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Background: Infection in acute pancreatitis (AP) is associated with nutritional therapies including naso-gastric (NG), naso-jejunal (NJ), and total parenteral nutrition (TPN). To examine infections among NG, NJ, TPN, and no nutritional support (NNS) in treating patients with AP. Methods: The investigators completed comprehensive search in the Cochrane library, EMBASE, PubMed, Web of Science, and ClinicalTrials.gov without restriction on language and publication date before January 21, 2019. They also searched the reference lists of relevant studies for randomized controlled trials (RCTs) comparing NG, NJ, TPN, and NNS among patients with AP. Quantitative synthesis was conducted in a contrast-based network meta-analysis. To clarify effects, a network meta-analysis was conducted to calculate the surface under the cumulative ranking curve (SUCRA). Beside of overall infections, the event rates of infected pancreatic necrosis, bacteremia, line infection, pneumonia, urinary tract infection, and other types of infections were measured. Results: The network meta-analysis of 16 RCTs showed that NJ had significantly lower overall infection rates compared with TPN (risk ratio: 0.59; 95% confidence interval: 0.38, 0.90); and NG had a larger effect size and higher rank probability compared with NJ, TPN, and NNS (mean rank = 1.7; SUCRA = 75.8). TPN was the least preferred (mean rank = 3.2; SUCRA = 26.6). Conclusions: NG and NJ may be preferred therapies for treating patients with AP. Clinicians may consider NG as a first-line treatment for patients with AP (including severe AP) and even in patients receiving prophylactic antibiotics. In addition, we found that NNS should be avoided when treating patients with severe AP. [ABSTRACT FROM AUTHOR]

The present study analyzed gene expression arrays to identify differentially-expressed genes (DEGs) between mycophenolate mofetil (MMF)‑treated and placebo‑treated patients with symptomatic carotid artery stenosis (SCAS). In addition, the key genes involved in the pharmacology of MMF treatment in patients with SCAS were identified. The gene expression dataset was obtained from a Gene Expression Omnibus database, which included 9 MMF‑treated and 11 placebo‑treated samples. The DEGs were identified between MMF and placebo groups using R software. Furthermore, a protein‑protein interaction (PPI) network of the identified DEGS was constructed. The Database for Annotation, Visualization and Integrated Discovery was used to perform Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses of the 19 most significant DEGs. A total of 210 DEGs between the MMF and placebo groups were screened and their PPI was constructed. GO function analysis revealed that the 19 DEGs were predominantly involved in the tyrosine phosphorylation of signal transducer and activator of transcription‑5 protein, which is closely associated with the activation of T cells. The KEGG pathway analysis suggested that the main metabolic pathways of the 19 DEGs were associated with the pharmacological functioning of MMF in activated T cells. In conclusion, the present study identified numerous key DEGs associated with SCAS, and the results suggested that v‑kit Hardy‑Zuckerman 4 feline sarcoma viral oncogene homolog and apelin may serve important roles in the MMF treatment of SCAS. [ABSTRACT FROM AUTHOR]

