Search

The β feeding probability of (102,104,105,106,107)Tc, 105Mo, and 101Nb nuclei, which are important contributors to the decay heat in nuclear reactors, has been measured using the total absorption technique. We have coupled for the first time a total absorption spectrometer to a Penning trap in order to obtain sources of very high isobaric purity. Our results solve a significant part of a long-standing discrepancy in the γ component of the decay heat for 239Pu in the 4-3000 s range.

A Penning trap-based purification process having a resolution of about 1 ppm is reported. In this context, we present for the first time a production method for the most complicated and crucially important nuclear weapons test signature, (133m)Xe. These pure xenon samples are required by the Comprehensive Nuclear-Test-Ban Treaty Organization to standardize and calibrate the worldwide network of xenon detectors., (Copyright 2009 Elsevier Ltd. All rights reserved.)

The superallowed beta-decay Q(EC) values of (34)Cl and (38)K(m) have been measured with an online Penning trap to be 5491.662(47) keV and 6044.223(41) keV, respectively. The new values are more precise than the previous high-precision reaction-based values but are consistent with them and establish that there are no significant systematic differences between the two types of measurements.

The Q value of the ;{112}Sn double-beta decay was determined by using a Penning trap mass spectrometer. The new atomic-mass difference between ;{112}Sn and ;{112}Cd of 1919.82(16) keV is 25 times more precise than the previous value of 1919(4) keV. This result removes the possibility of enhanced resonance capture of the neutrinoless double-EC decay to the excited 0;{+} state at 1871.00(19) keV in ;{112}Cd.

The nuclides 104-108Sn, 106-110Sb, 108,109Te, and 111I at the expected endpoint of the astrophysical rp process have been produced in 58Ni+natNi fusion-evaporation reactions at IGISOL and their mass values were precisely measured with the JYFLTRAP Penning trap mass spectrometer. For 106Sb, 108Sb, and 110Sb these are the first direct experimental mass results obtained. The related one-proton separation energies have been derived and the value for 106Sb, Sp=424(8) keV, shows that the branching into the closed SnSbTe cycle in the astrophysical rp process is weaker than expected.

Nuclides in the vicinity of 94Ag have been studied with the Penning trap mass spectrometer JYFLTRAP at the Ion-Guide Isotope Separator On-Line. The masses of the two-proton-decay daughter 92Rh and the beta-decay daughter 94Pd of the high-spin isomer in 94Ag have been measured, and the masses of 93Pd and 94Ag have been deduced. When combined with the data from the one-proton- or two-proton-decay experiments, the results lead to contradictory mass excess values for the high-spin isomer in 94Ag, -46 370(170) or -44 970(100) keV, corresponding to excitation energies of 6960(400) or 8360(370) keV, respectively.

Atomic masses of the neutron-rich isotopes (76-80)Zn, (78-83)Ga, (80-85)Ge, (81-87)As, and (84-89)Se have been measured with high precision using the Penning trap mass spectrometer JYFLTRAP at the IGISOL facility. The masses of (82,83)Ga, (83-85)Ge, (84-87)As, and 89Se were measured for the first time. These new data represent a major improvement in the knowledge of the masses in this neutron-rich region. Two-neutron separation energies provide evidence for the reduction of the N=50 shell gap energy towards germanium (Z=32) and a subsequent increase at gallium (Z=31). The data are compared with a number of theoretical models. An indication of the persistent rigidity of the shell gap towards nickel (Z=28) is obtained.

Using a new fast cleaning procedure to prepare isomerically pure ion samples, we have measured the beta-decay Q(EC) values of the superallowed beta emitters 5(0)Mn and (54)Co to be 7634.48(7) and 8244.54(10) keV, respectively, results which differ significantly from the previously accepted values. The corrected Ft values derived from our results strongly support new isospin-symmetry-breaking corrections that lead to a higher value of the up-down quark mixing element V(ud) and improved confirmation of the unitarity of the Cabibbo-Kobayashi-Maskawa matrix.

Background: Valyl-prolyl-proline (VPP), a bioactive peptide formed during the fermentation with Lactobacillus helveticus LBK-16H (L. helveticus), has been shown to increase bone formation in vitro. The aim of the study was to determine whether VPP and L. helveticus fermented milk prevent bone loss in ovariectomized (OVX) rats., Methods: During the 12-week intervention study, the OVX rats received VPP in water or L. helveticus fermented milk, containing VPP. Sham-operated rats receiving water acted as controls. The trabecular and cortical bone mineral density were determined by peripheral quantitative computed tomography before the operation and at 4 and 12 weeks. The mechanical testing and ash weight analysis as well as the static and dynamic histomorphometrical parameters were assessed at the end of the intervention., Results: VPP given in water showed no clear effect on bone loss. L. helveticus fermented milk prevented bone loss by decreasing bone turnover and increasing the bone mineral density. Ovariectomy caused a 57% loss in the trabecular bone, which was attenuated by 16% in the L. helveticus group., Conclusions: VPP peptide did not prevent ovariectomy-induced bone loss, which could be due to the poor bioavailability of VPP from water solution. L. helveticus fermented milk prevented bone loss, whether this is due to the VPP peptide cannot be concluded., (Copyright 2007 S. Karger AG, Basel.)

