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Patients with multiple myeloma (MM) who experience early relapse (ER) within 24 months of autologous stem cell transplantation (ASCT) have inferior overall survival and represent a functionally high-risk (HR) subgroup. To investigate immune features of functionally HR MM, we performed immunohistochemistry (IHC) of the bone marrow and high-dimensional flow cytometry-based phenotyping of peripheral blood to evaluate the T-cell compartment of patients with MM at day 100 after ASCT. An initial IHC-based analysis of a cohort of patients with MM (n = 110) with long-term follow-up implicated CD3+PD-1+ T cells as a marker of functionally HR disease independent of maintenance therapy or cytogenetics, suggesting a role for activated T cells as a biomarker of disease biology. Next, to further refine the immunophenotype associated with ER, we conducted flow cytometry of peripheral blood samples from Blood and Marrow Transplant Clinical Trials Network (BMT CTN) 0702 trial participants with ER (n = 45) or long-term remission (LR; n = 51), defined as no relapse for >4 years of follow-up. Unsupervised clustering followed by multivariate logistic regression identified the differential expression of HLA-DR, granzyme B, CTLA4, CD27, TIGIT, and CD38 within discrete T-cell subsets, distinguishing ER from LR patients. After variable reduction and validation, CD38 expression by CD8+Eomes+ effector memory T cells emerged as the most predictive feature segregating ER from LR patients, with an area under the curve (AUC) of 86%. This immunophenotype was corroborated in a separate standard-of-care cohort (n = 18). Thus, flow cytometric analysis of peripheral blood at day 100 after ASCT identified a CD8+CD38+ T-cell subpopulation as a key feature of immunologically HR MM.

Spinal surgery, particularly spinal decompression and fusion surgery, commonly encounters intraoperative bleeding. Deep bleeding in the narrow operative area (e.g. bone marrow cavity and venous plexus) is a significant challenge for achieving accurate hemostasis with traditional strategies, posing a life-threatening risk. Herein, a novel dual-form hemostatic material (CMC-Gelatin, CG) composed of carboxymethyl cellulose (CMC) and gelatin is developed for non-compressible hemostasis in spinal surgery. For minor bleeding, CG in powder form reduces blood loss by 69.06% within a mouse bleeding model, demonstrating hemostatic efficacy comparable to that of the commercial Surgicel® powder, while exhibiting superior cytocompatibility. Notably, CG powder rapidly forms an injectable gel upon mixing with saline, making it suitable for severe bleeding in a confined space during spinal surgery. Specifically, in a pig paraspinal microvenous hemorrhage model, CG gel exhibits excellent hemostatic performance, reducing blood loss by 78.44% compared with the untreated group. Importantly, CG demonstrated a comparable hemostasis time and reduced blood loss in vivo compared to the commercial Surgiflo®. The designed CG materials exhibit outstanding hemostatic properties in deep, narrow areas, making them a promising hemostatic material in spinal surgery.

A man in his early 50s with no significant prior renal history was admitted with acute kidney injury and sepsis secondary to right lower limb cellulitis, requiring prompt multidisciplinary management and further evaluation of the underlying etiology. Initial treatment included hemodialysis, following which the patient developed polyarticular septic arthritis (PASA), a rare condition. Examination revealed significant swelling and tenderness in multiple joints, and microbiological analysis confirmed a Staphylococcus aureus infection. Hemodialysis precipitated the bloodstream infection, as blood cultures were negative before hemodialysis but positive for Staphylococcus aureus post-dialysis. The patient underwent multiple joint washouts and was treated with intravenous vancomycin and linezolid. The patient's renal function normalized after treatment, and his symptoms resolved without recurrence. This case highlights the potential for PASA in an immunocompetent individual after a single hemodialysis session, emphasizing the role of catheter-related bloodstream infection (CRBSI) in its pathogenesis and underscoring the importance of timely diagnosis and treatment to prevent severe outcomes. Such presentations underscore the importance of heightened clinical vigilance, as delayed recognition can result in significant morbidity.

