This study is to investigate therapeutic effect of astaxanthin on acetic acid-induced gastric ulcer in rats. Rats were divided into control group, ulcer control group, and astaxanthin (5, 10, and 25 mg x kg(-1)) groups at random, 8 rats in each group. After administered for 10 days consecutively, all the rats were sacrificed. The area of ulcer and the levels of MDA, SOD, CAT and GSH-Px in gastric mucosa were measured. Compared with ulcer control group, in astaxanthin (5, 10, and 25 mg x kg(-1)) groups, the area of ulcer was decreased significantly. Level of MDA decreased while activities of SOD, CAT and GSH-Px increased (P < 0.05). Astaxanthin has good therapeutic effect on acetic acid-induced gastric ulcer in rats. Eliminating free radical and improving local blood circulation of the ulcer may be the mechanism of action.
Acetic Acid ; Animals ; Anti-Ulcer Agents ; therapeutic use ; Antioxidants ; therapeutic use ; Catalase ; metabolism ; Gastric Mucosa ; metabolism ; pathology ; Glutathione Peroxidase ; metabolism ; Male ; Malondialdehyde ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Stomach Ulcer ; chemically induced ; drug therapy ; metabolism ; pathology ; Superoxide Dismutase ; metabolism ; Xanthophylls ; therapeutic use

Objective To discuss the effect of positive nursing intervention on quality of life of patients with post-herpetic neuralgia.Methods 80 cases of patients with post-herpetic neuralgia from January 2011 to June 2012 were chosen and randomly divided into the control group and the treatment group,each with 40 cases.Both groups received neural stem closure therapy,and the treatment group was given positive nursing intervention in addition,including humane care,synchronized implementation of home care guidance by caregivers,hope nursing and telephone interviews.NRS and SF-36 were used to evaluate the curative effect and quality of life,and indexes were compared between two groups.Results The excellence rates 30 and 60 days after treatment were 100％ in the treatment group,obviously higher than 85.0％ in the control group,and the differences were statistically significant (x2 =5.1,7.6,respectively; P ＜ 0.05).There was no statistically significant difference of SF-26 between two groups before treatment (P ＞ 0.05).30 days after treatment,the score of physical function,body pain and general health was (56 ± 22.5),(79 ± 11.9),(73 ± 17.8) in the treatment group,higher than (44 ± 16.7),(63 ± 21.2),(59 ± 16.7) in the control group,and the differences were statistically significant (t =2.71,4.16,3.63,respectively; P ＜ 0.05).60 days after treatment,the score of physical function,body pain and general health was (68 ± 21.7),(82 ± 14.8),(79 ± 18) in the treatment group,higher than (46.6 ± 14.3),(70 ±22.3),(66 ± 18.2) in the control group,and the differences were statistically significant (t =5.21,2.84,3.21,respectively; P ＜ 0.05).Conclusions Positive nursing interventions can significantly improve the curative effect and quality of life of patients with post-herpetic neuralgia,which can also improve the quality of medical care obviously.

This study was aimed to establish the real-time fluorescent quantitative PCR (RT-qPCR) with erythrocyte Kidd blood group gene for detecting the hematopoietic chimera and to investigate the feasibility of this method. The TaqMan MGB probes and special primers were designed on basis of difference of erythrocyte Kidd blood group alleles, the hematopoietic chimerism was detected by RT-qPCR, the DNA chimerism was simulated by means of dilution of multiple proportions, and the sensitivity analysis was performed. The results showed that the RT-qPCR with erythrocyte Kidd blood group gene could effectively distinguish JK*A and JK*B alleles. There was no significant difference between the theoretic value and the practical measured value by this method (P > 0.05). As 156 donor's cells could be discriminated from 10(4) chimeric cells, this method may effectively detect donor's cells with correlation coefficient 0.998. It is concluded that the established RT-qPCR with erythrocyte Kidd blood group gene shows the feasibility for quantitative detection of hematopoietic chimera, and may be used to quantitatively detect chimera in a certain range.
Chimera ; Erythrocytes ; Humans ; Kidd Blood-Group System ; genetics ; Real-Time Polymerase Chain Reaction

