instruction:
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.
question:
Context: The purpose of this study was to examine the effectiveness of ankle bracing and taping in preventing recurrencess of ankle sprains, specifically in female athletes.', "Varsity soccer players' medical records over a five-year period were retrospectively reviewed at a Division III women's college. Data were extracted regarding any history of ankle sprain(s), type of intervention used as prophylaxis after the ankle sprain, number of exposures, and any incidence of recurrence.", 'All collegiate varsity soccer players who had suffered a previous sprain to either one or both ankles (38 players) were identified as subjects.', 'Each previously injured ankle (n = 56) was considered as a case for the analysis. Ankles that had a previous sprain received one of four interventions: 1) a canvas, laced ankle brace (n = 19), 2) taping (n = 12), 3) a combination of taping and ankle bracing (n = 8), or 4) no treatment (n = 17).', 'The four intervention groups had a total of 1717 practice exposures and 650 competitive game exposures; exposures did not differ among the 4 groups. Ankle sprain recurrence frequency was 0%, 25%, 25%, and 35% for the braced, taped, combination, and untreated groups, respectively. The recurrence incidence for the braced group was significantly lower than that of the other three groups. The ankle sprain recurrence frequency did not differ among the taped, combination, and no treatment groups.\Question: Does ankle brace effectively reduce recurrence of ankle sprains in female soccer players?
answer:
We suggest that prophylactic ankle bracing is effective in reducing the incidence of ankle sprains in female soccer players with a previous history of ankle sprains.

question:
Context: The current standard of care for glioblastoma (GBM) involves a combination of surgery, radiotherapy, and temozolomide chemotherapy, but this regimen fails to achieve long-term tumor control. Resistance to temozolomide is largely mediated by expression of the DNA repair enzyme MGMT; however, emerging evidence suggests that inactivation of MSH6 and other mismatch repair proteins plays an important role in temozolomide resistance. Here, we investigate endogenous MSH6 mutations in GBM, anaplastic oligodendroglial tumor tissue, and corresponding brain tumor-initiating cell lines (BTIC).', 'MSH6 sequence and MGMT promoter methylation were determined in human tumor samples and BTICs. Sensitivity to temozolomide was evaluated in vitro using BTICs in the absence and presence of O(6)-benzylguanine to deplete MGMT. The influence of MGMT and MSH6 status on in vivo sensitivity to temozolomide was evaluated using intracranial BTIC xenografts.', 'We identified 11 previously unreported mutations in MSH6 in nine different glioma samples and six paired BTIC lines from adult patients. In addition, MSH6 mutations were documented in three oligodendrogliomas and two treatment-naive gliomas, both previously unreported findings. These mutations were found to influence the sensitivity of BTICs to temozolomide both in vitro and in vivo, independent of MGMT promoter methylation status.\Question: Do novel MSH6 mutations in treatment-naive glioblastoma and anaplastic oligodendroglioma contribute to temozolomide resistance independently of MGMT promoter methylation?
answer:
These data demonstrate that endogenous MSH6 mutations may be present before alkylator therapy and occur in at least two histologic subtypes of adult glial neoplasms, with this report serving as the first to note these mutations in oligodendroglioma. These findings broaden our understanding of the clinical response to temozolomide in gliomas.

question:
Context: Age-related cataract (ARC) is the leading cause of visual impairment worldwide, and -crystallin (CRYAA) is the predominant structural protein involved in the maintenance of lens clarity and refractive properties. We previously demonstrated that CRYAA genes undergo epigenetic repression in the lens epithelia in ARC. We further analyze the underlying mechanism in the current study.', 'The transcription factor binding sites of the CpG island of CRYAA promoter were predicted by TESS website. An electrophoretic mobility shift assay (EMSA) was used to analyze the impact of the methylation of CpG sites on transcription factors. Human lens epithelial B-3 (HLE B-3) Cells were treated with demethylation agent zebularine in the concentrations of 0 (PBS as control), 10M, 20M, 50M, 100M and 200M, respectively. After treatment in the above concentrations for 24h, 48h and 72h, respectively, CRYAA mRNA expression levels were detected by Quantitative Real-Time RT-PCR.', 'The methylation of the CpG site of the CRYAA promoter decreased the DNA-binding capacity of transcription factor Sp1. Zebularine increased CRYAA expression in HLE B-3 Cells in a dose- dependent and time- dependent pattern.\Question: Do cpG site methylation in CRYAA promoter affect transcription factor Sp1 binding in human lens epithelial cells?
answer:
The evidence presented suggests that the methylation of the CpG sites of the CRYAA promotor directly affect Sp1 binding, leading to down expression of CRYAA in human lens epithelial cells. Zebularine treatment could restore CRYAA expression in a dose- dependent and time- dependent pattern.