Search Results (1,963)

Reproductive emergencies in male dromedary camels (Camelus dromedarius) threaten fertility, health, and welfare but remain poorly documented. This review consolidates knowledge on the diagnosis, management, and prognosis of acute reproductive pathologies, including traumatic injuries (testicular trauma, penile hematoma, and preputial laceration), obstructive conditions (urethral obstruction, phimosis, and paraphimosis), vascular emergencies (spermatic cord torsion, priapism), inflammatory diseases (orchitis, epididymitis, pizzle rot), congenital anomalies (persistent frenulum), iatrogenic complications, and pharmacologic-induced dysfunction. Systematic breeding soundness examination and ultrasonography are indispensable for assessing testicular perfusion and guiding intervention. Given the scarcity of camel-specific literature, this narrative clinical review integrates evidence from published camelid studies, relevant reports from other domestic species, and representative clinical observations documented by the authors to provide a practical framework for diagnosis and management. Field constraints, the stoic nature of camels, and harmful ethnoveterinary practices often delay diagnosis and compromise outcomes. Prognosis varies considerably depending on the condition and timeliness of intervention; early aggressive management can preserve reproductive function, while delayed treatment frequently results in permanent infertility or death. Given the economic and cultural importance of camels in arid regions, improving outcomes for reproductive emergencies is essential for sustaining breeding programs and enhancing animal welfare. This narrative clinical review integrates published literature with representative clinical observations and retrospective field cases to summarize the diagnosis, management, and prognosis of reproductive emergencies in male dromedary camels. It also provides a structured clinical framework to support veterinarians in managing these acute conditions and highlights critical gaps requiring further research. Full article

Background: Synaptic plasticity in neurodegenerative disorders (NDs), cognitive impairment, and mental health conditions is regulated by brain-derived neurotrophic factor (BDNF). Even healthy individuals have different levels, which are affected by complex epigenetic, inflammatory, and metabolic regulation. BDNF expression changes are associated with both typical and abnormal aging, as well as mental health conditions. These changes affect brain areas that are crucial for memory, such as the hippocampus and the parahippocampal cortex. Neurotrophins (NTs), including nerve growth factor (NGF) and BDNF, are essential for neuronal differentiation via tropomyosin receptor kinase B (TrkB) and the p75 neurotrophin receptor (p75NTR). Dysregulated NTs signaling contributes to synaptic dysfunction and neuroinflammation. Objective: This systematic review synthesizes preclinical evidence of the potential of naturally derived compounds to modulate NTs for neuroprotection and their incorporation into novel foods. Methodology: A review of major databases found studies that examined the impact of dietary polyphenols and other bioactive substances on NT signaling oxidative stress, inflammation, and neuronal plasticity. Results: Compounds such as epigallocatechin gallate, resveratrol, curcumin, quercetin, and flavanols, can positively impact NTs, reducing reactive oxygen species/reactive nitrogen species, enhancing cell survival, and increasing the expression of trophic factors such as nuclear factor erythroid 2-related factor 2 (Nrf2), NGF, and vascular endothelial growth factor in neural stem cells. However, their bioavailability, optimal dosage, and dietary interactions require further research. Conclusions: The consumption of BDNF-promoting foods can potentially stimulate BDNF synthesis, support optimal neurotransmission, and fortify neural plasticity. Evidence supports a polyphenol-rich diet for preventing NDs and promoting brain health. Observational studies consistently support the protective effects of polyphenols on brain health through their impact on the gut–brain axis. Full article

