A new study meticulously sampled different lung regions in people with cystic fibrosis to understand why infections persist after treatment with new drugs called modulators. These drugs are not curative, but help improve symptoms by addressing the underlying physiological flaw in this genetic condition. Unexpectedly, the new findings suggest that lung damage might not be the main cause of infection persistence. It might be possible that the bacteria is adapting in new ways to resist clearance even when the lungs are being treated with the best drugs available. 

Lithium-based batteries (LiBs) are integral components in operating electric vehicles to renewable energy systems and portable electronic devices, thanks to their unparalleled energy density, minimal self-discharge rates, and favorable cycle life. However, the inherent safety risks and performance degradation of LiB over time impose continuous monitoring facilitated by sophisticated battery management systems (BMS). This review comprehensively analyzes the current state of sensor technologies for smart LiBs, focusing on their advancements, opportunities, and potential challenges. Sensors are classified into two primary groups based on their application: safety monitoring and performance optimization. Safety monitoring sensors, including temperature, pressure, strain, gas, acoustic, and magnetic sensors, focus on detecting conditions that could lead to hazardous situations. Performance optimization sensors, such as optical-based and electrochemical-based, monitor factors such as state of charge and state of health, emphasizing operational efficiency and lifespan. The review also highlights the importance of integrating these sensors with advanced algorithms and control approaches to optimize charging and discharge cycles. Potential advancements driven by nanotechnology, wireless sensor networks, miniaturization, and machine learning algorithms are also discussed. However, challenges related to sensor miniaturization, power consumption, cost efficiency, and compatibility with existing BMS need to be addressed to fully realize the potential of LiB sensor technologies. This comprehensive review provides valuable insights into the current landscape and future directions of sensor innovations in smart LiBs, guiding further research and development efforts to enhance battery performance, reliability, and safety.

Postmenopausal osteoporosis (PMOP) is framed as a systemic bone disease driven by estrogen withdrawal, but emerging evidence positions gut dysbiosis and its fermentation products—short-chain fatty acids (SCFAs)—as equally influential regulators of skeletal fate. Estrogen loss elevates gut permeability, allowing lipopolysaccharide and pro-inflammatory T cells to traffic from intestine to bone marrow, tipping the Th17/Treg balance toward osteoclast-promoting cytokines such as IL-17, TNF-α and RANKL. Germ-free or T-cell–depleted mice do not lose bone after ovariectomy, underscoring the microbiota-immune axis as a mechanistic core.

Lactic acid (LA) has transitioned from being perceived as a mere glycolytic waste product to a pivotal regulator of tumor–immune crosstalk. Historical milestones—from Scheele’s 1780 isolation from sour milk to Zhao’s 2019 discovery of histone lactylation—reveal an expanding biochemical repertoire that now encompasses pH control, G-protein-coupled receptor (GPR81/132) signaling, post-translational modification via lysine lactylation, and multi-directional metabolic shuttling between cytoplasm, mitochondria, and neighboring cells. Within the tumor microenvironment (TME), high glycolytic flux exports lactate and protons through monocarboxylate transporter 4 (MCT4), acidifying the extracellular milieu to ~6.5–6.8. This acidity degrades extracellular matrix, blunts drug uptake, and, via protonation, neutralizes weak-base chemotherapeutics. Cancer cells exploit the same molecule as fuel: MCT1-mediated uptake drives tricarboxylic acid cycle oxidation, NADPH generation via IDH1, and lactylation of DNA-repair proteins NBS1 and MRE11, enhancing genomic stability and chemoresistance. Concurrently, GPR81-cAMP-PKA-TAZ/TEAD signaling elevates PD-L1 expression, facilitating immune escape.

HOXB13, a B-class homeobox transcription factor, sits at the hub of developmental gene networks yet has emerged as a double-edged sword in human cancer. While indispensable for embryonic patterning and androgen-dependent organogenesis, its expression is frequently hijacked or extinguished by epigenetic, mutational and post-translational events that drive tumour initiation, progression and therapy resistance. Across more than twenty malignancies, the protein acts as either oncogene or tumour suppressor, depending on tissue context, interacting partners and mutational status.