Search Results (17,882)

Background: Sub-Saharan Africa is undergoing a rapid epidemiological transition marked by a growing burden of non-communicable diseases, including breast, cervical, ovarian, and uterine cancers, which constitute major causes of morbidity and mortality among women in the region; however, comprehensive assessments of long-term trends and regional heterogeneity remain limited. This study examines the burden and temporal trends of breast, cervical, ovarian, and uterine cancers across sub-Saharan Africa from 1990 to 2023. Methods: A retrospective ecological analysis was conducted using data from the latest Global Burden of Disease 2023 study. Age-standardised incidence rates, mortality rates, and disability-adjusted life year rates were estimated for breast, cervical, ovarian, and uterine cancers across 48 sub-Saharan African countries and four sub-regions. Temporal trends were assessed from 1990 to 2023, with percentage changes calculated to characterise epidemiological transitions. Geographic variation and age-specific patterns were examined to identify high-burden settings and priority populations. Results: Between 1990 and 2023, the burden of all four cancers increased substantially across sub-Saharan Africa, with significant regional and country-level heterogeneity. Breast cancer exhibited the largest absolute burden, with incidence increasing by over 120 percent and mortality by more than 80 percent, particularly in Central and Western Africa. Cervical cancer remained the leading cause of cancer-related mortality among women in Eastern and Southern Africa, despite evidence of stabilisation or decline in selected countries. Ovarian and uterine cancers demonstrated sustained upward trends, especially in Central Africa, with high mortality-to-incidence ratios indicating late diagnosis and limited treatment access. Across all cancer types, Central and Eastern sub-Saharan Africa consistently experienced the highest disability-adjusted life year burdens. Conclusions: The burden of the selected cancers in sub-Saharan Africa has increased markedly over the past three decades, with persistent regional inequities reflecting gaps in prevention, early detection, and treatment capacity. Strengthening cancer surveillance systems, expanding equitable access to screening and vaccination programmes, and improving diagnostic and treatment infrastructure are critical to reversing current trends. These findings provide region-specific evidence to guide cancer control priorities and resource allocation across sub-Saharan Africa. Full article

Background/Objectives: Group A Streptococcus (GAS) pharyngitis is a frequent cause of morbidity in pediatric populations, which requires timely identification to prevent complications such as acute rheumatic fever. Rapid antigen detection tests (RADTs) are practical alternatives to throat culture. This study evaluates the diagnostic performance of the RapidFor™ Strep A test. Methods: This prospective clinical study enrolled 389 pediatric patients aged < 18 years with symptoms suggestive of streptococcal pharyngitis. Two throat swabs were collected from each patient: one for rapid antigen testing with RapidFor™ Strep A and one for culture. Sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) were calculated. Results: Throat culture was positive in 95 of 389 patients (24.4%). The RapidFor™ Strep A test demonstrated a sensitivity of 98.95% (95% confidence interval [CI]: 94.28–99.81%) and a specificity of 96.26% (95% CI: 93.43–97.90%). The PPV was 89.52%, and the NPV was 99.65%. Agreement with culture was excellent (κ = 0.919); in particular, false-positive results accounted for 2.8% and false-negative results accounted for 1.05%. Fever was the strongest clinical indicator associated with positive results. Conclusions: The RapidFor™ Strep A test showed very high diagnostic accuracy compared with throat culture, including an excellent NPV (99.6%), which supports its reliability for ruling out GAS pharyngitis in pediatric settings. The test is an effective screening tool that facilitates timely antibiotic therapy. Full article

