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.
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Question: Beta defensins are secreted from ovine oviduct epithelial cells (OOECs) in response to microbial infection, and are potential alternatives to antibiotic agents in the treatment of microorganism infection, particularly given the abuse of antibiotic agents and the increasing number of drug-resistant bacteria. The aberrant expression of defensins may result in disorders involving organ and oviduct inflammation, such as salpingitis.', 'In the present study, we investigated the effects of LPS on the mRNA expression levels of sheep β-defensin-1 (SBD-1) in ovine oviduct epithelial cells. The OOECs in vitro culturing system were established and treated with different concentrations of LPS for indicated time. In addition, MAPK inhibitors and TLR4 antibodies were pretreated to investigate the potential mechanism which involves in LPS regulating SBD-1 expression.', 'LPS markedly upregulated SBD-1 expression in a concentration- and time-dependent manner. Treatment with 100\xa0ng/mL LPS resulted in the phosphorylation of JNK, ERK and P38 MAPK. Interestingly, the LPS stimulated SBD-1 expression was attenuated by pretreatment with the P38 MAPK inhibitors SB203580 and SB202190 but not the JNK inhibitor SP600125, while the ERK inhibitor PD98059 had a minor effect. Furthermore, treatment with a Toll-like receptor 4 (TLR4) neutralizing antibody significantly decreased P38 MAPK phosphorylation and LPS induced SBD-1 expression.

Answer: Does lipopolysaccharide induce SBD-1 expression via the P38 MAPK signaling pathway in ovine oviduct epithelial cells?


Question: Angiotensin II (Ang II) signaling has been implicated in cardiac arrhythmogenesis, which involves induction of reactive oxygen species (ROS). It was shown that Ang II can activate Ca/Calmodulin kinase II (CaMKII) by oxidation via a NADPH oxidase 2 (NOX2)-dependent pathway leading to increased arrhythmic afterdepolarizations. Interestingly, cAMP-dependent protein kinase A (PKA) which regulates similar targets as CaMKII has recently been shown to be redox-sensitive as well.', 'This study aims to investigate the distinct molecular mechanisms underlying Ang II-related cardiac arrhythmias with an emphasis on the individual contribution of PKA vs. CaMKII.', 'Isolated ventricular cardiac myocytes from rats and mice were used. Ang II exposure resulted in increased NOX2-dependent ROS generation assessed by expression of redox-sensitive GFP and in myocytes loaded with ROS indicator MitoSOX. Whole cell patch clamp measurements showed that Ang II significantly increased peak Ca and Na current (ICa and INa) possibly by enhancing steady-state activation of ICa and INa. These effects were absent in myocytes lacking functional NOX2 (gp91phox(-/-)). In parallel experiments using PKA inhibitor H89, the Ang II effects on peak INa and ICa were also absent. In contrast, genetic knockout of CaMKIIδ (CaMKIIδ(-/-)) did not influence the Ang II-dependent increase in peak ICa and INa. On the other hand, Ang II enhanced INa inactivation, increased late INa and induced diastolic SR (sarcoplasmic reticulum) Ca leak (confocal Ca spark measurements) in a CaMKIIδ-, but not PKA-dependent manner. Surprisingly, only the increase in diastolic SR Ca leak was absent in gp91phox(-/-)myocytes suggesting that Ang II regulates INa inactivation in a manner dependent on CaMKII- but not on NOX2. Finally, we show that Ang II increased the propensity for cellular arrhythmias, for which PKA and CaMKII contribute, both dependent on NOX2.

Answer: Does nADPH oxidase 2 mediate angiotensin II-dependent cellular arrhythmias via PKA and CaMKII?


Question: Mark/recapture (or capture-recapture) is a simple technique commonly applied to estimate the hypothetical total (including undercount) in a register composed of cases from two or more independent and separately incomplete case lists. This paper seeks to illustrate serious drawbacks in the use of the mark/recapture technique when applied to injuries.', 'Northumbrian children under 15 years of age who were seriously injured in motor vehicle accidents (MVAs) over a five year period ascertained from two data sources: police reports and hospital inpatient records.', 'Individuals (n) appearing in both police (S) and hospital (H) case lists are identified using various matching criteria. The separate and combined influence of age, sex, and casualty class (cyclist, passengers, pedestrians) on the probability of such matching is estimated using multivariate techniques. The hypothetical total incidence of child MVA victims (N) is calculated from N = (S x H)/n.', 'Estimates of the incidences of "serious" injuries in MVAs under various conditions of stratification and matching. The overall procedure is tested for conformity with accepted criteria for valid use of mark/recapture.', 'About one third of the 1009 police and 836 hospital records could be exactly matched. There were significant variations in matching proportions by class of accident (pedestrian v passenger v cyclist). This selective recapture or "heterogeneity" was not affected by sex, but was independently influenced by the age of the child. Further uncertainty was introduced when matching criteria were slightly relaxed. Estimates of the total population of children with serious injuries vary accordingly from 1729 to 2743. A number of plausible reasons why these two data sources might not be unbiased or mutually independent samples of the total target population are proposed as explanations for this heterogeneity.

Answer:
Are children goldfish -- mark/recapture techniques and their application to injury data?