Lactate Contributes to Remote Ischemic Preconditioning-Mediated Protection Against Myocardial Ischemia Reperfusion Injury by Facilitating Autophagy via the AMP-Activated Protein Kinase-Mammalian Target of Rapamycin-Transcription Factor EB-Connexin 43 Axis.

Remote ischemic preconditioning (RIPC) exerts a protective role on myocardial ischemia/reperfusion (I/R) injury by the release of various humoral factors. Lactate is a common metabolite in ischemic tissues. Nevertheless, little is known about the role lactate plays in myocardial I/R injury and its underlying mechanism.

Sodium butyrate alleviates right ventricular hypertrophy in pulmonary arterial hypertension by inhibiting H19 and affecting the activation of let-7g-5p/IGF1 receptor/ERK.

Pulmonary arterial hypertension (PAH) is a complex and fatal cardio-pulmonary vascular disease. Decompensated right ventricular hypertrophy (RVH) caused by cardiomyocyte hypertrophy often leads to fatal heart failure, the leading cause of mortality among patients. Sodium butyrate (SB), a compound known to reduce cardiac hypertrophy, was examined for its potential effect and the underlying mechanism of SB on PAH-RVH.

Synergistic Effects of Multiple Environmental Factors on Degradation of Silicone Rubber Seals under Marine Atmosphere.

In this research, the degradation behavior and failure mechanism of silicone rubber seal rings under the synergistic effects of multiple factors in the marine atmosphere are fully investigated. Firstly, four aging factors of air, temperature, compressive stress, and chemical medium were determined by analyzing the service environment profile of silicone rubber seal under a marine atmosphere environment. Secondly, to better simulate the actual service environment of silicone rubber and shorten the test period, an artificially accelerated aging test was designed and carried out in the laboratory.

A ring N(CH)-based derivative of resveratrol inhibits pulmonary vascular remodeling in hypoxia pulmonary hypertension.

Pulmonary artery smooth muscle cells (PASMCs) phenotypic switching and pulmonary artery endothelial cells (PAECs) endothelial-mesenchymal transition (EndMT) are important in promoting pulmonary hypertension (PH)-pulmonary vascular remodeling (PVR). Resveratrol can efficiently inhibit the proliferation of PASMCs, but its application is limited due to its low bioavailability and solubility. In this study, we modified resveratrol to assess the role of A ring N(CH)-based derivatives of resveratrol (Res4) in PVR-PASMCs phenotypic switching and PVR-PAECs EndMT.

Erythropoietin promotes myocardial infarction repair in mice by improving the function of Sca-1 stem cells.

Myocardial infarction (MI) is one of the leading causes of death in the world. With the improvement of clinical therapy, the mortality of acute MI has been significantly reduced. However, as for the long-term impact of MI on cardiac remodeling and cardiac function, there is no effective prevention and treatment measures.

LncRNA H19 deficiency protects against the structural damage of glomerular endothelium in diabetic nephropathy via Akt/eNOS pathway.

This study aimed to investigate the functions of lncRNA H19 on glomerular endothelial structural damage of diabetic nephropathy (DN). Rats were fed a high sugar and fat high feed die, and intraperitoneally administrated with streptozotocin (30 mg/kg) to induce DN model. Meanwile, rat glomerular endothelial cells (rGEnCs) were treated with high a level of glucose （HG, 30 mM glucose）to induce structural damage.

Clinicopathological characteristics and prognosis of breast cancer patients with lung cancer: A study based on 19,807 breast cancer patients.

This study was conducted to investigate the clinicopathological characteristics and prognosis of breast cancer and lung cancer (BC-LC) and provide a theoretical basis for the diagnosis and treatment of BC-LC in clinical work. A retrospective study was conducted on breast cancer (BC) patients in our center from September 2009 to November 2020. The patients were divided into the BC-LC group and the control group.

Diagnostic value of F-FDG PET/CT versus contrast-enhanced MRI for venous tumour thrombus and venous bland thrombus in renal cell carcinoma.

The purpose of this study was to compare the ability of F-FDG PET/CT and contrast-enhanced MRI (CEMRI) to detect and grade venous tumour thrombus (VTT) and venous bland thrombus (VBT) in RCC and assess invasion of the venous wall by VTT. The PET/CT and CEMRI data of 41 patients with RCC were retrieved. The difference in maximum standardized uptake value (SUVmax) between VTT and VBT was analysed.

