Accurate diagnosis of bacterial meningitis is critical, particularly in young febrile infants. Although commercially available multiplex PCR assays enable rapid pathogen detection, these typically do not include Salmonella spp. or other Enterobacteriaceae, which may result in missed diagnoses and/or inappropriate treatment duration. We report the case of a 2-month-old female infant with Salmonella enteritidis meningitis and concurrent bacteremia. The patient initially presented with fever, lethargy, and a bulging anterior fontanelle. Cerebrospinal fluid (CSF) analysis was highly suggestive of bacterial meningitis. However, both CSF culture and the FilmArray ME Panel were negative, likely due to prior empirical antibiotic therapy at another hospital. The causative organism was isolated on blood cultures. The infant was treated with intravenous ceftriaxone for 24 days and discharged in excellent clinical condition. Twelve days later, she was readmitted with a relapse of meningitis and bacteremia caused by the same pathogen. She received combination therapy with cefotaxime and cotrimoxazole for 37 days, followed by cefotaxime monotherapy for another 26 days. Immunological evaluation, including assessment of immunoglobulin levels, lymphocyte subsets, and interferon-γ receptor and Interleukin-12 receptor expression, was normal. The patient had a favorable outcome with complete clinical and laboratory recovery and a normal neurodevelopmental outcome at follow-up. Salmonella meningitis is a rare but life-threatening condition in infants, which may be overlooked when relying on molecular diagnostic panels that do not include this pathogen. Negative CSF PCR results should be interpreted with caution in the presence of typical cytological and biochemical findings of bacterial meningitis. Prolonged antimicrobial therapy of at least 4-6 weeks is essential to prevent relapse and ensure optimal microbiologic and clinical outcomes.

Gaucher disease is a rare autosomal recessive lysosomal storage disorder that is caused by a deficiency of the enzyme "β-glucocerebrosidase", leading to the accumulation of glucocerebroside within macrophages. It commonly presents with hepatosplenomegaly, cytopenias, and bone marrow infiltration. Gaucher disease is a pan-ethnic lysosomal storage disorder reported worldwide. Although few cases have been described in Pakistan and other South Asian countries, limited awareness and restricted access to diagnostic testing may contribute to underdiagnosis and delayed recognition in this region. We report the case of a 2-year-old girl who presented with fever and cough of 1 week's duration. Her mother reported normal birth and development until 6 months of age, after which she developed progressive weakness and abdominal distension. She had a history of recurrent hospitalizations for anemia, chest infections, and abdominal swelling. Family history revealed consanguinity and early childhood deaths of two siblings and one cousin with similar complaints. The clinical examination revealed pallor, weakness, and marked hepatosplenomegaly. A complete blood count showed features of pancytopenia; therefore, a bone marrow examination was advised, which demonstrated characteristic Gaucher cells, supporting a presumptive diagnosis of Gaucher disease. Symptomatic treatment was initiated, and the patient was referred to Children Hospital, Lahore, Pakistan.

Seasonal affective disorder (SAD) and bipolar disorder (BD) with a seasonal pattern are conventionally framed as disorders of photoperiod and circadian timing, yet affected individuals also show a striking, reproducible metabolic rhythm-carbohydrate craving and weight gain in winter, appetite reduction and weight loss in summer-that has rarely been integrated into mechanistic models of seasonal mood cycling. Building on an evolutionary "metabolic plasticity" view, in which seasonal shifts in energy storage are conserved adaptations that can become maladaptive in predisposed individuals, we propose the Seasonal Metabolic Oscillation (SMO) hypothesis: that the seasonal expansion and contraction of adipose tissue is not merely a passive symptom but a candidate mediator and amplifier of seasonal mood cycling. We advance two claims of deliberately unequal evidentiary strength. The better-supported core claim is that winter adiposity amplifies and helps maintain the depressive phase, by promoting low-grade neuroinflammation and indoleamine 2,3-dioxygenase (IDO1) activation, which diverts tryptophan into the kynurenine pathway, and by adding leptin resistance and stress-axis dysregulation that together bias the brain toward depression. The more tentative, exploratory claim is that the spontaneous loss of adiposity in summer relieves this inflammatory burden and, through photoperiod-driven changes in dopaminergic and circadian signaling, may lower the threshold for mood elevation in predisposed individuals. Pleiotropic circadian and metabolic variants, including ZBTB20 and NPAS2, are proposed to confer joint vulnerability to SAD, obesity, and bipolar spectrum illness. The model yields a central, falsifiable prediction-that within the same individuals seasonal swings in adiposity statistically precede and account for a defined share of seasonal mood change-and is directly testable through weight-stabilization experimental-medicine trials, within-subject longitudinal biomarker tracking, and Mendelian randomization. We stress that the model's two central assumptions-that seasonal adiposity change temporally precedes mood change, and that a swing of the modest magnitude typical of SAD is quantitatively sufficient to move central neurochemistry-remain experimentally undemonstrated, and that photoperiod is a plausible common cause of both adiposity and mood that only designs decoupling the two can exclude. If supported, SMO would reframe seasonal mood disorders as recurrent metabolic-neuroimmune-mood conditions and motivate metabolically informed screening, pharmacotherapy, and chronotherapy.

