Objective To investigate the distribution status of coal-burning fluorosis (endemic fluorosis) areas in Luoyang and to provide scientifc evidence for making strategies in prevention and control. Methods In 2006, a household per village was chosen to carry the general survey so as of disease condition, living habits and housing structure among 941 coal-burning pollution fluorine sickness natural villages in Yanshi, Mengjin, Xin'an, Luanchuan counties and Geely area which were under the jurisdiction of Luoyang. In the general survey, the sampled village having a population of more than 500 person was considered as a major survey village, and water fluoride, 8 - 12 year-old child fluorine spot on tooth and the urinary fluoride were surveyed. Water fluoride and the child urinary fluoride determination used the fluoride ion selective electrode method, and the children's dental fluorosis used Dean method. Results The endemic fluorosis of Luoyang existed 742 in endemic fluomsis villages, compared with history, a decrease of 199 in number. Ninety-six point seven per cent( 142 543/147 419) of the households were consuming smoke-free coal. Households using intact kitchens accounted for 93.6%( 137 919/147 419). Of which 63.0%(86 889/137 919) of kitchens were mixed up with bedrooms. Total 125 060 people were using coal- fired furnace for heating, of which 87.8%(109 802/125 060) had smoke-free facilities, 12.2%(15 258/125 060) had none. Among 52 endemic villages with population of more than 500 people surveyed, a total of 183 water samples were collected, 2 had water fluoride exceeding 1.0 rag/L, the highest water fluoride being 1.04 rag/L, averaging 0.39 mg/L Sixteen villages had a prevalence rate of dental fluorosis for children less than 30.00%, accounting for 30.8% (16/52), 36 endemic villages the prevalence of dental fluorosis detection rate of more than 30.00%, accounting for 69.2%(36/52). Twenty-thrce villages had a dental fluorosis index greater than 0.6, severe dental fluorosis was not found. Real-time measurement of 1408 urine samples of children aged 8 - 12 showed that urine fluoride highest value 6.88 nag/L, the minimum value of 0.10 mg/L, geometric mean 1.10 mg/L. The prevalence rate of dental fluorosis for children was 36.06%. Conclusions In Luoyang city, numbers of coal-burning endemic fluorosis villages are less than before, children's dental fluorosis has significantly declined, however some people still use kitchens connecting with bedrooms and lack smoke-free facilities, they need to be educated to change lifestyle and improve furnace to reduce soot fluoride pollution.

Objective To study the value and effectiveness of surgical management and mapping in supratentorial tumoral complicated with epilepsy and to study the correlations between tumor and the epileptogenic focus.Methods The clinical data of 121 patients with supratentorial cerebral tumor but epilepsy as initial symptom were retrospectively analyzed for the incidence of pre-and postoperative epileptic seizures,including grade Ⅰ glioma in 1 5 cases and grade Ⅱ glioma in 35 cases,grade Ⅲ-Ⅳglioma in 12 cases,menigoma in 32 cases,metastases in 10 cases,cavernous angiomas in 15 cases,and ependymomas in 2 cases.Results Surgery based on CT/MRI,seizure type and EEG changes was conducted.There was no death in operation.The highest incidence was in frontal lobe and the lowest in occipital lobe.Correlations between localization of tumor and the epileptogenic focus:there were 50 cases in the same location,near or beside tumors in 28 cases,far separate apart(＞2 cm)from tumors in 25 cases,no relationship was found in 18 cases.103 patients were followed up for one to nine years.31 patients had a few seizures in the early postoperative period.Epileptic seizures were cured without anti-epilepsy drugs in 83 cases.Conclusion There are some differences between tumors'location and epileptogenic focus in supratentorial tumoral epilepsy.The location and size of epileptogenic zone should be detected before and during operation.The resection of the tumor combined with the resection of the epileptogenic zone"epilepsy surgery"can provide good results.

OBJECTIVETo study the influence of micrometastasis in lymph node on staging and prognosis of non-small-cell lung cancer (NSCLC).

METHODSIn 39 NSCLC patients, micrometastasis in pathologically negative lymph nodes were tested through immunohistochemical cytokeratin (CK) analysis and the relationship between CK(+) and staging, survival were analyzed.

