Objective To evaluate the intervention effects of low-fluoride brick tea in the population, and to provide data for the prevention and control of the brick-tea type fluorosis. Methods Eighty-six Kazakh families with 5-12 years old children were selected and divided into two groups in the severe brick-tea type fluorosis areas of Akesai County of Gansu Province. Forty-six households were intervened by drinking low-fluoride brick tea as intervention group and another 40 households drank general brick tea as control group. The fluoride content in water, tea and urine was monitored and the total daily fluoride intake of adults and children was calculated by the fluoride content of the tea before and during intervention. The baseline prevalence of dental fluorosis was surveyed in all Kazakh school students aged 5 - 12 years before intervention, dental fluorosis prevalence were surveyed in two groups after the intervention. The fluoride content in water, urine,tea, and brick-tea samples was detected by iron electrode method, and dental fluorosis was diagnosed by Dean's method. Results The fluoride content of water were 0.36,0.50 mg/L respectively before and 42 months after intervention. The total daily fluoride intake of adults and children in the intervention group (being 4.39,5.12,5.38,4.49 mg in adults and 1.90,2.33 in children, 2.33, 1.94 mg for four calculations) were lower than those in control group (8.42,9.07,8.35,7.92 and 3.65,3.93, 3.62,3.43 mg). Except the second batch (530.4 mg/kg), the average fluoride content of the other 3 batches of low-fluoride brick tea(239.3,222.88,154.7 mg/kg) was lower than that of 4 batches of market brick tea(366.9,412.2, 286.0,379.6 mg/kg). The fluoride content of low-fluoride brick tea samples was in accordance with the national standard(< 300 mg/kg) in 16 of 21 samples in 4 the batches, and the qualifying rate was 76.19%(16/21). Only 5 of 21 market brick tea samples in 4 batches was qualified, accounting for 23.80%(5/21), both were significantly different(χ2= 11.52, P < 0.01). In 12, 36, 42 months after intervention, urine fluoride content in the intervention group of adult(1.84,1.23,1.77 mg/L) and children(1.55,0.65,1.10 mg/L) was less than that of the control group (adults: 3.37,3.68,3.02 mg/L, children: 2.64,1.64,2.62 mg/L), both being statistically significant (t value were 2.94,2.43,3.91,3.29,2.31,4.42, P < 0.01 or 0.05). The detective rate of dental fluorosis was 69.02%(127/184)at baseline among children. After the intervention, it lowered to [44.83% (13/29) in the intervention group, significantly lower than that in the control group[71.88%(23/32), χ2 = 4.60, P < 0.05]. Conclusion Low-fluoride brick tea can reduce the fluoride intake of the residents who drink brick tea, and alleviate excessive fluoride and the damage of high-fluoride.

Child ; Child, Preschool ; Female ; Humans ; Infant ; Injections ; Male ; Pneumonia ; drug therapy ; Quinuclidines ; therapeutic use ; Respiratory Insufficiency ; complications

OBJECTIVETo provide evidence for illustrating the molecular mechanism of nickel carcinogenesis, and to identify the differential expression of protein in crystalline NiS-induced neoplastic transformation of human bronchial epithelial cell by proteomics technology.

METHODSTwo dimensional electrophoresis (2-DE) and the ImageMaster 3.10 software were used to analyze the differential expression of protein, matrix-assisted laser desorption/ionization-time of flight mass spectrometry (MALDI-TOF-MS) combined with database search was applied to identify protein peroxiredoxin 2 (PDX2) related to malignant transformation.

RESULTSThe good 2-DE pattern including resolution and reproducibility was obtained. Nearly 700 expressed proteins per 2-D gel were isolated with molecular weights (MW) ranging from 14,400 to 94,000 KD and pI 3 - 10. A protein PDX2 with MW 21,890 KD, pI 5.66, which was highly expressed in malignantly transformed cell, was identified using MALDI-TOF-MS.

CONCLUSIONPDX2 was involved in malignant transformation of human bronchial epithelial cell induced by crystalline nickel sulfide.

