Objective To research in the effect of pertinent nursing method on therapeutic effect of postoperative intractable affective disorder. Methods We drew out all the patients who were in accordance with inclusion and exclusion criteria and accepted surgical treatment from June to September in 2008,and obtained 45 patients which were divided into the experimental group(21 participants) and the control group (24 participants) randomly.The experimental group adopted pertinent nmsing intervention in different periods,the control group accepted routine nursing measures.Two psychiatrists evaluated these patients' symptoms using the Brief Psychiatric Rating Scale (BPRS), Bech-Rafaelsen Mania Rating Scale (BRMS), and Hamilton Depression Scale (HAMD). Results The difference of total efficiency between the two groups had no statistical significance at 1 week and 1 month after operation, yet, obvious statistical significance was seen on 3 and 6 months after operation.The total points of all scales had no statistical significance at 1 week and 1 month after operation; however, obvious statistical significance appeared on 3 month and 6 month after operation.The improvement of symptoms of the experimental group was better than the control group. Conclusions The nurs-i ng interventions used in this research could improve the therapeutic effect of the postoperative intractable affective disorder, and the effects were reflected mainly in the long term effectiveness.

Objective To study the current situation of human brucellosis infection in a population at high risk in Qian'an,and to provide a scientific basis for prevention and control of the disease.Methods Towns with centralized residents working in sheep breeding,transporting,slaughtering and processing in Jianchangying,Muchangkou and Xiaguanying of Qian'an were selected.In each selected town,2-3 villages with relatively centralized households working in sheep farming,transportation and slaughtering were chosen.All of the people who contacted the sheep or their excrement were chosen as monitoring objects,and serological antibody was tested with rose Bengal plate test(RBPT) and serum agglutination test(SAT).Regional,gender,age and occupational distribution of brucellosis were analyzed.Results A total of 367 blood samples were tested,46 of them were positive in both RBPT and SAT with a ratio of 12.53％ (46/367).Male positive rate [13.51％ (30/222)] was slightly higher than that of females [11.03％(16/145)].The rate in Jianchangying was higher than that of other two towns with a ratio of 13.38％(40/299).The veterinary population had the highest ratio of 33.33％(1/3).Conclusions It is necessary to carry out the surveillance on brucellosis and to further strengthen communication with the animal husbandry department,and strengthen protection on key population.At the same time,in order to control the spread of the disease,extensive health education and intervention measures should be carried out.

OBJECTIVETo investigate the T13254C polymorphism frequency in GPVI gene among Chinese Han population and its relevance to the arterial thrombotic diseases.

METHODSThe enrolled population in this study consisted of 314 healthy subjects and 274 patients with myocardial or cerebral infarctions. GPVI T13254C genotypes were determined by PCR amplification of a 355 bp fragment encompassing exon 5 of GPVI gene, followed by Msp I digestion of the product. The digested products were analyzed in 15% polyacrylamide gel electrophoresis (PAGE).

RESULTSThe frequencies of the T allele and C allele in the T13254C polymorphism were 0.9809 and 0.0191, respectively, with a frequency of heterozygous of 0.0319, which were significantly different from those reported in western population (P < 0.01). As compared with controls, no significant difference in T13254C genotype distribution was found in the arterial thrombotic diseases group.

CONCLUSIONThe GPVI T13254C polymorphism appears in a low frequency in Chinese Han population. No relationship is found between T13254C polymorphism and the risk for thrombotic diseases.

Adult ; Aged ; Aged, 80 and over ; Alleles ; Asian Continental Ancestry Group ; genetics ; Base Sequence ; Brain Infarction ; ethnology ; genetics ; China ; Female ; Gene Frequency ; Genotype ; Humans ; Male ; Middle Aged ; Molecular Sequence Data ; Myocardial Infarction ; ethnology ; genetics ; Platelet Membrane Glycoproteins ; genetics ; Polymorphism, Single Nucleotide

OBJECTIVETo identify the genetic defect underlying congenital afibrinogenemia in a Chinese family.

METHODSPlasma fibrinogen (Fg) was assessed by both Clauss method and immunonephelometry. Genomic DNA was isolated from peripheral blood of the proband and 13 members of her family. All the exons and exon-intron boundaries of the three fibrinogen genes (FGA, FGB, FGG) were amplified by PCR followed by direct sequencing. Restriction endonuclease analysis was performed for the PCR products of the family members and 50 healthy donors to exclude gene polymorphism.

