Severe hypokalemia is a rare but potentially reversible cause of malignant arrhythmias and cardiac arrest. Early recognition of significant fluid, electrolyte, and acid-base disturbances in patients with intestinal urinary diversion may be life-saving. We present the clinical course of a 55-year-old woman who developed severe hyperchloremic metabolic acidosis and extreme hypokalemia following prolonged vomiting and high-output fluid loss through a Bricker ureteroileocutaneostomy. The patient was admitted to the intensive care unit in a peri-arrest condition, where cardiac arrest occurred shortly thereafter. The monitored rhythm was ventricular fibrillation alternating with "torsade de pointes" ventricular fibrillation. During advanced life support, targeted high-dose intravenous potassium replacement, magnesium sulfate administration, and bicarbonate substitution were performed. A total of 120 mL of 7.4% potassium chloride was administered during resuscitation, resulting in return of spontaneous circulation after approximately 18 minutes. During the first 24 hours, a total of 460 mmol potassium chloride replacement was required. Following the return of spontaneous circulation, intermittent hemodialysis was performed to correct severe metabolic acidosis. During subsequent intensive care treatment, sepsis and bilateral pneumonia developed; however, with targeted antimicrobial therapy, organ support, and continuous electrolyte correction, the patient's condition gradually improved. Successful extubation was performed on day 7, and the patient was transferred back to the nephrology ward with favourable neurological outcome. This case highlights that rapidly developing severe hypokalaemia and metabolic acidosis in patients with Bricker urinary diversion may lead to malignant arrhythmias and cardiac arrest; however, prompt recognition of reversible metabolic abnormalities and aggressive targeted potassium replacement can be life-saving. Orv Hetil. 2026; 167(41): 1664-1668.

G is present on virtually all red blood cells expressing either D or C; thus, identification of anti-G, anti-D, and anti-C in a patient's plasma can be challenging. While identification of anti-G is usually of little clinical significance, it becomes increasingly important in the context of prenatal care. Proper antibody differentiation is necessary to determine candidacy for Rh immune globulin administration to prevent anti-D immunization during pregnancy. We conducted an analytical experimental study of 18 plasma samples from donors and patients with apparent anti-D and anti-C upon initial antibody identification. Samples were tested in duplicate using two established anti-G differentiation methods. Method A consisted of sequential adsorption and elution techniques, and Method B consisted of double adsorption and elution techniques. Of the 18 samples obtained, 14 fit the criteria for inclusion in this study. Both methods successfully identified anti-G and anti-D when present. Method A failed to identify anti-C in one sample. Our results generated a percent positive agreement of 92.9 percent with a 95 percent confidence interval of 68.5-98.7. Our findings demonstrated that Method B detected more antibodies than Method A and allowed for a reduction in testing time, making it the preferred method in this study.

TXNDC11 is an endoplasmic reticulum-associated redox protein involved in protein quality control, but its relevance in acute myeloid leukemia remains incompletely understood. This study examined the expression pattern, prognostic value, and stress-related functional role of TXNDC11 in acute myeloid leukemia using public transcriptomic datasets and experimental validation. Bioinformatic analyses were used to evaluate TXNDC11 expression, survival association, protein interaction networks and pathway enrichment. Loss-of-function experiments were performed in acute myeloid leukemia cell lines to assess cell viability, oxidative stress status, endoplasmic reticulum stress signaling, and responses to the chemical chaperone 4-phenylbutyric acid. TXNDC11 expression was relatively elevated in acute myeloid leukemia samples and higher expression was associated with shorter overall survival. Protein interaction and enrichment analyses connected TXNDC11-associated networks with endoplasmic reticulum-associated degradation, unfolded protein response, endomembrane organization, and apoptosis-related pathways. In THP-1 and HL-60 cells, TXNDC11 knockdown reduced cellular viability and was accompanied by increased reactive oxygen species and malondialdehyde levels, decreased ATP content, reduced glutathione availability, and a lower GSH/GSSG ratio, indicating disruption of redox homeostasis. At the molecular level, TXNDC11 depletion increased GRP78/BiP, p-eIF2α/eIF2α, ATF4, p-IRE1α/IRE1α, cleaved ATF6 p50/full-length ATF6, DDIT3/CHOP mRNA, XBP1s mRNA, HSPA5/BiP mRNA, and cleaved caspase-3, supporting activation of multiple UPR-associated signals and apoptosis-associated marker expression. Treatment with 4-phenylbutyric acid partially attenuated these stress-related molecular and redox changes. Repeated local si-TXNDC11 administration suppressed AML xenograft growth and reduced TXNDC11 expression in endpoint tumor tissues. These findings suggest that TXNDC11 is linked to adverse prognosis in acute myeloid leukemia and may support leukemic cell stress adaptation by limiting endoplasmic reticulum stress-associated redox imbalance and apoptotic signaling.