RESULTSIn these 39 patients, the survival of CK(+) and CK(-) patients were 32 months and 48 months respectively (P = 0.0178). Multivariate analysis of Cox regression model showed: clinical stage (P = 0.0288) and relapse or metastasis (P = 0.0053) affected the prognosis while micrometastasis in lymphnodes (P = 0.7740) did not.

CONCLUSIONThe detection of micrometastasis in the lymphnodes may serve as a supplement to the present staging system for lung cancer. Even though the prognosis of patients with micrometastasis being poorer than those without, micrometastasis in the lymph nodes should not be regarded as an independent prognostic factor.

Adult ; Aged ; Carcinoma, Non-Small-Cell Lung ; diagnosis ; metabolism ; secondary ; Female ; Humans ; Keratins ; metabolism ; Lung Neoplasms ; diagnosis ; metabolism ; pathology ; Lymph Nodes ; pathology ; Male ; Middle Aged ; Neoplasm Staging ; Prognosis

Objective To explore whether puerarin induced apoptosis of SKOV3 ovarian cancer cells by microRNA-125b.Methods Using the qRT-PCR technique to detect the change of microRNA-125b after puerarin pretreated SKOV3.Using RNA interference technology to inhibit microRNA-125b expression in SKOV3 cells.Using Western blot technique to detect apoptosis related proteins after microRNA-125b lower expression.Results Puerarin could significantly inhibit ovarian cancer cell SKOV3 proliferation activity and promote its apoptosis related proteins expression.And puerarin can promote the expression of microRNA-125b.Inhibition of microRNA-125b expression in ovarian cancer cell SKOV3 could reduce apoptosis protein expression in SKOV3 cell.Conclusion MicroRNA-125b was involved in puerarin induced SKOV3 cell apoptosis,and prompt microRNA-125b is key molecular of the drug resistance in SKOV3.

OBJECTIVETo measure the thickness of facial bone wall of maxillary anterior teeth and premolars based on cone beam computed tomography (CBCT) images.

METHODSCBCT images from 118 patients were collected from the Affiliated Stomatology Hospital of Zhejiang University. The thickness perpendicular to the long axis of facial bone wall was measured at two locations: 4 mm apical to the cementoenamel junction (point 1) and the middle of the root (point 2).

RESULTSThe thickness of the facial bone walls of central incisors, lateral incisors and canines ranged from 0.5 to 1.5 mm. A thin facial bone wall (<1.0 mm) was quite frequent in central incisors (44.1% at point 1, 56.8% at point 2), lateral incisors (65.2% at point 1, 89.8% at point 2) and canines (45.8% at point 1, 61.0% at point 2). In contrast, the majority of examined first premolars (77.1% at point 1, 68.7% at point 2) and second premolars (94.1% at point 1, 94.1% at point 2) exhibited a thick facial bone wall (>1.0 mm).

CONCLUSIONA thin facial bone wall of teeth in the anterior maxilla is common. Radiographic analysis of facial bone wall using CBCT is recommended for selection of appropriate treatment approach.

Adult ; Bicuspid ; diagnostic imaging ; Cone-Beam Computed Tomography ; Female ; Humans ; Incisor ; diagnostic imaging ; Male ; Maxilla ; diagnostic imaging ; Young Adult

OBJECTIVEBased on establishment of four rat models of experimental pulmonary hypertension (PH), the authors examined the inhibition of matrix metalloproteinases (MMPs) by doxycycline and its effect on the development of PH and associated pulmonary vascular remodeling.

METHODHealthy male Sprague-Dawley rats (weight 350 g to 400 g) were randomly divided into nine groups: Normal control group (N), four model groups (H, M, P, PM) and their corresponding drug intervention groups (HD, MD, PD, PMD) in which doxycycline was given by gavage at a 20 mg/kg daily dosage. On day 28 (day 35 for PM and PMD models), the animals were catheterized to record mean pulmonary arterial pressure (mPAP) and then sacrificed. Fulton Index [RV/(LV + S)] was measured immediately. Morphometric parameters, including percent vascular wall thickness and muscularization of non-muscularized peripheral pulmonary arterioles were determined microscopically. The activity of MMPs was measured by gelatin zymography in the lung tissue.

