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Biomedical subjects

S Lindal

Publications and source records attributed to S Lindal.

At least 37 records · Page 2Linked to original sources
PubMed1999

A novel and efficient regimen for producing chronic relapsing experimental autoimmune encephalomyelitis (CR-EAE) in SJL mice.

We report that SJL mice developed chronic relapsing experimental autoimmune encephalomyelitis (CR-EAE) when injected with a mixture of mouse spinal cord homogenate (MSCH), killed mycobacteria tuberculosis (M. tb), and mycobacteria butyricum (M. b) in PBS 2 months before a conventional acute experimental autoimmune encephalomyelitis (EAE) induction injection. The altered progression of the disease involved an accelerated but less severe acute attack and development of a chronic course with relapsing-remitting episodes. Histological examination revealed inflammatory cell infiltration and demyelination in the brain. The dose of neuroantigen as well as the anatomical sites of injections were found to be crucial for the development of the disease.

Animals↗
PubMed1998

Progressive central and peripheral demyelinating disease of adult onset in a Norwegian family.

OBJECTIVE: To describe the clinical features of a Norwegian family with a combined central and peripheral demyelinating disease. DESIGN: Multiple case report. SUBJECTS AND MATERIALS: Three generations of a Norwegian family. Medical records were available for all 9 members of the second generation and 5 affected members in the third generation. RESULTS: At least 5 members had clinical features, neuroimaging findings, and electrophysiologic signs indicating a chronic progressive disorder affecting both the central and peripheral nervous systems. The clinical symptoms developed between the ages of 30 and 70 years in affected family members, who gradually developed sensory loss, muscle deterioration, and distal weakness in all extremities, unsteady gait, and dysarthria. Five of 9 persons in the second generation had strokes and experienced mental deterioration. The initial stroke episodes were recognized between the ages of 54 and 68 years, and death occurred between the ages of 62 and 75 years. In 7 subjects, cerebrospinal fluid protein levels were increased, and in 5 agar gel electrophoresis indicated blood-brain barrier dysfunction. Seven family members had neuroimaging signs of a widespread white matter disorder. In 4 subjects, neurophysiological investigations indicated a polyneuropathy, and in 3 subjects, results from a sural nerve biopsy showed a demyelinating neuropathy. There was no evidence of co-inheritance with genetic markers of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (19p), PMP22 (17q), APP (21q), CMTX1 (Xq), or PLP (Xq). CONCLUSIONS: Progressive central and peripheral demyelinating disease seems to be a distinct type of hereditary adult-onset demyelinating disorder affecting both the peripheral and central nervous systems. Its exact nature remains unknown.

Adult↗
PubMed1998

Insulin kinetics, insulin action, and muscle morphology in lean or slightly overweight persons with impaired glucose tolerance.

Glucose intolerance is influenced by body fat mass, as well as muscle fiber composition. To examine the relation between the metabolic profile and muscle morphology in this condition, we performed muscle biopsies and hyperglycemic clamps to determine insulin secretion and clearance, and the insulin effects on glucose disposal and nonesterified fatty acids (NEFA) in 45 glucose intolerant persons (body mass index [BMI], 27.8 +/- 3.0 kg/m2) and 45 normoglycemic controls (BMI, 25.8 +/- 2.7 kg/m2) (P = .001). After adjustment for BMI, glucose-intolerant subjects had lower first-phase insulin release (726 v 954 pmol/L, P = .04). Glucose-intolerant subjects and controls differed in fasting insulin, insulin clearance, and insulin sensitivity to glucose disposal before, but not after, standardizing for BMI. During the clamp, glucose-intolerant subjects had less NEFA suppression and elevated levels of NEFA compared with controls (85% +/- 9% v 90% +/- 6%, P = .02; and 70 +/- 42 micromol/L v 45 +/- 28 micromol/L, P = .01). Glucose-intolerant subjects also had a higher percentage of insulin-insensitive, type 2b muscle fibers, which are not adapted for fat oxidation (7% +/- 9% v 9% +/- 9%, P = .003). BMI was not associated with NEFA suppression or the percentage of type 2b muscle fibers in either group. In conclusion, glucose-intolerant persons have impaired first-phase insulin release, an elevated percentage of type 2b muscle fibers, and increased NEFA availability. Reduced insulin clearance, hyperinsulinemia, and insulin resistance were associated with small increments in BMI.

