Life-Basel最新文献

Light-induced membrane fusion has become a pivotal technique for constructing and functionalizing synthetic cells by enabling precise control over membrane merging events. Traditional fusion approaches that rely on chemical, physical, and mechanical stimuli frequently lack both specificity and reversibility, limiting their utility in mimicking dynamic cellular processes. Here, we review advances employing photosensitive molecules and optogenetic tools that facilitate spatiotemporally controlled fusion of lipid and polymer vesicles, enabling dynamic content exchange and membrane remodeling. These approaches have enhanced synthetic cell assembly, molecular transport, and signal transduction, with applications extending to drug delivery and biosensing. Despite challenges in efficiency and biocompatibility, ongoing innovations in photosensitizer design and light activation strategies promise to expand the capabilities of synthetic biology platforms. This work underscores the potential of light-induced fusion to advance the development of intelligent nanomaterials and functional synthetic cellular systems.

Isolated, confined, and extreme environments hold the opportunity to collect unique biomedical data. These often-remote places present specific medical challenges for deployed expeditioners. Here we report a case of acute severe high altitude pulmonary oedema (HAPE) and its management at a remote research station in Antarctica. At the beginning of the 2023 summer campaign at Concordia Station (3200 m AMSL), a technician presented with shortness of breath and compromised circulation three days after arrival on site. Immediate diagnostics and medical treatments with high-flow oxygen and the use of a mobile hyperbaric chamber after initial resuscitation were administered. Within a time window of 24 h, evacuation to sea level was organised via aircraft (flight duration 4 h, non-pressurised cabin) inside the mobile hyperbaric chamber. The patient was discharged from medical treatment 48 h later in Christchurch (NZ). We conclude that despite rigorous pre-deployment screening, even experienced expeditioners can develop critical medical conditions that require prompt reaction and rescue. Structured assessment tools can aid in their recognition and management.

Childhood obesity has emerged as a major global health challenge, with a marked increase in prevalence. Defined by excessive fat accumulation, it is associated with an increased risk of developing metabolic syndrome (MetS) and metabolic dysfunction-associated steatotic liver disease (MASLD). These conditions share common pathophysiological mechanisms, involving chronic low-grade inflammation, adipose tissue dysfunction, and insulin resistance. Excess weight contributes to the development of MetS even in the pediatric population through abdominal fat accumulation, dyslipidemia, hypertension, and hyperglycemia, while also creating a pro-inflammatory state that enhances hepatic fat accumulation, leading to MASLD. It is a bidirectional relationship, with MASLD increasing the risk of hypertension and the development of MetS individual components and as a whole. Adipose tissue, especially visceral fat, acts as a metabolic and immunologic organ, producing pro-inflammatory cytokines, which further accentuate insulin resistance and hepatic injury. The "three-strike" hypothesis illustrates the progression of MASLD. Several inflammatory biomarkers, including C-reactive protein, interleukins, adipokines, and serum ferritin, have been studied to monitor and predict disease progression in pediatrics. However, their diagnostic value in children remains limited due to age-related variability and lack of standardized pediatric cut-off points. A unified definition of pediatric MetS and MASLD is crucial to improve study comparability and clinical applicability. Such standardization would support the development of targeted strategies for early identification and intervention.

Over the past 30 years, cardiovascular diseases (CVD) have become the dominant contributor to the global disease burden, accounting for approximately 93% of prevalence, 54% of mortality, and 60% of disability-adjusted life-years lost [...].

Background: Patients with benign prostatic hyperplasia (BPH) have an increased risk of developing cardiovascular disease. Taking alpha-1 blockers is associated with an increased risk of major adverse cardiovascular events. Patients suffering from ischemic stroke (IS) may develop baroreflex and parasympathetic dysfunction-induced cerebral autoregulation impairment. The relationship between pharmacotherapy for BPH and the risk of recurrent IS remains unclear. The purpose of this study was to determine whether medications for BPH increase the risk of recurrent IS.

Methods: This is a retrospective cohort study. Data from patients diagnosed with IS between 2000 and 2015 was collected from Taiwan National Health Insurance Database. Newly diagnosed IS patients were identified (International Classification of Diseases, Ninth Edition, Clinical Modification (ICD-9-CM): 433-437). BPH patients with an ICD-9-CM of 600 were identified. The event observed was recurrent IS after the firstever IS. The factors associated with recurrent IS were assessed via Cox proportional hazards regression.

