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Biomedical subjects

J Reimers

Publications and source records attributed to J Reimers.

At least 37 records · Page 2Linked to original sources
PubMed1993

[Incidence of short hamstrings and leg muscles at ages 3-17 years].

In 1991, 769 children and adolescents, 98% of the pupils in the various age groups in seven schools and ten kindergartens on Funen, were examined. Seventy-five percent of the boys and 35% of the girls over the age of ten proved to have such short hamstrings that one knee had a extension deficit without violence of > or = 40 degrees when the hip was flexed 90 degrees. More than 10% of the boys over the age of ten had an extension deficit of > or = 60 degrees. Forty-five children had a difference > or = 15 degrees between the two legs. The triceps surae muscles are too short if the corrected foot can only be pressed slowly to the right angle. This was found to be the case for 25-64% of the children from the age of three to 17. Therefore, we must conclude that it is necessary to allow time in kindergarten and school for the children to stretch their muscles a few minutes daily.

Adolescent↗
PubMed1993

Involvement of interleukin 1 and interleukin 1 antagonist in pancreatic beta-cell destruction in insulin-dependent diabetes mellitus.

In this review we propose that the balance between the action of interleukin 1 (IL-1) and its natural antagonist IL-1ra on the level of the insulin-producing pancreatic beta-cell may play a decisive role in the pathogenesis of insulin-dependent diabetes mellitus (IDDM). We argue that IL-1 potentiated by other cytokines (tumor necrosis factor alpha, interferon gamma) is an important effector molecule involved in both early and late events in the immune-mediated process that leads to beta-cell destruction and IDDM. We also point out that surprisingly high molar excesses of IL-1ra over IL-1 are necessary to block the action of IL-1 on islet beta-cells compared to islet alpha-cells in vitro and in animals. We suggest that the selectivity of beta-cell destruction in IDDM may be conferred on several levels: (1) homing of beta-cell antigen specific T cells, (2) targeted delivery of cytokines by lymphocytic and monocytic cells beta-cells, (3) high molar excesses of IL-1ra over IL-1 needed to prevent IL-1 mediated beta-cell toxicity, (4) increased beta-cell sensitivity to free nitric oxide and oxygen radical formation induced by IL-1 and (5) inadequate oxidative stress response by beta-cells to cytokines. Further studies are needed to establish the in vivo role of an imbalance between the amounts of IL-1 and IL-1ra produced relative to their action in the pathogenesis of IDDM.

Animals↗
PubMed1992

Repetitive in vivo treatment with human recombinant interleukin-1 beta modifies beta-cell function in normal rats.

It is unknown whether interleukin-1 exerts a bimodal effect on Beta-cell function in vivo, and whether interleukin-1 has a diabetogenic action in normal animals. We therefore studied: (a) acute effects 2 h after an intraperitoneal bolus injection of 4 micrograms of recombinant human interleukin-1 beta per kg body weight on blood glucose, plasma levels of insulin, glucagon and corticosterone in Wistar Kyoto rats, either untreated or pre-treated with 4 micrograms/kg of interleukin-1 daily for 3 or 5 days; (b) the cumulative effects of repetitive intraperitoneal injections of 4 micrograms/kg interleukin-1 on blood glucose, glucose tolerance, plasma levels of insulin, glucagon and corticosterone, pancreatic insulin content and pancreatic ultrastructure; and (c) blood glucose and plasma concentrations of insulin, glucagon and corticosterone 10 h after the last of five intraperitoneal injections of interleukin-1, at which time point the inhibitory effect of short-term interleukin-1 exposure on insulin secretion reaches its nadir in vitro. A single injection of 4 micrograms/kg of interleukin-1 caused a slight, but significant lowering of blood glucose 2 h after interleukin-1 injection with no significant changes in plasma insulin and in spite of increases in plasma glucagon and corticosterone. A lowering of blood glucose 2 h after interleukin-1 administration was reproduced with 40, but not 0.4 micrograms/kg of interleukin-1, and was also seen in interleukin-1 pre-treated rats. Two hours after the fifth injection of interleukin-1, intraperitoneal glucose tolerance was impaired with elevated plasma insulin and corticosterone levels and increased pancreatic insulin content, indicating a state of insulin resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

The pharmacokinetics, distribution and degradation of human recombinant interleukin 1 beta in normal rats.