The beta-decay Q(EC) values of the superallowed beta emitters 26Alm, 42Sc, and 46V have been measured with a Penning trap to a relative precision of better than 8 x 10(-9). Our result for 46V, 7052.72(31) keV, confirms a recent measurement that differed from the previously accepted reaction-based Q(EC) value. However, our results for 26Alm and 42Sc, 4232.83(13) keV and 6426.13(21) keV, are consistent with previous reaction-based values. By eliminating the possibility of a systematic difference between the two techniques, this result demonstrates that no significant shift in the deduced value of Vud should be anticipated.

Human serum tartrate-resistant acid phosphatase exists as two enzyme isoforms (TRACP 5a and 5b), derived by differential, post-translational processing of a common gene product. Serum TRACP 5b is from bone-resorbing osteoclasts (OC) and becomes elevated in diseases of increased bone resorption. TRACP 5a is secreted by macrophages (MPhi) and dendritic cells (DC) and is increased in many patients with rheumatoid arthritis. Our purpose was to fully characterize the properties of human TRACP isoforms and to produce an antibody specific to TRACP 5a for use as a biomarker in chronic inflammatory diseases. Partially purified, natural serum TRACP isoforms and recombinant TRACP 5a (rTRACP 5a) were compared with respect to specific activity and subunit structure and presence of sialic acid. Mice were immunized with rTRACP 5a, and resulting hybridomas were screened for monoclonal antibody to serum TRACP 5a. One antibody, 220, was tested for its epitope specificity and use in various immunological techniques. rTRACP 5a had properties identical to serum TRACP 5a. Antibody 220 was specific for the trypsin-sensitive epitope in the loop peptide, present only in TRACP 5a. Antibody 220 was effective for specific immunoprecipitation, immunoassay, and immunoblot of TRACP 5a. Intact TRACP was present in MPhi, DC, and OC. TRACP 5a was the predominant isoform secreted by MPhi and DC, whereas TRACP 5b was the predominant isoform secreted by OC. TRACP isoforms 5a and 5b may have different functions inside and outside of monocyte-derived cells. Antibody 220 is an important resource for studies of the biosynthetic relationship among TRACP isoforms and of the significance of serum TRACP 5a as a marker in diseases of bone metabolism and inflammation.

The need for high-throughput assays in molecular biology places increasing requirements on the applied signal processing and modelling methods. In order to be able to extract useful information from the measurements, the removal of undesirable signal characteristics such as random noise is required. This can be done in a quite elegant and efficient way by the minimum description length (MDL) principle, which treats and separates 'noise' from the useful information as that part in the data that cannot be compressed. In its current form the MDL denoising method assumes the Gaussian noise model but does not require any ad hoc parameter settings. It provides a basis for high-speed automated processing systems without requiring continual user interventions to validate the results as in the conventional signal processing methods. Our analysis of the denoising problem in mass spectrometry, capillary electrophoresis genotyping, and sequencing signals suggests that the MDL denoising method produces robust and intuitively appealing results sometimes even in situations where competing approaches perform poorly.

In human tissues, the laminin (Ln) alpha1 chain shows a restricted and developmentally regulated distribution in basement membranes (BMs) of a subset of epithelial tissues, including those of renal proximal convoluted tubules. The present study investigated the distribution of the Ln alpha1 chain in renal cell carcinomas (RCCs) and oncocytomas as well as in xenografted tumours induced in nude mice with four characterized RCC cell lines. These cell lines were also used in cell adhesion studies with purified laminins. By immunohistochemistry it was found that the Ln alpha1 chain is widely present in the BMs of RCCs, all of the specimens presenting immunoreactivity. High-grade RCCs tended to contain more BM-confined and stromal immunoreactivity than low-grade tumours, none of the grade 3 (G3) carcinomas being negative and all of the metastatic specimens showing partial or overall BM immunoreactivity. Double immunolabelling experiments showed that in RCC BMs but not in vessel walls, the Ln alpha1 chain was co-distributed with Ln alpha5, beta1, and beta2 chains, implying the presence of Ln-1/Ln-3 and Ln-10/Ln-11. In papillary RCCs, the Ln alpha1 chain co-localized with Ln-5. The oncocytomas lacked immunoreactivity for the Ln alpha1 chain. Xenografted tumours induced in nude mice showed BM-like deposition of the Ln alpha1 chain. In cell adhesion studies, mouse and human Ln-1 were equally effective in promoting cell adhesion of all RCC cell lines. For each cell line, Ln-10 and Ln-10/11 were equally effective adhesive substrates, all cell lines adhering more avidly to these laminins than to mouse or human Ln-1. As judged by inhibition assays employing specific integrin antibodies, adhesion of normal human renal proximal tubular epithelial (RPTE) cells and RCC cells from a G1 tumour to human Ln-1 was mediated mainly by alpha(6)beta(1) integrin, while only the G1 RCC cells adhered to mouse Ln-1 by using alpha(6)beta(1) integrin. For adhesion to Ln-10, RPTE cells and RCC cells from a G1 tumour used an unidentified beta(1) integrin. Cells from G3 tumours mainly used an alpha(3)beta(1) integrin complex for adhesion to mouse Ln-1 and to human Ln-1 and Ln-10. For all cells, adhesion to the Ln-10/11 mixture was mediated by an unidentified integrin complex or by other adhesion molecules. These results show that laminin trimers containing the alpha1 chain are, in contrast to oncocytomas, abundant in the BMs of RCCs. This is in keeping with their suggested origin from renal proximal tubular epithelium known for its capacity to produce the Ln alpha1 chain. The results also show that RCC cells utilize complex, mainly integrin alpha(3)beta(1)- and integrin alpha(6)beta(1)-mediated, mechanisms for adhesion to laminins. The adhesion to Ln-1 changes from integrin alpha(6)beta(1) to integrin alpha(3)beta(1) upon increasing malignancy and, especially for Ln-10 and Ln-10/11, other adhesion molecules of non-integrin type may contribute to the adhesion., (Copyright 2003 John Wiley & Sons, Ltd.)

