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Comment by Dr. Krishna Kumari Challa on December 7, 2024 at 9:20am

Quality of parent-child relationships predicts adulthood well-being

The link between early life experiences and mental health has been widely explored by psychology researchers. One key aspect of human early life experiences is the relationship that people develop with their parental figures, which is at the center of attachment theory and various other psychological models.

Past studies suggest that the quality of relationships between parents and their children plays a role in the subjective well-being of these children when they reach adulthood. While this finding is well-documented, many past studies were conducted on relatively small samples of participants residing in a single country.

The countries included in this study were selected carefully, to maximize religious and ethnic diversity in the sample. The objective was to include people living in all the broader geographical regions on Earth.

Now two researchers at Gallup, recently carried out a study aimed at exploring the link between parent-child relationships and an adult's self-reported well-being in a larger and more varied sample that spanned across 21 countries.

Their paper, published in Communications Psychology, suggests that the quality of parent-child relationships predicts the well-being of adults residing in all of the countries they studied.

The researchers  found a substantial effect of parent-child relationships on both flourishing and mental health. The effect was larger than any other variable they tested, including parental socio-economic status, current education level, current household income, gender, and financial security.

The relationship was positive in every country, and it reached conventional levels of significance in all but one. Even that exception seemed to be explained by the relatively young population in the survey. When the researchers re-weighted the data to make the ages similar across countries, they found a significant effect in every country.

Overall, the findings of this research study suggest that there is a universal link between parent-child relationships and lifelong well-being, which applies to all people, irrespective of where they were raised.

 Jonathan T. Rothwell et al, Parent-child relationship quality predicts higher subjective well-being in adulthood across a diverse group of countries, Communications Psychology (2024). DOI: 10.1038/s44271-024-00161-x.

Comment by Dr. Krishna Kumari Challa on December 6, 2024 at 11:49am

Does CPR help both the conditions of cardiac arrest and heart attacks?

CPR is primarily used to treat cardiac arrest, not a heart attack; while chest compressions might be used in some situations during a heart attack, full CPR is typically not recommended unless the heart attack progresses to cardiac arrest, where the heart stops beating completely, meaning CPR is used to keep blood circulating until further medical intervention is available. 

Cardiopulmonary resuscitation (CPR) plays an important role in the early treatment of a heart attack if the heart stops beating.

CPR is an emergency treatment. It helps keep blood moving throughout a person’s body when their heart stops beating, which healthcare professionals refer to as cardiac arrest. CPR helps extend the opportunity for successful resuscitation.

Not everyone who has a heart attack needs CPR. It is only necessary if a person goes into cardiac arrest.

Comment by Dr. Krishna Kumari Challa on December 6, 2024 at 11:38am

Researchers reprogram immune cells to decrease rejection of medical implants

Researchers have discovered that using a drug that is a metabolic inhibitor  makes the body more receptive to medical devices such as pacemakers, replacement joints and dental implants.

When doctors surgically place an implant into a human, there will always be an immune response and there's a chance the implant will be rejected.

Scientists used a drug that signals the body to boost or inhibit a particular reaction, called a metabolic modulator. This drug was incorporated into an amorphous polylactide—a biomaterial used to make medical implants—and then the material was implanted in mice.

Using intravital microscopy—a technique that allows us to look inside a living subject under a microscope—the researchers imaged different kinds of immune cells around the implant site for up to 10 weeks.

Their paper is published in the journal Nature Biomedical Engineering.

These findings have significant implications for improving patient recovery times, reducing postsurgical complications like chronic inflammation and implant rejection and potentially saving costs. And they may eventually affect the way medical device manufacturers and pharmaceutical scientists approach medical implants.

Chima V. Maduka et al, Immunometabolic cues recompose and reprogram the microenvironment around implanted biomaterials, Nature Biomedical Engineering (2024). DOI: 10.1038/s41551-024-01260-0

Comment by Dr. Krishna Kumari Challa on December 6, 2024 at 11:33am

Researchers studied the flocculus and paraflocculus' role in the brain to better understand how their malformation could influence behavior. They found that the neural circuits within the flocculus and paraflocculus are dysfunctional.
The regions also control a reflex that ensures stable vision during head movements and is crucial for face recognition. The researchers found that this reflex is impaired in 22q. This may be a valuable lead for schizophrenia research because patients with schizophrenia have a deficit in face recognition.
The paraflocculus is also connected to the auditory cortex.