RESULTS(1) Rats in all model groups (H, M, P, PM) developed significant pulmonary arterial hypertension and right ventricular hypertrophy in comparison with their corresponding drug intervention groups (HD, MD, PD, PMD) and normal control group (N) (P < 0.01). For example, mPAP (mm Hg)(1 mm Hg = 0.133 kPa):N: 18.10 +/- 1.45, H: 27.20 +/- 1.55, HD: 23.90 +/- 2.13; Fulton Inedx(%):N: 23.41 +/- 1.84, H: 34.44 +/- 2.70, HD: 27.55 +/- 2.45. (2) The percent vascular wall thickness (WT%) and percentage of muscularization of non-muscular pulmonary arterioles were significantly increased in all model groups compared with drug intervention groups and normal group (P < 0.01). For example, WT%:N: 10.90 +/- 3.11, H:41.41 +/- 5.21, HD: 17.73 +/- 3.12; Muscularization(%):N: 13.83 +/- 3.72, H: 44.93 +/- 2.43, HD: 29.89 +/- 4.45. (3) The activity of MMPs was inhibited by doxycycline effectively as assessed by gelatin zymography (P < 0.01). For example, the activity of MMP2 (A x 10(3)):N: 1.43 +/- 0.24, H: 3.58 +/- 0.28, HD: 2.29 +/- 0.31.

CONCLUSIONDoxycycline attenuated PH and associated pulmonary vascular remodeling in all rat PH models. The study suggests that high expression and enhanced activity of MMPs may play a brutial role in the development of PH. Such phenomenon seems to be common in a variety of PH models of different etiology.

Animals ; Disease Models, Animal ; Doxycycline ; pharmacology ; Hypertension, Pulmonary ; metabolism ; physiopathology ; Male ; Matrix Metalloproteinases ; metabolism ; Pulmonary Artery ; metabolism ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo explore the role of expression of connective tissue growth factor (CTGF) in pulmonary vascular remodeling of pulmonary hypertensive rats, and investigate the regulation of CTGF expression by simvastatin in this animal model.

METHODSEighty male Sprague-Dawley rats (350 to 400 g) were randomized to 7 groups. The rats in group PM(1 - 21) (n = 10) and PM(1 - 35) (n = 12) were treated with pneumonectomy + monocrotaline (MCT), and sacrificed at the 21st or 35th experimental day;those in groups PMS(1 - 35) (n = 12), PMS(21 - 35) (n = 12), PMV(1 - 35) (n = 12) and PMV(21 - 35) (n = 12) were given daily lavage of simvastatin (or vehicle) as intervention measure which began from the 1st and 21st experimental days, respectively; additional 10 rats were used as control without any intervention. The animals were sacrificed at the end of experiment (35 th day) as hemodynamic measurements and study on the morphological parameters relevant to pulmonary vascular remodeling were performed on each group of rats. The expression of ET-1 mRNA, CTGF mRNA and protein, and synthesis of collagen in these pneumonectomized, MCT-treated rats were compared between control and rats treated with simvastatin.

RESULTSRats in PM(1 - 35) Group developed severe PAH (mPAP = 39.75 +/- 3.62 mm Hg) (1 mm Hg = 0.133 kPa), right ventricular hypertrophy [RV/(LV + S) ratio = 0.627 +/- 0.040], and arterial medial hypertrophy (WT% = 61.73 +/- 5.39), these parameters of the control animals were 17.10 +/- 1.20 mm Hg, 0.262 +/- 0.018 and 14.71 +/- 1.16, respectively. CTGF mRNA and protein were mainly located in pulmonary arterial smooth muscle cells and interstitial macrophage shown by in situ hybridization and immunohistochemistry, respectively. The expression of ET-1 mRNA and CTGF mRNA detected by fluorescent quantitative RT-PCR in Group PM(1 - 35) were significantly increased in comparison with controls, and so did the CTGF protein expression determined by Western blotting in these diseased rats. The content of hydroxyproline (1.30 +/- 0.19 microg/mg wet lung) was remarkably higher than that of control animals (0.56 +/- 0.10 microg/mg wet lung). The up-regulation of ET-1 and CTGF gene expression, and elevated synthesis of hydroxyproline were reversed in rats intervened with simvastatin. The pulmonary hypertension, right ventricular hypertrophy and medial hypertrophy were attenuated in all simvastatin-treated rats no matter the intervention was initiated from the beginning or midway of the study.

