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Molecular mechanism underlying peripartum cardiomyopathy

Scientists have identified a previously unknown molecular safeguard that protects the heart during pregnancy, shedding new light on the causes of peripartum cardiomyopathy (PPCM), a rare and life-threatening form of pregnancy-related heart failure.

In a study published in Nature Communications, the team reveal that the gene the peptidyl-tRNA hydrolase 2 (PTRH2) plays a critical role in helping the maternal heart adapt to pregnancy-induced stress.

In wild-type female mice hearts, Ptrh2 protein levels significantly increase during pregnancy and decrease postpartum, demonstrating a protective role in response to pregnancy-initiated cardiac stresses.

Using advanced mouse models, the researchers showed that loss of PTRH2 leads to severe postpartum heart failure. “During pregnancy, the heart increases in size to account for increased blood flow—but without PTRH2, the heart doesn’t return to normal,” explained a co-first author. “That kind of enlargement can be extremely dangerous and, in many cases, fatal.”

The authors also demonstrate that infusion of a caspase 3-specific inhibitor attenuated the PPCM phenotype. Thus, Ptrh2 act as a negative regulator of pregnancy-induced cardiac stresses by activating pro-survival signals and blocking apoptotic signals.

The findings point to new therapeutic possibilities and underscore the urgent need for better treatments. ScienceMission sciencenewshighlights.

Game-Changing Blood Pressure Drug Works for Patients Not Controlled by Standard Treatments

Blood pressure is one of the most common health problems worldwide, yet it remains difficult to control for many patients even with daily medication. New research from the United Kingdom suggests a different approach could help. Scientists report that a treatment given just twice a year may offer sustained blood pressure reductions for people whose hypertension has proven hard to manage.

The findings come from a large international clinical trial published in JAMA and led by researchers at Queen Mary University of London. The study focused on a long-acting injectable therapy designed to work alongside existing blood pressure medications rather than replace them.

The cytokine TNF is a driver of rheumatoid arthritis, but the signaling-pathway details remain incomplete

Here, Sarah Gaffen & team report on the noncanonical RNA binding protein Arid5a as an activator of TNF signaling that is elevated in human RA tissues. And in mice… its loss results in resistance to collagen-induced arthritis:

The figure shows TNF stimulation causes Arid5a accumulation in the cytoplasm in a murine stromal fibroblast cell line untreated (left) and treated (right); Arid5a (red); RPL7A (green); nuclei (blue).


1Division of Rheumatology & Clinical Immunology, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.

2BIOCEV, First Faculty of Medicine, Charles University, Vestec, Czech Republic.

3School of Medicine, Tsinghua Medicine, Tsinghua University, Beijing, China.

An organ-conformal, kirigami-structured bioelectronic patch for precise intracellular delivery

Now online! Organ-level localized delivery is a long-standing challenge, especially for gene therapy. This study establishes a universal conformality theory that enables POCKET—a kirigami-structured bioelectronic patch—to integrate seamlessly with organs and realize precise intracellular electro-delivery of therapeutics without off-target effects.

Bitly: Among adults with treatment-refractory

HER2-positive BiliaryTractCancer, zanidatamab produced sustained, meaningful clinical responses and extended survival compared to prior standards.

In patients with immunohistochemistry (IHC) 3+ tumors, response rates and overall survival were notably higher than those with IHC 2+ tumors, substantiating the use of reflex IHC testing to identify candidates for HER2-targeted therapy.

Safety remained consistent over 33 months of follow-up, and the ongoing HERIZON-BTC-302 phase 3 trial is assessing zanidatamab alongside first-line standard care in this setting.


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Brain Scans Reveal an “Inflamed Brain Type” Across Major Psychiatric Disorders

Individuals with psychiatric disorders exhibiting seemingly similar symptoms often respond very differently to the same treatment, suggesting that distinct biological processes are at work beneath the surface of similar clinical presentations. Researchers have now identified a distinct immuno-inflammatory biomarker across major psychiatric disorders that can be detected using non-invasive brain imaging. Patients exhibiting this brain signature showed systemic inflammation and poorer response to standard treatments. The findings of the new study in Biological Psychiatry, published by Elsevier, lay the foundation for a biology-augmented diagnostic framework in psychiatry and detail the potential for biomarker-guided, anti-inflammatory precision therapies.

Neuroimaging links diverse biological mechanisms to clinical manifestations, providing compelling insights into the neural mechanisms underlying brain function implicated in psychiatric diseases. Through neuroimaging, shared neural correlates have been increasingly identified across major psychiatric disorders such as schizophrenia, major depressive disorder, and bipolar disorder. While subtypes within and across psychiatric diagnoses have been identified, the biological underpinnings remain unclear. This study aimed to uncover these hidden “biotypes,” focusing particularly on brain inflammation—a mechanism thought to drive illness in a subset of patients, but which is difficult to measure directly in the living brain.

The research was conducted in two independent cohorts. In the first stage, brain connectivity scans were combined with blood-based molecular (DNA methylation) data to identify a brain network pattern linked to immune system dysfunction. In the second longitudinal stage, investigators validated that patients with this brain marker had higher blood inflammation indices—such as neutrophil-to-lymphocyte ratios—and showed less improvement with conventional treatments during hospitalization.

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