[An investigation of occupational exposure to welding fume, manganese, and manganese compounds in a large container manufacturing enterprise].

Objective: To investigate the current status of the occupational hazards of welding fume, manganese, and manganese compounds in the welding environment of a large container manufacturing enterprise, as well as the status of occupational health examination of workers, and to provide a basis for improving the welding environment of this enterprise. Methods: In August 2016, July 2017, and August 2018, convenience sampling was used to perform an on-site occupational hygiene survey of the welding workshop for three consecutive years, and welding fume, manganese and, manganese compounds (counted as manganese dioxide) were measured for their workplace exposure concentrations and exposure levels in workers. A comprehensive analysis was performed for the results of occupational health examination. Results: Welding fume, manganese, and manganese compounds in the welding environment gradually increased from 2016 to 2018 (χ(2)(trend)=5.14 and 5.54, P<0.05). The maximum over-standard rate of concentration-short term exposure limit was 43.3% (13/30) for welding fume and 40.0% (12/30) for manganese and its compounds, and the maximum over-standard rate of time-weighted average concentration was 26.7% (8/30) for welding fume and 23.3% (7/30) for manganese and its compounds. Abnormalities were observed in the occupational health examination of welding workers in 2016-2018, among which respiratory system abnormalities (cough, expectoration, and wheezing), nervous system abnormalities (dizziness, fatigue, sleep disorders, amnesia, hyperhidrosis, and palpitations), and electrocardiogram abnormalities (bundle conduction block) had an incidence rate of above 10.0%, and the incidence rate of abnormalities on posterior-anterior X-ray high-kV chest radiograph was close to 8.9% (30/336) . Conclusion: There is severe exposure to welding fume, manganese, and manganese compounds among workers in this enterprise, which cause great hazards to the health of workers. It is necessary to strengthen occupational health management, take measures to improve the welding environment, and enhance occupational disease prevention.

[Determination of methyl ethyl ketone in urine by headspace gas chromatography].

Objective: To establish a method for determination of methyl ethyl ketone in urine by headspace gas chromatography. Methods: In the urine sample(hereinafter referred to as urine sample), methyl ethyl ketone is pretreated by headspace technology, and a certain amount of head air is injected into the gas chromatograph, separated by capillary column, detected by hydrogen flame ionization detector, and the retention time is qualitative and the peak height is high. Peak area. Results: Good linearity was in the range of 0.01 to 6.0 µg/ml with a regression equation of y=13.316x+0.8497 and γ=0.9997.The minimum detectable concentration of methyl ethyl ketone was 0.01 µg/ml. The range intra-day RSD and inter-day RSD were 2.2%-5.5% and 2.5%-6.1% respectively. Urine samples can be stored for 20 days in the refrigerator at 4 ℃. Conclusion: The method has a high advantage of sensitivity and accuracy, and also easy to operate. Therefore, it is suitable for the determination of methyl ethyl ketone in urine.

[Determination of diethyl phthalate in the air of workplace by gas chromatography].

Objective: To establish a method for the determination of diethyl phthalate by gas chromatography in the air of workplaces. Methods: Diethyl phthalate in the air of workplace was collected throµgh glass fiber filter, eluted with methylbenzene, and detected by gas chromatography coupled with FID detectors. Results: The linear range of diethyl phthalate determined by this method was 14.0~1 400 µg/ml, y=2.09801x-3.66229, and the coefficient correlation was 0.999 99. The detection limit was 1.10 µg/ml, and the minimum detection concentration was 0.18mg/m(3) (collected sample volume was 30 L) . The within-run precisions were 1.04%~2.75%, and the between-run precisions were 0.34%~1.30%. The recovery rates were 98.72%~103.21%, and sampling efficiency was 97.2%~100.0%. The elution efficiencies were 97.25%~98.68%. The samples could be stored at room temperature for 15 days. Conclusion: The indicators established in this study were conformed with the requirements of GBZ/T210.4-2008, "The Guidelines for the Development of Occupational Hygiene Standards Methods Part 4: Determination of Chemical Substances in the Air of Workplaces" . Diethyl phthalate in the workplace air could be rapidly collected, accurate separated and determinated. This method is applicable to the determination of diethyl phthalate in the workplace air.

[Determination of tributyl phosphate in the air of workplace by gas chromatography].

Objective: To establish a practical method forsampling and detectingtributyl phosphate intheworkplace. Methods: The samples were extracted by glass fiber membrane, eluted with ether, separated by gas chromatography, and detected by flame photometric detector. Results: There were good linear relationship in the minimum detection concentration was 7.2-720.0 µg/ml, and the correlation coefficient was 0.999 92. The detection limit was 0.86 µg/ml, and the minimum detection concentration was 0.14 mg/m(3) (sample volume was 30 L) . Recovery rates were 99.8%-100.2%. The with-in relative standard deviations were 4.0%-5.4% and the between relative standard deviations were 2.0%-5.5%, and average samplingefficiency was about 99.1%-100.0%. Conclusion: This method conforms with the requirements of "Standardization of Methods for Determination of Toxic Substance in Workplace" . Tributyl phosphate in air could be determined accurately using this method.

