Objective To investigate the cause of an outbreak that with fever,chest tightness,cough as the main symptoms in a production enterprise of solar cells,and to provide suggestrons for the on -site disposal and preventing of re -issued. Methods Clinical features and epidemiological characteristics of the cases were analyzed.The workplaces and treatment of industrial wastes were investigated.Legionella in the throat swab sample and residual water during the processes were detected.Simulation test for poisonous gas from waste incineration was performed using a portable GC -MS detector. Results 52 cases were found and the attack rate was 42.76%.The case distribution was consistent with the characteristics of the outbreak of a homologous exposure.Legionella test result was negative.Clinical symptoms of patients were similar to those of fume fever.In the 1 2 jobs,the higher the amount of compressed air used in the job,the higher the incidence rate was,and there were statistical correlation between the two (P <0.01 ).A large number of fluorine -containing solid waste was burned in the evening before the onset of the disease.The compressed air station was downwind from the location of waste incineration,and the simulation test showed that the concentrations of fluobenzene and two -fluobenzene were 435 and 51 3 mg/m3 ,respectively.Conclusion The toxic smoke produced by illegal incineration of fluorine -containing solid waste,from the compressed air station into the workshop,causing the workers exposed to organic fluoride poisoning,and then the fluoropolymer fume fever outbreak.Fortunately,we disposed it timely and effectively,and all cases quickly recovered and no secondary occurred.

Objective To evaluate the efficacy of segmental tracheal resection with end-to-end anastomosis for cicatricial cervical tracheal stenosis.Methods The clinical outcomes of 40 patients treated with tracheal resection were retrospectively reviewed.There were 28 male patients and 12 female patients with the age ranged from 6 to 64 years (mean 33.7 years).The degree of stenosis was classified according to Myer-Cotton classification as follows:grade Ⅱ (n =7),grade Ⅲ (n =22) and grade Ⅳ (n =11).The stenosis extension ranged from 1.0 to 4.3 cm (mean 2.5 cm).The causes of the stenosis were postintubation (n =33),cervical trauma (n =6) and resection of tracheal neoplasm (n =1).Results Thirty-four(85.0％) patients were decannulated and 6 failed.Of the 6 patients failed,4 were decannulated after reoperation with the sternohyoid myocutaneous flap or thyroid alar cartilage graft.Complications occurred in 10 patients.In 8 patients granulation tissues formed at the site of the tracheal anastomosis,which needed endoscopic resction,and in 2 patients anastomosic dehiscence occurred.No injury to recurrent laryngeal nerve or trachoesophageal fistula occurred.Conclusion Segmental tracheal resection with end-to-end anastomosis is an effective surgical method for tracheal stenosis,which has a higher successful rate for primary operation and shorter therapeutic period.

Objective To determine the roles and underlying molecular mechanism of MicroRNA-203 on the migration of human hypo-pharyngeal carcinoma cells. Methods The potential MicroRNA-203 target genes were searched by bioinformatic miRNA target prediction tools and KEGG database,and a large number of candidates was identified. The MEKK1 was selected for further investigation. This gene is known to play a role in tumor metastasis. The MicroRNA-203’s binding sites in MEKK1’s mRNA 3’UTR were analyzed by luciferase report-er assays. Nextly,the protein expression of MEKK1 in Fadu-Lv-MicroRNA-203 cells was determined by Western blot assay. The regulation of MEKK1’s mRNA expression by MicroRNA-203 was analyzed by qRT-PCR. Transwell cell migration assays were performed to confirm the im-pact of MicroRNA-203 on hypopharyngeal carcinoma metastasis. Results The expression level of endogenous MicroRNA-203 was negatively correlated with the mRNA and protein expression levels of MEKK1 in hypopharyngeal carcinoma cells. Transwell migration assay results showed that MicroRNA-203 overexpression inhibited hypopharyngeal carcinoma cell migration ability. Furtherly,MEKK1 can promote hypo-pharyngeal carcinoma cell migration ability. Conclusion MEKK1 is a direct target of MicroRNA-203. MicroRNA-203 plays a role in hypo-pharyngeal carcinoma cell migration ability through MEKK1.

Macrophages are heterogeneous and diversified, and can be polarized into different phenotypes in various microenvironments and physiological or pathological conditions. Major macrophage subpopulations including classically activated(M1) and alternatively activated(M2) macrophages, which represent different surface receptors, secret different cytokines and chemokines, are regulated by different signal paths of transcriptions and epigenetic levels, and play distinctive roles in tumor progress. TCMs may improve the microenvironment by regulating phenotype polarization of macrophages. So far, specific biomarkers and polarized molecules mechanisms generated through the macrophage polarization approach are still unclear. In this article, we merely summarize the advance in domestic and foreign studies on phenotype polarization of macrophages and regulatory mechanisms and look into the future of intervention with TCMs.
Animals ; Cell Polarity ; Humans ; Macrophages ; physiology ; Medicine, Chinese Traditional ; Neoplasms ; drug therapy ; immunology ; Phenotype

