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: Mast cells play a central role in allergic and inflammatory diseases. Several reports indicated role of peroxisome proliferator-activated receptor gamma (PPARgamma) on mast cell function. However, there is no report about the role of PPARgamma on differentiation of mast cells from the progenitors. In this study, we investigated the role of PPARgamma in regulating bone marrow-derived mast cell maturation and the therapeutic implications for mast cell-related diseases such as atopic or contact dermatitis.', 'We used in vitro cell culture system for mast cell differentiation from bone marrow-progenitors using specific ligands and lentiviral-mediated short hairpin RNA of PPARgamma, and in vivo murine dermatitis models.', 'Activation of PPARgamma inhibited the maturation of bone marrow progenitors into connective tissue-type mast cells (CTMCs) through up-regulation of GATA-4 and GATA-6 resulting in a decrease in expression of histidine decarboxylase and mast cell histamine content. In comparison, the differentiation of bone marrow progenitors into CTMCs was significantly accelerated by the knockdown of PPARgamma expression by lentiviral-mediated short hairpin RNA. Peroxisome proliferator-activated receptor gamma ligand administration to mice inhibited the maturation of mast cells resulting in attenuation of atopic and contact dermatitis via diminishment of the number of mature mast cells.\Question: Does activation of peroxisome proliferator-activated receptor gamma suppress mast cell maturation involved in allergic diseases?
[A]: Our results indicate that PPARgamma is one of master regulators on mast cell maturation and potentially useful for the therapy in various disorders involving mast cell activation.

[Q]: Context: The development of human leukocyte antigen (HLA) antibody responses has been associated with worse clinical outcomes, such as bronchiolitis obliterans syndrome (BOS) and death, in lung transplant recipients (LTRs). However, the role of donor-specific HLA antibody (DSA) responses as a risk factor for poor outcomes remains controversial.', 'We prospectively screened 445 LTRs for DSA at our institution at the time of surveillance bronchoscopies for the first 2 years after transplantation between 2003 and 2008, and evaluated clinical outcomes. For this purpose, we used the combination of panel-reactive antibodies (PRA) by enzyme-linked immunosorbent assay (ELISA) and the Luminex single-antigen bead (SAB) assay (One Lambda, Canoga Park, CA).', 'We detected de novo DSA (dnDSA) in 58 of 445 (13%) LTRs in our cohort. Freedom from BOS was significantly reduced in LTRs with dnDSA versus those without dnDSA (p < 0.001). Using a Cox proportional hazards model, the development of dnDSA was associated with a significantly increased hazard ratio (HR = 6.59 [4.53 to 9.59]; p < 0.001) for BOS and high-grade BOS (Stage 2) (HR = 5.76 [3.48 to 9.52]; p < 0.001). Freedom from death was significantly reduced in LTRs with dnDSA (p < 0.001), including mortality attributable to BOS (HR = 9.86 [4.91 to 19.78]; p < 0.001).\Question: Are de novo donor-specific HLA antibodies associated with early and high-grade bronchiolitis obliterans syndrome and death after lung transplantation?
[A]: Taken together, our findings provide evidence that dnDSA is associated with accelerated BOS kinetics and severity, as well as death due to BOS after lung transplantation. In addition, these data support regular monitoring for the development of dnDSA in LTRs and underscore the need for novel strategies to mitigate the increased risk of poor outcomes associated with dnDSA.

[Q]: Context: Cisplatin is a commonly used chemotherapeutic agent which causes apoptosis or necrosis of renal tubular epithelial cells in vitro. Caspases are a family of cysteine proteases that mediate apoptosis (caspase-3) and inflammation (caspase-1). Although well studied in vitro, caspases have not been previously studied in cisplatin-induced acute renal failure (ARF) in vivo.', 'Cisplatin (30 mg/kg) was injected intraperitoneally into wild-type and caspase-1-deficient (-/-) C57BL/6 mice. Serum creatinine and blood urea nitrogen (BUN), and renal caspase-1, -3, -8 and -9 activity were measured on days 1, 2, and 3 after cisplatin injection. Kidneys were examined for acute tubular necrosis (ATN), neutrophils, and apoptosis on days 1, 2, and 3.', 'After cisplatin injection, serum creatinine and BUN were normal on day 1, began to increase on day 2, and peaked on day 3. Similarly, ATN scores and neutrophil counts peaked on day 3. In contrast, renal apoptosis significantly increased on day 2. Renal dysfunction, apoptosis, ATN scores and neutrophil infiltration were all reduced in the caspase-1(-/-) mice. In wild-type mice, caspase-1 and -3 activity increased on days 2 and 3. Caspase-3 activity was reduced by approximately 50% in caspase-1(-/-) mice; active caspase-3 detected by immunoblot was also reduced in caspase-1(-/-) mice. In vitro, addition of recombinant caspases to kidney cytosolic extracts determined that caspase-1 activates caspase-3 in renal tissue.\Question: Are caspase-1-deficient mice protected against cisplatin-induced apoptosis and acute tubular necrosis?
[A]:
These results indicate that caspase-1 contributes to cisplatin-induced ARF and ATN (day 3). Furthermore, caspase-1 affects caspase-3 activation and apoptosis in cisplatin-induced ARF (day 2).