Objective　To observe the change of lipidemia and lipoprotein in wistar rats with fluorosis.Methods　14 wistar rats were fed normal food with hyper concentration of NaF water (100 mg/L) for six months,the TC,TG,HDL-c,LDL-c,APO AI APO B and AI,R-CHE were measured in serum.Results　The result show that there are an increace of T C,TG,HDL-c,LDL-c,APO AI，APO B and AI,R-CHD compared with normal rats (P <0.05).Conclusions　The result indicate that the fluorosis can increase the lipidemia and lipoprotein in rats with fluorosis and lead to athero selerosis.

Adult ; Back Muscles ; physiopathology ; Fasciitis ; physiopathology ; therapy ; Female ; Humans ; Male ; Moxibustion ; Muscular Diseases ; physiopathology ; therapy

Objective To investigate the changes of reactive oxygen species(ROS) level and mitochondria fission-fusion-balance in cortical neurons of rats with chronic fluorosis and reveal the correlation between these two factors. Methods One hundred and twenty rats were randomly divided into 3 groups(control group, low-dose fluorosis group, high-dose fluorosis group) and 40 rats were in each group according to body weight and the experiments were carried out for 3 months or 6 months. The rats were fed with different concentrations of fluoride (NaF) to establish fluorosis models. Controls were fed with tap water( < 0.5 mg/L), experimental animals in low- or high-dose group were fed with water containing NaF 10.0,50.0 mg/L, respectively. The level of ROS and the morphology in mitochondria fission-fusion balance in neurons of the cortex of rat brains prepared with cortical frozen sections were detected with ROS fluorescent probe and MitoTracker RED probe, respectively. Results Significant differences of the level of ROS and the numbers of abnormal mitochondria in morphology in the cortical neurons were found between 3 groups at the experiment period of 3 month and 6 month(F= 3.07,3.06,3.05,3.07, all P < 0.05). As compared with control group(10.43 ± 5.98,4.12 ± 3.86) at the experiment period of 3 month, the level of ROS and the numbers of abnormal mitochondria in morphology in the cortical neurons were obviously increased in high-dose fluorosis group(25.48 ± 6.09,20.47 ± 6.09, all P < 0.05), whereas no significant changes were found in low-dose fluorosis group(11.67 ± 3.49,6.68 ± 3.48, all P> 0.05). Furthermore, the increases in both ROS level and abnormal numbers of mitochondria were significant observed in the cortical neurons of low-dose fluorosis group (63.02 ± 8.15, 49.33 ± 8.61) and high-dose fluorosis group(65.60 ± 7.40,53.10 ± 6.95) as compared with the control group (25.26 ± 6.41,20.26 ± 6.41) at the experimental period of 6 month (all P < 0.05). The abnormal numbers of mitochondria correlated with ROS level(r = 0.93,0.81, all P < 0.05). Conclusions Taking excessive amount of fluoride results in high level of oxidative stress and impaired the balance of mitochondrial fission-fusion,which is dependent on the feeding times and doses of fluoride. The mechanism of the mitochondrial abnormalities might be associated with the high level of oxidative stress induced by chronic fluorosis.

Objective To evaluate quantitatively the spasticity of elbow flexor biceps in stroke patients using integrated EMG (IEMG),and to correlate the IEMG with Ashworth scale.Methods The IEMG data was recorded from the biceps while passively stretch the elbow joint of a group of 90 subjects,and was correlated with the varying levels of Ashworth category(20 cases with grade 0,6 cases gradeⅠ,16 cases gradeⅠ~+,20 cases gradeⅡ,and 18 ca- ses gradeⅢ).Results The IEMG data were positively correlated with simultaneous Ashworth scale categories.The range of IEMG value corresponding to the Ashworth category is as follows:1.3～12.1 (6.7?5.4)?V?s vs Ash- worth grade 0;4.6～12.3 (8.5?3.9)?V?s vs Ashworth gradeⅠ.15.3～28.4(21.8?6.6)?V?s vs Ashworth gradeⅠ~+;37.2～68.9 (53.1?15.6)?V?s vs Ashworth gradeⅡ;82.3～144.1 (113.2?30.9)?V?s vs Ash- worth gradeⅢ.Conclusion The IEMG value can be used to quantify the spasticity of elbow flexor in stroke pa- tients.

