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Healthcare access in Latin America is highly unequal, with rural and peri-urban populations disproportionately excluded from essential and specialized services. To address the persistent gaps often obscured by conventional urban–rural classifications, this study developed a machine learning framework integrating the Functional Urban Area (FUA) model with Density-Based Spatial Clustering of Applications with Noise (DBSCAN) and Shannon entropy optimization to refine urbanization gradients and quantify inequities across 11 countries. High-resolution population density data from the Meta High Resolution Settlement Layer (HRSL, 2020) and CIESIN’s Gridded Population of the World (GPWv4, rev. 11), combined with healthcare facility locations from Healthsites.io, were processed in R to generate population-facility networks. Entropy optimization dynamically determined country-specific DBSCAN distance thresholds, ensuring representative clustering of functional urban and rural areas. Facilities were categorized by care level, and per-capita densities were compared across clusters. Results showed that entropy-optimized DBSCAN improved spatial precision over traditional approaches and revealed systemic urban bias: Peru, Chile, and Venezuela had the lowest hospital densities, while Ecuador, Bolivia, and Paraguay displayed the strongest rural deficits in primary care. Specialized services were overwhelmingly concentrated in urban clusters. This reproducible framework establishes a quantitative baseline for healthcare inequities, providing data-driven insights to inform the design of decentralized strategies to improve equitable access to care across Latin America.

Despite the growing evidence in the cardiology literature that transradial approach has substantial benefits over transfemoral access, this technique is rarely used during interventions in the systemic circulation. The aim of this study was to evaluate the feasibility of transradial approach for hepatic radioembolization and to compare it with transfemoral approach. Sixty-four hepatic radioembolizations performed in 50 patients were included in the study. Thirty-three procedures were performed via radial access in 27 patients, and 31 procedures were performed via femoral access in 23 patients. There was 100% technical success in performing hepatic radioembolization in both groups. The majority (97%) of the patients who underwent transradial radioembolization reported preference for radial artery access. The fluoroscopy time was significantly longer (9.45±5.09 min vs. 5.72±3.67 min, P < 0.01) and the radiation dose was significantly higher (597.8±585.2 mGy vs. 302.8±208.3 mGy, P < 0.01) in the radial group compared with the femoral group. The direct cost savings using radial access versus femoral access is approximately $100/procedure. In addition, there was a one hour (50%) shorter postprocedural stay for patients who underwent the transradial procedure. Transradial access is feasible for hepatic radioembolization. The transradial approach is cheaper and offers improved patient comfort. However, it is technically challenging, with longer fluoroscopy times and higher radiation doses. Transradial approach should be considered as a primary choice in patients with low platelet count and/or morbid obesity. Transradial access should be in the procedural repertoire of every interventional radiologist.

Endovascular coil embolization is an effective, minimally invasive technique used to treat visceral pseudoaneurysms. Although rare, post-procedural infections such as bacteremia and infective endocarditis (IE) can occur, particularly in patients with underlying malignancy, valvular abnormalities, or immunosuppression. Early recognition and intervention are critical to preventing serious complications. A 52-year-old male with a history of renal cell carcinoma (post left nephrectomy) and a known heart murmur presented to the hospital with worsening left-sided abdominal pain. Imaging revealed multiple visceral pseudoaneurysms involving the hepatic, splenic, and mesenteric arteries. He underwent successful coil and glue embolization. Further workup with transesophageal echocardiography (TEE) revealed severe mitral regurgitation with vegetations and a flail posterior mitral leaflet. Blood cultures obtained after the embolization procedure were positive for , confirming IE, and the patient subsequently underwent mitral valve replacement and pacemaker implantation at a cardiac hospital. He completed intravenous antibiotic therapy and was discharged in stable condition. Eighteen-month follow-up imaging showed evolving splenic infarcts without evidence of visceral pseudoaneurysms. This case highlights a rare but serious complication of coil embolization. While the causal link cannot be definitively confirmed, the sequence of events and known mechanisms of post-procedural bacteremia support a strong association. Factors such as the introduction of foreign material, ischemia-induced tissue vulnerability, and the presence of underlying malignancy may increase the risk of hematogenous bacterial seeding. , though classically associated with dental flora, can exhibit invasive potential in vulnerable hosts. Cancer patients face elevated risks due to frequent vascular instrumentation and immunosuppressive treatments. High-risk patients may benefit from close post-procedural monitoring and early infectious workup. This case highlights the importance of species-level identification and clinical vigilance in preventing delayed diagnosis and complications.