Foodborne diseases remain a major public health challenge. Among them, salmonellosis is one of the most frequently reported illnesses, associated with clusters and outbreaks and with considerable morbidity, potentially severe in vulnerable populations. Children are more susceptible due to biological, behavioral, and dietary factors. This study aimed to summarize and describe national surveillance data from the Mandatory Notification System, combined with serotyping data, on reported salmonellosis cases in Greece during the period 2005–2024, with a focus on children aged 0–14 years. During the study period, a total of 7340 salmonellosis cases were reported among children aged 0–14 years. Notification rates declined gradually until 2021, followed by an increase through 2024. The mean annual notification rate was 23.0 cases per 100,000 population, with the highest incidence observed among children aged 0–4 years. A clear seasonal pattern was observed, with a peak during summer months, alongside notable geographical variation. The most frequently identified serovars were Salmonella Enteritidis and Salmonella Typhimurium. These findings indicate that salmonellosis remains a public health concern in the pediatric population, highlighting the need for enhanced surveillance, improved food hygiene practices, and targeted prevention strategies to reduce disease burden. Full article

Background/Objectives: Sarcopenia (SP) and osteoporosis (OP) are common yet underrecognized complications of liver cirrhosis, contributing to increased morbidity and mortality. Their coexistence, termed osteosarcopenia (OS), represents a compounded musculoskeletal impairment. Insulin-like growth factor 1 (IGF-1), synthesized in the liver, has been implicated in muscle and bone metabolism. This study aimed to assess the prevalence and association of laboratory and clinical parameters with SP, OP, and OS in cirrhotic patients, with a focus on IGF-1 deficiency and their impact on mortality. Methods: This cross-sectional study included 100 cirrhotic patients at a tertiary center. Sarcopenia was diagnosed using CT-derived L3 skeletal muscle index and osteoporosis via the DEXA scan. IGF-1 levels and metabolic parameters were measured. Multivariate logistic regression identified laboratory and clinical factors associated with musculoskeletal complications. However, due to the cross-sectional design, causal relationships could not be inferred. Results: SP, OP, and OS were present in 41%, 22%, and 11% of patients, respectively. IGF-1 levels were significantly lower in patients with SP, OP, and OS (p < 0.05) and were independently associated with increased risk of SP (OR = 1.797, p = 0.006), OP (OR = 1.873, p = 0.045), and OS (OR = 2.326, p = 0.003). Mortality rates were significantly higher among patients with OS (72.7%), OP (77.3%), and SP (56.1%). OS conferred the highest adjusted mortality risk (OR = 2.739, p = 0.009), followed by SP (OR = 2.278, p = 0.015) and OP (OR = 1.958, p = 0.036). Conclusions: Musculoskeletal complications are highly prevalent and predictive of mortality in cirrhosis. IGF-1 deficiency is a strong independent biomarker for SP, OP, and OS. Routine screening and early intervention targeting IGF-1 pathways and nutrition may improve outcomes in this population. Full article

Background/Objectives: The study’s goal is to assess the association between long-term statin therapy and influenza incidence, influenza severity, and all-cause mortality. Methods: Two population-based dynamic cohorts (exposed and unexposed to statins) were followed from 2010 to 2019. Participants were 60 years or older; frail patients were excluded. The primary outcomes were influenza incidence, influenza-related intensive care unit (ICU) admission as a proxy for severity, and all-cause mortality. The exposed cohort comprised new statin users with a minimum of two pharmacy invoices within 90 days of enrollment. Adjusted risk ratios (aRRs) for influenza incidence, ICU admission, and mortality rate were calculated using Poisson regression. Results: The initial study population of 639,564 individuals was evenly split into exposed (319,782) and unexposed (319,782) cohorts; mean age was 71 years (standard deviation: 8 years), and 57% were women. Compared to non-users, new statin users showed a higher influenza incidence [9.39 (95% confidence interval: 9.36–9.42) vs. 7.64 (7.61–7.66) per 1000 person-years], ICU admission [1.65 (1.65–1.66) vs. 1.36 (1.35–1.36) per 1000 person-years], and overall mortality rate [97.09 (96.75–97.43) vs. 94.15 (93.82–94.47) per 1000 person-years]. Adjusted analysis revealed no significant association between statin use and influenza incidence [aRR: 1.04 (0.98–1.10)] or influenza-related ICU admission [aRR: 1.03 (0.89–1.19)] and shifted the effect on mortality from harmful to beneficial [aRR: 0.88 (0.87–0.89)]. Conclusions: Despite new users’ greater vulnerability at the start of treatment, our findings indicate that statins do not influence influenza incidence or severity but reduce all-cause mortality, warranting further exploration of their anti-inflammatory properties. Full article