RESULTSNo Fg was detected in the plasma of the proband and her father by Clauss method, while low levels (< 0.02 g/L) were detected by immunonephelometry. A homozygous C to T mutation was found in the two cases at nucleotide 3108 in exon 4 of FGA gene, resulting in a null mutation which encoded severely truncated alpha-chains owing to its premature termination at the Gln 150 codon. The C-->T mutation eliminated a unique recognition site for restriction enzyme RsaI. The PCR amplified fragments of the proband and her father could not be digested by RsaI, showing that they are homozygous. Her mother and some family members are heterozygous at this site since the fragment could partly be digested, while the same fragment of controls could be completely digested as expected.

CONCLUSIONThe Gln (CAG)-->150stop (TAG) nonsense mutation in FGA gene is a novel genetic defect of congenital afibrinogenemia which, to our knowledge, has not been described before.

Adolescent ; Afibrinogenemia ; congenital ; genetics ; Base Sequence ; Codon, Nonsense ; DNA Mutational Analysis ; Exons ; genetics ; Female ; Fibrinogen ; genetics ; Humans ; Male ; Pedigree

OBJECTIVETo construct the expression vectors of vWF73 and vWF114 fragments of von Willebrand factor (vWF) A2 domain, and to express glutathione S-transferase (GST) fusion proteins in E. coli, and to explore their values in measuring ADAMTS13 activity as substrates.

METHODSThe DNA fragments encoding vWF73 and vWF114 were generated using PCR and separately cloned into pGEX-6P-1, a Schistosoma japonicum GST fusion expression vector. The expression of GST-vWF73-H and GST-vWF114-H was induced in liquid culture, followed by purification with Ni-NTA agarose column. The cleavage of two GST fusion proteins by recombinant ADAMTS13 (rADAMTS13) or plasma from normal individuals and thrombotic thrombocytopenic purpura (TTP) patients were identified by Western blot. Based on an enzyme-linked immunosorbent assay (ELISA) with anti-GST and anti-His monoclonal antibodies, GST-vWF73-H and GST-vWF114-H were used to measure plasma ADAMTS13 activity as substrates.

RESULTSTwo small molecular substrates of ADAMTS13, GST-vWF73-H and GST-vWF114-H, are expressed and purified, which could be specifically cleaved by rADAMTS13 or plasma from healthy individuals, but not by plasma from congenital or idiopathic TTP patients. An ELISA assay was established to detect plasma ADAMTS13 activity using GST-vWF73-H and GST-vWF114-H as substrates.

CONCLUSIONSTwo GST fusion proteins in vWF A2 domain, vWF73 and vWF114, were expressed effectively using a prokaryotic expression system and could be used to detect ADAMTS13 activity as substrates.

ADAM Proteins ; blood ; genetics ; ADAMTS13 Protein ; Enzyme-Linked Immunosorbent Assay ; Escherichia coli ; metabolism ; Glutathione Transferase ; metabolism ; Humans ; Male ; Purpura, Thrombotic Thrombocytopenic ; blood ; genetics ; metabolism ; von Willebrand Factor ; genetics ; metabolism

OBJECTIVETo explore the biological effect on NB4 cells proliferation, all-trans retinoic acid (ATRA) inducing differentiation and resistance to apoptosis by vascular endothelial growth factor (VEGF)-C cDNA transfection.

METHODSThe recombinant eukaryotic expression plasmid pcDNA3.1-VEGF-C and the vacant pcDNA3.1 vector were introduced separately into NB4 cells by lipofectamine mediation. The positive clones were screened by G418 and identified by reverse transcriptase-PCR (RT-PCR) and Western blotting. The proliferation capacity of NB4/VEGF-C cells was analysed by MTT assay and colony forming assay in vitro. After NB4/VEGF-C cells were induced by ATRA, the expression level of C/EBPalpha gene, CD11b on cells surface and morphological alteration were analysed by real-time quantitative PCR (RQ-PCR), flow cytometry (FCM), and Wright-Giemsa staining, respectively. FCM Annexin V-FITC/PI dual labeling technique was performed to investigate the etoposide (Vp16) induced NB4/VEGF-C cells apoptosis and bcl-2 gene expression level in these cells was analysed by RQ-PCR. The NB4/pcDNA3.1 cells was used as control in the above experiments.

RESULTSA stable NB4 cell line that secrets VEGF-C and its control lines were established. The proliferation capacity of the former was stronger than that of the latter. The expression level of C/EBPalpha gene of NB4/VEGF-C cells on ATRA treatment was only 1/32 that of NB4/pcDNA3.1 cells. The CD11b level and the degree of differentiation of NB4/VEGF-C were weaker than that of NB4/pcDNA3.1 cells. The percentage of apoptotic NB4/VEGF-C cells induced by Vp16 [(7.20 +/- 2.52)%] was significantly lower than that of NB4/pcDNA3.1 cells [(16.07 +/- 3.58)%] (P = 0.005), but the bcl-2 gene expression level of NB4/VEGF-C cells is 2.28-fold that of NB4/pcDNA3.1 cells.