CONCLUSIONThe up-regulation of CTGF gene expression may play an important role in the development of pulmonary vascular remodeling in PAH. Simvastatin can prevent and, to some extent, reverse the vascular remodeling via down-regulation of CTGF gene expression.

Animals ; Connective Tissue Growth Factor ; metabolism ; Down-Regulation ; Hypertension, Pulmonary ; metabolism ; physiopathology ; Male ; Rats ; Rats, Sprague-Dawley ; Simvastatin ; pharmacology

OBJECTIVETo investigate the role of matrix metalloproteinase-9 (MMP-9) and its tissue inhibitor (TIMP-1) in the pathogenesis of bronchial asthma and assess the effect of steroid treatment on MMP-9 and TIMP-1 levels. Matrix metalloproteinases are a family of zinc and calcium-dependent endopeptidases. Many MMPs such as MMP-1, MMP-2, MMP-3 are associated with asthma, in which MMP-9 is the key factor in asthma. Tissue inhibitor-1 of metalloproteinases is a specific inhibitor of MMP-9; the MMP-9 and TIMP-1 imbalance could lead to airway inflammation and remodeling in lung disease such as asthma.

METHODSForty Wistar rats were divided into 4 groups randomly: control, asthma model 7 days (7-day group), asthma model 21 days (21-day group) and steroid treatment groups. Asthma model of rats were established by ovalbumin (OVA) sensitization and challenge with mist inhalation. The expression of MMP-9 and TIMP-1 in lung tissues was detected by immunocytochemistry, RT-PCR and Western blotting.

RESULTS(1) By observing the changes of action, tracing respiratory curves, detecting level of serum IgE level and observing the lung tissues sections, the authors demonstrated that the rat asthmatic models were successfully established. (2) The lung tissue sections of the asthma groups stained with hematoxiline and eosin (HE) showed many inflammatory cell infiltrations around the bronchioli and accompanying arterioles, hyperplasia of caliciform cells, broken bronchial mucous membrane and thickening of submucosal layer. The hyperplasia of airway smooth muscle and basement membrane were more significant in asthma model 21-day group than that in 7-day group. These changes were improved after treatment. (3) The expression of MMP-9 in rat's lung tissues: the expression was 2.71 +/- 0.37 in 7-day group, 1.76 +/- 0.27 in 21-day group, 0.88 +/- 0.18 in the treatment group and 0.52 +/- 0.10 in the control group (F = 151.52, P < 0.01). The expression of TIMP-1 in rat's lung tissues was 1.13 +/- 0.19 in the 7-day group, 1.55 +/- 0.24 in 21-day group, 0.77 +/- 0.15 in the treatment group and 0.47 +/- 0.08 in the control group (F = 69.46, P < 0.01). (4) The results of immunocytochemistry and protein expression were consistent with those of RT-PCR.

CONCLUSIONThe protein and mRNA expression level of MMP-9 and TIMP-1 was high in asthmatic rat's lung tissues. Down-regulation of the expression of MMP-9 and TIMP-1 by steroids may be one of the mechanisms by which airway inflammation and remodeling are inhibited in asthma.

Administration, Inhalation ; Animals ; Asthma ; drug therapy ; metabolism ; Blotting, Western ; Bronchi ; metabolism ; pathology ; Disease Models, Animal ; Enzyme-Linked Immunosorbent Assay ; Gene Expression Regulation, Enzymologic ; Glucocorticoids ; administration & dosage ; therapeutic use ; Immunohistochemistry ; Inflammation ; drug therapy ; metabolism ; pathology ; Lung ; drug effects ; metabolism ; pathology ; Male ; Matrix Metalloproteinase 9 ; genetics ; metabolism ; Rats ; Rats, Wistar ; Respiratory Mucosa ; drug effects ; metabolism ; pathology ; Reverse Transcriptase Polymerase Chain Reaction ; Tissue Inhibitor of Metalloproteinase-1 ; genetics ; metabolism

OBJECTIVETo research the effects of glycogen synthase kinase (GSK3β) overexpression and GSK3β inhibitor SB-216763 on the proliferation of hepatic oval cells in rats and its regulatory mechanisms by Wnt signaling pathway.

