Network pharmacology study of Gardeniae Fructus in regulating ferroptosis for the treatment of cerebral ischemia-reperfusion injury / 中国药师

Objective To investigate the molecular mechanism of Gardeniae Fructus regulating ferroptosis in the treatment of cerebral ischemia-reperfusion injury(CIRI)by network pharmacology methods.Methods The effective active ingredients of Gardeniae Fructus and their predicted targets were obtained from the TCMSP database.Cerebral ischemia-reperfusion injury were collected and obtained from the GeneCards database.The active ingredients of Gardeniae Fructus and the intersection genes of CIRI injury were obtained through Venny.The Cytoscape 3.9.1 software was utilized to construct a relationship network among Gardeniae Fructus,its active components and predicted targets.The gene ontology(GO)enrichment and the Kyoto encyclopedia of genes and genomes(KEGG)analyses of the"gardenia-CIRI"intersection genes were performed using R software.The ferroptosis-related genes were obtained from the FerrDb database,and the common targets among the active components of Gardeniae Fructus,CIRI and ferroptosis were comprehensively analyzed to predict the effective components and targets involved in the regulation of ferroptosis in the context of CIRI.Results Sixty-five active components with corresponding gene targets were identified from Gardeniae Fructus,and the correlating prediction was conducted.HIF-1α,TP53,MAPK8,HMOX1,NOS2,RELA and IL-6 were identified as potential targets of Gardeniae Fructus in regulating ferroptosis and preventing cerebral ischemia-reperfusion injury.KEGG analysis suggested that Gardeniae Fructus may mediate HIF-1,TNF,MAPK and Toll-like receptor signaling pathways to regulate the ferroptosis process,thus exerting therapeutic effects on CIRI.Conclusion Gardeniae Fructus may treat cerebral ischemia-reperfusion injury by regulating the ferroptosis pathway.

Analysis of 1 case of convulsion death caused by large dose of diquat poisoning / 中华劳动卫生职业病杂志

A retrospective analysis of a case of death from sudden convulsions caused by oral high-dose diquat was conducted, and the mechanism and treatment of central damage caused by diquat were investigated to lay the foundation for increasing the success rate of treatment of high-dose diquat poisoning. At the same time, at the same time, our clinical treatment experience has also been accumulated.

Association of vitamin D receptor gene haplotypes and genotype combinations with susceptibility to occupational elevated blood lead / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the association of the haplotypes and genotype combinations of vitamin D receptor (VDR) BsmI (rs1544410), Tru9I (rs757343), ApaI (rs7975232), and TaqI (rs731236) with the susceptibility to elevated blood lead in Chinese Han population.</p><p><b>METHODS</b>According to Diagnostic Criteria of Occupational Chronic Lead Poisoning (GBZ 37-2002) and Occupational Exposure Limits for Hazardous Agents in the Workplace Part 1: Chemical Hazardous Agents (GBZ 2.1-2007), the workers were divided into high-exposure group (lead dust ≥ 0.05 mg/m(3), lead fume ≥ 0.03 mg/m(3)) and low-exposure group based on the concentrations of lead fume and lead dust in the workplace. The high-exposure group was further divided into normal-blood lead subgroup and high-blood lead subgroup. Fasting peripheral venous blood (5 ml) was collected using a heparin tube; genomic DNA was extracted from the peripheral blood cells with a Qiagen kit; single nucleotide polymorphisms were detected by allelic discrimination assay using TaqMan probes (carrying fluorescent dyes); haplotypes were analyzed and compared by Haploview.</p><p><b>RESULTS</b>VDR BsmI, Tru9I, ApaI, and TaqI were in Hardy-Weinberg equilibrium between the normal-blood lead subgroup and high-blood lead subgroup (P > 0.05). Compared with haplotype CCCA which had the highest distribution frequency, haplotypes CCAA and CTCA were the high-risk factors for elevated blood lead (OR = 1.814, 95%CI = 1.055 ∼ 3.119; OR = 1.919, 95%CI = 1.040 ∼ 3.540). Compared with genotype combination CC + CC + CC + AA which had the highest distribution frequency, genotype combination CC + CC + AC + AA was the high-risk factor for elevated blood lead (OR = 2.800, 95%CI = 1.282 ∼ 6.116).</p><p><b>CONCLUSION</b>As for VDR BsmI, Tru9I, ApaI, and TaqI, haplotypes CCAA and CTCA and genotype combination CC + CC + AC + AA are associated with the susceptibility to elevated blood lead.</p>