HIF-1α promotes the proliferation and migration of pulmonary arterial smooth muscle cells via activation of Cx43.

The proliferation of pulmonary artery smooth muscle cells (PASMCs) is an important cause of pulmonary vascular remodelling in hypoxia-induced pulmonary hypertension (HPH). However, its underlying mechanism has not been well elucidated. Connexin 43 (Cx43) plays crucial roles in vascular smooth muscle cell proliferation in various cardiovascular diseases.

MicroRNA-137 Inhibited Hypoxia-Induced Proliferation of Pulmonary Artery Smooth Muscle Cells by Targeting Calpain-2.

The proliferation of pulmonary artery smooth muscle cells (PASMCs) is an important cause of pulmonary vascular remodeling in pulmonary hypertension (PH). It has been reported that miR-137 inhibits the proliferation of tumor cells. However, whether miR-137 is involved in PH remains unclear.

Glucagon-Like Peptide-1 Analog Liraglutide Attenuates Pressure-Overload Induced Cardiac Hypertrophy and Apoptosis through Activating ATP Sensitive Potassium Channels.

Purpose: This study aimed to investigate whether inhibition of glucagon-like peptide-1 (GLP-1) on pressure overload induced cardiac hypertrophy and apoptosis is related to activation of ATP sensitive potassium (KATP) channels.

Methods: Male SD rats were randomly divided into five groups: sham, control (abdominal aortic constriction), GLP-1 analog liraglutide (0.3 mg/kg/twice day), KATP channel blocker glibenclamide (5 mg/kg/day), and liraglutide plus glibenclamide.

Stenosing tenosynovitis : Evaluation of percutaneous release with a specially designed needle vs. open surgery.

Purpose: The purpose of this study was to evaluate the effectiveness of conventional open surgery and percutaneous release with a specially designed needle for treating stenosing tenosynovitis in terms of cure, relapse and complication rates.

Methods: In this study 89 fingers from 76 patients were randomly assigned and allocated to one of the treatment groups. A total of 37 patients were treated with open surgery in group 1 and 39 patients with percutaneous release using a specially designed needle in group 2.

MicroRNA-140-5p targeting tumor necrosis factor-α prevents pulmonary arterial hypertension.

Background: Pulmonary arterial hypertension (PAH) is characterized by the apoptosis resistance and hyperproliferation of pulmonary artery smooth muscle cells (PASMCs). Its pathogenesis has not been revealed. Here, we carried out experiments to investigate the functions of miR-140-5p and tumor necrosis factor-α (TNF-α).

F-FDGPET/CT in fever of unknown origin and inflammation of unknown origin: a Chinese multi-center study.

Purpose: To evaluate the clinical value of F-FDG-PET/CT for the diagnosis of fever of unknown origin (FUO) and inflammation of unknown origin (IUO) in Chinese population, as well as the characteristics of PET/CT in different category of etiological disease.

Methods: A total of 376 consecutive patients with FUO/IUO who underwent FDG-PET/CT at 12 hospitals were retrospectively studied. FDG uptake was quantitatively and visually evaluated, by using SUV and a 4-grade scale respectively.

Early life esophageal acid exposure reduces expression of NMDAR1 in the adult rat dorsal hippocampus and medial prefrontal cortex: Potential relationship with hyperlocomotion.

Objective: Early life esophageal acid exposure causes long-term molecular alterations in the rostral cingulate cortex; however, whether it induces behavioral changes remains unverified. Little is known about the molecular changes resulting from this event in the developing hippocampus and medial prefrontal cortex (mPFC). This study aimed to investigate the influence of early life esophageal acid exposure on spontaneous locomotor behavior and N-methyl-D-aspartate receptor (NMDAR), expression in these brain regions of adult rats.

Knockdown of metadherin inhibits cell proliferation and migration in colorectal cancer.

Metadherin (MTDH) is a multifunctional oncogene involved in tumor cell migration and metastasis through regulating a number of oncogenic signaling pathways in various human malignancies. Previous studies have demonstrated that MTDH is overexpressed in human colorectal cancer (CRC) and associated with cancer progression and a poor prognosis. However, the underlying mechanisms remain largely unknown.