Body Mass Index↗
PubMed1997

Human leukocyte antigen class I in polymyositis: leukocyte infiltrates, regeneration, and impulse block.

In polymyositis (PM), T-cell mediated myocytotoxicity is directed against strongly human leukocyte antigen class I positive (HLA-I+) muscle fibers. Fiber regeneration probably is partly responsible for this HLA-I up-regulation. We have evaluated regeneration, denervation/impulse blockade, and focal leukocyte infiltrates as possible HLA-I inducing factors in PM. Distinctive patterns of HLA-I, nerve cell adhesion molecule (NCAM), and vimentin expression accompany denervation and regeneration. Regenerating fibers also have centralized nuclei. Using semiquantitative methods, we examined strongly HLA-I+ fibers in PM muscle biopsies for these markers. Sarcoplasmic HLA-I levels were related to the presence of leukocyte infiltrates and invasion of fibers. Strongly HLA-I+ fibers were frequently invaded, and regeneration-associated changes were usually observed at sites of fiber damage. Sarcoplasmic HLA-I levels were stable along intact fibers, also adjacent to leukocyte infiltrates. A majority of the strongly HLA-I+ fibers were nonregenerating (NCAM+ only). Though other mechanisms cannot be excluded, this suggests that impulse blockade or denervation may contribute to extra HLA-I up-regulation in these fibers.

Aged↗
PubMed1996

[Tamoxifen and endometrial cancer. A case report].

Tamoxifen is an oestrogen antagonist with partial agonistic effects that is used extensively in the treatment of mammary carcinoma. We report a case of an 80 year old woman who was operated on for carcinoma of the mammary gland and developed endometrial carcinoma after ten years of tamoxifen treatment. Tamoxifen has been noted for its reportedly low incidence of side effects. Since 1985, however, several reports have associated tamoxifen with higher risk of endometrial carcinoma. We also review the relevant literature published during the last decade.

Adenocarcinoma↗
PubMed1996

High-dose 7-hydromethotrexate: acute toxicity and lethality in a rat model.

To elucidate mechanisms for methotrexate (MTX)-induced renal and hepatic toxicity, we investigated the acute effects of bolus plus continuous infusion of up to 0.4 g/kg 7-hydroxymethotrexate (7-OH-MTX) in the rat. We demonstrate for the first time in any species the occurrence of acute lethal toxicity within a few hours after 7-OH-MTX administration. Serum concentrations of 7-OH-MTX measured at the time of death were 1.4 mM (mean), about one-half of those achieved in some patients after infusion of high-dose MTX (HD-MTX) in the clinic. The data suggest an approximate LD50 (the dose lethal to 50% of the study population) of 0.3 g/kg and a steep dose/lethality curve for 7-OH-MTX. Moreover, acute renal and hepatic toxicity occurred as evidenced by severe morphological findings and increased serum levels of creatinine and liver transaminases. In all rats subjected to continuous infusion of 7-OH-MTX, yellow microscopic precipitations were apparent in the kidney tubules. Crystallization was also seen in bile ducts of the liver in some of the rats. These results further support that the formation of 7-OH-MTX is disadvantageous and that reported attempts to prevent its formation during MTX treatment are warranted.

Animals↗
PubMed1996

Endothelin-1 causes sequential trapping of platelets and neutrophils in pulmonary microcirculation in rats.