Based upon in vivo rat experiments it was recently suggested that interleukin 1 in the circulation may be implicated in the initial events of beta-cell destruction leading to insulin-dependent diabetes mellitus (IDDM) in humans. The aim of the present study was to estimate half-lives of distribution (T1/2 alpha) and elimination phases (T1/2 beta) of human recombinant interleukin 1 beta (rIL-1 beta), and its tissue distribution and cellular localization by means of mono-labelled, biologically active 125I-rIL-1 beta. After intravenous (i.v.) injection, 125I-rIL-1 beta was eliminated from the circulation with a T1/2 alpha of 2.9 min and a T1/2 beta of 41.1 min. The central and peripheral volume of distribution was 20.7 and 19.1 ml/rat, respectively, and the metabolic clearance rate was 16.9 ml/min/kg. The kidney and liver showed the highest accumulation of tracer, and autoradiography demonstrated that 125I-rIL-1 beta was localized to the proximal tubules in the kidney and to the hepatocytes in the liver. Furthermore, grains were localized to the islets of Langerhans in the pancreas. Tracer-bound proteins corresponding to intact 125I-rIL-1 beta were found in the circulation after i.v., intraperitoneal (i.p.) and subcutaneous (s.c.) injections, as demonstrated by high performance size exclusion chromatography, trichloracetic acid precipitation and SDS-PAGE until 5 h after tracer injection. Pre-treatment with 'cold' rIL-1 beta enhanced degradation of a subsequent injection of tracer. The route of administration was of importance for the biological effects of rIL-1 beta, as demonstrated by a reduced food intake, increased rectal temperature and blood glucose after s.c. injection of rIL-1 beta compared with i.p. The present demonstration of intact rIL-1 beta in the circulation and the islets of Langerhans supports the hypothesis that systemic IL-1 beta may be involved in the initial beta-cell destruction leading to IDDM in humans.

Animals↗
PubMed1991

Repeated intraperitoneal injections of interleukin 1 beta induce glucose intolerance in normal rats.

Previous in vitro findings suggest the involvement of interleukin 1 (IL-1) in the pathogenesis of insulin-dependent diabetes mellitus. The aims of the present study were to investigate the effects of single or repeated ip injections of recombinant IL-1 beta on blood glucose and glucose tolerance in vivo. Normal Wistar Kyoto rats were injected ip with a single injection of 4 micrograms/kg of the mature form of recombinant IL-1 beta (amino acids 117-269) or once daily on 5 consecutive days. Control rats were given vehicle and were fed ad libitum or pair-fed together with the rIL-1 beta treated rats. An ip glucose tolerance test (0.2 g D-glucose/100 g) was performed 2 h after injection of rIL-1 beta. A single injection of rIL-1 beta caused a mild depression in blood glucose and an improved glucose tolerance. Multiple injections of rIL-1 beta induced a diminished weight gain, a 24-28% reduction in food intake, a lasting mild depression of blood glucose (7 days) and a transiently impaired glucose tolerance on day 5. We conclude that systemic IL-1 should be considered an important regulator of glucose homeostasis in vivo.

Animals↗
PubMed1991

[Improvement of chronic regionally impaired myocardial function immediately after coronary angioplasty].

UNLABELLED: The effect of PTCA on chronically impaired, regional wall motion was studied in 40 patients with stable angina and stenoses in the left anterior descending artery. Left-ventricular angiograms were obtained before, 15 min after PTCA and, additionally, in eight patients 15 +/- 5 weeks after PTCA. Left-ventricular ejection fraction and regional myocardial function were assessed by the centerline method. Patients with no (n = 18) or non-Q-wave (n = 12) infarction were compared to patients with Q-wave infarction (n = 10). After PTCA, ejection fraction increased from 54 +/- 8% to 59 +/- 8% (p less than 0.05) and regional function improved significantly (maximal standard deviation before PTCA: 2.8 +/- 0.8; after PTCA: 1.9 +/- 0.9- segments below the first standard deviation before PTCA: 31 +/- 16; after PTCA: 19 +/- 17). The improvements were found in patients with no or non-Q-wave infarction. The benefit on regional function was unchanged at follow-up. CONCLUSIONS: PTCA reduced chronic regional myocardial dysfunction in 78% of the patients with stable angina within 15 min. Reversible myocardial dysfunction is most likely related to hibernating myocardium.

Aged↗
PubMed1990

[Referral pattern, diagnoses and occurrence of short muscles in children and adolescents in an orthopedic specialist practice].