Six2 is negatively correlated with good prognosis and decreases 5-FU sensitivity via suppressing E-cadherin expression in hepatocellular carcinoma cells.

This work aims to study the roles and related mechanisms of six2 in 5-FU sensitivity of hepatocellular carcinoma (HCC) cells. KM-Plotter analysis showed that HCC patients with higher six2 expression levels had shorter overall survival. Six2 expression was higher in clinical HCC tissues than in normal tissues, and was negatively correlated with E-cadherin expression.

Curcumin inhibits cardiac hypertrophy and improves cardiovascular function via enhanced Na/Ca exchanger expression after transverse abdominal aortic constriction in rats.

Background: This study tested the hypothesis that inhibition of cardiac hypertrophy and preservation of cardiac/endothelial function by the natural yellow pigment curcumin are associated with upregulated expression of Na/Ca exchanger (NCX) after transverse aortic constriction (TAC).

Methods: Male Wistar rats were subjected to TAC for 10 weeks and curcumin (50 mg/kg/day) was fed by gastric gavage during TAC. Expression of NCX and endothelial nitric oxide synthase (eNOS) was analyzed by Western blot and immunohistochemistry.

[Role of autophagy in TXNIP overexpression-induced apoptosis of INS-1 islet cells].

Thioredoxin (Trx) interacting protein (TXNIP) is a Trx-binding protein that inhibits the antioxidative function of Trx and is highly expressed in the serum and tissue samples from diabetes patients. This study was to explore whether TXNIP overexpression could cause INS-1 cell autophagy under normal glucose and lipid concentrations, and to analyze the role of autophagy in the apoptosis of INS-1 cells. The INS-1 cells cultured under normal conditions were divided into three groups: normal control, empty adenovirus vector (Ad-eGFP) and TXNIP overexpression (Ad-TXNIP-eGFP) groups.

Epigallocatechin-3-gallate ameliorates hypoxia-induced pulmonary vascular remodeling by promoting mitofusin-2-mediated mitochondrial fusion.

Pulmonary hypertension (PH) mainly results from excessive proliferation of pulmonary artery smooth muscle cells (PASMCs) and displays mitochondrial abnormalities such as mitochondrial fragmentation. Epigallocatechin-3-gallate (EGCG), an efficient antiproliferative compound in green tea, has recently been demonstrated to inhibit PASMCs proliferation. However, the pre-clinical issues as to whether EGCG attenuates PH and the underlying mechanisms have yet to be addressed.

Involvement of epithelial-mesenchymal transition afforded by activation of LOX-1/ TGF-β1/KLF6 signaling pathway in diabetic pulmonary fibrosis.

Background And Objective: Diabetic pulmonary fibrosis is a severe disease that increases mortality risk of diabetes. However, the molecular mechanisms leading to pulmonary fibrosis in diabetes are poorly understood. This study investigated the roles of epithelial-mesenchymal transition (EMT) and the associated molecular mechanisms in streptozotocin (STZ)-induced rat pulmonary fibrosis.

LOX-1 promotes right ventricular hypertrophy in hypoxia-exposed rats.

Aim: Chronic hypoxia leads to right ventricular hypertrophy (RVH). RVH is believed to result from hypoxia-induced pulmonary hypertension. However, if hypoxia impacts RVH directly awaits clarification.

Negative feedback regulation between microRNA let-7g and LOX-1 mediated hypoxia-induced PASMCs proliferation.

Background: Pulmonary hypertension (PH) is a proliferative disorder associated with enhanced proliferation and suppressed apoptosis of pulmonary artery smooth muscle cells (PASMCs). Our lately study demonstrated that let-7g inhibited hypoxia-induced proliferation of PASMCs via repressing c-myc-Bmi-1-p16 signaling pathway. However, the upstream of let-7g has not yet been fully defined.

MicroRNA let-7g inhibited hypoxia-induced proliferation of PASMCs via G/G cell cycle arrest by targeting c-myc.

Aims: Pulmonary hypertension (PH) is a proliferative disorder characterized by enhanced proliferation and suppressed apoptosis of intrapulmonary vascular smooth muscle cells. Recently, network-based bioinformatics have identified let-7 family, a tumor suppressive microRNA, regulate multiple interacting targets relevant to PH. However, the role of let-7 in vascular homeostasis in PH remains unknown.