Objective To observe glucose metabolism in C57 mice treated with different doses of fluoride.Methods Forty male C57 mice (body weight 20-24 g) were divided into four groups which were exposed to 0,50,100 and 150 mg/L sodium fluoride (NaF) by random number table according to body weight,each group had 10 mice.At 2,4,6,8,10 and 12 weeks after fluoride exposure,body weight was measured,blood glucose and glycosylated hemoglobin were detected by blood glucose meter and glycosylated hemoglobin meter,serum insulin and glucagon were detected by enzyme-linked immunosorbent assay (ELISA).Results At 10 and 12 weeks after fluoride exposure,the differences of fasting glucose between groups of C57 mice were statistically significant (F =35.12,21.92,all P ＜ 0.05),the fasting glucose of 100,150 mg/L fluoride groups [(7.7 ± 0.2),(7.3 ± 0.3),(8.6 ± 0.5),(9.1 ± 0.7)mmol/L] were higher than those of the control group [(5.4 ± 0.3),(5.0 ± 0.3)mmol/L,all P ＜ 0.01].The differences of glycosylated hemoglobin,glucagons between groups were statistically significant (F =3.85,8.74,all P ＜ 0.05).The glycosylated hemoglobin of 100,150 mg/L fluoride groups [(7.73 ± 0.76),(7.80 ± 1.15) mmo]/L] were higher than those of the control group [(5.43 ± 1.27) mmol/L,all P ＜ 0.05]; serum glucagon levels of 50,100,150 mg/L fluoride groups [(19.15 ± 11.84),(26.55 ± 15.97),(20.05 ± 7.29)ng/L] were lower than that of the control group [(48.35 ± 2.79)ng/L,all P ＜ 0.01].Conclusion Long term excess fluoride intake can reduce the function of sugar metabolism in C57 mice.

Objective:Ciliary neurotrophic factor (CNTF) plays important roles in the maintenance and survival of motor neurons. This study attempted to explore the expression and distribution of CNTF mRNA and its protein in the ambiguous nucleus(Amb) motoneuron in order to clarify its functional state after long term laryngeal denervation. Methods: The recurrent laryngeal nerves were obtained from dogs. Brain stems were removed and sectioned for histochemistry, immunohistochemistry and in situ hybridization of CNTF. Amb motoneurons were identified by Nissl staining. The count and intensity of positive reactive motoneurons were measured by computer image processing system. Results: Transection of the laryngeal nerve led to a very marked reduction in the count and intensity of CNTF mRNA positive reactive motoneurons, and reached minimal levels at week 3. CNTF immunoreactivity increased rapidly and reached maximal levels also at week 3. At week 4, a significant increase in CNTF mRNA expression and decrease in CNTF immunoreactivity were observed. At week 6, both CNTF mRNA and its protein expression were significantly less than those of unlesioned contraletaral sides. Although a difference between week 6 and 12 was observed, the motoneurons were generally stable in the expression level of CNTF mRNA and its protein, and in the size and count after 12 weeks, with 78%, 84.4%, 80.9% and 83.7% respectively as compared with the unlesioned contralateral Amb. Conclusion: The results indicate that although degenerating changes occurre in the Amb motoneurons after long term laryngeal denervation, the ciliary neurotrophic factors activity of the lesioned motoneurons is still maintained at a certain level. [

Objective To investigate the association between cumulative exposure blood to pressure (cum BP) and new-onset chronic kidney disease (CKD).Methods In this prospective cohort study,101 510 employees of Kailuan Group receiving annual health examination during 2006 to 2007 were observed.The participants received the second,third,and fourth annual health examinations during 2008 to 2009,2010 to 2011,and 2012 to 2013 year respectively.Their urinary and serum creatinine were tested,and participants with incomplete SBP,DBP data and CKD were excluded.Further excluding those who somehow failed to take annual health examination,with incomplete data,or new-onset CKD 27 809 participants were selected in the analysis.According to cum BP exposure quintile grouping:Q1 ＜ 3.70 scores;Q2:3.70-6.16 scores;Q3:6.17-8.45 scores;Q4:8.46-10.95scores;Q5 ≥ 10.96 scores.Multivariate Logistic regression was used to analyze the association between cum BP level and new-onset CKD by cum BP exposure quintile grouping.Results The rise of cum BP exposure level caused the increased incidence of CKD.The incidences of CKD in the five quintile groups were 2.59％,3.11％,4.19％,5.81％,and 7.73％ respectively (P＜ 0.01).Compared with Q1 group,multivariate logistic regression analysis showed that after the adjustment of age,gender,education,income,smoking,drinking,BMI,FBG,TC,TG,LDL,HDL,UA and CRP,the incidences of CKD gradually increased in the Q2,Q3,Q4,and Q5 cum BP quintile groups,and OR(95％CI) values were 1.08(0.86-1.35),1.26(1.01-1.58),1.57(1.27-1.95),1.78(1.43-2.21) respectively (P for trend ＜0.01).Similar results were obtained in different genders.For each single point increase of cum BP exposure level,the incidence of CKD increased 6％ in the general population (P for trend ＜ 0.01),increased 8％ in male (P for trend ＜ 0.01),and 3％ in female (P for trend=0.12).Conclusion As the cumulative exposure to blood pressure increases,the risk of CKD incidence rises,especially in men.

OBJECTIVETo identify the small supernumerary marker chromosomes (sSMC) and guide the genetic counseling and medical treatment in two patients with Turner syndrome.

