Migration of Intrauterine Device Into the Bladder: A Case Report.

Complications associated with intrauterine contraceptive devices (IUDs), particularly those involving migration into the bladder, are infrequent occurrences yet clinically significant. The clinical presentation of patients with IUD displacement into the bladder is frequently vague and non-specific, posing a challenge for timely and accurate diagnosis. This report details the case of a patient who presented with an IUD malpositioned into the bladder, initially manifesting solely as urinary frequency.

miR-124a Involves in the Regulation of Wnt/-Catenin and P53 Pathways to Inhibit Abdominal Aortic Aneurysm via Targeting BRD4.

Background: Abdominal aortic aneurysm (AAA) belongs to a progressive, gradual aortic rupture, which can lead to death without surgical intervention. The key factors regulating the occurrence and progress of AAA are not clear. Increasing studies have indicated that microRNA (miRNA) plays an important role in cancer development.

Correlations of AQP4 expression and polymorphism with diabetic retinopathy.

Objective: The aim of this study was to investigate the relationships of aquaporin 4 (AQP4) rs200498749, rs149465 and rs650217 polymorphisms and gene expression with diabetic retinopathy (DR).

Patients And Methods: A total of 400 patients with diabetes mellitus (DM) treated in our hospital were enrolled in this study. All subjects were divided into two groups, including DM group (n=200, without DR) and DR group (n=200, with DR).

Daphnetin suppresses experimental abdominal aortic aneurysms in mice via inhibition of aortic mural inflammation.

Rupture of abdominal aortic aneurysm (AAA) is a devastating event that can be prevented by inhibiting the growth of small aneurysms. Therapeutic strategies targeting certain events that promote the development of AAA must be developed, in order to alter the course of AAA. Chronic inflammation of the aortic mural is a major characteristic of AAA and is related to AAA formation, development and rupture.

Circular RNA circ-PRKCI promotes lung cancer progression by binding to microRNA-1324 to regulate MECP2 expression.

Objective: We aimed to investigate the expression and specific molecular mechanism of circ-PRKCI in lung cancer (LCa).

Patients And Methods: The relationship between the expression level of circ-PRKCI and the prognosis of patients was analyzed. The impacts of circ-PRKCI on the invasiveness of LCa cells were examined by Cell Counting Kit-8 (CCK-8) experiments, clone formation experiments, and transwell invasion experiments.

LncRNA UCA1 inhibits proliferation and promotes apoptosis of cervical cancer cells by regulating β-catenin/TCF-4.

Objective: The aim of this study was to explore the regulatory effect of long non-coding ribonucleic acid (lncRNA) urothelial carcinoma antigen 1 (UCA1) on the proliferation and apoptosis of HeLa cells and to elucidate its potential regulatory mechanism.

Materials And Methods: HeLa cells were cultured in vitro and randomly divided into three groups, including blank control group (Control group), lncRNA UCA1 negative control (NC) group, and lncRNA UCA1 interference group [lncRNA UCA1 small interfering RNA (siRNA) group]. The expression level of lncRNA UCA1 in HeLa cells was detected by quantitative reverse transcription-polymerase chain reaction (qRT-PCR).

LINC00858 facilitates the malignant development of Wilms' Tumor by targeting miR-653-5p.

Background: To uncover the clinical significance of LINC00858 in the development of Wilms' Tumor and the potential molecular mechanism.

Methods: LINC00858 levels in Wilms' Tumor species and cell lines were determined by quantitative real-time polymerase chain reaction (qRT-PCR). The clinical significance of LINC00858 in influencing pathological features and prognosis in patients with Wilms' Tumor was analyzed.

Triad3A displays a critical role in suppression of cerebral ischemic/reperfusion (I/R) injury by regulating necroptosis.

Ischemic stroke is a major cause of death and disability worldwide. Necroptosis is known as a form of cell death, playing an essential role in regulating ischemia-induced brain injury. Triad3A is a ubiquitin ligase of the RING-in-between-RING family, and regulates necroptotic cell death under different pathological conditions, including neurodegenerative disorders.

A gene mutation in RNA-binding protein 10 is associated with lung adenocarcinoma progression and poor prognosis.

RBM10 regulates the expression of various genes, which are often mutated in male lung adenocarcinoma. The present study confirmed the association of the mutation at exon 10 with the clinicopathological data and prognosis of lung adenocarcinoma. The effect of mutant on regulating lung cancer cell growth and invasion was investigated .

MiR-181a mediates Ang II-induced myocardial hypertrophy by mediating autophagy.

Objective: To investigate the relationship between miR-181a and cardiac hypertrophy and autophagy in rats with myocardial hypertrophy, and whether miR-181a regulates the autophagy through ATG5, thereby participating in the occurrence and development of myocardial hypertrophy.

Materials And Methods: The rat model of myocardial hypertrophy was established via the abdominal aortic coarctation. The expression of miR-181a in cardiac tissues was detected via reverse transcription-polymerase chain reaction (RT-PCR).

miR-101 Enhances Cisplatin-Induced DNA Damage Through Decreasing Nicotinamide Adenine Dinucleotide Phosphate Levels by Directly Repressing Tp53-Induced Glycolysis and Apoptosis Regulator Expression in Prostate Cancer Cells.

Tp53-induced glycolysis and apoptosis regulator (TIGAR) enhances the pentose phosphate pathway, thereby contributing directly to DNA repair due to generation of nicotinamide adenine dinucleotide phosphate (NADPH) and ribose-5-phosphate, two key precursors of DNA synthesis and repair. Targetscan database showed that miR-101 was predicted to potentially target TIGAR. Therefore, we speculated that miR-101 could enhance cisplatin-induced DNA damage by directly repressing TIGAR expression in prostate cancer cells.

Hypermethylation of CDH13, DKK3 and FOXL2 promoters and the expression of EZH2 in ovary granulosa cell tumors.

Aberrant epigenetic modification is associated with the development and progression of cancer. Hypermethylation of tumor suppressor gene promoters and cooperative histone modification have been considered to be the primary mechanisms of epigenetic modification. Ovary granulosa cell tumors (GCTs) are relatively rare, accounting for ~3% of all ovarian malignancies.