instruction:
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.
question:
Context: Current diagnostic tests for gastroesophageal reflux disease (GERD) do not consistently measure chronicity of reflux. Mucosal impedance (MI) is a minimally invasive measurement to assess esophageal conductivity changes due to GERD. We aimed to investigate MI pattern in patients with symptoms of extraesophageal reflux (EER) in a prospective longitudinal cohort study.', 'Patients with potential symptoms of EER undergoing esophagogastroduodenoscopy (EGD) with wireless pH monitoring were studied. Participants included those with erosive esophagitis (E+), normal EGD/abnormal pH (E-/pH+), and normal EGD/normal pH (E-/pH-). MI was measured from the site of injury in patients with E+, as well as at 2, 5, and 10 cm above the squamocolumnar junction (SCJ) in all participants.', 'Forty-one patients with symptoms of EER were studied. MI measurements at 2\u2009cm above the SCJ were significantly (P\u2009=\u20090.04) different among the three groups, with MI lowest for E+ and greatest for E-/pH- patients. Although not statistically significant, there is a graded increase in median (interquartile range) MI axially along the esophagus at 5\u2009cm (P\u2009=\u20090.20) and at 10\u2009cm (P\u2009=\u20090.27) above the SCJ, with those with reflux (E+ and E-/pH+) having a lower MI than those without.
Answer: Patients with symptoms of EER and evidence of acid reflux have an MI lower than those without at 2 cm above the SCJ, with a trend at 5 cm and 10 cm as well. MI may be a tool to assess presence of GERD in patients presenting with EER symptoms.
answer:
Is esophageal Mucosal Impedance Pattern Distinct in Patients With Extraesophageal Reflux Symptoms and Pathologic Acid Reflux?


question:
Context: Cigarette smoke disrupts the protective barrier established by the airway epithelium through direct damage to the epithelial cells, leading to cell death. Since the morphology of the airway epithelium of smokers does not typically demonstrate necrosis, the most likely mechanism for epithelial cell death in response to cigarette smoke is apoptosis. We hypothesized that cigarette smoke directly up-regulates expression of apoptotic genes, which could play a role in airway epithelial apoptosis.', 'Microarray analysis of airway epithelium obtained by bronchoscopy on matched cohorts of 13 phenotypically normal smokers and 9 non-smokers was used to identify specific genes modulated by smoking that were associated with apoptosis. Among the up-regulated apoptotic genes was pirin (3.1-fold, p < 0.002), an iron-binding nuclear protein and transcription cofactor. In vitro studies using human bronchial cells exposed to cigarette smoke extract (CSE) and an adenovirus vector encoding the pirin cDNA (AdPirin) were performed to test the direct effect of cigarette smoke on pirin expression and the effect of pirin expression on apoptosis.', 'Quantitative TaqMan RT-PCR confirmed a 2-fold increase in pirin expression in the airway epithelium of smokers compared to non-smokers (p < 0.02). CSE applied to primary human bronchial epithelial cell cultures demonstrated that pirin mRNA levels increase in a time-and concentration-dependent manner (p < 0.03, all conditions compared to controls). Overexpression of pirin, using the vector AdPirin, in human bronchial epithelial cells was associated with an increase in the number of apoptotic cells assessed by both TUNEL assay (5-fold, p < 0.01) and ELISA for cytoplasmic nucleosomes (19.3-fold, p < 0.01) compared to control adenovirus vector.
Answer: These observations suggest that up-regulation of pirin may represent one mechanism by which cigarette smoke induces apoptosis in the airway epithelium, an observation that has implications for the pathogenesis of cigarette smoke-induced diseases.
answer:
Is upregulation of pirin expression by chronic cigarette smoking associated with bronchial epithelial cell apoptosis?


question:
Context: This study is to evaluate the effect of high-volume hemofiltration (HVHF) and early goal-directed therapy (EGDT) on alveolar-arterial oxygen exchange in patients with refractory septic shock.', 'Patients were classified into two groups by a prospective cohort study: 86 received both HVHF and EGDT (the HVHF group), and 81 treated with EGDT only (the control group). Alveolar-arterial oxygen pressure was taken at baseline and at days 1, 3, and 7, and respiratory index (RI, ratio of P(a)O2 alveolar-arterial oxygen pressure difference (P(A-a)DO2) to arterial oxygen pressure (P(a)O2) was calculated.', 'At day 7, the levels of central venous and arterial blood oxygen content were significantly higher in the HVHF vs. the control group (both with p < 0.05). The level of oxygen extraction ratio (O2ER) was significantly higher in the HVHF than the control group (p < 0.01). The levels of P(A-a)DO2 and RI were significantly lower in the HVHF than the control group (p < 0.05 and p < 0.01, respectively). RI and the ratio of P(a)O2 to the fraction of inspired oxygen were significantly higher in the HVHF than the control group (p < 0.05 and p < 0.01, respectively). The acute physiology and chronic health evaluation score and the sequential organ failure assessment score in the HVHF group were significantly lower compared to the control group (p < 0.01 and p < 0.05, respectively). At day 28, the mortality rate was lower in the HVHF vs. the control group (p < 0.01).
Answer: These findings demonstrated that HVHF, when used as an adjunctive therapy to the EGDP protocol, could improve alveolar-arterial oxygen exchange, clinical outcome and survival in patients with refractory septic shock.
answer:

Does high-volume hemofiltration combined with early goal-directed therapy improve alveolar-arterial oxygen exchange in patients with refractory septic shock?