Zhi-Long-Huo-Xue-Tong-Yu modulates mitochondrial fission through the ROCK1 pathway in mitochondrial dysfunction caused by streptozotocin-induced diabetic kidney injury.

Zhi-Long-Huo-Xue-Tong-Yu (ZLHXTY) is a defined mixture of 5 herbs developed by Professor S.J. Yang according to the Buyang Huanwu decoction method, which has been recorded in the Yilingaicuo. This study investigated the renoprotective effects of ZLHXTY on mitochondrial dysfunction induced by diabetic kidney injury in a diabetic rat model. Diabetes was induced by a single intravenous injection of streptozotocin. Rats were daily fed either ZLHXTY or vehicle beginning in the 1st week after injection. Levels of mitofusin 2 (mfn2), dynamin-related protein 1 (Drp1), caspase-9, and rho-associated, coiled-coil-containing protein kinase 1 (ROCK1) were detected using Western blotting. Levels of intracellular calcium and adenosine triphosphate (ATP) were examined using an enzyme-linked immunosorbent assay. An electron microscopic examination of kidney tissue was performed. The levels of mfn2 and ATP in the diabetes and ZLHXTY groups decreased from the 4th week after modeling. The expression levels of Drp1, ROCK1, and caspase-9 increased in the diabetes group but decreased in the ZLHXTY group from the 4th week after modeling. Compared with the diabetes group, ZLHXTY treatment decreased the mesangial expansion index and proteinuria levels, and improved the pathological changes typical of diabetic kidney injury. Furthermore, ZLHXTY treatment inhibited the activation of ROCK1 and expression of Drp1 and caspase-9, but did not affect the expression of mfn2. This study indicates that ZLHXTY treatment could protect kidney tissue from diabetic injury through the ROCK1 pathway response to mitochondrial dysfunction induced by diabetes.

Novel PRRT2 mutations in paroxysmal dyskinesia patients with variant inheritance and phenotypes.

Paroxysmal dyskinesias (PDs) are a group of episodic movement disorders with marked variability in clinical manifestation and potential association with epilepsy. PRRT2 has been identified as a causative gene for PDs, but the phenotypes and inheritance patterns of PRRT2 mutations need further clarification. In this study, 10 familial and 21 sporadic cases with PDs and PDs-related phenotypes were collected. Genomic DNA was screened for PRRT2 mutations by direct sequencing. Seven PRRT2 mutations were identified in nine (90.0%) familial cases and in six (28.6%) sporadic cases. Five mutations are novel: two missense mutations (c.647C>G/p.Pro216Arg and c.872C>T/p.Ala291Val) and three truncating mutations (c.117delA/p.Val41TyrfsX49, c.510dupT/p.Leu171SerfsX3 and c.579dupA/p.Glu194ArgfsX6). Autosomal dominant inheritance with incomplete penetrance was observed in most of the familial cases. In the sporadic cases, inheritance was heterogeneous including recessive inheritance with compound heterozygous mutations, inherited mutations with incomplete parental penetrance and de novo mutation. Variant phenotypes associated with PRRT2 mutations, found in 36.0% of the affected cases, included febrile convulsions, epilepsy, infantile non-convulsive seizures (INCS) and nocturnal convulsions (NC). All patients with INCS or NC, not reported previously, displayed abnormalities on electroencephalogram (EEG). No EEG abnormalities were recorded in patients with classical infantile convulsions and paroxysmal choreoathetosis (ICCA)/paroxysmal kinesigenic dyskinesia (PKD). Our study further confirms that PRRT2 mutations are the most common cause of familial PDs, displaying both dominant and recessive inheritance. Epilepsy may occasionally occur in ICCA/PKD patients with PRRT2 mutations. Variant phenotypes INCS or NC differ from classical ICCA/PKD clinically and electroencephalographically. They have some similarities with, but not identical to epilepsy, possibly represent an overlap between ICCA/PKD and epilepsy.

The role of programmed cell death in streptozotocin-induced early diabetic nephropathy.

The mechanism of autophagy in diabetic nephropathy (DN) is still unclear. The study was performed on streptozotocin (STZ) rats to investigate whether programmed cell death contribute to the pathogenesis and progression of DN. STZ rats were induced by an single intravenous injection of STZ dissolved in citrate buffer, early DN (E-DN) for STZ rats was defined as the stage from modeling to the end of the 8th week according to previous studies. A total of 36 male Sprague-Dawley rats were randomly divided into two groups: an E-DN group and a control group. After the 1st, 4th, and 8th week, the rats were sacrificed. Beclin1 and microtubule associated protein 1 light chain 3 (LC3) were examined, apoptosis level in renal tissue was detected by Tunnel assay detected as the apoptotic index. An electron microscopic examination of kidney tissues was performed at end of the 4th and 8th week. Compared with the control group, Beclin1 expression increased since the 1st week after modeling in STZ rats kidney and peaked at the end of the 8th week in western blotting and immunohistochemical stain. Meanwhile the level of LC3-II in DN group was significantly lower from the end of the 1st to the 8th week. A small amount of autophagosomes were observed in both E-DN group and control group under electron microscopic examination, and there was no significant difference between the groups. These findings indicate that an abnormality on autophagy may play an important role in the pathogenesis of E-DN.