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Orbea is a morphologically diverse lineage within the subtribe Stapeliinae, yet plastome evolution in Arabian taxa remains insufficiently characterized. This study reports the first complete chloroplast genomes of Orbea sprengeri subsp. commutata and O. wissmannii var. eremastrum and investigates plastome structure, sequence variability, and phylogenetic relationships across tribe Ceropegieae. Chloroplast genomes were assembled, annotated, and compared with 13 published plastomes representing major Ceropegieae lineages. Both Arabian plastomes displayed the typical quadripartite structure and identical gene content of 114 unique genes, including 80 protein-coding genes, 30 transfer RNA genes, and four ribosomal RNA genes. However, O. wissmannii var. eremastrum exhibited pronounced structural divergence, possessing the largest plastome recorded for the tribe (170,054 bp), an 8.9 kb expansion of the inverted repeat regions, and an 8.4 kb inversion spanning the ndhG–ndhF region. Comparative analyses revealed conserved gene order across Ceropegieae but identified six highly variable loci (accD, clpP, ndhF, ycf1, psbM–trnD, and rpl32–trnL) as potential DNA barcodes. Selection pressure analyses indicated strong purifying selection across most genes, with localized adaptive signals in accD, ndhE, ycf1, and ycf2. Phylogenomic reconstruction consistently resolved the two Arabian Orbea taxa as a distinct clade separate from the African O. variegata. This study fills a gap in Ceropegieae plastid genomics and underscores the importance of sequencing additional Orbea species to capture the full extent of genomic variation within this diverse genus. Full article

Background: Catechol-O-methyltransferase (COMT) catalyzes catecholamine O-methylation and contributes to dopamine turnover, potentially influencing levodopa requirements in Parkinson’s disease (PD). We evaluated whether the Gothelf COMT haplotype—and its constituent variants rs2075507, rs4680 (Val158Met), and rs165599—differ in frequency between PD cases and controls. We then tested associations between these variants and clinical phenotypes, with a prespecified focus on levodopa equivalent daily dose (LEDD). Finally, we examined whether haplotype structure and allele-specific context (e.g., background-dependent effects) help explain observed genotype–phenotype relationships in the PD cohort. Aim: Analysis of the rs2075507, rs4680 and rs165599 at individual and haplotype level between control and diseased groups. Furthermore, analysis of association of individual SNPs or haplotype level with clinical outcomes. Subjects and methods: Fifty-five individuals with Parkinson’s disease (PD) and fifty-three neurologically healthy controls were enrolled at a single center. Genomic DNA was isolated from peripheral blood, and three COMT variants—rs2075507 (promoter), rs4680/Val158Met (coding), and rs165599 (3′UTR)—were genotyped by Sanger sequencing. Allele, genotype, and tri-marker haplotype frequencies were estimated, and case–control differences were evaluated. Within the PD cohort, associations with clinical outcomes—primarily levodopa equivalent daily dose (LEDD)—were analyzed using multivariable linear models. Statistical tests were two-sided, with multiplicity control as specified in the corresponding tables. Results: The rs2075507 polymorphism showed a robust additive association with LEDD; each A allele predicted higher dose (LEDD ≈ +1331 mg/day, p = 0.001) after adjusting for age and sex. The tri-haplotype test did not show significant association with LEDD. Nevertheless, rs2075507 SNP strongly marked downstream backgrounds: in AA carriers, rs4680–rs165599 haplotypes were enriched for Val (G) and rs165599-G; in GG carriers, for rs165599-A with mixed Val/Met; and GA was A-loaded at both loci. Exact tests confirmed that AA and GG differed in rs4680–rs165599 composition, whereas GA vs. GG was not significant. Conclusions: The promoter variation at rs2075507 may represent the genetic contributor to levodopa dose requirements when modeled with SNP–SNP interactions, with its effect is modified mostly by rs165599 polymorphism. Tri-haplotypes do not independently predict LEDD. The rs4680 (coding) and rs165599 (3′UTR) context appears to fine-tune rather than determine dosing needs, mainly via interaction with rs2075507 SNP. Full article

