Peptide PDRPS6 attenuates myocardial ischemia injury by improving mitochondrial function.

Mitochondrial dynamics play a crucial role in myocardial ischemia-reperfusion (I/R) injury, where an imbalance between fusion and fission processes occurs. However, effective measures to regulate mitochondrial dynamics in this context are currently lacking. Peptide derived from the 40 S ribosomal protein S6 (PDRPS6), a peptide identified via peptidomics, is associated with hypoxic stress.

Comprehensive analysis of the expression and prognosis for APOE in malignancies: A pan-cancer analysis.

Apolipoprotein E (), a gene identified as one of the strongest genetic factors contributing to the risk determinant of developing late-onset Alzheimer's disease (AD), may also contribute to the risk of cancer. However, no pan-cancer analysis has been conducted specifically for the gene. In this study, we investigated the oncogenic role of the gene across cancers by GEO (Gene Expression Omnibus) and TCGA (The Cancer Genome Atlas).

The influence of gender and wealth inequality on Alzheimer's disease among the elderly: A global study.

This study was designed to explore the relationship between Alzheimer's disease (AD) rates and socioeconomic conditions in 120 countries. We used mixed effect models to investigate the relationship between the rates of AD and socioeconomic data. This study is among the first studies to put forward statistical evidence of a significant association between AD and other dementias among the elderly and socioeconomic inequality.

A novel peptide HSP-17 ameliorates oxidative stress injury and apoptosis in H9c2 cardiomyocytes by activating the PI3K/Akt pathway.

Background: Oxidative stress and cell apoptosis play pivotal roles in the pathogenesis of doxorubicin (DOX)-induced myocardial injury. Heat shock protein-derived peptide (HSP-17) is a peptide which is low-expressed in DOX treated mouse heart tissue. It has high bioactivity and interspecies sequence consistency, and is predicted to have myocardial protective effect.

ELA-11 protects the heart against oxidative stress injury induced apoptosis through ERK/MAPK and PI3K/AKT signaling pathways.

Increasing evidence revealed that apoptosis and oxidative stress injury were associated with the pathophysiology of doxorubicin (DOX)-induced myocardial injury. ELABELA (ELA) is a newly identified peptide with 32 amino acids, can reduce hypertension with exogenous infusion. However, the effect of 11-residue furn-cleaved fragment (ELA-11) is still unclear.

Genetic alterations, RNA expression profiling and DNA methylation of HMGB1 in malignancies.

The high mobility group box 1 (HMGB1) is a potential biomarker and therapeutic target in various human diseases. However, a systematic, comprehensive pan-cancer analysis of HMGB1 in human cancers remains to be reported. This study analysed the genetic alteration, RNA expression profiling and DNA methylation of HMGB1 in more than 30 types of tumours.

Identification of a novel native peptide derived from 60S ribosomal protein L23a that translationally regulates p53 to reduce myocardial ischemia-reperfusion.

Myocardial ischemia-reperfusion (I/R) is a severe disease，but its underlying mechanism is not fully elucidated and no effective clinical treatment is available. Utilizing intracellular peptidomics, we identified a novel native peptide PDRL23A (Peptide Derived from RPL23A), that is intimately related to hypoxic stress. We further show that PDRL23A effectively alleviates hypoxia-induced cardiomyocyte injury in vitro, along with improvements in mitochondrial function and redox homeostasis, including ROS accumulation, oxidative phosphorylation, and mitochondrial membrane potential.

Exercise-induced peptide TAG-23 protects cardiomyocytes from reperfusion injury through regulating PKG-cCbl interaction.

Recent studies have revealed that proper exercise can reduce the risk of chronic disease and is beneficial to the body. Peptides have been shown to play an important role in various pathological processes, including cardiovascular diseases. However, little is known about the role of exercise-induced peptides in cardiovascular disease.

The Impact of COVID-19 on Primary Care General Practice Consultations in a Teaching Hospital in Shanghai, China.

The COVID-19 (2019 novel coronavirus disease) pandemic is deeply concerning because of its massive mortality and morbidity, creating adverse perceptions among patients likely to impact on their overall medical care. Thus, we evaluated the impact of the COVID-19 pandemic on the pattern of primary care consultations within a Shanghai health district. A retrospective observational cohort study was performed, with data analyzed concerning the pattern of patient visits to general practitioners within the Tongren Hospital network (the sole provider of general practice to the population of 700,000).

Exercise-induced peptide EIP-22 protect myocardial from ischaemia/reperfusion injury via activating JAK2/STAT3 signalling pathway.

Recent studies have revealed that exercise has myocardial protective effects, but the exact mechanism remains unclear. Studies have increasingly found that peptides play a protective role in myocardial ischaemia-reperfusion (I/R) injury. However, little is known about the role of exercise-induced peptides in myocardial I/R injury.

Peptidomics analysis revealed that a novel peptide VMP‑19 protects against Ang II‑induced injury in human umbilical vein endothelial cells.

Vascular endothelial dysfunction is a vital pathological change in hypertension, which is mainly caused by apoptosis and oxidative stress injury of vascular endothelial cells. Peptidomics is a method for the direct analysis of small bioactive peptides in various biological samples using liquid chromatography‑mass spectrometry (MS)/MS. Given the advantages of the low molecular weight, optimum targeting and easy access to cells, peptides have attracted extensive attention in the field of drug research.

Peptide Szeto‑Schiller 31 ameliorates doxorubicin‑induced cardiotoxicity by inhibiting the activation of the p38 MAPK signaling pathway.

