Background/Objectives: Damage Control Resuscitation (DCR) is a critical strategy in the management of severe trauma, focusing on the optimisation of the patient’s physiological condition. This study reviews current DCR strategies, emphasizing the mitigation of the “diamond of death”—hypothermia, acidosis, coagulopathy, and hypocalcemia—while addressing complex disturbances like respiratory distress syndrome (ARDS) and (acute kidney injury) AKI in high-ISS (Injury Severity Score) patients. Methods: A systematic review of 59 contemporary sources was conducted, encompassing clinical trials (e.g., CRASH-2), military-to-civilian protocol translations, and guidelines from the C and European Resuscitation Council. The analysis focused on pre-hospital interventions, in-hospital transfusion protocols, and the impact of transport logistics on survival. Results: Evidence highlights that aggressive crystalloid resuscitation (over 5 L) significantly increases mortality, favoring balanced blood component therapy (1:1:1 ratio) or Whole Blood guided by viscoelastic testing like rotational thromboelastometry (ROTEM) or thromboelastography (TEG). Pre-hospital success is driven by rapid hemorrhage control via tourniquets, early administration of Tranexamic Acid (TXA), no aggressive crystalloids, permissive hypotension, proactive calcium supplementation is recommended in early care. Furthermore, the integration of Helicopter Emergency Medical Services (HEMS) is independently associated with improved survival in multi-organ trauma by reducing time to definitive care and facilitating “en-route” damage control. Conclusions: The evolution of rescue strategies focused on mitigating the effects of the diamond of death, combined with the implementation of permissive hypotension and optimized HEMS logistics, constitutes the foundation of a modern model aimed at minimizing mortality in multi-organ trauma.

Background/Objectives: Asthma exacerbations are among the most frequent causes of pediatric emergency department (ED) visits, with over 700,000 annual cases in the United States and a significant number in Europe. Children under five years of age are particularly vulnerable to hospitalization. Methods: As timely assessment of exacerbation severity in the ED is critical, this review synthetizes data about tools such as the Pediatric Respiratory Assessment Measure (PRAM) and the Asthma Severity Score (ASS) aid in evaluating clinical status based on respiratory rate, oxygen saturation, accessory muscle use, and response to treatment. We also analyzed the proper management following established guidelines from GINA, NAEPP and other articles. Results: First-line therapy includes oxygen supplementation, short-acting beta-agonists (SABAs) administered frequently during the first hour, and early systemic corticosteroids. In moderate to severe cases, ipratropium bromide is added. For refractory or life-threatening presentations, intravenous magnesium sulfate, epinephrine, or ventilatory support may be required. Discharge is appropriate when symptoms resolve, oxygen saturation remains >94% on room air, and the child demonstrates adequate inhaler use. Hospitalization is indicated in cases of persistent hypoxemia, poor response, feeding difficulties, or social concerns. Post-discharge care includes thorough caregiver education, medication access, and a personalized asthma action plan to reduce recurrence risk. Conclusions: The effective diagnosis, appropriate exacerbation treatment, monitoring of patients in the post-attack period, as well as successful preventive medication play a key role in the management of pediatric patients with asthma.

Current scientific research demonstrates that cutaneous melanoma and mucosal melanoma are two distinct disease entities, considering the complexities of their diagnosis and treatment. Mucosal melanoma is characterized by a significantly poorer prognosis than cutaneous melanoma, with a 5-year overall survival (OS) rate of less than 20%. Surgical resection remains the gold standard of management; however, there is currently a paradigm shift away from routine, complication-prone completion lymph node dissection toward selective surveillance using serial ultrasound. This approach significantly improves patients’ quality of life without negatively impacting OS. Due to anatomical constraints (e.g., oral cavity, paranasal sinuses), narrow resection margins are supplemented with radiotherapy. Although this effectively reduces the risk of local recurrence, it does not prolong OS due to rapid distant metastasis, which occurs in approximately half of the patients within the first year. In systemic treatment, the standard of care involves dual immune checkpoint blockade (nivolumab plus ipilimumab) as well as BRAF/MEK and tyrosine kinase inhibitors (imatinib, nilotinib). The efficacy of immunotherapy in mucosal melanoma is significantly lower compared to that in cutaneous melanoma. The application of nivolumab plus ipilimumab yields slightly better outcomes than anti-PD-1 monotherapy; however, the proportion of patients achieving a durable response to treatment and the long-term survival rates remain highly unsatisfactory. The insufficient efficacy of current treatment paradigms highlights a critical need for the development of novel strategies. These include the broader application of Mohs micrographic surgery and the implementation of experimental therapies currently under investigation, such as anti-angiogenic treatments, oncolytic viruses, vaccines, adoptive T-cell therapies (e.g. CAR-T), bispecific antibodies (e.g. brenetafusp), and gut microbiome modulation.

