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Biomedical subjects

G J Johnson

Publications and source records attributed to G J Johnson.

At least 109 records · Page 6Linked to original sources
PubMed1989

Effect of dietary fish oil on lung lipid profile and hypoxic pulmonary hypertension.

The effects of dietary polyunsaturated fats on chronic hypoxic pulmonary hypertension were assessed in rats fed fish oil, corn oil, or a lower fat, "high-carbohydrate" diet (regular) beginning 1 mo before the start of hypoxia (0.4 atm, n = 30 for each). Mean pulmonary arterial pressures were lower in the chronically hypoxic rats fed fish oil (19.7 +/- 1.8 mm Hg) than in the rats fed corn oil (25.3 +/- 1.6 mm Hg) or regular diets (27.5 +/- 1.5 mm Hg, P less than 0.05). The fish oil diet increased lung eicosapentaenoic acid 50-fold and depleted lung arachidonic acid 60% (P less than 0.0001 for each). Lung thromboxane B2 and 6-ketoprostaglandin F1 alpha levels were lower, and platelet aggregation, in response to collagen, was reduced in rats fed fish oil. Chronically hypoxic rats fed fish oil had lower mortality rates than the other hypoxic rats. They also had lower blood viscosity, as well as less right ventricular hypertrophy and less peripheral extension of vascular smooth muscle to intra-acinar pulmonary arteries (P less than 0.05 for each). The mechanism by which dietary fish oil decreases pulmonary hypertension and vascular remodeling during chronic hypoxia remains uncertain. The finding that a fish oil diet can reduce the hemodynamic and morphological sequelae of chronic hypoxia may have therapeutic significance.

Animals↗
PubMed1988

Chemotherapy followed by consolidation radiation therapy for the treatment of clinical stage II aggressive histologic type non-Hodgkin's lymphoma.

Sixty-three eligible patients with Ann Arbor clinical Stage II or IIE aggressive histologic type non-Hodgkin's lymphomas received combination chemotherapy (cyclophosphamide, doxorubicin, vincristine, and prednisone [COPA]) as the primary treatment technique. Moderate-dose radiation therapy (2500 to 3000 cGy in 2 to 3 weeks) was given to anatomic areas involved initially by lymphoma in patients demonstrated to be in complete remission after chemotherapy. Fifty-seven percent of the patients were free of lymphoma clinically after induction chemotherapy. The minimum patient follow-up from the start of chemotherapy is 3.7 years, and the median follow-up for patients still alive is 4.7 years. The progression-free survival is projected to be 62% at 4 years, and 86% of the patients achieving a complete response are projected to be in continuous remission at 4 years from the completion of all therapy. There were no treatment-related fatalities. This treatment sequence has produced durable tumor control in the majority of patients with acceptable toxicity. The need for consolidation radiation therapy is being studied currently in a controlled clinical trial.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1988

Sonographic and urographic correlation in Bardet-Biedl syndrome (formerly Laurence-Moon-Biedl syndrome).

To determine the spectrum of urologic disease and the value of ultrasound as a screening mechanism, renal imaging was performed on 23 patients with Bardet-Biedl syndrome. On intravenous urography (IVU), abnormal calices were present in 22 patients, with communicating cortical cysts/diverticula in 17. Ultrasound detected caliceal or cystic changes in 70%. On IVU, 21 patients had fetal-type lobular outlines that were detected on sonography in 95%. Renal structural abnormalities are characteristic of the Bardet-Biedl syndrome, and are still best imaged by urography.

Adolescent↗
PubMed1988

Dihydropyridine agonist Bay K 8644 inhibits platelet activation by competitive antagonism of thromboxane A2-prostaglandin H2 receptor.

