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.

[EX Q]: Context: Thus far, live attenuated SIV has been the most successful method for vaccinating macaques against pathogenic SIV challenge; however, it is not clear what mechanisms are responsible for this protection. Adoptive transfer studies in mice have been integral to understanding live attenuated vaccine protection in models like Friend virus. Previous adoptive transfers in primates have failed as transferred cells are typically cleared within hours after transfer.', 'Here we describe adoptive transfer studies in Mauritian origin cynomolgus macaques (MCM), a non-human primate model with limited MHC diversity. Cells transferred between unrelated MHC-matched macaques persist for at least fourteen days but are rejected within 36 hours in MHC-mismatched macaques. Cells trafficked from the blood to peripheral lymphoid tissues within 12 hours of transfer.\Question: Do allogeneic lymphocytes persist and traffic in feral MHC-matched mauritian cynomolgus macaques?
[EX A]: MHC-matched MCM provide the first viable primate model for adoptive transfer studies. Because macaques infected with SIV are the best model for HIV/AIDS pathogenesis, we can now directly study the correlates of protective immune responses to AIDS viruses. For example, plasma viral loads following pathogenic SIV challenge are reduced by several orders of magnitude in macaques previously immunized with attenuated SIV. Adoptive transfer of lymphocyte subpopulations from vaccinated donors into SIV-naïve animals may define the immune mechanisms responsible for protection and guide future vaccine development.

[EX Q]: Context: To examine whether trichostatin A (TSA), a histone deacetylase inhibitor (HDACI), can induce up-regulation of peroxisome proliferator-activating receptor gamma (PPAR gamma) and to see whether LG100268, a retinoid X receptor (RXR) ligand, can inhibit proliferation of endometriotic cells alone or in synergy with ciglitazone, a PPAR gamma agonist.', 'One endometrial stromal cell line and two endometriotic cell lines used as a model system: Western blot analysis to determine whether TSA can up-regulate PPAR gamma expression, and MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide) proliferation assay to see whether ciglitazone and LG100268 have any antiproliferative effects individually or jointly.', 'Academic.', 'None.', 'Culture of immortalized endometrial and endometriotic cell lines with TSA, or ciglitazone or LG100268.', 'PPAR gamma protein expression levels in cells treated with or without TSA, and number of viable cells treated with or without ciglitazone, LG100268, or both.', 'The TSA treatment resulted in up-regulation of PPAR gamma expression in all cell lines in a dose-dependent fashion. Both ciglitazone and LG100268 inhibited proliferation in a dose-dependent manner, and the antiproliferative effects appeared to be synergistic. In addition, endometriotic cells were more sensitive than endometrial stromal cells to LG100268 treatment.\Question: Do peroxisome proliferator-activated receptor-gamma and retinoid X receptor agonists synergistically suppress proliferation of immortalized endometrial stromal cells?
[EX A]: The up-regulation of PPAR gamma induced by TSA indicates that the action of HDACIs also includes the PPAR gamma signaling pathway, suggesting that the activation of PPAR gamma is a desirable way to contain endometriosis phenotypes. The higher sensitivity of endometriotic cells than their endometrial counterpart to LG100268 treatment suggests that the sensitivity differential could be exploited effectively to eradicate unwanted ectopic endometrial tissues while minimizing the collateral damage to the normal endometrial tissues.

[EX Q]: Context: Residual disease (RD) at definitive resection of incidental gallbladder cancer (IGBCA) influences outcome, but its clinical relevance with respect to anatomic site is incompletely characterized.', 'Consecutive patients with IGBCA undergoing re-exploration from 1998 to 2009 were identified; those submitted to a complete resection were analyzed. Demographics and tumor- and treatment-related variables were correlated with RD and survival. Cancer-specific survival was stratified by site of RD (local [gallbladder bed]; regional [bile duct, lymph nodes]; distant [discontiguous liver, port site, peritoneal]).', 'Of the 135 patients submitted to re-exploration, RD was found in 82 (61%) overall and in 63 (54%) of 116 patients submitted to resection; the most common site was regional (n\xa0=\xa027, 43%). The T stage of the gallbladder specimen was the only independent predictor of RD (T1b\xa0= 35.7%, T2\xa0= 48.3%, T3\xa0= 70%, p\xa0= 0.015). The presence of RD at any site dramatically reduced median disease-free survival (DFS) (11.2 vs 93.4 months, p < 0.0001) and disease-specific survival (DSS) (25.2 months vs not reached, p < 0.0001) compared with no RD, respectively. Disease-specific survival did not differ according to RD location, with all anatomic sites being equally poor (p\xa0= 0.87). Residual disease at any site predicted DFS (hazard ratio [HR] 3.3, 95% CI 1.9 to 5.7, p\xa0= 0.0003) and DSS (HR 2.4, 95% CI 1.2 to 4.6, p\xa0= 0.01), independent of all other tumor-related variables.\Question: Does residual disease predict outcomes after definitive resection for incidental gallbladder cancer?
[EX A]:
Survival in patients with RD at local or regional sites was not significantly different than that seen in stage IV disease, with neither subgroup clearly benefiting from reoperation. Outcomes were poor in all patients with RD, regardless of location.