CONCLUSIONThe VEGF-C via VEGFR-3 signaling pathway could promote the proliferation of leukemic cells by autocrine pathway and inhibit the cell differentiation mediated by ATRA and chemotherapy-induced apoptosis. VEGF-C/VEGFR-3 signaling loops might play an important role in disease progression and be potential therapeutic target for the treatment of leukemias.

Apoptosis ; drug effects ; genetics ; physiology ; Blotting, Western ; CCAAT-Enhancer-Binding Protein-alpha ; genetics ; metabolism ; CD11b Antigen ; genetics ; metabolism ; Cell Differentiation ; genetics ; physiology ; Cell Line, Tumor ; Cell Proliferation ; DNA, Complementary ; genetics ; Drug Resistance, Neoplasm ; Flow Cytometry ; Genetic Vectors ; Humans ; Leukemia, Promyelocytic, Acute ; genetics ; metabolism ; pathology ; Reverse Transcriptase Polymerase Chain Reaction ; Transfection ; Tretinoin ; pharmacology ; Vascular Endothelial Growth Factor C ; genetics ; metabolism ; physiology

OBJECTIVETo investigate the antigen levels and activity of von Willebrand factor cleaving protease ADAMTS13 in thrombotic thrombocytopenic purpura (TTP) patients and carriers.

METHODS28 samples from 13 TTP patients and 10 samples from the carriers were examined. The activity of ADAMTS13 was measured by residue collagen binding assay, and antigen by a newly developed sandwich ELISA.

RESULTSThe mean ADAMTS13 level in Chinese normal controls (CN) was (600.93 +/- 145.36) mU/ml (n = 26) comparable to the level (1000 mU/ml) in pooled normal Caucasian plasma, and the activity was (74.79 +/- 11.81)%. Both the antigen level and activity of ADAMTS13 in congenital TTP patients either before plasma exchange (pre-PE) or interval relapse were quite lower than those in normal control, but were increased after PE (post-PE). The antigen was (331.40 +/- 109.85) mU/ml (P < 0.01, n = 10), and activity was (66.79 +/- 12.82)% (P > 0.05). The ADAMTS13 levels pre-PE in idiopathic TTP was (98.7 +/- 82.08) mU/ml (n = 11, P < 0.01), and that post-PE was up to (449.4 +/- 232.33) mU/ml (P < 0.01, n = 10). The activity of ADAMTS13 in patients pre-PE and post-PE were (22.23 +/- 19.07)% (P < 0.01) and (60.92 +/- 22.33)% (P > 0.05) respectively. In a secondary TTP patient the ADAMTS13 antigen was much higher than that in CN, and the activity was 6.00%.

CONCLUSIONThe antigen and activity of ADAMTS13 in most TTP patients pre-PE are deficient, and these two indices in most TTP patients are paralleled. The reason for ADAMTS13 deficiency is congenital shortage or clearance by immune system, but it is unknown that why in some patients the ADAMTS13 antigen is extremely high but its activity is quite low.

ADAM Proteins ; blood ; immunology ; ADAMTS13 Protein ; Adult ; Female ; Humans ; Male ; Purpura, Thrombotic Thrombocytopenic ; blood ; immunology

OBJECTIVETo identify the genetic defect of inherited coagulation factor (F) deficiency in a Chinese family and to explore its molecular mechanism.

METHODSThe activity and antigen of plasma F were measured by photometric test and enzyme-linked immunosorbent assay, and rocket-electrophoresis, respectively. All the exons and exon-intron boundaries of the FA subunit gene were amplified by PCR and then DNA sequencing was performed. Restriction endonuclease analysis was used for the PCR products of the family members and 80 healthy donors to exclude gene polymorphism.

RESULTSRapid dissolution of the proband's fibrin clot occurred within 30 minutes, and antigen of his plasma F was significantly decreased, two compound heterozygous missense mutations (a C to T transition at nucleotide 177,246 which caused Arg703Trp, and a A to G transition at nucleotide 177,286 which caused His716Arg) in exon 15 of FA subunit gene were found. The possibility of gene polymorphism was excluded by restriction endonuclease analysing. Each of these two missense mutations was respectively found in his mother and father. Molecular modeling based on 3D crystallographic data predicted that the mutant protein decreased stability and was likely to be rapidly degraded.

CONCLUSIONSThe inherited F deficiency in the Chinese family is caused by two compound heterozygous missense mutations-Arg703Trp and His716Arg in the FA subunit, which to our knowledge, are reported for the first time.

