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.

Example Input: Context: To investigate the role of S100A3 and the effect of S100A3 inhibition on human castration-resistant prostate cancer (CRPC) cells by using in vitro and in vivo functional assays.', 'Using human CRPC cells (PC3 and DU145), S100A3 expression levels were assessed by reverse transcription-polymerase chain reaction and Western blot analysis. After S100A3-specific small interfering ribonucleic acid (RNA) treatment, cell viability was determined by Cell Counting Kit-8 assay, and apoptotic cell fractions were evaluated by flow cytometry. The invasive properties of these cells and the expression pattern of matrix metalloproteinases (MMPs) were assessed using transwell migration assays, reverse transcription-polymerase chain reaction, and gelatin zymography. Finally, the in vivo efficacy of S100A3 inhibition on human CRPC cells was investigated using human tumor xenograft models in nude mice.', 'Human CRPC cells showed overexpression of S100A3, and its suppression reduced cell viability owing to apoptotic cell death. Additionally, S100A3 inhibition decreased the invasiveness of human CRPC cells. Moreover, MMP-2 and MMP-9 were downregulated in PC3, whereas only MMP-9 was downregulated in D145 after S100A3 inhibition. In human CRPC xenograft models, we noted a marked reduction in tumor growth in mice injected with S100A3 short hairpin RNA-transfected PC3 and DU145 cells.\Question: Does s100A3 suppression inhibit in vitro and in vivo tumor growth and invasion of human castration-resistant prostate cancer cells?
Example Output: Human CRPC cells showed upregulation of S100A3 expression, and S100A3 inhibition reduced tumor cell viability. S100A3 inhibition reduced invasion capability with downregulation of MMP expression. More importantly, S100A3 inhibition resulted in tumor growth suppression in human CRPC xenograft models, suggesting S100A3 could serve as a novel therapeutic target for the treatment of human CRPC.

Example Input: Context: Re-stenosis after percutaneous coronary angioplasty (PTCA) is related to clinical and angiographic features.', 'To describe the clinical and angiographic characteristic of our patients with coronary cardiopathy subjected to PTCA and the predictor factors for re-stenosis.', 'We gathered the clinical and angiographic characteristics of all patients who underwent a successful PTCA of a native coronary artery. All patients had a clinical assessment one year after the procedure. Patients were classified in Group 1, if they did not have angina or coronary events after the angioplasty or Group 2, if they had angina or a coronary event after the procedure. Only Group 2 patients were subjected to a coronary angiogram.', 'We collected 383 PTCA procedures. Follow up information was obtained in 92.2%. Three hundred forty two patients (89.3%) were assessed one year the procedure. Nine patients (2.3%) died of a cardiovascular cause. Ninety patients (26.3%) were classified in Group 2. In 65 patients, angiographic re-stenosis was demonstrated (19%). Re-stenosis occurred in 36 and 13% of patients with an without Diabetes Mellitus, respectively (p <0.01). The other clinical predictor variables were a history of myocardial infarction (p =0.007), obesity (p =0.041) and hypercholesterolemia (p =0.050). None of the angiographic characteristics predicted restenosis. Stents were protective factors against restenosis (15.6% in stented lesions vs 25.4% in nonstented; p =0.01).\Question: Do [ One year follow up of successful coronary angioplasty in non selected patients ]?
Example Output: Re-stenosis after angioplasty occurred in 19% of our patients with angina or coronary events. The clinical variables associated with a higher risk of re-stenosis were diabetes (the main risk factor), previous myocardial infarction, obesity and hypercholesterolemia. Angiographic variables were not associated with re-stenosis. The use of stents decreases the incidence of re-stenosis in all groups).

Example Input: Context: DNA transcription is regulated, in part, by acetylation of nuclear histones that are controlled by 2 groups of enzymes: histone deacetylases (HDAC) and histone acetyl transferases (HAT). Whether an imbalance in HDAC/HAT system plays a role in hemorrhage/resuscitation is unknown. The goals of this study were to determine whether hemorrhage results in deacetylation of cardiac histones and whether this can be corrected through the application of different resuscitation strategies or specific HDAC inhibitors.', "In the first experiment, rats (n = 6 per group) were subjected to volume-controlled hemorrhage and resuscitated with racemic lactated Ringer's solution, L-lactated Ringer's solution, 7.5% hypertonic saline solution, ketone Ringer's solution, and pyruvate Ringer's solution. Control groups included no hemorrhage (sham) and hemorrhage with no resuscitation. In the second experiment (n = 5 per group), 3 HDAC inhibitors (valproic acid, trichostatin A, and suberoylanilide hydroxamic acid) were added to saline solution resuscitation. Heart tissue was collected at the end of resuscitation. Isolated subcellular protein fractions were used in Western blotting to analyze the patterns of total protein acetylation and histone acetylation specifically. HDAC and HAT activity was measured in tissue extracts.", "Hemorrhage led to partial histone deacetylation. Resuscitation resulted in protein hyperacetylation in nuclear fractions only. A detailed analysis of histones (on 10 acetylation sites) revealed that ketone Ringer's solution hyperacetylated histones H2B, H3, and H4. The addition of suberoylanilide hydroxamic acid hyperacetylated histones more effectively than other resuscitation strategies, presumably by direct inhibition of HDAC activity.\Question: Are cardiac histones substrates of histone deacetylase activity in hemorrhagic shock and resuscitation?
Example Output:
Hemorrhage/resuscitation is associated with HDAC/HAT activity misbalance, and the acetylation status of cardiac histones is influenced by the choice of resuscitation strategy. Shock-induced changes can be reversed through the infusion of pharmacologic HDAC inhibitor, even when it is administered after the insult for a limited period of time.