Cerebral venous thrombosis (CVT) is an uncommon cerebrovascular condition with highly variable clinical presentations and a wide spectrum of underlying causes. Iron deficiency anemia (IDA) has been increasingly recognized as a significant predisposing factor for CVT. We describe the case of a 45-year-old woman who presented with a gradually intensifying headache, followed by acute onset of left facial palsy and left-sided weakness. Laboratory tests demonstrated microcytic, hypochromic anemia, consistent with IDA. Computed tomography (CT), magnetic resonance imaging (MRI), and magnetic resonance venography (MRV) revealed thrombosis of the right transverse sinus, accompanied by venous infarction and intracranial hemorrhage. An extensive workup showed no evidence of hereditary thrombophilia or autoimmune disease. Subsequent evaluation identified a uterine fibroid causing chronic menorrhagia, which was considered the primary source of her IDA. Anticoagulation therapy was started with low-molecular-weight heparin (LMWH) and later transitioned to apixaban. She also received iron supplementation and blood transfusion. Her neurological deficits gradually improved, with no progression of the intracranial hemorrhage and no new thrombotic events. Follow-up imaging showed substantial resolution of venous edema and mass effect; however, MRV continued to demonstrate persistent occlusion of the right transverse sinus. Anticoagulation was stopped four months after disease onset, and no recurrence occurred during subsequent follow-up. This case underscores several key clinical considerations. First, IDA resulting from chronic gynecologic blood loss should be recognized as a modifiable risk factor for CVT. Second, anticoagulation can be used safely in patients with hemorrhagic CVT, even in the presence of severe anemia. Third, good clinical and radiologic outcomes are possible despite incomplete venous recanalization. Collectively, these observations suggest that restoration of overall cerebral venous hemodynamics, rather than recanalization by itself, may be crucial for recovery from CVT.

This study aimed to identify and validate potential endoplasmic reticulum stress-related biomarkers of focal segmental glomerulosclerosis(FSGS). Five microarray datasets were downloaded from the GEO database. The endoplasmic reticulum stress-related genes were extracted from GeneCards database. GSE104948, GSE129973, and GSE121233 datasets were used to identify DEGs by limma R package. WGCNA was performed to obtain hub gene modules. We intersected the DEGs, genes from hub module of WGCNA, and ERSRGs. GO and KEGG pathway enrichment analyses were performed. LASSO, SVM-RFE, and RF algorithms were used to screen characteristic genes. Further, GSE108109 and GSE104066 were used as validated datasets. Box plots, ROC curves, and AUC were created to identify potential biomarkers. A novel nomogram model was constructed using potential biomarkers. Immunohistochemistry validated the expression of the potential biomarkers, and correlation analysis was used to assess the correlation between the integrated optical density(IOD) value of GADD45A and the levels of 24-hour urinary protein, eGFR, and blood urea nitrogen. Intersecting DEGs, the brown module genes, and ERSRGs, we identified 15 hub ERSRGs of FSGS. AGO2, CCND1, GADD45A, TRAM2, and PTPN1 genes were screened by using Lasso, SVM-RFE, and RF. Further, CCND1, GADD45A, and TRAM2 were validated as significant in training and validation datasets. A nomogram based on CCND1, GADD45A, and TRAM2 expression was constructed. The calibration curves, decision analysis curve, and clinical impact curve showed that the nomogram had good consistency and clinical practical benefit. The expression of GADD45A is higher in FSGS than controls in immunohistochemical(IHC) results(P&#x202f;<&#x202f;0.0001). The integrated optical density value of GADD45A shows a strong correlation with 24-hour urinary protein(r 2&#x202f;=&#x202f;0.8459,P&#x202f;<&#x202f;0.0001), eGFR(r 2&#x202f;=&#x202f;-0.8233,P&#x202f;<&#x202f;0.0001), and blood urea nitrogen(r 2&#x202f;=&#x202f;0.8695,P&#x202f;<&#x202f;0.0001). GADD45A may be a potential biomarker associated with endoplasmic reticulum stress in FSGS.With its potential applicability spanning both biomarker identification and therapeutic intervention, GADD45A offers a compelling avenue for improving FSGS detection and clinical management in subsequent investigations.