We investigated the significance of the variants of the IRS-2 gene in patients with type 2 diabetes. The entire coding part of the IRS-2 gene was screened by single-strand conformation polymorphism analysis in 40 Chinese and 40 Finnish patients with late-onset type 2 diabetes. The association of the variants of the IRS-2 gene with type 2 diabetes was studied in 85 Finnish diabetic patients and 82 Finnish control subjects and in 100 Chinese diabetic patients and 85 Chinese control subjects. The four variants predicting structural changes in the insulin receptor substrate (IRS)-2 protein included an insertion of AAC (Asn) in the Asn repeat sequence centered around codons 29-36 (allele frequencies of 0 vs. 0.6% and 1.5 vs. 0%), the Ala157Thr substitution (0 vs. 0% and 0.5 vs. 0%), the Leu647Val substitution (0.6 vs. 0% and 0 vs. 0%), and the Gly1057Asp polymorphism (31 vs. 31% and 35 vs. 30%) (P = NS for all comparisons). Furthermore, six silent variants were observed (CGC147CGG, CCC155CCG, GCC156GCT, AGT723AGC, TGT816TGC, and CCC829CCT). The Gly1057Asp polymorphism was not associated with insulin resistance or impaired insulin secretion in Finnish subjects with normal glucose tolerance (n = 295) or impaired glucose tolerance (n = 38). These data indicate that structural variants of the IRS-2 gene were uncommon in Finnish and Chinese patients with type 2 diabetes. Thus, the variants in the coding part of the IRS-2 gene are unlikely to have a major role in the development of type 2 diabetes in Finnish or Chinese subjects.

We have studied the synthesis of laminins (Ln) and determined the specific integrins mediating the adhesion of immortalized human corneal epithelial cells to mouse Ln-1, and human Lns-5 and -10. Immunofluorescence microscopy of the cells demonstrated integrin alpha(2), alpha(3), alpha(6), beta(1)and beta(4)subunits, integrins alpha(6)and beta(4)being found in a typical 'leopard-skin' like manner. Immunoprecipitation studies showed that the cells produced alpha 3, beta 3 and gamma 2 chains of Ln-5, but not Lns-1 or -10. In culture Ln-5 was found as small plaques beneath the adhering cells within 1 hr, while in 4 hr widely spread Ln-5 plaques were observed in colocalization with beta(4)integrin subunit. By using a quantitative cell adhesion assay and function-blocking monoclonal antibodies we showed that integrin beta(1)subunit plays a role in mediating corneal epithelial cell adhesion to mouse Ln-1. However, none of the available function-blocking antibodies to integrin alpha-subunits inhibited the adhesion. Integrin alpha(3)beta(1)complex mediated the adhesion of corneal epithelial cells to human Lns-5 and -10. Integrin complex alpha(3)beta(1), as well as laminin alpha(3)chain, was also shown to mediate cell adhesion to newly produced endogenous Ln-5. The present results show that integrin alpha(3)beta(1)complex mediates the adhesion of corneal epithelial cells to Lns-5 and -10, while a yet unknown integrin alpha subunit appears to play a role in the adhesion to Ln-1. The results also show that among corneal basement membrane laminins, Ln-5 is synthetized by epithelial cells while Ln-10 may be a product of keratocytes., (Copyright 2001 Academic Press.)

