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To evaluate the exported risk of novel coronavirus pneumonia (NCP) from Hubei Province and the imported risk in various provinces across China. Data of reported NCP cases and Baidu Migration Indexin all provinces of the country as of February 14, 2020 were collected. The correlation analysis between cumulative number of reported cases and the migration index from Hubei was performed, and the imported risks from Hubei to different provinces across China were further evaluated. A total of 49 970 confirmed cases were reported nationwide, of which 37 884 were in Hubei Province. The average daily migration index from Hubei to other provinces was 312.09, Wuhan and other cities in Hubei were 117.95 and 194.16, respectively. The cumulative NCP cases of provinces was positively correlated with the migration index derived from Hubei province, also in Wuhan and other cities in Hubei, with correlation coefficients of 0.84, 0.84, and 0.81. In linear model, population migration from Hubei Province, Wuhan and other cities in Hubei account for 71.2%, 70.1%, and 66.3% of the variation, respectively. The period of high exported risk from Hubei occurred before January 27, of which the risks before January 23 mainly came from Wuhan, and then mainly from other cities in Hubei. Hunan Province, Henan Province and Guangdong Province ranked the top three in terms of cumulative imported risk (the cumulative risk indices were 58.61, 54.75 and 49.62 respectively). The epidemic in each province was mainly caused by the importation of Hubei Province. Taking measures such as restricting the migration of population in Hubei Province and strengthening quarantine measures for immigrants from Hubei Province may greatly reduce the risk of continued spread of the epidemic.
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Objective To discuss the effects of polybrominated diphenyl ethers （PBDEs） exposure in e-waste dismantling region on the human body and provide data support for the identification of environmental health damage to residents in the e-waste dismantling region. Methods Adults in an e-waste dismantling region （exposed group, 54 participants） and a control region （control group, 58 participants） were selected, questionnaires were carried out and blood and urine samples were collected. Blood PBDEs, blood lipids, blood routine, blood lead, urine cadmium, urine chromium and urine nickel were detected. T-test was utilized to compare the differences of PBDEs between the two groups. Multivariate analysis were utilized to compare the differences between the two groups in blood routine indexes. Linear regression was used to analyze the relationship between PBDEs and blood routine. Results Exposure levels of PBDEs were significantly higher in the exposed group （240.00 ng/g, adjusted mass fraction of blood lipids, thereafter） than in the control group （93.00 ng/g, P<0.05）. There was no statistical significance in the differences in most blood routine indexes of the two groups （ P>0.05）, and their reference values were all within normal ranges. Mean platelet volume, plateletcrit, basophils percentage, absolute value of basophils, and mean corpuscular hemoglobin concentration were higher in the exposed group than in the control group （P<0.05）. Platelet distribution widths were lower in the exposed group than in the control group and below the normal reference range （P<0.05）. Conclusion PBDEs exposure in e-waste dismantling region tend to change platelet morphology, the number of basophils, and mean corpuscular hemoglobin concentration, and may pose potential health hazards to local residents.
Subject(s)
Adult , Humans , China , Electronic Waste/analysis , Environmental Monitoring , Halogenated Diphenyl Ethers/toxicity , Human BodyABSTRACT
Purpose To investigate the clinicopathological features, the diagnosis and differential diagnosis of spindle cell lipoma/pleomorphic lipoma (SCL/PL). Methods Eight cases of SCL/PL were studied by HE staining and immunohistochemistry. The literature was reviewed. Results Microscopically, the neoplasm consisted of spindle cells, mature adipocytes and thick rope-like collagen bundles in variable proportions with mucinous degeneration. The floret-like multinucleated giant cells were easy to be seen in the pleomorphic lipoma. Immunohistochemical analysis revealed that the tumor cells were positive for CD34 and vimentin. The Ki-67 was approximately 2％. The patients were followed up for 3 ～ 74 months, and no recurrence or metastasis occurred. Conclusion The SCL/PL is a special subtype of benign lipoma, surgery is considered the first choice, and outcome is favorable. The diagnosis and differential diagnosis of SCL/PL are important.
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Purpose To investigate the expression of globular C1q receptor (gC1qR) in ovarian cancer and to explore its potential molecular mechanism.Methods Retrospective analysis was made on 48 ovarian cancer tissues and ovarian cancer cell line SKOV3.Real time PCR and Western blot analysis were applied to detect the levels of gC1qR mRNA and gC1qR protein expression.The abilities of SKOV3 cells proliferation activity and quantity,migration and apoptosis were respectively assessed by M'TT,transwell assay and flow cytometry.Besides,the intracellular ROS was estimated via the fluorescence of H2DCFDA,the mitochondrial membrane potential was tested using a JC-1 probe,and the intracellular Ca2+ was assessed via Fluo-3/AM.Results The expressions of gC1qR gene was obviously decreased in the group of ovarian cancer tissues when compared with normal ovarian tissues group (2.61 ±0.34 vs 7.32 ± 1.25,0.20 ± 0.02 vs 0.67-± 0.06,P ＜ 0.001).Overexpression of gC1qR gene could result in significant up-regulation of ovarian cancer cell apoptosis and down-regulation in proliferation and migration,and showed significant cell apoptosis morphology.Simultaneously,the intracellular ROS and Ca2+ were obviously increased,and the mitochondrial membrane potential was obviously decreased.Conclusion gC1qR gene may play an important role in the apoptosis of ovarian cancer cells.In this process,gC1qR gene can induce apoptosis of ovarian cancer cells by inducing mitochondrial dysfunction.
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Welder's siderosis was traditionally described as "benign pneumoconiosis" because of the absence of associated symptoms, functional impairment or pulmonary fibrosis. Although several authors have reported evidence of fibrosis in the lungs of welders, siderosis with local massive fibrosis has been rarely described. In this paper, we present a case of Welder's siderosis with local massive fibrosis mimicking lung cancer.
Subject(s)
Humans , Male , Middle Aged , Fibrosis , Diagnosis , Diagnostic Imaging , Radiography , Siderosis , Diagnosis , Diagnostic ImagingABSTRACT
<p><b>OBJECTIVE</b>To establish a model of human monocytic leukemia with CNS infiltration in BALB/c nude mice.</p><p><b>METHODS</b>BALB/c nu/nu mice pre-treated by splenectomy, cytoxan intraperitoneal injection, and sublethal irradiation (SCI), were transplanted intravenously with 1 x 10(7) of human monocytic leukemic SHI-1 cells. The leukemic cells engrafted in the mice were detected by RT-PCR, histopathological examination, immunohistochemistry and FCM.</p><p><b>RESULTS</b>The survival time of SCI-nu/nu mice was 33-46 d. Paraplegia occurred in some of the mice. 5 weeks after transplantation, SHI-1 cells engrafted in SCI-nu/nu mice, multi-organs were involved and green solid neoplasms were formed in some organs. Histopathological examination found that SHI-1 cells infiltrated in liver, lung, kidney and testis of the mice and vertebral and skull bone marrow was replaced by leukemic cells. Leukemic cell penetrated through the surface of vertebrae, formed neoplasm, and entered the subdural space, but seldom involved the spinal parenchyma. In brain leukemia cells were filled in the subdural space and pia-arachnoid, covered the surface of cerebrum, cerebellum, spread along the virchow-robin space on the surface of pia mater, and eventually invaded the brain parenchyma.</p><p><b>CONCLUSION</b>SHI-1 cells could engrafted in the SCI-nu/nu mice, form an efficient and reproducible experimental model of CNSL and systematic leukemia. This model may be useful for studying the pathogenesis of CNSL.</p>