Norrin, secreted by retinal M&#xfc;ller cells, activates canonical Wnt signaling via Frizzled-4 and co-receptors. Loss-of-function mutations abolish intraretinal capillary formation in mice. In humans, mutations in NDP, which encodes norrin, cause Norrie disease, characterized by retinal hypovascularization and congenital blindness, and X-linked familial exudative vitreoretinopathy (FEVR), resembling retinopathy of prematurity (ROP). We evaluated adeno-associated viral (AAV) vectors expressing norrin as gene therapy for Norrie disease, FEVR, and ROP. AAV2-7m8 and AAV-ShH10 were tested in juvenile wild-type and norrin-deficient (Ndp KO) mice via intravitreal injection at postnatal day 7, with some mice subjected to oxygen-induced retinopathy (OIR). AAV2-7m8 transduced M&#xfc;ller glia, while AAV-ShH10 targeted retinal ganglion cells. Both vectors fully restored intraretinal capillary growth in Ndp KO mice, normalizing vessel density and plexus organization, preserving the blood-retinal barrier, and rescuing visual function. In OIR, scAAV2-7m8-huNorrin reduced vaso-obliteration and neovascular tuft formation, increasing deep plexus coverage, and suppressed Vegfa164 and Ang-2 upregulation. The findings demonstrate that AAV-mediated norrin delivery efficiently targets retinal glia and neurons, restores vascular structure and function, stabilizes the blood-retinal barrier, and mitigates OIR-induced pathological angiogenesis, supporting its potential as a therapeutic strategy for Norrie-related retinopathies and ROP.

Cadmium (Cd) is a non-essential and highly toxic heavy metal widely present in aquatic environments. However, studies investigating the toxic effects of Cd on crucian carp (Carassius auratus) are relatively few. This study aimed to evaluate the toxic effects of Cd by assessing hematological parameters, antioxidant responses, and the expression of stress-related genes in C.&#xa0;auratus exposed to waterborne Cd. A total of 180 healthy C.&#xa0;auratus (19.43 &#xb1;&#xa0;1.5 cm and 170.00 &#xb1;&#xa0;3.04 g) were exposed to Cd at concentrations of 0, 2, and 4 mg/L for 8 weeks, with three replicates per treatment. The exposure to Cd resulted in significant reductions in red blood cell (RBC) count, hemoglobin (Hb) concentration, and hematocrit (Hct) values. Moreover, the levels of total superoxide dismutase (T-SOD), catalase (CAT), and glutathione peroxidase (GPx) in the liver also decreased significantly, whereas malondialdehyde (MDA) content was increased significantly. The expression levels of CAT, copper (Cu)/zinc (Zn)-superoxide dismutase (Cu/Zn-SOD), heat shock protein 70 (HSP70), heat shock protein 90 (HSP90), and metallothionein (MT2) genes were significantly upregulated. Overall, Cd exposure adversely affected the hematological parameters, induced oxidative stress, and altered the expression levels of stress-related genes. This study not only provides new insights into the toxic effects of Cd in C. auratus but also contributes to environmental monitoring research.

Heart failure (HF) patients exhibit autonomic dysfunction. Orthostatic hypotension occurs often in HF and may be linked with altered cardiovascular responsiveness in HF. However, the cardiovascular response to acute hypotension in HF patients compared to healthy adults is unknown. Therefore, data were retrospectively analysed from eight patients with HF with reduced ejection fraction (7 male/1 female) and seven healthy adults (CON; 6 male/1 female) who underwent acute hypotension via thigh cuff deflation following 7.5 min of unilateral lower limb occlusion. Mean arterial blood pressure (MAP; photoplethysmogram) and heart rate (HR; electrocardiogram) were continuously recorded. Statistical analysis involved independent-samples t-tests. Baseline cardiovascular values were not different between groups (all p > 0.05). The magnitudes of the MAP peak decrease during acute hypotension and consequent HR peak increase were not different between groups (MAP: HF -11 &#xb1; 3&#x2009;mmHg vs. CON -12 &#xb1; 5&#x2009;mmHg, p = 0.756; HR: HF 3 &#xb1; 2b &#xb7; min-1 vs. CON 4 &#xb1; 3b &#xb7; min-1, p = 0.243). However, the MAP time to peak decrease and HR time to peak increase were longer in HF than CON (MAP: HF 11 &#xb1; 5&#x2009;s vs. CON 6 &#xb1; 3&#x2009;s, p = 0.041; HR: HF 10 &#xb1; 4&#x2009;s vs. CON 6 &#xb1; 2&#x2009;s, p = 0.044). HF patients exhibit a delayed cardiovascular response to acute hypotension compared to healthy adults, which may be linked with more frequent orthostatic hypotension in HF.