Background: Obesity is fundamentally characterized by low-grade chronic inflammation (LGCI), driven by hypertrophic adipocytes and macrophage infiltration that release pro-inflammatory cytokines (e.g., TNF-α, IL-6). Vitamin D, recognized as a potent immunomodulator, holds significant potential in mitigating this inflammatory cascade. This review evaluates the impact of vitamin D supplementation on the pro-inflammatory cytokine profile and metabolic parameters in patients with obesity and metabolic syndrome. Methods: A comprehensive literature review was conducted using PubMed and Google Scholar databases. The analysis encompassed 31 scientific articles, including recent meta-analyses and randomized controlled trials (RCTs), focusing on the interplay between vitamin D, systemic inflammation, and obesity-related metabolic disturbances. Results: Current evidence indicates that vitamin D supplementation significantly reduces systemic inflammatory markers (IL-6, hs-CRP, TNF-α) and improves insulin resistance indices (HOMA-IR) and lipid profiles. However, supplementation alone does not induce significant reductions in body mass index (BMI) or total adipose tissue volume. Furthermore, owing to vitamin D sequestration in adipose tissue and volumetric dilution, patients with obesity require personalized, high-dose regimens (often ≥4,000 IU/day) to achieve optimal serum 25(OH)D levels (30–50 ng/mL) necessary for clinical immunomodulation. Conclusions: While vitamin D is not a standalone weight-loss intervention, it serves as a crucial adjunctive therapy for modulating the LGCI associated with obesity. Current data do not support extrapolating these anti-inflammatory effects to a definitive reduction in cardiometabolic risk. However, achieving optimal serum levels requires personalized dosing to address altered pharmacokinetics, alongside essential lifestyle modifications, including diet and exercise.

Background: The microbiota-gut-brain axis provides a biologically plausible framework for bidirectional communication between intestinal microorganisms and the central nervous system. Human studies have reported gut microbiota differences in autism spectrum disorder (ASD), attention-deficit hyperactivity disorder (ADHD), and schizophrenia, but the reproducibility and clinical meaning of these observations remain uncertain. Objective: To critically summarize human evidence on gut microbiota composition in ASD, ADHD, and schizophrenia, and to assess clinical evidence for probiotic and synbiotic formulations and fecal microbiota transplantation (FMT) in these disorders. Methods: A focused narrative review was conducted using PubMed and supplementary Google Scholar searches. Publications from 1 January 2012 to 31 December 2024 were considered, and the final search update was completed on 28 February 2025. Forty-two publications were purposively selected and synthesized; original human studies were prioritized whenever available. Evidence was interpreted with attention to study design, sample size, medication exposure, diet, gastrointestinal symptoms, stool characteristics, sequencing and bioinformatics methods, outcome selection, safety reporting, and risk of reverse causality. Because this was a narrative rather than a systematic review, no PRISMA flow diagram, duplicate independent screening, formal study-level risk-of-bias instrument, or new quantitative pooling was used. Results: Across all three disorders, individual studies and meta-analyses report group-level microbiota differences, but no reproducible disorder-specific microbial signature has been established. In ASD, dietary selectivity, gastrointestinal symptoms, and stool consistency explain an important proportion of reported associations. ADHD studies are generally small and yield conflicting diversity and taxonomic findings. In schizophrenia, associations are influenced by antipsychotic exposure, metabolic status, smoking, diet, and illness chronicity. Controlled trials and meta-analyses have not shown consistent improvement in core symptoms with probiotic or synbiotic products. Early uncontrolled microbiota-transfer studies in ASD suggested possible benefits, but a 2024 randomized placebo-controlled FMT trial did not demonstrate improvement in its primary clinical outcome. Evidence for FMT in ADHD is limited to a case report, and no controlled human efficacy evidence was identified for schizophrenia. FMT carries infectious, procedural, and uncertain long-term risks. Conclusions: Gut microbiota differences in ASD, ADHD, and schizophrenia should currently be regarded as associated features rather than established causes, diagnostic biomarkers, or validated therapeutic targets. Routine microbiome testing, probiotics or synbiotics for core symptoms, and FMT cannot be recommended as standard treatments for these disorders. Future studies require longitudinal designs, careful control of diet and medication, standardized laboratory methods, preregistered clinical outcomes, adequate power, external validation, and systematic safety monitoring.

Attention-Deficit/Hyperactivity Disorder (ADHD) is a prevalent neurodevelopmental disorder traditionally linked to monoaminergic dysregulation within the brain’s reward circuitry. Recent evidence points to the potential role of the gut-brain axis (GBA), a bidirectional communication network linking the central nervous system with the enteric microbiota. This narrative review explores the proposed associations between intestinal dysbiosis and ADHD symptoms, as well as the potential for GBA-targeted therapeutic interventions. Research suggests that individuals with ADHD may exhibit distinct microbial profiles, characterized by an increased abundance of genera such as Bifidobacterium and Bacteroides , and a depletion of anti-inflammatory taxa like Faecalibacterium . These shifts are hypothesized to contribute to “leaky gut” syndrome, potentially triggering systemic inflammation and neuroinflammation that could disrupt neural circuits responsible for executive function. Furthermore, experimental models indicate that gut microbes may modulate the availability of dopamine precursors, indirectly influencing reward processing. Preliminary clinical data suggest that “psychobiotics,” synbiotics, and targeted micronutrient supplementation (e.g., iron, zinc, and magnesium in cases of confirmed deficiencies) might serve as supportive interventions and potentially improve quality of life. While standard pharmacotherapy remains the primary treatment, GBA-focused strategies are being investigated as adjunctive therapies, offering a promising yet preliminary avenue for personalized management. Integrating these interventions may help manage common comorbidities across the lifespan, though further robust clinical trials are required.