This study was aimed to investigate the distribution of rare blood group in Zhejiang Han population. The H(-) (H system), GPA(-) and s(-) (MNS), Rhnull, Rhmod, D--, CCDEE, CCdEE (variations of Rh), GPC(-) (Gerbich), i(+) (I), Lu(b-) (Lutheran), Js(b-) and k(-) (Kell), Fy(a-) (Duffy), Ok(a-) (Ok), Di(b-) (Diego) phenotypes were screened by serological or molecular methods. Jk (a-b-) phenotype was detected by urea hemolytic test. The results showed that one Di (a+b-) individual was found in 1618 blood donors, three Fy (a-b+) individuals in 1007 donors and one CCdEE individual in 633 Rh negative donors. No Jk (a-b-), H(-), GPA(-), s(-), GPC(-), i(+) (adult), Lu(b-), k(-), Js(b-), Lu(b-) and Ok(a-) phenotypes were found in this large scale survey. It is concluded that Di (a+b-), Fy (a-b+), CCdEE phenotypes are confirmed in the blood donors and this study provides the distribution data of erythrocyte rare blood group in Zhejiang Han population.
Asian Continental Ancestry Group ; genetics ; Blood Group Antigens ; genetics ; Blood Grouping and Crossmatching ; methods ; Erythrocytes ; immunology ; Humans ; Molecular Biology ; Phenotype

OBJECTIVETo study the mechanism underlying the effect of combined use of cyclonpamine and hydroxycamptothecin in inducing the apoptosis of human oral squamous cell carcinoma cell line (OSCC) HSQ-89.

METHODSCCK8 assay was used to investigate the inhibitory effect of cyclopamine on HSQ-89 cells. Flow cytometry (FCM) was employed to examine the cell apoptosis following combined treatment with cyclonpamine and hydroxycamptothecin. Reverse transcription polymerase chain reaction (RT-PCR) was applied to detect the mRNA expressions of Bcl-2, Bcl-xl, and Bid in HSQ-89 cells after the treatments.

RESULTSCombined treatment with cyclonpamine and hydroxycamptothecin significantly inhibited the cell proliferation compared with hydroxycamptothecin treatment alone, also resulting in a significantly higher apoptosis rate of the cells (P<0.05). The mRNA level of Bcl-2 was significantly decreased after the treatments, especially after the combined treatment. Cyclopamine produced no significant effect on the mRNA levels of Bcl-xl and Bid in the cells.

CONCLUSIONThe combined use of cyclopamine and hydroxycamptothecin significantly down-regulates the expression on of bcl-2 to induce the apoptosis of human OSCC cell line HSQ-89.

Antineoplastic Agents ; pharmacology ; Apoptosis ; drug effects ; Camptothecin ; analogs & derivatives ; pharmacology ; Carcinoma, Squamous Cell ; pathology ; Cell Line, Tumor ; Drug Synergism ; Humans ; Mouth Neoplasms ; pathology ; Proto-Oncogene Proteins c-bcl-2 ; genetics ; metabolism ; RNA, Messenger ; genetics ; metabolism ; Veratrum Alkaloids ; pharmacology

OBJECTIVETo analyze the molecular basis for an individual with ABx09 phenotype of ABO subtype.

METHODSThe ABO group antigens on red blood cells of the proband were identified by monoclonal antibodies, and the ABO antibody in serum was detected by standard A, B, O cells. The exons 1 to 7 of ABO gene were amplified by polymerase chain reaction (PCR) respectively and the PCR products were sequenced directly. The amplified products for exons 5 to 7 were also cloned by TOPO TA cloning sequencing kit to split the two alleles apart, selected colonies were sequenced bidirectionally for exons 5 to 7 of the ABO gene. The samples of the proband's parents were collected, then serological test of the blood group and sequence analysis for exons 6 and 7 of ABO gene were preformed.