MicroRNAs (miRNAs) are small non-coding regulatory RNAs, which are involved in the post-transcriptional regulation of gene expression. miRNA (miR)-155, which has previously been reported to be overexpressed in lung cancer, is correlated with poor patient prognosis. The present study aimed to investigate the effects of miR-155 on the radiosensitivity of human non-small cell lung cancer (NSCLC) cells. To explore the roles of miRNAs in the regulation of irradiation sensitivity of human lung cancer cells, the expressions of miR-155 in response to irradiation, have been studied by RT-qPCR, and the putative direct target of miR-155 was identified by western blot and luciferase assays. The results of the present study revealed that the expression of miR-155 was induced by irradiation, thus suggesting a positive correlation between miR-155 and radiosensitivity. Furthermore, overexpression of miR-155 rendered lung cancer cells resistant to irradiation. In addition, hexokinase 2 (HK2) was identified as an indirect target of miR-155; exogenous overexpression of miR-155 upregulated the expression of HK2, whereas inhibition of miR-155 by antisense miRNA suppressed HK2 expression. In addition, HK2-modulated glucose metabolism was significantly upregulated by overexpression of miR-155. Notably, inhibition of miR-155 sensitized lung cancer cells to irradiation via suppression of glucose metabolism. In conclusion, the present study reported a novel function for miR-155 in the regulation of NSCLC cell radiosensitivity, thus suggesting that miR-155 may be considered a therapeutic target for the development of anticancer drugs. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate the effect of erythropoietin (EPO) on the inflammatory response and the mechanism analysis of the Τoll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB) signaling pathway of NEC. A total of 94 patients with necrotizing enterocolitis (NEC) were randomly divided into the control (42 cases) and observation (52 cases) groups, The control group received the standard medical treatment plan, whereas for the observation group this treatment plan was combined with the application of recombinant EPO for intramuscular injection treatment. The clinical effect was subsequently compared. The results showed that the complication and death rates in the observation group were significantly lower than those in the control group with statistically significant differences (P<0.05). Following treatments, the levels of tumor necrosis factor-α (TNF-α) and interleukin (IL)-6 in the observation group were significantly lower than those in the control group. The expression levels of mRNA of TLR4 and NF-κB in the observation group were significantly lower than those in the control group, with statistically significant differences (P<0.05). In summary, EPO was able to reduce the levels of inflammatory response of TNF-α and IL-6 through the TLR4/NF-κB signaling pathway, and improve the NEC, thus providing a basis for the clinical treatment of NEC. [ABSTRACT FROM AUTHOR]

The prevalence of diabetes mellitus (DM) continues to increase each year. However, the efficacy of glucose-lowering therapies remains unsatisfactory. Moreover, the clinical characteristics and manifestations of DM in Chinese patients are different from those in Western patients. Thus, it is imperative to develop an optimal treatment protocol for lowering blood glucose levels in Chinese patients with DM. Sitagliptin has been used in People's Republic of China, and sitagliptin and metformin combination therapy may not alter their individual pharmacokinetics. To date, several clinical trials undertaken to investigate the efficacy of sitagliptin and metformin combination therapy have revealed that it effectively controlled glycated hemoglobin, fasting plasma glucose, and postprandial plasma glucose levels to a greater extent than sitagliptin or metformin alone. In addition, the combined therapy was well tolerated and induced few side effects, which were largely mild. Furthermore, the combined therapy was easy to administer, and the patients receiving this therapy showed good compliance. Therefore, for Chinese patients with type 2 DM, sitagliptin and metformin combination therapy is preferred. [ABSTRACT FROM AUTHOR]

There is lack of consensus regarding the prognostic significance of primary tumor location of upper tract urothelial carcinoma(UTUC). We performed a meta-analysis to evaluate the impact of primary tumor location on prognosis in patients with UTUC who had undergone radical nephroureterectomy(RNU). We included eligible studies that reported hazard ratios(HRs) estimates with 95% confidence intervals(CIs) for the association between tumor location and recurrence-free survival(RFS) and cancer-specific survival(CSS) of UTUC. The local advanced tumors(pT3/4) and nodal positive(pN1) tumors in patients stratified by tumor location were also estimated. The review contained 17 studies including a total of 12094 patients were identified. Although it was not significant in univariable analysis, meta-analysis demonstrated that ureteral tumors had a worse prognosis than renal pelvic tumors on RFS and CSS in multivariable analysis after adjusted for all covariates. Multifocal tumors also showed a significantly association with both disease progression and cancer-specific mortality in univariable and multivariable analyses. However, no statistically significant differences were found between renal pelvic and ureteral tumors in presentation of pT3/4 and pN1 tumors. Our meta-analysis indicated that ureteral and multifocal tumors are independent prognosticators of disease progression and cancer-specific survival in patients with UTUC treated with RNU. [ABSTRACT FROM AUTHOR]