Phosphatidylinositol (PI) 3-kinase is a key signaling molecule in insulin-stimulated glucose transport. Therefore, we investigated the catalytic subunit p110beta, of human PI 3-kinase as a candidate gene for type 2 diabetes. Human p110beta gene was cloned from the placental genomic library. All 22 exons, intronic regions flanking the exons and 1.5 kb of the proximal/5' region of the p110beta gene, were screened for variants by single-strand conformation polymorphism analysis in 79 Finnish patients with type 2 diabetes . Allele frequencies of the variants were also determined in 77 nondiabetic control subjects. No variants were found in exons in diabetic patients. However, we identified two nucleotide polymorphisms in the proximal/5' region of the p110beta gene and a variation in the number of 2-bp repeat sequence (TA)n in intron 4. The allele frequencies did not differ between diabetic and control subjects. Our results may indicate that the catalytic subunit p110beta of PI 3-kinase plays such a fundamental role in the insulin-signaling pathway that structural variants are not likely to exist in that gene. The importance of the polymorphisms in the proximal/5' region of the p110beta gene for insulin signaling remains to be determined.

Objective: To determine the role of the hepatocyte nuclear factor (HNF)-1alpha and HNF-4alpha genes in the etiology of late-onset type 2 diabetes in Finnish and Chinese subjects., Research Design and Methods: The whole coding regions of the genes encoding for HNF-1alpha and HNF-4alpha, including approximately 800 bp of the HNF-1alpha promoter, were investigated in 40 Finnish subjects (fasting C-peptide 50-570 pmol/l) and 47 Chinese subjects with type 2 diabetes by single-strand conformation polymorphism (SSCP) analysis. Frequencies of the variants of these genes were analyzed by restriction fragment-length polymorphism analysis in additional samples of 100 Finnish diabetic patients and 82 Finnish control subjects and in 58 Chinese diabetic patients and 51 Chinese control subjects., Results: No previously reported gene defects were detected, but one novel functionally silent GCC-->GCG variant (nucleotide 73, exon 10) was observed in the HNF-4alpha gene in a Chinese diabetic patient. Interestingly, the Ala98Val substitution of the HNF-1alpha gene occurred at a significantly higher frequency in 140 Finnish diabetic patients compared with 82 control subjects (P = 0.014). The Ala98Val variant was not, however, associated with abnormalities in insulin secretion evaluated by oral and intravenous glucose tolerance tests in subjects with normal (n = 295) or impaired (n = 38) glucose tolerance., Conclusions: Variants in the HNF-1alpha and HNF-4alpha genes are unlikely to play a major role in the pathogenesis of late-onset type 2 diabetes in Finnish and Chinese subjects. However, the association of the Ala98Val variant of the HNF-1alpha gene with type 2 diabetes in Finnish subjects may indicate a diabetogenic locus close to the HNF-1alpha gene.

Two novel monoclonal antibodies were raised and used to study the expression of laminin (Ln) alpha1-chain in developing and adult human tissues. In both fetal and adult kidney, a distinct immunoreactivity was seen in basement membranes (BM) of most proximal tubules but not in the distal tubular or glomerular BM or in the basal laminae of blood vessels. Immunoprecipitation of metabolically labeled cultured human renal proximal tubular cells showed an abundant production and deposition of Ln alpha1-chain to the extracellular matrix, suggestive of an epithelial origin of kidney Ln-1. Quantitative cell adhesion experiments with JAR choriocarcinoma cells showed that purified human Ln-1 is a good substrate for cell adhesion that it is differently recognized by integrin receptors when compared to mouse Ln-1. In fetal and adult testes immunoreactivity was solely confined to BM of the seminiferous epithelium. In the airways BM-confined reaction was only seen in fetal budding bronchial tubules (16-19 weeks) at the pseudoglandular stage of development. In the skin a distinct immunoreactivity was confined to BM of developing hair buds but not in epithelial BMs of adult epidermis or of epidermal appendages. In other adult tissues, immunoreactivity was found in BMs of thyroid, salivary, and mammary glands as well as in BMs of endometrium and endocervix, but not of ectocervix or vagina. No immunoreactivity was found in BMs of most of the digestive tract, including the liver and pancreas, except for BMs of esophageal submucosal glands and duodenal Brunner's glands. In fetal specimens, BMs of the bottoms of the intestinal and gastric glands were positive. Basal laminae of blood vessels were generally negative for Ln alpha1 chain with the exception of specimens of both fetal and adult central nervous system in which immunoreactivity for Ln alpha1 chain was prominently confined to capillary walls. The results suggest that outside the central nervous system, Ln alpha1 chain shows a restricted and developmentally regulated expression in BMs of distinct epithelial tissues., (Copyright 2000 Academic Press.)

