Shanghai Blood Center

The authors have disclosed no conflicts of interest. Research data are not shared. TABLE S1. The primer sequences and their respective concentrations for TGS. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.

Acute kidney injury (AKI), characterized by inflammation and oxidative stress, is a life-threatening clinical presentation. We previously demonstrated the role of miR-382 in the progression of chronic kidney disease (CKD). However, the role of miR-382 in AKI is unknown. Genetic depletion of miR-382 exacerbated renal dysfunction, histologic lesions, apoptosis of epithelial cells, and oxidative stress in kidneys in ischemia-reperfusion (I/R)- and sepsis-induced AKI. In vitro, downregulation of miR-382 accompanied with activation of phosphorylation of signal transducer and activator of transcription 1 (STAT1) were induced in mouse renal tubular epithelial cells (mTECs) with hypoxia/reoxygenation (H/R) and lipopolysaccharide (LPS) treatments. Colocalization of phosphorylated STAT1 (p-STAT1) and Lotus tetragonolobus lectin (LTL) suggested the activation of STAT1 signaling in renal epithelial after I/R injury (IRI). Overexpression of miR-382 in mTECs abrogated phosphorylation of STAT1, generation of interleukin-6 (Il-6), tumor necrosis factor-α (Tnf-α), and Il-1β as well as reactive oxygen species (ROS) and apoptosis after H/R- and LPS treatments. Additionally, loss of miR-382 was found in isolated macrophages from kidney during I/R-induced AKI. Upregulation of miR-382 in Raw264.7 cells inactivated STAT1 signaling and hindered polarization of M1 macrophages inhibiting Il-6 and inducible nitric oxide synthase (iNos). Inhibition of STAT1 pharmacologically reduced Il-1β, Il-6, and Tnf-α in Raw264.7 after H/R. Taken together, these results demonstrated the protective role of miR-382 in I/R- and sepsis-induced AKI, suggesting miR-382 as a novel therapeutic strategy for AKI.

Plain Language SummaryPeople with chronic kidney disease (CKD) are more likely to develop heart problems, including a condition called left ventricular hypertrophy (LVH), where the heart’s main pumping chamber becomes thickened. This study looked at whether a simple blood test value – the hemoglobin-to-red cell distribution width ratio (HRR) – could help identify CKD patients at higher risk of LVH. A lower HRR may reflect anemia or poor nutrition, both common in CKD. We reviewed data from 195 patients with moderate to severe CKD who were not on dialysis. We found that patients with lower HRR were more likely to have LVH, even after accounting for other health factors. We also explored how two biological markers – parathyroid hormone and N-terminal pro-brain natriuretic peptide – may partially explain the link between HRR and LVH. Our findings suggest that HRR, a routine and inexpensive blood test, may help doctors better assess heart risk in people with CKD.

BackgroundThe Monopterus albus serves as a unique model for studying sex reversal, transitioning naturally from female to male. However, the origins of male germline stem cells (GSCs) and the roles of somatic cells during sex reversal remain poorly understood.MethodsWe performed single-cell RNA sequencing (scRNA-seq) on ovarian, ovotestis, and testicular tissues to construct a gonadal cell atlas. RNA fluorescence in situ hybridization (RNA-FISH) validated cell subpopulations.ResultsCell types of germ cells and somatic cells in gonads were identified, and their differentiation trajectories during sex reversal were depicted. Our results show that GSCswdr17+tep1− in the ovaries possess bipotential differentiation capacity and can transform into GSCswdr17+ tep1+ with the capability to differentiating into sperm during sex reversal. Two theca cell subpopulations cooperate to synthesize steroid precursors in ovaries, with Leydig cells in testes likely originating from theca cell transitions. Proliferative gdf9+ follicle cells promoted folliculogenesis and persisted in male gonads with reduced hsd17b1 expression. Stromal heterogen-eity analysis revealed bmp4+ mesenchymal stem cells (MSCsbmp4+) as potential precursors for Sertoli cells in testes.ConclusionsThis study provides a comprehensive cellular roadmap of gonadal cell dynamics during sex reversal in Monopterus albus. Our findings unveil the molecular mechanisms underlying germline and somatic cell fate determination, offering novel insights into vertebrate sex reversal and potential therapeutic strategies for disorders of sex development (DSD).Supplementary InformationThe online version contains supplementary material available at 10.1186/s13287-025-04810-8.