Results: Recurrent IS was associated with BPH with an adjusted hazard ratio (HR) of 1.505 and a 95% confidence interval (CI) of 1.112-1.829, p < 0.001), and a competing risk model showed an adjusted HR of 1.544 (95% CI: 1.128-1.896, p < 0.001). The adjusted HR for treatment with alpha-1 blockers was 1.581 (95% CI: 1.16-1.915, p < 0.001), and increased risk with adjusted HR for treatment with high doses of 5-alpha reductase inhibitors over a long period of time are also at risk of recurrent IS.

Conclusions: These findings highlight the association between BPH incidence and the risk of recurrent IS. The pharmacotherapy for BPH in IS patients should take great care.

Background: Advanced stages of peripheral arterial disease, particularly chronic limb-threatening ischemia, are characterized by unfavorable limb outcomes and a substantial risk of major amputation. Clinical evaluation traditionally focuses on arterial obstruction; however, venous dysfunction may coexist and contribute to local limb pathophysiology in advanced PAD, remaining insufficiently recognized in routine practice. Methods: We performed a retrospective cohort analysis of consecutive patients with advanced peripheral arterial disease managed at the First Surgical Clinic of the Emergency County Clinical Hospital of Craiova over a five-year period (January 2020 to December 2024). Venous disease was defined using a clinically oriented composite definition incorporating imaging-confirmed venous pathology, prior deep venous thrombosis, and persistent lower-limb edema attributable to venous dysfunction. Arterial disease severity was assessed using multimodal imaging. Analyses were performed at both patient and limb levels to evaluate associations between venous disease, arterial severity markers, and clinical outcomes. Results: Among 241 patients (482 limbs), concomitant venous disease was identified in 68.9% at the patient level and was predominantly unilateral. At the limb level, venous disease was significantly associated with markers of severe arterial involvement, including inflow disease, higher segment occlusion scores, impaired tibial runoff, and absence of a patent pedal arch. Despite greater arterial severity, patients with venous disease exhibited a lower unadjusted rate of major amputation compared with those without venous involvement. Conclusions: Concomitant venous disease is highly prevalent in patients with advanced PAD and is closely linked to arterial disease severity. These findings suggest that venous dysfunction represents an integral component of advanced limb-threatening ischemia rather than an isolated comorbidity. Incorporating clinically oriented venous assessment may improve understanding of limb pathophysiology and support a more integrated arterio-venous approach to advanced PAD management.

Despite progress in understanding the molecular mechanisms of diseases, the dominant paradigm in explaining pathogenesis remains the concept of a pathogen's direct damaging effect on parenchymal cells. Based on years of research, the authors of this article propose a revision of traditional views on disease pathogenesis. We emphasize the pivotal role of the microvasculature. Existing morphological studies provide insufficient insight into the role of these structures in the development of the pathological process. We conducted a search in international databases to find literary sources current as of December 2025. As an evidence base for the presented concept, we used the results of our own studies published from 1989 to the present. Data from the literature on non-infectious diseases are also separately presented. Our novel data from investigation of infectious and non-infectious diseases demonstrate that even in the initial stages of a pathological process, the microvessels of organs become the primary target of damage. The cascade of pronounced changes in parenchymal cells triggered by this initial event determines the development of the disease. The work examines the cellular and molecular aspects of the interaction between microvessels, pathogens, and the surrounding tissue. The proposed concept provides an objective and fundamentally new explanation for known facts. An important contribution of this concept is its potential to reveal promising directions for further research and for developing innovative approaches to disease therapy.

Background: Advances in genome-wide DNA-based technologies have fundamentally transformed prenatal genetic diagnostics, enabling detection of clinically significant submicroscopic chromosomal abnormalities that are not identifiable by conventional cytogenetic methods. These developments have important implications for the diagnosis and management of pregnancies complicated by fetal structural abnormalities, as they enable more accurate etiological diagnosis, improved prognostic assessment, and more informed clinical decision-making and reproductive counselling.