Objective: To investigate the possible association of the variants in the nucleotide binding fold regions of the sulfonylurea receptor 1 (SUR1) gene with gestational diabetes mellitus (GDM), type 2 diabetes, and altered insulin secretion in Finnish subjects., Research Design and Methods: The nucleotide binding fold regions of the SUR1 gene were amplified with polymerase chain reaction and screened by the single-strand conformational polymorphism analysis in 42 subjects with GDM and 40 subjects with type 2 diabetes. Detected variants were further investigated in 377 normoglycemic subjects by restriction fragment-length polymorphism analysis. The effect of the variants of the SUR1 gene on first-phase insulin secretion was studied in 295 normoglycemic subjects., Results: In subjects with GDM or type 2 diabetes, one amino acid change (S1369A), four silent substitutions (R1273R, L829L, T759T, and K649K), and three intron variants were identified in the nucleotide binding fold regions of the SUR1 gene. A tagGCC allele of exon 16 splice acceptor site was more frequent in subjects with GDM (0.55 allele frequency, n = 42) and type 2 diabetes (0.60, n = 40) than in normoglycemic subjects (0.43, n = 377) (P1 = 0.024 and P2 = 0.009, respectively). Similarly, an AGG allele of the R1273R polymorphism was more common in subjects with GDM (0.87) and type 2 diabetes (0.87) than in normoglycemic subjects (0.74) (P1 = 0.009 and P2 = 0.001, respectively). However, the S1369A, R1273R, and cagGCC-->tagGCC variants of the SUR1 gene were not associated with altered first-phase insulin secretion in 295 normoglycemic subjects., Conclusions: These results suggest that a functional variant that contributes to the risk of GDM and type 2 diabetes may locate close to the SUR1 gene.

Familial combined hyperlipidemia (FCHL) is characterized by variable expression of dyslipidemias and insulin resistance. Because the genetic background for FCHL is unknown, we investigated the effect of the Trp64Arg polymorphism of the beta3-adrenergic receptor (beta3-AR) gene and the promoter variant A --> G (-3826) of the uncoupling protein 1 (UCP1) gene on glucose and lipid metabolism in FCHL families. Both polymorphisms were screened in 228 members from 27 families with FCHL and in 82 control men from a random population sample. The frequency of the polymorphisms of the beta3-AR and UCP1 genes did not differ between patients with FCHL and controls. Although the rate of insulin-stimulated whole-body glucose uptake evaluated by the euglycemic clamp in family members of patients with FCHL was unaffected by both polymorphisms, subjects with the Trp64Arg genotype of the beta3-AR gene had higher rates of glucose oxidation (17.6+/-4.5 v 15.8+/-4.1 micromol/kg/min, P=.017) and lower levels of free fatty acids (FFAs) in the fasting state (0.56+/-0.27 v 0.61+/-0.28 mmol/L, P=.027) and during the euglycemic clamp (0.12+/-0.10 v 0.21+/-0.15 mmol/L, P=.041) than subjects with the Trp64Trp genotype. We conclude that in FCHL families, codon 64 polymorphism of the beta3-AR gene may influence the rate of glucose oxidation via FFA levels.

We conducted a randomized, double-blind, placebo-controlled trial to assess the atrophogenicity of tacrolimus ointment. In a combined group of atopic dermatitis patients (n = 14) and healthy volunteers (n = 12), 0.3% tacrolimus, 0.1% tacrolimus, betamethasone-valerate, and a vehicle control were applied in a randomized order to nonsymptomatic, 4 cm x 4 cm regions of abdominal skin. After 7 d of treatment under occlusion, the carboxy- and amino-terminal propeptides of procollagen I (PICP, PINP) and the amino-terminal propeptide of procollagen III (PIIINP) were measured from suction blister fluid with specific radioimmunoassays. In addition, ultrasound measurements of skin thickness were taken. Betamethasone-treated areas showed median PICP, PINP, and PIIINP concentrations of 17.0%, 17.6%, and 39.5% of the vehicle control at the end of the treatment period, respectively, whereas the 0.1% and 0.3% tacrolimus-treated areas showed median concentrations of approximately 100% of the vehicle control (p < 0.001). Betamethasone was also the only treatment to reduce skin thickness; the median decrease in skin thickness was 7.4% relative to 0.1% tacrolimus, 7.1% relative to 0.3% tacrolimus, and 8.8% relative to the vehicle control (p < 0.01). Results for atopic dermatitis patients and healthy volunteers were similar. These findings suggest that tacrolimus does not cause skin atrophy.

Objective: To investigate the effect of the islet promoter region variant (G-->A) at nucleotide -30 of the glucokinase (GCK) gene on insulin levels in subjects with normal glucose tolerance (NGT), impaired glucose tolerance (IGT), and NIDDM., Research Design and Methods: The study population included 294 subjects with NGT, 83 subjects with IGT, and 36 subjects with NIDDM. Oral glucose tolerance tests (OGTTs) were performed in all subjects, and intravenous glucose tolerance tests (IVGTTs) were performed in subjects with NGT. The islet promoter region of the GCK gene was amplified with polymerase chain reaction and screened for the variant (-30) using single-strand conformation polymorphism analysis., Results: The islet promoter variant (-30) of the GCK gene was found in 17% of subjects with NGT, 23% of subjects with IGT, and 14% of patients with NIDDM (NS between the groups). Fasting, 1-h, and 2-h insulin levels, measured by OGTT, did not differ between subjects with and without this variant in any of the three groups. Furthermore, first-phase insulin secretion, determined by an IVGTT in subjects with NGT, did not associate with presence of the islet promoter region variant (-30) of the GCK gene., Conclusions: These results indicate that the variant (-30) of the islet promoter region of the GCK gene does not have a significant effect on insulin secretion in Finnish subjects with NGT, IGT, or NIDDM.

