Environmental Exposure ; adverse effects ; Hearing Loss ; etiology ; Humans ; Noise, Occupational ; adverse effects ; Occupational Diseases ; etiology ; Occupational Exposure ; adverse effects ; Risk Factors ; Smoking ; adverse effects ; Vibration ; adverse effects

Humans ; Noise, Occupational ; adverse effects ; Occupational Exposure ; standards

AIM To study the central role of genistein (GST) in regulating cardiovascular function of nervous center by examining the effects of GST on the electrical activity of rat paraventricular nucleus neurons in slice preparation and to elucidate the mechanism involved. METHODS Using extracellular single-unit discharge recording technique to examine discharges of neurons in paraventricular nucleus of hypothalamic slices at the resting potential level. RESULTS ①In response to the application of GST 10, 50 and 100 μmol·L-1, respectively, in the perfusate for 2 min, the spontaneous discharge rates (SDR) of neurons in 25/26 hypothalamic slices were significantly decreased in a concentration-dependent manner. ②Pretreatment with L-glutamate 0.2 mmol·L-1 led to a marked increase in the SDR of slices in an epileptiform pattern. GST 50 μmol·L-1 significantly attenuated the increased SDR in all 7 slices. ③In 8/8 slices, the G protein-coupled inwardly rectifying K+ channels (GIRKs) antagonist, tetraethylammonium 1 mmol·L-1 completely blocked the inhibitory effect of GST 50 μmol·L-1. ④Pretreatment with nitric oxide synthase inhibitor Nω-nitro-L-arginine methyl ester 50 μmol·L-1 increased SDR in all 7 slices, but did not affect the inhibitory effect of GST 50 μmol·L-1. CONCLUSION GST can inhibit the electrical activity of paraventricular neurons, and play a protective role on the central neurons. The inhibitory effect of GST may be related to the activation of GIRKs which induce K+ outward current and then engender the cell membrane hyperpolarization, but be not due to the NO release.

A rapid, reliable and sensitive pressurized capillary electrochromatography-Laser induced fluorescence ( pCEC/LIF ) method with trifluoroacetic acid ( TFA ) pre-column derivation for simultaneous determination of four aflatoxin ( AFB1 , AFB2 , AFG1 , AFG2 ) was developed. This method included separation on a capillary column packed with 1. 8μm C18 particles using 0. 05% FA aqueous solution/methanol (55:45, V/V) as mobile phase at a pump flow rate of 0. 05 mL/min when the split ratio was 1:300. Under the optimum conditions including running voltage of 15 kV, excitation wavelength of 375 nm and emission wavelength of 450 nm, the baseline separation of four aflatoxins was achieved within 10 minutes. The limits of detection (LODs) were 0. 02, 0. 016, 0. 008 and 0. 01 μg/L for AFG1, AFB1, AFG2, AFB2(S/N=3), respectively. The linear detection ranges of AFG1 , AFB1 , AFG2 , AFB2 were 0. 1-10, 0. 1-10, 0. 1-3 and 0. 1-3 μg/L with correlation coefficients (R2) of 0. 9999, 1. 0000, 0. 9995 and 0. 9997, respectively. The established method was applied to analyze the peanut butter, and the recoveries of standard addition experiment were between 90 . 0% and 112 . 0% for all analytes ( RSDs=0 . 5%-1 . 9%) .

Extracellular single-unit discharge recording technique was used to examine the effects of Ginkgolide B (BN52021) on the discharges of neurons in CAI area of hippocampal slices and to elucidate the mechanisms involved.The results showed that:(1) In response to the application of ginkgolide B (0.1,1,10 βμmol/L; n =43) into the perfusate for 2 rain,the spontaneous discharge rates (SDR) of 42/43 (97.67%) neurons were significantly decreased in a dose-dependent manner; (2) Pretreatment with L-glutamate (L-Glu,0.2mmol/L) led to a marked increase in the SDR of all 10 (100%) neurons in an epileptiform pattern.The increased discharges were suppressed significantly after ginkgolide B (1 μmol/L) was applied into the perfusate for 2 rain; (3) In 8 neurons,perfusion of the selective L-type calcium channel agonist,Bay K 8644 (0.1 μmol/L),induced a significant increase in the discharge rate of 8/8 (100%) neurons.Ginkgolide B (1 μmoL/L) applied into the perfusate inhibited the discharges of 7/8 (87.5%) slices; (4) In 8 neurons,the broad potassium channels blocker,tetraethylammonium (TEA,1 mmol/L) completely blocked the inhibitory effect of ginkgolide B (1 μmol/L).These results suggest that ginkgolide B can inhibit the electrical activity of CAI neurons.The inhibitory effect may be related to the blockade of L-type voltage-activated calcium channel and may be concerned with delayed rectifier potassium channel (KDR),which indicated that ginkgolide B play a protective role on the central neurons.