Hepatocyte growth factor combined with autologous bone marrow mesenchymal stem cell transplantation for treatment of silicosis / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To evaluate the potential role of hepatocyte growth factor (HGF) combined with bone marrow mesenchymal stem cells (BMSC) autograft for the treatment of silicosis.</p><p><b>METHODS</b>Bone marrow (100 ml) was aspirated from a severe silicosis patient. BMSCs isolated, purified and cultured in vitro. When BMSC came to 70% confluence at passage 3, the culture medium was added liposomes (lipo2000) and plasmid-HGF (p-HGF) and cultured for 2 d. HGF-MSCSs (5 × 10(7) cells) were resuspended in 50 ml 0.9% sodium chloride (NS) and infused Intravenous drip at 3 consecutive times (once a week). Clinical follow-up were performed before and after treatment: (1) pulmonary high-kV X-ray, chest CT examination; (2) pulmonary function test; (3) determination of serum ceruloplasmin.</p><p><b>RESULTS</b>The symptoms such as coughing, chest tightness disappeared at 12 months after treatment. Pulmonary function tests showed significant changes after treatment: forced vital capacity (FVC) increased from 64.6% to 81.0%, forced expiratory volume in one second (FEV(1.0)) increased from 68.7% to 90.1%, 1 second rate (FEV(1.0)/FVC%) reduced from 111.6% to 107.1%, the maximum mid-expiratory flow (FEF(25%∼75%) decreased from 100.2% to 94.6%, forced expiratory vital capacity 75% of the moment bit of gas flow (MEF(75%)) increased from 99.2% to 113.5%, forced expiratory vital capacity 50% of the moment bit of gas flow (MEF(50%)) increased from 125.3% to 130.2%, forced expiratory vital capacity 25% of the moment bit of gas flow (MEF(25%)) reduced from 86.9% to 71.7%; serum ceruloplasmin levels decreased from 690 mg/L to 180.6 mg/L; lung high-kV X-ray at 1st review showed that diffuse lung nodules had been absorbed and getting smaller than before treatment; chest CT showed that the distribution and number of small nodules at double lung fields decreased than before treatment.</p><p><b>CONCLUSION</b>HGF combined with BMSC transplantation may have some potential role for the treatment of silicosis patients.</p>

Cytotoxicity of dichloroacetic acid in lymphocyte and expression of chemokine receptor CXCR2 and chemokine receptor CXCR3 mRNA / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To explore the effects of trichloroethylene (TCE) and its by-products (trichloroacetic acid, TCA; dichloroacetic acid, DCA) on the normal human peripheral blood lymphocyte and the role of DCA in dermatitis medicamentosa- like induced by trichloroethylene (DMLT).</p><p><b>METHODS</b>Lymphocyte was isolated from peripheral venous blood, and cytotoxicity of human lymphocytes treated with different concentrations (0.02 approximately 30.00 mmol/L) of DCA was determined at indicated times (2 h and 4 h) based on the MTS assay. Action of DCA on cell viability, membrane integrity was assessed by neutral red uptake (NRU) assay and lactate dehydrogenase (LDH) release test and measurement of superoxide dismutase (SOD) activity. Fluorescence quantitative reverse transcription polymerase chain reaction (FQ-RT-PCR) was employed for detection and quantization of the chemokine receptor CXCR2 and chemokine receptor CXCR3 mRNA in peripheral blood lymphocyte treated with different concentrations of DCA.</p><p><b>RESULTS</b>DCA had a more vital effect on peripheral blood lymphocyte than TCE and TCA. A concentration-dependent release of LDH was observed at 4 h after cells were exposed to different doses of DCA (0.88, 1.75, 3.50 and 7.00 mmol/L) (P < 0.05), and DCA also caused an inhibition of SOD activity in a concentration-dependent manner (P < 0.05). The results of FQ- RT- PCR indicated that CXCR2 and CXCR3 mRNA were all over- expression. At 48 h after the DCA of 0.5 mmol/L and 10.00 mmol/L was used, CXCR2 and CXCR3 mRNA were 10.34, 5.66-fold and 19.43, 8.75-fold of those in the control group (P < 0.01).</p><p><b>CONCLUSION</b>DCA is of a great cytotoxicity and may be one of crucial evocators on DMLT.</p>

