As one of the main appendages of skin, hair follicles play an important role in the process of skin regeneration. Hair follicle is a tiny organ formed by the interaction between epidermis and dermis, which has complex and fine structure and periodic growth characteristics. The hair growth cycle is divided into three continuous stages, growth (anagen), apoptosis-driven regression (catagen) and relative quiescence (telogen). And The Morphogenesis and cycle of hair follicles are regulated by a variety of signal pathways. When the signal molecules in the pathways are abnormal, it will affect the development and cycle of hair follicles, which will lead to hair follicle-related diseases.This article will review the structure, development, cycle and molecular regulation of hair follicles, in order to provide new ideas for solving diseases and forming functional hair follicle.

Morphogenesis, Growth Cycle and Molecular Regulation of Hair Follicles.

Frontiers in Cell and Developmental Biology

Chronic kidney disease (CKD) is a global public health issue characterized by progressive loss of kidney function, of which end-stage kidney disease (ESKD) is the last stage. The global increase in the prevalence of CKD is linked to the increasing prevalence of traditional risk factors, including obesity, hypertension, and diabetes mellitus, as well as metabolic factors, particularly insulin resistance, dyslipidemia, and hyperuricemia. Mortality and comorbidities, such as cardiovascular complications, rise steadily as kidney function deteriorates. Patients who progress to ESKD require long-term kidney replacement therapy, such as transplantation or hemodialysis/peritoneal dialysis. It is currently understood that a crucial aspect of CKD involves persistent, low-grade inflammation. In addition, increased oxidative and metabolic stress, endothelial dysfunction, vascular calcification from poor calcium and phosphate metabolism, and difficulties with coagulation are some of the complex molecular pathways underlying CKD-related and ESKD-related issues. Novel mechanisms, such as microbiome dysbiosis and apolipoprotein L1 gene mutation, have improved our understanding of kidney disease mechanisms. High kidney disease risk of Africa has been linked to APOL1 high-risk alleles. The 3-fold increased risk of ESKD in African Americans compared to European Americans is currently mainly attributed to variants in the APOL1 gene in the chromosome 22q12 locus. Additionally, the role of new therapies such as SGLT2 inhibitors, mineralocorticoid receptor antagonists, and APOL1 channel function inhibitors offers new therapeutic targets in slowing down the progression of chronic kidney disease. This review describes recent molecular mechanisms underlying CKD and emerging therapeutic targets.

Advances in kidney disease: pathogenesis and therapeutic targets.

Frontiers in Medicine

Treatment of patients with chronic kidney disease (CKD) requires implementation of prevention and management strategies that reduce the risk of kidney failure and CKD-associated cardiovascular risk. Metabolic syndrome is characterised by obesity, high blood pressure, dyslipidaemia and hyperglycaemia, and is common among patients with CKD. Large-scale randomised trials have led to significant advances in the management of CKD with five pharmacotherapies now proven to be nephroprotective and/or cardioprotective in certain types of patients. Renin-angiotensin system inhibitors and sodium-glucose co-transporter 2 inhibitors slow kidney disease progression and reduce heart failure complications for most patients with CKD. In addition, statin-based regimens lower low-density lipoprotein cholesterol and reduce the risk of atherosclerotic disease (with no clinically meaningful effect on kidney outcomes). For patients with type 2 diabetes and albuminuric CKD, the non-steroidal mineralocorticoid receptor antagonist finerenone and the glucagon-like peptide-1 receptor agonist semaglutide also confer cardiorenal benefits, with semaglutide additionally effective at reducing weight. Together, these randomised data strongly suggest that metabolic syndrome mediates some of the cardiorenal risk observed in CKD. Considered separately, the trials help elucidate which components of metabolic syndrome influence the pathophysiology of kidney disease progression and which separately modify risk of atherosclerotic and non-atherosclerotic cardiovascular outcomes. As we predict complementary and different mechanisms of nephroprotection and cardioprotection for these different interventions, it seems logical that they should be deployed together to maximise benefits. Even when combined, however, these therapies are not a cure so further trials remain important to reduce the residual cardiorenal risks associated with CKD.

THE PREVENTION AND MANAGEMENT OF CHRONIC KIDNEY DISEASE AMONG PATIENTS WITH METABOLIC SYNDROME.

Kidney International

Acute respiratory distress syndrome (ARDS) is a severe complication of critical illness, characterized by bilateral lung infiltrates and hypoxemia. Its clinical and pathophysiological heterogeneity poses challenges for both diagnosis and treatment. This review outlines the evolution of ARDS definitions, discusses the underlying pathophysiology of ARDS, and examines the clinical implications of its heterogeneity. Traditional ARDS definitions required invasive mechanical ventilation and relied on arterial blood gas measurements to calculate the PaO2 /FiO2 ratio. Recent updates have expanded these criteria to include patients receiving noninvasive respiratory support, such as high-flow nasal oxygen, and the adoption of the SpO2 /FiO2 ratio as an alternative to the PaO2 /FiO2 ratio. While these changes broaden the diagnostic criteria, they also introduce additional complexity. ARDS heterogeneity-driven by varying etiologies, clinical subphenotypes, and underlying biological mechanisms-highlights the limitations of a uniform management approach. Emerging evidence highlights the presence of distinct ARDS subphenotypes, each defined by unique molecular and clinical characteristics, offering a pathway to more precise therapeutic targeting. Advances in omics technologies-encompassing genomics, proteomics, and metabolomics-are paving the way for precision-medicine approaches with the potential to revolutionize ARDS management by tailoring interventions to individual patient profiles. This paradigm shift from broad diagnostic categories to precise, subphenotype-driven care holds promise for redefining the landscape of treatment for ARDS and, ultimately, improving outcomes in this complex, multifaceted syndrome.

