Given a passage with a context and an answer, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.

Context: In the past years the interaction of GH and 11beta hydroxysteroid dehydrogenase (11betaHSD) in the pathogenesis of central obesity has been suggested.', 'We studied the effects of 9 months of GH treatment on 11betaHSD activity and its relationship with body composition and insulin sensitivity in 30 men with abdominal obesity, aged 48-66 years, in a randomised, double-blind, placebo-controlled trial.', 'Urinary steroid profile was used to estimate 11betaHSD type 1 and 2 (11betaHSD1 and 11betaHSD2) activities. Abdominal s.c. and visceral adipose tissues were measured using computed tomography. Glucose disposal rate (GDR) obtained during a euglycaemic-hyperinsulinaemic glucose clamp was used to assess insulin sensitivity.', 'In the GH-treated group the 11betaHSD1 activity decreased transiently after 6 weeks (P < 0.01) whereas 11betaHSD2 increased after 9 months of treatment (P < 0.05). Between 6 weeks and 9 months, GDR increased and visceral fat mass decreased. Changes in 11betaHSD1 correlated with changes in visceral fat mass between baseline and 6 weeks. There were no significant correlations between 11betaHSD1 and 11betaHSD 2 and changes in GDR.
Answer: The study demonstrates that short- and long-term GH treatment has different effects on 11betaHSD1 and 11betaHSD2 activity. Moreover, the data do not support that long-term metabolic effects of GH are mediated through its action on 11betaHSD.
Is gH effect on enzyme activity of 11betaHSD in abdominal obesity dependent on treatment duration?

Context: The use of cultured keratinocyte (CK) allografts for burn wounds offers a potentially unlimited supply of skin. It is unknown, however, whether CK allografts induce rejection in vivo. This study investigated the induction of immune responsiveness to CK allografts as measured by mixed lymphocyte response and serum cytotoxic antibody.', 'Female CBA mice (n = 160) were randomized to four equal groups, each receiving a 3 cm2 flank graft of autologous CBA CK (Auto CK), allogeneic C57BL/6 CK (Allo CK), C57BL/6 full thickness skin (Allo FT), or Sham. Graft take was assessed by gross and histologic examinations. Unidirectional mixed lymphocyte response was measured with graft recipient and donor splenocytes by use of tritiated thymidine uptake. Stimulation indexes were calculated. Serum cytotoxic antibody was measured by coculturing graft recipient serum with donor splenocytes and rabbit complement and assessing resultant cell killing.', 'Overall graft take was 50% for Allo CK and 74% for Auto CK, Allo FT, but not Allo CK, were associated with significantly increased stimulation indexes compared with Auto CK and Sham (p < 0.01). Allo FT, but not Allo CK, resulted in elevated titers of alloantibody, reaching significant levels 10 days after grafting (p < 0.05).
Answer: CK allografts do not result in increased in vitro T cell responses or enhanced alloantibody formation, indicating that sensitization to major histocompatibility antigens by CK does not occur. These data suggest that CK allografts may provide a possible source of grafts for victims of large burn wounds.
Do cultured keratinocyte allografts fail to induce sensitization in vivo?

Context: One hypothesis for thyroid cancer development is its derivation from thyroid cancer stem cells (CSCs). Such cells could arise via different paths including from mutated resident stem cells within the thyroid gland or via epithelial to mesenchymal transition (EMT) from malignant cells since EMT is known to confer stem-like characteristics. Furthermore, EMT is a critical process for epithelial tumor progression, local invasion, and metastasis formation. In addition, stemness provides cells with therapeutic resistance and is the likely cause of tumor recurrence. However, the relevance of EMT and stemness in thyroid cancer progression has not been extensively studied.', 'To examine the status of stemness in thyroid papillary cancer, we employed a murine model of thyroid papillary carcinoma and examined the expression of stemness and EMT using qPCR and histochemistry in mice with a thyroid-specific knock-in of oncogenic Braf (LSL-Braf((V600E))/TPO-Cre). This construct is only activated at the time of thyroid peroxidase (TPO) expression in differentiating thyroid cells and cannot be activated by undifferentiated stem cells, which do not express TPO.', 'There was decreased expression of thyroid-specific genes such as Tg and NIS and increased expression of stemness markers, such as Oct4, Rex1, CD15, and Sox2 in the thyroid carcinoma tissue from 6-week-old BRAF(V600E) mice indicating the dedifferentiated status of the cells and the fact that stemness was derived in this model from differentiated thyroid cells. The decreased expression of the epithelial marker E-cadherin and increased EMT regulators including Snail, Slug, and TGF-β1 and TGF-β3, and the mesenchymal marker vimentin demonstrated the simultaneous progression of EMT and the CSC-like phenotype. Stemness was also found in a cancer thyroid cell line (named Marca cells) derived from one of the murine tumors. In this cell line, we also found that overexpression of Snail caused up-regulation of vimentin expression and up-regulation of stemness markers Oct4, Rex1, and CD15, with enhanced migration ability of the cells. We also showed that TGF-β1 was able to induce Snail and vimentin expression in the Marca cell thyroid cancer line, indicating the induction of EMT in these cells, and this induction of EMT and stemness was significantly inhibited by celastro a natural inhibitor of neoplastic cells.
Answer: Our findings support our earlier hypothesis that stemness in thyroid cancer is derived via EMT rather than from resident thyroid stem cells. In mice with a thyroid-specific knock-in of oncogenic Braf (LSL-Braf((V600E))/TPO-Cre), the neoplastic changes were dependent on thyroid cell differentiation and the onset of stemness must have been derived from differentiated thyroid epithelial cells. Furthermore, celastrol suppressed TGF-β1 induced EMT in thyroid cancer cells and may have therapeutic potential.

Is stemness Derived from Thyroid Cancer Cells?