RESULTSBoth A and B antigens were detected on red blood cells of the proband and there was anti-B antibody in the serum. There was no G deletion at position 261, while 297AG in exon 6, 467CT, 526CG, 657CT, 703GA, 796CA, 803GC, 889GA and 930GA heterozygote in exon 7 were detected by direct DNA sequencing, which can be assigned for A102Bx09 genotype. After cloning and sequencing, two alleles A102 and Bx09 were obtained. The sequence of Bx09 had one nucleotide changes (G to A) at position 889 compared with that of B101, which resulted in an amino acid change of Glu to Lys at 297 position. The Bx09 in the proband was inherited from her mother by family investigation.

CONCLUSIONG to A at nt889 of alpha-1,3 galactosyltransferasegene can result in Bx09 phenotype, with the presence of anti-B antibody in serum.

ABO Blood-Group System ; genetics ; metabolism ; Adolescent ; Alleles ; Base Sequence ; Blood Grouping and Crossmatching ; Female ; Gene Frequency ; Genotype ; Humans ; Molecular Sequence Data ; Pedigree ; Phenotype

OBJECTIVETo establish the eukaryotic cell expression system for the alpha-1,2 fucosyltransferase gene FUT1 293C to T and 658C to T mutations and explore the mechanism of FUT1 mutations resulting in the reduced expression of H antigen.

METHODSGenomic DNAs were extracted from individuals with para-Bombay phenotype and full coding region of FUT1 was amplified. The amplification fragments were ligated with pcDNA3.1 plasmid to construct the recombinant expression vectors. The recombinant plasmids were transfected into the COS-7 cells using lipofectamine transfection reagent and stable expression screening was performed. FUT1 mRNA expression was determined by real-time quantitative PCR. The activity of enzyme was measured by high performance liquid chromatography. Expressed protein was identified by SDS-PAGE and Western blotting.

RESULTSpcDNA3.1-FUT1 wildtype, pcDNA3.1-FUT1 293C to T and pcDNA3.1-FUT1 658C to T recombinant vectors were constructed, respectively. COS-7 cells with stable expression of FUT1 were obtained through recombinant plasmid transfection and screening with G418. The FUT1 mRNA level of transfected cells with 293C to T and 658C to T recombinant vectors reached 97.10% and 104.74% of the wildtype FUT1 transfected cell. A specific protein band with about 46 000 was confirmed in the transfected cell lysates by SDS-PAGE electrophoresis and Western blotting with 6×His Tag antibody. The wildtype FUT1 transfected cell lysates can catalyze the enzymatic reaction, while the enzyme activity of cell lysates from 293C to T and 658C to T were abolished.

CONCLUSIONThe results suggested that the 293C to T and 658C to T mutations of FUT1 gene did not affect the RNA and protein expression levels, but the enzyme activity of cells with FUT1 mutations was significantly decreased which resulted in the reduced expressin of H antigen.

Animals ; COS Cells ; Cercopithecus aethiops ; Fucosyltransferases ; genetics ; metabolism ; Gene Expression Regulation ; Genetic Vectors ; genetics ; Mutant Proteins ; genetics ; metabolism ; RNA, Messenger ; genetics

OBJECTIVETo investigate the distribution of translocation between chromosomes 4q35 and 10q26 in facioscapulohumeral muscular dystrophy (FSHD) patients and normal individuals.

METHODSThe Bgl II-Bln I dosage test was performed to study the distribution of translocation between chromosomes 4q35 and 10q26 in 70 cases of FSHD patients, 55 cases of kindred with FSHD, and 52 cases of normal controls.

RESULTS(1) In normal individuals, the frequency of translocation between chromosomes 4q35 and 10q26 is 19.23%. The frequency of translocation from chromosome 4q35 to 10q26 and that from chromosome 10q26 to 4q35 are both 9.62%. (2) In the FSHD patients, the frequency of translocation between chromosomes 4q35 and 10q26 is 18.57%. The frequency of translocation from chromosome 4q35 to 10q26 and that from chromosome 10q26 to 4q35 are 12.86% and 5.71% respectively.

