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Diabetes insipidus is characterized by polyuria and polydipsia, often resulting from central or nephrogenic causes. In diabetic emergencies, hyperosmolar hyperglycemic state (HHS), severe hypernatremia, and ventricular fibrillation are life-threatening conditions that require prompt intervention. This report describes a 47-year-old male with poorly controlled diabetes mellitus, who developed coma, excessive thirst, polyuria, hyperglycemia (47.29 mmol/L), hypernatremia (195.6 mmol/L), and plasma hyperosmolality (385 mOsm/kg). Despite fluid resuscitation and insulin therapy, refractory hypernatremia persisted, leading to a diagnosis of central diabetes insipidus (CDI). The patient also developed ventricular fibrillation, which was managed with defibrillation. Concurrently, desmopressin and blood purification were administered to address CDI and severe hypernatremia. This case emphasizes the importance of considering CDI when polyuria persists despite glucose control. The occurrence of ventricular fibrillation underscores the necessity of continuous cardiac monitoring in the context of hypovolemia and severe electrolyte imbalance. We propose that diabetes mellitus-related vascular injury impairs blood flow in the hypothalamus-pituitary tract, disrupting arginine vasopressin synthesis and secretion, contributing to CDI in poorly controlled diabetes mellitus.

Eleonora's falcon (Falco eleonorae) has a unique ecology that makes it ideal for studying predator-prey dynamics. Its diet shifts seasonally, with insects dominating the non-breeding and pre-laying periods, and birds becoming the main prey during chick-rearing. This systematic review explores the falcon's foraging behavior during the pre-breeding and breeding phases within its global breeding range, emphasizing insect prey. Following PRISMA guidelines, the review includes studies from ten Mediterranean countries and the Canary Islands. Literature was sourced from Web of Science, Google Scholar, PubMed, and Scopus, covering both peer-reviewed and grey literature up to 2024. From 18 scientific publications and personal observations, 120 insect species and morphospecies from 47 families were recorded as prey. Coleoptera, Hymenoptera, and Hemiptera were the most frequent insect orders. Migratory species such as Acherontia atropos, Anax parthenope, and Anax ephippiger were also documented. This review contributes valuable knowledge for future studies on the dietary ecology of Eleonora's falcon and similar raptors.

Water metabolism is fundamental to sustaining physiological functions in living organisms and plays a particularly vital role in poultry, especially laying hens. It directly influences their health status and production performance. Follicular development, a crucial phase in the reproductive cycle of laying hens, is highly sensitive to water availability. Insufficient hydration can lead to increased stress, reduced synthesis of ovarian hormones, and impaired follicular maturation, while excessive hydration may disturb osmotic balance and interfere with normal follicle growth. Although existing studies have preliminarily demonstrated a link between water metabolism and follicular function, the molecular mechanisms - particularly those involving aquaporins, hormonal receptors, and intracellular signaling pathways - have not been comprehensively elucidated. By integrating molecular biology techniques, physiological indicators, and imaging analysis, this study reveals how water status regulates follicular development through the modulation of AQP1 and AQP3 expression, activity of follicle-stimulating hormone and luteinizing hormone receptors, and the MAPK/ERK and PI3K/Akt signaling pathways. It was found that water restriction significantly downregulated AQP1 and AQP3 expression and reduced FSH receptor and LH receptor activities. These molecular adjustments likely serve as adaptive responses to minimize water loss and preserve the stability of the follicular microenvironment. Meanwhile, water-restricted conditions enhanced MAPK/ERK activation and attenuated PI3K/Akt signaling, further influencing follicular growth. These findings contribute to a more refined understanding of the role of water metabolism in reproductive regulation and provide theoretical support for optimizing breeding strategies under hydration-related stress conditions.

