with the new code were indeed a living organism, but the researchers found that they grow around four times slower than the parent strain—a problem they hope to eventually fix. However, the new strain shows a distinct gene expression profile, which indicates broad physiological adaptation.

Some possible applications of this new strain include virus-resistant organisms for biotechnology and industry, and the synthesis of proteins and polymers with new properties. Overall, the researchers are optimistic about the potential for this new strain. Their work also raises questions about whether there are limits to reducing the number of codons or creating organisms with entirely novel biochemistries.

Wesley E. Robertson et al, Escherichia coli with a 57-codon genetic code, Science (2025). DOI: 10.1126/science.ady4368

Part 2

Comment by Dr. Krishna Kumari Challa on Saturday

Scientists shrink the genetic code of E. coli to contain only 57 of its usual 64 codons

The DNA of nearly all life on Earth contains many redundancies, and scientists have long wondered whether these redundancies served a purpose or if they were just leftovers from evolutionary processes. Both DNA and RNA contain codons, which are sequences of three nucleotides that either provide information about how to form a protein with a specific amino acid or tell the cell to stop (a stop signal) during protein synthesis.

Altogether, there are 64 possible codon combinations and these combinations are nearly universal for all life on Earth. But some codons are redundant. There are only 20 amino acids available for a cell to work with, and 61 of the 64 codons are available for protein synthesis, while 3 are used as stop signals. This makes for a lot of redundancy in codons.

Some studies suggest that these redundancies might help prevent mutations in DNA, but reducing the genetic code of certain organisms by removing unnecessary parts can also be beneficial. In 2019, a group of scientists reduced the genome of E. coli to 61 codons from 64 by making 18,214 changes. They called the resulting version Syn61 and this virus-resistant version is being used to create more reliable drugs and for manufacturing novel materials.

Now, another group of scientists, some of whom worked on Syn61, have managed to further reduce the genetic code of E. coli down to 57 codons, making Syn57. They recently published their work in Science.

Part 1

Comment by Dr. Krishna Kumari Challa on Friday

COVID and flu can ‘wake up’ cancer
Common respiratory illnesses such as COVID-19 or flu can awaken dormant cancer cells in mice. When a tumour grows, some cells can detach, travel round the body and ‘hide’ in tissues such as the lungs after treatment. Researchers found that the release of an immune molecule called interleukin-6, triggered by respiratory illnesses, wakes up these dormant cells — but only for a short time. This means that the infections do not directly cause cancer, but make it more likely that a future threat could revive the disease.

https://www.nature.com/articles/s41586-025-09332-0?utm_source=Live+...

Comment by Dr. Krishna Kumari Challa on Friday

Microplastics Alter Predator Preferences of Prey through Associative Learning

Exposure to microplastics can give roundworms (Caenorhabditis elegans) a taste for plastic-contaminated food.

When given the choice of plastic-laced or uncontaminated food, worms initially opted for the cleaner option. But after a few generations of worms were exposed to contaminated food, they developed an attraction to contaminated food. This behavior wasn’t seen in mutated worms that had a learning deficit, meaning that the preference for plastic was probably learned and passed down across generations.

https://pubs.acs.org/doi/10.1021/acs.estlett.5c00492

Exposure to microplastic makes animals want to eat it more

Over multiple generations, small nematode worms began preferring microplastic-contaminated food over cleaner options, which could have consequences for ecosystem health

https://www.newscientist.com/article/2488923-exposure-to-microplast...

Comment by Dr. Krishna Kumari Challa on Friday

Changes in diet drove physical evolution in early humans

As early humans spread from lush African forests into grasslands, their need for ready sources of energy led them to develop a taste for grassy plants, especially grains and the starchy plant tissue hidden underground.

But a new study  shows that hominins began feasting on these carbohydrate-rich foods before they had the ideal teeth to do so. The study provides the first evidence from the human fossil record of behavioral drive, wherein behaviors beneficial for survival emerge before the physical adaptations that make it easier, the researchers report in Science.

The study authors analyzed fossilized hominin teeth for carbon and oxygen isotopes left behind from eating plants known as graminoids, which include grasses and sedges. They found that ancient humans gravitated toward consuming these plants far earlier than their teeth evolved to chew them efficiently. It was not until 700,000 years later that evolution finally caught up, in the form of longer molars like those that let modern humans easily chew tough plant fibers.

The findings suggest that the success of early humans stemmed from their ability to adapt to new environments despite their physical limitations.

Isotope analysis overcomes the enduring challenge of identifying the factors that caused the emergence of new behaviors—behavior doesn't fossilize.

Anthropologists often assume behaviors on the basis of morphological traits, but these traits can take a long time—a half-million years or more––to appear in the fossil record.

These chemical signatures are an unmistakable remnant of grass-eating that is independent of morphology. They show a significant lag between this novel feeding behavior and the need for longer molar teeth to meet the physical challenge of chewing and digesting tough plant tissues.

 Luke D. Fannin et al, Behavior drives morphological change during human evolution, Science (2025). DOI: 10.1126/science.ado2359. www.science.org/doi/10.1126/science.ado2359.

Comment by Dr. Krishna Kumari Challa on Friday

Where did potatoes come from? Scientists answer this question in a new research work

Modern-day potato originated from hybridization event with tomatoes 9 million years ago, study reveals

An international research team has uncovered that natural interbreeding in the wild between tomato plants and potato-like species from South America about 9 million years ago gave rise to the modern-day potato.

In a study published in the journal Cell, researchers suggest this ancient evolutionary event triggered the formation of the tuber, the enlarged underground structure that stores nutrients found in plants like potatoes, yams, and taros.

These findings show how a hybridization event between species can spark the evolution of new traits, allowing even more species to emerge. 

As one of the world's most important crops, the potato's origin had long puzzled scientists. In appearance, modern potato plants are almost identical to three potato-like species from Chile called Etuberosum. But these plants do not carry tubers. Based on phylogenetic analysis, potato plants are more closely related to tomatoes.

To solve this contradiction, researchers analyzed 450 genomes from cultivated potatoes and 56 of the wild potato species.

They found that every potato species contained a stable, balanced mix of genetic material from both Etuberosum and tomato plants, suggesting that potatoes originated from an ancient hybridization between the two.

While Etuberosum and tomatoes are distinct species, they shared a common ancestor about 14 million years ago. Even after diverging for about 5 million years, they were able to interbreed and gave rise to the earliest potato plants with tubers around 9 million years ago.

The team also traced the origins of the potato's key tuber-forming genes, which are a combination of genetic material from each parent. They found the SP6A gene, which acts like a master switch that tells the plant when to start making tubers, came from the tomato side of the family. Another important gene called IT1, which helps control growth of the underground stems that form tubers, came from the Etuberosum side. Without either piece, the hybrid offspring would be incapable of producing tubers.

This evolutionary innovation coincided with the rapid uplift of the Andes mountains, a period when new ecological environments were emerging. With a tuber to store nutrients underground, early potatoes were able to quickly adapt to the changing environment, surviving harsh weather in the mountains.

 Ancient hybridization underlies tuberization and radiation of the potato lineage, Cell (2025). DOI: 10.1016/j.cell.2025.06.034. www.cell.com/cell/fulltext/S0092-8674(25)00736-6

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