BackgroundMoyamoya disease (MMD) is a cerebrovascular disease characterized by progressive stenosis or occlusion of the terminal portion of internal carotid arteries and the formation of a vascular network at the base of the brain. The pathogenesis of MMD is still unclear.Methodology/Principal FindingsWe retrospectively analyzed clinical data for 65 consecutive patients with MMD in our institutions and evaluated the histopathological and immunohistochemical findings of intracranial vessels from 3 patients. The onset age distribution was found to have 1 peak at 40–49 year-old age group, no significant difference was observed in the female-to-male ratio (F/M = 1.2). Intracranial hemorrhage was the predominant disease type (75%). Positive family history was observed in 4.6% of patients. Histopathological findings were a narrowed lumen due to intimal fibrous thickening without significant inflammatory cell infiltration, and the internal elastic lamina was markedly tortuous and stratified. All 3 autopsy cases showed vacuolar degeneration in the cerebrovascular smooth muscle cells. Immunohistochemical study showed the migration of smooth muscle cells in the thickened intima, and aberrant expression of IgG and S100A4 protein in vascular smooth muscle cells. The Complement C3 immunoreactivity was negative.Conclusion/SignificanceThis study indicated that aberrant expression of IgG and S100A4 protein in intracranial vascular wall of MMD patients, which suggested that immune-related factors may be involved in the functional and morphological changes of smooth muscle cells, and finally caused the thickened intima. A possible mechanism is that deposits of IgG in the damaged internal elastic lamina may underlie the disruption of internal elastic lamina, which facilitated S100A4 positive SMCs migrated into intima through broken portions of the internal elastic lamina, resulting in lumen stenosis or occlusion, leading to compensatory small vessels proliferation.

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Background. Diabetes mellitus (DM) can induce cardiomyocyte injury and lead to diabetic cardiomyopathy (DCM) which presently has no specific treatments and consequently increase risk of mortality. Objective. To characterize the therapeutic effect of 6-gingerol (6-G) on DCM and identify its potential mechanism. Methods. In vivo streptozotocin- (STZ-) induced DM model was established by using a high-fat diet and STZ, followed by low-dose (25 mg/kg) and high-dose (75 mg/kg) 6-G intervention. For an in vitro DCM model, H9c2 rat cardiomyoblast cells were stimulated with high glucose ( glucose = 33  mM) and palmitic acid (100 μM) and then treated with 6-G (100 μM). Histological and echocardiographic analyses were used to assess the effect of 6-G on cardiac structure and function in DCM. Western blotting, ELISA, and real-time qPCR were used to assess the expression of ferroptosis, inflammation, and the Nrf2/HO-1 pathway-related proteins and RNAs. Protein expression of collagen I and collagen III was assessed by immunohistochemistry, and kits were used to assay SOD, MDA, and iron levels. Results. The results showed that 6-G decreased cardiac injury in both mouse and cell models of DCM. The cardiomyocyte hypertrophy and interstitial fibrosis were attenuated by 6-G treatment in vivo and resulted in an improved heart function. 6-G inhibited the expression of ferroptosis-related protein FACL4 and the content of iron and enhanced the expression of anti-ferroptosis-related protein GPX4. In addition, 6-G also diminished the secretion of inflammatory cytokines, including IL-1β, IL-6, and TNF-α. 6-G treatment activated the Nrf2/HO-1 pathway, enhanced antioxidative stress capacity proved by increased activity of SOD, and decreased MDA production. Compared with in vivo, 6-G treatment of H9c2 cells treated with high glucose and palmitic acid could produce a similar effect. Conclusion. These findings suggest that 6-G could protect against DCM by the mechanism of ferroptosis inhibition and inflammation reduction via enhancing the Nrf2/HO-1 pathway.

It has previously been demonstrated that phospha-tidylinositol-3-kinase (PI3K)/Akt and cleaved caspase-3 serve critical roles in the apoptosis of cardiac myocytes following ischemia/reperfusion injury. Epigallocatechin-3-gallate (EGCG), the predominant catechin component of green tea, has been reported to have potential cardioprotective effects in primary cultures of cardiac myocytes exposed to I/R injury, mediated through inhibition of signal transducers and activators of transcription-1 activity. In addition, it is also known that the biological behavior of EGCG may be influenced by metal ions, for example the hepatoprotective activity of EGCG has been reported to be enhanced by zinc. In the present study, the protective effects of EGCG with zinc were assessed on cultures of rat cardiac myoblasts exposed to hypoxia/reoxygenation (H/R) injury. H9c2 cells were subjected to 3-h hypoxia, followed by 1-h reperfusion. EGCG and/or zinc were perfused prior to induced hypoxic stress. It was demonstrated that when EGCG interacted with zinc, the anti-apoptotic activity was significantly enhanced. To the best of our knowledge, the current study was the first to demonstrate that EGCG + Zn2+ protects H9c2 cells against H/R injury through activation of the PI3K/Akt pathway, as determined by western blotting. Since EGCG + Zn2+ may, at least in part, protect cardiac myocytes against H/R-induced apoptotic cell death, the PI3K/Akt pathway of EGCG may be enhanced by its interactions with zinc during H/R injury. Furthermore, it was suggested that a similar procedure may be implemented in a clinical setting, in order to maximize PI3K/Akt activation levels in patients with acute coronary artery disease. EGCG and zinc may therefore represent effective agents for use in the prevention of I/R injury in clinical practice.

Background: COVID-19(Corona Virus Disease 2019) outbreaks around the world and is highly infectious, which may cause people prone to anxiety and depression. Pregnant women, as a particular group, need more attention. The aim of this study is to investigate the mental health status of pregnant women during the outbreak of COVID-19, to analyze factors affecting their mental health status, to get wise to their cognition, behavioral responses and to provide solution guidance for psychological problems.Methods: Using a self-designed questionnaire, self-rated anxiety scale(SAS), self-rated depression scale (SDS), we conducted a web-based survey on 1160 pregnant women during the outbreak of COVID-19.Results: Compared with general adults in some regions of China during the outbreak of COVID-19, the scores of SAS and SDS of pregnant women were both significantly higher (P<0.05). The results of multivariate regression analysis unveiled that age, levels of education, and duration of pregnancy were factors influencing pregnant women’s psychological status. In terms of psychological problems, compared with pregnant women aged < 30 years old, the risk of psychological problems in pregnant women aged ≥ 30 years old was 0.646 times (95% CI:0.486-0.858). Besides, compared with women with a level of high school or below, those with a junior college degree or above had a poor mental health risk of 0.551 times (95%CI: 0.416-0.731). Compared with women in early pregnancy, women in middle pregnancy and in last pregnancy had a risk of 0.543 times (95% CI:0.398-0.739) and 0.636 times (95% CI: 0.466-0.867) in poor mental health.Conclusions: During the outbreak of COVID-19, pregnant women are prone to anxiety or depression, highlighting the necessity of further attention to mental health. It is of great significance to provide timely psychological counseling and intervention for pregnant women with poor mental health during the COVID-19 outbreak.