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Biomedical subjects

J Eriksson

Publications and source records attributed to J Eriksson.

At least 73 records · Page 4Linked to original sources

Internal derangement of the temporomandibular joint: correlation of arthrographic imaging with surgical findings.

Sixty-seven patients, who were surgically treated for internal derangement of the temporomandibular joint (TMJ), were retrospectively examined. The patients were evaluated preoperatively by clinical and arthrographic examinations and these results were compared with findings at surgery. Partial or complete dislocation of the disc was detected by arthrographic examination in 65 joints. Actual disc displacement was demonstrated at surgery in 57 TMJs, giving arthrography a positive predictive value of 88% for detecting disc dislocation. Arthrographic diagnosis of disc perforation was unreliable, as both false positive and false negative observations were recorded. Arthrography was found to have a positive predictive value of only 53% for assessing disc perforation. Based upon its proven inaccuracy, invasiveness and discomfort to the patient, it is recommended to replace arthrography by magnetic resonance imaging.

Adult↗

Resistance training in the treatment of non-insulin-dependent diabetes mellitus.

Aerobic endurance exercise has traditionally been advocated in the treatment of non-insulin-dependent diabetes mellitus (NIDDM). However, the effect of aerobic endurance exercise programs on long-term glycaemic control is small to moderate. The aim of the present study was to determine the effect of circuit resistance training on long-term glycaemic control (HbA1c) and to examine the potential association between muscle size and glycaemic control in NIDDM subjects. Eight NIDDM subjects participated in a 3 month individualized progressive resistance training program (moderate intensity, high-volume) twice a week with measurements of HbA1c, lipids, blood pressure, VO2max and thigh muscle cross-sectional area. There was a significant improvement in HbA1c (8.8% - 8.2%; p < 0.05). Muscle endurance increased by 32 +/- 23% (p < 0.05), and the cross-sectional area of m. vastus lateralis increased by 21% (p < 0.001). There was a strong inverse correlation between HbA1c and muscle cross-sectional area (knee extensors) after the exercise period (r = -0.73; p < 0.05). Circuit resistance training seems to be feasible in moderately obese, sedentary elderly NIDDM subjects and the inclusion of circuit resistance training in exercise training programs for NIDDM subjects should be considered.

Aged↗

Genetic and environmental components of interindividual variation in circulating levels of IGF-I, IGF-II, IGFBP-1, and IGFBP-3.

We assessed the magnitude of the genetic component in the variation of circulating levels of insulin-like growth factors I and II (IGF-I and IGF-II), and their binding proteins IGFBP-1 and IGFBP-3 by measuring their serum concentrations in 32 monozygotic and 47 dizygotic adult twin pairs of the same sex. The intrapair correlation for the IGF-I levels was r = 0.41 (P < 0.009) for monozygotic twins and r = 0.12 (P < 0.22) for dizygotic twins. For the IGF-II concentration the intrapair correlations were r = 0.66 (P < 0.0001) for the monozygotic and r = 0.34 (P < 0.01) for the dizygotic twins. No significant intrapair correlation was found for IGFBP-1 levels in either group. The correlations for IGFBP-3 concentration were r = 0.65 (P < 0.0001) and r = 0.23 (P < 0.06) for monozygotic and dizygotic twins, respectively. Women had higher IGF-II levels than men (635+/-175 vs. 522+/-144 microg/liter; P < 0.0001) and IGFBP-3 levels were also higher in women compared with men (5441+/-1018 vs. 4496+/-1084 microg/liter; P < 0.001). The proportion of variance attributable to genetic effects was 38% for the IGF-I concentration, 66% for the IGF-II concentration, and 60% for the IGFBP-3 concentration. No significant heritability was found for the IGFBP-1 concentrations. Our results show that, in adults, there is a substantial genetic contribution responsible for interindividual variation of the circulating levels of IGF-I, IGF-II, and IGFBP-3, but not for the IGFBP-1 levels.

Adult↗

Conformational studies of microcystin-LR using NMR spectroscopy and molecular dynamics calculations.

NMR spectroscopy in aqueous and dimethyl sulfoxide/water solutions is used to determine the three-dimensional structures of microcystin-LR, a cyclic cyanobacterial heptapeptide toxin which is a potent inhibitor of type 1 and type 2A protein phosphatases. The conformations of this toxic peptide are studied using a simulated annealing (SA) protocol followed by refined SA calculations in vacuo and free MD simulations in water. Only one conformational family in each solvent is found. The peptide ring has a saddle-shaped form, essentially the same in both solvents. The structural difference observed between the two solution structures is located to the part consisting of Mdha, Ala, and Leu. This peptide segment is not present in nodularin, a cyclic pentapeptide of similar toxicity. The Arg side chain is very flexible, while the side chain of Leu is well defined. The side chain of Adda, essential for toxicity, is constrained in the vicinity of the backbone ring but appears to be flexible in the more remote part.

Bacterial Toxins↗

Antispastic effects of L-dopa.

