Hidradenitis suppurativa is a cutaneous chronic inflammatory disease that is estimated to affect about 1% of the population and caused pain, malodorous discharge, disfigurement, and poor quality of life with psychosocial problems. The typical features are recurrent painful nodules, abscesses, and sinus tracts on the axillae, groins, gluteal areas, and anogenital regions since postpuberty. Smoking and obesity are two major triggering factors of hidradenitis suppurativa. Women are prone to have hidradenitis suppurativa than men in Western countries, but the male-to-female ratio is reversed in oriental countries. The disease severity can be affected by menstruation, pregnancy, and menopause. Furthermore, the phenotypes are different among men and women with hidradenitis suppurativa. Men are prone to have buttock involvement while women are prone to have axillary, groins, and submammary lesions. This review introduces the skin appendages and pathophysiology of hidradenitis suppurativa and then focuses on the sex difference and the effects of sex hormones on hidradenitis suppurativa and current hormone-associated treatments.

Nicotinamide adenine dinucleotide (NADH) has been reported to regulate synaptic plasticity recently, while its role in this process remains unclear. To explore the contribution and the underlying mechanisms of NADH regulating synaptic plasticity, here, we examined NADH's effect on immediate-early response genes (IEGs) expressions, including C-Fos and Arc in primary cultured cortical neurons and the frontal cortex of mouse brain. Our results showed that NADH promoted IEGs expression and that the C-Fos and Arc levels are increased in primary cultured cortical neurons, which is almost completely blocked by N-methyl-D-aspartate receptor (NMDAR) inhibitor, MK-801. Moreover, NADH significantly increased intracellular Ca²⁺ levels and the phosphorylation of Erk1/2, a downstream molecule of the NMDAR. Furthermore, NADH also significantly increased IEGs expression in vivo, accompanied by the changes of Ca²⁺ in neurons and activation of excitatory neurons in the mouse frontal cortex. In conclusion, this study indicates that NADH can promote the expression of synaptic plasticity-related IEGs through the NMDAR/Ca²⁺/Erk1/2 pathway, which provides a new way to understand the regulatory role of NADH in synaptic plasticity.

Oxysophoridine (OSR) is a main active alkaloid extracted from Sophora alopecuroides, which is a traditional Chinese herbal medicine that has been used widely. In this study, we used thoracic aorta rings isolated from Sprague–Dawley rats to explore the vasodilative activity of OSR and its potential mechanisms. The isolated rat thoracic aorta rings were used to observe the effects of different concentrations of OSR (0.4–2.0 g·L⁻¹) on the resting normal rings and the phenylephrine precontracted endothelium-intact or endothelium-denudedisolated thoracic aorta rings, respectively. The interactions among OSR and barium chloride (BaCl₂), tetraethylamine, 4-aminopyridine, glibenclamide (Gli), L-nitroarginine methyl ester (L-NAME), and cyclooxygenase (COX) inhibitor indomethacin (INDO) were evaluated. The experimental results show that OSR had no effect on the tension of resting vascular rings, but the vasodilating effect could be confirmed in a concentration-dependent manner on both endothelium-intact and endothelium-denuded vascular rings. This vasodilation effect of OSR on thoracic aorta vascular rings could be inhibited significantly by potassium channel blockers glibenclamide (Gli, 10 μmol·L⁻¹) and 4-aminopyridine (4-AP, 5 mmol·L⁻¹). In addition, vasodilatory effects of OSR were not inhibited in the presence of potassium channel blockers barium chloride (BaCl₂, 1 mmol·L⁻¹) and tetraethylamine (TEA, 10 mmol·L⁻¹), nitric oxide synthase inhibitor (L-NAME, 0.1 mmol·L⁻¹) and COX inhibitor (INDO, 10 μmol·L⁻¹). In conclusion, the vasodilatory effects of OSR on thoracic aorta rings is associated with K_V and K_ATP.

Acute myocardial infarction (AMI) is an instant death of cardiomyocytes that ends in a large mortality worldwide. Thus, there is a great interest to come up with novel protective approaches for AMI to mount cardiomyocyte survival, enhance postinfarcted cardiac function, and countermand the process of cardiac remodeling. Spermidine has vital roles in vast cellular processes under pathophysiological circumstances. This study aims to enhance our comprehension of the role of autophagy as a possible protective sequel of spermidine supplementation on postinfarction ventricular dysfunction in a rat model of AMI induced by isoproterenol (ISO). Thirty male rats were divided into three groups (control, AMI, and spermidine + AMI). AMI was induced by subcutaneous ISO injections for two consecutive days. Rats were pretreated with spermidine by intraperitoneal injection before induction of AMI. Electrocardiogram (ECG) was recorded in all rats 24 h after the second dose of ISO. Rats were sacrificed after ECG recording, and samples were taken for biochemical assessments. Spermidine intake before induction of AMI in rats significantly attenuated cardiac dysfunction where cardiac enzymes are decreased, and ECG changes induced by ISO are reversed in cardiomyocytes. Spermidine affects the autophagic flux of autophagy-related protein expression (LC3-II, TFEP, and p62). Furthermore, it increased the total antioxidant capacity.