METHODSThe hepatic oval cells WBF-344 were divided into the blank control group, GSK3β over-expression group, DMSO control group and GSK3β inhibitor groups, while the inhibitor groups set up three concentration gradients, that was 1, 5, 10 µmol/L. Using the GSK3β over-expression lentivirus, which had been identified correctly, and SB-216763 dealt with the cells WBF-344. The cells morphology of each group was observed under the phase contrast inverted microscope, and the expression of fluorescence in the lentivirus-transfected group was observed under the fluorescent microscope. The proliferation of each group cells was tested by CCK8 kits. The cells' apoptosis was detected by AnnexinV-FITC/PI kits. The expression of GSK3β, β-catenin and cyclin D1 were detected by Western blot.

RESULTSThe cells of GSK3β over-expression group were fewer and obvious aging. However, in each inhibitor added group, the cells' division and proliferation was vigorous, and the condition was good. Moreover, the cells' proliferation was getting stronger with the concentration of SB-216763 increasing. A large number of green fluorescence was expressed in the lentivirus-transfected cells. The cells' proliferation in GSK3β over-expression group restrained (t = 7.178, P < 0.01, as compared with control), while the cells' proliferation was vigorous in inhibitor groups (F = 45.030, P < 0.01, as compared with control). Flow Cytometry showed that the cells apoptosis was significant in GSK3β over-expression group. Western blot showed that the expression of GSK3β was increased, while the expression of β-catenin and cyclin D1 was decreased in the over-expression group. The expression of GSK3β had no significant difference among the control group and inhibitor groups. However, the expression of β-catenin and cyclin D1 was significantly increased with the concentration of SB-216763 increasing.

CONCLUSIONSThe overexpression of GSK3β can inhibit the Wnt signaling pathway, thus restrain the cells' proliferation and promotes apoptosis. SB-216763 can activate the Wnt pathway, thus promotes cells' proliferation.

Animals ; Cell Line ; Cell Proliferation ; drug effects ; Cyclin D1 ; metabolism ; Glycogen Synthase Kinase 3 ; metabolism ; Glycogen Synthase Kinase 3 beta ; Glycogen Synthase Kinases ; metabolism ; Hepatocytes ; drug effects ; Indoles ; pharmacology ; Male ; Maleimides ; pharmacology ; Rats ; Transfection ; Wnt Signaling Pathway ; beta Catenin ; metabolism

The aim of this project is to establish a fibroblast growth factor-21 (FGF-21) signaling pathway targeted cell model, for screening a class of FGF-21 receptor agonists as anti-diabetic candidates. FGF-21 requires beta klotho transmembrane proteins as co-receptor for the activation of tyrosine kinase FGF receptor (FGFR) signaling, thereby activating a series of intracellular signaling pathways and regulating gene transcription for glucose metabolism. Firstly a recombinant plasmid expressing co-receptor beta klotho and EGFP reporter genes was constructed. After introducing the recombinant plasmid into package cells, the cell culture supernatant was used to infect 3T3-L1 cells, which were then screened for stably expressing beta klotho gene. Administration of FGF-21 increased the expression of GLUT1 and stimulated GLUT1-mediated glucose uptake. This novel cell model can be conveniently used in high-throughput drug screening of FGF-21 or FGF-21 analogues.
3T3-L1 Cells ; Animals ; Drug Evaluation, Preclinical ; Fibroblast Growth Factors ; metabolism ; pharmacology ; Glucose ; metabolism ; Glucose Transporter Type 1 ; genetics ; metabolism ; Glucose Transporter Type 4 ; genetics ; metabolism ; HEK293 Cells ; Humans ; Hypoglycemic Agents ; metabolism ; Membrane Proteins ; genetics ; metabolism ; Mice ; NIH 3T3 Cells ; Plasmids ; RNA, Messenger ; metabolism ; Receptors, Fibroblast Growth Factor ; agonists ; Recombinant Proteins ; genetics ; metabolism ; Retroviridae ; genetics ; Signal Transduction ; Transfection