To study the mechanisms of total flavonoid from Glycyrrhizae Radix et Rhizoma (TFGR) and its ingredient isoliquiritigenin (ISL) on their regulation of M2 phenotype polarization of macrophages. IL-4 (60 μg x L(-1)) induced RAW264.7 cells for 6 h to establish the M2 macrophage model. TFGR and ISL restrained breast cancer cells migration with the aid of M2 macrophages in vitro. TFGR and ISL inhibited gene and protein expression of Arg-1, up-regulated gene of HO-1 and protein expression of iNOS, enhanced the expression of microRNA 155 and its target gene SHIP1, meanwhile down-regulated.the phosphorylation of STAT3 and STAT6. So TFGR and ISL were the bioactive fraction and ingredient in Glycyrrhizae Radix et Rhizoma to reverse M2 phenotype macrophages polarization. TFGR and ISL inhibited the promotion of M2 macrophages to breast cancer cells migration in vitro, STAT signal pathways and miR155 were partly involved.
Animals ; Cell Line, Tumor ; Cell Movement ; drug effects ; Cell Polarity ; drug effects ; Chalcones ; pharmacology ; Flavonoids ; pharmacology ; Glycyrrhiza ; chemistry ; Interleukin-4 ; genetics ; metabolism ; Macrophages ; cytology ; drug effects ; metabolism ; Mice ; RAW 264.7 Cells ; Rhizome ; chemistry

OBJECTIVETo investigate the optimal conditions for establishing insulin-resistant 3T3-L1 adipocytes.

METHOSDexamethason (DEX), 3-isobutyl-methylxanthine (IBMX) and different concentrations of insulin (10(-8), 10(-7), and 10(-6) mol·L(-1)) were used to induce 3T3-L1 preadipocytes into mature adipocytes identified by oil red O staining. We established insulin- resistant 3T3-L1 adipocytes cell model (IR-3T3-L1) by exposing the cells to 1µmol·L(-1) DEX, and the changes of glucose concen- tration in the cell culture were determined by glucose oxidase-peroxidase (GOD-POD) assay.

RESULTSTreatment of 3T3-L1 cells with DEX, IBMX and 10(-6) mol·L(-1)) insulin for 9 days resulted in the differentiation of >90% of the cells into mature adipocytes. IR-3T3-L1 cells cultured for 96 h in the culture media containing 1 µmol·L(-1) DEX showed significantly increased glucose consumption (P=0.0003) as compared with the control group at 36 h (P<0.001).

CONCLUSION3T3-L1 cells can be induced into mature adipocytes by exposure to 1 µmol·L(-1) DEX, 0.5 mmol·L(-1) IBMX and 10(-6) mol·L(-1)) insulin. A 96 h exposure to 1 µmol·L(-1) DEX can induce 3T3-L1 adipocytes to acquire insulin resistance that can be maintained for 36 h.

1-Methyl-3-isobutylxanthine ; chemistry ; 3T3-L1 Cells ; Adipocytes ; cytology ; Animals ; Cell Differentiation ; Culture Media ; chemistry ; Dexamethasone ; chemistry ; Glucose ; chemistry ; Insulin ; chemistry ; Insulin Resistance ; Mice

Objective To investigate the optimal conditions for establishing insulin-resistant 3T3-L1 adipocytes. Methods Dexamethason (DEX), 3-isobutyl-methylxanthine (IBMX) and different concentrations of insulin (10-8, 10-7, and 10-6 mol · L-1) were used to induce 3T3-L1 preadipocytes into mature adipocytes identified by oil red O staining. We established insulin-resistant 3T3-L1 adipocytes cell model (IR-3T3-L1) by exposing the cells to 1μmol· L-1 DEX, and the changes of glucose concen-tration in the cell culture were determined by glucose oxidase-peroxidase (GOD-POD) assay. Results Treatment of 3T3-L1 cells with DEX, IBMX and 10-6 mol· L-1 insulin for 9 days resulted in the differentiation of>90%of the cells into mature adipocytes. IR-3T3-L1 cells cultured for 96 h in the culture media containing 1 μmol · L-1 DEX showed significantly increased glucose consumption (P=0.0003) as compared with the control group at 36 h (P<0.001). Conclusion 3T3-L1 cells can be induced into mature adipocytes by exposure to 1μmol· L-1 DEX, 0.5 mmol· L-1 IBMX and 10-6 mol· L-1 insulin. A 96 h exposure to 1μmol· L-1 DEX can induce 3T3-L1 adipocytes to acquire insulin resistance that can be maintained for 36 h.

