International research led by Istanbul Technical University identifies a previously unrecognized magmatic system, providing new insights into the tectonic evolution of the Neo-Tethys 

Heart failure with preserved ejection fraction (HFpEF) accounts for approximately 50% of global heart failure cases yet lacks robust pharmacological options. This analysis maps HFpEF drug trials registered on ClinicalTrials.gov from 2003 to 2025. A systematic search conducted on November 10, 2025, identified HFpEF-specific drug trials (LVEF ≥50%). Data regarding geography, phases, status, time, and drug classes were descriptively analyzed using R (version 4.3.1). Of the 272 trials, 236 qualified, with a notable surge post-2016 (180 [76.3%]). The majority were U.S.-led (138 [58.5%]). Phase Ⅱ trials were predominant, comprising 92 trials (39.0%), with 111 trials completed (47.0%). The leading classes of drugs included SGLT2 inhibitors (SGLT2i) and novel/targeted therapies, each represented in 31 trials (13.1%). The period from 2021 to 2025 highlighted a focus on SGLT2i and an increase in GLP-1 receptor agonists (GLP-1RA), following recent approvals (sacubitril/valsartan in 2021; empagliflozin/dapagliflozin in 2022–2023; and finerenone by the FDA in 2025). The expansion of trials post-2016 favors metabolic and targeted agents. However, attrition rates underscore the need to prioritize phenotype-specific and combination trials.

Mycobacterial kinase PknG directly phosphorylates host lysine-tRNA ligase (KARS) at T592 and T595, modulating the MAPK/NF‑κB signaling axis and regulating host immunity. Targeting these phosphorylation sites offers a new host-directed therapy against drug-resistant tuberculosis.

While pyridoxal 5’-phosphate (PLP) is considered the bioactive form of vitamin B6 with context-dependent anticancer roles, we redefine its non-phosphorylated precursor, pyridoxal (PL), as a direct and potent cytotoxic agent against ovarian cancer. Using validated patient-derived organoids encompassing diverse histological subtypes and orthotopic in vivo models, we demonstrate that unmetabolized PL triggers lethal oxidative stress independent of PLP conversion. Mechanistically, PL induces PEX11A-dependent peroxisome fission and disrupts PEX5-dependent catalase import, fundamentally switching peroxisomal function from a protective hydrogen peroxide (H2O2) scavenger to a dominant H2O2 generator through accelerated fatty acid β-oxidation. This peroxisome-driven H2O2 surge propagates severe oxidative damage, causing mitochondrial dysfunction, DNA fragmentation, and intrinsic apoptosis. The cytotoxic cascade is significantly rescued by antioxidants, confirming redox imbalance as the primary death mechanism. Our findings reveal an unprecedented mechanism wherein PL exploits peroxisomal metabolism to create a lethal H2O2 overload, effectively repurposing a cellular detoxification organelle into a vulnerability. This work establishes unmodified PL as a novel cancer therapeutic agent by reprogramming redox homeostasis and positions peroxisomal H2O2 flux as a druggable target in ovarian cancer. Inhibiting PL phosphorylation enhances efficacy, offering a promising strategy for targeting therapy-resistant disease.

The tumor microenvironment (TME) is a complex and dynamic ecosystem that plays a pivotal role in cancer progression and therapy resistance. Its heterogeneity and constant remodeling present significant challenges for effective treatment. The emergence of nanomedicine integrates nanotechnology and medicine, aiming to overcome and ameliorate the limitations of conventional therapeutic agents in cancer treatment. Despite the broad biomedical applications of nanomaterials, the clinical translation of nanodrugs remains hindered by the complexity and heterogeneity of the TME as well as challenges related to the physicochemical properties of nanomaterials. This paper published in iMetaMed underscores key challenges and difficulties currently faced by nanomaterials in cancer treatment, including: issues related to nanomaterial biosafety and long-term toxicity assessment; uncertainties in vivo biotransformation and metabolic pathways; therapeutic efficacy variations caused by spatiotemporal heterogeneity of the TME; barriers from laboratory research to clinical translation; and insufficient selectivity in the precise modulation of TME components.

• BacSafe is a comprehensive, open-access bacterial biosafety database covering 20,630 species across 3,902 genera, with 89 biosafety-related attributes per entry compiled from 711,344 genome assemblies, over 2.5 million PubMed publications, and 20,437 food and pharmaceutical recall records.

Dr. Daniel Hajovsky, associate professor in the Department of Educational Psychology at Texas A&M University, studies human intelligence and the cognitive processes that affect learning. In a study published in the Journal of Intelligence, Hajovsky and his co-authors examined the relationship between cognitive abilities and mathematics skills. The findings point to fluid reasoning and comprehension knowledge as two of the most consistent cognitive predictors of math skills.

In a new expert review, researchers examine gaps in how muscle health is addressed in clinical nutrition and lay out a research agenda for moving the field forward. In the review, published in Clinical Nutrition, the experts draw on existing research on muscle health across aging, cancer, critical illness, diabetes and obesity to consider how muscle health can be better incorporated into clinical nutrition.

Ultimately, the authors propose that “muscle health should be recognized as a central and measurable target of clinical nutrition rather than a secondary or downstream outcome.”