Dentathalia scutellariae (Hymenoptera: Athaliidae) is a major pest of Scutellaria baicalensis, a plant of significant economic and medicinal value. To date, no genomic resources have been available for this species, limiting research into its biology and control. Here, we reported a genome assembly of D. scutellariae with high accuracy and contiguity, sequenced by PacBio HiFi long-read and MGI-Seq short-read methods. The genome assembly is 157.00 Mb in length with a contig N50 of 4.04 Mb. The complete BUSCO score was 98.8%. The genome contained 14.73 Mb of repetitive elements, representing 9.38% of the total genome size. We predicted 14,904 protein-coding genes, of which 12,327 genes were annotated functionally. Gene family analysis of D. scutellariae revealed 422 expanded and 113 contracted gene families. Notably, genes within expanded families were significantly enriched in retinol metabolism and drug metabolism–cytochrome P450 pathways. We present the first high-quality genome assembly of D. scutellariae, which serves as a foundational genomic resource. This dataset will facilitate future studies on the molecular basis of D. scutellariae’s pest status, host adaptation, and the development of targeted control strategies. Full article

Bovine mastitis remains a globally prevalent disease, with the limitations of antibiotic-based treatments—such as the rise in antimicrobial resistance and the presence of drug residues—highlighting the urgent need for alternative therapeutic approaches. Inflammation is intricately linked to various cytokines and immunomodulatory proteins, among which cyclophilin A (CypA) serves as a pivotal inflammatory mediator, significantly contributing to the initiation and amplification of inflammatory responses under such conditions. The acquisition of high-purity recombinant protein is a fundamental prerequisite for in vitro functional studies of bovine CypA. This study aimed to construct a eukaryotic expression vector for bovine CypA and verify its expression in CHO-K1 cells. Utilizing the bovine CypA gene sequence available in GenBank, the coding region was artificially synthesized and optimized for codon usage, subsequently being inserted into the pPB[Exp] backbone vector via BsrGI and BstEII double digestion. The resulting polycistronic expression vector contained a CAG promoter driving the CypA transcription, an EF1α promoter driving the EGFP reporter gene, a PGK promoter controlling the puromycin resistance gene, and a C-terminal His-tag. Restriction enzyme digestion and bidirectional Sanger sequencing confirmed that the inserted fragment sequence was completely consistent with the optimized design. Robust EGFP fluorescence was observed 24 h post-transfection and remained stable after puromycin selection. qPCR analysis showed that the Ct value of CypA in the experimental group was 16.20 ± 0.04, while no amplification signal was detected in the control group. Additionally, Western blot analysis identified a CypA-specific band at approximately 18 kDa, confirming the correct expression of the exogenous CypA protein in CHO-K1 cells. Collectively, these results demonstrate the successful construction and validation of a bovine CypA eukaryotic expression vector. The established CHO-K1 expression system exhibited stable and efficient expression, thereby providing a robust foundation for future research on the production and application of recombinant CypA protein. Full article

We introduce the Onco-Hem Connectome (OHC), a patient similarity network (PSN) designed to organize real-world hemato-oncology inpatients by exploratory phenotypes with potential clinical utility. Background: Polypharmacy and drug–drug interactions (DDIs) are pervasive in hemato-oncology and vary with comorbidity and treatment intensity. Methods: We retrospectively analyzed a 2023 single-center cohort of 298 patients (1158 hospital episodes). Standardized feature vectors combined demographics, comorbidity (Charlson, Elixhauser), comorbidity polypharmacy score (CPS), aggregate DDI severity score (ADSS), diagnoses, and drug exposures. Cosine similarity defined edges (threshold ≥ 0.6) to build an undirected PSN; communities were detected with modularity-based clustering and profiled by drugs, diagnosis codes, and canonical chemotherapy regimens. Results: The OHC comprised 295 nodes and 4179 edges (density 0.096, modularity Q = 0.433), yielding five communities. Communities differed in comorbidity burden (Kruskal–Wallis ${\epsilon }^2$: Charlson 0.428, Elixhauser 0.650, age 0.125, all FDR-adjusted p < 0.001) but not in utilization (LOS, episodes) after FDR (${\epsilon }^2$ ≈ 0.006–0.010). Drug enrichment (e.g., enoxaparin $\Delta$ = +0.13 in Community 2; vinblastine $\Delta$ = +0.09 in Community 3) and principal diagnoses (e.g., C90.0 23%, C91.1 15%, C83.3 15% in Community 1) supported distinct clinical phenotypes. Robustness analyses showed block-equalized features preserved communities (ARI 0.946; NMI 0.941). Community drug signatures and regimen signals aligned with diagnosis patterns, reflecting the integration of resource-use variables in the feature design. Conclusions: The Onco-Hem Connectome yields interpretable, phenotype-level insights that can inform supportive care bundles, DDI-aware prescribing, and stewardship, and it provides a foundation for phenotype-specific risk models (e.g., prolonged stay, infection, high-DDI episodes) in hemato-oncology. Full article

