Biomedical application of quercetin (QT) as an effective flavonoid has limitations due to its low bioavailability. Superparamagnetic iron oxide nanoparticle (SPION) is a novel drug delivery system that enhances the bioavailability of quercetin. The effect of short time usage of quercetin on learning and memory function and its signaling pathways in the healthy rat is not well understood. The aim of this study was to investigate the effect of free quercetin and in conjugation with SPION on learning and memory in healthy rats and to find quercetin target proteins involved in learning and memory using Morris water maze (MWM) and computational methods respectively. Results of MWM show an improvement in learning and memory of rats treated with either quercetin or QT-SPION. Better learning and memory functions using QT-SPION reveal increased bioavailability of quercetin. Comparative molecular docking studies show the better binding affinity of quercetin to RSK2, MSK1, CytC, Cdc42, Apaf1, FADD, CRK proteins. Quercetin in comparison to specific inhibitors of each protein also demonstrates a better QT binding affinity. This suggests that quercetin binds to proteins leading to prevent neural cell apoptosis and improves learning and memory. Therefore, SPIONs could increase the bioavailability of quercetin and by this way improve learning and memory.
Category: biotech/medical – Page 2,227
Circa 1998
CELL BIOLOGY
F or cells, aging and cancer are often opposite sides of a genetic coin: With “heads,” cells will eventually stop dividing, reaching a permanently quiescent stage called senescence, as do normal human cells in lab cultures. With “tails,” the cells with genetic defects can become immortal and never stop dividing—a common characteristic of cultured cancer cells. Now, a group at Baylor College of Medicine in Houston has found a gene that may help determine which side the coin lands on.
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Researchers have developed a method that could drastically accelerate the search for new drugs to treat mental health disorders such as schizophrenia.
Mental health disorders are the leading cause of disability worldwide, accounting for 31% of total years lived with disability. While our understanding of the biology behind these disorders has increased, no new neuropsychiatric drugs with improved treatment effects have been developed in the last few decades, and most existing treatments were found through luck.
This is mainly because doctors can’t take brain tissue samples from patients in the same way that they are able to do a biopsy on a cancer tumour elsewhere in the body for example, so it’s difficult for researchers to understand exactly what to target when designing new neuropsychiatric drugs.
Induced pluripotent stem (iPS) cells are among the most important tools in modern biomedical research, leading to new and promising possibilities in precision medicine. To create them requires transforming a cell of one type, such as skin, into something of a blank slate, so it has the potential to become virtually any other kind of cell in the body, useful for regenerative therapies for everything from heart disease to diabetes.
However, current methods to induce pluripotency are inefficient: In a batch of 100 cells slated for reprogramming, only five or so complete the transition. A new study published today in Cell Reports by a team of researchers at the University of Wisconsin-Madison’s Wisconsin Institute for Discovery (WID) and School of Medicine and Public Health could improve that efficiency.
It describes combined laboratory and computational methods that lead to better completion of pluripotency, a faster process, and improved understanding of how cells become reprogrammed from one cell type to another, for instance, transforming a skin cell to a cardiac cell. And it includes some surprises, the authors say.
A newly-discovered gene gives infectious bacteria the ability to survive even the strongest antibiotics.
Cornell University biologists found the bacterial gene mcr-9, which when activated makes bacteria resistant to an “antibiotic of last resort” called colistin, according to research published in the journal mBio on Tuesday. If bacteria with the gene were to spread, doctors could find themselves facing a dangerous and perhaps untreatable superbug.
A team of researchers led by Harvard University scientists has improved the laboratory process of converting stem cells into insulin-producing beta cells, using biological and physical separation methods to enrich the proportion of beta cells in a sample. Their findings, published in the journal Nature, may be used to improve beta cell transplants for patients with type 1 diabetes.
In 2014, Douglas Melton’s lab showed for the first time that stem cells could be converted to functional beta cells, taking a step toward giving patients their own source of insulin. In that initial process, beta cells made up 30 percent of the final cell mixture.
“To improve from 30 percent, we needed to really understand the other 70 percent of the resulting cells,” said Adrian Veres, a graduate student in the Melton lab and lead author of the current study. “Until recently, we couldn’t take a sample of our cells and ask what cell types were in there. Now, with the revolution in single-cell sequencing, we can go from nothing to the full list.”
Researchers from King’s College London have found that therapy that can induce heart cells to regenerate after a heart attack.
Myocardial infarction, more commonly known as a heart attack, caused by the sudden blocking of one of the cardiac coronary arteries, is the main cause of heart failure, a condition that now affects over 23 million population in the world, according to the World Health Organisation.
At present, when a patient survives a heart attack, they are left with permanent structural damage to their heart through the formation of a scar, which can lead to heart failure in the future. In contrast to fish and salamander, which can regenerate the heart throughout life.