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Reversing fibrosis: New research provides insight for novel therapies

Yale School of Medicine (YSM) researchers have made key breakthroughs in understanding how to treat fibrotic diseases such as scleroderma and graft-versus-host disease.

Fibrotic diseases are a group of conditions—often autoimmune—characterized by excessive tissue scarring. They can drastically hinder patients’ quality of life, and in some cases, they can be life-threatening— contributes to approximately 45% of all deaths in developed nations. However, there are no effective treatments.

Now, in a study published in Blood, researchers have developed a monoclonal antibody that is showing promise as a new therapy for patients. And in a Nature Communications study, the same team discovered a signaling pathway that may be mediating fibrosis and could be a target for future therapies.

Droplet-based bioprinting Reviews Methods Primers

(DBB) enables the fabrication of three-dimensional structures from biomaterials. In this Primer, Gupta and colleagues describe the various DBB modalities and their applications, considerations for the selection of bioinks and substrates, methods to assess printability, the limitations of DBB and their solutions, and potential advances that might be brought about by incorporating new technologies.

Masahiro Hara

After graduating from Hosei University, Hara worked at Denso, a Toyota Group subsidiary, where he began developing a barcode system. [ 6 ] In 1992, at Denso’s development department (later Denso Wave), he was tasked with creating a new 2D code to efficiently track automotive components. [ 7 ] [ 8 ] [ 9 ] [ 10 ] One day during a lunchtime game of go, he realized the black-and-white patterns could encode information. [ 6 ] He also researched publications to find a unique proportion for the position pattern to ensure readability. [ 11 ] The code was introduced in 1994. [ 12 ]

In 2021, QR codes were being used to book and track COVID-19 tests and contact tracing. [ 6 ] Hara has stated that he would like to develop QR codes for additional medical purposes, including imaging such as x-rays or electrocardiogram data. [ 2 ] Hara still works for Denso as of 2024. [ 1 ]

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Researchers reveal intricate control system for key immune gene

The immune system faces a delicate balancing act: It must be aggressive enough to fight infections and cancer, yet restrained enough to avoid attacking the body’s own tissues.

More than two decades ago, researchers identified a gene called FOXP3 as playing a critical role in maintaining this balance and preventing autoimmune disease—work that garnered this year’s Nobel Prize in Physiology or Medicine.

Now, scientists at Gladstone Institutes and UC San Francisco (UCSF) have mapped the intricate network of genetic switches that use to fine-tune levels of FOXP3. Their findings, published in Immunity, have important implications for developing immune therapies and address a long-standing mystery about why this gene behaves differently in humans than in mice.

Hints to the H.I.N.T.S. Exam for Acute Vestibular Syndrome

This Neurology Education Teaching Neurovisual by Sutherland and Gummerson details the Head-Impulse-Nystagmus-Test-of-Skew (HINTS) exam, which uses special maneuvers to identify central etiologies of acute vestibular syndrome with greater sensitivity than hyperacute MRI.


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The psychedelic psilocin suppresses activity of central amygdala corticotropin releasing factor receptor 1 neurons and decreases ethanol drinking in female mice

Alcohol use disorder (AUD) is a highly prevalent disorder with limited therapeutic options. The central amygdala (CeA) is a critical brain region as dysregulation within the CeA and the corticotropin-releasing factor (CRF) system are associated with AUD pathology. CeA CRF1 receptors regulate alcohol drinking and have served as a therapeutic target in alcohol treatment. One emerging potential therapeutic for AUD is psilocybin. Psilocybin has been shown to decrease drinking in some clinical studies however the effects are variable and mechanisms underlying these effects are poorly understood. Psilocybin can engage many brain regions, including the CeA, and may produce therapeutic effects on drinking through interactions with CeA CRF1 neurons. The current study explores the effects of psilocin, the active metabolite of psilocybin, on voluntary ethanol drinking and CeA CRF1 activity to understand the potential mechanisms underlying the therapeutic effects of psilocin. Psilocin acutely decreased ethanol consumption in mice exposed to two different models of chronic ethanol exposure without producing changes in locomotor behavior. Psilocin increased CeA activation and decreased relative CRF1 activation in CeA sub-regions from ethanol-naïve female CRF1:GFP mice. These results were also observed in chronic ethanol-exposed mice at 24hr and 72hr withdrawal timepoints. Psilocin increased corticosterone at 24hr withdrawal but not at 72hr withdrawal. Collectively, these results demonstrate that psilocin engages CeA circuitry and decreases relative CRF1 activation, in parallel with acute reductions in drinking. These results contribute to our understanding of the mechanisms underlying the actions of psilocin and inform the interpretation of therapeutic effects in clinical studies.

Significance Statement Alcohol is one of the most commonly-used substances that dysregulates brain regions involved in emotional processing and stress. An important regulator of the stress response is the neuropeptide known as corticotropin releasing factor (CRF). Alcohol can dysregulate brain regions through the engagement of corticotropin releasing factor receptor 1 (CRF1)-containing neurons and thus promote continued alcohol use. Although alcohol use disorder (AUD) is a highly prevalent condition, few treatment options are available. Psilocybin, a psychedelic prodrug that is broken down into the active metabolite, psilocin, has emerged as a potential treatment for AUD in recent studies. The current study explores the effects of psilocin on alcohol drinking and central amygdala CRF1-containing neurons in female mice to better understand potential therapeutic mechanisms.

Family history key to predicting antidepressant response

A new study from Queen Mary University of London shows that a family’s experience with certain medicines could help doctors predict how future generations will respond to the same drugs.

The researchers found that people were almost five times more likely to have a affecting how they process antidepressants if both they and a parent had stopped taking the same medication early.

Published in Communications Medicine, the study looked at 600 British, Bangladeshi and Pakistani families from the Genes and Health Project—one of the world’s largest community genetics studies.

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