Impaired glycogen synthesis after insulin stimulation accounts for most of the insulin resistance in patients with non-insulin-dependent diabetes mellitus (NIDDM). The glycogen synthase gene (GYS1), which encodes the rate-limiting enzyme for glycogen synthesis, is a promising candidate gene for NIDDM. Therefore, we screened all 16 exons of this gene by single-strand conformation polymorphism analysis in 40 patients with NIDDM (age 67 +/- 2 years, body mass index 28.2 +/- 0.6 kg/m2) from Taipalsaari, eastern Finland. The Gly464Ser variant (exon 11) and a silent polymorphism TTC342TTT (exon 7) have been reported previously. In addition, we found a new variant Gln71His (exon 2) and a new amino acid polymorphism Met416Val (exon 10). An additional sample of 65 patients with NIDDM and 82 normoglycaemic men (age 54 +/- 1 years, body mass index 26.3 +/- 1.4 kg/m2) were screened. The allele frequency of the TTC342TTT silent substitution was 0.29 in both NIDDM and normoglycaemic subjects. The Gln71His and Gly464Ser variants were found in 1 (1%) and 3 (3%) subjects, respectively, of the 105 NIDDM patients and in none of the 82 normoglycaemic men. The Met416Val polymorphism was found in 16 (15%) of the 105 NIDDM patients and in 14 (17%) of the 82 control subjects (all heterozygous). The Met416Val polymorphism was not associated with insulin resistance in two groups of normoglycaemic subjects. In conclusion, the new Gln71His and Met416Val substitutions and other variants of the glycogen synthase gene are unlikely to make a major contribution to insulin resistance and NIDDM in diabetic patients from eastern Finland.

Objective: To investigate the association of the Trp64Arg polymorphism of the beta3-adrenergic receptor gene with NIDDM and the features of insulin resistance syndrome in subjects from eastern Finland., Research Design and Methods: We determined the prevalence of the Trp64Arg polymorphism of the beta3-adrenergic receptor gene by restriction fragment length polymorphism analysis in 110 patients with NIDDM (54 men and 56 women, age 63 +/- 1 years, BMI 30.4 +/- 0.5 kg/m2), in 183 patients with features of insulin resistance syndrome (103 men and 80 women, age 44 +/- 0 years, BMI 31.1 +/- 0.4 kb/m2), and in 82 normoglycemic control men (age 54 +/- 1 years, BMI 26.3 +/- 0.4 kg/m2)., Results: The allele frequency of the Trp64Arg polymorphism of the beta3-adrenergic receptor gene was similar in patients with NIDDM, in patients with insulin resistance syndrome, and in control subjects (0.08, 0.07, and 0.07, respectively; NS). In addition, this polymorphism was not associated with low resting metabolic rate, abdominal obesity, increased lipid oxidation, hypertension, or earlier development of NIDDM as previously described. Furthermore, in 82 normoglycemic male control subjects the Trp64Arg polymorphism was not associated with insulin resistance evaluated by the euglycemic-hyperinsulinemic clamp., Conclusions: The Trp64Arg polymorphism of the beta 3-adrenergic receptor gene is unlikely to be a major genetic predisposer to NIDDM or insulin resistance syndrome in subjects from eastern Finland.

Familial combined hyperlipidemia (FCHL) is associated with variable expression of dyslipidemias and insulin resistance. In nondiabetic Pima Indians an A to G substitution in codon 54 of the fatty acid binding protein 2 (FABP2) gene has been shown to be associated with insulin resistance. We screened the entire coding region of this gene by single-strand conformation polymorphism analysis in 24 probands (17 men and 7 women; age, 63.0 +/- 7.4 years [mean +/- SD]; body mass index [BMI], 27.7 +/- 4.2 kg/m2) who had FCHL and in 40 healthy men from a random population sample of 82 men (age, 54.0 +/- 5.0 years; BMI, 26.3 +/- 3.2 kg/m2). Insulin resistance was assessed with the euglycemic clamp in 58 subjects from FCHL families (14 probands with FCHL and 44 first-degree relatives of probands; 38 men and 20 women; age, 51.5 +/- 12.6 years; BMI, 25.5 +/- 3.9 kg/m2). We found three nucleotide substitution in the FABP2 gene: GCT to ACT (Ala-->Thr) in codon 54, GTA to GTG in codon 118, and GCGCA to GCACA in the 3'-noncoding region. Frequencies of these variants did not differ between the patients and control subjects. The Ala to Thr substitution in codon 54 was associated with a high lipid oxidation rate (P = .011 after adjustment for sex and family relationship), high HDL triglycerides (P = .042), and high LDL triglycerides (P = .013) but not with insulin resistance in subjects from FCHL families. The FABP2 gene is unlikely to be a major gene for FCHL, but it might affect lipid metabolism in subjects with FCHL.