Peste des Petits Ruminants (PPR), a highly contagious disease of domestic and wild small ruminants, is characterized by severe morbidity and mortality. PPRV, the causative agent, is a morbillivirus in the family Paramyxoviridae. The virus poses a significant barrier to sustainable agricultural development in the developing world. Currently, no effective therapeutics agent for PPRV infection is available. Ginsenoside Rb3, the major bioactive constituent in the plants of ginseng, was reported to exert a wide range of pharmacologic and immunologic effects. However, it is unclear whether Ginsenoside Rb3 can act as an antiviral against PPRV infection. Here, we show that Ginsenoside Rb3 exhibits significant antiviral activity against PPRV in cell culture models. The mechanism of action of Ginsenoside Rb3 against PPRV is mainly attributed to its ability to inhibit PPRV-mediated autophagy, thus leading to promotion of interferon responses. In summary, our study establishes Ginsenoside Rb3 as a novel antiviral agent effective against PPRV, sheds light on its mode of action, and reveals a novel immunomodulatory strategy that may prove essential for combating both current and future viral outbreaks. Full article

Drug-induced kidney injury remains a major clinical challenge associated with diverse therapeutic agents and is an important cause of acute kidney injury, chronic renal dysfunction, and treatment-related morbidity. Growing evidence indicates that nephrotoxicity caused by anticancer, immunosuppressive, and anti-infective drugs is strongly driven by oxidative stress and redox homeostasis disruption. Excessive production of reactive oxygen species (ROS) in renal tubular cells overwhelms endogenous antioxidant defenses and triggers mitochondrial dysfunction, inflammatory signaling, and activation of stress-responsive pathways that culminate in tubular injury and renal functional decline. These processes promote apoptosis, necrosis, microvascular injury, and a reduction in the glomerular filtration rate, while dysregulation of redox-sensitive pathways involved in cell survival and repair further heightens renal vulnerability. This review summarizes current mechanistic insights into oxidative stress-mediated pathways of drug-induced nephrotoxicity, with emphasis on their translational relevance. In addition, it discusses emerging biomarkers for early detection and highlights recent advances in antioxidant-based and redox-modulating strategies that may help prevent renal injury and preserve kidney function. Full article

Background: Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by immune dysregulation and systemic inflammation, with the cardiovascular (CV) system representing a major yet frequently under-recognized target. Cardiac involvement spans from subclinical myocardial inflammation to overt pericardial disease, myocarditis, valvular abnormalities, coronary microvascular dysfunction, and accelerated atherosclerosis. Given that CV disease remains a leading cause of morbidity and mortality in SLE, early detection of silent cardiac injury is crucial. Aim: This review aims to provide a comprehensive and clinically oriented overview of CV involvement in SLE, focusing on the role of multimodal cardiac imaging in the detection, characterization, and risk stratification of cardiac abnormalities, as well as its potential implications for clinical management and preventive strategies. Methods: This narrative review is based on a structured, non-systematic search of PubMed (2013–2026), combining the term “systemic lupus erythematosus” with imaging-related keywords including “transthoracic echocardiography,” “cardiac magnetic resonance,” and “cardiac computed tomography.” English-language studies in adult populations were screened and selected according to clinical relevance, methodological robustness, and contribution to understanding SLE-related cardiac involvement. Discussion: Multimodal cardiac imaging plays a central role in the evaluation of SLE-related cardiac disease. Transthoracic echocardiography (TTE) represents the first-line modality for the assessment of ventricular function, pericardial disease, and valvular abnormalities, while deformation imaging enables the detection of subtle myocardial dysfunction. Cardiac magnetic resonance (CMR) provides comprehensive tissue characterization, allowing differentiation between active inflammation and chronic fibrosis. Cardiac computed tomography (cCT) identifies subclinical coronary atherosclerosis and high-risk plaque features, whereas nuclear imaging techniques offer insight into inflammatory activity and microvascular dysfunction. Conclusions: An integrated, imaging-based approach enables early diagnosis, refined CV risk stratification, longitudinal monitoring, and personalized therapeutic strategies. Multimodal imaging thus represents a key pillar of precision medicine in lupus-associated CV disease. Full article