To predict the risk of diabetic macular edema (DME) onset and to identify features of the risk subgroups. Population-based observational study with a case-control design. Health checkup and diagnosis data from the JMDC claims database (January 2005-July 2020), one of the largest Japanese epidemiological databases, were used. From 272 337 individuals diagnosed with type 2 diabetes (International Classification of Diseases, 10th Revision E11), we analyzed 2368 pairs of DME and non-DME individuals, which matched 1:1 by the balancing score calculated from regression analysis of DME with sex, age, months of observation, number of checkups, duration of diabetes, and months until the first checkup. We employed a multivariate Cox proportional hazards model, regularized Cox models, and a random survival forest (RSF). These models were trained via ID-level bootstrap resampling using 43 health checkup variables (missing ratio <50%) and 404 high-incidence diseases within 6 months, along with age, sex, and duration of diabetes mellitus, to assess DME risk. Temporal changes in RSF-predicted risk scores were analyzed using nonlinear modeling techniques. Concordance index (C-index), integrated Brier score (IBS), and cumulative/dynamic mean area under the receiver operating characteristic curve (AUC). Thirteen checkup items and 44 disease history variables were significantly associated with the onset of DME. The RSF identified 43.8% of DME cases >5 years prior to onset, with a specificity of 85.5%. The RSF achieved median C-index, IBS, and mean AUC values of 0.694 (95% confidence interval, 0.688-0.697), 0.181 (0.179-0.184), and 0.750 (0.739-0.756), respectively, outperforming both multivariate and univariate Cox models. Three distinct DME risk subgroups were suggested by temporal changes in the RSF-predicted risk score. Predictors of DME onset varied markedly among these subgroups. In the explicit high-risk subgroup, urinary protein and urinary sugar were highly important, and liver function-related blood tests, such as alanine transaminase and &#x3b3;-gultamyltransferase, were also ranked high in variable importance metrics. Anemia-related laboratory tests were associated with DME development only in this subgroup. Random survival forest demonstrated superior performance in relative risk prediction of DME using health checkup data. External validation remains an essential prerequisite before any clinical application. Proprietary or commercial disclosure may be found in the Footnotes and Disclosures at the end of this article.

Ch&#xe9;diak-Higashi syndrome (CHS) is a rare autosomal recessive disorder characterized by severe immunodeficiency, partial albinism, recurrent infections, and progressive neurologic dysfunction. Unless patients undergo successful hematopoietic cell transplantation (HCT), a majority of them die during childhood because of an accelerated phase of immune dysfunction and hemophagocytic lymphohistiocytosis (HLH). Herein, we aim to describe the laboratory diagnosis, clinical manifestations, and genetic findings in three patients with CHS. Three patients with partial albinism associated with CHS were included in this study. Immunological screening tests were done. Leukocyte granules in peripheral blood smear (PBS) and hair shafts were examined. Subsequently, genetic analyses were performed by Whole Exome Sequencing (WES) followed by Sanger sequencing for all patients and their parents. Initial immunology screening tests were within normal limits. Light microscopy studies of patients' PBS showed giant granules in the leukocyte cytoplasm. Furthermore, there were evenly distributed melanin granules in the patients' hair shafts. Variant analysis of the LYST gene identified three splicing site defects: one known variant, c.7060-1G>A in intron 24, and two novel variants, c.2363+2T>C in intron 5, and c.10702-3A>G in intron 47. Hair shaft assay and PBS are rapid and suitable tests in early diagnosis and differentiation in CHS patients. WES results revealed 2 novel splice site variants that might contribute to earlier and more accurate diagnosis. This facilitates early enrolment of CHS patients in the HCT protocol-the optimal treatment path-and enables prenatal diagnosis for affected families.