Orthohantavirus infections are classically associated with hemorrhagic fever with renal syndrome (HFRS) in Eurasia and hantavirus cardiopulmonary syndrome (HCPS) in the Americas. However, accumulating evidence indicates that the clinical spectrum is considerably broader, with frequent involvement of organ systems beyond the kidney and lung. Hepatic manifestations, in particular, may mimic acute viral hepatitis, leading to diagnostic challenges and underrecognition. This paper synthesizes published evidence on hepatic involvement in orthohantavirus infection, with a focus on clinical presentation, pathogenic mechanisms, differential diagnosis, biomarkers, and public health implications. Relevant literature was identified through searches of peer-reviewed articles, with emphasis on studies reporting hypertransaminasemia, hepatitis-like illness, and liver injury in confirmed hantavirus infections. Mild to moderate elevations in aminotransferases are common during acute orthohantavirus infection, and in some patients the clinical picture may be dominated by fever, thrombocytopenia, and hepatitis-like abnormalities, closely resembling dengue, leptospirosis, or classical viral hepatitis. Hepatic injury appears to result primarily from systemic endothelial dysfunction, immune-mediated inflammation, and microvascular leakage rather than direct hepatocytopathic effects. Emerging biomarkers of severity, including thrombocytopenia, neutrophil-to-lymphocyte ratio, soluble thrombomodulin, and IL-6 trans-signaling, reflect widespread vascular and inflammatory activation. Diagnostic delays are frequent, particularly in non-endemic regions, due to low clinical awareness and overlapping features with more common febrile hepatotropic syndromes. Orthohantavirus infection should be considered in the differential diagnosis of acute febrile illness with unexplained hypertransaminasemia and thrombocytopenia, especially when epidemiological clues suggest rodent exposure or compatible environmental contexts. Recognizing hepatic involvement as part of a systemic endothelial syndrome may improve diagnostic accuracy, reduce underreporting, and facilitate earlier supportive management. Increased awareness among hepatologists, infectious disease specialists, and emergency physicians is warranted. Full article

In recent years, bisphenol F (BPF) and bisphenol S (BPS) have been used in several everyday products to replace bisphenol A (BPA), since exposure to BPA has been associated with the development of several pathologies. However, recent studies have also been associating exposure to BPA substitutes with the development of various pathologies, including cardiovascular diseases, and the safety of BPA substitutes for human health has been questioned. Thus, this study aimed to investigate and compare BPA, BPF and BPS effects on arterial tone and to explore the mechanisms involved. The results suggest that BPA, BPS and BPF exert non-genomic and endothelium-independent relaxant effects on arteries and smooth muscle cells from the umbilical cord. Regarding genomic effects, the results suggest that BPA, BPF, and BPS disrupted the primary mechanisms underlying HUA relaxation by interfering with the cGMP signaling pathway and modulating the Ca²⁺ channels activity. Moreover, these results suggest that BPF alters the vasorelaxant response more than BPA and BPS. Therefore, replacing BPA with its substitutes does not appear to be beneficial for human cardiovascular health. Thus, in the future, the vascular effects of these bisphenols should be further evaluated to clarify their modes of action and future implications for maternal-fetal health. Full article

Background/Objectives: Hearing loss and dementia are highly prevalent conditions in older adults and represent a growing public health challenge. Over the past decade, a substantial body of epidemiological evidence has demonstrated a consistent association between age-related hearing loss and cognitive dysfunction, including incident dementia. However, the nature of this relationship remains incompletely understood. Methods: This narrative review provides a structured overview of current evidence, focusing on epidemiological findings, mechanistic pathways, and clinical implications. Hearing loss has been associated with both accelerated cognitive decline and increased dementia risk, with a clear severity–impact relationship. Results: Several interacting mechanisms have been proposed, including increased cognitive load, structural and functional brain changes, social isolation, and shared vascular and metabolic risk factors. Emerging concepts such as the “auditory brain” and central auditory dysfunction further suggest that hearing impairment may also represent an early manifestation of neurodegenerative processes. Intervention studies have yielded mixed results. While hearing rehabilitation improves communication and quality of life, randomized evidence has not consistently demonstrated a reduction in cognitive decline in the general population, but potential benefits may exist in higher-risk subgroups. Increasing attention has been directed toward the role of neuroplasticity, with evidence suggesting that delayed intervention may limit the effectiveness of rehabilitation due to long-standing auditory deprivation. Conclusions: Taken together, current evidence suggests that hearing loss may represent both a potentially modifiable risk factor and an early marker of cognitive decline. Early identification and timely management of hearing impairment may therefore play an important role in maintaining cognitive and brain health and improving quality of life in older adults. Full article