The patterns of referral for 600 consecutive children and adolescents under the age of 17 years were analysed and the symptoms were compared with the diagnoses. 40% were referred because of foot problems, 20% had mobility problems and 20% had pain in the back or extremities. Out of the 240 patients with foot problems, these could be confirmed in 44%. 30% had merely short muscles and 7% had, in addition, spasticity. 70% out of the 110 patients referred on account of flat foot had too short achilles tendons. 50% out of the 600 patients referred had short achilles tendons and/or hamstring muscles. In 20%, the short muscles alone could explain the symptoms experienced by the patients. Short heel tendons are found with broad fore-feet, cavus and valgus feet, loose subtaloid joints, heel exostoses, pain in the heel and in the calf. Short hamstrings result in a shuffling gait, high-riding patellae with periodic pain, pain on the posterior aspect of the thigh and a straight transition in the thoraco-lumbar region with subsequent Scheuermann's disease. The length of the muscles should, therefore, be investigated. If they are too short, they should be stretched for one minute every twelfth hour to obtain optimal elasticity and length.

Achilles Tendon↗
PubMed1990

Nonvalvular atrial fibrillation associated with cardioembolic stroke: the role of hypertensive heart disease.

Epidemiologists have not identified high risk groups nor the entire spectrum of heart disease, especially the subclinical forms underlying nonvalvular atrial fibrillation (NVAF) predisposing to cardioembolic (CE) stroke. We analysed 36 cases of 'isolated' NVAF among 106 consecutive cases of CE stroke after excluding cases of AF associated with valvular disease, myocardial infarcts, ischaemic and other cardio-myopathies (34 cases). This revealed echocardiographic left ventricular hypertrophy (LV mass index 136 +/- 25 g, vs normal 68 +/- 12 g p less than 0.001), enlarged left atria (left atrial area 27.4 +/- 3.6 cm2 vs normal 14.3+/- 1.6 cm2 p less than 0.001), normal systolic function and formed the largest group associated with CE stroke (34%), mean age 72.6 years--Study Group D. Eighty nine per cent had known or undetected hypertension compared to 60% in matched controls (x2 = 8.3 df = 1 p less than 0.01), and hypertension remained the predominant risk factor for left ventricular hypertrophy (LVH). Although all had echocardiographic LVH, 60% had neither electrocardiographic LVH nor cardiomegaly on chest X-ray. Hence usual epidemiologic methods may fail to detect these cases. Hypertensive heart disease is known to predispose to left atrial enlargement and AF. Progressive atrial enlargement is associated with increasing risk of embolic stroke. We conclude that NVAF associated with hypertensive heart disease forms a major component of the spectrum of heart disease associated with NVAF predisposing to CE stroke. Detection and treatment of hypertension to prevent or reverse LVH and atrial enlargement should be an important preventive measure.

Adult↗
PubMed1990

Intra-peritoneal administration of interleukin-1 beta induces impaired insulin release from the perfused rat pancreas.

Previous studies have demonstrated a stimulatory effect of interleukin-1 beta (IL-1 beta) on insulin and glucagon release from the perfused rat pancreas, accompanied by selective lysis of 20% of beta-cells as assessed by electronmicroscopy. However, we have not observed an inhibitory action of IL-1 beta on insulin release from the perfused pancreas as shown for isolated islets. To test whether periodical exposure of the endocrine pancreas to circulating IL-1 beta in vivo affects insulin release from the intact perfused pancreas, rats were treated with daily intraperitoneal injections of 4 micrograms IL-1 beta/kg or saline for 5 days. On day 5 the pancreata were isolated 2 h after the last injection and perfused from 0 to 72 min with 11 mmol/l D-glucose and from 72 to 84 min with 20 mmol/l D-glucose. Saline or IL-1 beta was added from 12 to 72 min. In pancreata from animals pre-treated with IL-1 beta glucose-stimulated as well as IL-1 beta potentiated glucose-stimulated insulin release was almost completely abolished. Furthermore, a decline in insulin release was observed at 11 mmol/l D-glucose, in contrast to an increase in insulin release in controls. The total extractable insulin content in pancreata from IL-1 beta pre-treated rats was higher than in pancreata from saline-treated controls. In contrast to the inhibitory effect of in vivo administration of IL-1 beta on beta-cell function glucagon secretion was stimulated. These observations suggest that circulating IL-1 beta is an important modulator of alpha- and beta-cell secretory function in vivo and that IL-1 beta should be considered a contributory pathogenetic factor in the development of insulin-dependent (type 1) diabetes mellitus.

Animals↗
PubMed1990

Functional changes in the antagonists after lengthening the agonists in cerebral palsy. I. Triceps surae lengthening.