BackgroundGlaucoma is the leading cause of irreversible blindness worldwide, with primary open-angle glaucoma (POAG) arising as the most common subtype. Recent studies have shown that muscarinic and prostaglandin pathways can modulate bone remodeling under systemic, context-dependent conditions. M3 muscarinic receptor activation has been linked to increased bone formation and decreased resorption, whereas continuous prostaglandin E2 (PGE2) administration inhibits bone resorption, with intermittent use inducing bone formation. Given the minimal systemic findings of topical ophthalmic medications, the clinical relevance of bone remodeling effects for patients treated with glaucoma eye drops, particularly in regard to osteoporosis, remains uncertain and warrants evaluation.Patients and MethodsA retrospective cohort study was conducted using the TriNetX network with approximately 100 million de-identified electronic medical records. Cohorts included POAG patients prescribed either prostaglandin analogs (e.g. latanoprost, bimatoprost, travoprost, tafluprost) without muscarinic agonist use, or muscarinic M3 agonists (e.g. pilocarpine, carbachol) without prostaglandin analog use. Propensity score matching was performed for age, sex, comorbidities, and concurrent glaucoma medications to limit possible cofounders. The outcome was defined as a diagnosis of osteoporosis without current pathological fracture (ICD code M81). Risk ratios (RR), odd ratios (OR), and 95% confidence intervals (CI) were calculated.ResultsAfter matching, each cohort included 6,743 patients. The incidence of osteoporosis is 13.3% in the prostaglandin cohort and 8.9% in the muscarinic cohort. Prostaglandin agonist use was associated with a statistically significant increase in osteoporosis risk (RR = 0.67, 95% CI 0.60-0.73; OR = 0.63, 95% CI 0.57-0.71; p < 0.0001).ConclusionProstaglandin agonist use was associated with an increased risk of osteoporosis compared with muscarinic agonist therapy in POAG patients. These findings suggest potential systemic effects (e.g. changes to bone health) of prostaglandin agonist use beyond previously known local, ocular effects and highlight the importance of considering osteoporosis risk in glaucoma management.

In light of the increasing exposure to folate and its unresolved relationship with skin cancer, experimental studies are warranted to better understand and define its role in skin carcinogenesis. The present study evaluated the effects of folic acid supplementation on cutaneous squamous cell carcinoma (cSCC) in mice and explored the underlying mechanisms. A two-stage skin carcinogenesis model was employed using 7,12-dimethylbenz[a]anthracene (DMBA) and 12-O-tetradecanoyl phorbol-13-acetate (TPA) as initiator and tumor promoter respectively. LACA mice were orally supplemented with folic acid (FA) at doses of 1 or 2 mg/kg body weight and divided into six groups: control, DMBA/TPA, FA1(1 mg/kg) + DMBA/TPA, FA2(2 mg/kg) + DMBA/TPA, FA1 and FA2 groups. Supplementation began 4 weeks prior to tumor induction and continued for twenty weeks. Histopathological analysis confirmed cSCC development. During the early stages, papilloma incidence was higher in FA1 + DMBA/TPA and FA2 + DMBA/TPA groups in comparison to DMBA/TPA group. However, by the end of the treatment period, lesion incidence reached 100% in all groups, with a greater total lesion count and lesion burden observed in the supplemented groups its indicating pro-carcinogenic effects. Enhanced cellular proliferation in these groups was evident from histomorphometric assessments and increased expression of proliferating cell nuclear antigen and folate transporters. Increase in tumorigenesis was also associated with enhanced activity of serum lactate dehydrogenase, oxidative DNA damage and inhibition in expression of MGMT gene. However, no noteworthy difference was observed between two levels of supplementation. These findings suggest that folic acid supplementation may promote skin tumorigenesis through increased proliferation, enhanced DNA damage, and impaired DNA repair mechanisms.

