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: Androgen-independent prostate cancer is today an incurable disease, but increased understanding of the mechanisms for the transition into an androgen-independent state may increase the possibilities for more efficient strategies in the future.', 'An androgen-independent subline, LNCaP-19, to the androgen-dependent prostate cancer cell line LNCaP was developed in vitro under standard culture conditions. The characteristics of LNCaP-19 regarding androgen responsiveness, PSA, and VEGF secretion was studied in vitro. The growth in vivo and the microvessel density (MVD) of the tumors were studied after inoculation in nude mice.', 'LNCaP-19 grows equally well in dextran-charcoal stripped FBS (DCC-FBS) as in normal FBS, and rapidly gives rise to tumors in both intact and castrated mice, indicating a true androgen-independent growth. The PSA secretion from LNCaP-19 cells was lower than from LNCaP cells, while the VEGF level was comparable to the secretion from LNCaP cells without androgen stimulation. The MVD was increased in the LNCaP-19 tumors, and the vessels also displayed a changed morphology with exclusively small microvessels without lumen.
Answer: LNCaP-19 shows characteristics resembling those of androgen-independent prostate cancer. An increased MVD and changed vessel morphology in the tumor, makes it an interesting model system for studies regarding angiogenesis in the context of the acquisition of androgen independence.
Is transition of an androgen-dependent human prostate cancer cell line into an androgen-independent subline associated with increased angiogenesis?

Context: Smoking cessation rapidly reduces cardiovascular risk. The pathophysiological mechanisms involved are still being debated. We measured structural and functional arterial wall properties of the femoral and carotid arteries after smoking cessation to investigate their possible role in cardiovascular risk reduction.', 'Out of 127 smokers, 33 proved to stop smoking for two years. They were compared with 50 nonsmokers and 55 persistent smokers in a prospective study. Cross-sectional compliance and distensibility coefficients as well as intima-media thickness of both carotid arteries and of the right common femoral artery were measured ultrasonographically at baseline and 3, 6, 12 and 24 months after smoking cessation. The nonsmoking and persistent smokers group were measured twice at an interval of 24 months.', 'Persistent smoking and two years of smoking cessation did not affect cross-sectional compliance and distensibility coefficients. Although at baseline intimal-medial layers were thicker in smokers, the change over time in intima-media thickness did not differ significantly between all three groups.
Answer: Two years of smoking cessation was not accompanied by a slower progression or a regression in intima-media thickness nor by an improved cross-sectional compliance or distensiblity coefficient. Nevertheless, smoking cessation should be recommended as it reduces cardiovascular risk rapidly after smoking cessation.
Does two years of smoking cessation reduce arterial wall thickness and stiffness?

Context: Inflammation triggered by infection or injury is tightly controlled by glucocorticoid hormones which signal via a dedicated transcription factor, the Glucocorticoid Receptor (GR), to regulate hundreds of genes. However, the hierarchy of transcriptional responses to GR activation and the molecular basis of their oftentimes non-linear dynamics are not understood.', 'We investigated early glucocorticoid-driven transcriptional events in macrophages, a cell type highly responsive to both pro- and anti-inflammatory stimuli. Using whole transcriptome analyses in resting and acutely lipopolysaccharide (LPS)-stimulated macrophages, we show that early GR target genes form dense networks with the majority of control nodes represented by transcription factors. The expression dynamics of several glucocorticoid-responsive genes are consistent with feed forward loops (FFL) and coincide with rapid GR recruitment. Notably, GR binding sites in genes encoding members of the KLF transcription factor family colocalize with KLF binding sites. Moreover, our gene expression, transcription factor binding and computational data are consistent with the existence of the GR-KLF9-KLF2 incoherent FFL. Analysis of LPS-downregulated genes revealed striking enrichment in multimerized Zn-fingers- and KRAB domain-containing proteins known to bind nucleic acids and repress transcription by propagating heterochromatin. This raises an intriguing possibility that an increase in chromatin accessibility in inflammatory macrophages results from broad downregulation of negative chromatin remodelers.
Answer: Pro- and anti-inflammatory stimuli alter the expression of a vast array of transcription factors and chromatin remodelers. By regulating multiple transcription factors, which propagate the initial hormonal signal, GR acts as a coordinating hub in anti-inflammatory responses. As several KLFs promote the anti-inflammatory program in macrophages, we propose that GR and KLFs functionally cooperate to curb inflammation.

Does glucocorticoid receptor coordinate transcription factor-dominated regulatory network in macrophages?