Objective To investigate the optimal conditions for establishing insulin-resistant 3T3-L1 adipocytes. Methods Dexamethason (DEX), 3-isobutyl-methylxanthine (IBMX) and different concentrations of insulin (10-8, 10-7, and 10-6 mol · L-1) were used to induce 3T3-L1 preadipocytes into mature adipocytes identified by oil red O staining. We established insulin-resistant 3T3-L1 adipocytes cell model (IR-3T3-L1) by exposing the cells to 1μmol· L-1 DEX, and the changes of glucose concen-tration in the cell culture were determined by glucose oxidase-peroxidase (GOD-POD) assay. Results Treatment of 3T3-L1 cells with DEX, IBMX and 10-6 mol· L-1 insulin for 9 days resulted in the differentiation of>90%of the cells into mature adipocytes. IR-3T3-L1 cells cultured for 96 h in the culture media containing 1 μmol · L-1 DEX showed significantly increased glucose consumption (P=0.0003) as compared with the control group at 36 h (P<0.001). Conclusion 3T3-L1 cells can be induced into mature adipocytes by exposure to 1μmol· L-1 DEX, 0.5 mmol· L-1 IBMX and 10-6 mol· L-1 insulin. A 96 h exposure to 1μmol· L-1 DEX can induce 3T3-L1 adipocytes to acquire insulin resistance that can be maintained for 36 h.

Cisplatin is a first-line anticancer drug widely used in clinic. However, its resistance reduces its efficacy. With a non-specific cell cycle, cisplatin's main targets are nucleophilic protein, DNA and RNA in cells. Among cisplatin's multi-factorial resistance mechanisms, abnormal expression of transport protein, intracellular detoxification enhancement, DNA repair capacity increase and apoptosis blocking are the main mechanisms. Because traditional Chinese medicines (TCMs) have unique advantages in cancer treatment, their combination with cisplatin can improve the efficacy. In this paper, the authors summarized the advance in studies on cisplatin's resistance and the combination of TCMs and cisplatin in recent years.
Antineoplastic Agents ; administration & dosage ; pharmacology ; Antineoplastic Combined Chemotherapy Protocols ; therapeutic use ; Apoptosis ; drug effects ; Cell Cycle ; drug effects ; Cisplatin ; administration & dosage ; pharmacology ; Drug Resistance, Neoplasm ; drug effects ; Drugs, Chinese Herbal ; administration & dosage ; Humans ; Medicine, Chinese Traditional ; methods ; trends ; Neoplasms ; drug therapy ; pathology ; therapy

It is now well established that inflammation plays an important role in the development of numerous chronic metabolic diseases including insulin resistance (IR) and type 2 diabetes (T2DM). Skeletal muscle is responsible for 75% of total insulin-dependent glucose uptake; consequently, skeletal muscle IR is considered to be the primary defect of systemic IR development. Our pre- vious study has shown that rutaecarpine (Rut) can benefit blood lipid profile, mitigate inflammation, and improve kidney, liver, pan- creas pathology status of T2DM rats. However, the effects of Rut on inflammatory cytokines in the development of IR-skeletal muscle cells have not been studied. Thus, our objective was to investigate effects of Rut on inflammatory cytokines interleukiri (IL)-1, IL-6 and tumor necrosis factor (TNF)-α in insulin resistant primary skeletal muscle cells (IR-PSMC). Primary cultures of skeletal muscle cells were prepared from 5 neonate SD rats, and the primary rat skeletal muscle cells were identified by cell morphology, effect of ru- taecarpine on cell proliferation by MTT assay. IR-PSMC cells were induced by palmitic acid (PA), the glucose concentration was measured by glucose oxidase and peroxidase (GOD-POD) method. The effects of Rut on inflammatory cytokines IL-1, IL-6 and TNF-α in IR-PSMC cells were tested by enzyme-linked immunosorbent assay (ELISA) kit. The results show that the primary skeletal muscle cells from neonatal rat cultured for 2-4 days, parallel alignment regularly, and cultured for 7 days, cells fused and myotube formed. It was shown that Rut in concentration 0-180. 0 μmol x L(-1) possessed no cytotoxic effect towards cultured primary skeletal muscle cells. However, after 24 h exposure to 0.6 mmol x L(-1) PA, primary skeletal muscle cells were able to induce a state of insulin resistance. The results obtained indicated significant decrease (P < 0.05 to P < 0.001) IL-1, IL-6 and TNF-α production by cultured IR-PSMC cells when incubating 24 hours with Rut, beginning from 20 to 180.0 μmol x L(-1). IL-1, IL-6 and TNF-α in the Rut treated groups were dose-dependently decreased compared with that in the IR-PSMC control group. Our results demonstrated that the Rut promoted glucose consumption and improved insulin resistance possibly through suppression of inflammatory cytokines in the IR-PSMC cells.
Animals ; Cell Proliferation ; drug effects ; Cytokines ; metabolism ; Female ; Glucose ; metabolism ; Indole Alkaloids ; pharmacology ; Inflammation ; metabolism ; Insulin Resistance ; Male ; Muscle, Skeletal ; cytology ; drug effects ; metabolism ; Quinazolines ; pharmacology ; Rats