BackgroundAdherence is important for the internal validity of randomized controlled trials (RCTs), but adherence-related reporting in oral Chinese herbal medicine (CHM) RCTs for cancer has not been systematically examined. This study assessed reporting practices before the release of the CONSORT 2025 statement and explored factors associated with intervention completion.MethodsPubMed, Web of Science, EMBASE, and the Cochrane Library were searched for eligible studies published between January 2010 and April 2025. Study characteristics, adherence-related reporting, monitoring methods, and intervention completion were extracted. Binary logistic regression identified factors associated with reporting of adherence-related information. In parallel-group RCTs using CHM only in the intervention group, beta-binomial regression was used as the primary model to assess factors associated with intervention completion.ResultsA total of 113 studies were included, and 51 (45.1%) reported adherence-related information. English-language publication, higher modified Jadad score, and reporting of adherence monitoring methods were associated with reporting of adherence-related information. Only 24 studies (21.2%) described adherence monitoring methods, with diary cards being the most common. Mean intervention completion across the 51 studies was 93.4%. In 43 parallel-group RCTs, placebo use (OR = 0.38, 95% CI: 0.24-0.60; P < 0.001) and syndrome differentiation-guided treatment adjustment (OR = 0.58, 95% CI: 0.37-0.91; P = 0.019) were associated with lower intervention completion in the CHM intervention group, whereas solid dosage forms were associated with higher intervention completion (OR = 2.11, 95% CI: 1.26-3.55; P = 0.005). The directions of the associations were generally consistent across sensitivity analyses.ConclusionBefore the release of CONSORT 2025, adherence-related reporting in oral CHM RCTs for cancer was inadequate and non-standardized. Placebo use, syndrome differentiation-guided treatment adjustment, and oral dosage form were associated with intervention completion. These findings may inform adherence reporting and the design of future CHM trials.

Conventional glofitamab step-up dosing reaches the 30-mg target dose approximately 3 weeks after obinutuzumab. This interval may be difficult to accommodate in patients with relapsed or refractory large B-cell lymphoma (R/R LBCL) who require disease control within days before cellular therapy. We retrospectively evaluated an accelerated bridging schedule of obinutuzumab 1000 mg on day 1 followed by glofitamab 2.5 mg on day 4, 10 mg on day 8, and 30 mg on day 11. Forty-one consecutive adults with R/R LBCL were included. All patients had a documented plan to proceed to chimeric antigen receptor (CAR) T-cell therapy after glofitamab initiation. The cohort was high risk: 90.2% had stage III-IV disease, 70.7% had an International Prognostic Index score of 3%-5%, and 46.3% had central nervous system (CNS) involvement. Cytokine release syndrome (CRS) occurred in 8 patients (19.5%), including 1 grade 3 event; immune effector cell-associated neurotoxicity syndrome (ICANS) occurred in 2 patients (4.9%), both grade 1-2. At the prespecified day-12 assessment, the overall response rate was 80.5% (33/41). Among 19 patients with CNS involvement, 18 (94.7%) responded, and cerebrospinal fluid cytology cleared in all evaluable patients with baseline positivity. After one cycle, 38 of 41 patients (92.7%) proceeded to planned CAR T-cell therapy. In this relatively small retrospective cohort, accelerated glofitamab bridging therapy showed rapid early antitumor activity and manageable toxicity, and a high response rate after subsequent CAR T-cell therapy. Longer-term outcomes could not be attributed to glofitamab alone. These findings are descriptive and require prospective validation.

The Japanese eel (Anguilla japonica) is a commercially important species whose captive reproduction remains challenging. Bone morphogenetic protein 15 (BMP15) is an oocyte-derived factor that plays a key role in regulating folliculogenesis; however, its function in Japanese eel is unclear. In this study, the full-length Japanese eel bmp15 cDNA was cloned and bioactive recombinant BMP15 protein was produced. Weekly co-administration of recombinant BMP15 with FSH and LHRHa for 10 weeks significantly promoted ovarian development, as indicated by increased gonadosomatic index (GSI), larger oocyte area, and elevated serum vitellogenin (VTG) levels compared to hormone treatment alone. Integrated multi-omics analyses suggested that BMP15 exerts its biological functions through a coordinated regulatory network involving anabolic metabolism, glycerophospholipid biosynthesis, nutrient transport, extracellular matrix remodeling, and suppression of steroidogenesis. These findings are consistent with a mechanistic model in which BMP15 simultaneously promotes growth, maintains follicular homeostasis, and optimizes oocyte quality by controlling maturation timing. Our findings identify BMP15 as a potential key regulator of ovarian development in Japanese eel and highlight its potential as a novel homologous factor for improving artificial maturation strategies in eel aquaculture.