Objective The aim of the study was to investigate the expression of P-glycoprotein (P-gp)and nuclear factor κB (NF-κB) in the cerebral cortex of rat with chronic fluorosis,and to reveal the mechanisms of damaged nervous system resulted from the toxicity of fluoride.Methods Sixty SD rats were randomly divided into three groups.The rats in each group were given drinking water containing different levels of fluoride:control group less than 0.5 mg/L,small amount of fluoride exposure group 10.0 mg/L and large amount of fluoride exposure group 50.0 mg/L.The animals were examined at the sixth month after initiating the experiment.Protein levels of P-gp and NF-κB in brain tissues were detected by immunocytochemistry and Western blotting,and the P-gp protein and mRNA level by quantitative real time PCR method.Results As compared to the control group(28.21 ±6.13),the numbers of positive staining cells by P-gp antibody in the cortex of rat brains were significantly increased in both the small and the large amount of fluoride exposure groups[(48.46 ± 8.00),(53.72 ± 9.15),respectively,all P ＜ 0.05] ; the protein levels in the control group(100.00 ± 3.86)％ detected by Western blotting were significantly increased in the cortex of rat brains treated with fluoride in both the small and the large amount of fluoride exposure groups[(189.47 ± 3.14)％,(191.36 ± 11.09)％,respectively,all P ＜ 0.05].The significantly increased expression of NF-κB at the protein level was observed in the cortex of rat brains of the small and the large amount of fluoride exposure groups[(365.97 ± 6.04)％ and (417.15 ± 10.89)％,respectively] as compared with the control group[(100.00 ± 10.07)％,all P ＜ 0.05].The mRMA level of P-gp in the cortex of rat brains of the small and the large amount of fluoride exposure groups(2396 ± 427,3479 ± 371,respectively) were higher than that of the control group(260 ± 106,all P ＜ 0.05).Conclusion The increased expressions of P-gp and NF-κB in the cortex of rat brains are induced by chronic fluorosis,which might be connected with the mechanism of brain damages.

Background Diabetic retinopathy (DR) leads to blindness because of the retinal angiogenesis caused by the ischemia of retina.Vascular endothelial growth inhibitor (VEGI) is a recently identified anti-angiogenic cytokine,which can suppress endothelial cell proliferation and angiogenesis.Objective The aim of this study was to detect the change of serum and vitreous VEGI/TL1A and its relative cytokines in patients with DR.Methods A non-randomized controlled clinical trial was performed.Fifty-five DR patients were enrolled in Tianjin Medical University General Hospital from November 2012 to March 2013 with the informed consent.The patients were divided into non-proliferative DR (NPDR) group (20 cases) and PDR group (35 cases).Eleven cataract patients served as normal control group,and 15 patients with diabetic mellitus (DM) were included as DM group.The demography was matched among the groups,but the course of DM and the blood glucose level were elevated in the PDR group and the DM group compared with DR group (all at P＜0.05).We collected the serum of all the patients above.Another 23 PDR patients (25 eyes) were enrolled in Tianjin Medical University General Hospital from November 2012 to March 2013 with the informed consent and served as PDR group,healthy corpse's eyes (n=7) as control group,the patients were assigned to the retinal photocoagulation group,surgery group and photocoagulation +surgery group according to different treatment procedures.Vitreous samples were collected during the progress of vitrectomy.TL1A/VEGI 251,VEGF,TNF-α,IL-1β and NF-κB p65 concentrations in the serum and vitreous specimens were detected using ELISA.The differences of serum and vitreous TL1A/VEGI 251,VEGF,TNF-α,IL-1β and NF-κB p65 in various groups were statistically analyzed by ANOVA and independent sample t test,respectively.The correlation between TL1A/VEGI 251 and VEGF,TNF-α,IL-1β,NF-κB p65 were calculated by Pearson correlation analysis.Results TL1A/VEGI 251 concentration was elevated in the DM group,NPDR group and PDR group compared with the normal control group,with significant difference among the 4 group (F =27.431,P =0.009),and TL1A/VEGI 251 concentration was higher in the PDR group than that in the DM group or the NPDR group (P＜0.05).VEGF,TNF-α,IL-1 β and NF-κB p65 concentrations in serum were increased in the PDR group in comparison with the DM group,NPDR group and the normal control group (P＜0.05).However,no significant difference among the DM group,NPDR group and the normal control group (P＞0.05).Serum TL1A/VEGI 251 concentration was significant correlated with VEGF,TNF-α,IL-1β and NF-κB p65 concentration (r=0.951,0.951,0.851,0.944,all at P＜0.01).Vitreous TL1A/VEGI 251,VEGF,TNF-α,IL-1 β concentrations were ascended in the PDR group compared with the normal control group (P =0.024,0.001,0.000,0.037),but there was no significantly difference in vitreous NF-κB p65 concentration between the two groups (P =0.073).Vitreous TL1A/VEGI 251 concentrations declined in the retinal photocoagulation group and the surgery group compared with the normal group (all at P＜ 0.05),and significant positive correlations were found between vitreous TL1A/VEGI 251 concentration and VEGF or TNF-α concentration (r =0.675,0.950,P ＜ 0.01) ;while Pearson correlation coefficient was not statistically significant between vitreous TL1A/VEGI 251 concentration and IL-1β or NF-κB p65 concentration (r=0.233,0.318,P＞0.05).Conclusions VEGI is involved in the pathogenesis of DR,and it interacts with VEGF,TNF-α,IL-1β and NF-κB to affect the development of DR.These results provide a new clue for the further study of DR.