Hypoglycemia is a frequent finding after simultaneous pancreas-kidney (SPK) transplantation, but its etiology is often multifactorial and challenging to interpret. We report a rare case of late-onset severe hypoglycemia secondary to a neuroendocrine tumor arising in a pancreatic allograft. A 60-year-old man with type 1 diabetes mellitus underwent SPK transplantation in 2007 with immediate graft function and long-term metabolic stability. Ten years post-transplant, partial pancreatic graft dysfunction and progressive vascular complications were noted. In 2024, 17 years after transplantation, the patient developed recurrent, documented hypoglycemic episodes despite withdrawal of glucose-lowering therapy, with fasting plasma glucose values as low as 40 mg/dL and a marked reduction in HbA1c. Biochemical evaluation suggested endogenous hyperinsulinism, with elevated chromogranin A levels. Imaging studies revealed a large hypervascular mass within the pancreatic graft, with high somatostatin receptor expression on 68Ga-DOTA-TOC PET-CT. Histology from biopsy and subsequent total graft pancreatectomy confirmed a well-differentiated grade 2 neuroendocrine tumor with focal insulin expression, consistent with insulinoma. Surgical resection resulted in complete resolution of hypoglycemia. This case highlights the need to consider rare but clinically significant causes of hypoglycemia in SPK recipients and underscores the importance of a comprehensive, multidisciplinary diagnostic approach integrating continuous glucose monitoring, biochemical markers, and advanced imaging.

Primary care clinics in Puerto Rico operate under compounding financial, workforce, infrastructural, and environmental constraints that threaten continuity and quality of care. Understanding how these clinics sustain operations under chronic systemic stress and recurrent disasters can yield resilience strategies applicable to safety-net and rural primary care settings more broadly.

This study investigates the latent motivational structure and qualitative manifestations of motivational withdrawal among some Chinese higher vocational college students learning College English within exam-oriented instructional contexts. Drawing on Self-Determination Theory (SDT) and Learned Helplessness Theory (LHT), the study investigates how diminished self-determined motivational support and perceived effort ineffectiveness are reflected in students' reported experiences and observable disengagement.

Post-pancreatitis diabetes mellitus after acute pancreatitis (PPDM-A) is increasingly recognized as a distinct metabolic complication rather than a simple subtype of type 2 diabetes. This narrative review summarizes current evidence on PPDM-A, with emphasis on terminology, diagnostic timing, epidemiology, pathophysiology, risk factors, clinical phenotypes, screening, prevention, and long-term follow-up. A structured literature search was conducted in PubMed/MEDLINE, Scopus, and Google Scholar to identify relevant studies. PPDM-A may develop after mild, moderately severe, or severe acute pancreatitis, although the risk is greatest in patients with pancreatic necrosis, recurrent attacks, exocrine pancreatic dysfunction, obesity, dyslipidemia, fatty liver disease, metabolic comorbidities, and marked in-hospital glycemic variability. A major diagnostic challenge is distinguishing transient stress hyperglycemia and previously unrecognized diabetes from incident PPDM-A. Formal diagnosis should generally be established no earlier than 90 days after the index episode of acute pancreatitis to minimize misclassification due to transient stress-related dysglycemia. Follow-up assessment should combine fasting plasma glucose and HbA1c, whereas a 75-g oral glucose tolerance test (OGTT) may provide greater sensitivity during early recovery, particularly when HbA1c is unreliable, results are borderline or discordant, or isolated postprandial dysglycemia is suspected. Current evidence indicates that PPDM-A develops through interacting pathogenic domains, including pancreatic endocrine injury with impaired β-cell reserve, metabolic dysregulation characterized by insulin resistance and persistent inflammation, exocrine pancreatic dysfunction with nutritional consequences, and emerging mechanisms involving gut microbiome alterations, bile acid-FGF19 signaling, and extracellular vesicle-mediated communication. Available data support a trajectory-based model in which some patients recover normal glucose metabolism, some develop persistent intermediate dysglycemia, and others progress to overt diabetes over months or years. Structured post-discharge surveillance, risk-stratified follow-up, assessment of exocrine dysfunction, and prevention of recurrent pancreatic injury are essential for improving early detection, reducing diagnostic misclassification, and optimizing long-term clinical outcomes.

Osteomyelitis (OM) is an infectious disease caused by the invasion of bone tissue by pathogenic microorganisms. It is frequently associated with biofilm formation, residual sequestra, local ischemia and hypoxia, elevated oxidative stress, and immune dysfunction. Conventional treatments rely on systemic antibiotics, surgical debridement, antibiotic-loaded bone cement, and bone transport techniques. Although these approaches can control infection in some cases, they remain limited by insufficient drug penetration, nondegradable materials, the need for secondary surgery, difficulty in repairing bone defects, and the risk of recurrence. In recent years, emerging biomaterials have provided new therapeutic strategies for OM by enabling the local delivery of antimicrobial agents, antimicrobial peptides, metal ions, or gaseous molecules, often in combination with photothermal therapy, sonodynamic therapy, pH/enzyme-responsive systems, and immunomodulation. The aim of this mini-review is to briefly summarize the pathological features of OM, outline the major design strategies of biomaterials currently used for OM treatment, and discuss the challenges associated with their clinical translation.