To investigate the causal relationship between two adverse reproductive outcomes (male infertility and spontaneous abortion) and COVID-19 infection using Mendelian randomization (MR) analysis. A two-sample MR study was conducted to examine potential causal links between COVID-19 infection severity and reproductive outcomes, using large-scale genome-wide association study (GWAS) summary statistics from European-ancestry populations. GWAS summary statistics were analyzed for COVID-19 phenotypes (infection: n = 1,683,769; hospitalized: n = 1,557,411; very severe respiratory-confirmed: n = 1,388,342; critical illness: n = 10,056) and reproductive outcomes (spontaneous abortion: n = 98,453; male infertility: n = 73,479). Causal estimates were calculated using inverse variance weighted (IVW), weighted median, MR-Egger regression, and weighted mode methods. IVW analysis revealed no significant association between genetic susceptibility to COVID-19 infection and male infertility (odds ratio [OR] = 0.7668; 95% confidence interval [CI]: 0.3798-1.5484; p = 0.4590) or spontaneous abortion (OR = 0.9936; 95% CI: 0.8066-1.2241; p = 0.8518). Similar null associations between COVID-19 severity phenotypes (hospitalized, very severe respiratory-confirmed, and critical illness) and male infertility or spontaneous abortion were observed. Sensitivity analyses using alternative methods confirmed the absence of pleiotropy and heterogeneity. This two-sample MR analysis provides robust evidence against a causal relationship between COVID-19 and increased risks of male infertility or spontaneous abortion.

The immunoproteasome regulatory component proteasome activator subunit beta (PSME2) plays a crucial role in immune regulation, yet its impact on intestinal barrier integrity in ulcerative colitis (UC) remains unclear. This study aimed to elucidate the involvement of PSME2 in UC pathogenesis. Clinical samples from UC patients and healthy controls were analyzed to assess PSME2 expression. A dextran sulfate sodium-induced colitis mouse model was employed to evaluate disease progression, colon histology, and PSME2 levels. In vitro, colonic cells were treated with lipopolysaccharide (LPS) to examine tight junction protein (claudin-1) expression and inflammatory mediators (IL-6, IL-10, TNF-α). Autophagy modulation was investigated using PSME2 silencing and chloroquine (CQ) treatment. PSME2 upregulation in UC and colitis mice correlated with disease severity. In vitro, LPS suppressed claudin-1 expression, while PSME2 knockdown restored claudin-1 levels and reduced inflammatory cytokines. PSME2 depletion enhanced autophagy, as indicated by an increased LC3-II/LC3-I ratio, reduced p62, and elevated LC3B puncta. CQ treatment reversed the protective effects of PSME2 silencing, confirming autophagy's role in barrier integrity. PSME2 exacerbates intestinal inflammation by promoting cytokine release and disrupting epithelial barrier function through autophagy dysregulation. Suggesting its potential as a therapeutic target.

Stüve-Wiedemann syndrome (SWS) is a rare autosomal recessive genetic disorder characterised by skeletal dysplasia, dysautonomia, and multi-system abnormalities. It is typically caused by variants in the leukaemia inhibitory factor receptor (LIFR) gene. This case report presents a novel and complex heterozygous variant in the LIFR gene in a 2-month-old Chinese infant, which contributes to the limited literature on SWS in the Chinese population and underscores the importance of early identification and intervention. The infant was born at 38 weeks of gestation via caesarean section due to breech presentation. He presented with multiple symptoms, including persistent pulmonary hypertension of the newborn, recurrent hyperthermia, and joint deformities. Whole exome sequencing identified a novel compound heterozygous variant in the LIFR gene. The infant underwent various interventions, including mechanical ventilation, inhaled nitric oxide, and nasogastric feeding. Despite these measures, the infant experienced recurrent hyperthermia episodes leading to multi-organ dysfunction. The infant was eventually stabilised, but follow-up revealed global developmental delay and persistent skeletal abnormalities. Early identification of the LIFR gene variant is crucial for timely intervention and management of multi-system complications. Further research is warranted to explore targeted therapies and improve outcomes for patients with this rare disorder.