The placenta is often described as the “window to the brain” due to its crucial role in fetal neurological development. In this study, we investigated a family where the older male offspring exhibited severe neurodevelopmental and mild motor coordination disorders. His brother displayed emotional and behavioral dysregulation along with mild motor coordination disorders. The father was asymptomatic, while the mother and daughter showed mild learning disabilities. Whole exome sequencing (WES) identified a disruptive X-linked pathogenic variant, c.1088_1089del p.Asp363GlyfsTer2, within the calpain-6 (CAPN6) gene. We have submitted this variant to the ClinVar database (RCV005234146.2). The variant was found in hemizygous condition in the affected male offspring and in heterozygous condition in both the mother and daughter. As predicted, the variant undergoes nonsense-mediated mRNA decay (NMD), preventing the translation of the CAPN6 gene into a functional protein. CAPN6 is a critical gene predominantly expressed in placental and trophoblast tissues. Although its function is not well characterized, CAPN6 is also expressed in several regions of the developing brain. Recent studies have shown that genetic variants in CAPN6 significantly influence vascular endothelial growth factor (VEGF) activity, thereby affecting angiogenesis and the blood supply essential for fetal growth and development. Although CAPN6 lacks an MIM phenotype code, we hypothesize that it might be enumerated as a novel candidate gene contributing to neurodevelopmental disorders. Functional studies are imperative to elucidate the role of CAPN6 in placental function and its potential implications for neurodevelopmental processes. This work aims to inspire further research into the role of CAPN6 in placental biology and its relevance to neurodevelopmental disorders. Full article

Melanocortin-2 receptor accessory protein 2 (MRAP2) is essential for the intricate regulation of energy balance. Although rare MRAP2 variants have been reported in obese individuals, their overall impact on human obesity risk remains uncertain because previous studies were small, heterogeneous, and often lacked systematic functional characterization. To address this gap, we conducted a comprehensive systematic review and cohort-level meta-analysis to quantify the association between rare coding variants in MRAP2 and obesity. We systematically searched five major databases (Embase, PubMed, Scopus, Google Scholar, and Web of Science) and identified five eligible publications comprising seven independent cohorts. In total, 27 rare coding MRAP2 variants were observed in 46 (1.01%) individuals with obesity and 18 (0.34%) individuals with normal weight, among 9771 individuals (5223 with normal weight and 4548 with obesity). Using inverse-variance–weighted random-effects models fitted with restricted maximum likelihood, carriers of rare coding MRAP2 variants had higher odds of obesity (OR = 2.61; 95% CI, 1.49–4.58; p = 8.0 × 10⁻⁴). Taken together, these findings, derived predominantly from European-ancestry cohorts, support MRAP2 as a biologically plausible susceptibility gene for human obesity and indicate that rare coding MRAP2 variants are associated with higher odds of obesity, providing a quantitative framework to guide future large-scale genetic and functional studies. Full article

Anti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis is an immune-mediated neurological disorder driven by dysregulated neuroimmune interactions, yet the molecular architecture linking tumor-associated immune activation, peripheral immunity, and neuronal dysfunction remains insufficiently understood. In this study, we established an integrative computational framework that combines multi-tissue transcriptomic profiling, weighted gene co-expression network analysis, immune deconvolution, and machine learning-based feature prioritization to systematically characterize the regulatory landscape of the disease. Joint analysis of three independent GEO datasets spanning ovarian teratoma tissue and peripheral blood transcriptomes identified 2001 consistently dysregulated mRNAs, defining a shared tumor–immune–neural transcriptional axis. Across multiple feature selection algorithms, ACVR2B and MX1 were reproducibly prioritized as immune-associated candidate genes and were consistently downregulated in anti-NMDAR encephalitis samples, showing negative correlations with neutrophil infiltration. Reconstruction of an integrated mRNA-miRNA-lncRNA regulatory network further highlighted a putative core axis (ENSG00000262580–hsa-miR-22-3p–ACVR2B), proposed as a hypothesis-generating regulatory module linking non-coding RNA regulation to immune-neuronal signaling. Pathway and immune profiling analyses demonstrated convergence of canonical immune signaling pathways, including JAK-STAT and PI3K-Akt, with neuronal communication modules, accompanied by enhanced innate immune signatures. Although limited by reliance on public datasets and small sample size, these findings delineate a systems-level neuroimmune regulatory program in anti-NMDAR encephalitis and provide a scalable, network-based multi-omics framework for investigating immune-mediated neurological and autoimmune disorders and for guiding future experimental validation. Full article