We previously showed that endothelin-1 (ET-1) causes accumulation of leukocytes in the pulmonary microvasculature and increases vascular permeability in isolated rat lungs provided the presence of leukocytes in the perfusate. In the present study, we examined the time sequence for morphological changes induced by ET-1 in rat alveolar tissue. For this purpose we used morphometric analysis based on lung transmission electron micrographs. Morphometry was performed by point counting, and data were expressed as relative volume density. ET-1 (0.06, 0.6, and 6 nmol/kg) was infused into the internal jugular vein, and the animals were killed at certain points of time. The lungs were fixed by endotracheal instillation of McDowell's fixative. Infusion of ET-1 (0.06 or 0.6 nmol/kg) caused no significant morphological changes in the rat alveolar tissue as assessed by morphometric examination. A sevenfold increase in volume density of platelets was seen 5 min after infusion of ET-1 6 nmol/kg. The platelets were loosely aggregated, adhered partly to the endothelium, and some of them had a spherical shape with vacuoles, indicating activation. The volume density of erythrocytes increased threefold, lasting 30 min. At 120 min, the volume density of polymorphonuclear leukocytes (PMN) increased 10-fold. The PMN adhered closely to the endothelium and partly occluded the capillary lumen. Simultaneously, the endothelial cell surface showed morphological signs of injury. No significant changes were observed in the volume density of alveolar macrophages or monocytes. No significant changes were seen in lung volumes or the volume of the alveolar tissue compartment. The results showed that ET-1 causes a time- and dose-dependent sequential entrapment of platelets and neutrophils in the pulmonary circulation.

Animals↗
PubMed1995

[Malignant hyperthermia--still a current and dangerous problem].

Malignant hyperthermia is a potentially fatal condition inducible by volatile anaesthetics and/or suxamethonium in genetically susceptible individuals. A disturbed calcium homeostasis in skeletal muscle (possibly in the ryanodin receptor) results in elevated myoplasmatic calcium. The latter causes muscle contraction and a hypermetabolic state, clinically observed as rigidity, fever, hypercarbia, metabolic acidosis and hyperkalemia. Arythmia ensues. Dantrolene inhibits the release of calcium and can halt the process if the diagnosis is made early. A fatal incident of probable malignant hyperthermia in a 13 year old boy is described and evaluated according to a multifactorial clinical grading scale. The value of the in vitro contracture test to diagnose malignant hyperthermia is discussed. Suggestions concerning the treatment of masseterspasm rigidity, an acute episode of malignant hyperthermia, and safe anaesthesia for susceptible patients are presented.

Adolescent↗
PubMed1995

Myocardial and microvascular injury following coronary surgery and its attenuation by mode of reperfusion.

In 14 patients undergoing coronary surgery, repeated atrial biopsies were obtained before and at the end of ischemia, and at 20 and 60 min of reperfusion. In half of the patients reperfusion was initiated with an abrupt rise in blood temperature and pressure, in the other half with a gradual rise. The biopsies were prepared for transmission electron microscopy and analyzed by stereological technique. In all biopsies, myocytic injury, as revealed by mitochondrial changes and intracellular edema, occurred following ischemia (P = 0.0003 and 0.007, respectively). The intracellular edema regressed following 20 min of reperfusion (P = 0.008). The myocytic mitochondrial changes persisted during reperfusion towards the end of the observation period (P = 0.0001). Interstitial edema increased following ischemia (P = 0.007) and persisted following 60 min of reperfusion (P = 0.009). The capillary part was significantly reduced after 20 min of reperfusion (P = 0.003), probably reflecting interstitial edema. Most changes were reversible in nature, although foci of irreversible changes were shown. In patients with a gradual start of reperfusion there was a significant regression of interstitial edema (P = 0.005) at 60 min reperfusion compared to the patients with an abrupt start, where the same changes seemed to persist or even increase. The study demonstrates that "reperfusion injury" occurs in human myocardium. It can be discerned from "ischemic" injury, and it may be reduced by a gentle mode of reperfusion.

Adult↗
PubMed1995

Metabolic effects of two regimens of growth hormone given before operation in piglets.

