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: Recently, extract of Ginkgo biloba leaves (GbE) have become widely known phytomedicines and have shown various pharmacological activities, including improvement of blood circulation, protection of oxidative cell damage, prevention of Alzheimer's disease, treatment of cardiovascular disease and diabetes complications. This study was designed to investigate the effects of an ethanolic GbE on renal fibrosis in diabetic nephropathy (DN) and to clarify the possible mechanism by which GbE prevents renal fibrosis.", 'We investigated the protective effects of GbE on renal fibrosis in STZ-induced diabetic rats. Rats were randomized into six groups termed normal control, diabetes mellitus, low dose of GbE (50\xa0mg/kg/d), intermediate dose of GbE (100\xa0mg/kg/d), high dose of GbE (200\xa0mg/kg/d) and rapamycin (1\xa0mg/kg/d).', 'After 12 weeks, the rats were sacrificed and then fasting blood glucose (FBG), creatinine (Cr), blood urea nitrogen (BUN), urine protein, relative kidney weight, glycogen and collagen accumulation, and collagen IV and laminin expression were measured by different methods. The amounts of E-cadherin, α-SMA and snail, as well as the phosphorylation of Akt, mTOR and p70S6K in the renal cortex of rats, were examined by western blotting.', 'Compared with diabetic rats, the levels of Cr, BUN, urine protein, relative kidney weight, accumulation of glycogen and collagen, and expression of collagen IV and laminin in the renal cortex were all decreased in GbE treated rats. In addition, GbE reduced the expression of E-cadherin, α-SMA, snail and the phosphorylation of Akt, mTOR and p70S6K in diabetic renal cortex.\Question: Does ethanolic Ginkgo biloba leaf extract prevent renal fibrosis through Akt/mTOR signaling in diabetic nephropathy?
[A]: GbE can prevent renal fibrosis in rats with diabetic nephropathy, which is most likely to be associated with its abilities to inhibit the Akt/mTOR signaling pathway.


[Q]: Context: An intact and fully functional multiprotein DNA replication complex (DNA synthesome) from human as well as from murine mammary carcinoma cells was first isolated and characterized in our laboratory. The human cell synthesome supports the in vitro origin-specific simian virus 40 (SV40) DNA replication reaction in the presence of the viral large T-antigen using a semiconservative mechanism and has been shown to contain all the proteins and enzymes required to support DNA synthesis. We are currently using the DNA synthesome as a unique model for analyzing the mechanism of action of anticancer drugs affecting DNA replication. The purpose of this study was to further investigate the mechanism of action of ara-C using the DNA synthesome isolated from the human breast cancer cell line MDA MB-468.', 'Synthesome-mediated SV40 DNA replication was performed in the presence of various concentrations of ara-CTP (the active metabolite of ara-C) and the types of daughter DNA molecules produced were analyzed lusing neutral and alkaline gel electrophoresis. We also examined the effect of ara-C on intact MDA MB-468 cell DNA synthesis and on cell proliferation. In addition, we studied the effect of ara-CTP on the activity of some of the synthesome target proteins (the DNA polymerases alpha and delta).', 'Full-length daughter DNA molecules were obtained in the presence of low concentrations of ara-CTP while at higher concentrations, there was an inhibition of full-length daughter DNA synthesis. The findings suggest that specifically the initiation phase of DNA synthesis was inhibited by ara-CTP since the production of the short Okazaki fragments was suppressed at all concentrations of the drug above 10 microM. In addition, it was found that the IC50 of ara-CTP for inhibition of synthesome-mediated in vitro DNA replication was comparable to that required to inhibit intact cell DNA synthesis. Further experimentation has shown that ara-CTP preferentially inhibits the activity of the synthesome-associated DNA polymerase alpha enzyme while the DNA polymerase delta seems to be resistant to the inhibitory effect of that drug.\Question: Does ara-C affect formation of cancer cell DNA synthesome replication intermediates?
[A]: Our results indicate that ara-C's action on DNA replication is mediated primarily through DNA polymerase alpha and suggest that this enzyme plays a key role in DNA synthetic initiation events. The results also provide definitive support for the use of the DNA synthesome as a unique and powerful model for analyzing the mechanism of action of anticancer drugs which directly affect DNA replication.


[Q]: Context: Intermountain Risk Score (IMRS) uses the admission complete blood count and basic metabolic profile to predict mortality. Intermountain Risk Score has been validated in medical patients but has not been evaluated in trauma. This study tested whether IMRS is predictive of mortality in a trauma population at a level I trauma center.', 'Admitted trauma patients with complete blood count and basic metabolic profile from October 2005 to December 2011 were evaluated. Thirty-day and 1-year IMRS were calculated using multivariable modeling. Mortality was determined using the medical record and Social Security Administration death data.', 'Three thousand six hundred thirty-seven females and 5901 males were evaluated. Intermountain Risk Score was highly predictive of death at 30 days (c-statistics, c = 0.772 for females; c = 0.783 males) and 1 year (c = 0.778 for females; c = 0.831 males). Cox regression analysis, adjusted for injury severity score, blunt vs penetrating, and length of stay, showed increased mortality risks among patients in the moderate- and high-risk IMRS-defined groups at both 30 days and 1 year, with hazard ratios ranging from 4.96 to 57.88 (all P < .001).\Question: Does the Intermountain Risk Score predict mortality in trauma patients?
[A]:
Intermountain Risk Score strongly predicts mortality in trauma patients at this single level I trauma center. The ability to accurately determine a patient's mortality risk at admission makes IMRS a potentially clinically important tool.