OBJECTIVETo map the regulatory domain of Escherichia coli T-protein.

METHODSFragmentation cloning was employed in cloning of 11 fragments from T-protein. The regulatory activity of each fragment was determined respectively.

RESULTSThe regulatory domain of T-protein was located in the C-terminal 270 amino acids, which was the same location as PDH domain.

CONCLUSIONT-protein has no independent regulatory domain.

Cloning, Molecular ; Deoxyribonucleases, Type I Site-Specific ; analysis ; chemistry ; genetics ; Escherichia coli Proteins ; analysis ; chemistry ; genetics ; Nucleic Acid Conformation ; Peptide Fragments ; chemistry ; genetics ; Protein Binding ; genetics ; Regulatory Elements, Transcriptional ; genetics

OBJECTIVE To investigate the relationship between the Nco I, Ava II polymorphism of low density lipoprotein receptor (LDL-R) gene in patients with the occurrence of atherosclerotic cerebral infarction (ACI) among the Han nationality in Liaoning province. METHODS The polymerase chain reaction technique was used to study the polymorphisms of LDL-R gene and allele frequencies in 77 patients with ACI and in 113 age-matched Chinese healthy controls. The levels of the lipid and lipoproteins were also compared among the cases with ACI and the controls. RESULTS A(+) frequencies of LDL-R gene in healthy controls and ACI group were 0.230 and 0.125 respectively, while the N(+) frequencies of healthy control and ACI group was 0.667 and 0.662 respectively. In case of the coexistence of A(-) A(-) and N(+) N(+), the relative risk (RR) of ACI was 5.56(P<0.001), while the RR of the increase of serum levels TG, TC, LDL-C, LP(a) were 4.29, 7.67, 9.33 and 3.09(P<0.05), respectively. CONCLUSION The coexistence of A(-) A(-) and N(+) N(+) can affect the concentration of lipid and lipoprotein and is in close relationship with the occurrence of ACI.
Apolipoprotein A-I ; blood ; Apolipoproteins B ; blood ; Binding Sites ; genetics ; Cerebral Infarction ; blood ; genetics ; Cholesterol ; blood ; Cholesterol, LDL ; blood ; DNA ; genetics ; metabolism ; Deoxyribonucleases, Type II Site-Specific ; metabolism ; Genotype ; Humans ; Intracranial Arteriosclerosis ; blood ; genetics ; Lipoproteins ; blood ; Receptors, LDL ; genetics ; Triglycerides ; blood

OBJECTIVE: To investigate the interaction between polymorphism of Toll-like receptor 4 (TLR4) gene G11367C in 3' untranslated region (UTR) and inhibitor of nuclear factor kappaB (IκB)-α 
Hae III in acute pancreatitis (AP) and the degree of severity.
 METHODS: A total of 450 patients with confirmed AP (AP group), who came from the First Affiliated Hospital of Xinxiang Medical College from May 2013 to June 2015, were divided into a mild AP subgroup (MAP subgroup), a moderately severe AP (MSAP subgroup), and a severe acute AP (SAP subgroup) (n=150 in each group). One hundred fifty healthy persons were served as a control group. There was no significant difference in age, gender, ethnicity and birthplace among all groups. The genetic polymorphisms of TLR4 gene G11367C in 3' untranslated region and IκB-α Hae III were analyzed by polymerase chain reaction (PCR). Eligible participants were personally interviewed by a questionnaire. Unconditional logistic regression model and single factor analysis were performed to calculate the adjusted odds ratios (OR) and 95% confidence intervals (95% CI) of G11367C and IκB-α Hae III polymorphisms, respectively. The interaction of nucleotide polymorphisms was analyzed.
 RESULTS: The frequencies of G11367C (GC), IκB-α Hae III (AG) and IκB-α Hae III (GG) were 69.56%, 33.78% and 36.22% in the AP group; 49.33%, 24.67% and 26.00% in the MAP subgroup; 70.67%, 34.67% and 36.67% in the MSAP subgroup; 88.67%, 42.00% and 46.00% in the SAP subgroup and 26.67%, 14.00% and 14.67% in the control group, respectively. There was significant difference in the frequencies betweenc the AP group and the control group, or among each AP subgroup (all P<0.01). The risk of AP was significantly increased in the subjects with G11367C (GC) genotype (ORAP=6.2828, ORMAP=2.6776, ORMSAP=6.6250, ORSAP=21.5147), which was also increased in those with IκB-α Hae III (AG) genotype (ORAP=5.7369, ORMAP=2.5277, ORMSAP=6.1824, ORSAP=17.8572) and in those with IκB-α Hae III (GG) genotype (ORAP=5.8724, ORMAP=2.5902, ORMSAP=6.4027, ORSAP=18.9022). The combined analysis of the polymorphisms showed that the percentage of G11367C (GC)/ IκB-α Hae III (GG) in the AP group, the MAP subgroup, the MSAP subgroup, the SAP subgroup and the control groups was 26.44%, 12.67%, 26.00%, 40.67% and 4.00%, respectively, with significant difference in the frequency among all groups (all P<0.01). The people who carried with Pro12Ala (AA)/Pro198Leu (LL) had a high risk of AP (ORAP=30.1314, ORMAP=6.7612, ORMSAP=39.5000, ORSAP=401.5833), and the statistical analysis suggested a positive interaction between Pro12Ala (AA) and Pro198Leu (LL) in increasing the risk of AP (All γ>1). Similarly, there were also positive interactions in the pathogenesis of AP between G11367C (GC) and IκB-α Hae III (AG) (All γ>1). 
 CONCLUSION These carriers of G11367C(GC), IκB-α Hae III(AG) and IκB-α Hae III (GG) genotypes may have a high risk of AP occurency, and there are significant interactions between genetic polymorphisms of G11367C and IκB-α Hae III, which increaes the risk of the occurrence and development of AP.
3' Untranslated Regions ; Acute Disease ; Deoxyribonucleases, Type II Site-Specific ; Ethnic Groups ; Genetic Predisposition to Disease ; Genotype ; Humans ; I-kappa B Kinase ; Logistic Models ; NF-KappaB Inhibitor alpha ; Odds Ratio ; Pancreatitis ; Polymerase Chain Reaction ; Polymorphism, Single Nucleotide ; Promoter Regions, Genetic ; Toll-Like Receptor 4