Mitochondrial genomes play a central role in fungal physiology and adaptation, yet their evolutionary dynamics during domestication remain poorly understood. Here, we performed a comparative mitogenomic and gene-expression analysis of three Pleurotus ostreatus dikaryotic strains differing in origin and degree of adaptation to laboratory conditions: the long-term commercial strain dkN001, the laboratory-maintained wild isolate dkF515, and the recently collected wild strain dkN009. High-throughput Illumina sequencing enabled complete assembly of circular mitochondrial genomes, revealing substantial size variation among strains, where the dkN001 strain exhibited the second smallest mitogenome reported for the genus Pleurotus. Comparative analyses showed >99% sequence identity between wild isolates and ~95% identity relative to the commercial strain. Variations in genome size among strains were associated with intron dynamics in the cox1 and rnl genes, as well as intron loss predominantly in the commercial strain dkN001, consistent with mitochondrial genome streamlining during domestication. Expression profiling of mitochondrial protein-coding genes (PCGs) under multiple culture conditions revealed conserved transcriptional responses in dkN001 and dkF515 that contrasted sharply with those of dkN009. The differences observed, which affected components of the electron transport chain, suggested shifts in energy metabolism associated with long-term laboratory maintenance. Therefore, our results demonstrate that domestication in P. ostreatus involves both structural remodelling of the mitogenome and changes in regulation of mitochondrial PCGs, highlighting the importance of mitonuclear interactions in fungal adaptation to controlled environments. Full article

Intraoperative assessment of pancreatic quality, followed by sampling for the potential isolation of Langerhans islets for subsequent autotransplantation, is currently a key component of post-total pancreatectomy diabetes mellitus treatment. The aim of this study was to quantitatively evaluate pancreatic parenchymal stiffness using optical coherence elastography (OCE) imaging, and to investigate the utility of the OCE method as a potential indicator of islet yield after pancreatectomy. A total of 41 freshly excised human pancreatic specimens, containing pancreatic ductal adenocarcinoma (PDAC) and surrounding non-tumorous tissues post-pancreatectomy, were studied. In this research, the stiffness (Young’s modulus, kPa) and its color-coded 2D distribution were calculated for various pancreatic samples using compression OCE. Stiffness values were compared between intact pancreatic parenchyma (islet-poor and islet-rich) and pancreatic lesion groups (parenchymal fibrosis and/or PDAC invasion). The data were confirmed by histological analysis. In addition, the measured stiffness values for various morphological groups of the pancreatic samples were compared with the number of isolated islets obtained from pancreatic samples after collagenase treatment. The study demonstrated that OCE can effectively distinguish areas of pancreatic lesions and identify intact pancreatic parenchyma containing Langerhans islets. A highly significant increase in mean stiffness (p < 0.0001) was observed in postoperative pancreatic samples exhibiting signs of parenchymal fibrosis or PDAC invasion compared to unaffected, intact pancreatic parenchyma. For the first time, a relationship between stiffness values and the number of isolated pancreatic islets was demonstrated; in particular, the number of isolated islets significantly decreased (≤110 pcs/g) in samples exhibiting stiffness values above 150 kPa and below 75 kPa. The optimal stiffness range for the efficient isolation of islets (≥120 pcs/g) from pancreatic tissue was identified as 75–150 kPa. The study introduces a novel approach for rapid and objective intraoperative assessment of pancreatic tissue quality using real-time OCE data. This technique facilitates the identification of regions affected by pancreatic lesions and supports the selection of intact pancreatic parenchyma, potentially enhancing the accuracy of Langerhans islet yield predictions during surgical resection. Full article

