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913). The highest number of patients who applied to the clinic was in the "45 and over" age group (317 patients); 270 patients were in the 25-44 age group. A maximum positivity of 10.3% was observed in the 7-14 age group.
Previously, fascioliasis was considered a rare infection in humans; however, it has emerged as an important public health problem in the world. Considering fascioliasis in patients with clinical symptoms, not only with direct observation but also using serological methods, would be effective in early diagnosis and treatment of the disease.
Previously, fascioliasis was considered a rare infection in humans; however, it has emerged as an important public health problem in the world. Considering fascioliasis in patients with clinical symptoms, not only with direct observation but also using serological methods, would be effective in early diagnosis and treatment of the disease.Gut microbiota is vital for human health. Shifts in the microbial diversity can affect bacterial function, and dysbiosis is associated with a variety of gastrointestinal disorders, including celiac disease (CD) and irritable bowel syndrome (IBS). The distinction between IBS and non-celiac gluten sensitivity (NCGS) is unclear, and it is conceivable that the gut microbiota profile of these patients may overlap. To our knowledge, no existing literature has evaluated the microbial characteristics in CD, IBS, and NCGS. Hence, this systematic review aims to compare the gut microbiota profile in these three diagnoses. A literature search was conducted in PubMed (Medline) until April 2019. Studies investigating bacterial diversity in the gut of patients with CD, IBS, and NCGS were eligible. Inclusion criteria were observational studies and randomized controlled trials reporting bacterial profile at baseline. Ninety-one articles were identified, of which 13 trials were eligible for inclusion. Overall, the bacterial composition of the gut microbiota of patients with CD and those with IBS shared the many similarities. The microbial richness was correspondingly reduced in these patient-groups compared with healthy controls, but this was not reported for NCGS. Our findings suggest that the bacterial profiles of patients with IBS and CD share certain disease-specific trends. Fewer similarities were observed between the bacterial profiles of patients with IBS and NCGS. Notably, the data are limited; thus, no solid conclusions can be made on the basis of these findings alone. The suggested trends can be a valuable basis for further research.The effect of miR-532-5p on human brain microvascular endothelial cells damage induced by ox-LDL is studied. HBMEC-3 were cultured and treated with ox-LDL for 24 h to establish a model of cell oxidative damage. The expression of miR-532-5p was detected by qRT-PCR and that of CLIC4 was detected by Western blot. miR-NC, miR-532-5p mimics, si-NC, si-CLIC4, miR-532-5p mimics and pcDNA, miR-532-5p mimics and pcDNA-CLIC4 were transfected into HBMEC-3 cells, respectively, using ox -LDL processing for 24 h. Flow cytometry was used to detect the apoptotic rate. The dual luciferase reporting experiment verified the relationship between miR-532-5p and CLIC4. The ox-LDL treatment led to lower expression of miR-532-5p (p less then 0.05), higher expression of CLIC4 (P less then 0.05), enhanced content of MDA (p less then 0.05), decreased activities of SOD and CAT (p less then 0.05), increased apoptosis rate (p less then 0.05), higher protein level of Bax (p less then 0.05), and lower protein level of Bcl-2 (p less then 0.05). Compared with ox-LDL + miR-NC group and ox-LDL + si-NC group, ox-LDL + miR-532-5p group and ox-LDL + si-CLIC4 group had decreased content of MDA (P less then 0.05), increased activities of SOD and CAT (p less then 0.05), decreased apoptosis rate (p less then 0.05), lower level of Bax (p less then 0.05), and higher level of Bcl-2 (p less then 0.05). The miR-532-5p mitigates human brain microvascular endothelial cells damage induced by ox-LDL via down-regulating CLIC4 expression.To study the effect of velvet antler polypeptides (VAP) on Alzheimer's disease (AD) cell model, Aβ25-35 was used to induce SK-N-SH cells to obtain AD cell model. The MDA, SOD, GSH-Px levels were determined using relevant kits. Flow cytometry was conducted to detect apoptosis, Western blot was employed to measure Bcl-2, Bax, HDAC6 protein expression, and qPCR was used to assay microRNA (miR)-613 and HDAC6 mRNA levels. Target Scan prediction combined with dual luciferase reporting experiments was conducted to analyze the targeting relationship between miR-613 and HDAC6. miR-613 was transfected in SK-N-SH cells; Alternatively, anti-miR-613 was transfected, followed by Aβ25-35 and 80 mg/L of VAP. The AD model cells showed increased MDA content, apoptosis rate, Bax protein expression, HDAC6 mRNA and protein expression, but lower SOD, GSH-Px activities, Bcl-2 protein level, and miR-613 expression (p less then 0.05). VAP reduced MDA content, apoptosis rate, Bax protein expression, HDAC6 mRNA and protein expression, but enhanced SOD, GSH-Px activities, Bcl-2 protein level, and miR-613 expression (p less then 0.05). Over-expression of miR-613 increased SOD, GSH-Px activities, and Bcl-2 protein expression in AD model cells, but reduced HDAC6 protein levels, MDA content, apoptosis rate, and Bax protein levels (p less then 0.05). VAP may regulate Aβ25-35-induced apoptosis so as to treat Alzheimer's disease.Tyrosine Kinase Inhibitors (TKIs) have significantly improved the clinical outcome of BCR-ABL+ Chronic Phase-Chronic Myeloid Leukemia (CP-CML). Nonetheless, approximately one-third of the CP-CML patient's progress to advanced phases of CML (accelerated and blast phase). Impaired DNA repair including mutations in Fanconi anemia (FA) pathway genes are responsible for progression