The choice of appropriate therapeutic plans for primary endocervical adenocarcinomas (ECA) and endometrial adenocarcinomas (EMA) depends on the tumor’s site of origin. Some panels of antibodies help to distinguish primary ECA from EMA. However, unexpected expressions of those markers often exist, which causes this diagnostic dilemma to be still unresolved. In this study, we investigate five commonly used monoclonal antibodies (p53, TTF1, CK7, CK20, and CK34βE12) to evaluate their potential use in distinguishing between these two gynecologic malignancies. A tissue microarray was constructed using paraffin-embedded, formalin-fixed tissues from 35 hysterectomy specimens, including 14 ECA and 21 EMA. Utilizing the avidin–biotin (ABC) technique, tissue array sections were immunostained with the five aforementioned commercially available antibodies. Immunohistochemical (IHC) expressions of p53, TTF1, CK7, CK20, and CK34βE12 were all nonsignificant ( P > 0.05) in frequency differences between the immunostaining results (positive vs. negative) in tumors from both the two primary adenocarcinomas (ECA vs. EMA). It is still uncertain which markers or panels would be the most appropriate for making diagnoses; hence, exploration of other useful markers, which make a definitive distinction between ECA and EMA merits further studies. This study, however, uncovered that the five commonly used monoclonal antibodies (p53, TTF1, CK7, CK20, and CK34βE12) are of no beneficial value in distinguishing between primary ECA and EMA. [ABSTRACT FROM AUTHOR]

Endocervical adenocarcinomas (ECA) and endometrial adenocarcinomas (EMA) are uterine malignancies that have differing biological behavior. The choice of appropriate therapeutic plan depends indeed on the tumor’s site of origin. In this study, we not only compare the individual expression status of five immunomarkers (ER, PR, Vim, CEA, and p16INK4a), but also evaluate whether p16INK4a adds value to the ER/PR/Vim/CEA panel characteristics in distinguishing between primary ECA and EMA. A tissue microarray (TMA) was constructed using paraffin-embedded, formalin-fixed tissues from 35 hysterectomy specimens, including 14 ECA and 21 EMA. TMA sections were immunostained with five anti-bodies, by avidin–biotin complex (ABC) method for antigen visualization. The staining intensity and area extent of the immunohistochemical (IHC) reactions were appraised by using the semi-quantitative scoring system. The four respective markers (ER, PR, Vim, CEA) and their combined panel expressions showed significant ( p < 0.05) frequency differences between ECA and EMA tumors. The p16INK4a marker also revealed a significant frequency difference ( p < 0.05) between the two sites of origin, but did not demonstrate to have any supplementary value to the 4-marker panel. According to our data, when there is histomorphological and clinical doubt as to the primary site of origin, we recommend that the conventional 4-marker (ER/PR/Vim/CEA) panel is appropriate. Ancillary p16INK4a-marker testing does not add value to the 4-marker panel in distinguishing between primary ECA and EMA. [ABSTRACT FROM AUTHOR]

Combinations therapy is often used in hypertensive patients whether combination therapy is necessary for preventing end-organ damage is not known. The objective of this study was to determine in four different hypertensive animal models the necessity of adding the calcium channel blocker amlodipine to therapy with the β-blocker atenolol to modulate end-organ damage. Spontaneously hypertensive rats, DOCA-salt hypertensive rats, two-kidney, one-clip renovascular hypertensive rats and Lyon genetically hypertensive rats were used to study this objective. These animal models have different sensitivities to atenolol and amlodipine. The dosages of therapy employed were 10 mg/kg atenolol alone, 1 mg/kg amlodipine, 10 mg atenolol + 1 mg/kg amlodipine and 5 mg/kg atenolol+0.5 mg/kg amlodipine. BP was continuously recorded in all animals. After determination of baroreflex sensitivity, rats were sacrificed for end-organ damage evaluation. The combination of amlodipine and atenolol had a synergistic inhibitory effect on blood pressure and blood pressure variability, and end-organ damage as compared with monotherapy with atenolol or amlodipine in all animal models. Baroreflex sensitivity also improved with the combination therapy more than with monotherapy. In conclusion, atenolol and amlodipine combination exerts a superior effect on blood pressure, blood pressure variability, baroreflex sensitivity and end-organ damage. The superior effect of the combination was observed in all four models of hypertension. [ABSTRACT FROM AUTHOR]