Bronchi ; cytology ; Cell Line ; Cell Transformation, Neoplastic ; chemically induced ; metabolism ; Epithelial Cells ; cytology ; drug effects ; metabolism ; Humans ; Nickel ; toxicity ; Peroxiredoxins ; metabolism ; Proteome

OBJECTIVETo study the alterations of FHIT gene and P16 gene in malignant transformed human bronchial epithelial cells induced by crystalline nickel sulfide using an immortal human bronchial epithelial cell line, and to explore the molecular mechanism of nickel carcinogenesis.

METHODS16HBE cells were treated 6 times with different concentrations of NiS in vitro, and the degree of malignant transformation was determined by assaying the anchorage-independent growth and tumorigenicity. Malignant transformed cells and tumorigenic cells were examined for alterations of FHIT gene and P16 gene using RT-PCR, DNA sequencing, silver staining PCR-SSCP and Western blotting.

RESULTSNiS-treated cells exhibited overlapping growth. Compared with that of negative control cells, soft agar colony formation efficiency of NiS-treated cells showed significant increases (P < 0.01) and dose-dependent effects. NiS-treated cells could form tumors in nude mice, and a squamous cell carcinoma was confirmed by histopathological examination. No mutation of exon 2 and exons 2-3, no abnormal expression in p16 gene and mutation of FHIT exons 5-8 and exons 1-4 or exons 5-9 were observed in transformed cells and tumorigenic cells. However, aberrant transcripts or loss of expression of the FHIT gene and Fhit protein was observed in transformed cells and tumorigenic cells. One of the aberrant transcripts in the FHIT gene was confirmed to have a deletion of exon 6, exon 7, exon 8, and an insertion of a 36 bp sequence replacing exon 6-8.

CONCLUSIONSThe FHIT gene rather than the P16 gene, plays a definite role in nickel carcinogenesis. Alterations of the FHIT gene induced by crystalline NiS may be a molecular event associated with carcinogen, chromosome fragile site instability and cell malignant transformation. FHIT may be an important target gene activated by nickel and other exotic carcinogens.

Acid Anhydride Hydrolases ; chemistry ; genetics ; metabolism ; Animals ; Base Sequence ; Bronchi ; cytology ; Cell Line ; Cell Transformation, Neoplastic ; chemically induced ; DNA Damage ; Exons ; Gene Deletion ; Genes, p16 ; Humans ; Mice ; Mice, Nude ; Molecular Sequence Data ; Mutagenicity Tests ; Neoplasm Proteins ; chemistry ; genetics ; metabolism ; Nickel ; toxicity ; RNA, Messenger ; metabolism ; Respiratory Mucosa ; cytology ; drug effects ; Reverse Transcriptase Polymerase Chain Reaction ; Sequence Analysis, DNA

To study the enzyme kinetics of schizandrin metabolism in different gender in rat liver microsomes, liver microsomes were prepared from male or female rats. Schizandrin was incubated with rat liver microsomes. Schizandrin and its metabolites were isolated and identified by HPLC-UV method. Vmax, Km and Cl(int) of schizandrin in male and female rat liver microsomes were (21.88 +/- 2.30) and (0.61 +/- 0.07) micromol x L(-1) x min(-1) x mg(-1) (protein), (389.00 +/- 46.26) and (72.64 +/- 13.61) micromol x L(-1), (0.0563 +/- 0.0007) and (0.0084 +/- 0.0008) min x mg(-1) (protein), respectively. The major metabolites of schizandrin in female and male rat liver microsomes were 7,8-dihydroxy-schizandrin (M1) and 7, 8-dihydroxy-2-demethyl schizandrin (M2b), respectively. Ketoconazole, quinidine, and orphenadrine had different level effects on schizandrin metabolism in both male and female rat liver microsomes, and cimetidine still had some inhibitory effect in male liver microsomes. CYP3A and CYP2C11 may be the main P450 enzymes in schizandrin metabolism and their difference in rat liver microsomes may be the main reason for the sex difference of metabolic enzyme kinetics and metabolites of schizandrin in rats.
Animals ; Chromatography, High Pressure Liquid ; Cimetidine ; pharmacology ; Cyclooctanes ; isolation & purification ; metabolism ; Enzyme Inhibitors ; pharmacology ; Female ; In Vitro Techniques ; Ketoconazole ; pharmacology ; Lignans ; isolation & purification ; metabolism ; Male ; Microsomes, Liver ; metabolism ; Orphenadrine ; pharmacology ; Plants, Medicinal ; chemistry ; Polycyclic Compounds ; isolation & purification ; metabolism ; Rats ; Rats, Sprague-Dawley ; Schisandra ; chemistry ; Sex Factors ; Spectrophotometry, Ultraviolet

OBJECTIVETo investigate the factors involved in the development of retinopathy of prematurity (ROP), and to provide the preliminary data for the evaluation of current criteria for ROP screening.

