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.

Q: Context: Osteoarthritis (OA) is associated with a gradual reduction in the interstitial osmotic pressure within articular cartilage. The aim of this study was to compare the effects of sudden and gradual hypo-osmotic challenge on chondrocyte morphology and biomechanics.', 'Bovine articular chondrocytes were exposed to a reduction in extracellular osmolality from 327 to 153 mOsmol/kg applied either suddenly (<5 s) or gradually (over 180 min). Temporal changes in cell diameter and the existence of regulatory volume decrease (RVD) were quantified along with changes in cortical actin and chromatin condensation. The cellular viscoelastic mechanical properties were determined by micropipette aspiration.', 'In response to a sudden hypo-osmotic stress, 66% of chondrocytes exhibited an increase in diameter followed by RVD, whilst 25% showed no RVD. By contrast, cells exposed to gradual hypo-osmotic stress exhibited reduced cell swelling without subsequent RVD. There was an increase in the equilibrium modulus for cells exposed to sudden hypo-osmotic stress. However, gradual hypo-osmotic challenge had no effect on cell mechanical properties. This cell stiffening response to sudden hypo-osmotic challenge was abolished when actin organization was disrupted with cytochalasin D or RVD inhibited with REV5901. Both sudden and gradual hypo-osmotic challenge reduced cortical F-actin distribution and caused chromatin decondensation.
Answer: Sudden hypo-osmotic challenge increases chondrocyte mechanics by activation of RVD and interaction with the actin cytoskeleton. Moreover, the rate of hypo-osmotic challenge is shown to have a profound effect on chondrocyte morphology and biomechanics. This important phenomenon needs to be considered when studying the response of chondrocytes to pathological hypo-osmotic stress.

A: Does the rate of hypo-osmotic challenge influence regulatory volume decrease ( RVD ) and mechanical properties of articular chondrocytes?
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Q: Context: Renal ischemia-reperfusion (I/R) injury is a major cause of acute renal failure (ARF). The transcription factor nuclear factor-kappaB (NF-kappaB) has been implicated as a key mediator of reperfusion injury. Activation of NF-kappaB is dependent upon the phosphorylation of its inhibitor, IkappaB, by the specific inhibitory kappaB kinase (IKK) subunit, IKKbeta. We hypothesized that ischemic preconditioning (IPC) reduces acute renal damage following I/R injury by inhibiting activation of IKKbeta. As neutrophil gelatinase-associated lipocalin (NGAL), an early predictive biomarker of acute kidney injury, is regulated by NF-kappaB, we approached the relationship between NGAL and IKKbeta.', 'Thirty male Sprague-Dawley rats were randomly divided into 3 groups after right kidney nephrectomy. Group A rats were sham-operated controls. Group B rats were 45-min ischemic in the left renal artery while Group C rats were pre-treated with 3 cycles of 2-min ischemia and 5-min reperfusion. All the rats were sacrificed at 24 h after reperfusion. We harvested kidneys and serum to do further analysis, including histological and functional parameters, expressions of NGAL and IKKbeta in renal tissues.', 'Compared with rats subjected to I/R injury, pre-treated rats had a significant decrease in serum creatinine level (Scr) and tubulointerstitial injury scores (Scr, 86.79 +/- 12.98 vs. 205.89 +/- 19.16 mircomol/l, p < 0.01; tubulointerstitial injury scores, 1.3 +/- 0.48 vs. 3.8 +/- 0.79, p < 0.01). In addition, expressions of IKKbeta (0.95 +/- 0.21 vs. 1.74 +/- 0.17, p < 0.05) and NGAL (1.71 +/- 0.032 vs. 2.66 +/- 0.078, p < 0.05) at renal tubule in pre-treated rats were attenuated significantly compared with rats subjected to ischemia-reperfusion injury. Moreover, our study showed that IKKbeta and NGAL were in positive correlation (R = 0.965 > R(0.01)(30) = 0.448, p < 0.01).
Answer: The evidence suggests that IKKbeta may play a role in renal I/R injury and give rise to the generation of NGAL. It appears that IPC may attenuate renal injury and the expression of NGAL following acute I/R injury. IKKbeta may offer a clinically accessible target for preventing renal injury following I/R.

A: Does ischemic preconditioning attenuate renal ischemia-reperfusion injury by inhibiting activation of IKKbeta and inflammatory response?
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Q: Context: Sophorae radix (SR) has been used for various diseases including atherosclerosis and arrhythmias. Atherosclerosis induced by hyperglycemia is an important factor in the promotion of diabetic complications. An early event in atherosclerosis is the adhesion of monocytes to endothelium via adhesion molecules. Among them, vascular cell adhesion molecule-1 (VCAM-1) expression mediates the binding of monocytes and lymphocytes to vascular endothelial cells.', 'The study was performed on vascular endothelial cells (ECV304 cells) that were pretreated with various concentrations of SR extract for 3 h before exposure with high glucose (55.5 mmol/l) for 48 h. The protein expression of VCAM-1 was measured by enzyme-linked immunosorbent assay (ELISA) and its mRNA expression was by reverse transcription polymerase chain reaction (RT-PCR).', 'SR extract significantly inhibited high glucose-induced expression of VCAM-1 in a dose-dependent manner and reduced the level of VCAM-1 mRNA through interfering with translocation of nuclear factor-kappaB (NF-kappaB). Decreased VCAM-1 expression by SR extract was associated reduction of adherence between high glucose-stimulated ECV304 cells and human monocyte-like HL-60 cells.
Answer: These data suggest that SR extract inhibits high glucose-mediated monocytes-endothelial cells adhesions and expression of VCAM-1 via inhibition of NF-kappaB translocation.

A:
Does sophorae radix extract inhibit high glucose-induced vascular cell adhesion molecule-1 up-regulation on endothelial cell line?
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