Stormwiggins1290

Acute myocardial infarction (AMI) is the main cause of cardiovascular events worldwide. AMI commonly occurs in elderly patients because of atherosclerotic process related to common risk factors. Consequently, the rupture of atheromatous plaque with deleterious sequela is the common etiology of the disease. However, there are less studied etiological factors in youth compared with the usual population. Therefore, this study aimed to examine the risk profile of Egyptian youth presenting with AMI.

A study was conducted in 106 patients aged ≤45 years admitted with AMI in our university hospital to explore their clinical profile risk factors.

In the study, 71 (67%) and 35 (33%) patients presented with ST elevation myocardial infarction (STEMI) and non-STEMI (NSTEMI). Anterior wall MI was predominant in 49 patients (46.2%). Moreover, 93 patients (88%) were smokers, 31 (29.2%) used tramadol, 43 (40.6%) smoked cannabis, 50 (47.2%) had poor sleeping habits, 29 (27.4%) had high stress levels, 37 (34.9%) had hypertension, and 22 (20.8%) had diabetes. Twenty (18.9%) patients had a family history of premature coronary artery disease. High and low high-density lipoprotein (HDL) levels were observed in 20 (18.9%) and 47 (44.3%) patients, respectively. The left anterior descending artery (LAD) was involved in 56% of the studied population associated with tramadol use. A significant association was found between both tramadol use and cannabis smoking and presence of heavy thrombus burden on coronary angiography.

AMI in Egyptian youth was predominantly observed in men, with anterior STEMI as the most common presentation. Cannabis and tramadol addiction were high risk factors for AMI in Egyptian youth.

AMI in Egyptian youth was predominantly observed in men, with anterior STEMI as the most common presentation. Cannabis and tramadol addiction were high risk factors for AMI in Egyptian youth.

TCF7L2 is a repressor and transactivator of genes, and its variants are strongly associated with diabetes. This study aimed to evaluate the sex-specific relationship between the most common TCF7L2 gene variants (-98368G>T, rs12255372 and -47833C>T, rs7903146) with diabetes and coronary heart disease in Turkish Adult Risk Factor (TARF) Study.

Single nucleotide variants (SNVs) have been genotyped using the TaqMan allelic discrimination assays in 2,024 (51.3% in women, age 55±11.8) Turkish adults participating in the TARF study. Statistical analyses were used to investigate the association of genotypes with clinical and biochemical measurements.

Among the TARF study participants, 11.7%, 24.3%, 14.1%, and 38.3% had diabetes, hypertension, coronary heart disease (CHD), and obesity, respectively. The frequencies of T allele for -47833C>T and -98368G>T in Turkish adults were determined to be 0.35 and 0.33, respectively. -47833C>T was significantly associated with higher fasting glucose concentrations in all participants, especially in men. Both SNVs were significantly associated with diabetes and CHD in all participants (p<0.05). When study population was stratified according to sex, -98368G>T was associated with diabetes in women (p=0.041) and -47833C>T was associated with diabetes and CHD in men (p=0.018 and p=0.032, respectively). Also, both SNVs and the diplotypes of common haplotype (H1) remained strongly associated with type 2 diabetes after risk factors were adjusted (p<0.05).

T allele homozygosity of two SNVs as well as the diplotype H1-/H1- reflects risk of diabetes primarily in men. Enhanced CHD risk is determined by the presence of diplotype H1-/H1- among nondiabetic participants.

T allele homozygosity of two SNVs as well as the diplotype H1-/H1- reflects risk of diabetes primarily in men. Enhanced CHD risk is determined by the presence of diplotype H1-/H1- among nondiabetic participants.

A strong correlation exists between myocardial fibrosis and heart failure (HF). Myocardial fibrosis can be detected by cardiac magnetic resonance (CMR), which is a crucial noninvasive imaging method with high specificity and sensitivity. Matrix metalloproteinases (MMPs) are primary proteases responsible for the degradation of extracellular matrix (ECM) components, and they play a vital role in maintaining the balance between anabolism and catabolism of ECM. This study aims to investigate the correlation between cardiac fibrosis detected on CMR and serum MMP-9 levels in patients with HF.

We enrolled 53 patients (age ≥18 years) with left ventricular ejection fraction (LVEF) ≤40%, who received CMR because of various indications. Protein Tyrosine Kinase inhibitor All patients were divided into two groups-with cardiac fibrosis (n=32) and without cardiac fibrosis (n=21)-detected by CMR with late-Gadolinium. Both groups were then compared according to MMP-9 levels.

