Investigating the impact of non-standard positioning on the accuracy of skull tracking algorithms using dual-panel imaging systems.

Objective: This study investigates the impact of non-standard positioning on the accuracy of 6D-skull tracking using dual-panel imaging systems. It explores whether positioning patients' heads at various angles during intracranial lesion treatment affects the accuracy of the CyberKnife 6D-skull tracking system.

Materials And Methods: A heterogeneous density skull phantom was used to simulate various patient skull positioning angles.

Plasma exosomes from patients with coronary artery disease promote atherosclerosis via impairing vascular endothelial junctions.

The underlying mechanism of vascular endothelial hyperpermeability caused by decrease of endothelial junctions occurring in atherosclerosis remains elusive. Our findings identified that plasma exosomes from patients with stable coronary artery disease (Exo) contain differentially expressed miRNAs that are clustered with genes related to cell junctions, prompting us to investigate the role of Exo in regulating vascular endothelial junctions and to elucidate the underlying mechanisms. Here, we show that Exo markedly impair vascular endothelial junctions via suppressing VE-Cadherin and ZO-1 in endothelial cells in vitro and in vivo, consequently increases endothelial permeability.

Renin and (pro)renin receptors induce vascular smooth muscle cell proliferation and neointimal hyperplasia by activating oxidative stress and inflammation.

Renin and prorenin promote the proliferation of vascular smooth muscle cells (VSMCs) through the (pro)renin receptor, or (P)RR, to promote restenosis occurrence. This study aimed to explore whether prorenin promoted the proliferation of VSMCs in a (P)RR-mediated Ang II-independent manner. : Losartan and PD123319 were used to block the interaction between (P)RR and angiotensin in vitro.

Association of the longitudinal trajectory of urinary albumin/creatinine ratio in diabetic patients with adverse cardiac event risk: a retrospective cohort study.

Objective: The baseline urinary albumin/creatinine ratio (uACR) has been proven to be significantly associated with the risk of major adverse cardiac events (MACE). However, data on the association between the longitudinal trajectory patterns of uACR, changes in glycated hemoglobin A1c (HbA1c), and the subsequent risk of MACE in patients with diabetes are sparse.

Methods: This is a retrospective cohort study including 601 patients with type 2 diabetes mellitus (T2DM; uACR < 300 mg/g) admitted to The First Hospital of Shanxi Medical University and The Second Hospital of Shanxi Medical University from January 2015 to December 2018.

Fibroblast-derived interleukin-6 exacerbates adverse cardiac remodeling after myocardial infarction.

Myocardial infarction is one of the leading causes of mortality globally. Currently, the pleiotropic inflammatory cytokine interleukin-6 (IL-6) is considered to be intimately related to the severity of myocardial injury during myocardial infarction. Interventions targeting IL-6 are a promising therapeutic option for myocardial infarction, but the underlying molecular mechanisms are not well understood.

Plasma-derived exosomal let-7c-5p, miR-335-3p, and miR-652-3p as potential diagnostic biomarkers for stable coronary artery disease.

Circulating exosomal microRNAs (miRNAs) have been identified as promising biomarkers for diagnosis of cardiovascular diseases. Nevertheless, the diagnostic potential of miRNAs in circulating exosomes for stable coronary artery disease (SCAD) remains unclear. We aim here to analyze the exosomal differentially expressed miRNAs (DEmiRNAs) in plasma of SCAD patients and investigate their diagnostic potential as SCAD biomarkers.

[Effects of PUMA knockout on the apoptosis of H9C2 cardiomyocytes induced by high glucose].

Objective: To investigate the effects of p53 upregulated modulator of apoptosis (PUMA) on the apoptosis of H9C2 cardiomyocytes induced by high glucose and its mechanisms.

Methods: H9C2 cardiomyocytes were treated with 5.5mmol/L (control group) or 35 mmol/L glucose (HG group) for 6 h, 12 h, 24 h or 48 h respectively to induce apoptosis, each group sets 5 multiple wells.

Evaluation of corrective effect of 6 degree of freedom couch on setup errors in intensity modulated radiotherapy for postoperative rectal cancer patients.