Astragalus membranaceus, a medicinal plant used in traditional Chinese medicine for centuries, has attracted growing scientific attention for its potential anti-aging and anticancer properties, particularly for skin and bone health. Its key bioactive compounds like astragalosides, cycloastragenol, and its commercial derivative TA-65, have been associated with telomerase activation and telomere maintenance, suggesting a possible role in modulating cellular senescence and tissue repair processes. In addition to the claimed telomere maintenance, A. membranaceus exhibits antioxidant, anti-inflammatory, and DNA-protective activities, properties that contribute to its anti-aging effects. Emerging evidence also suggests that telomerase modulation by A. membranaceus influences cancer cell dynamics, either suppressing tumor progression through immune regulation and apoptosis induction or, in some contexts, potentially promoting tumor growth. This duality highlights the importance of dose, formulation, and targeted application. Clinically, TA-65 has been reported to improve vascular health, bone mineral density, and skin elasticity in aging individuals. Preclinical studies further support its protective effects against osteoporotic bone loss and photoaging-induced dermal degeneration. This review summarizes the phytochemical composition of A. membranaceus and critically evaluates the mechanistic and therapeutic evidence underlying its anti-aging and anticancer actions on skin and bone tissues. It also discusses the pharmacokinetic properties of A. membranaceus, including its absorption, bioavailability, and safety profile. The integration of A. membranaceus into evidence-based senile therapeutic strategies holds promise, but further mechanistic and clinical studies are required to optimize its safety and efficacy. Full article

Adolescence is a developmental stage marked by dynamic interactions between diet, the gut microbiome and endocrine maturation, creating a physiological environment in which early metabolic disturbances can rapidly translate into long-term cardiovascular vulnerability. This narrative review summarises the latest research on the diet–microbiome–hormone axis in adolescents, focusing on the metabolic pathways through which microbial metabolites influence host physiology. Short-chain fatty acids (SCFAs), microbially transformed bile acids and postbiotic signalling molecules regulate enteroendocrine communication, insulin sensitivity, vascular function and inflammatory tone, thereby linking dietary exposures to early cardiometabolic alterations. Dysbiosis, driven by ultra-processed dietary patterns, low fibre intake and reduced microbial diversity, promotes metabolic endotoxemia, neuroendocrine imbalance and endothelial impairment, all of which are recognised as early indicators of cardiovascular disease. A distinctive contribution of this review is the integration of PF into the adolescent cardiometabolic framework. This emerging biotechnological process enables the controlled production of structurally defined bioactive compounds, including angiotensin-converting enzyme (ACE) inhibitory peptides, targeted prebiotic oligosaccharides, fermentable substrates that promote SCFA formation, microbially derived eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), phytosterols and purified postbiotics. These compounds modulate several regulatory pathways, such as the renin–angiotensin–aldosterone system, lipid and bile acid metabolism, gut barrier stability, inflammatory signalling and endocrine axes involving glucagon-like peptide-1 (GLP-1), peptide YY (PYY), leptin, insulin sensitivity and growth hormone/insulin-like growth factor-1 (GH/IGF-1) dynamics. By situating precision fermentation within the broader context of adolescent metabolic susceptibility, this review highlights its potential to support microbiome resilience, stabilise hormonal regulation and mitigate early cardiovascular risk. However, further adolescent-specific clinical trials and long-term safety assessments are required to translate these advances into effective public health strategies. Full article