Palmitic acid (PA) is a saturated free fatty acid which, when being excessive, accounts for lipotoxicity. Using human lung A549 cells as a model for lung alveolar type 2 epithelial cells, we found that challenge of A549 cells with PA resulted in apoptotic cell death, as reflected by positive annexin V and PI staining, and also appearance of cleaved caspase-3. PA treatment also caused depletion of intracellular Ca²⁺ store, endoplasmic reticulum (ER) stress, and oxidative stress. Tannic acid (TA), a polyphenol present in wines and many beverages, alleviated PA-induced ER stress, oxidative stress and apoptotic death. Thus, our results suggest PA lipotoxicity in lung alveolar type 2 epithelial cells could be protected by TA.

Cardiovascular disease (CVD) have multifactorial nature, and owing to their disparate etiological roots, it is difficult to ascertain exact determinants of CVD. In the current study, primary objective was to determine association of single nucleotide polymorphisms (SNP) in folate pathway genes, homocysteine, antihypertensive medication, and of known risk factors in relation to CVD outcomes. The participants numbered 477 (controls, n = 201, ischemic heart disease patients, n = 95, and myocardial infarction cases, n = 181, respectively). SNPs that were queried for homocysteine pathway genes included, “methylene tetrahydrofolate reductase (MTHFR)” gene SNPs rs1801133 and rs1801131, “methyltransferase (MTR)” SNP rs1805087, “paraoxonase 1 (PON1)” SNP rs662, and angiotensin-converting enzyme (ACE) gene polymorphisms rs4646994. Medication data were collected through questionnaire, and serum-based parameters were analyzed through commercial kits. The analysis of variance and multiple comparison scrutiny revealed that age, gender, family history, cholesterol, creatinine, triglyceride, high density lipoproteins (HDL), homocysteine, beta-blocker, ACE inhibitors, MTHFR and PON1 SNPs related to coronary artery disease (CAD). On regression, rs662 SNPs and C-reactive protein had nonsignificant odds ratio, whereas age, gender, creatinine, and HDL were nonsignificant. Family history, cholesterol, homocysteine, beta blocker, and ACE inhibitors, homocysteine, rs1801133 and rs1801131 SNP maintained significance/significant odds for CAD. The current study indicates an intricate relationship between genetic variants, traditional factors, and drug usage in etiogenesis of arterial disease. Differences in SNPs, their modulated effects in consensus with medicinal usage may be related to ailment outcomes affecting coronary vasculature.

Coronavirus disease 2019 (COVID-19) had caused a worldwide pandemic with public health emergencies since 2020. For the symptomatic patients, high mortality rate was observed if without timely and optimized management. In this study, we aimed to investigate the predictive and prognostic roles of hematologic and biochemical parameters obtained in the emergency department (ED) for COVID-19 patients. We conducted a retrospective study in a dedicated COVID-19 medical center, recruiting a total of 228 COVID-19 patients with 86 severe and 142 non-severe cases. Both the hematologic and biochemical parameters obtained in the ED upon arrival were analyzed to evaluate the association of the biomarkers with disease severity and prognosis among COVID-19 patients. Among these parameters, neutrophil-to-lymphocyte ratio (NLR), C-reactive protein (CRP), procalcitonin (PCT), lactate dehydrogenase (LDH), ferritin, and D-dimer were significantly higher in the severe group than the non-severe one, whereas the platelet count and lymphocyte-to-monocyte ratio were significantly lower. Receiver operating characteristic curve analysis revealed that the areas under curve of CRP, PCT, LDH, ferritin, D-dimer, and NLR for differentiating the severity of COVID-19 were 0.713, 0.755, 0.763, 0.741, 0.733, and 0.683, respectively, whereas the areas under curve of CRP, PCT, LDH, ferritin, D-dimer, and NLR for differentiating the mortality of COVID-19 were 0.678, 0.744, 0.680, 0.676, 0.755, and 0.572, respectively. Logistic regression analysis revealed that CRP, PCT, LDH, ferritin, D-dimer, and NLR were independent indicators for prediction of severe COVID-19, and LDH and ferritin were independent factors associated with the mortality in COVID-19. In conclusion, higher CRP, PCT, LDH, ferritin, D-dimer, and NLR were associated with severe COVID-19, whereas higher LDH and ferritin were associated with the mortality in COVID-19. These findings could help early risk stratification in the ED and contribute to optimized patient management.