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Biomedical subjects

J Olson

Publications and source records attributed to J Olson.

At least 127 records · Page 7Linked to original sources
PubMed1986

Two-dimensional echocardiographic identification of left ventricular pseudoaneurysm.

Nine patients with proved left ventricular pseudoaneurysm after transmural myocardial infarction were studied by two-dimensional echocardiography. In all patients two-dimensional echocardiography successfully displayed the pseudoaneurysm. The unique two-dimensional echocardiographic characteristics of pseudoaneurysm include: a sharp discontinuity of the endocardial image at the site of the pseudoaneurysm communication with the left ventricular cavity, and the presence of a relatively narrow orifice in comparison with the maximum diameter of the pseudoaneurysm fundus; visualization of the maximum diameter of the pseudoaneurysm fundus frequently required a slightly different tomographic view than that required for demonstration of the orifice. The distinctive echocardiographic features of pseudoaneurysm in these patients and technical implications for optimal visualization are described. Most of the pseudoaneurysms we encountered and many of those previously described were located posteriorly. We found the use of inferior angulated view modified from the standard apical four-chamber view extremely helpful in detecting the orifice in patients with posterior or posterolateral pseudoaneurysms. We conclude that two-dimensional echocardiography is an important technique for diagnosis of left ventricular pseudoaneurysm.

Aged↗
PubMed1986

Ultrasound differentiation of the competent from the incompetent cervix: prevention of preterm delivery.

To evaluate the feasibility of the use of serial ultrasound measurements of cervical length, membrane protrusion, and dilatation to discriminate between the competent and the incompetent cervix, 107 at-risk patients and 30 control subjects were examined prospectively. Patients were divided into five groups based on treatment and method of diagnosis. Epidemiologic, ultrasound, and outcome data were analyzed. Means and standard deviations for ultrasound measurements were established. Highly significant differences between all prediagnostic and postdiagnostic-pretreatment measurements were found (p less than 0.001). Highly significant differences were also found between all postdiagnostic-pretreatment and postdiagnostic-posttreatment measurements (p less than 0.001). No significant differences between prediagnostic and postdiagnostic-posttreatment measurements were noted. The incidence of preterm delivery was significantly higher among untreated diagnosed patients (p less than 0.01). By combined clinical and ultrasound criteria 51 patients (47.7%) were identified as not having cervical incompetency. Fifty-six patients (52.3%) were diagnosed.

Adolescent↗
PubMed1986

Basidiomycete mycelia and spore-allergen extracts: skin test reactivity in adults with symptoms of respiratory allergy.

One hundred fifty adults, with respiratory-allergic disease, and 14 control subjects, without symptoms of respiratory allergy, were skin prick tested with 16 common inhalant allergens, 12 extracts of mycelia from Basidiomycetes grown in vitro, and/or 10 to 15 basidiospore extracts. Eighty-three subjects (58%) had positive skin tests to two or more of the common inhalant allergens. Twenty-seven percent of the study subjects had positive skin reactions to one or more of the Basidiomycete mycelia extracts, and 32% demonstrated positive skin reactions to one or more basidiospore extracts. None of the 14 control subjects had positive skin reactivity to basidiospore extracts. Skin prick reactivity of study subjects to 15 different basidiospore extracts ranged from 5% for Cantharellus cibarius to 17% for Scleroderma sp. The prevalence of skin test reactivity to basidiospores did not differ significantly from the reactivity to commercial mold extracts of several common species of the Fungi Imperfecti (6% for Cladosporium herbarum or Penicillium notatum to 13% for Alternaria tenuis). These results demonstrate that a significant number of individuals reporting symptoms of respiratory allergy have skin test reactivity to basidiospores and suggest that these spores are important fungal aeroallergens in the New Orleans environment.

Adult↗
PubMed1986

Pathways for the reduction of oxidized glutathione in the Plasmodium falciparum-infected erythrocyte: can parasite enzymes replace host red cell glucose-6-phosphate dehydrogenase?