Background/Objectives: Angiogenic T (Tang) cells support endothelial repair and vascular homeostasis. This cross-sectional study compared circulating Tang cell levels in young adults with T1DM vs. healthy controls, and assessed associations between Tang cells and continuous glucose monitoring (CGM) metrics. Methods: Sixty-five young adults with T1DM and 55 healthy controls were enrolled at the University of Campania “Luigi Vanvitelli,” Naples, Italy. Clinical and biochemical data were collected. Tang cells (CD3⁺CD31⁺CD184⁺) were quantified by flow cytometry as absolute counts and percentage of CD3⁺ T cells. In T1DM, CGM metrics from the preceding 14 days were analyzed, including time in range (TIR), time above range (TAR), and time below range (TBR). Results: Individuals with T1DM had higher fasting glucose and HbA1c than controls. Total CD3⁺ T cell counts were lower in T1DM. Tang cells were significantly reduced in T1DM both as absolute number and percentage (21% [10–31] vs. 48% [39–62]; p < 0.001). In multivariable analyses, Tang cell percentage was positively associated with TIR and inversely associated with HbA1c and TAR. Conclusions: Young adults with T1DM exhibit significantly reduced circulating Tang cells. Associations with CGM metrics support a link between real-world glucose control and endothelial vascular health. Full article

There are a few molecules that are regularly used as markers for lymphatic endothelial cells (LECs) such as the adhesion molecule CD31/PEACAM1, the transcription factor PROX1, the Vascular Endothelial Growth Factor Receptor-3 (VEGFR3/FLT4), the glycoprotein podoplanin, and the hyaluronan receptor LYVE1. However, none of the molecules are exclusively expressed in LECs, and there is molecular and functional heterogeneity of LECs in initial lymphatics, lymphatic collectors and lymph nodes. Therefore, a combination of markers must be applied to identify lymphatics. This is particularly true for the characterization of conditions such as lymphatic malformations or cancers, in which the molecular profile of vessels may be variable or abnormal. Here we present two molecules that can help distinguish between endothelial cells of blood and lymphatic vessels: the scaffold protein liprin β-1 (PPFIBP1) and the intermediate filament synemin. We collected own data on the RNA and protein expression of the two molecules in humans, and studied publicly available databases. PPFIBP1 appears to be a suitable marker of LECs in initial lymphatics, collectors and lymph nodes, while synemin appears to be more restricted to initial lymphatics. We hope this will stimulate monoclonal antibody development and help expand the range of LEC markers in health and disease. Full article

Micro- and nanoplastics (MNPs) are emerging environmental contaminants of increasing relevance to human health. Growing evidence suggests that, following ingestion, inhalation, or, less convincingly, dermal exposure, MNPs may cross biological barriers, enter lymphatic and vascular compartments, and reach the liver. Owing to portal blood flow, sinusoidal architecture and Kupffer cell activity, the liver appears to be one of the principal sites of early particle sequestration. Human biomonitoring, ex vivo and postmortem studies have detected MNPs in blood and multiple organs, including the liver, although the currently available evidence remains limited and methodologically heterogeneous. Their identification relies on multistep analytical procedures that integrate sample pretreatment with FTIR, Raman spectroscopy, LD-IR, Py-GC-MS and supplementary imaging methods. However, each of these techniques presents significant limitations, particularly in the analysis of nanoplastics. Experimental studies indicate that MNPs may induce hepatic injury through oxidative stress, mitochondrial impairment, endoplasmic reticulum stress, inflammation, DNA damage, dysregulated lipid metabolism and disruption of the gut–liver axis, consequently contributing to steatosis, cholestatic anomalies and fibrosis. Consequently, MNPs should be considered potential contributors to liver pathology, although more comprehensive human data are still required. Full article

