Given a passage with a context and an answer, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.

Q: Context: The safety of Deltamethrin (DM) has been raised as a point of concern. The current investigation was envisaged to explore the responsiveness of oxidative stress parameters, DNA fragmentation and expression levels of TP53, cycloxygenase 2 (COX2) and cytochrome p4502E1 (CYP2E1) as toxicological endpoint in rats treated with DM. as well as attention was provided to the neuroprotective effect of vitamin E (VE).', 'Four different groups of rats were used in this study, group I served as control, group II received DM (0.6 mg/kg BW), group III received both DM plus VE and finally group IV received VE only (200 mg/kg BW). The treatment regimen was extending for one month for all groups and the brain tissues were collected for further analysis.', 'The obtained results showed a highly statistically significant increase in lipid peroxidation (LPO) content, nitric oxide concentration, and DNA fragmentation percentage and expression level of CYP2E1, TP53 and COX2 genes, in addition statistical significant reduction in total antioxidant capacity in DM treated group as compared to control were detected. Oral administration of VE attenuated the neurotoxic effects of DM through improvement of oxidative status, DNA fragmentation percentage and suppressing the expression level of CYP2E1, TP53 and COX2 genes.
Answer: From this study we concluded that VE supplementation has beneficial impacts on DM neurotoxicity in rats through its antioxidant and antiapoptotic properties.

A: Does vitamin E attenuate neurotoxicity induced by deltamethrin in rats?
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Q: Context: Increased concentrations of metalloproteinases are associated with the invasive and metastatic behavior of several human malignant tumors. Normally, enzymatic activity is tightly regulated by nonspecific mechanisms and specific inhibitors. The aim of the study was to determine the potential of a synthetic metalloproteinase inhibitor, batimastat, to show its in vitro effect on MatLyLu cancer cells and its in vivo effect on tumor growth in orthotopic cancer (R3327 Dunning tumor) in rats.', 'In vitro, a dose response curve of batimastat was generated over 4 days using the MTT assay. Prostate cancer was injected in vivo in male Copenhagen rats by inoculating R3327 Dunning tumor cells (MatLyLu) into the ventral prostatic lobe of 30 rats. Each of 10 rats received batimastat (30 mg/kg body weight) or vehicle administered once a day by i.p. application beginning the day of cell inoculation. Ten rats remained untreated. The effect on local tumor growth was evaluated by measuring tumor weights 20 days after tumor cell inoculation.', 'Significant inhibition of tumor cell proliferation in vitro occurred at 400 and 4,000 ng/ml batimastat. After orthotopic cell inoculation, tumors grew to mean weights of 18.9 g in the control group without treatment, to 22.3 g in the vehicle group, and to 11.1 g in the treated group. In comparison to the control group and to the vehicle group, tumor weights increased significantly less under treatment with batimastat.
Answer: Batimastat is able to reduce tumor growth in the standard prostate cancer model. Using this model, activity against cancer progression of future inhibitory agents can be reliably assessed.

A: Does synthetic inhibitor of matrix metalloproteinases ( batimastat ) reduce prostate cancer growth in an orthotopic rat model?
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Q: Context: To assess the predictive value of glycated albumin (GA) and other risk factors on a progression of diabetic retinopathy (DR).', 'In this retrospective longitudinal study, we enrolled the subjects with type 2 diabetes who had undergone fundus photography twice with a 5-years gap between January 2006 and December 2012, and had been measured consecutively for hemoglobin A1c (HbA1c) and GA levels every 3 or 6 months. The subjects were divided into two groups with or without a progression of DR. The mean HbA1c and mean GA were calculated separately by the sum of all measured values divided by the numbers of values throughout the study period.', 'Of the 359 subjects, progression group showed significantly higher diabetes duration (8.41±5.72 vs. 6.46±5.77, P<0.01), baseline HbA1c (9.13±2.71 vs. 8.41±2.32, P<0.05), fasting plasma glucose (8.71±2.78 vs. 7.94±2.63, P<0.05), 2h-postprandial glucose (15.12±11.20 vs.13.14±4.72, P<0.05), eGFR (114.81±39.15 vs. 103.23±32.18, P<0.01), mean HbA1c (8.32±1.69 vs. 7.39±1.35, P<0.01) and mean GA (22.66±5.92 vs. 19.83±5.18, P<0.01) than non-progression group. The frequencies of subjects with DR progression increased obviously with the increment of baseline HbA1c, mean HbA1c and mean GA according to quartile stratification of the above three glucose parameters. Multivariable binary logistic regression analysis investigated that the factors affected the DR progression were the presence of DR at baseline (OR=0.391, P=0.005), mean HbA1c (OR=1.389, P=0.021), mean GA (OR=1.087, P=0.039) and eGFR (OR=1.008, P=0.045). The optimal cut-off values of mean HbA1c and GA to predict DR progression were 7.27% and 21.85%, respectively.
Answer: The presence of DR at baseline, poor glycemic control, glycated albumin, and impaired renal function predicted DR progression in patients with type 2 diabetes.

A:
Does serum glycated albumin predict the progression of diabetic retinopathy -- a five year retrospective longitudinal study?
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