METHODSHigh resolution GTG and C banding, SRY amplification by PCR and fluorescence in situ hybridization (FISH) on metaphase chromosomes were performed to the two patients.

RESULTSThe karyotypes of the two patients were 45, X [29]/46,X, +mar[31] and 45,X[71]/46,X, +mar[29] respectively. SRY test indicated SRY-positive for patient 1, whose sSMC was originated from chromosome Y. The karyotype was confirmed as 45,X[29]/46,X,idic(Y)(q10)[31]. ish idic(Y)(q10)(RP11-115H13x2) (SRY+) by FISH. While in patient 2, the sSMC was originated from chromosome X, whose karyotype was determined as 45, X[71]/46,X, r(X)(p11.23q21)[29]. ish r(X) (p11.23q21)(AL591394.11xAC092268.3).

CONCLUSIONUsing cytogenetic and molecular cytogenetic analyses, we have identified the sSMCs in two patients with Turner syndrome, which was helpful to the clinical diagnosis and treatment.

Adolescent ; Child ; Chromosomes, Human, X ; genetics ; Chromosomes, Human, Y ; genetics ; Female ; Genetic Markers ; Humans ; In Situ Hybridization, Fluorescence ; Karyotyping ; Turner Syndrome ; genetics

Genome editing is a genetic engineering technique that uses site-directed cleavage activity of specific artificial nucleases and endogenous DNA damage repair activity to generate insertions, deletions or substitutions in the targeted genomic loci. As the accuracy and efficiency of genome editing is improving and the operation is simple, the application of genome editing is expanding. This article provides an overview of the three major genome editing technologies and genome editing types, and the regulatory frameworks for genome-edited products were summarized in the United States, the European Union, and other countries. At the same time, based on the Chinese safety management principles and systems for genetically modified organisms (GMOs), the authors proposed a regulatory framework for genome-edited products. Genome-edited products should first be classified according to whether containing exogenous genetic components such as Cas9 editing enzymes or not. They should be regulated as traditional genetically modified organisms if they do. Otherwise, the regulation of genome-edited products depends on targeted modifications.
CRISPR-Cas Systems ; Endonucleases ; Gene Editing ; Genome ; Mutagenesis, Site-Directed

The compounds of Ainsliaea yunnanensis were isolated and purified by various kinds of column chromatography methods and their structures were determined by spectroscopic data analysis. Twelve compounds were obtained from the petroleum ether of ethanolic extract of A. yunnanensis and elucidated as bauerenyl acetate (1), bauerenol (2), alpha-amyrin (3), psi-taraxasterol (4), beta-amyrin (5), echinocystic acid (6), multiflorenol (7), 3beta-hydroxy-olean-18-ene germanicol (8), 3beta-hexadecanoyl-12-oleanen-11-one (9), fernenol (10), fern-7-en-3beta-ol (11), and lupeol (12). All compounds were isolated from this genus for the first time except compound 1, 3, 5 and 10, and they were all isolated from this plant for the first time.
Asteraceae ; chemistry ; Drugs, Chinese Herbal ; chemistry ; isolation & purification ; Molecular Structure ; Spectrometry, Mass, Electrospray Ionization ; Triterpenes ; chemistry ; isolation & purification

To investigate the relationship between single nucleotide polymorphisms (SNPs) of CACNA1C (SNPs rs58619945, rs7316246 and rs216008) and susceptibility of chronic spontaneous urticaria (CSU) as well as the curative effect of non-sedating antihistamine drugs.
 Methods: Peripheral blood were extracted from 191 CSU patients to collect DNA. Urticaria Activity Score 7 (UAS7) and Dermatology Life Quality Index (DLQI) changes were collected from these patients with different non-sedating antihistamine drugs. PubMed retrieval system was used to select the 3 SNPs (rs58619945, rs7316246 and rs216008) of CACNA1C. Susceptibility of CSU and curative effect of non-sedating antihistamine drugs (desloratadine, mizolastine, fisofenadine) in 189 CSU patients and 105 controls with different SNPs were compared with Chi-squared test. Data of 105 southern Chinese controls were extracted from the 1 000 genome database.
 Results: Frequency of rs58619945 G allele in the CSU patients was significantly higher than that in the controls [OR(95%CI)=0.660(0.470-0.925), P=0.016]. However, there was no significant differences in rs7316246 and rs216008 between the CSU patients and the controls. Meanwhile there was no significant difference in general curative effect of the 3 drugs in the 3 SNPs (rs58619945: OR=0.843, P=0.454; rs7316246: OR=2.103, P=0.102; rs216008: OR=0.237, P=0.363). There was significant difference in different alleles of rs216008 in the patients administered by desloratadine [OR(95%CI)=0.480(0.247-0.933), P=0.029]. No difference was shown in the 3 SNPs in patients administered by mizolastine.
 Conclusion: The rs58619945 A/G might be related to susceptibility of CSU, and the rs216008 mutation might affect drug response of desloratadine.
Calcium Channels, L-Type ; genetics ; Chronic Disease ; Genetic Predisposition to Disease ; Histamine H1 Antagonists, Non-Sedating ; therapeutic use ; Humans ; Loratadine ; analogs & derivatives ; therapeutic use ; Polymorphism, Single Nucleotide ; Prognosis ; Retrospective Studies ; Urticaria ; drug therapy ; genetics