BackgroundLimited research has examined the direct or indirect effects of social isolation on anxiety symptoms. This study investigated the mediating effect of psychological capital (PsyCap) on social isolation and anxiety symptoms.MethodsThe study included 202 maintenance hemodialysis (MHD) patients from Shanghai Hospital in China. Data collection utilized basic data, social isolation, anxiety self-assessment, and psychological capital questionnaires. Statistical analysis employed PROCESS4.1 and SPSS26.0 for univariate and correlation analyses, with Model 4 being utilized for mediation effect assessment.ResultsSmoking history, heart failure, and dialysis time were identified as significant factors associated with anxiety in MHD patients. Social isolation score is positively correlated with PsyCap (r = 0.442, p < 0.001), and negative correlated with anxiety symptoms (r = −0.786, p < 0.001). The mediating effect of PsyCap accounts for 7.693% of the total effect.ConclusionPsychological capital plays a partial mediating role in the relationship between social isolation and anxiety in MHD patients. It is necessary to strengthen the assessment of social isolation in MHD patients to improve PsyCap and reduce the risk of anxiety symptoms.

HLA-DPB1*1790:01 differs from HLA-DPB1*02:02:01:01 by a single non-synonymous nucleotide change in exon 2.

Fetomaternal hemorrhage (FMH) is a rare perinatal condition characterized by the transplacental transfer of fetal erythrocytes into the maternal circulation. It poses significant risks, including fetal anemia, hydrops fetalis, and maternal alloimmunization, and often remains underdiagnosed due to non-specific clinical presentations and limited diagnostic accessibility. We present a case of a term neonate delivered via cesarean section at 38 weeks’ gestation who exhibited severe anemia and hyperbilirubinemia. Blood group analysis revealed maternal–neonatal Rh incompatibility, while flow cytometry quantified 2.0% fetal erythrocytes in maternal blood. This case underscores the diagnostic value of integrating blood group serology and flow cytometry in FMH confirmation, particularly when standard tests yield equivocal results. A multidisciplinary evaluation of the fetus is the key to early diagnosis and intervention to improve the clinical outcome of perinatal infants.

Passenger lymphocyte syndrome (PLS) is a hematological complication that can occur following transplantation, characterized by donor-derived memory B lymphocytes producing antibodies against the recipient’s blood cells. This review examines the pathophysiology, diagnostic approaches, and treatment strategies aimed at enhancing clinical management and standardizing therapeutic protocols for PLS. A literature search was conducted using Web of Science and PubMed to identify relevant publications on PLS, resulting in 79 studies. Studies were selected based on predefined criteria, including a focus on human donor-derived alloimmunity, documented blood group antigen-antibody interactions, transplantation context, clinical data on outcomes or management, and methodological validity. Only studies containing actual patient data and substantive discussions about PLS were included. PLS commonly presents as hemolytic anemia, accompanied by elevated lactate dehydrogenase (LDH) levels, indirect hyperbilirubinemia, and reduced haptoglobin levels. Diagnosis is primarily based on clinical manifestations and laboratory tests, including the direct antiglobulin test (DAT) and antibody screening. Differential diagnosis is crucial for excluding drug-induced hemolytic anemia and thrombotic microangiopathy. Current treatment strategies for PLS focus on halting hemolysis and restoring hematological balance. First-line treatment includes donor-compatible red blood cell transfusions and high-dose corticosteroids, while refractory cases may necessitate rituximab or plasmapheresis. Despite advancements in PLS management, challenges persist, including delayed diagnosis due to self-limiting cases and a lack of standardized treatment protocols. Future research should incorporate genomic and proteomic biomarkers for accurate diagnosis and risk prediction. Developing mechanism-driven therapies targeting donor lymphocytes and establishing global consensus frameworks can enhance monitoring, improve graft survival, and optimize transplant recipient outcomes.

The HLA-B*51:385 allele differs from HLA-B*51:285 by a single non-synonymous nucleotide change in exon 3.

The HLA-B*15:11:08 allele differs from HLA-B*15:11:01 by a single non-synonymous nucleotide change in exon 4.