Methods: This narrative review synthesizes contemporary international evidence on prenatal genetic diagnostic approaches, including conventional karyotyping, chromosomal microarray analysis (CMA), and genome-wide sequencing technologies. The review focuses on diagnostic performance, clinical utility, ethical considerations, and implementation within diverse healthcare systems.

Results: Accumulating evidence demonstrates that genome-wide approaches-particularly CMA and sequencing-based methods-provide a higher diagnostic yield in fetuses with structural anomalies, with an incremental yield of approximately 3-5% over conventional karyotyping. This is mainly due to their ability to detect pathogenic copy number variants below the cytogenetic resolution of karyotyping. These technologies improve etiological insight, enhance genotype-phenotype correlation, and support more precise prognostication and reproductive counselling, especially in pregnancies with fetal structural anomalies. Emerging sequencing platforms further expand the diagnostic spectrum by integrating copy number and sequence-level variant detection.

Conclusions: Genome-wide Copy Number Variation (CNV) analysis represents a critical component of contemporary prenatal diagnostics and should be integrated into invasive prenatal testing pathways in accordance with international recommendations. Genome-wide approaches need robust counselling frameworks and equitable health policy implementation to spread. The expense, lack of required experience, and variation in healthcare infrastructure across locations make widespread deployment difficult.

Background: Motor imagery (MI) and mirror therapy (MT) are widely used neurorehabilitation strategies to enhance motor recovery after stroke and are commonly applied as adjuncts to conventional rehabilitation therapy (CRT). However, direct comparative evidence between these interventions remains limited. This systematic review compared the effects of MI and MT on motor function, functional performance, spasticity, and gait-related outcomes in adults after stroke. Methods: A systematic comparative review with narrative synthesis was conducted following PRISMA guidelines and registered in PROSPERO (CRD420251274308). PubMed, Cochrane Library, CINAHL, Scopus, Web of Science, and ScienceDirect were searched up to July 2025. Clinical trials directly comparing MI and MT in adults with stroke were included. Methodological quality was assessed using the PEDro scale, and risk of bias was evaluated with the Cochrane RoB 2 tool. Results: Six clinical trials involving 206 participants were included. Both MI and MT were associated with significant pre-post improvements across motor function, functional performance, spasticity, and gait-related outcomes. Between-group comparisons yielded heterogeneous findings, with no consistent evidence supporting the superiority of either intervention. Isolated advantages of MI were reported for specific upper-limb subdomains, but these effects were not consistently replicated. Overall methodological quality ranged from low to moderate, and all included studies were judged to be at high risk of bias according to the RoB 2 tool. Conclusions: MI and MT appear to provide comparable benefits for motor and functional recovery after stroke when used as adjuncts to CRT. Current evidence does not support the preferential use of one intervention, highlighting the need for well-designed trials with improved methodological rigor.

Cardiometabolic and cardiovascular risks are commonly assessed using body mass index (BMI) and static measures of adiposity; however, individuals with similar BMI frequently exhibit markedly different metabolic and cardiovascular outcomes. This heterogeneity reflects not only differences in fat distribution but also variation in adipose tissue function and its temporal regulation. Adipose tissue contains intrinsic circadian clocks that coordinate daily rhythms in lipid storage and mobilization, insulin sensitivity, adipokine secretion, and immune activity in alignment with sleep-wake and feeding-fasting cycles. Circadian misalignment, as occurs with shift work, irregular sleep, or mistimed food intake, disrupts this coordination and promotes adipose tissue dysfunction characterized by impaired rhythmic lipid handling, altered endocrine signaling, inflammation, fibrosis, and oxidative stress. Emerging evidence suggests that circadian dysregulation may differentially affect adipose depots, including visceral, epicardial, and perivascular fat, thereby linking chronodisruption to insulin resistance, endothelial dysfunction, atherosclerosis, heart failure phenotypes, and arrhythmia susceptibility. This narrative review synthesizes human, experimental, and translational studies examining adipose tissue circadian regulation as a functional determinant of cardiometabolic and cardiovascular risk beyond BMI. We also discuss the clinical implications of circadian-informed strategies, including chrononutrition and time-restricted eating, as potential tools to improve risk stratification and cardiometabolic health.