Malnutrition disorders are associated with an enteropathy characterized by villus blunting, secretory cell loss, and mucosal inflammation. To investigate the contribution of undernutrition to enteropathy we conducted a case-control study of adult patients with starvation due to benign esophageal strictures, compared with non-malnourished community controls. Fasting blood samples and duodenal biopsies were collected from 34 cases and 66 controls. Duodenal biopsies were evaluated by morphometry while circulating C-reactive protein and hormones were measured by ELISA or Luminex. Multivariable models were adjusted for stricture, body mass index, HIV, and C-reactive protein. Epithelial surface area was reduced in cases (median 323&#x2009;&#x3bc;m (IQR 271, 392) per 100&#x2009;&#x3bc;m muscularis mucosae) compared to controls (448&#x2009;&#x3bc;m (IQR 384, 516); p&#x2009;=&#x2009;0.0001), even after adjustment in a linear regression model that included BMI, CRP, and HIV status. Hormonal analysis showed lower median concentrations of C-peptide (0.36&#x2009;ng/mL vs. 0.7&#x2009;ng/mL; p&#x2009;=&#x2009;0.003), insulin (639&#x2009;pg/mL vs. 2037&#x2009;pg/mL; p&#x2009;=&#x2009;0.0001), and GLP-2 (0&#x2009;ng/mL vs. 2.3&#x2009;ng/mL; p&#x2009;=&#x2009;0.0063) in cases compared to controls. Cases also had higher glucagon (52.4&#x2009;pg/mL vs. 36.6&#x2009;pg/mL; p&#x2009;=&#x2009;0.0012) and secretin concentrations (24.4&#x2009;pg/mL vs. 11.7&#x2009;pg/mL; p&#x2009;=&#x2009;0.009). Starvation and malnutrition consequent upon esophageal stricturing drives a further reduction in epithelial surface area, superimposed on environmental enteropathy. There was some evidence of abnormalities in secretion of pancreatic hormones and GLP-2.

A 76-year-old woman with a history of polymyalgia rheumatica, dyslipidemia, and osteoporosis was admitted due to a one-week history of productive cough and was initially diagnosed with bacterial pneumonia. Despite antibiotic therapy, her clinical condition worsened, leading to respiratory failure. Further history-taking revealed that she had been taking&#xa0;kakkonto, a Japanese herbal medicine (JHM), for the preceding 4.5 months as a self-initiated measure to prevent infection. The patient was eventually diagnosed with kakkonto-induced pneumonitis. Kakkonto was discontinued, and systemic corticosteroid therapy was initiated, resulting in rapid improvement. The peripheral blood drug-induced lymphocyte stimulation test was positive for kakkonto. Because the clinical and radiological findings of JHM-induced pneumonitis are nonspecific, careful medication history-taking, particularly for JHM, is essential for diagnosing unexplained pneumonitis.

Pulmonary arteriovenous fistula (PAVF) and hepatopulmonary syndrome (HPS) both cause right-to-left shunting, allowing pathogens to bypass the pulmonary filtration barrier and enter systemic circulation, leading to brain abscess. Despite distinct etiologies, both share the same pathological pathway-right-to-left shunt-resulting in the same devastating neurological complication. Two male patients with cryptogenic brain abscesses caused by PAVM (59 years old) and HPS (52 years old), respectively, are reported. The patient with PAVM presented with fever, dyspnea, and headache, and was diagnosed by contrast-enhanced chest computed tomography. Fusobacterium nucleatum was detected in cerebrospinal fluid (CSF). The patient recovered following anti-infective therapy combined with surgical resection of pulmonary lesions, achieving a favorable prognosis at the 3-month follow-up. The HPS patient had a history of hepatitis C complicated by liver cirrhosis. He presented with headache, fever, and orthostatic hypoxemia. Diagnosis was confirmed by a contrast-enhanced transcranial Doppler bubble test (c-TCD). Blood culture identified Streptococcus intermedius. The brain abscess recurred after antibiotic treatment due to refusal of liver transplantation. At the 3-year follow-up, the patient could maintain only a sedentary lifestyle. Both pulmonary arteriovenous fistula (PAVM) and hepatopulmonary syndrome (HPS) can cause cryptogenic brain abscess through right-to-left shunt. PAVM can be eradicated by intervention or surgery, while HPS fundamentally requires liver transplantation. Notably, Clinical and radiological improvement following antimicrobial therapy may not represent definitive cure if the underlying right-to-left shunt remains untreated, and recurrence remains possible.

