OBJECTIVETo investigate the modification of GSTM1, GSTT1 and GSTP1 gene polymorphisms on urinary 1-hydroxypyrene (1-OHP) excretions in workers under different exposure levels.

METHODSFour hundred and forty-seven occupationally exposed workers from two coking plants and 220 control workers from a wire rod plant were genotyped to analyze the modification of GSTM1, GSTT1 and GSTP1 gene polymorphisms on urinary 1-OHP excretions.

RESULTSThe urinary 1-OHP concentration in exposed group was much higher than that in control group (4.61 vs 0.34 µmol/mol Cr, P < 0.05). Occupational exposure levels and cigarette smoking were of the dominating factors affecting 1-OHP excretions in urine. After controlling potential confounders, decreased excretion of urinary 1-OHP was associated with GSTP1 I105V AG + GG genotype in coke oven workers (single-gene model, P = 0.012; multi-gene model, P = 0.011) and with GSTT1 null type in the analysis including all subjects (P = 0.055 in both single-gene and multi-gene models). GSTT1 and GSTP1 were interacted on the urinary concentrations of 1-OHP.

CONCLUSIONUrinary 1-OHP concentrations can be modified by GSTM1, GSTT1 and GSTP1 gene polymorphisms, indicating that these genes are involved in the metabolism of polycyclic aromatic hydrocarbons.

Adolescent ; Adult ; Control Groups ; Genotype ; Glutathione S-Transferase pi ; genetics ; Glutathione Transferase ; genetics ; Humans ; Male ; Middle Aged ; Occupational Exposure ; Polymorphism, Single Nucleotide ; Pyrenes ; analysis ; Urinalysis ; Young Adult

OBJECTIVETo investigate the interference effect of nicotinamide on UVA-induced cell proliferation in human skin melanocyte.

METHODSTo apply the optimum UVA dose expected to cause cell proliferation: 0.2 cm2, nicotinamide was added after the 0.2 cm2 UVA exposure immediately or 48 h later, then the rate of cell proliferation, calcium concentration and the activities of Na+-K+, Ca2+-ATP enzymes of melanocytes were measured respectively.

RESULTSAfter treatment with 1.000 mg/ml nicotinamide following UVA exposure, the rate of cell proliferation was decreased significantly 24 hours later. Treatment with 0.125 mg/ml nicotinamide 48 hours after UVA exposure also significantly inhibited the cell proliferation; 1.25 mg/ml nicotinamide increased calcium concentration in cells; 0.250 mg/ml nicotinamide increased the activities of Na+-K+, Ca2+-ATP enzymes in melanocytes (P < 0.05).

CONCLUSIONNicotinamide has more obvious effect on inhibiting melanocyte's proliferation if added immediately following UVA exposure. Our discovery indicated that nicotinamide may affect the melanocyte through modulating the calcium concentration. It is possible to consider nicotinamide as an efficient and safe sun screen to provide a certain level of protection for UVA exposed skin.

Cell Proliferation ; drug effects ; radiation effects ; Cells, Cultured ; Humans ; Melanocytes ; cytology ; Niacinamide ; pharmacology ; Skin ; cytology ; Ultraviolet Rays

OBJECTIVETo study the tolerance of rats induced by 28 day pretreatment with low dosage of dimthoate and the toxic effects challenged by higher dosage of dimethoate, and to investigate the change of M receptor and the mechanism of tolerance formation.

METHODSSD rats were given 25 mg/kg dimethoate daily(sc) while control group was given saline daily instead for 28 days. The activity of whole blood acetylcholinesterase (AChE) was examined. On the 29th day three groups of administrated rats were challenged by saline solution, 50 mg/kg and 100 mg/kg dimethoate, respectively. The density and mRNA level of brain M(1), M(2) receptor were determined. Lymphocytes of peripheral blood were isolated, and basal, inducible M(3) gene expression were measured by RT-PCR.

RESULTSDuring pretreatment, blood AChE activity decreased continually, it reached the lowest on the 13th day. And it decreased more after exposed to higher dosage of dimethoate. Brain AChE activity in the pretreated groups was lower than that in control group and decreased with the increase in challenging dosage. The density of M(1) receptor in negative control, pretreated, and 50, 100 mg/kg challenging groups were 979.15, 856.54, 539.46, 539.14 fmol/mg pro respectively. The change in relative levels of mRNA of M(1) receptor (2.59, 2.47, 2.20, 1.81) were consistent with the density of receptor but the level declined continually as the challenging dosage increased. The density of M(2) receptor were 507.38, 611.11, 548.42, 337.47 fmol/mg pro respectively, which were not obviously affected by pretreatment but decreased as the challenging dosage increased. The change in levels of M(2) receptor mRNA was not obvious. The basal gene expression of M(3) receptor mRNA was not different among all experimental groups while the inducible gene expression decreased with the increase in challenging dosage.