ObjectiveTo investigate the transcriptional changes of nitochondria fission and fusion gene loci and reactive oxygen species (ROS) level in cortical neurons of rats with chronic fluorosis,and to reveal their roles in mitochondria damage due to chronic fluorosis.MethodsSD rats were fed with different doses of fluoride through drinking water[＜ 0.5(control),10,50 mg/L,respectively] for 3 and 6 months.The level of ROS and mRNA contents of mitochondria fission gene loci Drp1/Fis1 and fusion gene locus Mfn1 in the cortical neurons of rat brains were detected with ROS fluorescent probe and real-time PCR,respectively.ResultsAs compared with control group [10.43 ± 5.98,(3.4 ± 0.6) × 103,(8.8 ± 1.4) × 10,(1.2 ± 0.2) × 102] at the experiment period of 3 months,the level of ROS and mRNA contents of mitochondria fusion gene locus Mfn1 and fission gene loci Drp1/Fis1 in the cortical neurons were obviously increased in the rats fed with 50 mg/L fluoride through drinking water[25.48 ± 6.09,(1.0 ± 0.2) × 1011,(3.0 ± 1.6) × 103,(8.9 ± 3.6) × 102,all P ＜ 0.05],whereas no significant changes were found in the rats fed with 10 mg/L fluoride[11.67 ± 3.49,(3.1 ± 0.3) × 104,(6.7 ± 2.7) × 10,(5.0 ± 0.9) × 10,all P ＞0.05].Furthermore,at 6 months of the experiment the increases in ROS level(63.02 ± 8.15,65.60 ± 7.40) and mRNA contents of mitochondria fission gene loci Drp1/Fis1 [(2.0 ± 0.8) × 106,(4.0 ± 0.6) × 105,(3.8 ± 1.3) × 103,(1.3 ± 0.2) × 103] and the decrease in mitochondrial fusion gene locus Mfn1[(3.0 ± 0.4) × 106、(4.0 ± 0.9) × 104]were observed in the cortical neurons of the rats fed with 10 mg/L and 50 mg/L fluoride as compared with the control group[25.26 ± 6.41,(3.0 ± 0.8) × 109,(5.1 ± 0.8) × 103,(2.8 ± 0.7) × 102,all P ＜ 0.05].Conclusions Excessive intake of fluorine leads to elevated ROS levels,and decreased transcription of mitochondrial fusion gene loci Mfn1,which is positively correlated with the time and dose-exposed to fluoride.The changes of mitochondrial fission and fusion gene loci in the cortical neurons may be related to high level of oxidative stress induced by chronic fluorosis.

Objective To investigate the deletion pattern of 4.8 kb mitochondrial DNA(mito-DNA) in liver,kidney,and brain of rats with chronic fluorosis and to explore the significance of mitochondria in the pathogenesis of chronic fluorosis.Methods Sixty SD rats were randomly divided into 3 groups according to body mass (20 in each group):control,low-fluoride and high-fluoride groups,and they were fed with different concentrations of fluoride in drinking water (0,10,50 mg/L,respectively) for 6 months.Mito-DNA in liver,kidney and brain was detected by real-time PCR.Results The amounts of 4.8 kb mito-DNA in liver(2.1 × 10-3,1.6 × 10-3),kidney (1.7 × 10-3,1.4 × 10-4) and brain cortex (1.5 × 10-5,1.3 × 10-5) in low-and high-fluoride groups were significantly reduced,as compared with that of control group (2.9 × 10-3,2.0 × 10-3,1.1 × 10-4,all P ＜ 0.05).The amount of 4.8 kb mito-DNA in kidney in high-fluoride group was lower than that in low-fluoride group (P ＜ 0.05).Conclusions Excessive fluoride intake can result in missing of 4.8 kb mito-DNA in liver,kidney and brain cortex.The abnormal of mito-DNA might be related to the dysfunction of mitochondrial respiratory chain.

