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OBJECTIVE: CircRNAs have been proven to be vital during the process of malignant tumors. Their functions in bladder cancer (BCa) process remain largely unclear. This study aims to elucidate the role of circ0041103 in affecting the malignant phenotypes of BCa, and the possible molecular mechanism. PATIENTS AND METHODS: Circ0041103 expression levels in BCa tissues and cell lines were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The clinical significance of circ0041103 in influencing tumor size, tumor staging and lymphatic metastasis of BCa was analyzed. Regulatory effects of circ0041103 on proliferative and metastatic capacities of T24 and UM-UC-3 cells were examined through functional experiments. The binding target of circ0041103 and its downstream protein were predicted by online bioinformatic tools, which were further confirmed by Dual-Luciferase reporter assay and Pearson correlation test. The role of circ0041103/miR-107/FOXK1 axis in regulating BCa process was explored by rescue experiments. RESULTS: Circ0041103 was abnormally upregulated in BCa tissues and cell lines. Its level was higher in BCa tissues with a larger tumor size, or worse tumor staging, or BCa cases with lymphatic metastasis. Knockdown of circ0041103 inhibited proliferative and metastatic capacities of T24 and UM-UC-3 cells. MiR-107 was the binding target of circ0041103, and FOXK1 was the downstream gene of miR-107. Overexpression of circ0041103 could reverse the inhibited proliferative and metastatic capacities of T24 and UMUC- 3 cells overexpressing miR-107. CONCLUSIONS: Circ0041103 is upregulated in BCa and predicts a poor prognosis in BCa. It stimulates BCa cells to proliferate and migrate via the miR-107/FOXK1 axis. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Whether patients with COVID-19 require invasive mechanical ventilation (MV) is not yet clear. This article summarizes the clinical treatment process and clinical data of patients with COVID-19 and analyzes the predictive factors for mechanical ventilation for these patients. MATERIALS AND METHODS: A retrospective study was carried out from January 5, 2020, to March 23, 2020, including 98 patients with COVID-19 treated at three designated hospitals in Huangshi City, Hubei Province. Data collection included demographics, previous underlying diseases, clinical manifestations, laboratory examinations, imaging examination results, diagnosis, and prognosis. This study presents a summary of the patients' overall clinical characteristics and clarifies the predictive factors for MV in patients with COVID-19. RESULTS: There were 56 males and 42 females included in this study. The mortality rate was 26.53% (26/98). Fever, cough, and chest tightness were the most common symptoms (64.3%, 37.8%, and 12.2%, respectively). Thirty cases required MV, 30.61% of the total cases, and the mortality rate was 73.33%. The univariate comparison showed that dyspnea, acute physiologic assessment, chronic health evaluation (APACHE II) score, and the ratio between arterial blood oxygen partial pressure (PaO2) and oxygen concentration (FiO2) (P/F) were statistically different between the MV group and the non-MV group (p < 0.05). CONCLUSIONS: Results showed the following: dyspnea; increased white blood cell count; decreased platelets; lowered albumin levels; increased urea nitrogen; increased levels of myocardial enzymes Creatine Kinase (CK), Creatine Kinase, MB Form (CKMB) and lactate dehydrogenase (LDH); increased lactate, and lowered blood calcium tests. These findings may indicate that the patients have an increased probability of needing MV support. A cutoff value for the initial APACHE II score of >11.5 and the initial PaO2/FiO2 ratio of <122.17 mmHg should be considered for MV support for patients with COVID-19. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The purpose of this study was to explore the influences of micro ribonucleic acid (miR)-708 on cerebral ischemia-reperfusion injury by regulating a disintegrin and metalloprotease 17 (ADAM17) in a targeted manner. MATERIALS AND METHODS: The rat model of middle cerebral artery occlusion (MCAO) was established, and the differentially expressed miR-NAs in the cerebral tissues of rats with ischemia-reperfusion injury were detected via sequencing. The research was performed in control group (PC12 cells received no treatment), inhibitor group (the expression of miR-708 in PC12 cells was down-regulated using miR-708 inhibitor), and interference + inhibitor group [PC12 cells were co-treated with miR-708 inhibitor and ADAM17 small interfering RNA (siRNA)]. Then, the expression of ADAM17 in cells, proliferation ability of cells, and number of apoptotic cells were detected in each group. RESULTS: A total of 225 differentially expressed miRNAs were obtained through miR-NA sequencing and bioinformatics analysis, of which miR-708, miR-169, miR-26, and miR-96 were highly expressed, whereas miR-122, miR-118, and miR-177 were lowly expressed in rats in ischemia-reperfusion group. Compared with that in control group, the level of miR-708 declined significantly in inhibitor group