Kangagger8251

To investigate the relationship between Transient Receptor Potential Vanilloid 6 (TRPV6) and ST-elevation acute myocardial infarction (STEMI) patients.

This observational research included a total of 221 patients with STEMI admitted during January 2017~August 2019. Additionally, 50 cases of non-ST-elevation acute myocardial infarction (NSTEMI) patients and 50 healthy individuals were enrolled as the control. Serum levels of TRPV6 were detected by ELISA method. The relationship between TRPV6, clinical characteristics, laboratory indices of CK-MB, TnI, NT-pro-B-type natriuretic peptide (NT-pro-BNP), C-reactive protein (CRP), and the left ventricular ejection fraction (LVEF%) was analyzed by statistical methods. K-M curve was performed for survival time.

Serum levels of TRPV6 were remarkably lower in STEMI and NSTEMI patients compared with the healthy control. Levels of NT-pro-BNP and CK-MB were significantly higher and serum levels of TRPV6 were dramatically lower in deceased STEMI patients in comparison with the surviving patients. The levels of TRPV6 were negatively correlated with CK-MB and NT-pro-BNP. Meanwhile, TRPV6 was negatively expressed in tissues of STEMI patients and positively expressed in normal tissues. Patients with lower TRPV6 levels had remarkably lower LVEF ratio, higher GRACE scores, higher CK-MB and NT-pro-BNP levels, as well as higher ratios of cardiovascular death, malignant arrhythmia, cumulative MACE, and shorter survival time than patients with higher TRPV6.

The lower expression of TRPV6 was associated with poor clinical outcomes and prognosis of STEMI patients.

The lower expression of TRPV6 was associated with poor clinical outcomes and prognosis of STEMI patients.

To investigate the possible role of Naringenin in AMPK signaling pathway in LPS-induced septic cardiac dysfunction in mice and to elucidate the inherent mechanism.

Male C57 mice were used in the establishment of mouse sepsis model. The effect of Naringenin on septic cardiac dysfunction was observed. Echocardiographic parameters were recorded. Western blot was employed to detect the expressions of BCL-2, BAX, cleaved caspase-3, pNF-kB and IkB-α. Myocardial mitochondria were isolated and extracted. Real-time PCR was applied to detect the expressions of Cox4i, Cox5a mRNA, mt-Nd1, mt-Nd2, mt-Co1 and mt-Co2 mRNA. Western blot was employed to detect the expressions of Complex I, Complex II, and OPA1 to evaluate the effects of Naringenin on myocardial mitochondrial biology and function in septic cardiac dysfunction.

The expressions of TNF-α, IL-6, pNF-κB and IκB-α have changed after Naringenin treatment. IκB-α expression was decreased, expressions of TNF-α, IL-6 and pNF-κB were increased. Naringenin has significantly inhibited AMPK and ACC phosphorylation, and decreased PGC1α expression. Moreover, Naringenin reversed the increased expressions of PGC1α and phosphorylation of AMPK and ACC by U75302 treatment, and decreased the expressions of complex I, complex II and OPA1.

Naringenin inhibits LTB4/BLT1 receptors to attenuate cardiomyocyte inflammation and apoptosis, which may mediate the protective effect of anti-septic cardiac dysfunction by activating AMPK signaling pathway and inhibiting NF-κB signaling and mitochondrial damage.

Naringenin inhibits LTB4/BLT1 receptors to attenuate cardiomyocyte inflammation and apoptosis, which may mediate the protective effect of anti-septic cardiac dysfunction by activating AMPK signaling pathway and inhibiting NF-κB signaling and mitochondrial damage.Toll-like receptor 4 (TLR4) is an important cellular transmembrane receptor and pattern-recognition signaling molecule for pathogens in the immune system. High mobility group box 1 protein (HMGB1) plays an important role in myocardial ischemia (MI) and reperfusion through a TLR4-mediated inflammatory response. T lymphocytes are involved in MI injury; however, the specific mechanisms underlying this role remain unclear. In this study, C57BL/6 wild-type (WT) mice and TLR4 knockout mice were divided into three groups, including a normal control group, an MI group that was generated using high doses of isoproterenol (ISO), and an ISO+rHMGB1 group that was generated using a combination of ISO and recombinant HMGB1 (rHMGB1). Echocardiography, hematoxylin and eosin staining, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), and flow cytometry were used to examine each group. The results showed that rHMGB1 could further aggravate myocardial injury and increase the CD4+/CD8+ ratio and the expression level of interleukin-17 (IL-17) (p less then 0.05) in vivo After the TLR4 gene was knocked out, myocardial ischemic injury in mice was alleviated, and the CD4+/CD8+ ratio and IL-17 expression level were both reduced (p less then 0.05) in vivo. Therefore, TLR4 knockout has a protective effect against MI in mice, which may involve the regulation of the ratio between CD4+ and CD8+ T lymphocytes and of the IL-17 expression level through the HMGB1-TLR4 signaling pathway.

Intrauterine hypoxia/asphyxia is not the cause, but a consequence of different pathological conditions that requires a more detailed study of the morphogenesis of perinatal death.

Structural changes in placentas of intrauterine fetal demise (IUFD) in different stages of intrauterine period and placentas in early neonatal death were reviewed and compared. Control group was composed of term placentas without evidence of perinatal asphyxia or other neonatal abnormalities. SH-4-54 Immunohistochemical investigation was performed by antibodies to Herpes simplex virus (HSV), Cytomegalovirus (CMV), and tumor necrosis factor (TNF). Morphometric analysis was performed using the Pannoramic Midi II histoscanner of "3DHISTECH" company.

The histologic examination of placentas revealed differences between IUFD and early neonatal death. Predominant localization of HSV and CMV antigens was noted in the walls of capillaries and in placental villous stroma in absolute majority of IUFD and early neonatal death cases; importantly, colocalization of TNF, HSV, and CMV antigens was also detected in cases of IUFD and early neonatal period.

Damage of placental vessels due to the influence of pathogenic factors (virus antigens, TNF) can cause acute or chronic intrauterine fetus hypoxia which is a leading pathogenetic factor of perinatal death.

Damage of placental vessels due to the influence of pathogenic factors (virus antigens, TNF) can cause acute or chronic intrauterine fetus hypoxia which is a leading pathogenetic factor of perinatal death.