The changes of kernel nutritive components and seed vigor in F1 seeds of sh2 sweet corn during seed development stage were investigated and the relationships between them were analyzed by time series regression (TSR) analysis. The results show that total soluble sugar and reducing sugar contents gradually declined, while starch and soluble protein contents increased throughout the seed development stages. Germination percentage, energy of germination, germination index and vigor index gradually increased along with seed development and reached the highest levels at 38 d after pollination (DAP). The TSR showed that, during 14 to 42 DAP, total soluble sugar content was independent of the vigor parameters determined in present experiment, while the reducing sugar content had a significant effect on seed vigor. TSR equations between seed reducing sugar and seed vigor were also developed. There were negative correlations between the seed reducing sugar content and the germination percentage, energy of germination, germination index and vigor index, respectively. It is suggested that the seed germination, energy of germination, germination index and vigor index could be predicted by the content of reducing sugar in sweet corn seeds during seed development stages.
Carbohydrates ; analysis ; Germination ; Seeds ; growth & development ; Zea mays ; chemistry ; growth & development

OBJECTIVETo explore the correlation between the recurrence of cerebral infarction and aspirin resistance (AR)/Chinese medical (CM) constitutions.

METHODSTotally 413 cerebral infarction patients took Aspirin Enteric-coated Tablet (100 mg per day) while receiving routine therapy, 5 days at least in a week. They were followed-up for 12 months. Aspirin sensitivity (AS) was determined using turbidimetry. CM constitutions among patients with different AS were compared. Ratios of AR patients and AS patients of different CM constitutions in cerebral infarction recurrent patients were compared. Platelet membrane glycoproteins (GP) II b HPA-3 gene polymorphism was detected by polymerase chain reaction (PCR) method. Correlation between recurrence of cerebral infarction and AR, bb genotypes, CM constitutions times AS were analyzed by Logistic regression.

RESULTSTotally 11 patients dropped out, 101 (25.12%)with recurrent cerebral infarction and 301 (74.88%) without recurrent cerebral infarction. There were 152 (37.81%) AR patients and 250 (62.19%) AS patients. AR accounted for 26.6% (80/ 301) and AS accounted for 73.4% (221/301) in non-recurrent cerebral infarction patients. AR accounted for 71.3% (72/101) and AS accounted for 28.7% (29/101) in recurrent cerebral infarction patients. There was statistical difference in AR and AS ratios (χ2 = 64.287, P = 0.000). The proportion of yin deficiency constitution (YDC) was the largest [28.3% (43/152)] in AR patients. The proportion of blood stasis constitution (BSC) was the largest [23.6% (59/250)] in AS patients. There was statistical difference in CM constitutions between AR patients and AS patients (χ2 = 21.574, P < 0.01). The former 4 recurrent rates occurred in AR patients of YDC, BSC, damp-phlegm constitution (DPC), qi deficiency constitution (QDC). YDC occupied the first place [22.4% (34/152)]. The former 4 recurrent rates occurred in AS patients of BSC, QDC, DPC, damp-heat constitution (DHC). BSC occupied the first place [3.2% (2/250)]. Compared with non-recurrent cerebral infarction patients and AS patients, bb gene occurred most often, but aa gene and ab gene occurred obviously lesser in non-recurrent cerebral infarction patients and AR patients (χ2 = 20.171, χ2 = 55.139, P < 0.01). AR and bb gene were positively correlated with recurrent cerebral infarction (OR = 18.423, P = 0.000; OR = 1.304, P = 0.028). Body constitutions interacted with AS (OR = 0.707, P = 0.000).

CONCLUSIONSRecurrent cerebral infarction was closely related to AR and constitutional types. The recurrence rate was higher in AR patients of YDC. GP I b HPA-3 bb genotype might be a risk factor for AR and recurrent cerebral infarction.

