Investigation into Information Release of Chinese Government and Departments on COVID-19.

Information release is an important way for governments to deal with public health emergencies, and plays an irreplaceable role in promoting epidemic prevention and control, enhancing public awareness of the epidemic situation and mobilizing social resources. Focusing on the coronavirus disease 2019 (COVID-19) epidemic in China, this investigation chose 133 information release accounts of the Chinese government and relevant departments at the national, provincial, and municipal levels, including Ministries of the State Council, Departments of Hubei Province Government, and Bureaus of Wuhan Government, covering their portals, apps, Weibos, and WeChats. Then, the characteristics such as scale, agility, frequency, originality, and impact of different levels, departments, and channels of the information releases by the Chinese government on the COVID-19 epidemic were analyzed. Finally, the overall situation was concluded by radar map analysis. It was found that the information release on the COVID-19 epidemic was coordinated effectively at different levels, departments, and channels, as evidenced by the complementarity between channels, the synergy between the national and local governments, and the coordination between departments, which guaranteed the rapid success of the epidemic prevention and control process in China. This investigation could be a reference for epidemic prevention and control for governments and international organizations, such as the World Health Organization (WHO), during public health emergencies, e.g. the COVID-19 pandemic.

Chlorogenic Acid Ameliorates Colitis and Alters Colonic Microbiota in a Mouse Model of Dextran Sulfate Sodium-Induced Colitis.

This study evaluated the mitigating effects of dietary chlorogenic acid (CGA) on colon damage and the bacterial profile in a mouse model of dextran sulfate sodium (DSS)-induced colitis. C57BL/6J mice were randomly assigned to receive one of the following treatments: (i) basal diet; (ii) basal diet with 2% CGA; (iii) basal diet with 2.5% DSS or (iv) basal diet with 2% CGA and 2.5% DSS. Following a 2-week pre-treatment period, mice in the DSS and CGA-DSS groups received 2.5% DSS in drinking water for 5 days, while the other two groups received sterile water. Compared to DSS alone, CGA was found to reduce the disease activity index, myeloperoxidase activity and tumor necrosis factor-α levels in colon tissues (P < 0.05). CGA also ameliorated DSS-induced inflammatory responses, reduced colon shortening and decreased the histological scores (P < 0.05). In an evaluation of the relative abundances of bacteria in the fecal microbiota, we found that CGA reversed the decrease in diversity caused by DSS and improved the relative abundance of organisms in the genus Lactobacillus (P < 0.05). These results indicate that CGA maintains intestinal health and reduces DSS-induced colon injury by decreasing the production of pro-inflammatory cytokines and restoring intestinal microbial diversity.

Identification of key regulators of pancreatic ductal adenocarcinoma using bioinformatics analysis of microarray data.

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal forms of cancer, and its etiology remains largely unknown. This study aimed to screen a panel of key genes and to identify their potential impact on the molecular pathways associated with the development of PDAC. Four gene expression profiles, GSE28735, GSE15471, GSE102238, and GSE43795, were downloaded from the Gene Expression Omnibus (GEO) database. The intersection of the differentially expressed genes (DEGs) in each dataset was obtained using Venn analysis. Gene ontology (GO) function and Kyoto Encyclopedia of Genes and Genomes pathway (KEGG) analysis were subsequently carried out. To screen for hub genes, a protein-protein interaction (PPI) network was constructed.The intersection of the DEGs revealed 7 upregulated and 9 downregulated genes. Upon relaxation of the selection criteria, 58 upregulated and 32 downregulated DEGs were identified. The top 5 biological processes identified by GO analysis involved peptide cross-linking, extracellular matrix (ECM) disassembly, regulation of the fibroblast growth factor receptor signaling pathway, mesoderm morphogenesis, and lipid digestion. The results of KEGG analysis revealed that the DEGs were significantly enriched in pathways involved in protein digestion and absorption, ECM-receptor interaction, pancreatic secretion, and fat digestion and absorption. The top ten hub genes were identified based on the PPI network.In conclusion, the identified hub genes may contribute to the elucidation of the underlying molecular mechanisms of PDAC and serve as promising candidates that can be utilized for the early diagnosis and prognostic prediction of PDAC. However, further experimental validation is required to confirm these results.

Emodin inhibits pancreatic cancer EMT and invasion by up­regulating microRNA­1271.