Occupational Medicine ; education

Objective To investigate the synergistic effect of methotrexate (MTX) and cyclophos phamide (CTX) on cell cycle and cyclin D1 of periphery blood lymphocytes (PBLs) and bone marrow byflow cytometry. Methods Wistar rats were randomly divided into four groups including normal control, MTX and cyclophosphamide combination group, MTX and CTX only treatment groups respectively. PBLs were isolated for flowcytometry analysis for the changes of cell cycle and the expression of cyclin D1 at week 0, week 3,week 9, week18 and week 27. Mice were dissected and the changes of lymphoeytes cell cycle and the expressions of cyclin D1 in the bone marrow were measured at week 0, week 3, week 9, week 18 and week 27 increased and the ratio of phase S cells was decreased (P>0.05). In the CTX treatment group, there was no statistical difference in ratios of each phase. In the MTX and CTX combination treatment group, the proportion of phase G0/G1 cells decreased significantly and the percentage of phase S cells increased in both PBLs and bone marrow ceils (P<0.05). And there was no statistical significant difference in different time points after marrow between different groups or different dissecting time points. Conclusion MTX combined with CTX has been shown to have antagonistic effect on cell cycle. However, this effect is not via the cyclin DI pathway.

Objective To investigate the therapeutic effect of intracerebral transplantation of mesenchymal stem cells(MSCs) derived from human umbilical cord blood(UCB) on hypoxic-ischemic brain damage(HIBD) in neonatal rat.Methods Twenty samples of human UCB were collected from healthy full-term newborns.MSCs were isolated from human UCB by density gradient centrifugation and purified by adhere cell selection method.For transplantation,P3 human UCB-derived MSCs were labeled by the 5-bromo-2-deoxyuridine (BrdU).Thirty SD rats of 7 d were built for neonatal HIBD model.One rat died and others were divided into transplant group(n=18) and control group(n=11).At the third day after building models,human UCB-derived MSCs were injected into left cortex in transplant group,while PBS of the same volume was injected into the same site in control group at the same time.The seventh day after transplantation,6 rats of transplant group were sacrificed to prepare brain tissue sections.The survival,migration and differentiation of the transplanted cells were investigated by brain tissue immunohistochemical analysis,and nervous function of 2 groups were evaluated by modified neurological severity score(mNSS) on the first,7th,14th,21th and 28th day after transplantation.Results MSCs were isolated from 5 of 20 human UCB samples.Immunocytochemical analysis of brain tissue showed that the transplanted human UCB-derived MSCs could survive and migrate around by the center of transplant site.There were (12.67?2.73)% of MSCs differentiated into astrocyte-like cells.mNSS showed that the score of transplant group was lower than that of control group on the first,7th,14th,21th and 28th day,and the differences of score points between 2 groups on the 14th,21th and 28thday were statistically significant(Pa

Antigens, CD20 ; analysis ; Bone Marrow Transplantation ; adverse effects ; CD79 Antigens ; analysis ; Female ; Humans ; Immunohistochemistry ; Liver Transplantation ; adverse effects ; Lymphoma, Large B-Cell, Diffuse ; etiology ; metabolism ; pathology ; Lymphoproliferative Disorders ; etiology ; metabolism ; pathology ; Male ; Middle Aged ; Postoperative Complications ; etiology ; metabolism ; pathology ; Young Adult

Alveolitis, Extrinsic Allergic ; Humans ; Occupational Diseases