Antispastic effects of the noradrenaline and dopamine precursor l-3,4-dihydroxyphelanine (L-dopa) were investigated in 11 subjects in which exaggerated stretch reflexes developed after spinal cord injuries. The effects were evaluated from changes in the electromyographic (EMG) response of the quadriceps muscle during tendon jerks evoked by standardized taps over the patellar tendon, in clonus and in resistance to passive movements of the limb. After administration of L-dopa, EMG responses occurring 30-150 ms after the tendon tap decreased to about 50% of control, and clinical tests revealed a marked decrease in the resistance to muscle stretches and in the degree of clonus. The effects were maximal within about 1 h. The depressive actions of L-dopa are interpreted as being exerted primarily at the spinal level, since they were evoked in paraplegics and tetraplegics. The results support the previous hypothesis that group II muscle afferents contribute to.the exaggerated stretch reflex in spastic patients because L-dopa depresses transmission from group II but not from group I muscle afferents. They also indicate the possibility of using L-dopa in the treatment of spastic patients.

Adolescent↗

Cellular events in Fas/APO-1-mediated apoptosis in JURKAT T lymphocytes.

In the present study we investigated the Fas-mediated cellular events using the human leukemic T cell line, JURKAT. Ligation of the Fas receptor with a monoclonal antibody (IgM) resulted in the rapid (within 3 h) induction of apoptosis and was characterized by a sequence of distinct morphological and biochemical events. Thus, plasma membrane blebbing, condensation of the chromatin, and formation of high-molecular-weight (HMW) DNA fragments were the earliest events observed (by 45 min). They were followed by cleavage of DNA into oligonucleosomal-length fragments (laddering pattern) and the formation of apoptotic bodies, and finally, rounding of the apoptotic cells and complete cleavage of DNA into oligonucleosomal-length fragments occurred. The mitochondria remained structurally intact up to the stage of oligonucleosomal-length DNA cleavage, and the ability of the cells to exclude trypan blue was not compromised throughout the time course of the experiments. In contrast to many other model systems, apoptosis in JURKAT cells after anti-Fas treatment did not require the presence of extracellular Ca2+ or Mg2+ and was only partially inhibited by Zn2+. In addition, Fas-mediated apoptosis was unaffected by the presence of free radical scavengers or inhibitors of protein phosphatases, protein kinases, and nitric oxide synthesis. However, the serine protease inhibitors, N-tosyl-L-phenylalanine chloromethyl ketone (TPCK) and 3,4-dichloroisocoumarin (DCI) prevented anti-Fas-induced apoptosis in JURKAT cells. Low concentrations of these inhibitors blocked oligonucleosomal-length, but not HMW, DNA fragmentation. The latter required a higher concentration of TPCK or DCI to block. In addition, low concentrations of DCI also prevented Fas-mediated plasma membrane blebbing. In summary, our results suggest that proteolysis plays a central role in Fas-mediated apoptosis and that distinct proteolytic enzymes are involved in HMW DNA fragmentation, and oligonucleosomal-length DNA fragmentation, as well as in plasma membrane blebbing.

Antibodies↗

Changes of lipolytic enzymes cluster with insulin resistance syndrome. Botnia Study Group.

The activities of hepatic and lipoprotein lipase and the levels of lipo- and apoproteins were compared in two groups of normoglycaemic men representing the highest (n = 18) and lowest (n = 15) fasting insulin quintiles of first degree male relatives of non-insulin-dependent diabetic patients. The high insulin group representing insulin-resistant individuals had significantly lower post-heparin plasma lipoprotein lipase activity than the low insulin group (14.2 +/- 4.0 vs 20 +/- 5.8 mumol NEFA.ml-1.h-1, p < 0.001); hepatic lipase activity did not differ between the two groups (24.2 +/- 11 vs 18.0 +/- 5.3 mumol NEFA.ml-1.h-1, NS). The lipoprotein lipase/hepatic lipase ratio in the high insulin group was decreased by 66% as compared to the low insulin group (0.75 +/- 0.57 vs 1.25 +/- 0.65, p < 0.01). In the high insulin group both total and VLDL triglycerides were higher than in the low insulin group (1.61 +/- 0.57 vs 0.86 +/- 0.26 mmol/l, p < 0.001 and 1.00 +/- 0.47 vs 0.36 +/- 0.16 mmol/l, p < 0.001, respectively) whereas HDL cholesterol and HDL2 cholesterol were lower (1.20 +/- 0.30 vs 1.43 +/- 0.22 mmol/l, p < 0.05 and 0.49 +/- 0.21 vs 0.71 +/- 0.17 mmol/l, p < 0.05, respectively). Total cholesterol, LDL cholesterol or HDL3 cholesterol did not differ between the two groups. The mean particle size of LDL was smaller in the high insulin group than in the low insulin group (258 +/- 7 vs 265 +/- 6 A, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗

Magnesium and ascorbic acid supplementation in diabetes mellitus.

