Pelvic organ prolapse (POP), a condition whose development is shaped by both genetic and clinical risk factors, significantly impairs women’s quality of life, yet genetic insights into non-European populations and comprehensive risk models that integrate genetic and clinical data remain insufficiently explored. To address this gap, the first polygenic risk score (PRS) for POP in the Chinese population was constructed, leveraging 20 disease-associated genetic variants derived from the largest available genome-wide association study (GWAS) on POP. The research analyzed two cohorts: a discovery cohort comprising 576 POP cases and 623 controls, and a validation cohort with 264 cases and 200 controls. Results confirmed that the POP case group had a significantly higher PRS than the control group; notably, women in the top 10% of PRS values (highest genetic risk) had an odds ratio of 2.6 for developing POP compared to those in the bottom 10% (lowest genetic risk). A high PRS was also found to correlate significantly with POP occurrence in specific subgroups: women over 50 years old and those with one or no childbirths. Additionally, an integrated prediction model combining PRS with clinical risk factors demonstrated better predictive accuracy than existing PRS-only models. This combined risk assessment tool proves robust for POP risk prediction and stratification, providing valuable guidance for personalized preventive measures and treatment strategies in future clinical practice.

Psoriasis, a chronic inflammatory skin disease, relies heavily on abnormal angiogenesis for its pathogenesis, and AlkB homolog 5 (ALKBH5)—an N⁶-methyladenosine (m⁶A) demethylase with known roles in regulating angiogenesis in cardiovascular and eye diseases—has emerged as a key player in this process. In imiquimod (IMQ)-induced psoriasis mouse models, ALKBH5 was found to be upregulated in skin lesions compared to control groups, with co-localization with cluster of differentiation 31 (CD31), an endothelial cell marker linked to angiogenesis. ALKBH5-deficient (ALKBH5-KO) mice showed reduced IMQ-induced psoriatic dermatitis, with histological improvements including thinner epidermis, less hyperkeratosis, fewer dermal capillaries, and decreased inflammatory cell infiltration. These mice also exhibited alleviated angiogenesis in psoriatic lesions, mediated by downregulation of the protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway. In vitro, human umbilical vein endothelial cells (HUVECs) treated with IL-17A— a cytokine critical to psoriasis pathogenesis—showed significant upregulation of ALKBH5, which further promoted the expression of angiogenesis-related cytokines and endothelial cell proliferation. ALKBH5 knockdown in HUVECs suppressed cell proliferation and angiogenesis, while overexpression had the opposite effect, with both processes regulated via the AKT-mTOR pathway. Collectively, these findings highlight ALKBH5’s pivotal role in psoriatic dermatitis and angiogenesis, identifying it as a potential therapeutic target for psoriasis.

Effective axon regeneration is critical for restoring nerve function in patients with axon injury-related neurological diseases, yet adult mammals show limited regenerative capacity in central axonal branches of dorsal root ganglion (DRG) neurons compared to their peripheral counterparts. To explore molecular drivers of this difference, rat sciatic nerve or dorsal root axotomy was performed to examine the expression of dysbindin domain containing 2 (DBNDD2) in DRGs after regenerative peripheral or non-regenerative central axon injury. Results revealed DBNDD2 is down-regulated in DRGs post-peripheral injury but up-regulated after central injury. Additionally, DBNDD2 expression varies between neonatal and adult rat DRGs, increasing gradually with development. Functional tests via DBNDD2 knockdown demonstrated that silencing this gene promotes neurite outgrowth in both neonatal and adult DRG neurons and stimulates robust axon regeneration in adult rats following sciatic nerve crush injury. Bioinformatic analysis further identified that transcription factor estrogen receptor 1 (ESR1) interacts with DBNDD2, exhibits a similar expression trend post-axon injury, and may target DBNDD2. These findings suggest that reduced DBNDD2 levels after peripheral injury and low neonatal DBNDD2 abundance contribute to axon regeneration, highlighting DBNDD2 manipulation as a promising therapeutic strategy for improving recovery after axon damage.

The Healthy China 2030 Plan established a key target of cutting premature deaths from diabetes by 30% by 2030, yet no assessment of diabetes-related premature mortality has been conducted since the plan’s launch. To address this gap, data from the Global Burden of Disease Study 2021 was utilized to calculate diabetes-related premature deaths by sex, province, and disease subtype across China from 1990 to 2021. The average annual percent change (AAPC) was employed to analyze temporal trends in premature mortality for different groups over this period, and projections of such mortality up to 2030 for the entire country and its individual provinces were made based on the average annual change rate observed between 2010 and 2021. Findings revealed that diabetes-related premature mortality first rose slowly, from 0.5% in 1990 to 0.6% in 2004, before declining through 2021, when it reached 0.4%. By 2030, only Fujian Province is expected to achieve the 30% reduction target, with merely seven provinces meeting the goal for females and none for males. Significant disparities in the decline rate exist between inland and coastal regions, highlighting obvious geographic differences and underscoring the need to balance the distribution of medical resources.

