In this task, you are given an abstract of article. Your task is to generate title for this article. Preferred titles are under thirty words.

[Q]: Patients with inflammatory bowel disease have an increased prevalence of osteoporosis, and suffer high rates of spinal bone loss. Hormone replacement therapy (HRT) is effective in the treatment and prevention of osteoporosis but has not been studied in patients with inflammatory bowel disease. A two year prospective study of HRT in inflammatory bowel disease was performed in 47 postmenopausal women aged 44 to 67 years with ulcerative colitis (25) or Crohn's disease (22). Patients had radial and spinal bone density measured annually by single photon absorptiometry and quantitative computed tomography respectively. The mean (95% confidence intervals) annual change in radial bone density was +1.42%/yr (+0.58 to +2.26; P < 0.005) and for spinal bone +2.60%/yr (+1.06 to +4.15; p < 0.005). There was no significant correlation between rates of change of bone density at the two sites, or between the rates of change and the initial bone density either in the radius or spine. Twelve patients were given prednisolone during the study, and their rates of change for spinal bone density were lower, but values were not statistically significantly different from those who did not receive corticosteroids. Changes in bone density for patients with ulcerative colitis and Crohn's disease were not significantly different. The change in bone density did not correlate with the patients' age or number of years after the menopause. It is concluded that HRT is effective in prevention of bone loss in postmenopausal women with inflammatory bowel disease.
[A]: Hormone replacement therapy prevents bone loss in patients with inflammatory bowel disease.

[Q]: Regulatory T (Treg) cells play a pivotal role in suppressing self-harmful T cell responses, but how Treg cells mediate suppression to maintain immune homeostasis and limit responses during inflammation is unclear. Here we show that effector Treg cells express high amounts of the integrin v8, which enables them to activate latent transforming growth factor- (TGF-). Treg-cell-specific deletion of integrin v8 did not result in a spontaneous inflammatory phenotype, suggesting that this pathway is not important in Treg-cell-mediated maintenance of immune homeostasis. However, Treg cells lacking expression of integrin v8 were unable to suppress pathogenic T cell responses during active inflammation. Thus, our results identify a mechanism by which Treg cells suppress exuberant immune responses, highlighting a key role for effector Treg-cell-mediated activation of latent TGF- in suppression of self-harmful T cell responses during active inflammation.
[A]: Integrin v8-Mediated TGF- Activation by Effector Regulatory T Cells Is Essential for Suppression of T-Cell-Mediated Inflammation

[Q]: The androgen receptor (AR) is overexpressed and hyperactivated in human castration-resistant prostate cancer (CRPC). However, the determinants of AR overexpression in CRPC are poorly defined. Here we show that retinoic acid receptor-related orphan receptor (ROR-) is overexpressed and amplified in metastatic CRPC tumors, and that ROR- drives AR expression in the tumors. ROR- recruits nuclear receptor coactivator 1 and 3 (NCOA1 and NCOA3, also known as SRC-1 and SRC-3) to an AR-ROR response element (RORE) to stimulate AR gene transcription. ROR- antagonists suppress the expression of both AR and its variant AR-V7 in prostate cancer (PCa) cell lines and tumors. ROR- antagonists also markedly diminish genome-wide AR binding, H3K27ac abundance and expression of the AR target gene network. Finally, ROR- antagonists suppressed tumor growth in multiple AR-expressing, but not AR-negative, xenograft PCa models, and they effectively sensitized CRPC tumors to enzalutamide, without overt toxicity, in mice. Taken together, these results establish ROR- as a key player in CRPC by acting upstream of AR and as a potential therapeutic target for advanced PCa.
[A]:
ROR- drives androgen receptor expression and represents a therapeutic target in castration-resistant prostate cancer