Emodin has a direct inhibitory effect on the growth and metastasis of a variety of malignant tumor cells. MicroRNA­1271 (miR­1271) has an extensive tumor­suppression effect by inhibiting epithelial mesenchymal transition (EMT) in tumor cells and induces tumor cell apoptosis. Proceeding with the EMT regulatory mechanism of pancreatic carcinoma, the present study aimed to examine the inhibitory effect of miR­1271 and emodin against invasion and metastasis of pancreatic carcinoma. The expression of EMT­related markers (E­cadherin, ZEB1 and TWIST1) was analyzed by western blotting. mRNA levels of miR­1271, E­cadherin, ZEB1 and TWIST1 in pancreatic tumor cells (SW1990) were measured through reverse transcription­quantitative polymerase chain reaction and cell invasiveness was detected using Transwell assays. In addition, a liver metastatic model was established with an implantation of pancreatic tumor tissue into the spleens of nude mice to study the effect of emodin on pancreatic cancer liver metastasis. In the present study, it was demonstrated that miR­1271 significantly decreased in pancreatic cancer cells and tissues. Twist1 may be a target gene of miR­1271. Emodin could inhibit the proliferation ability of pancreatic cancer cells and increased miR­1271 expression level. Further, we found that miR­1271 significantly inhibited SW1990 cell EMT and invasive ability. We also provided the evidence that emodin inhibited SW1990 cell EMT by raising the level of miR­1271. Moreover, the in vivo experiments have verified the inhibiting effect of emodin against liver metastasis of pancreatic cancer. The data in the present study indicated that emodin inhibited pancreatic cancer EMT and invasion by increasing the content of miR­1271.

Efficacy of the prophylactic use of octreotide for the prevention of complications after pancreatic resection: An updated systematic review and meta-analysis of randomized controlled trials.

BACKGROUND: The use of octreotide prophylaxis in the prevention of complications after pancreatic resection remains controversial. The aim of this systematic review and meta-analysis was to evaluate the efficacy of octreotide prophylactic treatment to prevent complications after pancreatic resection. METHODS: Five databases (PubMed, Medline, SinoMed, Embase, and Cochrane Library) were searched for eligible studies from 1980 to November 2016 with the limitation of human subjects and randomized controlled trials (RCTs). Data were extracted independently and were analyzed using RevMan statistical software version 5.3 (Cochrane Collaboration, http://tech.cochrane.org/revman/download). Weighted mean differences (WMDs), risk ratios (RRs), and 95% confidence intervals (CIs) were calculated. Cochrane Collaboration risk of bias tool was used to assess the risk of bias. RESULTS: Twelve RCTs comprising 1902 patients were identified as eligible. The methodological quality of the trials ranged from low to moderate. A pooled analysis of effectiveness based on the data from each study revealed that octreotide could significantly reduce the rate of pancreatic fistula (PF) after pancreatic resection (RR = 0.75, 95% CI = 0.57-0.98, P = .04). The same findings were discovered in multicenter and European subgroups with a subgroup analysis; no obvious differences were noted in American, Asian, and single-center subgroup analyses. An equal effect was observed between the use or non-use of octreotide groups regarding mortality (RR = 1.24, 95% CI = 0.77-2.02, P = .38). Octreotide had no advantages in regards to mortality improvement. The total numbers of complications associated with the use or non-use of octreotide were similar (RR = 0.77, 95% CI = 0.58-1.03, P = .08). Among the high-risk group, octreotide was more effective in reducing complications (RR = 0.61, 95% CI = 0.46-0.82, P = .0009). Compared with the patients who did not receive prophylactic treatment, the patients who underwent pancreatic resection benefited from octreotide because it had better efficacy in preventing fluid collection and postoperative pancreatitis. CONCLUSION: The prophylactic use of octreotide is suitable for preventing postoperative complications, especially PF and fluid collection as well as postoperative pancreatitis. However, no obvious differences were noted regarding mortality. In view of the clinical heterogeneity and varying definitions of PF, whether these conclusions are broadly applicable should be further determined in future studies.

Efficacy and Safety of Beclomethasone Dipropionate versus 5-Aminosalicylic Acid in the Treatment of Ulcerative Colitis: A Systematic Review and Meta-Analysis.