Clinical manifestation and influential factors in patients with acute arsenic poisoning / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the clinical characteristics of acute arsenic poisoning and its influential factors.</p><p><b>METHODS</b>Clinical data of 47 cases of arsenic poisoning were collected and analyzed. Two cases of observation, 40 cases of mild acute poisoning, and 5 severe acute poisoning were investigated in this group.</p><p><b>RESULTS</b>Myocardial enzyme activity was correlated with age and urine arsenic concentrations. Myocardial enzyme, the liver ALT, total bilirubin (TBil) and indirect bilirubin (IBil) were negatively correlated with vomiting frequency, with statistical significance (P < 0.05). Urine arsenic concentration was correlated with vomiting frequency and amount of soup drunk, with statistically significant difference (P < 0.05). Despite no statistical significance in age and amount of soup drunk, the patients with more vomiting or diarrhea had less urine arsenic concentrations, cardiac enzymes and liver enzyme concentration.</p><p><b>CONCLUSION</b>Acute arsenic poisoning can lead to multiple organ damage. The damage is relevant with amount of arsenic intake, vomiting, diarrhea and urinary frequency arsenic concentration. So early use of gastric lavage, vomiting, poison discharges, and adequate application of effective antidote (Na-DMPS) as soon as possible, symptomatic treatment and the reinforced monitoring, are the rescue key for patients with acute arsenic poisoning.</p>

Effects of lead exposure on thymic output naive T cells function / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the levels of T cell receptor rearrangement excision DNA circles (TRECs) within peripheral blood from workers exposed to lead, and thereby to evaluate the number of naive T cells and recent thymic output function.</p><p><b>METHODS</b>Quantitative detection of TRECs in peripheral blood mononuclear cells (PBMNC) from 10 cases of workers exposed to lead was performed by real time PCR analysis. 11 workers without exposure to lead served as unexposed controls. In addition, the relationship between TRECs, age, length of service, blood lead, urea lead, blood ZPP and urea delta-ALA was investigated.</p><p><b>RESULTS</b>The mean value of TRECs in workers exposed to lead was (2.44 +/- 1.87)/1000 PBMC, significantly under (5.60 +/- 3.96)/1000 PBMC in unexposed controls. A significant negative correlation was found between the TRECs and urea-ALA. But there was no significant correlation between them after controlling for blood lead, urea lead.</p><p><b>CONCLUSION</b>Lead exposure may damage thymic output naive T cells function. Furthermore, low-level exposure to lead may damage immune system and earlier than expected.</p>

Clinical experiment of cytokines induced killer cells for treatment of benzene poisoning / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To assess the reaction of cytokines induced killer (CIK) cells treatment in hematopoietic injury at different levels on patients with benzene poisoning and seek a novel, safe and effective immunotherapy for benzene poisoning.</p><p><b>METHODS</b>CIK cells were in vitro activated by interleukin-2 (IL-2) and granulocyte-macrophage-colony-stimulating factor (GM-CSF) from the peripheral blood mononuclear cells (PBMC). Thirty-two patients with benzene poisoning were treated with CIK cells. Nineteen patients with mild or moderate benzene poisoning in the control group were treated with VitB4, batilol, leucogen, inosine and stanozolol. The results for treatment of 12 patients with aplastic anemia induced by severe benzene poisoning (the efficacy rate and the case fatality rate) were analyzed. The change of T-lymphocyte subset analyzed by flow cytometry was also observed before and after treatment.</p><p><b>RESULTS</b>For mild or moderate benzene poisoning, the increase of WBC and RLT in CIK group was higher than that in the control group (P < 0.05). The CD(4)/CD(8) levels were significantly increased after CIK treatment. And for severe benzene poisoning, the effective rate of the CIK group was 91.7% and the mortality rate was 0%.</p><p><b>CONCLUSION</b>CIK treatment is safe and effective for hematopoietic injury caused by benzene poisoning. The mechanism may be related with the immune modulation of CIK treatment on immunodeficiency of patients with benzene poisoning.</p>