1. |
- Barclay, C J, et al.
(författare)
-
Initial mechanical efficiency of isolated cardiac muscle
- 2003
-
Ingår i: Journal of Experimental Biology. - 0022-0949 .- 1477-9145. ; 206:Pt 16, s. 2725-32
-
Tidskriftsartikel (refereegranskat)abstract
- The aim of this study was to determine whether the initial mechanical efficiency (ratio of work output to initial metabolic cost) of isolated cardiac muscle is over 60%, as has been reported previously, or whether it is approximately 30%, as suggested by an estimate based on the well-established net mechanical efficiency (ratio of work output to total, suprabasal energy cost) of 15%. Determination of initial efficiency required separation of the enthalpy output (i.e. heat + work) into initial and recovery components. The former corresponds to energy produced by reactions that use high-energy phosphates and the latter to energy produced in the regeneration of high-energy phosphates. The two components were separated mathematically. Experiments were performed in vitro (30 degrees C) using preparations dissected from rat left ventricular papillary muscles (N=13). Muscle work output and heat production were measured during a series of 40 contractions using a contraction protocol designed to mimic in vivo papillary muscle activity. Net mechanical efficiency was 13.3+/-0.7%. The total enthalpy output was 2.16 times greater than the initial enthalpy output, so that initial mechanical efficiency was 28.1+/-1.2%.
|
|
2. |
- Lindgren, Cecilia, et al.
(författare)
-
Contribution of known and unknown susceptibility genes to early-onset diabetes in scandinavia: evidence for heterogeneity.
- 2002
-
Ingår i: Diabetes. - : American Diabetes Association. - 1939-327X .- 0012-1797. ; 51:5, s. 1609-1617
-
Tidskriftsartikel (refereegranskat)abstract
- In an attempt to identify novel susceptibility genes predisposing to early-onset diabetes (EOD), we performed a genome-wide scan using 433 markers in 222 individuals (119 with diabetes) from 29 Scandinavian families with ≥2 members with onset of diabetes ≤45 years. The highest nonparametric linkage (NPL) score, 2.7 (P < 0.01), was observed on chromosome 1p (D1S473/D1S438). Six other regions on chromosomes 3p, 7q, 11q, 18q, 20q, and 21q showed a nominal P value <0.05. Of the EOD subjects in these 29 families, 20% were GAD antibody positive and 68% displayed type 1 diabetes HLA risk alleles (DQB*02 or 0302). Mutations in maturity-onset diabetes of the young (MODY) 1–5 genes and the A3243G mitochondrial DNA mutation were detected by single-strand conformation polymorphism and direct sequencing. To increase homogeneity, we analyzed a subsample of five families with autosomal dominant inheritance of EOD (greater than or equal to two members with age at diagnosis ≤35 years). The highest NPL scores were found on chromosome 1p (D1S438–D1S1665; NPL 3.0; P < 0.01) and 16q (D16S419; NPL 2.9; P < 0.01). After exclusion of three families with MODY1, MODY3, and mitochondrial mutations, the highest NPL scores were observed on chromosomes 1p (D1S438; NPL 2.6; P < 0.01), 3p (D3S1620; NPL 2.2; P < 0.03), 5q (D5S1465; NPL 2.1; P < 0.03), 7q (D7S820; NPL 2.0; P < 0.03), 18q (D18S535; NPL 1.9; P < 0.04), 20q (D20S195; NPL 2.5; P < 0.02), and 21q (D21S1446; NPL 2.2; P < 0.03). We conclude that considerable heterogeneity exists in Scandinavian subjects with EOD; 24% had MODY or maternally inherited diabetes and deafness, and ∼60% were GAD antibody positive or had type 1 diabetes-associated HLA genotypes. Our data also point at putative chromosomal regions, which could harbor novel genes that contribute to EOD.
|
|