of many cancers. Nevertheless, FA-pathways genes have never been reported in myeloid cancers. Hence, this study was aimed to discover DNA repair genes associated with CML progression. AP-CML patients were subjected to whole exome sequencing along with appropriate controls. A novel splice site FANCD2 mutation was detected. FANCD2 is a well-known FA-pathway gene with established role in DNA repair. This is first report of FA-pathway DNA repair genes in myeloid cancers that can serve as a novel marker of CML progression to clinically intervene CML progression. Further studies are needed to establish the functional role of FANCD2 in CML progression that can provide novel insights into CML pathogenesis. This study also indicates that a combination TKIs and Poly (ADP-ribose) polymerase (PARP) inhibitors like Olaparib (FDA approved anti-cancer drug for FA-pathway gene mutations) could improve the clinical outcome CML patients in accelerated and blast-crisis phases of the disease.To investigate the effect and mechanism of galactose on cerulean-induced pancreatic acinar cell injury. click here Acute pancreatitis cell injury model was established by arbusin-induced pancreatic acinar cell AR42J injury; galactose (25, 50, 100 mmol / L) was used to treat the injured cells, and the optimal concentration was 50 mmol / L; cell counting kit (CCK-8), enzyme linked immunosorbent assay (ELISA) to detect cell survival rate and necrosis rate; flow cytometry and Western blotting (Western blot) to detect cell apoptosis and autologous phage-related gene (Beclin1) and microtubule-associated protein 1 light chain 3 (LC3), apoptosis-related protein B-cell lymphoma / leukemia-2 (Bcl-2), Bcl-2-related X gene (Bax), and fibroblasts Expression of growth factor 21 antibody (FGF21) and anti-aging gene Klotho. A pancreatic acinar cell injury model was successfully established with cerana (100 nmol / L); galactose (25, 50, 100 mmol/L) In a concentration-dependent manner, the inhibitory effect of ceriferin on AR42J injury was inhibited at an optimal concentration of 50 mmol / L. Compared with the ceriferin group, the apoptosis rate of AR42J cells in the galactose group was significantly reduced. table Significantly increased, Bcl-2, FGF21 and Klotho protein expression was significantly increased, Bax protein was significantly decreased; the FGF21 inhibitor can be significantly reduced on galactose these caerulein-induced AR42J cells. Galactose can inhibit the apoptosis and autophagy of pancreatic acinar cells induced by cerana, and its potential mechanism is to up-regulate FGF21 and Klotho, providing a new potential drug for the treatment of acute pancreatitis.IAsp-N-Glc is a potential antitussive agent that is first reported to be isolated from Ginkgo Semen, but the bioavailability and excretion of IAsp-N-Glc are unknown. Therefore, we carried out our study to obtain the bioavailability and excretion profiles of IAsp-N-Glc in rats. Rapid, specific, and reliable quantification methods for the measurement of IAsp-N-Glc in rat plasma and fecal samples by using ultra-high-performance liquid chromatography coupled with triple quadrupole mass spectrometry were developed and validated. A C18 column was used for the separation of IAsp-N-Glc and internal standards, and water (containing 0.1% formic acid) and acetonitrile were chosen as the mobile phase for the separation in the flow-gradient mode. In the ranges of 37.5-7500 ng/mL and 120-30000 ng/mL, the calibration curves of IAsp-N-Glc exhibited satisfactory linearity for plasma and fecal samples with each linear correlation coefficient higher than 0.99, respectively. The methods were reproducible and reliable. The analytes were stable, and no apparent matrix effects were observed. The bioanalytical methods were successfully used to study the pharmacokinetics and excretion of IAsp-N-Glc in rats. Oral administration of IAsp-N-Glc exhibited a low absolute oral bioavailability (1.83±0.09%), and 59.63±6.29% of IAsp-N-Glc was excreted in feces. This report is the first to describe the bioavailability and excretion of IAsp-N-Glc in rats and will lay the foundation for the in-depth study and drug development of IAsp-N-Glc.The primary objective of the present clinical trial was to evaluate efficacy and safety of tramadol versus prednisone in Chinese patients with carpal tunnel syndrome (CTS) diagnosed by ultrasonography. A total of 60 patients' diagnosed with moderate CTS based on a clinical and electrophysiological parameters were enrolled in this clinical trial. The patients were randomly assigned to one of two groups in allocation ratio of 11. Test group was given controlled release Tramadol (100 mg every 12 hours) and Reference Group received Prednisone 20 mg once daily for 2 weeks (14 days). Ultrasound therapy (UT) was given as adjuvant therapy in both the group. CTS were evaluated before and after treatment through clinical findings, Boston Carpal Tunnel Questionnaire, visual analog scale (VAS) and electrophysiological data. The results were evaluated with Student's t test and chi-squared. A statistically significant difference was observed between both the treatment group regarding Durkan's test, Phalen's test, VAS and electrophysiological data after treatment. Improvement in patients treated with tramadol was significantly higher compared to prednisone group in all clinical and electrophysiological parameters. The Boston Questionnaire showed better results in tramadol groups, with a significant improvement in the symptom severity scale (SSS; p less then 0.005) and functional status scale (FSS; p less then 0.005). The results of this clinical trial suggest that treatment of CTS with tramadol along with UT as adjuvant therapy was associated with a significant improvement of clinical and electrophysiological parameters compared to Prednisone.
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