Plasmodium falciparum-infected human red cells possess at least two pathways for the generation of reduced nicotinamide adenine dinucleotide phosphate (NADPH): (1) the glucose-6-phosphate dehydrogenase (G6PD) pathway and (2) the glutamate dehydrogenase (GD) pathway using glutamate as a substrate. Uninfected erythrocytes lack the GD pathway. The NADPH generated can be used to reduce oxidized glutathione (GSSG), which accumulates in the presence of an oxidative stress. In red cell G6PD deficiency, this pathway is reduced or absent, and the host cells as well as the parasites within them are vulnerable to oxidant stress. In view of the presence of the GD pathway in parasitized red cells and the recent description of a parasite-derived G6PD enzyme, we have asked whether the pathways for the reduction of GSSG provided by the parasite can substitute for the host G6PD in red cells deficient in G6PD activity. We have devised a functional assay in which the reduction rate of GSSG is monitored in the presence of buffered infected or control red cell lysates and substrates. Infected G6PD-deficient erythrocytes were obtained from in vitro cultures after a single prior growth cycle of the parasites in G6PD deficient cells to eliminate contaminating normal red cells. The results show that only parasitized red cells can reduce GSSG via the GD pathway. In parasitized G6PD Mediterranean red cells (completely G6PD-deficient), there is a detectable GSSG reduction via the G6PD pathway, not found in uninfected lysates from the same individual. In G6PD A- (African type, featuring partial deficiency), a small increment in the G6PD-dependent reduction of GSSG can also be detected. However, when compared to G6PD normal red cells, the activities from the parasite-derived pathways are small and could not be considered substitutes for normal host enzyme activity. It is concluded that while the plasmodium provides additional pathways for the generation of NADPH that may serve its own metabolic needs, the host red cells and hence the parasite itself remain vulnerable to oxidant stress.

Erythrocytes↗
PubMed1986

Serum vitamin E levels in the very low birth weight infant during oral supplementation.

A prospective study was initiated to monitor serum tocopherol levels in all infants admitted to Indiana University Medical Center with birth weights less than 1,500 g. These infants routinely receive 100 mg/kg/d of oral vitamin E (Aquasol E tocopherol acetate) every six hours. Levels are determined weekly or semiweekly using a modification of the fluorometric method of Hanson and Warwick. Vitamin E dosage is adjusted regularly to achieve levels greater than or equal to 3.5 mg/dL. During the 6 months of this study, a total of 76 patients had 567 serum measurements. Of these, 220 levels (38%) were greater than or equal to 3.5 mg/dL, 71 (13%) were greater than or equal to 5.5 mg/dL, and 15 (2.7%) were greater than 8 mg/dL. Serum tocopherol levels often (1) remained greater than or equal to 3.5 mg/dL for several days after oral supplementation was discontinued or (2) again became greater than or equal to 3.5 mg/dL on a reduced dosage of 25 to 50 mg/kg/d. These data indicate that infants weighing less than 1,500 g at birth who are receiving oral vitamin E supplementation at 100 mg/kg/d will have varied serum levels with a significant percentage exceeding 3.5 mg/dL.

Age Factors↗
PubMed1984

Respiration in primary cultured cerebellar granule neurons and cerebral cortical neurons.

Respiration was measured polarographically in primary cultures enriched with cerebellar granule neurons or cerebral cortical neurons. The basal respiratory rate, measured on the sixth day after culturing, was 12.00 natom equiv. O/mg protein/min for the cortical neurons and 12.70 natom equiv. O/mg protein/min for the granule neurons. Maximal stimulation by 2,4-dinitrophenol produced a 20-40% increase over the basal rate for both neuronal types. Oligomycin inhibited neuronal basal respiration by 45%. These respiratory rates in neurons from primary culture are markedly lower than those measured in astrocytes grown under similar conditions.

Animals↗
PubMed1984

Deficiency of the iron-sulfur clusters of mitochondrial reduced nicotinamide-adenine dinucleotide-ubiquinone oxidoreductase (complex I) in an infant with congenital lactic acidosis.

We report the case of an infant with hypoglycemia, progressive lactic acidosis, an increased serum lactate/pyruvate ratio, and elevated plasma alanine, who had a moderate to profound decrease in the ability of mitochondria from four organs to oxidize pyruvate, malate plus glutamate, citrate, and other NAD+-linked respiratory substrates. The capacity to oxidize the flavin adenine dinucleotide-linked substrate, succinate, was normal. The most pronounced deficiency was in skeletal muscle, the least in kidney mitochondria. Enzymatic assays on isolated mitochondria ruled out defects in complexes II, III, and IV of the respiratory chain. Further studies showed that the defect was localized in the inner membrane mitochondrial NADH-ubiquinone oxidoreductase (complex I). When ferricyanide was used as an artificial electron acceptor, complex I activity was normal, indicating that electrons from NADH could reduce the flavin mononucleotide cofactor. However, electron paramagnetic resonance spectroscopy performed on liver submitochondrial particles showed an almost total loss of the iron-sulfur clusters characteristic of complex I, whereas normal signals were noted for other mitochondrial iron-sulfur clusters. This infant is presented as the first reported case of congenital lactic acidosis caused by a deficiency of the iron-sulfur clusters of complex I of the mitochondrial electron transport chain.