Base Sequence ; Child ; Exons ; Factor XIII ; genetics ; Factor XIII Deficiency ; genetics ; Heterozygote ; Humans ; Male ; Molecular Sequence Data ; Mutation, Missense ; Pedigree

OBJECTIVETo probe the mechanism of EEG activation and Xingnao Kaiqiao, evaluate the actions of cinnabaris and realgar in Xingnao Kaiqiao of Angong Niuhuang pill, guess the significance of cinnabaris and realgar in specific indication treatment of Angong Niuhuang pill, and provide experimental bases for the rationality of Angong Niuhuang pill building-up.

METHODSeventy SD rats were divided into seven groups: the control, the model, the Angong Niuhuang pill (0.4 g x kg(-1)), the Angong Niuhuang pill without cinnabaris and realgar (0.32 g x kg(-1)) , the cinnabaris and realgar (0.08 g x kg(-1)), the realgar (0.04 g x kg(-1)), and the cinnabaris (0.04 g x kg(-1)). Rats in the control and model groups were given distilled water. After three days of administration, the brain damage model was made by Lipopolysaccharides (LPS) injection through caudal vein and the catecholamine (CA) and its metabolites levels in cerebral cortex, included noradrenaline (NE), adrenaline (E), 3-methocy-4-hydroxyphenylglycol (MHPG), 5-hydroxytryptamine (5-HT), 5-hydroxyindoleacetic acid (5-HIAA), dopamine (DA), Homovanlic acid (HVA), 3,4-dihydroxyphenylacetic acid (DOPAC), were determined by high-performance liquid chromatography with electrochemical detector (HPLC-ECD). Influences of Angong Niuhuang pill, Angong Niuhuang pill without cinnabaris and realgar, cinnabaris and realgar on monoamine transmitters were observed in brain damage rats caused by LPS.

RESULTLPS could raise NE, 5-HT, 5-HIAA levels and reduce E, DOPAC levels, but had no influence on HVA, DA, MHPG levels. Angong Niuhuang pill had the trend of raising E, DOPAC levels and reducing NE level, and could reduce 5-HIAA level obviously comparing with models. But Angong Niuhuang pill without cinnabaris and realgar was different, NE level was significantly higher compared to models and Angong Niuhuang pill, DA level was also significantly higher compared to all groups. Cinnabaris and realgar had the same action trends with Angong Niuhuang pill, and separate realgar could obviously reduce 5-HT.

CONCLUSIONInfluence on CA and its metabolites levels in cerebral cortex may be one of the mechanisms of Angong Niuhuang pill's EEG activation, and cinnabaris and realgar have the same action on CA levels in cerebral cortex. The results of the present work allow us to put forward the hypothesis that cinnabaris and realgar are most likely one of the important material basis in Xingnao Kaiqiao of Angong Niuhuang pill.

Animals ; Arsenicals ; pharmacology ; Brain Injuries ; chemically induced ; metabolism ; physiopathology ; Catecholamines ; metabolism ; Cerebral Cortex ; metabolism ; physiopathology ; Drug Combinations ; Electroencephalography ; drug effects ; Lipopolysaccharides ; Male ; Medicine, Chinese Traditional ; Mercury Compounds ; pharmacology ; Norepinephrine ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Serotonin ; metabolism ; Sulfides ; pharmacology

OBJECTIVETo investigate the gene mutations of ADAMTS13 in a highly suspected hereditary thrombocytopenic purpura (TTP) patient, and then make a progressive diagnosis and adjust the plan of therapy.

METHODSADAMTS13 activity and inhibitor were determined by residual-collagen binding assay during several episodes. Genomic DNA extracted from the proband's peripheral blood was used for amplification of 29 exons and exon/intron boundaries of ADAMTS13 by PCR. The PCR products were screened by direct sequencing and the gene alterations were further confirmed by direct sequencing in her family members.

RESULTThe activity of the proband's ADAMTS13 was significantly reduced while no inhibitor was found. Two novel missense mutations were found in the TSPI repeated motif domain of ADAMTS13. In both mutations, thymine substituted for cytidine, resulting in the substitution of leucine for serine in nt 2708, exon 21 (codon S903L), and tryptophan for arginine in nt 3283, exon 25(codon R1095W). These two mutations were revealed as each heterozygote in the proband's parents.

CONCLUSIONThe deficiency of ADAMTS13 caused by two homozygote missense mutations might be responsible for episode of this TTP patient.

ADAM Proteins ; genetics ; Adult ; Exons ; genetics ; Female ; Humans ; Mutation ; Purpura, Thrombotic Thrombocytopenic ; genetics