MMP-9 levels were significantly higher in patients with cardiac fibrosis than tl in predicting left ventricular fibrosis. In clinical practice, the use of serum MMP-9 could provide early consideration of therapies for structural and functional pathology of the heart in patients with HF.Global prevalence of coronavirus disease 2019 (COVID-19) calls for an urgent development of anti-viral regime. Compared with the development of new drugs, drug repurposing can significantly reduce the cost, time, and safety risks. Given the fact that coronavirus harnesses spike protein to invade host cells through angiotensin-converting enzyme 2 (ACE2), hence we see if any previous anti-virtual compounds can block spike-ACE2 interaction and inhibit the virus entry. The results of molecular docking and molecular dynamic simulations revealed that remdesivir exhibits better than expected anti-viral invasion potential against COVID-19 among the three types of compounds including remdesivir, tenofovir and lopinavir. link2 In addition, a positive correlation between the surface area occupied by remdesivir and anti-viral invasion potential was also found. As such, the structure of remdesivir was modified by linking an N-benzyl substituted diamidine derivative to its hydroxyl group through an ester bond. It was found that this compound has a higher anti-viral invasion potential and greater specificity.Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive- fibrosing disease characterized by extensive deposition of extracellular matrix (ECM), scarring of the lung parenchyma. Despite increased awareness of IPF, etiology and physiological mechanism of IPF are unclear. Therefore, preclinical model will require relevant and recapitulative features of IPF. Recently, pluripotent stem cells (PSC)-based organoid studies are emerging as an alternative approach able to recapitulate tissue architecture with remarkable fidelity. Moreover, these biomimetic tissue models can be served to investigate the mechanisms of diverse disease progression. In this review, we will overview the current organoids technology for human disease modeling including lung organoids for IPF.Tendons are structures that connect muscles to the bones in our body and transmit the force generated by contraction of the muscles to the bones. link3 Ligaments are structures that connect bones to bones, with histological properties similar to tendons. In tendon and ligament tissue, there are very small amounts of cells similar to mesenchymal stem cells (MSCs) called tendon stem/progenitor cells (TSPCs), or tenogenic stem cells. While the role of specific growth factors and transcription factors is well established in the osteogenic and chondrogenic differentiation of stem cells, a consensus has not been established for tenogenic differentiation. Injuries to tendons and ligaments are very common, but natural healing is very slow and inefficient due to limited vascularization. Currently, there is no adequate method for restoring extensive tendon or ligament defects. Procedures addressing the unmet need for regeneration of these tissues are needed. In this review, the current knowledge, as well as the authors' ideas and perspective on stem cell and regenerative medicine for tendon and ligament defects are presented.

Embryonic stem (ES) cells have the capacity to self-renew and generate all types of cells. MUC1-C, a cytoplasmic subunit of MUC1, is overexpressed in various carcinomas and mediates signaling pathways to regulate intracellular metabolic processes and gene expression involved in the maintenance of cancer cells. However, the functional role of MUC1-C in ES cells is not well understood. In this study, we investigated the role of MUC1-C on growth, survival, and differentiation of mouse ES (mES) cells.

Undifferentiated mES cells expressed the MUC1-C protein and the expression level was decreased during differentiation. Inhibition of MUC1-C, by the specific inhibitor GO201, reduced proliferation of mES cells. However, there was no prominent effect on pluripotent markers such as Oct4 expression and STAT3 signaling, and MUC1-C inhibition did not induce differentiation. Inhibition of MUC1-C increased the G1 phase population, decreased the S phase population, and increased cell death. Furthermore, inhibition of MUC1-C induced disruption of the ROS balance in mES cells.

These results suggest that MUC1-C is involved in the growth and survival of mES cells.

These results suggest that MUC1-C is involved in the growth and survival of mES cells.

Liver cirrhosis is accompanied by abnormal vascular shunts. The Wnt pathway is essential for endothelial cell survival and proliferation. C-reactive protein (CRP), which is produced by hepatocyte, activates angiogenesis in cardiovascular diseases.

The expression of CRP in CCl4-injured rat livers was detected using qRT-PCR and Western blotting after transplantation of placenta-derived mesenchymal stem cells (PD-MSCs) into rats. To determine whether CRP functions in hepatic regeneration by promoting angiogenesis through the Wnt pathway, we detected VEGF and

-catenin in liver tissues and BrdU and

-catenin in hepatocytes by immunofluorescence. The expression levels of CRP, Wnt pathway-related and angiogenic factors were increased in CCl

-injured and PD-MSCs transplanted rat livers.

, the expression levels of Wnt signaling and angiogenic factors were decreased in siRNA-CRP-transfected rat hepatocytes.

CRP upregulation by PD-MSCs participates in vascular remodeling to promote liver regeneration via the Wnt signaling pathway during hepatic failure.

CRP upregulation by PD-MSCs participates in vascular remodeling to promote liver regeneration via the Wnt signaling pathway during hepatic failure.

This study shows the clinical data of 1-year follow-up of 8 patients with degenerative macular diseases who received suprachoroidal adipose tissue derived mesenchymal stem cell (ADMSC) implantation.

This prospective, single-center, phase 1/2 study enrolled 8 eyes of 8 patients with degenerative macular diseases of various reasons who underwent suprachoroidal implantation of ADMSCs. All patients had severe visual field defects and severe visual loss. All patients had defective multifocal electroretinography (mf ERG). The worse eye of the patient was selected for the operation. Patients were evaluated on the first day, first month, sixth month and at 1 year postoperatively. Best corrected visual acuity (BCVA), anterior segment and fundus examination, color photography, optical coherence tomography (OCT) and visual field (VF) examination were carried out at each visit. Fundus fluorescein angiography (FFA) and mfERG recordings were performed at the end of the sixth months. All 8 patients completed the 1 year follow-up.