CONCLUSIONSThe translocation between chromosomes 4q35 and 10q26 was frequently observed in both normal Chinese population and FSHD patients. No significant difference was observed between them.

Adolescent ; Adult ; Aged ; Aged, 80 and over ; Child ; Chromosomes, Human, Pair 10 ; genetics ; Chromosomes, Human, Pair 4 ; genetics ; Female ; Genotype ; Humans ; Male ; Middle Aged ; Muscular Dystrophy, Facioscapulohumeral ; genetics ; Translocation, Genetic

OBJECTIVETo investigate the molecular genetic basis of the B3 variant of ABO blood group system with mixed-field hemagglutination in Chinese.

METHODSSerological techniques were performed to characterize the erythrocyte phenotype of two discrepant samples. A sequential agglutination method and 13 short tandem repeat (STR) loci were tested to exclude the possibility of exogenous or endogenous DNA chimera. Mutations in exons 6 and 7, including partial intron of the ABO gene, were screened by polymerase chain reaction and DNA sequencing. Haplotypes of the two individuals were also analyzed by sequencing.

RESULTSA mixed-field hemagglutination of RBCs with anti-B and anti-AB antibodies was detected in the two unrelated individuals. Exogenous ABO-incompatible RBC transfusion and endogenous genetic chimera were excluded by sequential agglutination method and STR. The ABO phenotypes of the two individuals were classified as A1B3 according to the ABO subgroup definition. The sequence region from intron 5 to 3'-UTR of the B allele was identical to that of ABO*B101 allele, except for a T to C substitution at nucleotide position 425 in exon 7. This substitution resulted in an amino acid change of M142T in the B glycosyltransferase.

CONCLUSIONA novel B allele with 425T>C substitution resulting in B3 subgroup was identified in two Chinese individuals.

1,4-alpha-Glucan Branching Enzyme ; genetics ; ABO Blood-Group System ; genetics ; Alleles ; Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Asian Continental Ancestry Group ; genetics ; Cattle ; DNA Mutational Analysis ; Dogs ; Humans ; Methionine ; genetics ; Mice ; Molecular Sequence Data ; Mutation ; Phenotype ; Rats ; Sequence Alignment ; Sequence Analysis, DNA ; Threonine ; genetics

OBJECTIVETo explore the effects of epigallocatechin-3-gallate (EGCG) on the proliferation of human oral epithelial cancer cell line KB cells and the molecular mechanisms.

METHODKB cells were treated with various concentrations of EGCG for 24 or 48 h. MTT assay was used to test the cell viability. The changes of cell cycle in KB cells treated with EGCG for 48 h were analyzed using flow cytometry. The expressions of cyclin A, cyclin D1 and cyclin E were detected by RT-PCR and Western blotting.

RESULTThe viability of KB cells treated with various concentrations of EGCG (25, 50, 100, 200, 400, and 800 micromol/L) for 48 h were decreased to (85.4-/+2.4)%, (80.4-/+2.8)%, (51.5-/+4.5)%, (30.2-/+1.9)%, (25.3-/+1.5)%, (20.0-/+1.1)%, respectively, showing significant difference from that of the control group [(100.0-/+2.2)%, P<0.05). EGCG decreased the viabilities of KB cells in a dose-dependent manner. Flow cytometry demonstrated that treatment with EGCG significantly increased the cell percentage in sub-G1 phase, which was (73.5-/+4.4)% after a 48-h EGCG treatment, significantly different from that in the control group [(47.3-/+3.5)%, P<0.05). EGCG-induced G1 phase arrest was correlated to the down-regulation of cyclin A and cyclin E.

CONCLUSIONEGCG inhibits the proliferation of KB cells by inducing G1 phase arrest, which involves the downregulation of cyclin E.

Catechin ; analogs & derivatives ; pharmacology ; Cell Cycle ; drug effects ; Cell Proliferation ; drug effects ; Cyclin E ; metabolism ; Flow Cytometry ; G1 Phase Cell Cycle Checkpoints ; drug effects ; Humans ; KB Cells ; Oncogene Proteins ; metabolism