Telomerase reverse transcriptase (TERT) promoter mutations have been recognized as a common genetic event in bladder cancer (BC). Many studies have found the high TERT promoter mutations' prevalence in BC recurrence patients which may make the TERT promoter mutations become a potential prognosis prediction of BC. We performed a systematic search in Embase, PubMed, and Web of Science in January 2021. The aspects of evaluation, methods, validation, and results were used to evaluate the included studies' quality. We reviewed two of the most common mutations in types of TC, C288T and C250T and their relationship with prognosis of BC. Eight studies contained 1382 cases were enrolled in our study. The percentage of TERT promoter mutations in these cases was 62.5%. A statistically significant association was detected between TERT promoter mutation and recurrence (HR: 2.03, 95% CI: 1.53-2.68, p < 0.001). However, TERT promoter mutation was not significant associated with overall survival (HR: 1.077, 95% CI: 0.674--1.718, p = 0.757). No significant heterogeneities were observed (I 2 = 47.5%, P = 0.064; I 2 = 58.7%, p = 0.120, respectively). Bladder cancer patients with TERT promoter mutations take a higher risk of recurrence. TERT promoter mutations may become a potential prediction factor for bladder cancer recurrence.

<b><i>Introduction:</i></b> Salidroside (Sal) a bioactive component extracted from <i>Rhodiola rosea</i> is remarkable for its anti-asthmatic effects. The study aimed to explore the molecular mechanism of Sal in airway inflammation and remodeling in asthmatic mice and provide a novel theoretical basis for asthma treatment. <b><i>Methods:</i></b> An asthmatic mouse model was established via ovalbumin (OVA) treatment, followed by injection of Sal and transfection of miR-323-3p-mimic and sh- suppressor of cytokine signaling 5 (SOCS5). Expressions of miR-323-3p, SOCS5 mRNA, collagen (COL)-I, and COL-III were detected via reverse transcription quantitative polymerase chain reaction. SOCS5 protein level was detected via Western blot. Levels of IgE, IL-13, IL-4, and IL-5 were detected via enzyme-linked immunosorbent assay. Inflammatory cell infiltration was observed via hematoxylin-eosin staining. Collagen disposition was observed via Masson staining. Resistance index (RI) of airway hyperresponsiveness, and the number of total cells, inflammatory cells (eosinophil, macrophage, neutrophil, and lymphocyte) in bronchoalveolar lavage fluid (BALF) were observed. The binding relationship between miR-323-3p and SOCS5 was predicted through the RNA22 website and verified via dual-luciferase reporter assay. <b><i>Results:</i></b> miR-323-3p was highly expressed in OVA-treated mice. Sal treatment reduced inflammatory cell infiltration, COL disposition, miR-323-3p expression, and IgE, IL-13, IL-4, IL-5, COL-I, and COL-III levels, RI value, and the number of total cells and inflammatory cells in BALF. miR-323-3p inhibited SOCS5 transcription. miR-323-3p overexpression or SOCS5 downregulation reversed the protecting role of Sal in asthmatic mice. <b><i>Conclusion:</i></b> Sal inhibited miR-323-3p expression to promote SOCS5 transcription, thereby attenuating airway inflammation and remodeling in asthmatic mice.

Objective We conducted a pilot study of whether nonpathologists could accurately diagnose cervical precancer in biopsies using only a basic light microscope, evaluating p16INK4a immunohistochemistry (p16 IHC) of biopsies, and video-based training for both. Materials and Methods Using biopsies collected as part of a screening study conducted in rural China, we randomly selected 50 biopsies with a precancerous diagnosis of cervical intraepithelial neoplasia grade 2 (CIN2) or more severe (CIN2+) and 50 biopsies with diagnosis of CIN less severe than CIN2, and stained them for p16 using a commercial IHC kit. Twelve nonpathologists of varying educational backgrounds living in Beijing, China received video training and were assigned one of 4 sets of 25 CIN2+ and 25 CIN less severe than CIN2 for evaluation. A pathologist reviewed all 100 cases. Results The mean sensitivity and specificity of the p16 IHC staining scored by the nonpathologists were 91.7% and 94.1%, respectively, compared to scoring by the pathologist. The readers and the pathologist agreed on p16 IHC scoring for 42 (84%) of the 50 slides of CIN less severe than CIN2 and 37 (74%) of the 50 CIN2+ slides. The mean sensitivity and specificity for consensus CIN2+ of p16 IHC as scored by the readers were 88% and 87%, respectively, versus an overall sensitivity and specificity by the pathologist of 96% and 92%, respectively. Conclusions We demonstrated that nonpathologists can accurately diagnose CIN2+ using p16 IHC alone.