A narrative review on the future of ARDS: evolving definitions, pathophysiology, and tailored management.

Critical Care : the Official Journal of the Critical Care Forum

Malignant ST-Segment-Elevation in a Young Man With Syncope: Important Clues Hidden in Diagnostic Traps.

Circulation

Walking may appear to be a simple motor task, but is in fact a very complex behavior that involves virtually all levels of the nervous system. In daily clinical practice, subtle gait changes are commonly observed as we grow older, and these are often attributed to aging itself (the term "senile gait" was coined for this). However, growing evidence suggests that such age-related gait changes should not be regarded as a mere consequence of aging, but rather as indicators of underlying age-related disease. Numerous studies have shown that gait changes can be present for years during an otherwise prodromal phase of many progressive neurological disorders. As such, gait changes serve as clinical biomarkers of disease-related dysfunction in the neurological structures involved in gait control. We elaborate on the potential for gait to be exploited as an early warning system for underlying pathology. We also discuss the importance of such a proactive approach: an earlier diagnosis can lead to timely installment of symptomatic support, and sometimes start of prophylactic treatment. This can help reduce disability, and possibly increase survival because age-related gait disturbances are associated with increased mortality in the general population.

Gait changes with aging: an early warning sign for underlying pathology.

Journal of Neurology

Reproductive endocrine disorders, including infertility, polycystic ovary syndrome (PCOS), and endometriosis, significantly impact women's reproductive health and overall well-being. This comprehensive review explores the diagnosis and management strategies for these prevalent conditions. Infertility, affecting millions globally, is often linked to ovulatory dysfunction, PCOS, and endometriosis. PCOS is characterized by hyperandrogenism, menstrual irregularities, and insulin resistance, contributing to anovulation and infertility. The Rotterdam criteria are widely used for PCOS diagnosis, and management includes lifestyle modifications, pharmacological treatments like ovulation inducers, and, in some cases, surgical interventions. Endometriosis, caused by the presence of endometrial-like tissue outside the uterus, leads to chronic pain and infertility through inflammation, adhesions, and impaired ovarian function. Laparoscopy remains the gold standard for diagnosing endometriosis, and treatment focuses on pain relief, fertility preservation, and reducing recurrence. In cases of endometriosis-related infertility, assisted reproductive technologies (ARTs) like in vitro fertilization (IVF) are often recommended. In addition, the role of diet and lifestyle changes in managing these conditions is gaining recognition. This review emphasizes the complexity of reproductive endocrine disorders and underscores the need for individualized treatment plans, combining medical, surgical, and lifestyle approaches to improve fertility outcomes and enhance the quality of life for affected women. The review also highlights the importance of early diagnosis and advances in therapeutic interventions to ensure optimal patient care in the management of infertility, PCOS, and endometriosis.

Reproductive Endocrine Disorders: A Comprehensive Guide to the Diagnosis and Management of Infertility, Polycystic Ovary Syndrome, and Endometriosis.

Curēus

Both perineural and intravenous dexamethasone have been proposed as effective adjuncts that prolong the duration of peripheral nerve blocks. We sought to explore whether combining systemic with perineural dexamethasone yields any additive or synergistic effect on the characteristics and analgesic effects of peripheral nerve blocks.

Adult patients having distal radius open reduction and internal fixation and/or carpometacarpal arthroplasty under supraclavicular block were randomized to either intravenous dexamethasone; combination of perineural+intravenous dexamethasone; or no dexamethasone (control). Sensory block duration was set as the primary outcome. Secondary outcomes included motor block duration; post-operative rebound pain scores as well as worst pain at 8, 16, 24, 32, 40, and 48-hours; opioid consumption at 0-24 and 25-48 hours; incidence of nausea/vomiting; and presence of burning sensation in the blocked limb at 24 and 48-hours. Our null hypothesis was lack of difference in sensory block duration between the three groups.

A total of 104 patients were included in the analysis (37: intravenous dexamethasone; 34: intravenous+perineural dexamethasone; 33: control). Compared to intravenous dexamethasone alone, adding perineural dexamethasone did not yield any incremental benefits in any of the outcomes examined. The mean [SD] of sensory block duration was 21.3 [7.3] hours in the intravenous dexamethasone group, 20.6 [6.1] hours in the perineural+intravenous group, and 16.8 [6.8] hours in the Control group. The mean difference [95% CI] of sensory block duration was significantly prolonged by 4.5 hours [1.3, 7.7] (P=0.006) in intravenous dexamethasone group and 3.4 hours [0.8, 6.8] (P=0.015) in the perineural+intravenous dexamethasone group, when compared to control; however, no difference was observed when the two dexamethasone groups were compared to each other (0.7 hours [-2.5, 3.9](P=0.670)). Compared to control, both intravenous and intravenous+perineural dexamethasone similarly reduced 24-hour pain scores and opioid consumption and decreased incidence of rebound pain.

Our findings suggest that intravenous dexamethasone alone is sufficient to improve analgesic outcomes for patients receiving supraclavicular block for upper extremity surgery. Combining the intravenous and perineural dexamethasone routes does not yield additive or synergistic effect on the characteristics and analgesic effects of supraclavicular block.

EXPLORING THE ADDITIVE OR SYNERGISTIC EFFECTS OF THE SYSTEMIC AND PERINEURAL ROUTES OF DEXAMETHASONE AS ADJUNCTS TO SUPRACLAVICULAR BLOCK: A RANDOMIZED CONTROLLED TRIAL.

Morphogenesis, Growth Cycle and Molecular Regulation of Hair Follicles.

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