OBJECTIVE: To clarify the effects of growth hormone (GH) given three days before and at the start of a standard abdominal operation or at the start of the abdominal operation alone in piglets. DESIGN: Randomised experiment. SETTING: University hospital, Norway SUBJECTS: Twenty-four piglets. INTERVENTIONS: GH 24 IU was given intramuscularly for either three days before and on the morning of the operation or on the morning of a standard abdominal operation only (n = 8 in each group) A further 8 piglets acted as untreated controls. MAIN OUTCOME MEASURES: Diameter of fibres in the soleus and gastrocnemius muscles; urinary nitrogen excretion; and fat and carbohydrate oxidation measured by indirect calorimetry. RESULTS: Nitrogen excretion was reduced (in the three days group the mean (SEM) was 30.8 (4.2) mg/kg, corresponding figures from the one day group and the controls were 37.6 (5.8) and 55.4 (3.1) mg/kg, respectively, p = 0.004). Fat oxidation increased (for the whole period: p = 0.014) and carbohydrate oxidation decreased (p = 0.02) in the one day group only. The diameter of type I muscle fibres was increased in both muscles (soleus, three day group, mean (SEM) 37.5(1.4) microns compared with control, 30.4(0.6) microns, p = 0.001, and gastrocnemius, three day group 38.6(1.3) microns compared with control, 30.8(1.4) microns, p = 0.01). CONCLUSIONS: Three days treatment with GH enhanced nitrogen sparing and attenuated changes in fat and carbohydrate oxidation induced by one day treatment, but induced hypertrophy of type I muscle fibres.

Animals↗
PubMed1994

[Muscle tissue for diagnosis of neuromuscular diseases. Procedures of specimen taking, transport and preparation].

In this review we describe surgical methods for open muscle biopsy. In order to obtain optimal tissue quality, correct handling of the muscle specimens at all stages of the procedure is essential. A technologist who is familiar with the procedure should be present in the operating room. This is important to ensure that specimens for histochemical or biochemical studies are frozen immediately and specimens for electron microscopy are fixed without delay. We describe procedures for processing the specimens for cryostat sections, paraffin sections and electron microscopy, and a simple method for handling muscle specimens in local hospitals before transfer to a hospital with a neuropathological service.

Biopsy↗
PubMed1994

[Cystic lymphangioma of the mesentery].

Cystic lymphangioma of the mesentery is a rare congenital lesion with a relatively low growth potential. It is typically found in young adults, and thereby excluded from other, more aggressive lymphatic malformations seen in newborns. Symptoms of onset may be dramatic and sudden, but are often preceded by an interval of diffuse abdominal discomfort, possibly associated with loss of weight and a palpable abdominal mass. The multicystic architecture of the lesion is clearly visible on an abdominal CAT-scan and indicates the diagnosis. Percutaneous drainage of the cysts has neither diagnostic nor therapeutic effects. Radical excision of the expansion may include resection of the related intestinal segment. Lymphangioma of the mesentery is not malignant. We suggest an ultrasound follow-up six months after the intervention to establish whether the surgery has been successful.

Adult↗
PubMed1993

Mitochondrial disease and reduced sperm motility.

Mitochondrial dysfunction reduces aerobic energy production and results in symptoms from various tissues, depending on metabolic demands. Mitochondrial adenosine triphosphate (ATP) is essential for sperm motility. Sperm motility was investigated in a patient with a mitochondrial disease caused by reduced activity of the mitochondrial enzyme complexes I and IV, and in two control subjects. Spermatozoa were cultured in media containing various energy substrates. Motility was judged by light microscopy, and ultrastructure by transmission electron microscopy. In the patient with mitochondrial disease, 12% of the spermatozoa were motile in the medium containing only glucose. There was a three-fold increase in motile spermatozoa when pyruvate and succinate were present together with glucose. In contrast, the spermatozoa of both control subjects had best motility in the presence of substrates for complex I, and no further increase was observed when succinate was added. Glucose and pyruvate enter the respiratory chain at complex I, and succinate at complex II. Electron microscopy of spermatozoa from the patient with mitochondrial disease revealed mitochondria with increased matrix, thickening of membranes, parallelization of cristae and lipid inclusions, which are characteristic findings in mitochondrial disorders. Abnormal mitochondria were also found in a spermatid, suggesting that the ultrastructural changes of mitochondria are primary rather than secondary to degeneration of the spermatozoa. The results indicate that mitochondrial dysfunction causes reduced sperm motility in some men.