Purpose: To investigate the anti-asthmatic effect of Ping-Chuan Formula (PCF) in a mouse model, and the associated molecular mechanisms.Methods: Asthma mice were induced using ovalbumin (OVA), and PCF (600 mg/kg) was administered to the mice for 4 weeks. Sections of lung tissues were examined microscopically. The expressions of interleukins (ILs), interferon (IFN)-γ, transforming growth factor (TGF)-β were assayed, while lung tissue expressions of Toll like receptor (TLR)-4, GATA binding protein (GATA)-3, Ox40 ligand (OX40L), indoleamine 2,3-dioxygenase (IDO), and forkhead box P3 (Foxp3) determined. The T box expressed in T cells (T-bet) was evaluated using western blotting. The expressions of MHC II and co-stimulators (CD 11c, CD 80 and CD 86) of dendritic cells (DCs) were determined by flow cytometry.Results: PCF decreased inflammation in lung, and also down-regulated IL-4, -6, -17 and TGF-β (p < 0.01), whereas IL-10 and IFN-γ expressions were up-regulated (p < 0.01). Moreover, PCF decreased the expressions of TLR-4, GATA-3 and OX40L in lung tissue, and promoted Foxp3, IDO and T-bet. Besides, PCF decreased the levels of MHC II and co-stimulators (CD 80 and CD 86) on the surface of DCs.Conclusion: PCF exerts anti-asthmatic effect in mice via inhibition of inflammation, and modulation of MHC II and co-stimulators on the surface of DCs. These findings suggest that PCF is a promising candidate drug for treating asthma in humans.

Purpose: To investigate the effect of the Ma-Xin-Di-Tan (MXDT) decoction on ovalbumin-induced allergic asthma (AA) in mice. Methods: Asthma was induced in mice by ovalbumin (OVA) injection, and different doses of MXDT (150, 300, and 600 mg/kg/day) were administered orally for 28 days. Pathological changes in lung tissues were examined, while levels of cytokines, including interleukin (IL)-4, IL-6, IL-17, interferon (IFN)-γ, and transforming growth factor (TGF)-β, were determined using enzyme-linked immunosorbent assays (ELISAs) of the bronchoalveolar lavage fluid. Toll-like receptor (TLR)-4, GATA-binding protein (GATA)-3, Ox40 ligand (OX40L), indoleamine 2,3-dioxygenase (IDO), forkhead box P3 (Foxp3), and T box expressed in T cells (T-bet) levels were determined in lung tissues by western blot analysis. Results: MXDT inhibited the inflammatory reaction of lung tissues in OVA-challenged mice. After treatment with MXDT, levels of IL-4, IL-6, IL-17, and TGF-β were downregulated, whereas IFN-γ levels were upregulated. In addition, MXDT decreased TLR-4, GATA-3, and OX40L levels in lung tissues but increased the expression of Foxp3, T-bet, and IDO. Conclusion: MXDT has antiallergic effects on OVA-induced AA in mice; the possible molecular mechanisms might involve the inhibition of inflammatory reactions and modulation of Th1/Th2 cytokine balance.

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Purpose: To investigate the role and potential of miR-145 as a therapeutic target for the treatment of primary colon adenocarcinoma in cell lines Methods: The expression of miR145 was determined by quantitative real time-polymerase chain reaction (RT-PCR), while cell viability was determined by MTT assay. Apoptosis was assessed by 4',6diamidino-2-phenylindole (DAPI), acridine orange/ethidium bromide (AO/EB), and annexin V/PI double staining. Cell cycle analysis was performed by flow cytometry, while immunoblotting was used to determine protein expression. Results: The expression of miR-145 was significantly enhanced in all the colon adenocarcinoma cell lines investigated. On the other hand, suppression of miR-145 expression led to significant decrease in cell viability, activation of apoptosis, G2/M cell cycle arrest, and inhibition of migration of colon adenocarcinoma cells. Conclusion: These results indicate that miR-145 regulates the proliferation and metastasis of colon adenocarcinoma cells. Thus, it may be a prospective drug target for the treatment of this disease.