Fabry disease in mainland China is now mapped through the largest single-centre cohort to date, clarifying how α-galactosidase A deficiency, genotype and sex jointly sculpt the clinical spectrum. Retrospective analysis of 311 genetically confirmed individuals (200 males, 111 females) collected between 2012 and 2022 reveals that 76% present the classical phenotype and 24% the late-onset variant, with male predominance in the former (72%) and female skewing in the latter (62%). Limb pain (67%), hypohidrosis (63%), proteinuria (51%) and angiokeratomas (46%) emerge as the cardinal complaints, followed by renal (58%), cardiovascular (55%) and neuro-psychiatric (58%) involvement. Eye and ear lesions are also common, yet their frequency diverge sharply between sexes and phenotypes.

Ankylosing spondylitis (AS) is increasingly recognized as an independent risk factor for premature myocardial infarction (MI), yet the molecular bridge linking chronic axial inflammation to acute coronary events remains poorly mapped. Mining four public microarray cohorts (GSE128470, GSE73754, GSE100927, GSE122897) that profile peripheral blood mononuclear cells from AS patients, MI patients and healthy controls, integrative bioinformatics now delivers a concise pathogenic blueprint. Weighted gene co-expression network analysis identified one AS-related and one MI-related module that significantly overlap; machine-learning (LASSO + SVM-RFE) distilled these to two hub genes—S100A12 and MCEMP1—whose transcript levels rise concordantly across both diseases. ROC curves yield AUCs of 0.92–0.96 for distinguishing AS-MI cases from either disease alone, and a nomogram incorporating age, CRP and the two hubs achieves a net reclassification improvement of 34 %.

Despite significant advancements in medicine, cancer remains a major health challenge and the leading cause of mortality worldwide, highlighting the urgent need for continued research to identify robust biomarkers for the early detection, prognosis, and treatment across multiple cancer types.

Neutralizing antibodies that merely block receptor binding are losing ground against heavily mutated SARS-CoV-2 Omicron sub-variants. A new approach now exploits a llama-derived nanobody—VHH21—that does not just bind the spike (S) protein but actively tears the trimer apart within seconds. Bactrian camels were immunized with a cocktail of recombinant S proteins from ancestral and VOC strains, yielding a high-diversity VHH phage library. Multi-round biopanning and BLI screening singled out six nanomolar-affinity binders; VHH21, which spontaneously dimerizes, stood out by destroying 68 % of surface-immobilized S-trimers in 20 min, far outperforming ACE2 or conventional nanobodies.