The coronary slow flow phenomenon (CSFP) is delayed contrast progression through the epicardial coronary arteries in the absence of significant stenosis. The stress hyperglycemia ratio (SHR) normalizes admission glucose to the estimated average glucose derived from HbA1c, separating acute glycemic excursion from chronic hyperglycemia. Whether the SHR is independently associated with CSFP in patients with type 2 diabetes mellitus (T2DM) is not known. This retrospective case-control study enrolled 235 consecutive patients with T2DM who underwent coronary angiography between January 2022 and January 2025. Patients with epicardial stenosis exceeding 40% in any vessel, prior revascularization, or acute coronary syndrome within 30 days were excluded. Among the remaining patients, those with a corrected TIMI frame count (CTFC) above 27 in any epicardial vessel were classified as CSFP (n=112) and the rest as normal coronary flow (NCF) (n=123). The SHR was calculated as admission blood glucose (mmol/L) divided by (1.59 &#xd7; HbA1c% - 2.59). The SHR was higher in the CSFP group than in the NCF group (1.42 &#xb1; 0.31 vs. 1.08 &#xb1; 0.24, p<0.001). After multivariate adjustment, it remained independently associated with CSFP (odds ratio [OR] 2.84, 95% confidence interval [CI] 1.92-4.21, p<0.001). On receiver operating characteristic analysis the area under the curve (AUC) was 0.819 (95% CI 0.760-0.876); a cutoff of 1.21 gave 78.6% sensitivity and 74.0% specificity. The SHR correlated with mean CTFC (r=0.621, p<0.001) and outperformed admission glucose alone (AUC 0.724, p=0.003). In this cohort, the SHR was independently associated with CSFP and discriminated it better than admission glucose alone. Because it is calculated from two values routinely available at catheterization, admission glucose and HbA1c, the SHR is a practical candidate marker that warrants prospective validation for risk stratification in patients with T2DM undergoing coronary evaluation.

Hematopoietic stem cell transplantation (HSCT) of genetically engineered cells is a promising treatment modality for monogenic diseases. However, hematopoietic stem cell (HSC)-directed lentiviral vector (LV) gene therapies remain limited by genotoxicities associated with standard non-targeted conditioning using irradiation or alkylating chemotherapy. We and others developed an antibody drug conjugate (ADC) with anti-CD117 and saporin (sap), which selectively depletes CD117-expressing HSC and progenitor cells (HSPCs). Since anti-CD117-sap does not generally provide engraftment comparable to conventional conditioning, we investigated the hypothesis anti-CD117-sap is not effective as a single conditioning agent due to insufficient HSPC depletion. We show anti-CD117-sap induces nearly complete residual HSPC entry into a non-G0 proliferative state and postulated agents targeting cycling cells would enhance engraftment. When we administered the antimetabolite 5-fluorouracil with anti-CD117-sap, anti-thymocyte globulin, and an immunoglobulin-degrading enzyme, we achieved >90% peripheral blood chimerism of unmodified cultured donor cells. Additional immunosuppression combined with an increase in transplanted cells further permitted &#x223c;70% engraftment of HSPCs transduced with an LV encoding a high-expression, immunogenic factor VIII (FVIII) transgene. Copy numbers of &#x223c;1.0 and normal FVIII plasma activity levels (>50%) by 6 months post-HSCT were achieved. Collectively, we show ADC and antimetabolite administration can augment LV-engineered HSPC engraftment by targeting cycling cells.

This study sought to examine the correlation between antiretinal antibodies (ARAs) and OCT manifestations in patients diagnosed with nonparaneoplastic autoimmune retinopathy (npAIR). A retrospective, observational case series. Fifty-five patients (92 eyes) diagnosed with probable or possible npAIR. Patients underwent comprehensive evaluation, including best-corrected visual acuity (BCVA), slit-lamp biomicroscopy, fundus photography, autofluorescence, OCT scanning, and electroretinogram. Blood samples were analyzed for the presence of ARAs using Western Blot, including anti-recoverin (ARc), anti-&#x3b1;-enolase (AeNO), anti-carbonic anhydrase II (ACA), and anti-CRMP5 (AC5). Statistical analyses included the Kruskal-Wallis test (logarithm of the minimum angle of resolution BCVA) and 1-way analysis of variance (central retinal thickness [CRT]) for group comparisons. Diagnostic performance of key OCT features was assessed. Multimodal imaging, BCVA, and CRT of patients diagnosed with npAIR. Among the 55 npAIR patients, 52.7% were positive for a single tested antibody, while 25.5%, 14.5%, and 7.3% had two, three, or four of the tested antibodies, respectively. Central retinal thickness and BCVA were significantly worse in most ARA-positive groups versus controls. However, the AeNO(+) subgroup showed the best-preserved CRT and BCVA. The AeNO(+) eyes predominantly exhibited inner retinal (ganglion cell complex/retinal nerve fiber layer) thinning (66.7%). The ACA(+) and ARc(+) eyes showed patterns of diffuse outer retinal degeneration (50% and 75%, respectively). The AC5(+) eyes uniquely presented outer plexiform layer (OPL) "double-layer signs" (45.8%) and "retinitis pigmentosa-like" changes (25%). Analysis of diagnostic performance revealed that "inner retinal thinning" had moderate sensitivity (66.7%) for AeNO, while "OPL double-layer signs" showed perfect specificity (100%) for AC5 within our cohort. This study provides valuable insights into the correlation between ARA profiles and specific OCT patterns in npAIR patients. The findings advance our understanding of npAIR pathogenesis and highlight the potential of OCT imaging and ARA profiling in the diagnosis and management of this complex condition. The authors have no proprietary or commercial interest in any materials discussed in this article.