CONCLUSIONLow level dosage of dimethoate could induce animals to tolerate dimethoate toxicity. Reduction of M(1) receptor density which may be induced by the decrease in its gene expression may be the mechanism of tolerance. The change of M(3) receptor mRNA inducible expression in lymphocyte accorded with M(1) receptor mRNA expression in the brain.

Animals ; Brain ; metabolism ; Dimethoate ; toxicity ; Gene Expression ; drug effects ; Insecticides ; toxicity ; Lymphocytes ; metabolism ; Male ; Maximum Tolerated Dose ; RNA, Messenger ; genetics ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Receptors, Muscarinic ; genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Time Factors

OBJECTIVETo study the expression of muscarinic receptor M(3) gene in peripheral blood lymphocytes of workers exposed to organophosphorus pesticides (OPPs) and to explore its role in the adverse effects of OPPs.

METHODSThe lymphocytes of peripheral blood from 33 workers exposed to dimethoate and 15 control people were isolated and treated with saline and dimethoate respectively in vitro. RT-PCR technique was used to determine M(3) gene expression. Basal and inducible gene expression levels were measured.

RESULTSThere was no significant difference in basal gene expression level between exposed group and control group, while the inducible gene expression level was significantly higher in exposure group (1.92 +/- 1.07) than in control group (1.22 +/- 0.19) and basal level (1.49 +/- 0.45, P < 0.05). No differences in basal and inducible gene expression level were found between male and female people in both exposed and control group. The level of inducible M(3) gene expression increased with the increase in length of exposure time [< 5 a: (1.69 +/- 0.95), 5 - 25 a: (1.91 +/- 1.03), > 25 a: (2.09 +/- 1.25), the latter was significantly different from that of < 5 a (P < 0.05)].

CONCLUSIONAfter long-term exposure to OPPs, the basal M(3) receptor gene expression level in the exposed workers did not show any difference from the control group, but the inducible gene expression level (treated with dimethoate in vitro) was increased and related to the extent of exposure to dimethoate.

Dimethoate ; blood ; poisoning ; Female ; Gene Expression ; Humans ; Insecticides ; blood ; poisoning ; Lymphocytes ; cytology ; metabolism ; Male ; Occupational Exposure ; analysis ; RNA, Messenger ; genetics ; metabolism ; Receptor, Muscarinic M3 ; genetics ; Reverse Transcriptase Polymerase Chain Reaction

OBJECTIVETo investigate the effects of occupational lead exposure on the bone mineral density and the bone metabolism in exposed workers.

METHODSTwo hundred and ninety-eight lead-exposed workers in a storage battery plant in Shanghai were selected as the exposed subjects while eighty-one healthy officers in the plant who were not occupationally exposed to lead were treated as the control. The blood lead (BPb) and the urinary lead (UPb) were used as the exposure biomarkers while the Z score, the urinary hydroxyproline (HYP) the serum alkaline phosphatase (ALP) the serum alkaline phosphatase bone isoenzyme BALP and the serum osteocalcin BGP were used as the effect biomarkers for the bone effect caused by the lead. Bone mineral density (BMD) was measured by the single-photon absorptiometry (SPA-4).

RESULTSThe BPb, UPb, HYP, ALP, BALP in the occupational lead exposure group were higher than those in the control group with significantly statistical difference in male (P < 0.01). The levels of BGP in the exposure group was higher than that in the control group without significantly statistical difference (P > 0.05). The BMD in the exposure group was lower than that in the control group without significantly statistical difference (P > 0.05). The BMD was significantly decreased in the groups of the UPb 10 approximately microg/g Cr level compared with the 0 approximately microg/g Cr group with the significant difference (P < 0.01). In males, the BMD was significantly decreased in the group of the BPb 300 approximately microg/L level compared with the 0 approximately microg/L group with the significant difference (P < 0.01). The levels of HYP, ALP, BALP, BGP in the UPb 20 approximately microg/g Cr group were significantly higher than those in the UPb 0 approximately microg/g Cr group (P < 0.05). The levels of HYP, ALP, BALP, BGP in the BPb 300 approximately microg/L group were significantly higher than those in the BPb 0 approximately microg/L group (P < 0.05). The prevalence of both osteoporosis and the abnormal bone metabolisms indexes would increase significantly with the increase of the lead exposure (P < 0.01) with the linear correlation (P < 0.01). But the prevalence of higher BGP had no significant correlation with UPb (P > 0.05). BMDs were calculated using BMDS Version 1.3.2 software and BMDLs were also determined. The BMDLs of BPb and UPb for lead-induced osteoporosis were higher than those representing the change of bone metabolism induced by lead.