Therapeutic termination of pregnancy (TToP) represents an intervention that is performed for medical reasons, such as risks to maternal health or severe fetal anomalies. Advances in prenatal screening and diagnostic tools—including serum markers, ultrasound, cell-free fetal DNA, chorionic villus sampling and amniocentesis—have significantly improved early detection and clinical decision-making. This narrative review synthesizes current knowledge on the genetic, environmental and psychosocial determinants that influence the decision of the patients to pursue TToP. The literature search was performed primarily using PubMed database, while Scopus and Google Scholar were used to identify additional relevant studies. Some of the selected studies, as well as certain sections of this review, address both therapeutic and voluntary termination of pregnancy, whereas others focus exclusively on TToP. Moreover, this review describes the types of abortion (medical or surgical/aspiration) along with their management strategies to prevent or address potential complications. It is well known that demographic, cultural and socio-economic factors continue to influence the access to TToP, as well as the perceptions of it. Psychiatric comorbidities (such as anxiety, affective and psychotic disorders) are observed with a higher prevalence among women undergoing TToP and may influence both the decision and psychological outcomes post-procedure. While most women report emotional relief after TToP, some of them experience depression, post-traumatic stress disorder or substance misuse. Legal and ethical considerations further complicate access to safe abortion, leading to situations where patients may resort to unsafe procedures, which result in higher rates of morbidity and mortality. Data from the EUROCAT network show rising trends in congenital anomalies like trisomy 13, trisomy 18 and caudal regression syndrome (conditions commonly associated with TToP). Therefore, it is mandatory to form a multidisciplinary team in these cases, integrating medical, psychological and ethical dimensions. Ensuring safe, evidence-based and compassionate access to TToP remains a critical component of reproductive healthcare. Full article

Background/Objectives: Cardiorenal syndrome type 2 (CRS-2) is characterized by progressive renal dysfunction caused by chronic heart failure (HF) and is associated with increased morbidity and mortality. However, the prognostic value of renal biomarkers in patients with CRS-2 hospitalized for decompensated HF remains unclear. Methods: This prospective observational cohort study included 200 consecutive patients hospitalized for decompensated HF in the Intensive Care Unit of the Clinic for Internal Medicine at the University Clinical Centre Tuzla between April and October 2025. CRS-2 was defined as chronic HF with chronic kidney disease persisting for ≥3 months before admission according to KDIGO criteria. Patients were followed for three months. The primary composite outcome was all-cause mortality or initiation of renal replacement therapy. Results: CRS-2 was identified in 130 patients (65.0%) and was associated with higher in-hospital mortality (32.3% vs. 11.4%, p = 0.002) and three-month mortality (44.6% vs. 21.4%, p = 0.002). Within the CRS-2 subgroup, patients who experienced the primary composite outcome had higher admission levels of cystatin C and urinary albumin-to-creatinine ratio (UACR) and lower estimated glomerular filtration rate (eGFR). ROC analysis demonstrated moderate discriminative ability of cystatin C (AUC 0.739) and UACR (AUC 0.733). In Cox regression analysis, cystatin C (HR 1.534, 95% CI 1.263–1.863, p < 0.001) and UACR (HR 1.003, 95% CI 1.001–1.006, p = 0.001) were significantly associated with the primary composite outcome. Conclusions: Renal dysfunction markers, particularly cystatin C and albuminuria, are associated with early adverse outcomes in CRS-2 patients hospitalized for decompensated HF. Routine assessment of these biomarkers may provide additional prognostic information and support risk assessment in this high-risk population. Full article