METHODPremature infants with birth body weight (BBW) ≤ 2000 g or gestational age (GA) ≤ 34 weeks in the two hospitals in Zhejiang between March 2005 and November 2008 were recruited and examined by indirect ophthalmoscopy. The records were analyzed.

RESULTOne thousand two hundred and twenty-five premature infants were included. Of them, 713 were male and 512 female. There were 179 twins and 21 triplets in the premature infants. The incidence of ROP was 10.8% (132 in 1225 patients). There were 12 cases (0.98%) to the point of pre threshold ROP. 4 cases (0.3%) developed threshold ROP. Only one case developed pre threshold ROP of low risk among 65 cases without history of oxygen treatment (1.5%). The percentage has significant difference compared to that of cases with history of oxygen (χ(2) = 5.115, P < 0.01).Between ROP and Non-ROP groups, there was significant difference in BBW(F = 26.39, P < 0.001), gestational age (F = 19.73, P < 0.001), but there was no significant difference in sex (χ(2) = 0.279, P > 0.05) or twins and triplets (χ(2) = 3.449, P > 0.05). The incidence of ROP among premature infants with BBW ≤ 1000 g was more than three times of that with BBW > 1000 g, and the incidence of ROP among premature infants with GA ≤ 28 weeks was about 2.5 times of that with GA > 28 weeks. Logistic regression analysis indicated that less BBW or shorter GA or undulation of blood oxygen concentration was a significant risk factor involved in the development of ROP (r = 0.57, P < 0.05). All ROP patients were cured.

CONCLUSIONLess BBW, shorter GA and undulation of blood oxygen concentration are the important risk factors for the development of ROP. Premature infants with BBW ≤ 1000 g or GA ≤ 28 weeks, who had oxygen history, should be given very special attention in the ROP screening. The current criteria for ROP screening should be narrowed. In general, the ROP screening has lowered the incidence of blindness among children by investigating and treating ROP timely.

China ; epidemiology ; Female ; Humans ; Incidence ; Infant, Newborn ; Infant, Premature ; Male ; Neonatal Screening ; Retinopathy of Prematurity ; diagnosis ; epidemiology ; prevention & control ; Risk Factors

The medicinal fungi, which are of great importance in traditional medicine, are facing the problems of wild resources scarcity and low concentration of bioactive compounds. Velvet family and LaeA global regulator play a vital role in secondary metabolism and developmental programs, which are found in a wide variety of fungi ranging from Chytridiomycota to Basidiomycota. This review elaborates the structures and functions between Velvet family and LaeA protein. The Velvet family which shares the Velvet protein domain, including VeA (Velvet), VelB (Velvet like B), VosA (viability of spores A) and VelC (Velvet like C), acts on the regulation function is secondary metabolism and developmental programs such as asexual and sexual development. Furthermore, the function is affected by environmental factors such as light and temperature. LaeA protein which owns S-adenosylmethionine-dependent methyltransferase domain, coordinately regulates development and secondary metabolism by regulating and modifying the Velvet proteins. The regulation of LaeA is mediated by light receptor proteins. Therefore, clarifying the mechanism of Velvet and LaeA proteins in medicinal fungi will pave the way for nurturing medicinal fungi and improving production of bioactive compounds.
Fungal Proteins ; metabolism ; Fungi ; chemistry ; Gene Expression Regulation, Fungal ; Genes, Regulator ; Protein Structure, Tertiary ; Secondary Metabolism ; Structure-Activity Relationship