Oxidative stress serves a key role in doxorubicin (DOX)‑induced cardiotoxicity. The peptide Szeto‑Schiller (SS)31 is an efficacious antioxidant with the capacity to reduce mitochondrial reactive oxygen species (ROS) levels and scavenge free radicals. Although SS31 is involved in the pathophysiological process of various cardiovascular diseases, the role of SS31 in DOX‑induced cardiotoxicity remains unclear.

Circular RNA Arhgap12 modulates doxorubicin-induced cardiotoxicity by sponging miR-135a-5p.

Aim: This study aimed to investigate the regulatory role of differentially-expressed circular RNAs (circRNAs) in mouse cardiomyocytes during doxorubicin (DOX)-induced cardiotoxicity.

Main Methods: Two groups of mice were injected with equal volumes (0.1 mL) of normal saline and DOX.

Peptidomics Analysis Reveals Peptide PDCryab1 Inhibits Doxorubicin-Induced Cardiotoxicity.

Doxorubicin (DOX) is limited due to dose-dependent cardiotoxicity. Peptidomics is an emerging field of proteomics that has attracted much attention because it can be used to study the composition and content of endogenous peptides in various organisms. Endogenous peptides participate in various biological processes and are important sources of candidates for drug development.

A simulation training course for family medicine residents in China managing COVID-19.

Background And Objectives: As a result of the pandemic, family physicians face the additional challenge of navigating COVID-19. The aim of this study was to provide simulated training for best-practice management of COVID-19 presentations for residency program trainees in Shanghai, China.

Method: A simulated suspected COVID-19 case was designed on the basis of a real patient.

Role of lncRNA uc.457 in the differentiation and maturation of cardiomyocytes.

Congenital heart disease (CHD) is the most common type of birth defect, and the leading cause of fetal mortality. The long noncoding RNA (lncRNA) uc.457 is differentially expressed in cardiac tissue from patients with a ventricular septal defect; however, its role in cardiac development and CHD remains unknown.

Expression profile of long non‑coding RNAs in cardiomyocytes exposed to acute ischemic hypoxia.

Acute myocardial infarction (AMI) is a life‑threatening disease and seriously influences patient quality of life. Long non‑coding RNAs (lncRNAs), an emerging class of non‑coding genes, have attracted attention in research, however, whether lncRNAs serve a function in acute ischemic hypoxia remains to be elucidated. In the present study, an lncRNA microarray was used to analyze differential lncRNA expression in acute ischemic hypoxia.

Long noncoding RNA uc.4 inhibits cell differentiation in heart development by altering DNA methylation.

In previous studies, we have demonstrated that long noncoding RNA uc.4 may influence the cell differentiation through the TGF-β signaling pathway, suppressed the heart development of zebrafish and resulting cardiac malformation. DNA methylation plays a significant role in the heart development and disordered of DNA methylation may cause disruption of control of gene promoter.

An alternative under-valve approach to ablate right-sided accessory pathways.

Background: Right-sided accessory pathway (RAP) ablation is sometimes challenging.

Objective: Our study aimed to demonstrate an alternative ablation approach to RAPs under the tricuspid valve, especially when the conventional ablation attempts at the atrial side failed.

Methods: Twelve patients with RAPs were enrolled, 8 of whom had previously failed ablation.

Altered DNA Methylation of Long Noncoding RNA uc.167 Inhibits Cell Differentiation in Heart Development.

In previous studies, we have demonstrated the function of uc.167 in the heart development. DNA methylation plays a crucial role in regulating the expression of developmental genes during embryonic development.

Attenuation of Na/K-ATPase/Src/ROS amplification signal pathway with pNaktide ameliorates myocardial ischemia-reperfusion injury.

Objectives: Oxidative stress plays an important role in myocardial ischemia-reperfusion (I/R) injury. And pNaKtide is known to inhibit Na/K-ATPase/Src/reactive oxygen species (ROS) amplification signaling. Accordingly, we aimed to investigate the effect of pNaKtide on myocardial I/R injury.

The long non-coding RNA uc.4 influences cell differentiation through the TGF-beta signaling pathway.

In a previous study, we screened thousands of long non-coding RNAs (lncRNAs) to assess their potential relationship with congenital heart disease (CHD). In this study, uc.4 attracted our attention because of its high level of evolutionary conservation and its antisense orientation to the CASZ1 gene, which is vital for heart development.

Identification of differentially expressed lncRNAs involved in transient regeneration of the neonatal C57BL/6J mouse heart by next-generation high-throughput RNA sequencing.

Previous studies have shown that mammalian cardiac tissue has a regenerative capacity. Remarkably, neonatal mice can regenerate their cardiac tissue for up to 6 days after birth, but this capacity is lost by day 7. In this study, we aimed to explore the expression pattern of long noncoding RNA (lncRNA) during this period and examine the mechanisms underlying this process.

Peptidomics Analysis of Transient Regeneration in the Neonatal Mouse Heart.

Neonatal mouse hearts have completely regenerative capability after birth, but the ability to regenerate rapidly lost after 7 days, the mechanism has not been clarified. Previous studies have shown that mRNA profile of adult mouse changed greatly compared to neonatal mouse. So far, there is no research of peptidomics related to heart regeneration.

Peptidomic Analysis of Cultured Cardiomyocytes Exposed to Acute Ischemic-Hypoxia.

Background: Acute Myocardial Infarction (AMI) is a life-threatening cardiovascular disease involving disruption of blood flow to the heart, consequent tissue damage, and sometimes death. Peptidomics, an emerging branch of proteomics, has attracted wide attention.

Methods: A comparative peptidomic profiling was used to explore changes induced by acute ischemic-hypoxia in primary cultured neonatal rat myocardial cells.