Background: Optical genome mapping (OGM) detects genome-wide structural variants (SVs), including balanced rearrangements and complex copy-number alterations beyond standard-of-care cytogenomic assays. In chronic lymphocytic leukemia (CLL), cytogenetic and genomic risk stratification is traditionally based on fluorescence in situ hybridization (FISH), karyotyping, targeted next-generation sequencing (NGS), and immunogenetic assessment of immunoglobulin heavy chain variable region (IGHV) somatic hypermutation status, each of which interrogates only a limited aspect of disease biology. Methods: We retrospectively evaluated fifty patients with CLL using OGM and integrated these findings with cytogenomics, targeted NGS, IGHV mutational status, and clinical time-to-first-treatment (TTFT) data. Structural variants were detected using OGM and pathogenic NGS variants were derived from a clinical heme malignancy panel. Clinical outcomes were extracted from the electronic medical record. Results: OGM identified reportable structural variants in 82% (41/50) of cases. The most frequent abnormality was del(13q), observed in 29/50 (58%) and comprising 73% (29/40) of all OGM-detected deletions with pathologic significance. Among these, 12/29 (42%) represented large RB1-spanning deletions, while 17/29 (58%) were focal deletions restricted to the miR15a/miR16-1 minimal region, mapping to the non-coding host gene DLEU2. Co-occurrence of adverse lesions, including deletion 11q/ATM, BIRC3 loss, trisomy 12, and deletion 17p/TP53, were recurrent and strongly associated with shorter TTFT. OGM also uncovered multiple cryptic rearrangements involving chromosomal loci that are not represented in the canonical CLL FISH probe panel, including IGL::CCND1, IGH::BCL2, IGH::BCL11A, IGH::BCL3, and multi-chromosomal copy-number complexity. IGHV data were available in 37/50 (74%) of patients; IGHV-unmutated status frequently co-segregated with OGM-defined high-risk profiles (del(11q), del(17p), trisomy 12 with secondary hits, and complex genomes whereas mutated IGHV predominated in OGM-negative or structurally simple del(13q) cases and aligned with indolent TTFT. Integration of OGM with NGS further improved genomic risk classification, particularly in cases with discordant or inconclusive routine testing. Conclusions: OGM provides a comprehensive, genome-wide view of structural variation in CLL, resolving deletion architecture, identifying cryptic translocations, and defining complex multi-hit genomic profiles that tracked closely with clinical behavior. Combining OGM and NGS analysis refined risk stratification beyond standard FISH panels and supports more precise, individualized management strategies in CLL. Prospective studies are warranted to evaluate the clinical utility of OGM-guided genomic profiling in contemporary treatment paradigms. Full article

This paper proposes a resource optimized cascaded quantum surface repetition code architecture integrated with a Union Find (UF) enhanced hybrid decoder, which suppresses biased noise and improves the scalability of quantum error correction through synergistic inner outer quantum code collaboration. The hybrid architecture employs inner quantum repetition codes for local error suppression and outer rotated quantum surface codes for topological robustness, reducing auxiliary quantum qubits by 12.5% via shared stabilizers and compact lattice embedding. An optimized UF decoder employing path compression and adaptive cluster merging achieves near-linear time complexity $\mathcal{O}\left(n\alpha \right(n\left)\right)$, outperforming minimum-weight perfect matching (MWPM) decoders $\mathcal{O}\left(n^{2.5}\right)$. Under Z-biased noise $\eta =10$, simulations demonstrate a 28.2% error threshold, 2.6% higher than standard quantum surface codes, and 15% lower logical error rates via dynamic boundary expansion. At code distance $d=7$, resource savings reach 9.3% with maximum relative error below 8.5%, fulfilling fault-tolerance criteria. The UF decoder exhibits 38% threshold advantage over MWPM at low bias $\eta \approx {10}^{-3}$ and 15% less degradation at high noise $p=0.5$, enabling scalable real-time decoding. This framework bridges theoretical thresholds with practical resource constraints, offering a noise-adaptive QEC solution for near-term quantum devices including photonic quantum systems referenced in the paper’s background on repetition cat qubits. Full article