Tae-Yeon Eom et al, Tbx1 haploinsufficiency leads to local skull deformity, paraflocculus and flocculus dysplasia, and motor-learning deficit in 22q11.2 deletion syndrome, Nature Communications (2024). DOI: 10.1038/s41467-024-54837-3

Part 2

Comment by Dr. Krishna Kumari Challa on December 6, 2024 at 11:31am

Genetic risk for schizophrenia linked to a malformed skull

The chromosomal disorder 22q11.2 deletion syndrome (22q) has emerged as one of the strongest risks for schizophrenia. Scientists at St. Jude Children's Research Hospital identified malformed regions of the cerebellum in laboratory models and patients with 22q and found that these malformations were caused by improper skull formation. Further, the researchers linked the skull malformation to the loss of one gene: Tbx1.

The research shows that neurological disorders can stem from sources beyond the nervous system, such as improper skull development. The findings were published today in Nature Communications.

Gene removal blocks skull pocket from forming.

Previous work from scientists found that the deletion of only one 22q gene, Dgcr8, disrupts the flow of auditory information from a lower brain region called the thalamus to the auditory cortex, where sounds are interpreted. This region of the brain is also associated with auditory hallucinations, which are a hallmark symptom of schizophrenia. The researchers called this breakdown in information flow "thalamocortical disruption."

Although thalamocortical disruption occurs late in development, which is consistent with the onset of schizophrenia symptoms, it stays and doesn't go away. However, hallucinations are transient in nature—they come and go.

It seemed that this was just one of the hits that triggered symptoms.

The researchers noticed a part of the brain, the cerebellum, malformed in 22q animal models, specifically, the cerebellum's small lobules called the flocculus and paraflocculus. Most neurodevelopmental disorders arise from defects in genes that play a role in the brain, but the 22q gene the researchers linked to this malformation, Tbx1, was unexpected.

What is interesting about Tbx1 is that it is not very well expressed in the brain, especially the adolescent or adult brain. Rather, it's expressed in the surrounding tissues, namely bone, cartilage and vasculature tissues. It is very unlikely that Tbx1 directly affects the brain at all.

Instead, removing Tbx1 has an indirect but significant effect on brain development. Bone formation relies on immature osteoblast cells correctly growing into mature osteocytes. Tbx1 removal disrupted this cycle, resulting in an underdeveloped pocket in the skull which normally houses the flocculus and paraflocculus.

For a neurological syndrome, the findings are strikingly unusual—with no pocket in the skull for these structures to develop, they appear substantially smaller than normal. The reduction of the flocculus and paraflocculus was validated through magnetic resonance imaging studies of dozens of patients with 22q and a comparative control group.

Part 1

Comment by Dr. Krishna Kumari Challa on December 6, 2024 at 11:16am

Scientists have data representing genetic material from 50,000 E. coli samples gathered from four continents. When they studied these, they saw that the ability to produce the toxin is very limited and is primarily found in two particular genotypes of E. coli bacteria. Both of these circulate frequently in Norway and they are also the main genotypes causing infections in the bloodstream in the country.
In contrast, these genotypes of bacteria are rarely found in countries of South Asia.
The scientists involved in this study have therefore put forward a number of hypotheses on which ecological conditions drive these unwanted bacterial families away from certain population groups.
If scientists can succeed in developing vaccines against the harmful type of E. coli that produces colibactin, or a form of probiotics, this would result in notable public health benefits. These measures could eliminate the unwanted colibactin-producing bacteria from the intestines.

Tommi Mäklin et al, Geographical variation in the incidence of colorectal cancer and urinary tract cancer is associated with population exposure to colibactin-producing Escherichia coli, The Lancet Microbe (2024). DOI: 10.1016/j.lanmic.2024.101015. www.sciencedirect.com/science/ … ii/S2666524724002830

Part 2

Comment by Dr. Krishna Kumari Challa on December 6, 2024 at 11:09am

Scientists explore role of intestinal bacteria in cancer prevention

The link between intestinal bacteria and cancer

Certain intestinal bacteria are found more frequently in some countries such as Norway than in a number of other countries and there is also a higher incidence of bladder cancer, bowel cancer and prostate cancer. These findings may lead to new opportunities for preventing these types of cancer, according to a new study.

Previous studies have shown that a toxin produced by certain bacteria in order to dominate inside the intestine, causes damage to healthy cells and increases the risk of developing bowel cancer.

In a new study, scientists examined the incidence of bladder, colon, rectal and prostate cancer and compared this to the prevalence of two toxin-producing E. coli bacteria in the countries concerned. E. coli is the most common cause of urinary tract infections and bacterial infections in the bloodstream worldwide. Norway has a higher incidence of bladder cancer and colorectal cancer compared with many other countries.