Cancer immunotherapy has revolutionized oncologic treatment by harnessing and reprogramming the immune system to target malignant cells. This review provides a comprehensive picture of modern approaches to immunotherapy-based treatment strategies, such as immune checkpoint inhibitors (ICIs), chimeric antigen receptor T cells, mRNA vaccines, and biomaterials-based platforms, with a focus on their translational value and application to precision medicine. Emerging insights into the tumor microenvironment, immune resistance mechanisms, and T-cell subpopulation dynamics (e.g., γδ T cells, exhausted CD8⁺ T cells) are analyzed to elucidate immunotherapy response variability. Biomaterials such as injectable scaffolds, nanogels, and artificial antigen-presenting cells enable localized and sustained immune modulation, improving delivery precision and therapeutic efficacy. Personalized approaches, including neoantigen vaccine development and artificial intelligence (AI)-assisted biomarker prediction, are rapidly advancing individualized treatment regimens. Clinical trials illustrate how combination strategies with ICIs, chemotherapy, and nanomedicine enhance patient survival. Despite challenges including immune-related adverse events, manufacturing complexity, and global access disparities, integration of AI and multi-omics platforms promises to optimize patient stratification and therapeutic outcomes. This evolving paradigm positions personalized immunotherapy at the forefront of future oncologic care.

The long-term survival and quality of life of liver transplantation (LT) recipients has emerged as a critical focus, where managing sarcopenia (a syndrome of diminished muscle mass and strength) and perioperative nutrition is paramount. This study aimed to delineate the knowledge landscape and identify key research trends and potential molecular mechanisms linking LT and sarcopenia through bibliometric and bioinformatics analyses. This study employs bibliometric and bioinformatics analyses to evaluate research trends and molecular mechanisms linking LT and sarcopenia. Data were retrieved from Web of Science database, and tools such as CiteSpace, VOSviewer, and R were used for data analysis and visualization. A total of 448 studies published over the past two decades were analyzed. Our bibliometric analysis revealed geographical distribution patterns, authorship networks, journal contributions, and thematic trends related to both LT and sarcopenia. Bioinformatics analysis identified 78 biphenotypic target genes shared by LT and sarcopenia, with hub genes including IL1B, ADIPOQ, and TNF showing strong associations. Enrichment analyses further highlighted significant biological processes, such as "response to peptide hormone" and "regulation of glucose transmembrane transport," suggesting potential molecular mechanisms underlying the interaction between LT and sarcopenia. This study highlights the importance of incorporating routine sarcopenia assessments into the clinical management of LT candidates to optimize treatment strategies. Future research should focus on elucidating the molecular pathways connecting these conditions and developing targeted interventions to improve LT patients' outcomes and quality of life.

Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection. A rare but severe complication is haemophagocytic lymphohistiocytosis (HLH), an aggressive syndrome of excessive immune activation. Managing both conditions is particularly challenging in patients with multiple comorbidities. A 78-year-old male with a complex history, including myasthenia gravis and chronic kidney disease, was admitted with sepsis. Investigations confirmed infection with methicillin-resistant Staphylococcus aureus and human herpesvirus 8. He was subsequently diagnosed with HLH based on bone marrow findings of haemophagocytosis and elevated soluble CD25 levels. He was treated with a combination of antibiotics, immunomodulatory agents, and supportive care. After 21 days of treatment, the patient's condition improved significantly. This case highlights the importance of early recognition and timely intervention in the management of sepsis and HLH in patients with multiple comorbidities. A multidisciplinary approach and individualised treatment strategies are crucial for improving patient outcomes.

The development of lung squamous cell carcinoma (LUSC) is associated with the intratumoral microbiota. To facilitate faster clinical decisions and predict patient prognosis, we constructed an intratumoral microbial abundance prognostic scoring (MAPS) model for LUSC and analyzed its prognostic performance. Data on the LUSC tumor microbiome, patient survival, and clinical information were downloaded from The Cancer Microbiome Atlas and The Cancer Genome Atlas databases. Differentially abundant microbial genera in LUSC tumors were analyzed, and their prognostic value was evaluated. The differential abundance of key genera in the MAPS model was validated using lung adenocarcinoma (LUAD) tumors and normal tissues. Of 52 microbial genera with increased abundance and 437 with decreased abundance in LUSC tumors, 462 were highly related to the disease. Seven of 13 genera that were significantly related to prognosis were selected to construct the MAPS model. The MAPS risk grouping was identified as a prognostic risk factor for LUSC. Among the seven genera in the MAPS model, Indibacter, Oceanospirillum, Thalassomonas, and Thermopetrobacter differed in abundance between LUAD tumors and normal tissues and may be the key intratumoral microorganisms involved in LUSC and LUAD development. In conclusion, our MAPS model may be a powerful prognostic biomarker for LUSC.