A sensitive, rapid and specific liquid chromatographic-tandem mass spectrometric (LC-MS/MS) method for quantification of gabapentin in human plasma has been developed. After a single plasma protein precipitation with methanol, gabapentin and metformin (internal standard) were chromatographed on a Inertsil ODS-3 column (50 mm x 2.1 mm ID, 3 microm) with mobile phase consisting of methanol-0.2% formic acid aqueous solution (80:20, v/v) at a flow-rate of 0.2 mL x min(-1). Electrospray ionization (ESI) source was applied and operated in the positive ion mode. Multiple reaction monitoring (MRM) mode with the transitions of m/z 172 --> m/z 154 and m/z 130 --> m/z 71 were used to quantify gabapentin and metformin, respectively. The run time was 2.2 min. The linear calibration curve was obtained in the concentration range of 40.8-8.16x10(3) ng x mL(-1). The lower limit of quantification was 40.8 ng x mL(-1). The intra- and inter-day precision (RSD) was less than 12%, and the accuracy (RE) was within +/-6.4% calculated from quality control (QC) samples. The method was used to determine the concentration of gabapentin in human plasma after a single oral administration of 600 mg gabapentin capsule to 20 healthy male Chinese volunteers. The method was proved to be selective, sensitive, rapid and suitable for pharmacokinetic study of gabapentin in human plasma.
Administration, Oral ; Amines ; administration & dosage ; blood ; pharmacokinetics ; Anticonvulsants ; administration & dosage ; blood ; pharmacokinetics ; Area Under Curve ; Chromatography, High Pressure Liquid ; Cyclohexanecarboxylic Acids ; administration & dosage ; blood ; pharmacokinetics ; Humans ; Male ; Spectrometry, Mass, Electrospray Ionization ; Tandem Mass Spectrometry ; gamma-Aminobutyric Acid ; administration & dosage ; blood ; pharmacokinetics

OBJECTIVETo investigate the relationship between Transitional CK19 positive cells and hepatic precancerous lesion in chronic hepatitis B patients.

METHODSWe observed the expression of CK19 in liver tissue of chronic hepatitis B patients by LSAB immunohistochemical staining, and examined serum AFP and ultrasonography one time per 3 months for one year.

RESULTSWe observed a population of CK19 positive cells-with size and structure between those of human oval cells and mature hepatocytes-that usually occurred along with oval-cell proliferation. It was suggested that these transitional cells may partly account for the elevation of serum AFP. One patient occurred hepatic carcinoma, another patient had low-echogenic nodules in liver parenchyma within the 1 year follow-up period.

CONCLUSIONTransitional CK19 positive cells could be regarded as a new possible pathological marker of hepatic precancerous lesion.

Adolescent ; Adult ; Biomarkers, Tumor ; Female ; Humans ; Keratins ; analysis ; Liver Neoplasms ; chemistry ; pathology ; Male ; Middle Aged ; Precancerous Conditions ; chemistry ; pathology ; Tomography, X-Ray Computed ; alpha-Fetoproteins ; analysis

OBJECTIVETo detect the alteration of fragile histidine triad (FHIT) gene and p16 gene during malignant transformation of immortal human bronchial epithelial cell line (16HBE) induced by crystalline nickel sulfide, and study the molecular mechanism of nickel carcinogenesis.

METHODSMalignant transformed cells and tumorigenic cells were examined for the alteration of FHIT gene and p16 gene by RT-PCR, DNA sequencing and silver staining PCR-SSCP.

RESULTSCompared with those of control 16HBE, neither mutation of exon2 or exon2-3, abnormal expression in p16 gene nor mutation of FHIT exon5, 6, 7 and 8, exon1-4 or exon5-9 were observed in transformed cells and tumorigenic cells. But aberrant transcript or FHIT gene expression loss were observed in transformed cells and tumorigenic cells. One of the aberrant transcripts in FHIT gene, the deletion of exon6, exon7 and exon8 and an insertion of 36 bp sequence replacing exon6-8, was confirmed by sequencing.

CONCLUSIONFHIT gene, not p16 gene, could play a definite role in nickel carcinogenesis. Alterations of FHIT gene induced by crystalline NiS could be a molecular event associated with carcinogen, chromosome fragile site instability and cell malignant transformation, and FHIT gene could be one of the important target genes activated by exotic carcinogens.

Acid Anhydride Hydrolases ; Base Sequence ; Cell Transformation, Neoplastic ; chemically induced ; metabolism ; Cells, Cultured ; Gene Expression ; Genes, p16 ; physiology ; Humans ; Molecular Sequence Data ; Neoplasm Proteins ; genetics ; metabolism ; Nickel ; pharmacology