Objective: To explore the corrective effect of 6 degree of freedom couch on rotation errors in intensity modulated radiotherapy (IMRT) for postoperative rectal cancer patients, further to probe into the clinical application value of 6 degree of freedom couch in radiotherapy.

Methods: From January 1, 2020 to December 1, 2020, 30 patients with rectal cancer receiving postoperative intensity modulated radiotherapy in The First Hospital of Hebei Medical University were included in this retrospective study. The setup error values in all direction of patients before and after 6 degree of freedom correction were collected during each radiotherapy session.

Correlation between mechanism of oxidized-low density lipoprotein-induced macrophage apoptosis and inhibition of target gene platelet derived growth factor receptor-β expression by microRNA-9.

This study was to explore the effects of oxidized-low density lipoprotein (ox-LDL) on the proliferation and apoptosis of macrophages, and the role of miRNA-9 in the targeted regulation of platelet-derived growth factor receptor-β (PDGFR-β) expression. Macrophage RAW264.7 cells were cultured and foamed with 100 mg/L ox-LDL to detect the cell proliferation and apoptosis and target protein expression levels.

Glutamate Dehydrogenase as a Promising Target for Hyperinsulinism Hyperammonemia Syndrome Therapy.

Hyperinsulinism-hyperammonemia syndrome (HHS) is a rare disease characterized by recurrent hypoglycemia and persistent elevation of plasma ammonia, and it can lead to severe epilepsy and permanent brain damage. It has been demonstrated that functional mutations of glutamate dehydrogenase (GDH), an enzyme in the mitochondrial matrix, are responsible for the HHS. Thus, GDH has become a promising target for the small molecule therapeutic intervention of HHS.

Adiponectin improves amyloid-β 31-35-induced circadian rhythm disorder in mice.

Adiponectin is an adipocyte-derived hormone, which is closely associated with the development of Alzheimer's disease (AD) and has potential preventive and therapeutic significance. In the present study, we explored the relationship between adiponectin and circadian rhythm disorder in AD, the effect of adiponectin on the abnormal expression of Bmal1 mRNA/protein induced by amyloid-β protein 31-35 (Aβ31-35), and the underlying mechanism of action. We found that adiponectin-knockout mice exhibited amyloid-β deposition, circadian rhythm disorders and abnormal expression of Bmal1.

Adiponectin up-regulates the decrease of myocardial autophagic flux induced by β -adrenergic receptor autoantibody partly dependent on AMPK.

Cardiomyocytes autophagy is essential for maintaining cardiac function. Our previous studies have found that β -adrenergic receptor autoantibody (β -AA) induced the decreased myocardial autophagic flux, which resulted in cardiomyocyte death and cardiac dysfunction. And other studies demonstrated that β -AA induced the decrease of AMPK phosphorylation, the key hub of autophagy pathway, while adiponectin up-regulated autophagic flux mediated by AMPK.

Polypeptide Globular Adiponectin Ameliorates Hypoxia/Reoxygenation-Induced Cardiomyocyte Injury by Inhibiting Both Apoptosis and Necroptosis.

Adiponectin is a small peptide secreted and a key component of the endocrine system and immune system. Although globular adiponectin protects myocardial ischemia/reperfusion-induced cardiomyocyte injury, the protective mechanisms remain largely unresolved. Using a neonatal rat ventricular myocyte hypoxia/reoxygenation model, we investigated the role of its potential mechanisms of necroptosis in globular adiponectin-mediated protection in hypoxia/reoxygenation-induced cardiomyocyte injury as compared to apoptosis.

Intermedin protects thapsigargin‑induced endoplasmic reticulum stress in cardiomyocytes by modulating protein kinase A and sarco/endoplasmic reticulum Ca‑ATPase.

Intermedin (IMD) is a calcitonin/calcitonin‑related peptide that elicits cardioprotective effects in a variety of heart diseases, such as cardiac hypertrophy and heart failure. However, the molecular mechanism of IMD remains unclear. The present study investigated the effects of IMD on neonatal rat ventricular myocytes treated with thapsigargin.

Discovery of an Inhibitor for Bacterial 3-Mercaptopyruvate Sulfurtransferase that Synergistically Controls Bacterial Survival.

HS-producing enzymes in bacteria have been shown to be closely engaged in the process of microbial survival and antibiotic resistance. However, no inhibitors have been discovered for these enzymes, e.g.

