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.
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Question: Human cases of hypersensitivity pneumonitis (HP) have been reported among machinists for over 10 yr. Although mycobacteria have been implicated as causal agents, this has not been established in experimental studies and the mechanisms remain unclear. Other constituents of in-use metalworking fluids (MWFs) may also contribute to the development of lung disease. We investigated the potential for Mycobacterium immunogenum (MI) in MWFs to induce HP.', 'Mice were exposed intranasally for 3 wk to MI (isolated from MWFs), Saccharopolyspora rectivirgula (positive control), saline, endotoxin, MWFs spiked with endotoxin and/or MI, used MWFs, and particulate-fortified used MWFs. Responses were assessed 96 h after the last exposure.', 'Mice exposed to MI in MWFs developed lung pathology consistent with HP along with significantly more monocytes and neutrophils in lung lavage, increased CD4+/CD8+ T-lymphocyte ratio, and marked pulmonary lymphocytosis on histologic examination when compared with saline-treated control mice. Mice with Grade 2 or higher pathology (0-4 point scale) exhibited significantly elevated macrophage inflammatory protein-1alpha and IL-10 and a trend toward higher RANTES 96 h after the final dose. Endotoxin coexposure augmented lung pathology.

Answer: 0


Question: 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.

Answer: 0


Question: Cigarette smoking is a major risk factor for atherosclerotic cardiovascular disease, which is responsible for a significant proportion of smoking-related deaths. However, the precise mechanism whereby smoking induces this pathology has not been fully delineated. Based on observation of DNA double-strand breaks (DSBs), the most harmful type of DNA damage, in atherosclerotic lesions, we hypothesized that there is a direct association between smoking and DSBs. The goal of this study was to investigate whether smoking induces DSBs and smoking cessation reverses DSBs in vivo through examination of peripheral mononuclear cells (MNCs).', 'Immunoreactivity of oxidative modification of DNA and DSBs were increased in human atherosclerotic lesions but not in the adjacent normal area. DSBs in human MNCs isolated from the blood of volunteers can be detected as cytologically visible "foci" using an antibody against the phosphorylated form of the histone H2AX (γ-H2AX). Young healthy active smokers (n = 15) showed increased γ-H2AX foci number when compared with non-smokers (n = 12) (foci number/cell: median, 0.37/cell; interquartile range [IQR], 0.31-0.58 vs. 4.36/cell; IQR, 3.09-7.39, p<0.0001). Smoking cessation for 1 month reduced the γ-H2AX foci number (median, 4.44/cell; IQR, 4.36-5.24 to 0.28/cell; IQR, 0.12-0.53, p<0.05). A positive correlation was noted between γ-H2AX foci number and exhaled carbon monoxide levels (r = 0.75, p<0.01).

Answer:
1