This large outbreak of foodborne salmonellosis demonstrated the complexity of investigating outbreaks linked to poultry products. The outbreak also highlighted the importance of efforts to strengthen food safety policies related to Salmonella in chicken parts and has implications for future changes within the poultry industry. To investigate a large multistate outbreak of multidrug resistant Salmonella Heidelberg infections. Epidemiologic and laboratory investigations of patients infected with the outbreak strains of Salmonella Heidelberg and traceback of possible food exposures. United States. Outbreak period was March 1, 2013 through July 11, 2014. A case was defined as illness in a person infected with a laboratory-confirmed Salmonella Heidelberg with 1 of 7 outbreak pulsed-field gel electrophoresis (PFGE) XbaI patterns with illness onset from March 1, 2013 through July 11, 2014. A total of 634 case-patients were identified through passive surveillance; 200/528 (38%) were hospitalized, none died. Interviews were conducted with 435 case-patients: 371 (85%) reported eating any chicken in the 7 days before becoming ill. Of 273 case-patients interviewed with a focused questionnaire, 201 (74%) reported eating chicken prepared at home. Among case-patients with available brand information, 152 (87%) of 175 patients reported consuming Company A brand chicken. Antimicrobial susceptibility testing was completed on 69 clinical isolates collected from case-patients; 67% were drug resistant, including 24 isolates (35%) that were multidrug resistant. The source of Company A brand chicken consumed by case-patients was traced back to 3 California production establishments from which 6 of 7 outbreak strains were isolated. Epidemiologic, laboratory, traceback, and environmental investigations conducted by local, state, and federal public health and regulatory officials indicated that consumption of Company A chicken was the cause of this outbreak. The outbreak involved multiple PFGE patterns, a variety of chicken products, and 3 production establishments, suggesting a reservoir for contamination upstream from the production establishments. Sources of bacteria and genes responsible for resistance, such as farms providing birds for slaughter or environmental reservoir on farms that raise chickens, might explain how multiple PFGE patterns were linked to chicken from 3 separate production establishments and many different poultry products.

BackgroundImmune checkpoint therapy has achieved durable clinical responses, but only in a subset of cancer patients. Immunosuppressive myeloid cells, a heterogenous group of innate immune cells, have emerged as key contributors to resistance to T cell based immune checkpoint therapy. Leukocyte immunoglobulin-like receptor B4 (LILRB4), also known as immunoglobulin-like transcript 3 (ILT3), is an inhibitory receptor selectively expressed on myeloid cells, enriched in the tumor microenvironment and contributes to myeloid-driven immunosuppression. Recently, fibronectin has been identified as a functional ligand for LILRB4, and the LILRB4-fibronectin interaction was proposed as a stromal checkpoint suppressing myeloid cell anti-tumor activity. Targeting LILRB4 could represent a strategy to reprogram immunosuppressive myeloid cells and promote anti-tumor response. We developed JTX-1484, a highly selective, high-affinity humanized monoclonal antibody that binds to and antagonizes LILRB4 and blocks its interaction with fibronectin.MethodsA diverse panel of high affinity monoclonal antibodies that bind specifically to LILRB4 was generated. JTX-1484 activity alone or in combination with an anti-PD1 antibody was evaluated in vitro in different functional assays. Human primary myeloid-derived suppressor cells (MDSCs) were used in a T cell suppression assay and treated with JTX-1484. Primary monocyte-derived tolerogenic dendritic cells (tDCs) were utilized in mixed lymphocyte reactions with T cells and treated with JTX-1484 in combination with anti-PD1. JTX-1484’s ability to block fibronectin inhibitory activity on tDCs and THP-1 cells was also tested. Finally, the pharmacodynamic effect of anti-LILRB4 treatment in human tumor samples was evaluated by assessing gene expression changes in an ex vivo histoculture system.ResultsJTX-1484 reprogramed tDCs to a stimulatory phenotype as evidenced by increased pro-inflammatory cytokine production and increased ability to induce T cell activation in combination with anti-PD1. LILRB4 antagonism by JTX-1484 also reversed fibronectin-mediated inhibition of tDC activation and reduced MDSC-mediated T cell immunosuppression. Moreover, LILRB4 blockade in ex vivo human tumor samples induced pharmacodynamic responses consistent with increased immune activation and reduced myeloid immunosuppression.ConclusionsResults from our preclinical studies demonstrate that JTX-1484 is a highly specific and potent antagonist of LILRB4 that leads to myeloid cell reprogramming and more efficient T cell activation that could result in enhanced anti-tumor responses. JTX-1484 immunostimulatory properties towards myeloid cells could be complementary to immune checkpoint blockade therapy. Our data therefore support clinical development of JTX-1484. Indication selection will be guided by multiple factors including predictive biomarkers such as target and ligand abundance, as well as complementarity and combination potential with other therapies.Ethics ApprovalHuman blood and tumor samples were acquired from commercial providers and from the CHTN and NDRI networks respectively. Specimens were collected under each provider's human subject research institutional review board approved protocols and were fully anonymized or otherwise permanently de-identified to recipient investigators.

The Cockayne Syndrome B (CSB, ERCC6) protein, interacts with the exonuclease SNM1A during transcription-coupled DNA interstrand (ICL) repair, with CSB facilitating localisation of SNM1A to ICL damage. The functional and mechanistic details of this interaction in DNA repair, however, have not been defined. Here, we demonstrate that CSB enhances SNM1A resection through ICLs and identify a specific interaction between the winged-helix domain of CSB and the nuclease core of SNM1A that is crucial for recruitment and enhancement of nuclease degradation. Biochemical and single-molecule studies on DNA containing site-specific ICLs reveal that CSB increases the affinity of SNM1A to damaged DNA substrates and also alters the substrate conformation to enhance ICL processing by SNM1A. Notably, CSB was observed preferentially as a dimer when colocalised with SNM1A at ICLs, constrasting with its monomeric nature observed during repair initiation in classical transcription-coupled nucleotide excision repair. The combined results provide molecular insights into the basis of a direct contribution of CSB to a DNA repair reaction.