Cardiovascular diseases (CVDs) remain the primary cause of human morbidity and mortality in the world. Inflammation, oxidative stress, and vascular remodeling are the key factors that make CVDs worse. The nuclear factor κB (NF-κB) signaling pathway is a major regulator in the progression of CVDs. NF-κB activates wrongly, induces the secretion of pro-inflammatory cytokines (including TNF-α, IL-6, and IL-1β), and enhances reactive oxygen species (ROS) generation. These accelerate endothelial dysfunction, myocardial damage, and atherosclerotic plaque development. Natural products are structurally diverse, multi-targeted, and low toxicity. They offer a promising way to prevent and treat cardiovascular disease by modulating the NF-κB signaling pathway. This review summarizes the recent studies about using natural products (including flavonoids, terpenoids, alkaloids, polyphenols, and polysaccharides) to treat CVDs through the NF-κB pathway, with a critical analysis of evidence strength according to CVDs indication (atherosclerosis, myocardial ischemia/reperfusion injury, pulmonary arterial hypertension, etc.) and study type (in vitro, in vivo animal, and human clinical research). We detail their molecular mechanisms, such as inhibiting the nuclear translocation of NF-κB p65, downregulating IκB phosphorylation, blocking upstream signaling (e.g., TLR4/MyD88, PI3K/Akt, MAPK), and affecting with other pathways (e.g., Nrf2/HO-1, SIRT1) to reduce inflammation and oxidative stress together. We also detail the effects of these natural products in various CVDs models, including atherosclerosis, hypertension, myocardial ischemia/reperfusion injury, diabetic cardiomyopathy, and pulmonary arterial hypertension, highlighting the characteristics of their treatments. Finally, we discuss the challenges of bringing natural products into the clinic and share some ideas to solve difficulties, with an in-depth critical analysis of the translational bottlenecks (poor bioavailability, unclear structure–activity relationships, incomplete mechanistic elucidation, and lack of large-scale clinical trials) and their underlying causes across different natural product classes. In summary, this review offers new perspectives on developing natural product-based therapies targeting the NF-κB signaling pathway for CVDs. It offers useful references for both preclinical studies and clinical applications. Full article

Posttraumatic stress disorder (PTSD) has been linked to impaired physical function, which in turn predicts falls, morbidity, and mortality. However, few studies have used objective measures such as handgrip strength to assess physical function. In this cross-sectional study, we investigated associations of average PTSD symptom severity and symptom domain severity with measures of maximum handgrip strength and handgrip asymmetry from 11/2021–12/2023, among 381 male firefighters and emergency medical responders who responded to the World Trade Center disaster, using covariate-adjusted linear regression models. PTSD was diagnosed using the Structured Clinical Interview for the DSM-5 in 17% of responders. Greater overall PTSD average symptom severity was associated with weaker maximum handgrip strength (β = −4.43 lbs; 95%; CI: −8.77, −0.09; p = 0.045). Higher re-experiencing symptom severity was associated with weaker maximum handgrip strength (β = −4.17 lbs; 95% CI: −8.13, −0.22; p = 0.039). Avoidance symptoms were associated with weaker handgrip strength in adjusted models (β = −4.14 lbs; 95% CI: −7.56, −0.73; p = 0.018), and associated with a larger negative difference assessing for hand asymmetry (β = −2.20 lbs; 95% CI: −4.18, −0.22; p = 0.029). Findings suggest that PTSD may contribute to long-term physical decline, even in populations with high baseline fitness. Full article