Alzheimer’s disease (AD), the leading cause of dementia, is characterized by progressive cognitive decline along with hallmark brain pathologies including amyloid-beta accumulation, hyperphosphorylated tau, neuroinflammation and neuronal mitochondrial dysfunction. As current pharmaceutical treatments only provide modest symptomatic improvement, there is an urgent need for effective non-pharmaceutical treatment options for the prevention or slowing down of this disease. This review synthesizes results from randomized controlled trials, observational studies, and animal model research on the ability of exercise to influence cognitive functions, brain structural changes, inflammatory processes, and neuroplasticity-related pathways. Exercise has demonstrated the capacity to enhance neurotrophic signaling, improve the regulation of mitochondria, improve cerebrovascular function and reduce pro-inflammatory cytokine levels in preclinical and mild cognitive impairment (MCI) subjects. Additionally, aerobic and resistance training has been shown to enhance physical performance and functional capacity. Furthermore, mind–body, dual-task and multimodal types of interventions may also provide additional cognitive and psychological benefits. Although the overall cognitive effect of exercise in individuals with established AD is generally small, it has been demonstrated that exercise can contribute to maintaining brain health through multiple interconnected metabolic, vascular and molecular pathways, thereby preserving cognitive reserve and slowing disease progression, particularly when initiated during early to midlife prior to the onset of AD symptoms. Therefore, future research will require establishing stage-specific exercise recommendations based on modality type, intensity and duration to achieve optimal clinical outcomes. Full article

Background: Dementia and Type 2 diabetes (T2D) represent two of the most pressing global public health challenges of our time, both exacerbated by physical inactivity. These conditions disproportionately affect Global Majority populations, who experience earlier onset, higher prevalence, and poorer access to culturally appropriate preventive care. However, conventional research and interventions often overlook the sociocultural and structural factors that underpin this disparity. This study synthesises current evidence to understand how these three conditions intersect and to identify equitable pathways for prevention and support. Methods: A meta-narrative review approach was employed to integrate evidence from diverse biomedical, public health, sociocultural and intervention science traditions. Searches were undertaken across MEDLINE/PubMed-adapted searches, CINAHL, PsycINFO, Web of Science Core Collection, AMED and ASSIA, supplemented by grey literature searching and citation chasing. Five meta-narratives were identified: biomedical and epidemiological, public health, health disparities, sociocultural and behavioural, and intervention science. Cross-narrative synthesis produced a conceptual framework linking upstream determinants, lifestyle factors, and disease outcomes. Results: The review revealed that structural inequities such as deprivation, environmental barriers and sociocultural factors including stigma, gendered norms, limited access to culturally appropriate facilities that restrict physical activity (PA) opportunities within Global Majority communities. These constraints elevate T2D and dementia risk through biological pathways involving insulin resistance, vascular injury, and neuroinflammation. Community-based participatory research (CBPR) interventions particularly those delivered in trusted cultural or faith settings emerged as effective strategies to improve PA, glycaemic control, and cognitive well-being. Conclusions: This synthesis reframes dementia and diabetes as interlinked within a wider syndemic driven by structural and sociocultural inequities. The proposed framework underscores the importance of culturally grounded, community-led approaches to promote brain health, reduce risk, and achieve equitable healthy ageing among Global Majority populations. Full article