Background: Tic spectrum disorder (TSD), encompassing Tourette syndrome and chronic tic disorder, is a childhood-onset neurodevelopmental condition with complex genetic and environmental contributions. Heritable components have been implicated in TSD, but no clear genetic mechanisms have been identified. Significant aspects of TSD etiology remain unclear, with key uncertainties concerning the role of environmental influences in its development. In this study, we aimed to identify environmentally induced epigenomic and transcriptomic changes contributing to TSD pathology by investigating genetically similar monozygotic twins discordant for TSD. Methods: To investigate environmentally driven mechanisms, we analyzed peripheral blood from eleven monozygotic twin pairs, either discordant or concordant for TSD, using RNA sequencing and DNA methylation analysis. Results: Differential expression analysis identified a dozen differentially expressed genes between TSD and non-TSD individuals, most of which were long non-coding RNAs or pseudogenes. Expression of the small RNA gene RNY1 was significantly associated with tic severity, suggesting involvement of immune-related processes. DNA methylation (DNAm) analysis revealed ~30,000 probes with a nominal p < 0.05, however none of these were significant after multiple testing correction. Expression quantitative trait methylation (eQTM) analysis identified 236 methylation-associated genes. Gene set enrichment analysis demonstrated broad downregulation in TSD individuals for pathways related to translation, RNA processing, and neurobiological functions, with Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways including ribosome, nucleocytoplasmic transport, pluripotency signaling, and nicotine addiction. Conclusions: These results suggest that environmentally influenced gene expression may contribute to TSD pathogenesis through dysregulation of immune and neuronal pathways. Despite a small sample size, the monozygotic twin design provides strong control for genetic background and identifies significant differences that contribute to the understanding of the underlying molecular mechanisms of TSD. Full article

Background: Head and neck squamous cell carcinoma (HNSCC) remains the seventh most common cancer worldwide, characterized by late-stage diagnosis and poor 5-year survival rates. Oral squamous cell carcinoma (OSCC) is the most prevalent subtype. The identification of robust diagnostic, prognostic, and predictive markers is essential for personalized treatment monitoring. Methods: Following PRISMA and PICO standards, we conducted a comprehensive review of studies published over the past 10 years across PubMed/MEDLINE, Scopus, and Web of Science. The selection process was facilitated by AI-powered tools (Rayyan QCRI), and study quality was assessed using NOS or QUIPS. Results: 34 articles (including meta-analyses and original trials) were identified. Established clinical markers, such as p16-positivity (HR ≈ 0.55) and PD-L1 (CPS), remain significant. However, the molecular landscape is expanding to include high-risk lncRNA signatures (HR ≈ 2.50), immune checkpoints such as TIGIT (HR ≈ 1.85), and genomic alterations, including IL-10 promoter polymorphisms. We highlight that epigenetic silencing of p16 affects only about 25% of patients, while metabolic regulators (e.g., GLUT-1) and protein markers (e.g., MASPIN) offer critical predictive value for therapy response. Conclusions: The diagnostic and predictive paradigm is shifting toward a multi-omic approach that integrates DNA, RNA, proteins, and metabolic indicators. Future clinical use will rely on AI-driven multimarker panels and non-invasive liquid biopsies to enable real-time monitoring and de-escalation of treatment strategies. Full article

Background/Objectives: Sepsis is a critical medical emergency with significant morbidity and mortality, particularly in resource-limited countries. Effective strategies are essential to lower the high death rate. The sepsis code protocol recommends coordinated, structured, and prompt interventions for thorough patient care. This study aimed to compare in-hospital mortality rates after implementing the Sepsis Code protocol with those of a cohort of patients previously treated according to standard institutional guidelines. Methods: A pilot quasi-experimental study using a historical cohort design was conducted, involving patients with sepsis treated in an emergency department. Bivariate and multivariate analyses, as well as survival analysis, were conducted to evaluate the effectiveness of the intervention. Results: A total of 342 patients were analyzed. Among those who received the intervention, mortality was 13.4%, while in the control group, it was 22.5% (p = 0.042). Additionally, a protective association was found between the intervention and mortality (OR, 0.53; 95% CI, 0.29–0.94). Factors associated with increased mortality risk included lactate levels, SOFA score, septic shock presence, and history of diabetes. Conclusions: The implementation of the Sepsis Code in the emergency area showed an association with lower in-hospital mortality, especially in patients with septic shock. However, due to the study’s design, further research is needed to employ more robust methodologies and confirm the protocol’s applicability in the region. Full article