In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.

Q: Context: Hypoxia is associated with human non-small cell lung cancers (NSCLC), which are highly resistant to chemotherapy. The hypoxia inducible factor (HIF) as a transcription factor in response to hypoxia indicates that it could be a novel, tumor-specific target for anticancer therapy. We hypothesized that disruption of HIF pathway through lentiviral vector-mediated HIF-1alpha RNA interference (RNAi) could reverse the hypoxia-induced resistance to chemotherapy.', 'We transfected Human NSCLC cell lines, SPCA1 and A549 with HIF-1alpha specific RNAi lentiviral vectors as well as controls. HIF-1alpha silenced cells [SPCA1/HIF-1alpha(-) and A549/HIF-1alpha(-)] were screened by blasticidin. They were incubated in 19 or 0.5% O2 for 16 h followed by the assessment of chemosensitivity to cisplatin and doxorubicin with MTT and clonogenic assays. Quantitative RT-PCR and Western blot analysis were used to detect the expressions of HIF-1alpha mRNA and protein, respectively. Moreover, flow cytometry was used to monitor the expression of P-glycoprotein.', 'Exposure of SPCA1 and A549 cells to 0.5% O2 significantly increased resistance to cisplatin and doxorubicin, in contrast to cells incubated in normoxia. Transduction of SPCA1 with HIF-1alpha RNAi vector resulted in sequence specific silencing with 87.2 and 84.6% decreases of HIF-1alpha mRNA transcription and 97.3 and 94.8% of protein expressions in normoxia and hypoxia, respectively. Correspondingly, they are 89.2, 89.9% and 97.2, 88.4% decreases in A549 cells. Hypoxia-induced resistance to cisplatin and doxorubicin were reversed in SPCA1/HIF-1alpha(-) and A549/HIF-1alpha(-) cells. There was no significant P-glycoprotein increase induced by hypoxia in NSCLC cells.\Question: Is hypoxia-induced resistance to cisplatin and doxorubicin in non-small cell lung cancer inhibited by silencing of HIF-1alpha gene?

A: Our studies demonstrated that hypoxia-induced chemoresistance to cisplatin and doxorubicin in NSCLC cells is through the HIF pathway. MDR1 regulation may not be involved in hypoxia-induced chemoresistance. Combining delivery of HIF-1alpha RNAi lentiviral vector with cisplatin-related chemotherapy regimens may enable us to develop more effective strategy for NSCLC therapy.
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Q: Context: To assess the effect of six different enteral diets on the gut barrier.', 'Laboratory study.', 'University hospital, Germany.', '70 Specific pathogen free female Crl:CDR BR rats.', 'For 7 days, 6 groups of rats were fed orally with standard chow (n = 15); total parenteral nutrition solution (oral TPN, n = 15); elemental diet (ED, n = 10); nutrient-defined diet (NDD, n = 10); or the NDD supplemented with uracil (NDD+uracil, n = 10), or fibre (NDD+fibre, n = 10).', 'Bacterial translocation to mesenteric lymph nodes, numbers of Gram negative enterobacteria and total aerobic bacteria in the caecum, and intestinal concentrations of secretory IgA.', 'The incidence of bacterial translocation was significantly increased in the groups given oral TPN, ED, NDD, and NDD+uracil compared with the group given chow. Only NDD+fibre resulted in a similar degree of translocation to that in the chow group. All groups in which there was increased translocation had a highly significant overgrowth of aerobic bacteria in the caecum, mainly by Gram negative enteric organisms. The secretory IgA concentration was reduced in the group that had been given oral TPN, and that in the ED and NDD+uracil groups was similar to that in the chow group. NDD and NDD+fibre were associated with higher intestinal concentrations of secretory IgA than chow.\Question: Is fibre an essential ingredient of enteral diets to limit bacterial translocation in rats?

A: Fibre-free enteral diets do not protect the gut antimicrobial barrier whatever else is in them. The superiority of early enteral as opposed to parenteral nutrition after injury may, therefore, not be the result of a specific protective effect on the gut barrier. The supplementation of commercial enteral diets with bulk fibre should be tested in clinical trials.
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Q: Context: The study aimed to explore the alteration of autophagy in rat pancreas treated with exenatide.', 'Normal Sprague-Dawley rats and diabetes-model rats induced by 2-month high-sugar and high-fat diet and streptozotocin injection were subcutaneously injected with exenatide, respectively, for 10 weeks, with homologous rats treated with saline as control. Meanwhile, AR42J cells, pancreatic acinar cell line, were cultured with exenatide at doses of 5 pM for 3 days. The pancreas was disposed, and several sections were stained with hematoxylin-eosin. Immunohistochemistry was used to measure the expressions of glucagon-like peptide 1 receptor (GLP-1R) and cysteinyl aspartate specific proteinase-3 in rat pancreas, and Western blot was used to test the expressions of GLP-1R, light chain 3B-I and -II, and p62 in rat pancreas and AR42J cells. The data were expressed as mean (standard deviation) and analyzed by unpaired Student t test using SPSS 18.0 statistics software (SPSS China, Shanghai, China).', 'Exenatide can induce pathological changes in rat pancreas. The GLP-1R, p62, light chain 3B-II, and cysteinyl aspartate specific proteinase-3 in rat pancreas and AR42J cells treated with exenatide were significantly overexpressed.\Question: Does exenatide induce Impairment of Autophagy Flux to Damage Rat Pancreas?

A:
Exenatide can activate and upregulate its receptor, GLP-1R, then impair autophagy flux and activate apoptosis in the pancreatic acinar cell, thus damaging rat pancreas.This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially.
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