Aspirin ; therapeutic use ; Body Constitution ; Cerebral Infarction ; Drug Resistance ; Humans ; Medicine, Chinese Traditional ; Neoplasms ; Recurrence ; Yin Deficiency

Objective To study the mechanism of marcosomia by investigating insulin-like growth factor 2(IGF_2)imprinting status,expression level and the promoter usage in the placenta of macrosomia. Methods We selected heterozygous cases for Apa Ⅰ polymorphism in exon 9 of IGF_2 gene and then analyzed its imprinting status in 168 placentas of macrosomia and normal pregnancies.IGF_2 transcription levels and promoter usages in macrosomic and normal placenta were evaluated by using semi-quantitative RT- PCR assay.Results Thirty specimens of macrosomic placenta and 30 of normal placenta were identified as heterozygous for IGF_2.All of the heterozygous specimens showed maintenance of imprinting.The expression of placental IGF_2 mRNA(2.2?1.2)was significantly higher in macrosomia than that of normal weight group (1.6?0.6,P 0.05).Conclusion It is possible that over expression of IGF_2 in placenta contributes to macrosomia while the promoter usage and imprinting status are not associated with macrosomia.

To explore the possible linkage between telomerase and acute leukemia, we detected telomerase activity expressed in 3 leukemia cell lines, 22 acute leukemia bone marrow and 6 normal bone marrow with PCR ELISA assay. Results showed that telomerase activities of three leukemia cell lines were positive with the average (1.57 +/- 0.056) U, normal bone marrow samples average was (0.085 +/- 0.081) U, telomerase value from 22 acute leukemia patients was (0.512 +/- 0.294) U. Telomerase activity is higher expressed in acute leukemia than normal samples and decreased significantly after chemotherapy (P < 0.01). The results suggested that telomerase activity was related to some malignant diseases and might be used as a marker for tumor diagnosis and therapy.

OBJECTIVETo investigate the association among serous and cerebrospinal fluid (CSF) TNF-alpha level, gene polymorphisms of TNF-alpha and multiple sclerosis (MS) in Han nationality of southern China.

METHODSMS diagnosis was base on Poser (1983) criteria. Fifty-five patients with nonimmulogical diseases and 68 patients with MS from southern China were enrolled in the study, and their TNF-alpha level of serum and CSF were measured by double antibody sandwich ABC-ELISA. TNF-alpha -308G/A in 106 normal healthy subjects and 68 MS patients was genotyped with polymerase chain reaction-restriction fragment length polymorphism.

RESULTSThere was significant difference in the serous TNF-alpha level between nonimmune patients and active MS patients (234+/- 76 pg/mL vs 276+/- 71 pg/mL, P< 0.05), but not in the CSF (245+/- 83 pg/mL vs 265+/- 78 pg/mL, P> 0.05). The gene frequency distribution of TNF-alpha -308G/A was corresponding with Hardy-Weinberg equilibrium. The positive rate of genotype AA and the gene frequency of allele A of TNF-alpha were 4.4% and 14.0% in MS group, and 0 and 8.50% in healthy subjects, there was no statistical significance (P> 0.05).

CONCLUSIONThe TNF-alpha level in serum is associated with active MS, but not in the CSF. The gene polymorphisms of TNF-alpha -308G/A is not associated with MS in Han nationality of southern China.

Adolescent ; Adult ; Aged ; Asian Continental Ancestry Group ; genetics ; China ; Enzyme-Linked Immunosorbent Assay ; Female ; Gene Frequency ; Genotype ; Humans ; Male ; Middle Aged ; Multiple Sclerosis ; blood ; cerebrospinal fluid ; genetics ; Polymorphism, Genetic ; Tumor Necrosis Factor-alpha ; blood ; cerebrospinal fluid ; genetics

Objective To analyze the risk factors for the formation of carotid atherosclerotic plaque. Methods The clinical data of 279 hospitalized patients undergoing carotid artery color Doppler ultrasonography between June 2005 and December 2006 were collected. Multiple regression of the common carotid intimal-medial thickness (IMT) was used to screen the potential risk factors of carotid plaque formation. The patients were divided into two groups according to the presence of carotid plaque, and binary logistic regression and univariate analysis were used to identify the risk factors. The carotid plaque score and index were compared between the subgroups with different risk factors. Results The common carotid IMT was subjected to influences by age (β=0.242, P=0.000), systolic blood pressure (SBP) (β=0.152, P=0.013) and the level of low-density lipoprotein (LDL) (β=0.115, P=0.048). Age (OR=1.087, P=0.000) and SBP (OR=1.036, P=0.000) were identified as the main factors that affected the formation of carotid plaque. In patients above 60 years old, the detection rate of carotid plaque was significantly higher than that in patients below 60 years (X2=58.379, P=0.000), and the rate was significantly higher in hypertensive patients than in the normotensive patients (X2=18.206, P=0.000). The carotid plaque score and index were significantly higher in patients over 60 years old than in those below 60 years (F=69.353, P=0.000;F=64.826, P=0.000, respectively), and also significantly higher in hypertensive patients than in the normohypertensive patients (F=4.866, P=0.028;F=6.927, P=0.009, respectively). Conclusion Age and SBP are the major risk factors of carotid atheroselerotie plaque formation, and LDL is a factor of lesser risk.