Healthcare professionals must acquire and maintain both declarative knowledge and fine psychomotor skills across a wide range of clinical procedures. Human working memory is physiologically limited, and the high cognitive demands of clinical environments frequently contribute to medical errors and adverse events. Intra-individual performance variability—driven by fatigue, stress, and motivation—represents a further challenge that conventional medical safety education has not adequately addressed. According to the World Health Organization, patient harm ranks fourteenth in the global burden of disease, with approximately 10% of hospitalised patients in high-income countries experiencing harm within healthcare facilities. This study reports the design, theoretical rationale, and preliminary outcomes of an augmented reality (AR) glasses system for hands-free, self-directed medical procedural training, developed from a human factors and ergonomics (HFE) perspective. The system integrates a see-through head-mounted display (HMD; Epson Moverio BT-40S), bone-conduction earphones (Shokz OpenComm), and an industrial-grade voice recognition application (NEC Solution Innovators), achieving fully hands-free operation compatible with aseptic technique. Content design is grounded in cognitive load theory (CLT) and the cognitive theory of multimedia learning (CTML), extended by neuroscientific evidence on multisensory integration and memory consolidation. More than 40 procedure-specific modules have been developed in-house at Tokyo University of Technology, spanning airway management, vascular access, respiratory therapy, dialysis, and cardiac support. In a four-year longitudinal survey (virtual reality (VR) simulator; n = 286), major satisfaction items consistently exceeded the scale midpoint. In an AR endotracheal suctioning cohort (n = 38/22), procedural flow understanding was rated 3.95/5.0. A peer-reviewed randomised controlled trial (Clinical Simulation in Nursing, n = 36) demonstrated significantly superior skill improvement (p < 0.001) and learning motivation (p = 0.001) in the AR group versus textbook self-practice. Principal ergonomic limitations of current HMD hardware—excessive weight, narrow field of view, and absence of medical-grade certification—are documented, and AI-based real-time procedural assessment is identified as a priority for the next research phase. Full article

Endothelial dysfunction is a key characteristic of many diseases, including atherosclerosis, hypertension, heart failure, stroke, cancer, acute respiratory distress syndrome (ARDS), peripheral vascular disease, coronavirus 2019 (COVID-19), and pulmonary arterial hypertension (PAH). To improve understanding of the roles of endothelial cells (ECs) in health and disease, EC-specific genome editing technologies have been developed in recent years. Therapeutic strategies that aim to restore a healthy endothelial monolayer include the inhibition of endothelial genes that cause EC injury and dysfunction and the induction or activation of endothelial genes that drive EC repair and regeneration. In this review, we describe established recombinase-mediated genetic modification technologies and emerging EC-specific genome editing technologies including viral and non-viral delivery of the CRISPR/Cas9 genome editing system, and we summarize the strengths and limitations of each technology. We then discuss possible avenues for future research, including the development of organ-specific EC genome editing technologies. In short, EC-specific genome editing technologies can be used to modulate gene expression selectively in ECs and even within a specific vascular bed and/or distinctive EC subtype, and, in doing so, greatly improve the understanding of vascular biology and help develop precision genetic medicine targeting the disease-causing vascular bed(s) to effectively treat diseases caused by vascular endothelial dysfunction. Full article

Chronic exposure to fine particulate matter (PM_2.5) derived from wood combustion represents a major environmental health burden, particularly during pregnancy. However, the impact of pregestational and gestational (PM_2.5) exposure on the maternal great vasculature remains largely unexplored. This study evaluates the effects of wood smoke-derived (PM_2.5) on the structural architecture of the maternal aortic arch and associated hemodynamic changes during pregnancy in second-generation Sprague–Dawley rats. Animals were allocated into four groups (n = 12) according to filtered (FA) or non-filtered air (NFA) exposure during pregestational and gestational periods: FA/FA, FA/NFA, NFA/FA, and NFA/NFA. Morphometric analysis revealed significant reductions in tunica media (p = 0.0251) and adventitia thickness (p = 0.0014) in exposed groups, without changes in integrated optical density, suggesting alterations in elastic matrix organization without evidence of net mass loss. Histological analysis supported exposure-dependent structural heterogeneity, including elastic lamellae fragmentation and extracellular matrix disorganization. Each exposed group exhibited a distinct systolic blood pressure trajectory across gestation, with FA/NFA reaching the highest values at day 18 (151.0 ± 17.0 mmHg) and NFA/FA displaying sustained elevations despite gestational low-exposure conditions. Principal component analysis (49.2% explained variance) revealed a structured multivariate distribution of vascular and hemodynamic variables across exposure conditions, consistent with an exposure-window-dependent pattern. These findings suggest that (PM_2.5) exposure is associated with coordinated structural and hemodynamic changes in the aortic arch and support the hypothesis that the pregestational period may represent a window of increased susceptibility. Full article