TASK DEFINITION: Given a passage classify if the passage has a definite objective/aim/goal or not. Output '1' if the passage has a defininte objective/aim/goal and output '0' if the passage does not have a definite objective/aim/goal.
PROBLEM: Lung inflation causes cardiovascular suppression via an increase in intrathoracic pressure and neural mechanisms. To examine the mechanisms involved, we mea-sured the heart rate (HR) and arterial blood pressure (AP) responses to lung inflation before and after spraying the bronchi with lidocaine to suppress airway reflex. Thirty women participated in the study. One group (n = 20, Group BT) had their tracheas intubated by using double-lumen tubes. The other group (n = 10, Group TT) received an ordinary endotracheal tube. They were all studied under general anesthesia by using nitrous oxide, isoflurane, and muscle relaxation after a thiopental induction. In each patient, airway pressure was increased for 3 s, and changes in HR and AP were measured. Lung inflation was repeated after 5 mL of 4% lidocaine had been sprayed into the main bronchi unilaterally in Group BT or bilaterally in Group TT. There were no significant differences in cardiovascular responses between left and right lung inflation with the pressure at 20 and 30 cm H(2)O. Both lungs inflated at 20 cm H(2)O caused an increase in HR with a significantly greater decrease in AP than with unilateral inflation. Anesthesia of the bronchi abolished the HR increase, but not the AP decrease. Lung inflation at 30 cm H(2)O caused significant decreases in HR and AP which were not affected with topical anesthesia. These results indicate that the cardiovascular responses elicited by lung inflation in anesthetized humans are predominantly the direct effect of the increase in intrathoracic pressure, although sympathetic afferent activity induced via stimulation of mechanoreceptors in the airways contributes.

SOLUTION: 0

PROBLEM: Patients with frequent premature ventricular complexes (PVCs) might be at risk for the developing or exacerbation of left ventricular (LV) dysfunction. However, some patients with a high-PVC burden do not develop cardiomyopathy, while other patients with low-PVC burden can develop cardiomyopathy. The purpose of this study was to evaluate the positive predictors of idiopathic PVCs-induced cardiomyopathy.', 'We investigated 214 patients undergoing successful ablation of PVCs who had no other causes of cardiomyopathy. We divided the study cohort into 2 groups: ejection fraction (EF) ≥ 50% (normal LV) and EF < 50% (LV dysfunction). We analyzed the clinical characteristics, including the electrocardiogram and findings at electrophysiology study. Among these patients, 51 (24%) had reduced LVEF and 163 (76%) had normal LV function. Patients with LV dysfunction had significantly longer coupling interval (CI) dispersion (maximum-CI-minimum-CI) and had significantly higher PVC burden compared to those with normal LV function (CI-dispersion: 115 ± 25 milliseconds vs. 94 ± 19 milliseconds; P < 0.001; PVC burden: 19% vs. 15%; P = 0.04). Furthermore, patients with LV dysfunction had significantly higher body mass index (BMI) compared to those with normal LV function (BMI > 30 kg/m(2) ; 37% vs. 13%; P = 0.001). Logistic regression analysis showed that CI-dispersion, PVC burden, and BMI (>30\xa0kg/m(2) ) are independent predictors of PVC-induced cardiomyopathy.

SOLUTION: 0

PROBLEM: Ulcerative colitis and Crohn's disease frequently cause epithelial damage in the intestine, leading to gut inflammation accompanied by areas of ulceration. The regeneration of damaged mucosa as well as the restoration of intestinal homeostasis involve induced and coordinated proliferation and migration of intestinal epithelial cells. Commensal bacterial colonization of the intestine is essential for normal intestinal development, renewal, and repair. N-formyl peptide receptors (FPRs) are widely expressed pattern recognition receptors that can specifically bind and induce responses to host-derived and bacterial peptides and small molecules during repair of mucosal injury in a redox dependent manner. However, little is known about the host-microbiota crosstalk mediated by FPRs during repair of gut mucosal injuries. Herein, purpose of this study is to exploit the mechanism of mucosal healing promoted by a consortium of gut microbiota that preferentially colonizes ulcerated mucosa undergoing resealing.", 'The regeneration of injured epithelial was studied using defined mechanical wounds inflicted in the mouse distal colon by employing a miniature endoscope and forceps. Microbiota studies were performed by high throughput sequencing of the V4 region of 16s rRNA gene of the bacteria harvested from mucosal wounds undergoing different stages of regenerative events.', 'The high throughput sequencing analysis of bacterial 16s rDNA determined rapid, reversible spatiotemporal alterations in the composition and diversity of microbiota in the wound microenvironment. Our data demonstrated that these ecological changes are dependent on FPR1/NOX2-mediated local tissue hypoxia, depletion of muc2 mucin, and compensatory effect of the over expression of HIF1-regulated MUC3 mucin. Our data show that these events of mucosal regeneration enrich a dominant member of this wound-associated consortium, Akkermansia muciniphila, which is associated with the pro-restitutive function. A. muciniphila, an anaerobic, mucinophilic commensal bacterium, enhanced proliferation and migration of enterocytes adjacent to the colonic wound beds in a process involving FPR1/NOX1 dependent redox signaling.

SOLUTION:
0