Activating transcription factor 3 is a potential target and a new biomarker for the prognosis of atherosclerosis.

ATF3 (activating transcription factor 3) is a member of the mammalian activation transcription factor/cAMP-responsive element-binding (CREB) family. It plays a role in inflammation and innate immunity, and suggests that ATF3 is associated with atherosclerosis. In our study, we analyzed datasets of atherosclerosis from the NCBI-GEO (Gene Expression Omnibus) database and found that expression levels of ATF3 were lower in macrophages from ruptured atherosclerotic plaques than from stable atherosclerotic plaques.

Long Non-Coding RNA SNHG8 Plays a Key Role in Myocardial Infarction Through Affecting Hypoxia-Induced Cardiomyocyte Injury.

BACKGROUND The objective of the study was to explore the role of long non-coding RNA SNHG8 (lncRNA SNHG8) in myocardial infarction (MI) and the related mechanism of action. MATERIAL AND METHODS In vitro model of MI was established by hypoxia induction in cardiomyocyte line H9c2 cells. H9c2 cells were transfected with control-plasmid, SNHG8-plasmid, control-shRNA and SNHG8-shRNA.

Circ_BMP2K enhances the regulatory effects of miR-455-3p on its target gene and thereby inhibits the activation of cardiac fibroblasts.

Research has shown that some circular RNAs (circRNA) are abnormally expressed in the process of myocardial fibrosis, but the mechanism behind this was unknown. In the process of inducing cardiac fibroblast (CF) activation with TGF-β1 or Ang II, the expression of circRNA circ_BMP2K and miR-455-3p were significantly inhibited, whereas the expression of was promoted. The results from our dual luciferase reporter gene assays, RIP assays, and pull-down assays show that miR-455-3p directly binds circ_BMP2K, thereby mutually promoting their expression levels.

MicroRNA-20a/b regulates cholesterol efflux through post-transcriptional repression of ATP-binding cassette transporter A1.

ATP-binding cassette transporter A1 (ABCA1) plays a crucial role in reverse cholesterol transport and exhibits anti-atherosclerosis effects. Some microRNAs (miRs) regulate ABCA1 expression, and recent studies have shown that miR-20a/b might play a critical role in atherosclerotic diseases. Here, we attempted to clarify the potential contribution of miR-20a/b in post-transcriptional regulation of ABCA1, cholesterol efflux, and atherosclerosis.

Effect of adiponectin on macrophage reverse cholesterol transport in adiponectin-/- mice and its mechanism.

The objective of the present study was to investigate the effect of adiponectin (APN) on macrophage reverse cholesterol transport (RCT) in adiponectin-/- knockout mice (APN-/-mice) and its possible anti-atherosclerotic mechanism. A total of 30 male APN-/-mice were randomly divided into the control group and four intervention groups. The intervention groups were treated with intraperitoneal injections of APN, at doses of 50, 150, 200 and 250 µg/(kg/day), respectively, for 4 weeks.

Correlation between the High Density Lipoprotein and its Subtypes in Coronary Heart Disease.

Background/aims: To detect the changes of high density lipoprotein (HDL) and its subtypes in serum of patients with coronary heart disease (CHD).

Methods: 337 hospitalized patients were selected from our hospital during August, 2014 - January, 2015, and divided into CHD group (n = 190) and control group (n = 127). Lipoprint lipoprotein analyzer was used to classify low density lipoprotein (LDL) particle size and its sub-components, as well as HDL particle size and its sub-components.

P‑selectin increases angiotensin II‑induced cardiac inflammation and fibrosis via platelet activation.

Platelet activation is important in hypertension‑induced cardiac inflammation and fibrosis. P-selectin expression significantly (P<0.05) increases when platelets are activated during hypertension.

Globular adiponectin reduces vascular calcification via inhibition of ER-stress-mediated smooth muscle cell apoptosis.

Objective: This study aims to explore the mechanism of globular adiponectin inhibiting vascular calcification.

Methods: We established drug-induced rat vascular calcification model, globular adiponectin was given to observe the effect of globular Adiponectin on the degree of calcification. The markers of vascular calcification and apoptosis were also investigated.