Asian Science Citation Index is committed to provide an authoritative, trusted and significant information by the coverage of the most important and influential journals to meet the needs of the global scientific community.  
ASCI Database
308-Lasani Town,
Sargodha Road,
Faisalabad, Pakistan
Fax: +92-41-8815544
Contact Via Web
Suggest a Journal
 
Articles by T Hansen
Total Records ( 4 ) for T Hansen
  T Sparso , A Bonnefond , E Andersson , N Bouatia Naji , J Holmkvist , L Wegner , N Grarup , A. P Gjesing , K Banasik , C Cavalcanti Proenca , M Marchand , M Vaxillaire , G Charpentier , M. R Jarvelin , J Tichet , B Balkau , M Marre , C Levy Marchal , K Faerch , K Borch Johnsen , T Jorgensen , S Madsbad , P Poulsen , A Vaag , C Dina , T Hansen , O Pedersen and P. Froguel
  OBJECTIVE

Genome-wide association studies have identified several variants within the MTNR1B locus that are associated with fasting plasma glucose (FPG) and type 2 diabetes. We refined the association signal by direct genotyping and examined for associations of the variant displaying the most independent effect on FPG with isolated impaired fasting glycemia (i-IFG), isolated impaired glucose tolerance (i-IGT), type 2 diabetes, and measures of insulin release and peripheral and hepatic insulin sensitivity.

RESEARCH DESIGN AND METHODS

We examined European-descent participants in the Inter99 study (n = 5,553), in a sample of young healthy Danes (n = 372), in Danish twins (n = 77 elderly and n = 97 young), in additional Danish type 2 diabetic patients (n = 1,626) and control subjects (n = 505), in the Data from the Epidemiological Study on the Insulin Resistance Syndrome (DESIR) study (n = 4,656), in the North Finland Birth Cohort 86 (n = 5,258), and in the Haguenau study (n = 1,461).

RESULTS

The MTNR1B intronic variant, rs10830963, carried most of the effect on FPG and showed the strongest association with FPG (combined P = 5.3 x 10–31) and type 2 diabetes. The rs10830963 G-allele increased the risk of i-IFG (odds ratio [OR] 1.64, P = 5.5 x 10–11) but not i-IGT. The G-allele was associated with a decreased insulin release after oral and intravenous glucose challenges (P < 0.01) but not after injection of tolbutamide. In elderly twins, the G-allele associated with hepatic insulin resistance (P = 0.017).

CONCLUSIONS

The G-allele of MTNR1B rs10830963 increases risk of type 2 diabetes through a state of i-IFG and not through i-IGT. The same allele associates with estimates of β-cell dysfunction and hepatic insulin resistance.

  V Radha , J Ek , S Anuradha , T Hansen , O Pedersen and V. Mohan
 

Context: Mutations in the HNF 1A gene are the most common cause of maturity-onset diabetes of the young (MODY) in most populations. India currently has the largest number of people with diabetes in the world, and onset of type 2 diabetes occurs at a younger age with possible overlap with MODY. There are very few data on MODY mutations from India.

Objective: The objective was to screen coding and promoter regions of HNF1A gene for mutations in unrelated South Indian subjects in whom a clinical diagnosis of MODY was made.

Design: This was an observational cross-sectional study.

Setting: The study was conducted at a diabetes specialties centre in Chennai in southern India.

Patients: Ninety-six unrelated south Indian subjects in whom clinical diagnosis of MODY was made were included in the study. The control population comprised of 57 unrelated nondiabetic subjects selected from the Chennai Urban Rural Epidemiology Study, a study conducted on a representative population (aged ≥20 yr) of Chennai.

Results: We identified nine novel variants comprising seven mutations (one novel mutation –538G>C at promoter region and six novel coding region mutations) and two polymorphisms in the HNF1A gene. Functional studies revealed reduced transcriptional activity of the HNF1A promoter for two promoter variants. We also observed cosegregation with diabetes of the Arg263His coding region mutation in eight members of one MODY family, whereas it was absent in nondiabetic subjects of this family.

Conclusion: This study suggests that mutations in the HNF1A gene comprise about 9% of clinically diagnosed MODY subjects in southern India and a novel Arg263His mutation cosegregates with MODY in one family.

  J Javidpour , J. C Molinero , A Lehmann , T Hansen and U. Sommer
 

The sudden occurrence of the ctenophore Mnemiopsis leidyi has been reported recently from different regions of the Baltic Sea and it has been suggested that the species has invaded the whole basin. Here we provide the first set of quantitative data of seasonal diet composition and life history traits of M. leidyi and its predatory role in the pelagic ecosystem of the Western Baltic Sea. The size structure of the species appeared to be dominated by small size classes and only a few adults were as large as those reported in the native region of the species and in other invaded areas. We show that the species has a high preference for small-sized and slow swimming prey, mainly during the winter low temperature period. Barnacle nauplii appeared to be the main source of carbon for the over-wintering population of M. leidyi. A preference for copepods was only found during August when these prey contributed up to 20% of the gut composition. In summer, planula larvae of the jellyfish Aurelia aurita were the most abundant prey in the gut content (feeding rate of 621 ind. ctenophore–1day–1). We further found that at highest densities of the species, in summer, a significant predation on its larvae occurs, this being the major carbon source of adults. Overall, these results are discussed in the context of trade-offs M. leidyi faces in the new environment and adverse environmental conditions, which are likely forcing the species toward reduced sizes and also probably reducing its potential predatory impact in the Baltic Sea.

  T Hansen , D New , R Reeve , R Donne and W. Stephens
 

We report a man with type 1 diabetes mellitus, autoimmune hypothyroidism and a tentative diagnosis of multiple sclerosis. Following treatment with beta interferon, he developed systemic lupus erythematosus with pericarditis, pleural effusions, cerebral infarction associated with anti-phospholipid antibody and acute renal failure due to thrombotic microangiopathy. He responded well to immunosuppression and anticoagulation. These complications may represent the most severe autoimmune reaction to beta interferon reported to date.

 
 
 
Copyright   |   Desclaimer   |    Privacy Policy   |   Browsers   |   Accessibility