The effects of diet only (DO) and diet combined with either aerobic (DA) or resistance (DR) exercise on subcutaneous adipose tissue (SAT), visceral adipose tissue (VAT), lean tissue (LT), and skeletal muscle (SM) tissue were evaluated in 33 obese men (DO, n = 11; DA, n = 11; DR, n = 11). All tissues were measured by using a whole body multislice magnetic resonance imaging (MRI) model. Within each group, significant reductions were observed for body weight, SAT, and VAT (P < 0.05). The reductions in body weight (approximately 10%) and SAT (approximately 25%) and VAT volume (approximately 35%) were not different between groups (P > 0.05). For all treatments, the relative reduction in VAT was greater than in SAT (P < 0.05). For the DA and DR groups only, the reduction in abdominal SAT (approximately 27%) was greater (P < 0.05) than that observed for the gluteal-femoral region (approximately 20%). Conversely, the reduction in VAT was uniform throughout the abdomen regardless of treatment (P > 0.05). MRI-LT and MRI-SM decreased both in the upper and lower body regions for the DO group alone (P < 0.05). Peak O2 uptake (liters) was significantly improved (approximately 14%) in the DA group as was muscular strength (approximately 20%) in the DR group (P < 0.01). These findings indicate that DA and DR result in a greater preservation of MRI-SM, mobilization of SAT from the abdominal region, by comparison with the gluteal-femoral region, and improved functional capacity when compared with DO in obese men.

Objective: The first objective was to determine the associated sensitivity (true positives) and specificity (false positives) associated with the use of waist circumference (WC) to predict specific visceral adipose tissue (VAT) levels. Because WC is a strong correlate of VAT, and, a WC of 100 cm and a VAT area of 130 cm2 (L4-L5) have been suggested as thresholds for increased disturbances in insulin-glucose homeostasis and lipid metabolism, we assessed the sensitivity and specificity when using a WC of 100 cm to identify a VAT of 130 cm2 or greater. A second objective was to evaluate the effects of diet and exercise induced weight loss on VAT and WC to establish the utility of using WC to follow reductions in VAT., Research Design and Methods: The sensitivity between WC and VAT was assessed using 50 male (BMI: 30.9 +/- 4.7, age: 41.0 +/- 11.2 y) and 49 female (BMI: 33.3 +/- 5.0, age: 36.9 +/- 7.4 y) subjects. The effects of weight loss on WC and VAT were evaluated in a subgroup of 20 male and 38 female subjects. VAT was measured by magnetic resonance imaging., Results: The sensitivity associated with the prediction of a VAT of 130 cm2 or greater using a WC of 100 cm was high (83%), however, so too was the incidence of false positives (38%). Significant (p < 0.01) correlations were obtained between concurrent reductions in VAT and WC for both the male (r = 0.69) and female (r = 0.47) groups. For the two groups combined, regression analysis indicated that a 1 cm reduction in WC was associated with a 4% reduction in VAT mass (p < 0.01)., Conclusions: The misclassification of individuals with VAT accumulation above 130 cm2 suggest that WC alone lacks the sensitivity required to identify specific VAT values. The diet and exercise induced reductions in visceral adiposity are positively related to corresponding reductions in WC for both genders is a positive result, and demonstrates the potential utility of using WC to follow changes in the AT depot that conveys the greatest health risk.

Inspired by theoretical results on universal modeling, a general framework for sequential modeling of gray-scale images is proposed and applied to lossless compression. The model is based on stochastic complexity considerations and is implemented with a tree structure. It is efficiently estimated by a modification of the universal algorithm context. Several variants of the algorithm are described. The sequential, lossless compression schemes obtained when the context modeler is used with an arithmetic coder are tested with a representative set of gray-scale images. The compression ratios are compared with those obtained with state-of-the-art algorithms available in the literature, with the results of the comparison consistently favoring the proposed approach.

We evaluated the effects of energy restriction and resistance exercise on lean tissue (LT), skeletal muscle (SM) and adipose tissue (AT) in fourteen obese women. The prescribed diet created a daily 1000 kilocalorie (4.18 MJ) deficit. LT, SM and AT were measured using a magnetic resonance imaging (MRI) model whereby 41 transverse images were acquired over the entire body. Although significant (P < 0.01) losses were observed for bodyweight (-10.4 +/- 2.7 kg), and total AT volume (-9.8 +/- 2.5 l), no significant changes were observed for whole body LT (P > 0.05). For MRI-LT this observation remained true for upper and lower body regions. Measurement of MRI-SM in the appendicular region revealed that SM was preserved in both the arm and leg regions (P > 0.05). These findings provide evidence that lean tissues, in particular skeletal muscle, are preserved and adiposity is substantially reduced in response to weight loss induced by the combination of resistance exercise and moderate energy restriction.

