Given a passage, 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.

To determine the role of factor V Leiden and prothrombin gene mutation in the pathogenesis of unexplained second and third trimester nonrecurrent fetal loss.', 'One hundred and fourteen women with unexplained nonrecurrent late fetal loss made up the study group, and 106 normal pregnant women with a history of delivery of at least one healthy fetus and no history of late fetal loss made up the control group. The study group was further divided into two subgroups: second (n = 36) and third (n = 78) trimester fetal loss. All women were tested for factor V Leiden and G20210A prothrombin gene mutations.', 'Twenty-one (18.4%) of the women in the study group and seven (6.6%) of the women in the control group were heterozygous carriers of factor V Leiden mutation (OR = 3.19). Eleven (9.6%) of the women in the study group and three (2.8%) of the women in the control group were heterozygous carriers of prothrombin gene mutation (OR = 3.66). In assessing with regard to trimesters, 18 (23%) factor V Leiden and 10 (12.8%) prothrombin gene mutations were present in the group of third trimester fetal loss (OR = 4.24 and OR = 5.04, respectively). Three (8.3%) factor V Leiden and one (2.7%) prothrombin gene mutation were detected in women with second trimester fetal loss (OR = 1.28 and OR = 0.40, respectively).
Is third trimester nonrecurrent fetal loss associated with factor V Leiden and prothrombin gene mutations?

To evaluate whether the relationship between dietary composition and plasma lipid levels is genetically determined.', 'We have evaluated the influence of common apolipoprotein A5 (APOA5) variants (T-1131 > C, Ser19 > Trp and Val153 > Met) on plasma lipid concentrations in 117 males for whom dietary composition markedly changed and total cholesterol decreased (from 6.21 +/- 1.31 mmol/L in 1988 to 5.43 +/- 1.06 mmol/L in 1996) over an 8 year follow-up study.', 'APOA5 T-1131 > C and Val153 > Met variants did not influence the change in lipid measures over time. In Ser/Ser19 homozygotes, the plasma cholesterol was relatively stable over the years (6.1 +/- 1.2 mmol/L in 1988 and 5.6 +/- 1.0 mmol/L in 1996, -8%, P < 0.01). In contrast, in the Trp19 carriers, the decrease of the plasma cholesterol was more than 20% (6.5 +/- 1.6 mmol/L in 1988 and 5.1 +/- 1.0 mmol/L in 1996) (P < 0.001). The difference of the changes is significant (8% vs. 20%, P < 0.005). Changes in other analyzed lipid parameters have not been significantly associated with APOA5 variants.
Does aPOA5 variant Ser19Trp influence a decrease of the total cholesterol in a male 8 year cohort?

We examined the effects of cilostazol on mitogen-activated protein kinase (MAPK) activity and its relationship with cilostazol-mediated protection against apoptosis in lipopolysaccharide (LPS)-treated endothelial cells.', 'Human umbilical vein endothelial cells (HUVECs) were exposed to LPS and cilostazol with and without specific inhibitors of MAPKs; changes in MAPK activity in association with cell viability and apoptotic signaling were investigated.', 'Cilostazol protected HUVECs against LPS-induced apoptosis by suppressing the mitochondrial permeability transition, cytosolic release of cytochrome c, and subsequent activation of caspases, stimulating extracellullar signal-regulated kinase (ERK1/2) and p38 MAPK signaling, and increasing phosphorylated cAMP-responsive element-binding protein (CREB) and Bcl-2 expression, while suppressing Bax expression. These cilostazol-mediated cellular events were effectively blocked by MAPK/ERK kinase (MEK1/2) and p38 MAPK inhibitors.

Does cilostazol protect endothelial cells against lipopolysaccharide-induced apoptosis through ERK1/2- and P38 MAPK-dependent pathways?