In the course of the study, scientists also found that the prevalence of these two E. coli bacteria was higher in Norway. When they compared equivalent data from several different countries, they discovered a clear pattern: the fewer of these E. coli bacteria that circulate in the population, the lower the incidence of these types of cancer, and vice versa, and the study recently published in The Lancet Microbe confirms this.

In recent years, intense research has been carried out internationally on the link between the toxin produced by these bacteria, called colibactin, and several types of cancer. The research was initiated after groundbreaking studies revealed that colibactin damages DNA in intestinal cells and scientists produced models of intestinal organs and saw that the toxin-producing E. coli resulted in cancer in the models.

Part 1

Comment by Dr. Krishna Kumari Challa on December 6, 2024 at 10:37am

How hummingbirds fly and feed

Comment by Dr. Krishna Kumari Challa on December 6, 2024 at 9:42am

Engineered immune cells to tame inflammation

When the immune system overreacts and starts attacking the body, the only option may be to shut the entire system down and risk developing infections or cancer. But now, scientists  may have found a more precise way to dial the immune system down.

The technology uses engineered T cells that act as immune "referees" to soothe overreacting immune responses. They also can mop up inflammatory molecules.

The new approach could be used to stop the body from rejecting transplanted organs and tissues, such as pancreatic islet cells, which are sometimes used to treat type 1 diabetes. That way, recipients would not need to take harsh immunosuppressant drugs.

This technology can put the immune system back into balance.

The research The team adapted the suppressor cells' anti-inflammatory abilities to work in CD4 immune cells. These are the same cells that are used to make cancer-killing CAR T cells. They also gave these cells a molecular sensor to guide them to their target tissue in the body.

Proof of principle in type 1 diabetes :

The scientists tailored a batch of immune referees to search for human pancreatic islet cells and then produce TGF-Beta and CD25, molecules that can muzzle killer T cells.

They introduced the engineered referee cells into mice that had received a transplant of human islet cells, modeling the treatment for type 1 diabetes.

The referee cells found the vulnerable islet cells and stopped the killer T cells from attacking, and the islet cells survived.

 Nishith R. Reddy et al, Engineering synthetic suppressor T cells that execute locally targeted immunoprotective programs, Science (2024). DOI: 10.1126/science.adl4793. www.science.org/doi/10.1126/science.adl4793

Comment by Dr. Krishna Kumari Challa on December 5, 2024 at 2:19pm

To get the cell to use homology-directed repair, the researchers recently began using a molecule called AZD7648, which blocks fast repair and forces the cell to use homology-directed repair. This approach is expected to accelerate the development of more efficient gene therapies. Initial studies with these new therapies have been good. Too good to be true, as it turned out.

A research group led by Corn has discovered that the use of AZD7648 has serious side effects. The study has been published in the journal Nature Biotechnology.

Although AZD7648 promotes precise repair and thus precise gene editing using the CRISPR-Cas9 system as hoped, in a significant proportion of cells this has led to massive genetic changes in a part of the genome that was expected to be modified without scarring.

The ETH researchers found that these changes resulted in the simple deletion of thousands and thousands of DNA building blocks, known as bases. Even whole chromosome arms broke off. This makes the genome unstable, with unpredictable consequences for the cells edited by the technique.

When the researchers analyzed the genome at the sites where it had been edited, it looked correct and precise. But when they analyzed the genome more broadly, they saw massive genetic changes. These are not seen when you only analyze the short, edited section and its immediate neighborhood.

The extent of the negative effects surprised the researchers. In fact, they suspect that they do not yet have a complete picture of the full extent of the damage because they did not look at the entire genome when analyzing the modified cells, only partial regions.

New tests, approaches and regulations are therefore needed to clarify the extent and potential of the damage.

The development of any new technology is a rocky road. One stumble does not mean we give up on the technology, say the researchers.

Gene therapies based on the CRISPR-Cas system have already been successfully used in clinical practice. In recent years, for example, a hundred patients suffering from the hereditary disease sickle cell anemia have been treated with CRISPR-Cas-based therapeutics—without AZD7648.

"All patients are considered cured and have no side effects".

Grégoire Cullot et al, Genome editing with the HDR-enhancing DNA-PKcs inhibitor AZD7648 causes large-scale genomic alterations, Nature Biotechnology (2024). DOI: 10.1038/s41587-024-02488-6

Part 2

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