People have long given up on the search for the Fountain of Youth, a mythical spring that could reverse aging. But for some scientists, the hunt has not ended—it’s just moved to a different place. These modern-day Ponce de Leóns are investigating whether gut microbes hold the secret to aging well.
The gut microbiome refers to the vast collection of microscopic organisms—bacteria, fungi, and viruses—that largely inhabit the colon. These microbes aid in digestion and produce molecules that affect your physiology and psychology. The composition of the microbiome is influenced by a combination of factors, including genetics, diet, the environment, medications, and age.
I’m a microbiology professor and author of “Pleased to Meet Me: Genes, Germs and the Curious Forces That Make Us Who We Are,” which describes how the gut microbiome contributes to physical and mental health. The discovery that the gut microbiome changes with age has ignited studies to determine whether the Fountain of Youth might be right under your nose, down inside your gut.
【Evaluation of Pirfenidone for the Treatment of Acute Respiratory Distress Syndrome: A Case Report】 Full article: (Authored by Carlie Cressey Brown, et al., from University of Colorado Skaggs School of Pharmacy and Pharmaceutical Sciences (USA), etc.)
Acute respiratory distress syndrome (ARDS) is an acute hypoxemic lung injury typically caused by a predisposing factor such as infection, aspiration, transfusion or shock. While accepted management includes lung protective ventilation strategies, there is currently no mainstay pharmacologic treatment for ARDS. Due to its anti-inflammatory, antioxidant, and antifibrotic properties, pirfenidone presents as a potential therapeutic option for patients with ARDS. This paper presents a case of a patient with ARDS secondary to pneumonia who was refractory to standard therapies and effectively treated with pirfenidone.
Background: Acute respiratory distress syndrome (ARDS) is an aggressive, inflammatory lung injury with a high mortality rate. While accepted management includes lung protective ventilation strategies, there is currently no mainstay pharmacologic treatment for ARDS. Adjunctive pharmacologic treatment may include glucocorticoids, neuromuscular blockade and inhaled pulmonary vasodilators. Due to its anti-inflammatory, antioxidant, and antifibrotic properties, pirfenidone presents as a potential therapeutic option for patients with ARDS. Case Report: We present a patient treated with pirfenidone for ARDS. Our patient was a 31-year-old man who presented to the hospital with dyspnea on exertion and concern for relapsed acute myeloid leukemia. After a complex hospital course, the off-label use of pirfenidone 801 mg three times daily was pursued to treat his ARDS. The patient’s ARDS resolved after 10 days of pirfenidone, with no adverse effects, and he was discharged. Conclusions: This case illustrates the potential utility of pirfenidone in the management of ARDS. After no improvement with widely accepted strategies including lung protective ventilation and steroids, the patient demonstrated recovery after the initiation of pirfenidone. We can infer correlation but not causation in this setting, prompting the need for further prospective randomized clinical trials to establish pirfenidone as a therapeutic option in ARDS.
Exhaustion creeps in. Appetite vanishes. Hair thins. The person in the mirror looks gaunt. It’s the paradox of cancer treatment: The same drugs meant to save a life can also wear the body down. Nick Housley, assistant professor in Georgia Tech’s School of Biological Sciences, wants to change that. He studies where cancer drugs go once they’re inside the body, including places they were never intended to reach. Some of the medicine finds the tumor. The rest interacts with healthy tissue.
This approach has saved millions of lives. It can also create punishing side effects. “The problem isn’t that these drugs don’t work,” said Housley. “It’s that they affect far more of the body than they need to.”
Obesity is an independent driver of cardiovascular disease (CVD), mediated through adverse haemodynamic loading, insulin resistance, systemic inflammation, endothelial dysfunction and prothrombotic pathways. Contemporary obesity therapies show cardiovascular (CV) benefits beyond improvements in traditional risk factors. Across large CV outcome trials, glucagon-like peptide 1 receptor agonists consistently reduce three-point major adverse CV events (MACE) in patients with overweight, obesity and established CVD with and without diabetes. In obesity-related heart failure of preserved ejection fraction, semaglutide and tirzepatide improve symptoms and functional capacity and reduce worsening heart failure events, while effects on CV mortality remain uncertain.
Drug delivery researchers have vastly improved the potential of genetic therapies by overcoming the challenge of consistently getting genes and gene-editing tools where they need to be within cells. Findings of the study spearheaded by Oregon State University College of Pharmacy graduate student Antony Jozić are published in Nature Biotechnology.
When gene therapies enter a cell, they are often sent to lysosomes, the cell’s trash and recycling centers, where therapeutic genetic material is broken down before it can work. For gene therapies to succeed, they must avoid disposal and reach the part of the cell where they can function.
Drug addiction carries an extremely high risk of relapse, as cravings can be reignited by minor stimuli even long after one has stopped using. Previously, this phenomenon was attributed to a decline in the function of the prefrontal cortex (PFC), which regulates impulses. However, a joint international research team has recently revealed that the cause of addiction relapse is not a simple decline in brain function, but rather an imbalance in specific neural circuits.
New research on 175,000 women—the largest NHS study to date—on the use of AI in breast cancer screening shows that AI detected more cases of invasive cancer, more cases overall, had fewer false positives, and recalled fewer women having their first scan than humans did. For one part of the study, AI reduced the time spent reading scans by almost a third.
Through their study, the researchers tracked fluorescently tagged resident tissue macrophages in mouse eyes. When they selectively removed these cells, the eye’s drain, or outflow, became clogged, fluid built up, and eye pressure increased.
The discovery could lead to the development of future glaucoma treatments. The next step will be research to identify these resident macrophages in human eye tissue. “This research helps us understand the role of the immune system in regulating eye pressure,” said Katy Liu, MD, PhD, assistant professor in the department of ophthalmology at Duke University School of Medicine. “Our findings show that resident macrophages are essential for maintaining healthy eye pressure,” said Liu. “Disruption of this system may contribute directly to the development of glaucoma.”
Added W. Daniel Stamer, PhD, the Joseph A.C. Wadsworth Distinguished Professor of Ophthalmology, and co-vice chair for basic science research, “Now we have a specific target for developing new therapies that can normalize the eye pressure and stop vision loss, in contrast to current medications that do not target the source of disease.”