ABSTRACT
Objective:By exploring the management of subject complaints by the ethics committee, to identify and correct the problems that damage the rights of subjects in clinical drug trials, in order to improve the ability of the ethics committee of protecting the rights and interests of the subjects.Methods:We conducted a retrospective analysis of 13 cases of subject complaints accepted by the Ethics Committee of Peking University People′s Hospital from January to December 2021, analyzed the causes of complaints, and proposed countermeasures and suggestions.Results:Problems exist in the subject complaints regarding the payment of compensation, investigators′ communication attitude and skills, subjects′ understanding bias, etc.Conclusions:The ethics committee should attach great importance to subject complaints, adopt a closed-loop management process, carry out hierarchical management, strict ethical review, improve the ability of continuous supervision, conduct targeted training for investigators, and provide counseling services for subjects, to improve the communication between investigators and subjects, effectively reduce and avoid the occurrence of complaints. Relevant functional departments of medical and health institutions should work together to protect the rights and interests of the subjects.
ABSTRACT
The application of electronic informed consent has the advantages of speeding up the recruitment of subjects, helping the less educated to understand research and recruit groups, facilitating direct communication between subjects and researchers, minimizing human omissions and errors, and effectively improving the efficiency of clinical research. However, there are also some challenges, such as privacy, ethical censorship, hardware costs and so on. On the basis of the above discussion, this paper believed that electronic informed consent, as a new form, would provide a more powerful tool for clinical research in an era full of opportunities and challenges, with research value and potential.
ABSTRACT
Objective@#To explore the role of lysophosphatidic acid, vascular endothelial growth facor and endothelin in the pathogenesis of pulmonary fibrosis in coal workers’pneumoconiosis patients, the relationship of lysophosphatidic acid, VEGF and ET in serum was studied.@*Methods@#Sixty two pneumoconiosis patients were selected as cases group, which included 23 cases of stage Ⅰ, 25 cases of stageⅡand 14 cases of stageⅢ. Twenty workers were selected as dust exposure group who exposed to coal dust for more than 2 years and had not been diagnosed as pneumoconiosis. Ten healthy people who had no occupational dust exposure were simultaneously selected as the control group. The serum levels of LPA, VEGF and ET were measured by ELISA.@*Results@#The serum levels of VEGF and ET in coal dust exposed group and pneumoconiosis group were much higher than in the control group. The differences were statistically significant among the three groups (P<0.01) . The serum levels of LPA increased in the dust exposed group, stage Ⅰand stage Ⅱgroup. The serum levels of LPA correlated positively with the levels of VEGF and ET (P<0.05) .@*Conclusions@#The serum levels of LPA, VEGF and ET had evident correlation with the pulmonary fibrosis caused by coal dust, which indicate that LPA, VEGF and ET may play a pivotal role in the process of pulmonary fibrosis. The study will throw light on both pathogenesis and early intervention for pneumoconiosis.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the plasma level of extracellular histones in patients with silicosis, and to explore the role of extracellular histones in the pathogenesis of pulmonary fibrosis in silicosis.</p><p><b>METHODS</b>Sixty-two patients with silicosis were enrolled as the silicosis group, consisting of 23 patients with stage I silicosis, 25 with stage II silicosis, and 14 with stage III silicosis; sixty workers who had a history of occupational exposure to silica dust for more than 2 years and had not been diagnosed with silicosis were enrolled as the silica dust exposure group; sixty-five healthy workers without a history of occupational exposure to dust were enrolled as healthy controls. Enzyme-linked immunosorbent assay was applied to measure the plasma levels of plasma extracellular histone (H4) and transforming growth factor-β(TGF-β).</p><p><b>RESULTS</b>Compared with healthy controls [(0.82±0.67) μg/ml], the silica dust exposure group[(4.14±2.85) μg/ml] and silicosis group[(9.50±5.04) μg/ml] had significant increases in plasma level of H4 (P<0.01). The plasma level of H4 was significantly correlated with the stage of silicosis(r=0.8955, P=0.0388). The silicosis group had a significantly higher plasma level of TGF-β than the silica dust exposure group and healthy controls(P <0.05). In the patients with silicosis, the plasma level of H4 was significantly correlated with that of TGF-β(r=0.5375, P<0.01).</p><p><b>CONCLUSION</b>The plasma level of extracellular histones increases significantly in the pathogenesis of silicosis, and extracellular histones may play an important role in the progression of fibrosis in silicosis.</p>
Subject(s)
Humans , Case-Control Studies , Disease Progression , Dust , Histones , Blood , Occupational Exposure , Silicon Dioxide , Silicosis , Blood , Pathology , Transforming Growth Factor beta , BloodABSTRACT
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.