Objective To investigate the effect of nimesulide (NIM), a selective cyclooxygenase-2 (COX-2) inhibitor, on angiopoietins (Ang) gene expression of human glioma xenografts in nude mice and its significance. Methods Human SHG44 glioma cells were inoculated subcutaneously in 16 nude mice to establish xenograft models, and then these mouse models were randomly divided into NIM treatment group and control group. NIM (6 mg/kg) and saline were poured into the stomachs of the mice in each group, respectively, once daily for 35 d. The mRNA expressions of Ang-1 gene and Ang-2 gene in the xenografts were determined by RT-PCR. Microvessel density (MVD) in the xenografts was assessed by immunohistochemical technique. The tumor growth curve was drawn and the inhibition ratio of tumor growth was calculated. Results NIM could significantly inhibit the glioma xenografts growth with its inhibition rate reaching 42.03%. The mRNA expression of Ang-2 gene in NIM treatment group (0.2032±0.0185) was significantly lower than that in control group (0.6024±0.0289, P＜0.05), but that of Ang-1 gene showed no significant changes; therefore, the mRNA ratio of Ang-2/Ang-1 genes was decreased (0.5825±0.0621 vs. 1.5847±0.1948, P＜0.05). MVD in the xenografts of the NIM treatment group was significantly lower than that in the control group (P＜0.05). Conclusion NIM, by down-regulating the mRNA expression ofA ng-2 gene and changing the mRNA ratio of Ang-2/Ang-1 genes, can inhibit the tumor growth

OBJECTIVETo provide methods and alert thresholds which are scientific, sensitive, specific and practical for Early Warning System in Public Health Surveillance.

METHODSAlert data was based on historical infectious diseases reports. Control chart was used to detect outbreaks or epidemics. An epidemic was defined by consulting Specialists. After calculating sensitivity, specificity, positive predictive value and describing receiver-operating characteristic curve (ROC), the optimal model and thresholds were chosen.

RESULTSAt 80 percentile, the sensitivities and the specificities of epidemic haemorragia fever, hepatitis A, dysentery, epidemic cerebrospinal meningitis and malaria were over 90%, and there was a high efficacy of early warning. At 90 percentile, the sensitivities and the specificities of tuberculosis and measles were over 85%, and there was a high efficacy of early warning also.

CONCLUSIONControl chart based on five years was chose as a essential method in early warning system. The alert threshold for epidemic haemorragia fever, hepatitis A, dysentery, epidemic cerebrospinal meningitis and malaria was 80 percentile. The alert threshold for tuberculosis and measles was 90 percentile.

China ; epidemiology ; Communicable Diseases ; epidemiology ; Databases, Factual ; Disease Notification ; Dysentery, Bacillary ; epidemiology ; Environmental Monitoring ; methods ; Epidemiological Monitoring ; Female ; Hemorrhagic Fever with Renal Syndrome ; epidemiology ; Hepatitis A ; epidemiology ; Humans ; Male ; Meningitis, Meningococcal ; epidemiology ; Population Surveillance

OBJECTIVETo investigate the molecular mechanism of adiponectin inhibiting activation of hepatic stellate cells in non-alcoholic fatty liver fibrosis.

METHODSThe rat models of non-alcoholic fatty liver fibrosis were successfully established by fat-rich diet administration. The expression of adiponectin mRNA and protein were respectively detected by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot. LX-2 cells were cultured in an adipogenic differentiation mixture to induce quiescent adipocytic phenotypes, and then they were treated with TGFβ1, adiponectin and TGFβ1 + adiponectin, respectively. RT-PCR and Western blot were used to determine the expressions of mRNAs and proteins of a-smooth muscle actin (a-SMA), Collagen, adenosine monophosphate-activated protein kinase (AMPK), inducible nitric oxide synthase (iNOS), and endothelial NOS (eNOS). The results were analyzed using one-way ANOVA, Student-Newman-Keuls test, and linear correlation analysis. A P value of less than 0.05 was considered as statistically significant.

