Notes

Quick postpartum evaluation with the arschfick sphincter by endovaginal ultrasound: a fresh complex approach.
nt study showed good level of knowledge for HPV prevention regardless of occupation and is characterized by a high degree of awareness of the usefulness of prevention in adhering to the annual Pap smear test and gynaecological examination. The study shows the need for more information workshops for healthcare professionals, because physicians and midwives had high levels of knowledge, but not excellent as expected and required due to health-related profession.
Familial hypertrophic cardiomyopathy (HCM) is the most common genetic cardiac disease. While sarcomeric gene mutations explain many HCM cases, the genetic basis of about half of HCM cases remains elusive. Here we aimed to identify the gene causing HCM in a non-consanguineous Saudi Arabian family with affected family members and a history of sudden death. The impact of the identified mutation on protein structure and potential drug targets were evaluated in silico.

Triplets (two HCM subjects and one patent ductus arteriosus (PDA) case) and unaffected parents were screened by targeted next-generation sequencing (NGS) for 181 candidate cardiomyopathy genes. In silico structural and functional analyses, including protein modeling, structure prediction, drug screening, drug binding, and dynamic simulations were performed to explore the potential pathogenicity of the variant and to identify candidate drugs.

A homozygous missense mutation in exon 1 of TMP1 (assembly GRCh37-chr15 63340781; G>A) was identifie homozygous missense variation p.Gly3Arg in TPM1 associated with familial autosomal recessive pediatric HCM and PDA. The identified candidate TPM1 inhibitors warrant further prospective investigation.
To investigate astaxanthin (AST) protecting myocardial cells from hypoxia/reoxygenation (H/R) injury by regulating miR-138/HIF-1α axis.

Myocardial cells were collected and divided into a control group, a H/R group, and a H/R+AST group. The H/R injury model was established, and cells in the H/R+AST group were given AST before modeling. The cell survival rate, contents of myocardial enzymes, and apoptosis were detected.

The survival rate in the H/R group reduced and was lower than that in the H/R+AST group (p<0.05). Compared with the control group, activities of myocardial enzymes significantly increased in the H/R group but those were inhibited in the H/R+AST group (p<0.05). The apoptotic rate in the H/R group significantly increased compared with the control group but that significantly decreased compared with the H/R+AST group (p<0.05). The expression of cleaved caspase-9 and caspase-3 increased in the H/R group (p<0.05), and was higher than that in the H/R+AST group (p<0.05). The expreslating the expression of miR-138/HIF-1α axis.
Wellens syndrome is a typical electrocardiographic and clinical pattern that correlates with a severe proximal stenosis of the left anterior descending artery (LAD). It is associated with previous angina, no or slightly increased cardiac markers, and two ECG patterns diphasic T wave in V2-V3 (Type A) or deep negative T waves from V1 to V4 (type B). In this paper, we described two cases with asymptomatic Wellens patterns.

We describe two cases of Wellens syndrome ECG pattern that we observed in our Emergency Department not accompanied by chest pain or angina equivalents.

Both patients presented significant stenosis of LAD at the coronary angiography.

Asymptomatic patients presenting with Wellens ECG pattern should perform a coronary arteriography cause of the risk of a severe LAD stenosis. We need further studies to confirm if all "silent" Wellens syndromes deserve angiographic study.
Asymptomatic patients presenting with Wellens ECG pattern should perform a coronary arteriography cause of the risk of a severe LAD stenosis. We need further studies to confirm if all "silent" Wellens syndromes deserve angiographic study.
Long noncoding RNAs (lncRNAs) play critical roles in osteosarcoma (OS) progression. LncRNA DSCAM-AS1 has been reported to function as a tumor promoter in various cancers. However, the potential mechanism of DSCAM-AS1 in OS remains rarely know.

The expression levels of DSCAM-AS1 and miR-101 were detected by RT-qPCR. The correlation between DSCAM-AS1 and miR-101 expression was analyzed by Pearson's correlation. Kaplan-Meier analysis was used to assess the overall survival rate. Cell viability and invasion were assessed by MTT assay and transwell assays, respectively. A Luciferase reporter assay was used to identify the relationship between DSCAM-AS1 and miR-101.

In the present study, it was demonstrated that DSCAM-AS1 expression was significantly upregulated in OS tissues and cells and high expression of DSCAM-AS1 predicted poor prognosis in OS patients. In addition, the silencing of DSCAM-AS1 suppressed the viability and invasion of OS cells, while DSCAM-AS1 overexpression promoted cell viability and invasion. Furthermore, we found that DSCAM-AS1 inhibited miR-101 expression by direct interaction and DSCAM-AS1 promoted OS progression by sponging miR-101. GSK690693 In addition, miR-101 expression was negatively correlated with DSCAM-AS1 expression. Patients with low miR-101 expression had a shorter overall survival time compared with those with high miR-101 expression.

The present study demonstrated that DSCAM-AS1 accelerated OS cell progression by sponging miR-101, which might provide a new sight in the treatment of OS.
The present study demonstrated that DSCAM-AS1 accelerated OS cell progression by sponging miR-101, which might provide a new sight in the treatment of OS.
While Long Noncoding RNAs (LncRNAs) are well-known to modulate human cancer progression, the specific function of DBH-AS1 in melanoma remains to be fully established. The study will investigate the role of DBH-AS1 in melanoma cell.

The expression profiles of DBH-AS1, miR-223-3p, and IGF-1R in melanoma tissues and cell lines were determined by RT-qPCR analysis. CCK-8 assay, colony assays and transwell assay were employed to analyze the effects of DBH-AS1 on the proliferation, migration, and invasion in GC cells. Bioinformatics analysis and Dual-Luciferase reporter assay determined the direct binding relation between DBH-AS1, miR-223-3p and IGF-1R in GC.

Herein, we observed significant reductions in DBH-AS1 expression in melanoma tumor tissues and cell lines. Knockdown DBH-AS1 in melanoma cells impaired their proliferative, migratory, and invasive potential. We determined that DBH-AS1 was able to modulate insulin growth factor receptor (IGF-1R) expression as a competing endogenous RNA for DBH-AS1. In line with this finding, the knockdown DBH-AS1 was associated with decreases in the expression of glucose transporter (GLUT)-1 and a consequent inhibition of glucose uptake, lactate production, and ATP generation by melanoma cells.
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