In this Review, Zelniker and Braunwald summarize the cardioprotective effects of empagliflozin and other sodium–glucose cotransporter 2 inhibitors and discuss the underlying mechanisms of these effects, including haemodynamic modulation, improved mitochondrial bioenergetics and activation of cytoprotective pathways that inhibit oxidative stress, inflammation and fibrosis.
To delineate HDAC10’s function in T cells, we engineered CD4+ T cell-specific Hdac10 knockout (KO) mice (Hdac10fl/fl-CD4Cre) by crossing Hdac10fl/fl mice with CD4Cre mice (Figure S2 A), which were genotyped using PCR (Figure S2 B). The deletion of HDAC10 in CD4+ T cells was confirmed by western blotting (WB) and RT-qPCR (Figures S2 C and S2D). We observed that Hdac10 absence in CD4+ T cells had no effects on T cell development and differentiation in thymus (Figure S2 E and S2F) and T cells composition, apoptosis, or proliferation in spleen and mesenteric lymph nodes (mLN) (Figures S2 G–S2R) at steady state. Collectively, these data demonstrate that HDAC10 is dispensable for steady-state T cell development.
To determine HDAC10’s role in CD4+ T cells during allergic airway inflammation, we employed a neutrophilic asthma mouse model. Hdac10fl/fl-CD4Cre asthmatic mice exhibited lowered airway resistance compared with Hdac10fl/fl asthmatic mice (Figure 2A). Total cell counts and the number of neutrophils in BALF were profoundly reduced in Hdac10fl/fl-CD4Cre asthmatic mice compared with the littermates (Figures 2B and 2C). Hematoxylin and eosin (HE) staining confirmed attenuated inflammation score in Hdac10fl/fl-CD4Cre asthmatic mice (Figures 2D and 2E). Peribronchial trichrome (Masson) and periodic acid Schiff (PAS) staining showed a reduction in collagen deposition and mucus production in Hdac10fl/fl-CD4Cre asthmatic mice (Figures 2F–2I). Furthermore, IHC for myeloperoxidase (MPO) showed reduced neutrophil infiltration in lung tissues of Hdac10fl/fl-CD4Cre asthmatic mice (Figures 2J and 2K).
Mechanical forces regulate development, homeostasis, and repair in the skin, lung, and cornea—external barrier organs that are exposed to stretch, shear, and stiffness. Dysregulated mechanotransduction drives fibrosis, inflammation, and impaired repair via conserved pathways [Piezo1 (Piezo-type mechanosensitive ion channel 1), TRPV4 (transient receptor potential vanilloid 4), and integrin–YAP (Yes-associated protein)]. Targeting these circuits with small molecules, biologics, or stiffness-tuned biomaterials offers a novel category of cross-organ therapies. As mechanosensitive pathways and mechanically informed biomaterials advance toward clinical testing, an integrated cross-organ perspective is urgently needed to address unmet therapeutic needs in chronic barrier diseases. This review unifies disparate insights into biophysics, molecular biology, and clinical practice to reveal how shared mechanisms underpin barrier pathologies and enable breakthrough mechanomedicine treatments.
Fox News senior medical analyst Dr. Marc Siegel discusses how artificial intelligence is advancing medical research and a new drug that may help slow the aging process on ‘America’s Newsroom.’
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After AAV directed evolution led to discovery of a new blood-brain-barrier (BBB) receptor (carbonic anhydrase IV) which facilitates transcytosis, Ding et al. linked a small molecule binder of CA-IV to antibodies, allowing the antibodies to traverse the BBB. This is a major advance since it represents the first time that a receptor target discovered via AAV directed evolution has been adapted to transport other types of molecules across the BBB.
Existing receptor targets to direct delivery of biologics across the blood−brain barrier are ubiquitously expressed in the central nervous system (CNS) and peripheral tissues. Now, carbonic anhydrase IV (CA-IV) is identified as a brain-enriched receptor, enabling selective and prolonged delivery of large molecules to the CNS through conjugation of a small molecule targeting CA-IV.
AI’s business case is no longer hypothetical. AI enhances human potential by managing repetitive tasks at scale, freeing up humans to concentrate on strategy, judgment, and creativity. Organizations in many industries use it to speed up research, streamline operations, and make quicker, more informed decisions. Gains in productivity are genuine and compound.
AI is no longer a luxury in cybersecurity but a necessity. These days, attacks happen at machine speed, and only machine-speed defenses can keep up. AI-driven security solutions are a force multiplier, especially for companies without sizable security staffs, as they identify anomalies, pursue threats, and contain incidents far more quickly than human teams alone.
Above all, AI is a competitive advantage. Businesses that grasp it early will define their markets; those that hesitate will face upending by competitors who do. Financial literacy and AI fluency are quickly becoming equally essential to business leadership.
A remarkably detailed study of Maria Branyas, who lived past 117, reveals that extreme longevity may involve both intense aging and powerful biological protection at the same time. Researchers found signs of advanced aging, but also low inflammation, beneficial gut bacteria, protective genetic features, and a biological age younger than her chronological age. Because she avoided major disease, the study offered a rare look at aging itself rather than the illnesses that often accompany it.
