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Category: biotech/medical – Page 2,218

We’re tantalizingly close to growing organs in the lab, but the biggest remaining challenge has been creating the fine networks of blood vessels required to keep them alive. Now researchers have shown that a common food dye could solve the problem.

In the US there are currently more than 100,000 people on organ transplant waiting lists. Even if you’re lucky enough to receive a replacement, you face a lifetime on immunosuppressant drugs. That’s why scientists have long dreamed of growing new organs from patients’ own cells, which could simultaneously tackle the shortage and the risk of organ rejection.

The field of tissue engineering has seen plenty of progress. Lab-grown skin has been medically available for decades, and more recently stem cells have been used to seed scaffolds—either built form synthetic materials or made by stripping cells from natural support structures—to reproduce more complex biological tissue.

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Michigan State University senior vice president Stephen Hsu, a theoretical physicist and the founder of Genomic Prediction, demonstrates how the machine learning revolution, combined with the dramatic fall in the cost of human genome sequencing, is driving a transformation in our relationship with our genes. Stephen and Azeem Azhar explore how the technology works, what predictions can and cannot yet be made (and why), and the ethical challenges created by this technology.

In this podcast, Azeem and Stephen also discuss:

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Cardiovascular disease is a major cause of death worldwide, and treating it isn’t easy. The disease wreaks havoc on patients’ blood vessels and can require complex bypass surgery.

Scientists at the Morgridge Institute for Research are working toward a dream of creating artery banks—similar to banks common today—with readily-available material to replace diseased arteries during surgery.

The latest work in the lab of Morgridge regenerative biologist James Thomson puts the science one step closer to that goal.

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Most antibiotics work by interfering with critical functions such as DNA replication or construction of the bacterial cell wall. However, these mechanisms represent only part of the full picture of how antibiotics act.

In a new study of antibiotic action, MIT researchers developed a new machine-learning approach to discover an additional mechanism that helps some antibiotics kill bacteria. This secondary mechanism involves activating the bacterial metabolism of nucleotides that the cells need to replicate their DNA.

“There are dramatic energy demands placed on the cell as a result of the drug stress. These energy demands require a , and some of the metabolic byproducts are toxic and help contribute to killing the cells,” says James Collins, the Termeer Professor of Medical Engineering and Science in MIT’s Institute for Medical Engineering and Science (IMES) and Department of Biological Engineering, and the senior author of the study.

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Newly identified subsets of cell types present in joint tissue in people with rheumatoid arthritis and how they interact may explain why only some people respond to existing medications, according to two studies by co-senior author Laura Donlin, Ph.D., Co-Director of the Derfner Foundation Precision Medicine Laboratory at Hospital for Special Surgery (HSS) and collaborating colleagues. The findings suggest exciting new targets for developing precision medicine strategies in the future.

Rheumatoid arthritis (RA) is an autoimmune disease that affects the joints. The immune system mistakenly perceives as a harmful invader, like a bacteria or virus, and attacks it, causing inflammation, pain and swelling. RA affects an estimated 1.3 million Americans, about 1% of the population. Critical unmet needs in RA treatment are medications that effectively treat all people with RA, especially those who do not respond to disease-modifying (DMARDs) or biologics.

RA involves a complex interplay between many different types of cells—including T cells, B cells, monocytes and fibroblasts—but the specific subtypes that drive disease progression are largely undefined. Understanding these cell types more precisely may hold valuable information in developing new treatments.

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Deep brain stimulation (DBS), an experimental technology that involves implanting a pacemaker-like device in a patient’s brain to send electrical impulses, is a hotly debated subject in the field of medicine. It’s an inherently risky procedure and the exact effects on the human brain aren’t yet fully understood.

But some practitioners believe it could be a way to alleviate the symptoms of depression or even help treat Alzheimer’s — and now they suspect it could help with drug addiction as well.

In a world’s first, according to the Associated Press, a patient in Shanghai’s Ruijin Hospital had a DBS device implanted in his brain to treat his addiction to methamphetamine.

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Scientists know that age and weight are risk factors in the development of cancer. That should mean that whales, which include some of the largest and longest-lived animals on Earth, have an outsized risk of developing cancer.

But they don’t. Instead, they are less likely to develop or die of this enigmatic disease. The same is true of elephants and dinosaurs’ living relatives, birds. Marc Tollis, an assistant professor in the School of Informatics, Computing, and Cyber Systems at Northern Arizona University, wants to know why.

Tollis led a team of scientists from Arizona State University, the University of Groningen in the Netherlands, the Center for Coastal Studies in Massachusetts and nine other institutions worldwide to study potential cancer suppression mechanisms in cetaceans, the mammalian group that includes whales, dolphins and porpoises. Their findings, which picked apart the genome of the humpback whale, as well as the genomes of nine other cetaceans, in order to determine how their cancer defenses are so effective, were published today in Molecular Biology and Evolution.

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Neuroleptic malignant syndrome (NMS) is rare but one of the most serious adverse effects of antipsychotics. Here, we report a case of risperidone-associated NMS in which a successful rechallenge of risperidone was observed with a positive follow-up. A 47-year-old female with schizophrenia was treated with risperidone 4 mg/d for 8 months in 2009 and was admitted to our hospital in 2015 owing to violent behavior under persecutory delusions. Risperidone 2 mg/d was initiated and increased to 4 mg/d 54 days later. Further, long-acting injectable (LAI) risperidone 25 mg per 2 weeks was added on hospital day 15. On hospital day 116, NMS occurred and thus we discontinued all antipsychotics including LAI risperidone, then NMS improved. We resumed LAI risperidone 25 mg per 2 weeks on hospital day 148, thus we waited for 22 days before re-starting the drug treatment. She was discharged on hospital day 371, then switched to LAI paliperidone 150 mg per 4 weeks 2 months later. At the time of a follow-up 3 years later, NMS had not reoccurred. This case reports on an unusual presentation of NMS in which no hyperthermia was observed. Furthermore, this case indicated that NMS may occur in a dose-dependent manner. In conclusion, this case reported important information for clinicians with regard to antipsychotic drug rechallenges and proper dosing of APs to avoid or reverse NMS.

A 47-year-old female with schizophrenia and without other neuropsychiatric or systemic illnesses was treated with risperidone 4 mg/d for 8 months in 2009. In 2015, she was admitted owing to the violent behavior of attacking her mother-in-law under persecutory delusion with the belief that her mother-in-law was going to murder her and auditory hallucination of hearing her mother-in-law criticize her behind her back. Risperidone 2 mg/d was initiated and increased to 4 mg/d 54 days later. Further, long-acting injectable (LAI) risperidone 25 mg per 2 weeks was added on hospital day 15. She did not receive any mood stabilizers on admission, such as lithium, carbamazepine, valproate. During treatment, the patient complained of soreness and weakness of her whole body, and refused to eat or ambulate on hospital day 116, at which point she was tachycardic with a bpm of 116, but afebrile (36.4°C) with stable blood pressure (113÷72 mm Hg).

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