ABSTRACT
OBJECTIVE: To study the literature characteristics and research status of occupational hand-arm vibration disease in China. METHODS: Literature information on occupational hand-arm vibration disease published before 2018 in China were searched and collected through the China National Knowledge Infrastructure(CNKI) and Wanfang Database. The bibliometrics was used to analyze the publication time, type, journal sources, authors and their institutions, citation situation, funds and high-frequency key words. RESULTS: From 1975 to 2018, a total of 349 papers on occupational hand-arm vibration disease were published. The main article type was monograph, with a total of 179 articles(accounting for 51.3%). The articles were distributed in 79 kinds of journals, among them, 10 journals including China Occupational Medicine and Industrial Health and Occupational Diseases were the main carriers to publish related articles(237 papers, accounting for 67.9%). The main research institutions of the literature were Jining Medical College and Guangdong Province Hospital for Occupational Disease Prevention and Treatment, with 134 papers(accounting for 38.4%) published. Among the 5 core authors of the literature, 4 were from the above 2 research institutions. A total of 121 articles(accounting for 34.7%) were cited, and 77 articles(accounting for 22.1%) were supported by research fund. The top 3 high-frequency key words used were arm vibration disease, hand-transmitted vibration/local vibration and occupational disease. CONCLUSION: Occupational hand-arm vibration disease has attracted the attention of Chinese researchers, however, follow-up research, literature quality and funding support still need to be improved.
ABSTRACT
Objective@#In order to explore the role of heparan sulfate (HS) during the pathogenesis of acute respiratory distress syndrome (ARDS) , the protective effect of HS and its fragments against extracellular histones was compared.@*Methods@#Calf thymus histones (CTH) were injected via femoral vein to induce ARDS in rats. HS, HS fragments or saline was intraperitoneally injected (10mg/kg, Q6h, 24h) to test the protective effect against CTH. The ratio of wet/dry lung weight, protein content in bronchoalveolar lavage fluid (BALF) , total leukocyte and neutrophil count in BALF were measured.@*Results@#After CTH injection, the ratio of wet/dry lung weight (5.7±0.95) was much higher than the saline control group (3.1±0.15). The protein content (0.47±0.086mg/ml) , total leukocyte[ (97.4±15.6l) ×104/ml] and neutrophil (18±3.4/LPF) in BALF were obviously increased compared with the saline control group. The intervention of HS evidently decreased ratio of wet/dry lung weight (4.2±0.41) , protein content[ (0.26±0.019) mg/ml], leukocyte[ (61.3±5.74) ×104/ml] and neutrophil (12±1.8/LPF) in BALF. HS fragments also decreased ratio of wet/dry lung weight, protein content, leukocyte and neutrophil count in BALF though the strength was much less than HS.@*Conclusion@#HS and its fragments could provide protection against extracellular histones during the pathogenesis of ARDS. For the protective effect full length HS was much better than HS fragments.
ABSTRACT
Objective@#To investigate the effect of baicalin on the changes in hemorheology and its mechanism during the development of Acute Respiratory Distress Syndrome(ARDS) induced by oleic acid (OA) in rats.@*Methods@#Rats were randomized into 3 groups: control, ARDS (OA induction, 0.12 mg/kg) and ba-icalin-treated group (300 mg/kg). The blood samples were collected at 30 min, 1, 2, 3, 6, 12 and 6 h after OA injection. The whole blood viscosity, plasma viscosity, Maximum erythrocyte deformability index (DImax) were detected. Meanwhile, blood gas analysis and Routine blood test were also performed.@*Results@#The level of arte-rial oxygen partial pressure and oxygenation index decreased (P<0.01 vs. control) and oxygenation index (178 mm Hg, 1 mm Hg=0.133 kPa) reached the diagnostic standard of ARDS at 2 h in ARDS group. In baicalin-treated group, the level of arterial oxygen partial pressure and oxygenation index increased versus the ARDS group. The platelet count (PLT) decreased in baicalin-treated and ARDS groups. Compared with the ARDS group, the level of PLT increased significantly in baicalin-treated group at 30min, 1, 2, and 3 h. Hematocrit (HCT) increased in baicalin-treated and ARDS groups. Compared with the ARDS group, the level of HCT de-creased significantly in baicalin-treated group at 2, 3, 6 and 12 h. Meanwhile, all the index of hemorheology improved in baicalin-treated group.@*Conclusion@#Baicalin may improve hypoxemia of ARDS induced by OA in rats. It may be due to the Improvement of microcirculation of lung.
ABSTRACT
Objective To investigate whether chlorophyllin could protect human umbilical vein endothelial cell (HUVEC) against oxidative damage by inducing the expression of heme oxygenase-1 (HO-1) and to explore the underlying mechanism.Methods The cellular protection of chlorophyllin against oxidative damage was detected by cell-survival assay with flow cytometry.The level of free radicals was detected directly by electron spin resonance spectra.The induced expression of HO-1 was shown by RT-PCR,Western blot,immunofluorescence confocal laser microscopy and enzymatic activity test.Whether the activation of PI3K/Akt pathway was involved was detected by Western blot.Results Chlorophyllin could protect HUVEC against oxidative damage caused by H2O2 via scavenging the excessive free radicals.Chlorophyllin treatment could induce expression of HO-1 in a dose- and time-dependent manner.The activation of PI3K/Akt pathway was required in the induction of HO-1.LY294002,the specific inhibitor of PI3K,could suppress the activation of PI3K/Akt and the induced expression of HO-1 in a dose-dependent manner.Conclusions Chlorophyllin shows cellular protection against oxidative damage by counteracting the excessive free radicals.Up-regulation of HO-1 expression plays a pivotal role in the protection of chlorophyllin,while the activation of PI3K/Akt signaling pathway is required in the induction of HO-1.