The effect of magnesium (Mg) and ascorbic acid (AA) supplementation on metabolic control was assessed in 56 outpatient diabetics. A 90-day run-in period was followed by two 90-day treatment periods, during which Mg (600 mg/day) and AA (2 g/day) were administered in a randomized double-blind cross-over fashion. A decrease in systolic and diastolic blood pressure (132 +/- 3 vs. 138 +/- 4 and 77 +/- 2 vs. 82 +/- 2 mm Hg; p < 0.05) was observed in insulin-dependent diabetes mellitus subjects during Mg supplementation. No beneficial effect of Mg supplementation was observed on glycemic control, lipids or blood pressure in non-insulin-dependent diabetes mellitus (NIDDM) subjects. AA supplementation improved glycemic control among NIDDM subjects and both fasting blood glucose (9.1 +/- 0.5 vs. 10.1 +/- 0.6 mmol/l; p < 0.05) and HbA1c (8.5 +/- 0.3 vs. 9.3 +/- 0.3%; p < 0.05) improved. Beneficial effects of AA supplementation on cholesterol (5.9 +/- 0.2 vs. 6.2 +/- 0.2 mmol/l; p < 0.05) and triglycerides (2.2 +/- 0.2 vs. 2.5 +/- 0.2; p < 0.05) were also observed in NIDDM subjects. The results suggest that high-dose AA supplementation may have a beneficial effect in NIDDM subjects on both glycemic control and blood lipids.

Adult↗

Hyperproinsulinemia of type II diabetes is not present before the development of hyperglycemia.

OBJECTIVE: To examine proinsulin and insulin levels in first-degree relatives of patients with non-insulin-dependent diabetes mellitus (NIDDM). RESEARCH DESIGN AND METHODS: Comparison of insulin and proinsulin responses to an oral glucose tolerance test in four groups of individuals: 1) 31 patients with newly diagnosed NIDDM treated with diet alone, 2) 34 first-degree relatives of NIDDM patients with impaired glucose tolerance (IGT), 3) 26 relatives with normal glucose tolerance (NGT), and 4) 30 subjects without a family history of diabetes. RESULTS: Both fasting and post-glucose levels of proinsulin were elevated in patients with diabetes, but not in the relatives with IGT or NGT. Levels of true insulin were highest in the diabetic group, followed by the subjects with IGT, and were lowest among relatives with NGT. Proinsulin levels correlated with glucose levels, suggesting that hyperglycemia is the main stimulus for increased proinsulin secretion. CONCLUSIONS: First-degree relatives of NIDDM patients, who have a high risk of developing diabetes, do not exhibit elevated levels of fasting or glucose-stimulated proinsulin as long as their fasting glucose levels remain normal.

Blood Glucose↗

Insulin receptor isotype expression correlates with risk of non-insulin-dependent diabetes.

Skeletal muscle insulin resistance plays a pivotal role in the pathogenesis of non-insulin-dependent diabetes mellitus (NIDDM), as individuals with this defect are at increased risk of developing the disease later in life. To assess whether the abnormal expression of the structurally distinct human insulin receptor isoforms, HIR-A and HIR-B, which has been found in skeletal muscle of NIDDM patients, is a feature of a prediabetic state, skeletal muscle biopsies from nondiabetic individuals ranging from high insulin sensitivity to insulin resistance were examined. Polymerase chain reaction analysis of mRNA from muscle biopsies detected exclusive or predominant expression of HIR-A in 13 patients with normal insulin sensitivity. In contrast, 7 subjects with various degrees of insulin resistance exhibited abnormally increased HIR-B RNA expression. This association suggests the abnormal expression of receptor isoforms as a characteristic of the prediabetic state and supports the notion of a connection of this aberration with the pathogenesis of NIDDM. Changes in HIR-A/B expression in the skeletal muscle may thus provide a prognostic criterion for the development of NIDDM.

Adult↗

Association between polymorphism of the glycogen synthase gene and non-insulin-dependent diabetes mellitus.

BACKGROUND: The storage of glucose as glycogen in skeletal muscle is frequently impaired in patients with non-insulin-dependent diabetes mellitus (NIDDM) and their nondiabetic relatives. Despite an intensive search for candidate genes associated with NIDDM, no data have been available on the gene coding for the key enzyme of this pathway, glycogen synthase. METHODS AND RESULTS: Using a human complementary DNA probe, the restriction enzyme Xbal, and Southern blot analysis, we identified two polymorphic alleles, A1 and A2, in the glycogen synthase gene. The gene was localized to chromosome 19. The A1A2 or A2A2 genotype was found in 30 percent of 107 patients with NIDDM but in only 8 percent of 164 nondiabetic subjects without a family history of NIDDM (P < 0.001). The diabetic patients with the A2 allele had a stronger family history of NIDDM (P = 0.019), a higher prevalence of hypertension (P = 0.008), and a more severe defect in insulin-stimulated glucose storage (P = 0.001) than the diabetic patients with the A1 allele. The concentration of the glycogen synthase protein in biopsy specimens of skeletal muscle from the patients with the A2 allele was normal, however, suggesting that expression of the gene was unaltered. The Xbal polymorphism was due to a change of a single base in an intron. CONCLUSIONS: The Xbal polymorphism of the glycogen synthase gene identifies a subgroup of patients with NIDDM characterized by a strong family history of NIDDM, a high prevalence of hypertension, and marked insulin resistance.

Alleles↗