Acidosis↗
PubMed1984

Maturation of resistance to lead encephalopathy: cellular and subcellular mechanisms.

The rat pup fed inorganic lead has been studied extensively as an animal model of human lead encephalopathy. As in man, the sensitivity of the brain to lead toxicity is age-dependent. Pups given daily lead feedings for one week beginning in the first week of life show pathologic changes (i.e., hemorrhage, edema, and neuronal necrosis) throughout the brain including the cerebral cortex and cerebellum. Pups begun on daily lead feedings for two weeks between 10-18 days of age show similar pathologic changes almost entirely confined to the cerebellum. Pups receiving very large quantities of lead for two weeks beginning at 20 or 24 days of age develop only minimal edema or no changes by light microscopy. We have proposed that the effects of lead on cellular aerobic energy metabolism are important in the pathogenesis of the encephalopathy in the developing brain. Early in the course of lead feedings begun at 14 days of age, isolated cerebellar mitochondria show a loss of respiratory control. During the second week of lead feedings, respiration with NAD-linked substrates is inhibited in cerebellar mitochondria, but not in cerebral mitochondria, from these animals. Cerebral mitochondrial respiration in pups fed lead from birth also is inhibited while both cerebral and cerebellar mitochondrial respiration in lead-fed adults is not affected. Isolated brain mitochondria exposed to lead in vitro show similar changes; an initial respiratory stimulation (probably reflecting an energy-coupled uptake of lead) and a secondary inhibition of dehydrogenases located in the mitochondrial matrix. Lead also may compete with calcium for brain mitochondrial carrier or binding sites. During maturation, the brain appears to become resistant to lead toxicity by sequestering lead away from the mitochondrial site of action. This hypothesis is based upon the observations that: 1. the in vitro effects of lead are the same in immature and mature cerebellar mitochondria; 2. the cerebral and cerebellar lead concentrations are the same in immature encephalopathic and mature encephalopathy-resistant lead-fed animals and; 3. cerebellar mitochondria from animals fed lead from 14 days of age contain much more lead than cerebral mitochondria from these animals and cerebellar mitochondria from lead-fed adults. This hypothesis is supported further by the results of recent electron microscopic and elemental microprobe studies of lead distribution in the brains of animals fed lead beginning at 14-18 days of age.(ABSTRACT TRUNCATED AT 400 WORDS)

Age Factors↗
PubMed1983

In vitro translation of canine mitochondrial creatine kinase messenger RNA.

The cell-free translation products of mRNA from canine myocardium were immunoprecipitated using antiserum specific for either the MM or mitochondrial creatine kinase subunit. The two subunits were shown to be encoded by the nuclear genome and translated from separate mRNAs. The mitochondrial subunit was translated as a polypeptide with a molecular weight approximately 6,000 greater than the mature form of the enzyme. In contrast, the M-subunit was translated as a polypeptide having a molecular weight identical to that of the mature cytosolic M-subunit. It is assumed that the mitochondrial subunit precursor must be proteolytically processed during translocation from the cytoplasm into mitochondria.

Animals↗
PubMed1983

Factors affecting the ambulatory status of patients with spina bifida cystica.

Sixteen different factors that might affect the ambulatory status of patients with myelodysplasia after the age of five years were analyzed in ninety-eight patients using a linear regression technique (the Pearson correlation coefficient). Included in the study were fifty male and forty-eight female patients; the average age was fourteen years and four months (range, five years and nine months to thirty-one years and ten months). The sacral and fifth-lumbar paraplegics, with one exception, were all community ambulators. Fourth-lumbar paraplegics were usually functional ambulators, whose ability to walk was significantly influenced by musculoskeletal deformity of the spine, pelvis, hips, knees, feet, and ankles. Third-lumbar, first and second-lumbar, and thoracic level paraplegics usually were not functional ambulators. Ambulatory function was significantly influenced in third-lumbar paraplegics by hip deformity, in first and second-lumbar paraplegics by obesity and possibly by age, and in thoracic level paraplegics by age and by knee-foot-ankle deformities. Transitions in ambulatory status were usually to a lower functional level and were related to motivation, obesity, and musculoskeletal deformity. Ultimately, ambulatory status is probably related in large measure to the energy expenditure that is necessary to walk, but studies of energy requirements were not done. These findings emphasize the importance of controlling obesity as well as any musculoskeletal deformities that will influence the patient's ultimate walking ability.

Adolescent↗