Adenosine Triphosphate↗
PubMed1993

Experimental lovastatin myopathy.

Lovastatin (LS) is a potent HMG-CoA inhibitor used in the treatment of hypercholesterolemia. In humans it can cause a severe, necrotizing myopathy with myoglobinuria and renal failure. To investigate the pathogenesis of LS-induced myopathy we studied the effects of LS on rat skeletal muscle. Lewis rats were gavage-fed 1 mg/g body weight/day of LS. Control rats received carboxymethylcellulose-based suspension by gavage. Gastrocnemius and soleus, fast and slow twitch muscles respectively, were studied by light and electron microscopy. By day 10 LS-treated rats became severely weak. Gastrocnemius was severely affected with degeneration of membranous organelles and microvacuole formation, but soleus was spared. Eventually, 20-50% of the gastrocnemius but none of the soleus fibers became necrotic. Non-necrotic fibers showed no increases of acid phosphatase, indicating that autophagy was not excited. We conclude that LS causes muscle injury by inducing degeneration of membranous organelles, and fast twitch muscle fibers are selectively vulnerable to LS myopathy.

Acid Phosphatase↗
PubMed1992

[Perinatal listeriosis].

Human listeriosis is a rare disease. It may be foodborne. Listeric infection during pregnancy may give a fatal fetal outcome, caused by transplacental passage of organisms from the maternal gastrointestinal tract. We describe a case of perinatal listeriosis which resulted in preterm stillbirth. Perinatal listeriosis should be considered when flue-like symptoms are presented during pregnancy. Early diagnosis and treatment may improve the outcome.

Adult↗
PubMed1991

[Mitochondrial diseases. Diagnostic light and electron microscopic changes in muscle biopsies from patients with mitochondrial myopathy].

Mitochondrial myopathy can be caused by several metabolic defects in the mitochondria. Cells with high levels of oxidative metabolism, such as skeletal muscle, myocardium and brain cells, are particularly vulnerable to these defects. We describe the structural changes in muscle biopsies from 49 patients with mitochondrial myopathy. The younger patients were often symptom-free, but the possibility of a genetic defect was suggested by the family history. "Ragged-red fibres" were found in 10% of the biopsies. Typical paracrystalline inclusions were seen in the mitochondria of the oldest patients. Electron-lucent matrix and increased thickness of the inner membranes of the mitochondria in particular were found in the younger patients. Disorganization of cristae, with cristolysis and unfolding of the cristae was also found. We suggest that structural mitochondrial changes in mitochondrial myopathy constitute a stepwise process and that the mitochondrial alterations of the cristae may represent an early stage in the morphogenesis of mitochondrial disease.

Age Factors↗
PubMed1991

Mitochondrial myopathy in Marinesco-Sjögren syndrome.

Myopathy represents one of the major features of Marinesco-Sjögren syndrome (MSS). Seven patients with MSS from three different families were studied with morphological and neurophysiological methods. In two patients ragged-red fibres were found after Gomori trichrome staining. Transmission electron microscopy (EM) showed that subsarcolemmal accumulation of abnormal mitochondria regularly occurred and in one patient paracrystalline inclusion bodies were found. The EMG showed myopathic changes while the nerve condition velocities were normal. A delayed normalization of exercised-induced hyperlactatemia was noted. These findings show that mitochondrial myopathic changes are present in MSS.

Adolescent↗