Solid organ transplant (SOT) recipients undergoing total joint arthroplasty (TJA) may face elevated perioperative risk because of chronic immunosuppression, medical comorbidity, and organ-specific physiologic considerations. Although intravenous tranexamic acid (TXA) is widely used during TJA to reduce perioperative blood loss, evidence regarding outcomes among SOT recipients receiving TXA remains limited. A retrospective review was performed of 29,240 consecutive primary TJA patients who all received intraoperative intravenous TXA between June 2011 and March 2025. Patients undergoing unicompartmental knee arthroplasty, hemiarthroplasty, TJA for fracture, bilateral procedures, revision procedures, or those with less than 90 days of postoperative follow-up were excluded. SOT history was identified using diagnosis and procedural codes and verified by manual review. Outcomes included 90-day deep vein thrombosis (DVT), pulmonary embolism (PE), myocardial infarction (MI), operative time, and hospital length of stay (LOS). Sixty-six patients with verified SOT were identified. The most common transplant types were kidney (59%), liver (24%), and heart (9%). One SOT patient experienced a 90-day VTE event compared with 95 control patients (1.5% versus 0.3%, P&#xa0;=&#xa0;0.20). There were no PEs or MIs in the SOT cohort, compared with PE and MI rates of 0.2% and 0.01% in controls, respectively (P&#xa0;>&#xa0;0.05 for both). Operative times were similar between groups (100.8 versus 108.5&#xa0;min, P&#xa0;=&#xa0;0.11), while LOS was significantly longer among SOT recipients (86.2 versus 43.8&#xa0;h, P&#xa0;<&#xa0;0.001). In this retrospective cohort of primary TJA patients who all received intraoperative intravenous TXA, SOT recipients had low observed rates of VTE, PE, and MI. Because all patients received TXA and the SOT cohort was small, these findings should be interpreted as comparative observational safety data rather than evidence that TXA independently increases or does not increase thromboembolic risk in this population.

Eosinophilic colitis (EC) is a rare clinical entity. Advanced cases with severe inflammation may develop severe abdominal pain and distension, malabsorption, intestinal obstruction, and even GI hemorrhage. Once diagnosed early, EC responds to steroid therapy. We report the case of a 46-year-old male who presented with acute-onset left upper abdominal pain, enlargement of the right scrotal sac, and hemoperitoneum. A contrast-enhanced CT scan of the abdomen revealed an irregular hypoechoic lesion measuring approximately 6.5 &#xd7; 4.8 cm, likely a transverse mesocolon hematoma in the epigastric region with hemoperitoneum and right-sided hematocele with persistent processus vaginalis. USG-guided ascitic tap yielded bloody aspirate. Ascitic fluid analysis showed sheets of eosinophils (60%) with a hemorrhagic background. CBC showed eosinophilia (38%). He underwent diagnostic laparoscopy and laparoscopic left hemicolectomy; histopathological examination of the resected colon revealed EC (transmural type). He was given oral corticosteroids for two weeks after discharge. EC is a rare condition. It may present acutely and give rise to potentially severe and fatal complications like hemorrhage and perforation. With early diagnosis and appropriate treatment, we may be able to avoid serious complications in such patients.