BACKGROUND: Ulcerative colitis (UC) is a chronic and remitting inflammatory disease that is characterized by chronic idiopathic inflammation of the colon and bloody diarrhea. Currently drug treatment is the main intervention for patients with mild to moderate UC. Mesalazine (5-ASA) and beclomethasone dipropionate (BDP) have been widely used for the treatment of UC and have yielded satisfactory results. This study compared the effectiveness of 5-ASA and BDP in the treatment of UC. METHODS: The PubMed, Medline, SinoMed, Embase, and Cochrane Librinary databases were searched for eligible studies. Data were extracted by two of the coauthors independently and were analyzed using RevMan statistical software, version 5.3. Weighted mean differences (WMDs), odds ratios (ORs), and 95% confidence intervals (CIs) were calculated. Cochrane Collaboration's Risk of Bias Tool was used to assess the risk of bias. RESULTS: Seven randomized controlled trials that compared BDP with 5-ASA in treating UC were identified as eligible. The methodological quality of the trials ranged from low to moderate. A pooled analysis of effectiveness based on the Disease Activity Index (DAI) or other assessment method after treatment revealed that in the treatment of UC, there are no obvious differences between BDP and 5-ASA in inducing remission and clinical improvement (OR = 0.76, 95% CI = 0.56-1.03, P = 0.08). The total numbers of adverse events associated with BDP and 5-ASA treatments for UC were similar (OR = 1.21, 95% CI = 0.71-2.09, P = 0.48). The safety profiles for these two drugs are good. According to subgroup-analysis, we found no obvious differences of clinical efficacy between BDP and 5-ASA no matter oral or enema administration was used in the treatment of UC. A sensitivity analysis demonstrated the stability of the pooled results. CONCLUSION: During induction treatment of mild to moderate UC, there is no obvious difference between the two groups with respect to remission and clinical improvement. Given that the upper confidence limit for the OR barely exceeds 1.0 and that the p-value is close to 0.05 for this primary efficacy outcome as well as that the horizontal block lies to the left of the vertical line, it indicates that the clinical efficacy of BDP may be better than 5-ASA. However, taking into account that BDP has the risk of hypothalamic-pituitary-adrenal axis (HPA) suppression, 5-ASA has a potential advantage of safety in the treatment of mild to moderate UC.

O-GlcNAcylation enhances the invasion of thyroid anaplastic cancer cells partially by PI3K/Akt1 pathway.

BACKGROUND: The PI3K family participates in multiple signaling pathways to regulate cellular functions. PI3K/Akt signaling pathway plays an important role in tumorigenesis and development. O-GlcNAcylation, a posttranslational modification, is thought to modulate a wide range of biological processes, such as transcription, cell growth, signal transduction, and cell motility. O-GlcNAcylation is catalyzed by the nucleocytoplasmic enzymes, OGT and OGA, which adds or removes O-GlcNAc moieties, respectively. Abnormal O-GlcNAcylation has been implicated in a variety of human diseases. However, the role of O-GlcNAcylation in tumorigenesis and progression of cancer is still under-investigated. Understanding the O-GlcNAc-associated molecular mechanism might be significant for diagnosis and therapy of cancer. METHODS: Human thyroid anaplastic cancer 8305C cells were used to evaluate the role of O-GlcNAcylation in tumorigenesis and progression of cancer. The global O-GlcNAc level of intracellular proteins was up-regulated by OGA inhibitor Thiamet-G treatment or OGT over-expression. Cell proliferation was assessed by MTT assay. Invasion in vitro was determined by Transwell assay, and phosphorylation of Akt1 at Ser473 was assessed by Western blot for activity of Akt1. PI3K-specific inhibitor LY294002 and RNA interference of Akt1 were used to investigate the impact of PI3K/Akt signaling on the regulation of O-GlcNAcylation during tumor progression. RESULTS: Cell models with remarkably up-regulated O-GlcNAcylation were constructed, and then cell proliferation and invasion were determined. The results indicated that the proliferation was not affected by OGA inhibition or OGT overexpression, while the invasion of 8305C cells with OGA inhibition or OGT overexpression was obviously increased. Akt1 activity was stimulated by elevated O-GlcNAcylation by mediating phosphorylation at Ser473. The enhanced invasion of thyroid cancer cells by Thiamet-G treatment or OGT overexpression was significantly depressed by PI3K inhibitor LY294002. Moreover, silence of Akt1 remarkably attenuated the increase of cell invasion induced by Thiamet-G treatment, but the invasion was still higher compared to Akt1-silenced only cells. In other words, Thiamet-G restored the invasion of Akt1-silenced thyroid cancer cells, but it was still lower relative to Thiamet-G-treated only cells. CONCLUSION: Taken together, our findings suggested that O-GlcNAcylation enhanced the invasion of thyroid anaplastic cancer cells partially by PI3K/Akt signaling, which might be a potential target for the diagnosis and treatment of thyroid anaplastic cancer.

Pancreas-sparing duodenectomy with regional lymph node dissection for early-stage ampullary carcinoma: A case control study using propensity scoring methods.