The remarkable evolution of oncological therapies has dramatically improved cancer survival rates but has simultaneously introduced a significant burden of cardiovascular complications. Cardio-oncology has emerged as a critical multidisciplinary field focused on mitigating the “collateral damage” of life-saving anticancer treatments, ranging from traditional chemotherapeutics to novel immunotherapies. This review provides a comprehensive analysis of the pathophysiological mechanisms, clinical phenotypes, and evolving management strategies for cancer therapy-related cardiac dysfunction (CTRCD). An extensive synthesis of the current literature was conducted, focusing on the molecular pathways of cardiotoxicity, including Topoisomerase IIβ inhibition by anthracyclines, HER2 signaling disruption by targeted agents, and immune-mediated myocarditis triggered by checkpoint inhibitors (ICIs). Cardiotoxicity is increasingly recognized as a spectrum of phenotypes. Heart failure with reduced ejection fraction (HFrEF) remains a primary concern with cytotoxic agents, while heart failure with preserved ejection fraction (HFpEF) is emerging as a critical complication of radiation therapy and tyrosine kinase inhibitors (TKIs). The integration of advanced diagnostic tools—specifically Global Longitudinal Strain (GLS) and Cardiac Magnetic Resonance (CMR) mapping—has shifted the clinical focus toward subclinical detection. Furthermore, pivotal clinical trials such as PRADA and SUCCOUR have validated early pharmacological prophylaxis and strain-guided interventions. Emerging challenges, including the management of CAR-T cell-induced cytokine release syndrome and the specific cardiovascular needs of pediatric and geriatric populations, are also explored. The future of cardio-oncology lies in precision medicine, leveraging genomic profiling and artificial intelligence to identify high-risk individuals. A proactive, multidisciplinary approach is essential to ensure that the success of modern oncology is not compromised by irreversible cardiovascular morbidity. Full article

Wild mushroom consumption is widespread worldwide and remains an important cause of foodborne intoxication. This concise review analyzes recent literature on the geographic distribution of poisonous wild mushrooms and the epidemiological patterns of intoxication reported in Asia, Europe, and the Americas. Most poisoning incidents occur as a result of the misidentification of toxic species as edible during mushroom foraging. Alongside well-known poisonous mushrooms, several newly identified toxic species have been reported in recent years. The available epidemiological evidence demonstrates clear regional clustering of poisoning incidents, pronounced seasonal peaks associated with mushroom growth, and a predominance of cases in populations where wild mushroom foraging is a traditional practice. Amatoxin-containing species of the genus Amanita remain the leading cause of severe and fatal intoxications worldwide. Overall, the analyzed studies indicate that wild mushroom poisoning continues to represent a significant food safety and public health concern, particularly in Asia and parts of Europe. Improved toxicological surveillance, public awareness, and timely clinical management are essential for reducing morbidity and mortality associated with these intoxications. Full article

Stroke remains a major cause of morbidity and mortality worldwide. Although reperfusion therapies and secondary prevention have advanced, the global stroke burden continues to rise, driven by increasing rates of hypertension and diabetes mellitus. Type 2 diabetes (T2DM) increases the risk of acute ischemic stroke (AIS) through mechanisms involving chronic hyperglycemia, endothelial dysfunction, inflammation, and accelerated atherogenesis. In recent years, glucagon-like peptide-1 receptor agonists (GLP-1RAs) have emerged as promising agents for cardiovascular and cerebrovascular risk reduction in patients with T2DM. Beyond their glucose-lowering properties, GLP-1RAs improve blood pressure regulation and lipid metabolism, as mentioned in the 2025 AHA Journal guidelines for the prevention, detection, evaluation, and management of high blood pressure in adults. Emerging preclinical and clinical evidence indicates that GLP-1RAs also provide direct neurovascular protection by stabilizing the blood–brain barrier, modulating neuroinflammation, and promoting neuronal survival. These mechanisms may reduce ischemic injury, improve recovery after stroke, and protect against cognitive decline. Major cardiovascular outcome trials have demonstrated significant reductions in major adverse cardiovascular events and, to a lesser degree, non-fatal stroke among patients receiving GLP-1RAs. This narrative review evaluates current evidence on the neurovascular, cardiometabolic, and anti-inflammatory actions of GLP-1RAs and their potential role in mitigating stroke risk and promoting cerebrovascular health. Additionally, it highlights gaps in the literature, explores clinical and guideline implications, and outlines future directions for integrating GLP-1RA therapy into comprehensive stroke prevention and recovery strategies. Full article