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Comment by Dr. Krishna Kumari Challa on August 5, 2025 at 11:58am

When the first repair attempt stalls at the separating strands (known as the "replication fork"), a set of proteins tasked with stabilizing the fork adds a phosphate—that's the label—to a "signaling" protein. The signal results in the release of the damaged chromosome from a physical tether, allowing it more freedom to move within the nucleus. This release also triggers the formation of microtubules—long polymerized "tracks" of proteins that lead right to the nuclear periphery. The damaged DNA is carried along those tracks to where repair can be completed.

Having uncovered how this backup mechanism for DNA repair works, the scientists who conducted this work points to a potential strategy for treating cancer: Cancer cells have to replicate their genomes really fast, and they may be relying heavily on these backup mechanisms of DNA repair to survive. If we can target DNA repair vulnerabilities, we might have a way to preferentially kill a cancer cell.
That is why we study everything in detail, to use the knowledge in controlling the situations and curing the diseases!

Isn't this more amazing?

Tyler M. Maclay et al, The DNA replication checkpoint targets the kinetochore to reposition DNA structure-induced replication damage to the nuclear periphery, Cell Reports (2025). DOI: 10.1016/j.celrep.2025.116083

Part 2

Comment by Dr. Krishna Kumari Challa on August 5, 2025 at 11:55am

Cells have a second DNA repair toolbox for difficult cases

The human genome consists of 3 billion base pairs, and when a cell divides, it takes about seven hours to complete making a copy of its DNA. That's almost 120,000 base pairs per second. At that breakneck speed, one might expect errors to occur, and they do, at a rate of about two per second in every dividing cell. But cells have a "DNA repair kit" of enzymes that can correct those errors at a rate matching that at which they occur. 

That is amazing!

However, a bigger problem happens when there is a barrier to DNA replication, the process of copying the DNA. It can lead to a break in the chromosome, which will lead to loss of vital genetic information if not repaired. Gaps or breaks in DNA can be potentially harmful or fatal, should they lead to genetic diseases or cancer.

Researchers have  been examining cell DNA repair response to these critical events in yeast cells as an analog to human cells, and has discovered that the process is more elaborate and layered than previously thought.

In a recent study published in Cell Reports,  scientists looked at areas of the DNA that are particularly susceptible to breakage.

Those areas are where the sequence consists of long stretches of repeated triplets like CAGCAGCAG, or couplets like ATATATAT, which continue from just a few to hundreds of units long. When that occurs, the DNA may not always fold neatly into a long double helix, but may twist on itself to form hairpins and cruciform structures—like a tangled electric cord.

This is not a minor issue because repetitive DNA makes up about 10% of our genome, which is even greater than the portion that codes for protein.

When the strands become twisted, the repair proteins that scan the length of DNA can hit a snag and fail to carry out their task. That's when a second set of DNA repair proteins  comes into play.  Scientists are learning that there are backup mechanisms, and now it seems there is a place in the cell where the particularly difficult repairs go to get fixed.

That location is at the inner edge of the cell's nucleus, and a   recent paper by scientists describes how the damaged DNA gets there. The way the DNA gets to the periphery of the nucleus depends on the nature of the damage. For CAG repeats, to use an analogy, it's like adding a shipping label to the damaged goods and sending them out to the repair shop.

Part 1

Comment by Dr. Krishna Kumari Challa on August 5, 2025 at 11:08am

While this work might be groundbreaking, there are still some possible issues that need to be ironed out in future studies. For example, the experiment relies on post selection—where only certain photons are detected, possibly giving misleading results.

Another possible issue comes from a locality loophole due to the phase settings of the detectors not being separated properly. However, the study authors are aware of this study's limitations and are eager to find fixes to these issues and try again.

 Kai Wang et al, Violation of Bell inequality with unentangled photons, Science Advances (2025). DOI: 10.1126/sciadv.adr1794

Part 2

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Comment by Dr. Krishna Kumari Challa on August 5, 2025 at 11:07am

Scientists produce quantum entanglement-like results without entangled particles in new experiment

In the everyday world that humans experience, objects behave in a predictable way, explained by classical physics. One of the important aspects of classical physics is that nothing travels faster than the speed of light. Even information is subject to this rule. However, in the 1930s, scientists discovered that very small particles abide by some very different rules. One of the more mind-boggling behaviors exhibited by these particles was quantum entanglement—which Albert Einstein termed "spooky action at a distance."

In quantum entanglement, two particles can become entangled—meaning their properties are correlated with each other and measuring these properties will always give you opposite results (i.e., if one is oriented up, the other must be down). The strange part is that you still get correlated measurements instantaneously, even if these particles are very far away from each other.

If information cannot travel faster than the speed of light, then there should not be a way for one particle to immediately know the state of the other. This "spooky" quantum property is referred to as "nonlocality"—exhibiting effects that should not be possible at large distances in classical mechanics.

Up until recently, it was thought that only entangled particles could exhibit this nonlocality. But a new study, published in Science Advances, has used Bell's inequality to test whether nonlocal quantum correlations can arise from other non-entanglement quantum features.

The experiment used photons generated by laser light hitting a particular type of crystal in such a way that it is impossible to determine their source. The setup ensures that the photons cannot become entangled before their detection at two separate detectors. The researchers used Bell's inequality to determine if the experiment resulted in violations of local realism.

According to their calculations, the experiment resulted in a violation of the Bell inequality, exceeding the threshold by more than four standard deviations. This kind of violation using unentangled photons had not been seen before. The researchers say these violations of Bell's inequality arise from a property called quantum indistinguishability by path identity, instead of entanglement.

This work establishes a connection between quantum correlation and quantum indistinguishability, providing insights into the fundamental origin of the counterintuitive characteristics observed in quantum physics, the study authors write.

Part 1

Comment by Dr. Krishna Kumari Challa on August 5, 2025 at 10:51am

Scientists design superdiamonds with theoretically predicted hexagonal crystal structure

The brilliantly shiny diamond is more than just pretty; it's one of the hardest minerals on Earth, with a name derived from the Greek word adámas, meaning unbreakable. Scientists have now engineered a harder form of diamond known as bulk hexagonal diamond (HD)—a crystalline structure that has been theorized for over half a century to have physical properties superior to those of conventional diamond.

In a study published in Nature, researchers  synthesized bulk hexagonal diamond, ranging from 100-µm-sized to mm-sized, with a highly ordered structure by compressing and heating high-quality graphite single crystals under pressure conditions as uniform as possible.

The designed material, which was recoverable under ambient conditions, unveiled the previously elusive structural world of HD, opening new avenues for exploring its potential as a technologically superior material.

 Liuxiang Yang et al, Synthesis of bulk hexagonal diamond, Nature (2025). DOI: 10.1038/s41586-025-09343-x

Comment by Dr. Krishna Kumari Challa on August 2, 2025 at 12:17pm

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 August 2, 2025 at 11:06am

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 August 2, 2025 at 10:02am

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 August 2, 2025 at 10:00am

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 August 2, 2025 at 9:52am

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

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