Leonurus japonicas Houtt., a medicinal herb with a history dating back to the ancient classical text Shennong Bencao Jing—where it was noted for properties associated with "light body and long life"—has long been valued in traditional medicine under the names Chinese Motherwort or Siberian Motherwort. Renowned as the "sacred medicine of gynecology," it is recognized for effects including activating blood circulation, regulating menstruation, promoting diuresis, reducing swelling, and clearing heat and detoxifying, making it a common choice in clinical settings for treating various gynecological diseases. Within this herb, leonurine stands out as a key alkaloid, endowed with multiple biological activities such as anti-oxidation, anti-inflammation, and anti-apoptosis. Given that cardiovascular and central nervous system diseases pose significant "major health threats" to human life and health globally, and considering the side effects of many existing drugs, a comprehensive exploration of leonurine’s potential therapeutic role in these areas becomes highly relevant. This work focuses on reviewing the potential molecular therapeutic effects of leonurine on diseases affecting the cardiovascular and central nervous systems, emphasizes the latest findings in current research progress, and centers on its therapeutic impacts across different disease conditions. Currently, leonurine is in the clinical experiment stage, and the insights compiled aim to offer guidance for future studies into its molecular mechanisms and its broader clinical application.

Chemotherapy-induced nausea and vomiting (CINV) represents one of the most distressing and debilitating side effects experienced by cancer patients undergoing treatment, significantly impacting quality of life, treatment adherence, and overall therapeutic outcomes. Neurokinin-1 receptor antagonists (NK1RAs) have emerged as cornerstone agents in the modern management of CINV, particularly for delayed-phase symptoms that occur 24-120 hours after chemotherapy administration. These agents target substance P binding to NK-1 receptors in both central and peripheral nervous system pathways, addressing the complex neurotransmitter mechanisms underlying CINV pathophysiology.

Hydrogen sulfide (H₂S)-based mitochondrial energy metabolism blockade is an attractive tumor therapeutic modality. However, it is limited owing to metabolic plasticity, which allows tumors to shift their metabolic phenotype between oxidative phosphorylation and glycolysis for energy compensation. Herein, a hollow-hierarchical H₂S-multistage blasting nanomedicine was designed for a dual-pathway strategy targeting the blockade of energy metabolism and the imbalance of redox homeostasis. Achieved acidic and high glutathione (GSH)-responsive cascade release, presenting a long-term blast of in situ H₂S and calcium overload, coupled with in situ Prussian blue with heat-enhanced peroxidase enzyme activity and loaded glucose oxidase with H₂O₂ self-supply properties, thus exacerbating mitochondrial dysfunction in multiple pathways, disrupting intracellular redox homeostasis, and completely blocking the tumor cell's energy supply of tumor cells. This dual-pathway strategy utilizes H₂S gas-calcium overload to block energy metabolism and induce redox imbalance, providing new insights into exploring energy metabolism blockade as a therapeutic tool for tumor therapy.

Triboelectric nanogenerators (TENGs) are emerging devices with the ability to harvest energy in the environment. TENG usually consists of electrode and polymer layer, and the electrode could use the recyclable materials. However, the polymers commonly used in TENG, such as polydimethylsiloxane (PDMS), Kapton, and so on, which are difficult to degrade completely and prone to release dangerous chemicals in the natural environment. Due to the abundant sources, low cost, and biodegradability, natural biomaterials as friction layers for developing the degradable TENG have attracted considerable attention. However, achieving high electrical output performance and degradability simultaneously in a TENG remains challenging.

Researchers developed a self-assembly, carrier-free prodrug nanoplatform with dual PEGylation and tumor cell membrane coating. The system exhibits high drug loading, strong tumor selectivity, and long in vivo circulation, offering a promising solution to the long-standing challenges of stability and specificity in cancer nanomedicine.

The new release work in Nano Research reveals the critical role of initial lattice distortion (quantified by atomic size difference, δ) in defect formation and capacity decay of vanadium (V)-based alloys. High-δ alloys exhibited greater hydrogen capacity loss, accompanied by increased plateau slopes (S_f) and defect concentrations High-resolution microscopy uncovered a two-stage defect evolution in high-δ alloys: (1) misoriented nanograins formed at the first cycle, generating dislocations; (2) alternating layered nanostructures emerged in subsequent cycles, creating subgrain boundaries and localized strain. Notably, low-δ alloys avoided layered structure formation. These findings propose a design principle—minimizing δ—to develop stable hydrogen storage alloys.