CONCLUSIONSThe occupational exposure to lead could cause the decrease of the bone mineral density, lead to the osteoporosis, and may affect the bone metabolism.

Adult ; Aged ; Biomarkers ; blood ; urine ; Bone Density ; drug effects ; Bone and Bones ; drug effects ; metabolism ; Case-Control Studies ; Female ; Humans ; Lead ; adverse effects ; blood ; urine ; Male ; Middle Aged ; Occupational Exposure ; adverse effects ; Osteoporosis ; chemically induced ; Young Adult

OBJECTIVETo assess the risk of renal dysfunction caused by occupational lead exposure through epidemiological investigation.

METHODSThe workers in a battery factory were selected as the subjects for the exposure and effect assessment. The occupational environmental monitoring data was collected and used to calculate the total external dose of lead. The relationship between external dose and internal dose of lead was analyzed. The external dose, blood lead (BPb) and urinary lead (UPb) were used as exposure biomarkers while the urinary N-acetyl-D-glucosaminidase (UNAG), and urinary albumin (UALB) were used as the effect biomarkers for the renal dysfunction caused by lead. Software of BMDS (BMDS 11311) was used to calculate BMD.

RESULTSThe external and internal does of lead was positively correlated (BPb: r = 0.466, P < 0.01; UPb: r = 0.383, P < 0.01). The levels of BPb, UPb in exposure group (654.03 microg/L, 143.45 microg/g Cr) were significantly higher than those in the control group (57.12 microg/L, 7.20 microg/g Cr), so were UALB, UNAG; in addition, all of them presented significant dose-response relationship. The BPb BMD of UALB, UNAG were 607.76, 362.56 microg/L respectively and the UPb BMD of UALB, UNAG were 117.79, 78.79 microg/gCr respectively.

CONCLUSIONOccupational lead exposure can cause renal dysfunction, which presents dose-response relationship; the risk assessment of renal dysfunction caused by occupational lead exposure is performed by BMD calculation of BPb and UPb.

Adolescent ; Adult ; Biomarkers ; blood ; urine ; Environmental Monitoring ; Female ; Humans ; Kidney ; drug effects ; Kidney Diseases ; chemically induced ; Lead ; blood ; urine ; Male ; Middle Aged ; Occupational Exposure ; Risk Assessment ; Surveys and Questionnaires ; Young Adult

OBJECTIVETo explore the dose-effect relationship between lead exposure and nerve conduction velocity, and to assess risk characteristics of nerve conduction velocity induced by lead exposure.

METHODSThe external dose, internal dose (blood lead, urine lead) and the conduction velocity of peripheral nerve were examined. The benchmark dose of a population exposed to occupational lead was estimated to develop risk assessment of nerve conduction velocity in worker exposed to lead by use of BMDS (version 1.3.3). The BMDL in terms of blood lead and urine lead was calculated.

RESULTSThere was correlation between blood lead and urine lead. The sense nerve conduction velocity was decreased significantly in the group of lead exposure workers (P < 0.05). The BMDLs-05 for median nerve conduct velocity, ulnar nerve conduction velocity, and superficial peroneal nerve conduction velocity in terms of blood lead were 456.99, 332.36 and 468.38 microg/L respectively; the BMDLs-05 in terms of urine lead were 14.1, 9.2 and 13.6 microg/gCr respectively.

CONCLUSIONThe internal dose is the better index to reflect the level of lead exposure. Blood lead is identified as a specific and sensitive biomarker for sense nerve conduction velocity reduction. Ulnar nerve conduction velocity can be used as highly sensitive biomarkers to screen the high risk population of lead exposure.

Adolescent ; Adult ; Aged ; Biomarkers ; blood ; Female ; Humans ; Lead ; adverse effects ; blood ; Lead Poisoning ; blood ; Male ; Middle Aged ; Neural Conduction ; drug effects ; Occupational Exposure ; Risk Assessment ; Surveys and Questionnaires ; Young Adult

