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Category: biotech/medical – Page 116

ETH Zurich researchers have investigated how tiny gas bubbles can deliver drugs into cells in a targeted manner using ultrasound. For the first time, they have visualized how tiny cyclic microjets liquid jets generated by microbubbles penetrate the cell membrane, enabling the drug uptake.

The targeted treatment of brain diseases such as Alzheimer’s, Parkinson’s or brain tumors is challenging because the brain is a particularly sensitive organ that is well protected. That’s why researchers are working on ways of delivering drugs to the brain precisely, via the bloodstream. The aim is to overcome the blood–brain barrier, which normally only allows certain nutrients and oxygen to pass through.

Microbubbles that react to ultrasound are a particularly promising method for this sort of therapy. These microbubbles are smaller than a , are filled with gas and have a special coating of fat molecules to stabilize them. They are injected into the bloodstream together with the drug and then activated at the target site using ultrasound. The movement of the microbubbles creates tiny pores in the cell membrane of the blood vessel wall that the drug can then pass through.

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A team of engineers and physicists at Southern University of Science and Technology, in China, has created a nickel-based material that behaves as a superconductor above the −233°C (40 K) threshold under ambient pressure. In their study published in Nature, the researchers synthesized thin films of bilayer nickelate (La₂.₈₅Pr₀.₁₅Ni₂O₇) and found one that behaved as a high-temperature superconductor.

The −233°C threshold (40 K), often associated with the McMillan limit, marks a boundary beyond which conventional superconductivity theories become less predictive.

Scientists have been searching for a room-temperature superconductor that could revolutionize a wide range of technologies. The ability to achieve superconductivity without the need for costly and complex cooling systems would significantly reduce energy loss due to heat conversion in electrical transmission, leading to dramatic improvements in efficiency and cost reduction. This breakthrough could lead to advancements in numerous fields, including maglev trains, fusion reactors and MRI machine components. This new effort by the team in China represents another step in reaching the ultimate goal.

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Scientists are exploring gene editing as a way to correct trisomy at the cellular level. Using CRISPR-Cas9, researchers successfully removed extra copies of chromosome 21 in Down syndrome cell lines, restoring normal gene expression.

This breakthrough suggests that, with further development, similar approaches could be applied to neurons and glial cells, offering a potential treatment for those with the condition.

Gene Editing for Trisomy Treatment.

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Basically fungi foods can cure nearly all diseases it just requires the right mushroom for the ailment.

Bioactive compounds and metabolites in mushrooms Mushrooms in ancient healing Edible mushrooms with therapeutic potency References Further reading

Fungi have gained significant attention in the field of phytomedicine as potential natural sources of bioactive compounds and secondary metabolites. Fungi that produce visible fruiting bodies are called macrofungi. Mushrooms are edible macrofungi mainly found in rainy and snow-melting seasons.

Mushrooms form macroscopic fruiting bodies that eventually produce and disperse spores. Mushroom spores contain all the essential components that are needed to produce a new fungus. Mushrooms can exist in nature in many forms, including leathery or woody, fleshy, or sub-fleshy forms.

Mushrooms are probably the most miraculous entities because each mushroom can aid in a different way to cure each illness in the human biology. Much like cannabis is actually a cure all for so many ailments in humans so in turn are mushrooms able to do the same.

Alzheimer’s disease (AD) stands as a formidable neurodegenerative ailment and a prominent contributor to dementia. The scarcity of available therapies for AD accentuates the exigency for innovative treatment modalities. Psilocybin, a psychoactive alkaloid intrinsic to hallucinogenic mushrooms, has garnered attention within the neuropsychiatric realm due to its established safety and efficacy in treating depression. Nonetheless, its potential as a therapeutic avenue for AD remains largely uncharted. This comprehensive review endeavors to encapsulate the pharmacological effects of psilocybin while elucidating the existing evidence concerning its potential mechanisms contributing to a positive impact on AD. Specifically, the active metabolite of psilocybin, psilocin, elicits its effects through the modulation of the 5-hydroxytryptamine 2A receptor (5-HT2A receptor). This modulation causes heightened neural plasticity, diminished inflammation, and improvements in cognitive functions such as creativity, cognitive flexibility, and emotional facial recognition. Noteworthy is psilocybin’s promising role in mitigating anxiety and depression symptoms in AD patients. Acknowledging the attendant adverse reactions, we proffer strategies aimed at tempering or mitigating its hallucinogenic effects. Moreover, we broach the ethical and legal dimensions inherent in psilocybin’s exploration for AD treatment. By traversing these avenues, We propose therapeutic potential of psilocybin in the nuanced management of Alzheimer’s disease.

Alzheimer’s disease (AD) is a progressive neurodegenerative disease that is the leading cause of dementia in the elderly population (Anonymous, 2021). It is characterized by the deposition of amyloid-beta (Aβ) plaques, tau neurofibrillary tangles, and neuroinflammation (Scheltens et al., 2021). The prevalence of dementia is expected to rise as the global population grows and ages, with projections estimating a significant increase in the number of cases (Anonymous, 2022b). In 2019, the total cost of healthcare, long-term care, and hospice services for individuals aged 65 years and older with dementia in the United States was estimated at $2.2billion, so AD imposes a substantial burden on individuals, families, society, and the economy (Anonymous, 2022a). The U.S. Food and Drug Administration (FDA) has approved seven drugs for the treatment of AD, including rivastigmine, donepezil, galantamine, memantine, memantine combined with donepezil, aducanumab and lecanemab.

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Many aspects of inflammation increase with aging in mice and humans. Transcriptomic analysis revealed that many murine anti-aging interventions produce lower levels of pro-inflammatory proteins. Here, we explore the hypothesis that different longevity interventions diminish NF-κB levels, potentially mediating some of the anti-inflammatory benefits of lifespan-extending interventions. We found that the NF-κB protein p65 is significantly downregulated in the liver of several kinds of slow-aging mice. These included both sexes of GHRKO and Snell Dwarf mutant mice, and in females only of PAPPA KO mice. P65 is also lower in both sexes of mice treated with rapamycin, canagliflozin, meclizine, or acarbose, and in mice undergoing caloric restriction. Two drugs that extend lifespan of male mice, i.e. 17α-estradiol and astaxanthin, however, did not produce lower levels of p65.

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Gladstone researchers create a drug that replicates the cellular effects of low-oxygen therapy to treat inherited mitochondrial diseases.

For most people, living at high altitudes—where oxygen levels are lower than at sea level—can offer health benefits, such as reduced rates of heart disease and improved endurance. However, for individuals with inherited mitochondrial diseases, who often do not survive beyond childhood, low-oxygen environments like those at high elevations could be life-saving, potentially prolonging their lifespan and alleviating symptoms.

Now, researchers at Gladstone Institutes have developed a drug that replicates the effects of low-oxygen exposure. In mice with Leigh Syndrome—the most common childhood mitochondrial disease—the drug, called HypoxyStat, extended lifespan more than threefold and reversed brain damage and muscle weakness, even when administered in the disease’s late stages.

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