after treatment with miR-708 inhibitor. After treatment with miR-708 inhibitor, the protein expression level of ADAM17 in inhibitor group was evidently higher than that in control group, while its protein expression level in interference + inhibitor group was significantly decreased and restored, after interference of ADAM17 siRNA with protein expression. In comparison with control group, inhibitor group had increased apoptotic cells after miR-708 inhibitor treatment (p<0.05). Besides, after interference of ADAM17 siRNA with protein expression, there were a smaller number of apoptotic cells in interference + inhibitor group (p<0.05), showing mitigated apoptosis. Moreover, the proliferation ability of cells treated with miR-708 inhibitor in inhibitor group was weaker than that in control group (p<0.05), whereas the proliferation ability of cells in interference + inhibitor group was restored to a certain degree after ADAM17 siRNA interfered with the protein expression (p<0.05). CONCLUSIONS: MiR-708 can modulate ADAM17 in a targeted manner to affect cellular proliferation and apoptosis in cerebral ischemia-reperfusion injury. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To explore the associations of interleukin-18 (IL-18) and IL-9 gene polymorphisms with susceptibility to asthma, and to study the associations between IL-18 and IL-9 expression levels and polymorphisms. PATIENTS AND METHODS: A total of 200 asthma patients in our hospital were collected as disease group, while 200 healthy people were taken as control group. The deoxyribonucleic acid (DNA) was extracted from peripheral blood and sent to the company for the detection of IL-18 and IL-9 gene polymorphisms via sequencing. The levels of serum IL-18 and IL-9 were determined using enzyme-linked immunosorbent assay (ELISA), and arterial blood gas analysis was performed for patients. RESULTS: The allele distributions at IL-18 gene loci rs189667 and rs360715 had no differences between control group and disease group. The allele distributions at IL-9 gene loci rs1859430 and rs2066758 were different between the two groups (p=0.001, p=0.022), among which the G allele frequency was the highest in disease group [245 (0.613)], and the T allele frequency was also the highest in disease group [240 (0.600)]. There was a difference in the genotype distribution at IL-9 gene locus rs1859430 between the two groups, and the GG genotype frequency in disease group [82 (0.410)] was significantly higher than that in control group (p=0.005). The CC genotype frequency at rs2066758 was significantly lower in disease group [27 (0.135), p=0.044]. In disease group, the frequency of heterozygous model CT (p=0.047) at IL-18 gene locus rs360715, and recessive model GA+AA (p=0.021) and heterozygous model GA (p=0.031) at IL-19 gene locus rs1859430 was significantly lower than that in control group. In disease group, the AC haplotype frequency at IL-18 gene loci rs189667 and rs360715 was evidently lower than that in control group (p=0.048). Disease group had evidently lower AT haplotype frequency (p=0.006) and evidently higher GT haplotype frequency (p=0.000) at IL-9 gene loci rs1859430 and rs2066758. Moreover, the level of serum IL-18 in patients with TT genotype at IL-18 gene locus rs360715 was higher than that in those with other genotypes in disease group (p<0.05), and the level of serum IL-9 in patients with AG genotype at IL-9 gene locus rs1859430 was also higher than that in those with other genotypes in disease group (p<0.05). There was a remarkable association between CT genotype at IL-18 gene locus rs360715 and partial pressure of oxygen (PaO2) (p=0.035), and between CC genotype at IL-9 gene locus rs2066758 and partial pressure of carbon dioxide (PaCO2) (p=0.041). CONCLUSIONS: The expression levels of serum IL-18 and IL-9 and their gene polymorphisms are significantly associated with asthma. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To elucidate the function of MOTS-c in accelerating bone fracture healing by inducing BMSCs differentiation into osteoblasts, as well as its potential mechanism. MATERIALS AND METHODS: Primary BMSCs were extracted from rats and induced for osteogenesis. The highest dose of MOTS-c that did not affect BMSCs proliferation was determined by CCK-8 assay. After 7-day osteogenesis, the relative levels of ALP, Bglap, and Runx2 in MOTS-c-treated BMSCs influenced by FOXF1 were examined. ALP staining and alizarin red S staining in BMSCs were performed as well. The interaction between FOXF1 and TGF-β was analyzed by ChIP assay. At last, rescue experiments were performed to uncover the role of FOXF1/TGF-β axis in MOTS-c-induced osteogenesis. RESULTS: 1 μM MOTS-c was the highest dose that did not affect BMSCs proliferation. MOTS-c treatment upregulated the relative levels of ALP, Bglap, and Runx2, and stimulated mineralization ability in BMSCs, which were attenuated by the silence of FOXF1. TGF-β was proved to interact with FOXF1, and its level was positively mediated by FOXF1. The silence of FOXF1 attenuated the accelerated osteogenesis and TGF-β upregulation in BMSCs because of MOTS-c induction, and these trends were further reversed by the overexpression of TGF-β. CONCLUSIONS: MOTS-c treatment markedly induces osteogenesis in BMSCs. During MOTS-c-induced osteogenic progression, the upregulated FOXF1 triggers the activation of TGF-β pathway, thus accelerating bone fracture healing. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Growing studies indicated that long non-coding RNAs (lncRNAs) acted as imperative players in neoplasms initiation and progression. This research was designed to study the potential involvements of lncRNA FEZF1-AS1 (FEZF1-AS1) in the pathogenesis of prostate cancer (PCa). PATIENTS AND METHODS: Real-time PCR was performed to detect the expressions of FEZF1-AS1 in PCa specimens and cell lines. Correlations between G- FEZF1-AS1 expressions and clinical characteristics and overall survivals were determined using statistical methods. The CCK-8 assays, colony formation assay, flow cytometry, transwell, and wound scratch assays were carried out to study cells viability, cells migration, and invasion. Western blot and RT-PCR were used for the determination of the influence of FEZF1-AS1 on Notch signaling pathway. RESULTS: We found that FEZF1-AS1 expressions were distinctly reduced in human PCa tissues and cell lines compared with their non-tumor counterparts, and its higher levels were strongly associated with lymph node metastasis (p=0.012) and Angiolymphatic invasion (p=0.022). Then, Kaplan-Meier assays showed that patients with higher expressions of FEZF1-AS1 were shown to predict unfavorable overall survival. Cox proportional hazards risks assays revealed that FEZF1-AS1 acted as an independent prognostic factor for PCa. Functional investigations suggested that knockdown of FEZF1-AS1 could suppress cells proliferation, trigger late apoptosis, and inhibit cells invasion and migration. Mechanistic assays demonstrated that FEZF1-AS1 exhibited its tumor-promotive roles by activating the Notch signaling pathway. CONCLUSIONS: We suggested that FEZF1-AS1 served as a tumor promoter in PCa and may develop a novel therapeutic target for PCa patients. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To explore the effect of neurotrophin-3 (NT-3) messenger ribonucleic acid (mRNA) in the hippocampus on infection-induced memory impairment of neonatal rats. MATERIALS AND METHODS: 80 female Sprague-Dawley (SD) rats in the neonatal stage were selected to establish memory impairment model by bacterial meningitis infection. Rats were randomly divided into experimental group (n=40) and control group (n=40). Rats in experimental group were injected with β-amyloid precursor protein 319-335 peptide APP17p into brain tissue to up-regulate the expression of NT-3, and the rats in control group didn't receive treatment. Behavioral changes of rats were observed in Morris water maze and passive avoidance experiment. Apoptosis of nerve cells was detected by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL) method and Fluoro-Jade B method. NT-3 mRNA expression level was measured via reverse transcription polymerase chain reaction (RT-PCR). RESULTS: NT-3 expression level in experimental group was higher than that in control group (p<0.05). Apoptosis rate of nerve cells in experimental group was lower than that in control group, but the learning and memory ability of rats in experimental group was better than that in control group (p<0.05). CONCLUSIONS: Reduced NT-3 expression level may be correlated with the occurrence of meningitis because NT-3 can suppress nerve cell apoptosis and ameliorate learning and memory impairment to a certain extent to exert neuroprotective effects. [ABSTRACT FROM AUTHOR]

OBJECTIVE: We aimed to detect the role and function of microRNA-431 (miR-431) in lung cancer, and to investigate the underlying mechanism in regulating the development of lung cancer. PATIENTS AND METHODS: Quantitative Real- time polymerase chain reaction (qRT-PCR) was utilized to measure the relative expression level of miR-431 in lung cancer tissues and cell lines. Cell counting kit-8 (CCK-8) and colony formation assays were employed to measure the proliferative ability of lung cancer cells. Meanwhile, transwell assay was recruited to detect the invasive and migratory abilities of lung cancer cells. Furthermore, dual-luciferase reporter gene assay was designed to verify the target gene of miR- 431. Western blot assay was used to gauge the protein level of DDX5 (DEAD box polypeptide 5). RESULTS: MiR-431 expression was significantly lower in 122 lung cancer tissue samples or cell lines compared to the adjacent normal tissues or lung bronchial epithelial cell line, respectively. Over-expression of miR-431 significantly inhibited proliferation, invasion and migration of A549 cells. Down-regulation of miR-431 accelerated cell growth and metastasis of H1650 cells. DDX5 was proved to be a direct target for miR- 431 in lung cancer. CONCLUSIONS: MiR-431 expression decreased in lung cancer tissues and cells. MiR-431 suppressed proliferation, invasion and migration of lung cancer cells via inhibiting the expression of DDX5. Our study might provide a novel target for the biological therapy of lung cancer. [ABSTRACT FROM AUTHOR]