The genetic diversity of Schistosoma haematobium remains largely unstudied in comparison to that of Schistosoma mansoni. To characterize the extent of genetic diversity in S. haematobium among its definitive host (humans), we collected S. haematobium eggs from the urine of 73 infected schoolchildren at 5 primary schools in White Nile State, Sudan, and then performed a randomly amplified polymorphic DNA marker ITS2 by PCR-RFLP analysis. Among 73 S. haematobium egg-positive cases, 13 were selected based on the presence of the S. haematobium satellite markers A4 and B2 in their genomic DNA, and used for RFLP analysis. The 13 samples were subjected to an RFLP analysis of the S. haematobium ITS2 region; however, there was no variation in size among the fragments. Compared to the ITS2 sequences obtained for S. haematobium from Kenya, the nucleotide sequences of the ITS2 regions of S. haematobium from 4 areas in Sudan were consistent with those from Kenya (> 99%). In this study, we demonstrate for the first time that most of the S. haematobium population in Sudan consists of a pan-African S. haematobium genotype; however, we also report the discovery of Kenyan strain inflow into White Nile, Sudan.
Adolescent ; Animals ; Base Sequence ; Child ; DNA, Helminth/genetics ; Female ; *Genetic Variation ; Genotype ; Humans ; Male ; Molecular Sequence Data ; Ovum/classification/cytology ; Parasite Egg Count ; Polymorphism, Restriction Fragment Length ; Schistosoma haematobium/*genetics/*isolation & purification/physiology ; Schistosomiasis haematobia/diagnosis/epidemiology/*parasitology/urine ; Students ; Sudan/epidemiology ; Urine/*parasitology

OBJECTIVETo evaluate the efficacy and safety of zoledronic acid in the treatment of bone pain in patients with bone metastasis from solid tumor or multiple myeloma.

METHODSA randomized, double-blind, double-simulated and multi-center phase III clinical trail with pamidronate as control was conducted. Patients with moderate to severe bone pain (VAS > 50 mm) induced by solid tumor or multiple myeloma were randomized to receive intravenous zoledronic acid 4 mg or pamidronate 90 mg. Then the change of VAS and urinary NTX/Cr and CTX/Cr were observed in two groups.

RESULTSFrom July 2005 to September 2006, 228 patients with bone pain induced by bone metastasis from 15 cancer centers were randomize into two groups: 116 patients in zoledronic acid group and 112 patients in pamidronate group. The VAS value was decreased gradually after treatment in these two groups. Significant improvement in bone pain after treatment were observed both in zoledronic acid group and the control group when compared with baseline VAS on D8 (-11.77% vs. -10.87%), D15 (-24.60% vs. -21.06%) and D28 (-32.37% vs. -31.26%) (P< or =0.0001), but no significant difference existed between two groups (P =0.6587). Compared with baseline, urine NTX/Cr and CTX/Cr level were decreased rapidly after treatment in both groups, the nadir was on D8, the median decreased on D28, which was -36.9% vs. -32.1% for NTX/Cr (P = 0.7922) and -63.2% vs. -47.9% for CTX/Cr (P =0.834). The frequently observed adverse events were pyrexia (19.0% vs. 31.3%), vomiting (6.0% vs. 8.9%), nausea (4.3% vs. 4.5%), fatigue (3.4% vs. 2.7%) and constipation (2.6% vs. 1.8%) in the two groups. Compared with baseline, the serum creatinine level was not significantly increased throughout the study.

CONCLUSIONIntravenous injection of 4 mg zoledronic acid can significantly reduce bone pain and bone resorption marker in urine in the Chinese patients with bone metastasis from solid tumor or multiple myeloma, which is tolerable and also comparable to pamidronate in the efficacy and safety.

Adult ; Aged ; Analgesics ; adverse effects ; therapeutic use ; Bone Density Conservation Agents ; adverse effects ; therapeutic use ; Bone Neoplasms ; complications ; secondary ; Breast Neoplasms ; pathology ; Collagen Type I ; urine ; Colorectal Neoplasms ; pathology ; Creatinine ; urine ; Diphosphonates ; adverse effects ; therapeutic use ; Double-Blind Method ; Female ; Fever ; chemically induced ; Humans ; Imidazoles ; adverse effects ; therapeutic use ; Lung Neoplasms ; pathology ; Male ; Middle Aged ; Multiple Myeloma ; complications ; Pain Measurement ; Pain, Intractable ; drug therapy ; etiology ; urine ; Peptides ; urine ; Prospective Studies ; Vomiting ; chemically induced

Objective: To investigate the expression of miR-218 and its clinical significance in osteosarcoma tissues and explore its effect on proliferation and apoptosis in osteosarcoma cells. Methods: miR-218 expression was detected in 76 samples of surgically resected osteosarcoma and matched normal tumor-adjacent tissues using quantitative reverse transcription polymerase chain reaction (qRT-PCR). MiR-218 was over-expressed by exogenous miR-218 plasmids in Saos-2 cells, and then BrdU cell proliferation assay and flow cytometry were used to determine cell proliferation and apoptosis. Results: The expression of miR-218 in osteosarcoma tissues was significantly lower than those in normal tumor-adjacent tissues (t=8.735, P<0.001). MiR-218 expression in tumor tissues was significantly correlated with tumor size (χ