The effects of energy restriction alone (diet alone, DO) and energy restriction combined with endurance exercise (diet and exercise, DE) on lean tissue (LT), skeletal muscle (SM), and adipose tissue (AT) were evaluated in 24 obese women (DO, n = 12; DE, n = 12). The prescribed diet created an estimated daily deficit of 4.19 MJ (1000 kcal). LT, SM, and AT were measured by using magnetic resonance imaging (MRI). The weight loss observed for the DO group (-10.0 +/- 4.0 kg) was not significantly different from that of the DE group (-11.7 +/- 3.0 kg). However, the composition of the weight loss was significantly different between groups because the DE group lost significantly greater (P = 0.05) quantities of AT (-11.3 +/- 3.8 L) than the DO group (-8.3 +/- 3.6 L). Furthermore, whereas LT measured by MRI was maintained in the DE group, a modest (approximately 4%) but significant (P < 0.01) reduction in LT was observed in the DO group. Similarly, measurement of SM by MRI in the appendicular region revealed a preservation of SM in the DE group, but a significant (P < 0.01) reduction in the DO group. Maximal oxygen consumption (L) was significantly improved (approximately 9%) in the DE group (P < 0.01). These findings provide evidence that the combination of energy restriction and exercise result in a greater reduction of AT and preservation of LT and SM compared with energy restriction alone.

The effects of energy restriction (diet) in combination with either aerobic (DA) or resistance exercise (DR) on adipose tissue (AT) distribution were evaluated in 24 obese women (DA, n = 10; DR, n = 14). AT distribution was measured by magnetic resonance imaging (MRI). Comparison between groups demonstrated that the relative losses observed for body weight, subcutaneous AT (SAT), and visceral AT (VAT) volume were not significantly different (P > 0.05). A significant reduction in the volume ratio of VAT to SAT was observed for both groups (P < 0.01). Comparison of arm, abdomen and torso, and lower-body regions revealed that the regional mobilization of SAT was not significantly different between groups (P > 0.05) and that for both groups there was a preferential mobilization of SAT from the abdominal region (P < 0.05). Within the VAT depot, significant reductions were observed for both intraperitoneal and extraperitoneal AT (P < 0.01). These findings suggest that the combination of moderate energy restriction and either resistance or aerobic exercise induces significant reductions in VAT and SAT, with a preferential loss of VAT, and are thus effective means of reducing total and upper-body obesity in obese women.

The primary purpose of this study was to investigate the relationships between adipose tissue (AT) distribution, particularly visceral adipose tissue (VAT), circulating androgens, and plasma lipids in a group of 17 obese (body mass index [kg/m2], 31.8 +/- 3.8) android (waist to hip ratio [WHR], 1.01 +/- 0.05) men. AT distribution was measured by magnetic resonance imaging (MRI) using a multislice model in which 41 equidistant images were acquired from head to foot. Although the subjects were homogenous with respect to total adiposity, a sevenfold variation in VAT was observed. VAT and the visceral to subcutaneous ratio (VSR) were significantly correlated with triglyceride (TG) levels and the ratio of apolipoprotein (apo) B to low-density lipoprotein cholesterol ([LDL-C] P < .05). Neither proximal-thigh AT area nor lower-body subcutaneous adipose tissue (SAT) volume was significantly related to any lipid variable. However, the ratio of visceral AT area to thigh AT area (VTH) was positively correlated with TG (P < .05), and the ratio of VAT volume to lower-body SAT volume (VLBS) was positively correlated with TG, total cholesterol (TC), LDL-C (P < .05), and apo B (P = .057). Total testosterone (TT), free testosterone (FT), and sex hormone-binding globulin (SHBG) were not significantly related to any of the plasma lipid variables; however, the percentage of FT (%FT) was positively correlated with high-density lipoprotein cholesterol ([HDL-C]P < .01) and HDL-C/LDL-C (P < .05). TT, FT, %FT, and SHBG were not related to MRI-measured VAT. Age waa not related to either VAT or androgen levels.(ABSTRACT TRUNCATED AT 250 WORDS)

This study compared total and regional adipose tissue (AT) and lean tissue (LT) distribution measured by magnetic resonance imaging (MRI) in obese, android women (n = 40) and mean (n = 17). Women had significantly (P < 0.01) greater subcutaneous AT (39.6 +/- 11.6 vs 30.7 +/- 7.5 L) but significantly (P < 0.01) less visceral AT (2.5 +/- 1.1 vs 4.8 +/- 2.1 L) and LT (42.8 +/- 4.7 vs 58.2 +/- 6.2 L) compared with men. Segmentation of the visceral AT volume demonstrated that women had significantly (P < 0.01) less intraperitoneal (1.98 +/- 0.84 vs 3.74 +/- 1.61 L) and extraperitoneal AT (0.51 +/- 0.23 vs 1.04 +/- 0.47 L). When the legs, hip and pelvic region, and abdomen and torso regions were compared, women had significantly greater absolute quantities of subcutaneous AT and significantly less LT in all regions (P < 0.01); however, in all regions the relative distribution of both was similar. Anthropometric prediction of MRI-measured total AT gave SEs of 7.7% for women and 7.5% for men, for visceral AT 30% for women and 19% for men. Anthropometric prediction of LT gave SEs of 6.5% for women and 3.6% for men.