The application of deep learning in early enamel demineralization detection.

Objective: The study aims to develop a diagnostic model using intraoral photographs to accurately detect and classify early detection of enamel demineralization on tooth surfaces.

Methods: A retrospective analysis was conducted with 208 patients aged 14 to 44. A total of 624 high-quality digital images captured under standardized conditions were used to construct a deep learning model based on the Mask region-based convolutional neural network (Mask R-CNN).

FABP5+ macrophages contribute to lipid metabolism dysregulation in type A aortic dissection.

Type A aortic dissection (TAAD) is an acute onset disease with a high mortality rate. TAAD is caused by a tear in the aortic intima and subsequent blood infiltration. The most prominent characteristics of TAAD are aortic media degeneration and inflammatory cell infiltration, which disturb the structural integrity and function of nonimmune and immune cells in the aortic wall.

Pulsed field ablation as a precise approach for cardiac arrhythmia treatment via cardiac microenvironment remodeling.

PFA uses short-duration, high-voltage electrical pulses to induce transient or irreversible electroporation on cell membranes, causing cell death. Selective inhibition of chaotic electrical signals in morbid cardiomyocytes significantly aids the treatment of atrial fibrillation, ventricular tachycardia, and other heart arrhythmias. Recent preclinical and clinical studies have only investigated physical changes, such as lesion size and myocardial scar.

Integrative analysis of key microRNA-mRNA complexes and pathways in aortic aneurysm.

Background: This study investigated the therapeutic targets of aortic aneurysm (AA) and provided insights into the pathogenesis and molecular mechanisms of AA.

Methods: The messenger RNA (mRNA) datasets, GSE9106 (blood samples) and GSE7084 (tissue samples), and the microRNA (miRNA) datasets, GSE92427 (blood samples) and GSE110527 (tissue samples), were obtained from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) and differentially expressed miRNAs (DE-miRNAs) were analyzed by limma.

Association of NFE2L2 Gene Polymorphisms with Risk and Clinical Characteristics of Acute Type A Aortic Dissection in Han Chinese Population.

The present study is aimed at investigating the association of NFE2L2 gene polymorphisms with risk and clinical characteristics of acute type A aortic dissection (AAAD) in a Han Chinese population. Six SNPs (rs1806649, rs13001694, rs2364723, rs35652124, rs6721961, and rs2706110) in NFE2L2 were genotyped using SNaPshot Multiplex Kit in 94 adult patients diagnosed with AAAD at our hospital, and 208 healthy Han Chinese subjects from the 1000 Genomes Project were served as the control group. The CC genotype of rs2364723 (CC versus (GC+GG), OR = 2.

Iron deficiency promotes aortic medial degeneration via destructing cytoskeleton of vascular smooth muscle cells.

Background: Aortic dissection (AD) and aortic aneurysm (AA) are critical illnesses with an unclear pathogenetic mechanism that seriously threaten human life. Aortic medial degeneration (AMD) is the main pathological feature of AD and AA. Diseases of iron metabolism can cause a variety of physiological dysfunctions.

The sympathetic transmitter norepinephrine inhibits VSMC proliferation induced by TGFβ by suppressing the expression of the TGFβ receptor ALK5 in aorta remodeling.

The sympathetic system is involved in the arterial diseases, but its mechanism remains poorly understood. The present study aimed to explore the impact of the sympathetic neurotransmitter norepinephrine (NE) on transforming growth factor (TGF) β signaling and the role of NE in aortic remodeling. Guanethidine was used to induce a regional chemical sympathetic denervation (CSD) in angiotensin II (AngII) and β‑aminopropionitrile (BAPN)‑induced aortic aneurysm models.

Inhibition of CACNA1H attenuates doxorubicin-induced acute cardiotoxicity by affecting endoplasmic reticulum stress.

Background: Doxorubicin (DOX) is an anticancer drug that has been widely used in the clinic. However, recently its application has been limited due to the cardiotoxic effects it has caused. Severe cardiotoxicity of DOX causes cardiac hypertrophy that may lead to heart failure.

Comprehensive analysis of non-small-cell lung cancer microarray datasets identifies several prognostic biomarkers.

To find accurate and effective biomarkers for diagnosis of non-small-cell lung cancer (NSCLC) patients. We downloaded microarray datasets GSE19188, GSE33532, GSE101929 and GSE102286 from the database of Gene Expression Omnibus. We screened out differentially expressed genes (DEGs) and miRNAs (DEMs) with GEO2R.

Abnormal Ribosome Biogenesis Partly Induced p53-Dependent Aortic Medial Smooth Muscle Cell Apoptosis and Oxidative Stress.

Ribosome biogenesis is a crucial biological process related to cell proliferation, redox balance, and muscle contractility. Aortic smooth muscle cells (ASMCs) show inhibition of proliferation and apoptosis, along with high levels of oxidative stress in aortic dissection (AD). Theoretically, ribosome biogenesis should be enhanced in the ASMCs at its proliferative state but suppressed during apoptosis and oxidative stress.

Up regulation of isoleucyl-tRNA synthetase promotes vascular smooth muscle cells dysfunction via p38 MAPK/PI3K signaling pathways.

The pathogenesis of abdominal aortic aneurysm remains unclear. The aim of the present study was to establish whether isoleucyl-tRNA synthetase (Iars) regulates the differentiation and apoptosis of vascular smooth muscle cells (VSMCs) during the development of abdominal aortic aneurysm (AAA). In addition, the contribution of various signaling pathways towards this process was ascertained.

The deregulation of STIM1 and store operative calcium entry impaired aortic smooth muscle cells contractility in aortic medial degeneration.

Microarray analysis of clinical aortic samples suggested a potential role for stromal interaction molecule 1 (STIM1) in the modulation of aortic medial degeneration (AMD), despite the uncertainty about STIM1 in normal aortic smooth muscle cells (ASMCs). Here, we aimed to explore changes in STIM1 expression in AMD, and the possible mechanisms.  An AMD model was established using auto-delivery of angiotensin II (Ang II) into ApoE mice.