In a recent study, children with spastic cerebral palsy (median age, five years) were examined before and up to a median of 14 months after 52 operations involving elongation of the tendo Achillis or aponeurotomy of the gastrocnemius. On removal of the cast four weeks postoperatively, strength in the dorsiflexors had increased by more than 50%, as evaluated by the ability to raise a weight from a scale. Postoperative function was correlated with preoperative function. Strength had increased more than 200% by 14 months postoperatively, with no instance of excessive lengthening of the triceps. In 13 cases, the dorsiflexors had been without function preoperatively. Two of those cases again lost the dorsiflexor function achieved postoperatively, when dynamic shortening recurred after one year. The study thus confirms the view that antagonist function improves when spasticity in the agonist is reduced by tendon lengthening.

Adolescent↗
PubMed1990

Functional changes in the antagonists after lengthening the agonists in cerebral palsy. II. Quadriceps strength before and after distal hamstring lengthening.

In a recent study, 38 patients with spastic cerebral palsy (median age, 5.6 years) were examined before and at a median 13 months after distal lengthening of the hamstrings. Four weeks after operation, the strength of the quadriceps was reduced by a median value of 70%. Seven months after operation, the strength had been regained; by 13 months after operation, it had increased by a median value of 22%. In 20 cases, strength had increased by more than 50%. The present study confirms the theory that quadriceps function is strengthened when the antagonist function is weakened. The study also explains (1) why it often takes six months for gait to become better than before operation and (2) why spasticity of the rectus often increases after the hamstrings are lengthened.

Adolescent↗
PubMed1988

Lack of insulinotropic effect of endogenous and exogenous cholecystokinin in man.

Intraduodenal phenylalanine administration (333 mg/min over 60 min) released endogenous cholecystokinin in healthy young subjects as demonstrated radioimmunologically and by intraduodenal bilirubin and pancreatic enzyme output. Concomitantly, there was only a small increase over basal in circulating immunoreactive-insulin and immunoreactive-C-peptide concentrations. In healthy volunteers intraduodenal infusions of saline (10 ml/min), glucose (333 mg/min) or phenylalanine (333 mg/min) were performed for 60 min when plasma glucose was clamped at approximately 8 mmol/l. Phenylalanine enhanced immunoreactive-insulin and immunoreactive-C-peptide responses three-fold more than did the same amount of glucose. Immuno-reactive gastric inhibitory polypeptide responses were small and not different after glucose and phenylalanine administration. Immunoreactive cholecystokinin was significantly stimulated to 9.4 +/- 1.4 pmol/l only by intraduodenal phenylalanine. Plasma phenylalanine concentrations increased into the supraphysiological range (approximately 1.5 mmol/l). Intravenous infusions of phenylalanine achieving plasma concentrations of 1.2 mmol/l stimulated insulin secretion at elevated plasma glucose concentrations (approximately 8 mmol/l clamp experiments), but had no effect at basal plasma glucose concentrations. A small increase in cholecystokinin also was observed. Intravenous infusions of synthetic sulphated cholecystokinin-8 leading to plasma concentrations in the upper postprandial range (8-12 pmol/l) did not augment the immunoreactive-insulin or immunoreactive-C-peptide levels during hyperglycaemic clamp experiments, in the absence or presence of elevated plasma phenylalanine concentrations. It is concluded that the augmentation of the glucose-induced insulin release by intraduodenal administration of phenylalanine cannot be related to cholecystokinin release, but rather is explained by the combined effects of elevated glucose and phenylalanine concentrations. In man, cholecystokinin does not augment insulin secretion caused by moderate hyperglycaemia, elevations of phenylalanine concentrations, or combinations thereof.

Adult↗
PubMed1987

Lacunar infarction: a 12 month study.

Identification of lacunar infarction as a cause of stroke is important, as investigation, treatment and outcome differ from those in the other stroke categories. In this study of 121 acute strokes admitted over a period of 12 months, 28 patients (23%) were found to have lacunar infarction and 93% of patients with lacunes had either a past history of hypertension or echocardiographic evidence of left ventricular hypertrophy. The degree of left ventricular hypertrophy tended to be moderate to severe with an average left ventricular mass on echocardiography of 120 g/m2. Pure motor hemiparesis was the commonest clinical presentation and lacunar infarction overall has a low mortality.

Cerebral Infarction↗
PubMed1984

Adductor transfer versus tenotomy for stability of the hip in spastic cerebral palsy.

Two groups of children with cerebral palsy are compared with respect to the migration of the hip before and after 36 adductor transfers and 29 adductor tenotomies. The results in the two series are positive, with no significant difference (4 and 7%/year, respectively). Adductor transfer is a more stressful intervention for the child, with no proven advantage as yet. Therefore, we have for the time being withdrawn this procedure in favor of adductor tenotomy.

Adolescent↗