instruction:
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.
question:
Context: In maternal trauma, the Kleihauer-Betke (KB) test has traditionally been used to detect transplacental hemorrhage (TPH), so that Rh-negative women could receive appropriate Rh immune prophylaxis. Reasoning that the magnitude of TPH would reflect uterine injury, we evaluated Kleihauer-Betke testing as an independent predictor of preterm labor (PTL) after maternal trauma.', 'Admissions to the Shock Trauma Center, University of Maryland, from January 1996 to January 2002, were reviewed. Of 30,362 trauma patients admitted, 166 were pregnant, and 93 of these underwent electronic fetal monitoring. Their records were abstracted for demographics, injury type, three separate trauma scores, documented uterine contractions, PTL (contractions with progressive cervical change), and serious perinatal complications. In 71 cases, transplacental hemorrhage was assessed by maternal KB test.', 'TPH, defined as KB-positive for greater than 0.01 mL of fetal blood in the maternal circulation, occurred in 46 women. Forty-four had documented contractions (25 had overt PTL) and 2 had no contractions. In 25 women with a negative KB test, none had uterine contractions. All patients with contractions or PTL had positive KB tests. By logistic regression, KB test result was the single risk factor associated with PTL (p < 0.001; likelihood ratio, 20.8 for positive KB test). Compared with other sites, abdominal trauma was associated more often with uterine contractions (p < 0.001), PTL (p = 0.001), and a positive KB test (p < 0.001, chi). None of the trauma scoring systems predicted PTL.\Question: Is kleihauer-betke testing important in all cases of maternal trauma?
answer:
Kleihauer-Betke testing accurately predicts the risk of preterm labor after maternal trauma. Clinical assessment does not. With a negative KB test, posttrauma electronic fetal monitoring duration may be limited safely. With a positive KB test, the significant risk of PTL mandates detailed monitoring. KB testing has important advantages to all maternal trauma victims, regardless of Rh status.


question:
Context: Activation of NF-kappaB signaling pathway plays a critical role in the initiation and progression of carcinogenesis. However, the role of NF-kappaB pathway in esophageal squamous cell carcinoma (ESCC) has not been fully elucidated. Studies have shown that curcumin possesses anti-infection and anti-oxidation effects. This study was to evaluate whether curcumin could induce apoptosis through inhibition of NF-kappaB signaling pathway in ESCC cells.', 'Expressions of pIkappaBalpha and Bcl-2 were detected using Western blott after incubation of ESCC cells with curcumin (50 micromol/L) at different time points. Apoptosis and the number of viable ESCC cells were analyzed using flow cytometry and MTT, respectively, after the treatment of curcumin, 5-FU, or the combination of curcumin and 5-FU.', 'In two ESCC cell lines, EC9706 and Eca109,curcumin inhibited IkappaBalpha phosphorylation and Bcl-2 in a time-dependent manner; curcumin alone increased cell apoptosis (P<0.05), and the effect became more prominent when it was combined with 5-FU (P<0.05); curcumin plus 5-FU exerted a stronger inhibition effect on cell proliferation than curcumin alone (P<0.05) or 5-FU alone (P<0.05).\Question: Does [ Curcumin promote apoptosis of esophageal squamous carcinoma cell lines through inhibition of NF-kappaB signaling pathway ]?
answer:
Curcumin inhibits the phosphorylation of IkappaBalpha, leading to suppression of proliferation, induction of apoptosis and an increase of the sensitivity of ESCC cell lines towards 5-FU.


question:
Context: In humans, glucocorticoid-induced osteoporosis is the most common cause of medication-induced osteoporosis. Recent clinical data suggest that glucocorticoid therapy increases the risk of vertebral fractures within a short treatment period. Therefore, this study aimed at investigating vertebral bone in a rat model of glucocorticoid-induced postmenopausal osteoporosis.', 'Fifty Sprague-Dawley rats were randomly assigned into three groups: 1) untreated controls, 2) Sham-operated group, and 3) ovariectomized rats treated with glucocorticoid (dexamethasone) for 3 months (3M) after recovery from bilateral ovariectomy. Osteoporotic bone status was determined by means of the gold standard dual energy X-ray absorptiometry (DEXA) scan. Vertebral bodies were examined using µCT, histological analysis, mRNA expression analysis, and biomechanical compression testing. Further systemic effects were studied biochemically using serum marker analysis.', 'Dexamethasone treatment showed at 3M a significantly lower bone mineral density in ovariectomized rats compared to Sham-operated control (p < 0.0001) as analyzed in vivo by DEXA. Furthermore, Z scores reached levels of -5.7 in the spine indicating sever osteoporotic bone status. Biomechanical testing of compression stability indicated a lower functional competence (p < 0.0001) in the spine of treated rats. µCT analysis showed significant reduction of bone volume density (BV/TV%; p < 0.0001), significantly enhanced trabecular spacing (Tb.Sp; p < 0.0001) with less trabecular number (Tb.N; p < 0.001) and complete loss of trabecular structures in glucocorticoid-treated ovariectomized rats. Histological analysis by osteoblast and osteoclast activities reflected a higher bone catabolism reflected by osteoclast counts by TRAP (p < 0.019) and lower bone catabolism indicated by ALP-stained area (p < 0.035).Serum analysis showed a significant increase in osteocalcin (p < 0.0001), osteopontin (p < 0.01) and insulin (p < 0.001) at 3M. Expression analysis of molecular markers in the vertebral body revealed lower expression in tenascin C in the OVX-steroid animals at 3M.\Question: Does short-term glucocorticoid treatment cause spinal osteoporosis in ovariectomized rats?
answer:

Short-term glucocorticoid treatment of ovariectomized rats indicates according to DEXA standards a severe osteoporotic bone status in vertebral bone. Nonetheless, dysfunctional bone anabolism and enhanced bone catabolism are observed. Alterations of bone extracellular matrix proteins that correlate to inferior mechanical stability and affected microstructure were noticed and suggest further investigation. Treatment with dexamethasone was also seen to affect insulin and osteopontin levels and thus osteoblast function and maturation. This described animal model presents a recapitulation of clinically obtained data from early phase glucocorticoid-induced osteoporosis observed in patients.