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Genetic engineering in non-human primates has long been limited by the need for virus-based gene delivery methods. Recently, researchers in Japan successfully used a nonviral system to introduce a transgene—that is, a gene that has been artificially inserted into an organism—into cynomolgus monkeys, which is a species of primate closely related to humans. The paper is published in the journal Nature Communications.

Small animal models such as mice do not fully replicate the complexity of human diseases, particularly in areas like infectious disease and neuropsychiatric disorders. This limitation has made non-human primates an essential model for .

However, genetic modification of these primates has been challenging. For example, conventional virus-based methods require specialized containment facilities and are limited in terms of the size of transgenes that the viruses can carry. Also, these methods do not allow for precise selection of modified embryos before implantation.

This nonrandomized clinical trial reports outcomes for children with low-risk relapsed Hodgkin lymphoma treated with second-line chemotherapy and involved-field radiotherapy without autologous stem cell transplant.

A joint team of professors—Hajun Kim, Taejoon Kwon, and Joo Hun Kang—from the Department of Biomedical Engineering at UNIST has unveiled a novel diagnostic technique that utilizes artificially designed polymers known as peptide nucleic acid (PNA) as probes. The research is published in the journal Biosensors and Bioelectronics.

The fluorescence in situ hybridization (FISH) technique works by detecting fluorescent signals generated when probe molecules bind to specific genetic sequences in bacteria. This innovative FISH method employs two PNA molecules simultaneously. By analyzing the of 20,000 bacterial species, the research team designed PNA sequences that specifically target the ribosomal RNA of particular species.

The method is significantly faster and more accurate than traditional bacterial culture and (PCR) analysis, and it holds promise for reducing mortality rates in critical conditions such as sepsis, where timely administration of antibiotics is crucial.

Description: The American College of Physicians (ACP) developed this guideline based on the best available evidence on the comparative benefits and harms of pharmacologic treatments of acute episodic migraine headache, patients’ values and preferences, and economic evidence about these pharmacologic treatments. Methods: This guideline is based on a systematic review and network meta-analysis of the comparative benefits and harms of pharmacologic treatments of acute episodic migraine headaches, as well as systematic reviews of patients’ values and preferences and comparative cost-effectiveness analyses. The Clinical Guidelines Committee evaluated the following clinical outcomes using the GRADE (Grading of Recommendations, Assessment, Development and Evaluation) approach: pain freedom and pain relief at 2 hours; sustained pain freedom and sustained pain relief up to 48 hours; need for rescue medication within 24 hours; nausea, vomiting, and restored physical function at 2 hours; and overall and serious adverse events (AEs). Additional data on AEs were captured through U.S. Food and Drug Administration medication labels. Audience and Population: The audience for this clinical guideline is physicians and other clinicians. The population is adults with acute episodic migraine headache (defined as 1 to 14 headache days per month) managed in outpatient settings. Recommendation 1: ACP recommends that clinicians add a triptan to a nonsteroidal anti-inflammatory drug to treat moderate to severe acute episodic migraine headache in outpatient settings for nonpregnant adults who do not respond adequately to a nonsteroidal anti-inflammatory drug (strong recommendation; moderate-certainty evidence). Recommendation 2: ACP suggests that clinicians add a triptan to acetaminophen to treat moderate to severe acute episodic migraine headache in outpatient settings for nonpregnant adults who do not respond adequately to acetaminophen (conditional recommendation; low-certainty evidence).

Sleep isn’t just a luxury, it’s a vital process that helps our bodies repair and rejuvenate. Researchers have started to uncover how the quality and timing of sleep can affect more than just how rested we feel—it might also affect the very blueprint of our cells: our DNA.

A new study from Canada found that melatonin, a hormone known for its role in regulating sleep, might help reverse some of the DNA damage caused by years of poor sleep.

Melatonin is produced by the pineal gland in our brains when darkness falls. It signals to our bodies that it’s time to wind down and prepare for sleep. Beyond its sleep-inducing properties, melatonin is also a powerful antioxidant.

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Can you implant lab-grown brain tissue to heal brain damage? Kind of. What if you also implant an electrical stimulation device? The next generation of brain implants may be the Organoid Brain-Computer Interface (OBCI).

Learn about: brain organoids, dendritic spines, synapses, presynaptic and postsynaptic neurons, neurotransmitters.

Story of Einstein’s Brain: https://www.npr.org/2005/04/18/4602913/the-long-strange-jour…eins-brain

Dr. Michael Levin is on the verge of revolutionizing medicine by unlocking the bioelectric code that governs how cells communicate, heal, and build complex structures. His work reveals that intelligence exists at every level of biology—allowing us to reprogram tissues, regenerate limbs, and even suppress cancer by restoring cellular memory and connection.

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Sporotrichosis, a neglected tropical disease caused by Sporothrix species, is a growing concern, particularly due to the emergence of highly virulent, cat-transmitted S. brasiliensis. Rapid diagnosis and surveillance are crucial for controlling sporotrichosis. This study investigated the 3-carboxymuconate cyclase (CMC) gene, which encodes the major Sporothrix antigen (Gp60–70), as a molecular marker to understand the genetic diversity and evolution of these fungi. Analysis of 104 isolates (S. brasiliensis, S. schenckii, S. globosa, and S. luriei) revealed 79 unique haplotypes, demonstrating superior discriminatory power over traditional molecular markers. High–CMC polymorphisms, especially in S. brasiliensis and S. schenckii, suggest recent population expansion or positive selection, potentially driven by environmental pressures such as polyaromatic hydrocarbon pollutants. The conserved chromosomal location of CMC in pathogenic Sporothrix and its absence in less virulent species suggest a role in virulence. Identifying conserved residues within predicted B-cell epitopes provides targets for diagnostics and therapeutics. Additionally, we identified N-linked glycosylation sequons (e.g. NGS at 62, NNT at 225, and NGT at 373/374) conserved in pathogenic Sporothrix but absent in environmental Sordariomycetes, possibly contributing to pathogenicity and niche adaptation. This study establishes CMC as a valuable marker for understanding Sporothrix evolution and virulence, aiding in sporotrichosis management.

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