Objective To explore the risk factors of coal-burning-borne endemic fluorosis (endemic fluorosis) and to provide a scientific basis for making prevention and control strategy.Methods One hundred children with dental fluorosis and 30 adults with skeletal fluorosis who lived in Wushan county and Fengjie county,the endemic fluorosis regions northeast of Chongqing were randomly selected as the case group in 2010.One hundred healthy children and 30 healthy adults were selected from the population where the cases were selected from as the control group and 30 healthy external adults control were selected from Yubei district,a non-endemic fluorosis area.Fasting venous blood was draw from all subjects and the content of zinc (Zn),copper(Cu),calcium (Ca),magnesium(Mg),and ferrum(Fe) in venous blood was measured by atomic spectrophotometric.Instant urine was collected from all subjects and urinary fluorine was measured by fluorine selective electrode.We also did questionnaire survey to 100 dental fluorosis children and 100 control children about their situation of fluorine pollution and knowledge related to endemic fluorosis.Results Children's blood Zn of the ease group[(70.88 ±9.28) μmol/L] was lower than that of the control group [(75.53 ± 10.78)μmol/L],and the difference was statistically significant(P ＜ 0.05).But the average blood Cu content[(30.28 ± 2.58)μ mol/L] and the average urinary fluorine of the case group [(0.74 ± 0.36)mg/L] were significantly higher than that [Cu (28.45 ± 4.05)μmol/L and urinary fluorine (0.48 ± 0.21)mg/L] of the control group in children,respectively,and the differences was statistically significant(P ＜ 0.05).The average blood Zn content of adults in the case group[(91.13 ± 10.29)μ mol/L] was lower than that of the control group[(99.57 ± 11.73)μmol/L],and the difference was statistically significant (P ＜ 0.05).The average content of Mg[(1.57 ± 0.19)mmol/L],Fe[(8.17 ± 1.01) mmol/L] and urinary fluorine[(2.37 ± 1.01)mg/L] in the case group were higher than that [Mg(1.46 ± 0.16) mmol/L,Fe(7.72 ± 0.96) mmol/L and urinary fluorine(0.92 ± 0.85)mg/L] of the control group,respectively,and the differences were statistically significant(P ＜0.05).In the questionnaire survey,we found that the following were important related factors (OR values were 2.7335,0.3339,2.8428,0.4633,0.5439,0.4009,0.4805 and 0.3994,P ＜ 0.05) between the case group and the control group:using local coal for heating,furnaces and stoves improvement,eating local coal fire baked food,knowing the harm of endemic fluorosis to the health of human body,knowing endemic fluorosis can be prevented,knowing consuming baked food can cause endemic fluorosis,knowing drinking milk can prevent endemic fluorosis and having the habit of eating calcium tablets.Conclusions In addition to the main pathogenic element of fluorine,body Zn content is closely related to the process of coal-burning-borne endemic fluorosis in the two counties,fluorosis patients have lower blood Zn levels,Zn deficiency is an auxiliary factor in the etiology of fluorosis.Reduce the use of local coal for heating,do not consume the baked food,improve stoves,learn more knowledge about endemic fluorosis and ingest anti-fluoride elements can reduce the risk of endemic fluorosis.

Objective To explore the main influence factors of attention deficit hyperactivity disorder ( ADHD) and evaluate the clinical effect of Yi-gan-san modified.Methods Questionnaire survey consisting of home environment, living habits and exposure to environmental toxicant was used to investigate and evaluate children in the two groups, one of them was the study group with 120 cases of ADHD children, and the other was the control group with 120 cases of healthy children.A total of 75 cases with the pi-xu-gan-kang type were found among the ADHD children, and they were randomly divided into 2 groups:the experimental group ( n =38 ) , using drug therapy of Yi -gan -san modified ( 150 mL, twice a day ) and behavioral therapy (3 times a week);the control group, using behavioral therapy alone.The treatment lasted for all 8 weeks.The data of the line integral of traditional Chinese medicine symp-tom assessment was used to evaluate the curative effect before treatment and 4, 8 weeks after treatment.Results The survey found that the family environment such as low education level of parents, parenting methods, family income less than three thousand yuan each month, parenting and feeding patterns, whether both parents were the only child in the family were significantly associated with the occurrence of ADHD.We also found the exposure to DEHP, children′s rest hobbies, sleep habits, eclipse snack times and playing phone were significantly re-lated with the occurrence of ADHD.The CR of the treatment group was 52.63% and the total effective rate was 86.84%, and there was 24.32%and 43.24%in the control group respectively.The TCM syndrome score between the two groups had significant statistical significance ( P<0.01 ) , and the curative effect of the treatment group was better than that in the control group.The TCM syndrome score were significantly lowered after 8 weeks of treatment in the two groups (P<0.01).Conclusion The family environment, lifestyle and children′exposure to environmental toxicants were susceptible to the occurrence of ADHD.Using Yi-gan-san modified intervention for the treatment of ADHD is effective.