AIM: To investigate the outcomes of pancreas-sparing duodenectomy (PSD) with regional lymph node dissection vs pancreaticoduodenectomy (PD). METHODS: Between August 2001 and June 2014, 228 patients with early-stage ampullary carcinoma (Amp Ca) underwent surgical treatment (PD, n = 159; PSD with regional lymph node dissection, n = 69). The patients were divided into two groups: the PD group and the PSD group. Propensity scoring methods were used to select patients with similar disease statuses. A total of 138 matched cases, with 69 patients in each group, were included in the final analysis. RESULTS: The median operative time was shorter among the patients in the PSD group (435 min) compared with those in the PD group (481 min, P = 0.048). The median blood loss in the PSD group was significantly less than that in the PD group. The median length of hospital stay was shorter for patients in the PSD group vs the PD group. The incidence of pancreatic fistula was higher among patients in the PD group vs the PSD group. The 1-, 3-, and 5-year overall survival and disease-free survival rates for patients in the PSD group were 83%, 70%, 44% and 73%, 61%, 39%, respectively, and these values were not different than compared with those in the PD group (P = 0.625). CONCLUSION: PSD with regional lymph node dissection presents an acceptable morbidity in addition to its advantages over PD. PSD may be a safe and feasible alternative to PD in the treatment of early-stage Amp Ca.

Protective effect of Lai Fu Cheng Qi decoction on severe acute pancreatitis-induced myocardial injury in a rat model.

The aim of the present study was to evaluate the effects of Lai Fu Cheng Qi decoction on myocardial injury in rats with severe acute pancreatitis (SAP). In total, 30 rats were randomly divided into sham, SAP and decoction treatment groups. SAP was induced by a retrograde pancreatic duct injection of 5% sodium taurocholate in the SAP and decoction treatment groups. Rats in decoction treatment group also received intragastric administration of Lai Fu Cheng Qi decoction. The serum levels of creatine kinase isoenzyme (CK-MB) and lactate dehydrogenase (LDH) were detected using an automatic biochemical analyzer. In addition, myocardial Na+-K+-ATPase activity was analyzed using a spectrophotometric method and the mitochondrial membrane potential was measured by flow cytometry. Myocardial apoptosis was assessed using a TUNEL assay and pathological changes to the heart and pancreas were detected by hematoxylin and eosin staining. Compared with the rats in the sham group, rats in the SAP and decoction treatment groups exhibited significantly higher levels of serum CK-MB and LDH, apoptosis index and pathological scores, and had significantly lower levels of Na+-K+-ATPase activity and mitochondrial membrane potential. However, when compared with the SAP group, the serum levels of CK-MB and LDH, the pathological scores of the pancreas and heart, and the myocardial cell apoptosis index in the decoction treatment group were significantly lower. Furthermore, the Na+-K+-ATPase activity and mitochondrial membrane potential were significantly increased in the decoction treatment group when compared with the SAP group. Therefore, Lai Fu Cheng Qi decoction was shown to exert a protective effect on myocardial injury induced by SAP in rats.

Rosiglitazone inhibits hepatic insulin resistance induced by chronic pancreatitis and IKK-ß/NF-κB expression in liver.

OBJECTIVES: This study aimed to investigate the influence of rosiglitazone on hepatic insulin resistance and the expressions of IκB kinase-ß (IKK-ß)/nuclear factor-κB (NF-κB) in chronic pancreatitis (CP). METHODS: After CP was induced in rats, rosiglitazone and GW9662 were administered at the doses of 4 and 2 mg/kg per day for 4 weeks, respectively. Then, glucose and insulin tolerance tests were performed. Hepatocytes were isolated for the glucose release experiments. Determination of the IKK-ß, NF-κB, and Ser307p-insulin receptor substrates-1 (Ser307p-IRS-1) expression in the liver was performed. RESULTS: The increased plasma glucose, reduced insulin sensitivity, and the capacity of insulin to suppress glucose release in hepatocytes were observed in CP rats. The IKK-ß, NF-κB, and Ser307p-IRS-1 expressions were significantly higher in the liver of CP rats than in sham-operated rats (P < 0.05). Rosiglitazone treatment significantly improved hepatic insulin sensitivity and inhibited the IKK-ß, NF-κB, and Ser307p-IRS-1 expressions in the liver (P < 0.05). Counteraction with peroxisome proliferator-activated receptor-γ by GW9662 attenuated the aforementioned effects of rosiglitazone. CONCLUSIONS: Rosiglitazone attenuates hepatic insulin resistance induced by CP. The inhibition of hepatic IKK-ß and NF-κB expressions via peroxisome proliferator-activated receptor-γ may be involved in the therapeutic effect of rosiglitazone.