RESULTSIn vivo, with the progress of non-alcoholic fatty liver fibrosis, the model rats gradually showed hepatic steatosis, inflammation, necrosis and fibrosis. Compared with the control group, the level of serum adiponectin (2.49 ± 0.86 vs 5.81 ± 0.87, P < 0.05) and hepatic expressions of adiponectin mRNA and protein (0.26 ± 0.04 vs 0.72 ± 0.08; 0.64 ± 0.07 vs 0.21 ± 0.07, all P < 0.05) were all decreased in the 24th week group, and were negatively correlated with the level of Collagen which increased gradually. In vitro, TGFβ1 could activate quiescent LX-2 cells by decreasing mRNA and protein expression of eNOS (0.30 ± 0.10 vs 0.44 ± 0.08; 0.30 ± 0.09 vs 0.46 ± 0.07, all P < 0.05) and increasing the expression of iNOS (0.53 ± 0.07 vs 0.37 ± 0.04; 0.55 ± 0.07 vs 0.39 ± 0.05, all P < 0.05). Recombinant adiponectin not only maintained the quiescent phenotype of LX-2 cells but also inhibited LX-2 cells activation due to TGFβ1 by increasing the expression of eNOS (0.43 ± 0.08 vs 0.30 ± 0.10; 0.42 ± 0.07 vs 0.30 ± 0.09, all P < 0.05) and phosphorylation of AMPK (0.43 ± 0.07 vs 0.24 ± 0.04, P < 0.05) and decreasing the expression of iNOS (0.44 ± 0.05 vs 0.53 ± 0.07; 0.46 ± 0.07 vs 0.55 ± 0.07, all P < 0.05).

CONCLUSIONSData suggested that adiponectin could play a protective role on the pathogenesis of non-alcoholic fatty liver fibrosis by inhibiting the activation of hepatic stellate cells via up-regulating the expression of eNOS, which might associate with increased phosphorylation of AMPK.

Adiponectin ; metabolism ; pharmacology ; Animals ; Disease Models, Animal ; Fatty Liver ; metabolism ; Hepatic Stellate Cells ; metabolism ; Liver Cirrhosis ; metabolism ; pathology ; Nitric Oxide Synthase Type III ; metabolism ; Non-alcoholic Fatty Liver Disease ; Rats ; Rats, Wistar ; Reverse Transcriptase Polymerase Chain Reaction ; Transforming Growth Factor beta1 ; metabolism ; pharmacology

OBJECTIVESerum p53 protein overexpression was detected in population exposed to traffic exhaust gas to study the relation between traffic exhaust gas and the increased risk in p53 gene mutation.

METHODSSerum p53 protein expression was measured by enzyme-linked immunosorbent assay. Relationship between different types of job and serum p53 protein overexpression were studied by pearson Chi-square tests.

RESULTSResults on serum p53 protein overexpression on jobs outside of office (5.74%) were not significantly higher than jobs inside the office. However, it suggested that traffic police men (12.12%) working outside of office, with whose length of service longer than 30 years had a significant overexpression of serum p53 protein than the others (5.36%) whose length of service was less than 30 years (P < 0.05, OR = 2.43, 95% CI: 1.11 - 5.33). Overexpression rate of p53 protein appeared to be 6.89% in the group whose average weekly exposure hours were more than 40 hours, which was significant higher than the group whose exposed hours were less than 40 hours (P < 0.05, OR = 1.71, 95% CI: 1.03 - 2.81).

CONCLUSIONThe result suggested that traffic exhaust gas was likely to cause mutation of p53 gene and increasing the incidence of lung cancer.

Adult ; Aged ; Aged, 80 and over ; Female ; Genes, p53 ; Humans ; Lung Neoplasms ; etiology ; Male ; Middle Aged ; Mutation ; Occupational Exposure ; Tumor Suppressor Protein p53 ; blood ; Vehicle Emissions ; adverse effects