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: Oral tacrolimus, approved for the prophylaxis of organ rejection in liver or kidney transplants, has been reported to be effective in anecdotal cases of refractory inflammatory bowel disease.', 'To evaluate the usefulness of low-dose oral tacrolimus in refractory inflammatory bowel disease.', "Thirty-one adult Caucasian patients with steroid-dependent (n = 15) or steroid-refractory (n = 16) inflammatory bowel disease (Crohn's disease, n = 6; ulcerative colitis, n = 23; pouchitis, n = 2) were enrolled. Tacrolimus (0.1 mg/kg body weight per day) was administered orally in 30 patients and initially intravenously in one patient (0.01 mg/kg body weight per day), aiming for serum trough levels of 4-6 ng/mL. The median treatment duration was 12 months (range, 1-137 months).", "Twenty-eight patients (90.3%) experienced a clinical and laboratory response and 20 (64.5%) went into remission. One ulcerative colitis patient and two Crohn's disease patients did not improve. Three ulcerative colitis patients (9.7%) were colectomized at 1, 12 and 24 months after tacrolimus initiation. In 19 of 23 patients (82.6%) taking steroids, steroids were reduced or discontinued. Side-effects included a temporary rise of creatinine (n = 3, 9.7%), tremor or paraesthesias (n = 3, 9.7%), hyperkalaemia (n = 1, 3.2%), hypertension (n = 1, 3.2%) and an opportunistic infection (n = 1, 3.2%).\Question: Is rescue therapy with tacrolimus effective in patients with severe and refractory inflammatory bowel disease?

A: Oral tacrolimus is safe and effective in refractory inflammatory bowel disease.
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Q: Context: Celastrol is an active ingredient of traditional herbal medicine and has recently been identified as a potent natural proteasome inhibitor. In the present study, we evaluated the radiosensitizing potential of celastrol in the human prostate cancer PC-3 model.', 'Clonogenic assays were performed to determine the radiosensitizing effect of celastrol. Apoptosis was examined by flow cytometry using Annexin V and propidium iodide staining and by a caspase-3 activation assay. DNA damage processing was examined by immunofluorescent staining and Western blot for phosphorylated H2AX (gammaH2AX). The PC-3 xenograft model in the athymic nude mouse was used for the determination of the in vivo efficacy of celastrol combined with radiotherapy. The tumor samples were also analyzed for apoptosis and angiogenesis.', 'Celastrol sensitized PC-3 cells to ionizing radiation (IR) in a dose- and schedule-dependent manner, in which pretreatment with celastrol for 1 h followed by IR achieved maximal radiosensitization. Celastrol significantly prolonged the presence of IR-induced gammaH2AX and increased IR-induced apoptosis. Celastrol, combined with fractionated radiation, significantly inhibited PC-3 tumor growth in vivo without obvious systemic toxicity. The combination treatment increased gammaH2AX levels and apoptosis, induced cleavage of poly(adenosine diphosphate-ribose)polymerase and Mcl-1, and reduced angiogenesis in vivo compared with either treatment alone.\Question: Does celastrol potentiate radiotherapy by impairment of DNA damage processing in human prostate cancer?

A: Celastrol sensitized PC-3 cells to radiation both in vitro and in vivo by impairing DNA damage processing and augmenting apoptosis. Celastrol might represent a promising new adjuvant regimen for the treatment of hormone-refractory prostate cancer.
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Q: Context: To investigate the effect of high glucose on insulin-induced vascular endothelial growth factor (VEGF) expression in bovine retinal microvascular endothelial cells (BRECs) and to probe into related mechanisms.', 'BRECs were isolated as primary cultures and identified by immunostaining. Passage cells were initially exposed to normal (5 mM) or high glucose (30 mM) for 3 days, and equimolar L-glucose was supplemented for osmotic equation. BRECs were then treated with 100 nM insulin for 24 h or not, and cells were prepared for the determination of VEGF mRNA expression by real-time PCR. VEGF protein was determined by human umbilical vein endothelial cell proliferation assay, immunofluorescence, and ELISA. BRECs were treated with 5 or 30 mM glucose for 3 days and then cells cultured with 5 mM glucose were exposed to the PI3-K inhibitor wortmannin (100 nM), the P42/44 mitogen-activated protein kinase (MAPK) inhibitor U0126 (50 microM), or to the protein kinase C (PKC) inhibitor GF109203X (2 microM) 1 h before addition of 100 nM insulin. Twenty-four hours after incubation with insulin, the cells were subjected to real-time PCR and ELISA analyses.', 'Insulin or high glucose alone markedly increased VEGF mRNA and protein levels in BRECs (P<0.05, two-way ANOVA). However, the combination of insulin and high glucose displayed a weaker effect in promoting VEGF expression than did insulin alone (P<0.05, t-test). Pretreatment of cells with PI3-K inhibitor significantly (P<0.05, one-way ANOVA) suppressed the insulin-induced VEGF expression; neither pretreatment with the PKC inhibitor nor with the P42/p44 MAPK inhibitor showed an effect on the expression of VEGF at the mRNA or protein level (P>0.05, one-way ANOVA).\Question: Does high glucose attenuate insulin-induced VEGF expression in bovine retinal microvascular endothelial cells?

A:
Both insulin and high glucose can markedly increase VEGF expression in BRECs at the mRNA and protein level. We propose that insulin may upregulate VEGF expression through the PI3-K signalling pathway in BRECs, and high glucose may attenuate insulin-induced VEGF expression by impairing PI3-K signalling pathways.
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