Relationship between quality of life and disability level in patients with occupational disease / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the relationship between the quality of life (QOL) and disability level in patients with occupational disease and to investigate the influencing factors for QOL.</p><p><b>METHODS</b>A total of 255 patients with occupational disease were selected from three specialized hospitals dedicated to occupational disease and the department of occupational medicine of one comprehensive hospital using cluster sampling from December 2013 to May 2014. A survey was carried out using WHOQOL-BREF and general questionnaire (including disability level), and statistical analysis was also performed using t test, F test, analysis of variance, and multivariate stepwise regression analysis.</p><p><b>RESULTS</b>The QOL scores of patients with occupational diseases, from high to low, were social domain (11.48 ± 2.86), psychological domain (10.60 ± 2.28), physiological domain (10.54 ± 1.65), and environmental domain (10.50 ± 2.55), scores of which were significantly lower than the normal levels (P<0.05). QOL showed no significant differences between patients with occupational diseases of different disability levels (P>0.05). Also, QOL showed no significant differences between stage I, II and III patients with pneumoconiosis (P>0.05). The patients with pneumoconiosis were divided into mild, moderate, and severe groups, and the QOL scores of patients with mild pneumoconiosis in psychological and environmental domains were significantly higher than those of the patients with moderate or severe pneumoconiosis (P< 0.05). Patients with occupational poisoning was divided into mild, moderate and severe groups, and the three groups showed no significant differences in QOL score (P>0.05). Multivariate regression analysis showed that the QOL score of each domain was mainly influenced by the degree of lung injury, complications, course of disease, age of onset, income, and employment status.</p><p><b>CONCLUSION</b>The QOL of patients with occupational disease is significantly reduced, and disability level cannot accurately reflect their QOL. The treatment of patients with occupational disease should focus on their complications, and at the same time QOL should also be improved.</p>

Adenosine alleviates hypoxia-induced rat right ventricular hypertrophy through the NHE-1/CaN signal pathway / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the effect of adenosine and its agonist on hypoxia-induced right ventricular hypertrophy (RVH) and explore the underlying mechanism.</p><p><b>METHODS</b>Fifty-six rats were randomly divided into normoxia group, hypoxia group, and treated hypoxia groups (with different treatments with adenosine, A1 receptor agonist CPA, A2 receptor agonist NECA, CPA plus A1 receptor inhibitor DPCPX, or NECA plus A2B receptor inhibitor MRS1754). The rats except for those in normoxia group were exposed to normobaric chronic hypoxia (9.5%-10.5% oxygen) for 21 days, and the corresponding treatments were administered since the 7th day of hypoxia till day 21 via implantable capsule with a pressure pump. After the treatments, the right ventricles were then removed and weighed for evaluation of hypertrophy, and the expressions of NHE-1 and CnAβ mRNA in the myocardial tissue were detected using RT-PCR.</p><p><b>RESULTS</b>After a 21-day hypoxia, the rats showed significantly increased RV/(LV+S) ratio (0.369∓0.033) and RV/BW ratio (0.75∓0.095) compared to those in normoxia group (0.271∓0.010 and 0.59∓0.039, respectively; P<0.001), adenosine treatment group (0.281∓0.022 and 0.65∓0.077, respectively; P<0.001, P=0.025), hypoxia with CPA group (0.313∓0.021 and 0.66∓0.067, respectively P<0.001), and hypoxia with NECA group(0.333∓0.019, and 0.68∓0.074, respectively P<0.001). The NHE-1 and CnAβ mRNA levels in hypoxia group were significantly higher than those in normoxia group, adenosine treatment group, hypoxia with CPA group, and hypoxia with NECA group(P<0.001).</p><p><b>CONCLUSION</b>Adenosine and its agonist can inhibit hypoxia-induced RVH in rats through the NHE-1/CaN signal pathway.</p>