The dihydropyridine calcium channel antagonists, such as nifedipine, inhibit platelet aggregation in vitro and ex vivo, but the mechanism by which this occurs is uncertain. Bay K 8644 (BAY) is a substituted dihydropyridine that has effects on voltage-dependent calcium channels in cardiac and smooth muscle that are opposite the effects of nifedipine. To evaluate the mechanism responsible for dihydropyridine-induced inhibition of platelet function, we studied the in vitro effects of BAY on human platelet aggregation and secretion plus several related biochemical parameters, including cytoplasmic ionized calcium ([Ca2+]i). BAY exerted concentration-dependent effects on platelet aggregation and secretion of [14C]serotonin. BAY (1-10 microns) inhibited the second wave of platelet aggregation and secretion stimulated by adenosine diphosphate or epinephrine and blocked shape change, aggregation, and secretion induced by the thromboxane A2 (TXA2) mimic, U46619. BAY also inhibited U46619-induced phosphorylation of the approximately 40,000-dalton cytoplasmic protein substrate of protein kinase C (40K protein), formation of TXA2, and rise in [Ca2+]i, all biochemical consequences of platelet activation. The (+)-(R) enantiomer of BAY [BAY(+)] was predominantly responsible for the inhibitory effects of racemic BAY. Nifedipine had the same inhibitory effects on platelet function and biochemistry, except it was approximately 10 times less potent than BAY. Since these results suggested inhibition of the TXA2-prostaglandin H2 (PGH2) receptor, we measured binding of [3H]U46619 to intact platelets. BAY, BAY(+), and nifedipine all functioned as competitive antagonists of [3H]U46619 binding (BAY Ki = 1.47 microM). They did not inhibit binding of [3H]yohimbine to platelet alpha 2-adrenergic receptors. At 1-10 nM BAY, BAY(+) and the (-)-(S) enantiomer of BAY [BAY(-)] all resulted in slight stimulation of platelet function and biochemical events. No significant increase in [3H]U46619 binding was demonstrable, however. Therefore, dihydropyridines that function as either calcium channel agonists or antagonists in cardiac or smooth muscle exert concentration-dependent effects on platelet function. In nanomolar concentrations, they augment, and in micromolar concentrations, they inhibit platelet activation induced by TXA2 or U46619. These data indicate that dihydropyridines do not inhibit TXA2-induced platelet activation by an effect on voltage-dependent calcium channels; they define the mechanism of inhibition as competitive antagonism of the TXA2-PGH2 receptor. The mechanism responsible for augmentation of platelet activation is uncertain.(ABSTRACT TRUNCATED AT 400 WORDS)

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1988

The epidemiology of trachoma in southern Malawi.

A population-based prevalence survey of ocular disease was conducted in the Lower Shire River Valley of Malawi in 1983. A total of 5,436 children less than 6 years of age and 1,664 persons greater than or equal to 6 years were examined. The prevalence of inflammatory trachoma peaked in the 1-2-year-old age group at 48.7% and declined rapidly with age to less than 5% by age 15. The prevalence of cicatricial trachoma was low in young children and climbed gradually with age to greater than 40% among those greater than or equal to 50 years. Risk factors for inflammatory disease in young children included low socioeconomic status of the family, long walking distance to the household's primary source of water, absence of a latrine in the family compound, and presence of trachoma among siblings. Indices of crowding practices were not associated with inflammatory disease. An apparent inverse association of facewashing and inflammatory trachoma in children did not hold up when adjusted for other risk factors.

Adolescent↗
PubMed1988

Band-3 polymers and aggregates, and hemoglobin precipitates in red cell aging.

As part of our systematic ongoing studies of mechanisms of cellular and molecular aging, we developed a "biochemical profile" of senescent human red cells. This "red cell aging" panel allows us to assess functional red cell age independent of chronologic age. The panel used to obtain this profile includes IgG binding, phagocytosis, enzyme activity, anion transport, ankyrin binding, and immunoblotting with antibodies to band 3. We used this panel to compare the biochemical profile of glucose 6-phosphate dehydrogenase-deficient and hemoglobin Köln cells containing high molecular weight protein polymers or hemoglobin precipitates with that of normal senescent cells. We found no evidence in support of the concept that aggregation of band 3 plays a role in the mechanism for generating senescent cell antigen. Observations such as these support the hypothesis that degradation of band 3, rather than aggregation is a critical event in IgG binding and normal erythrocyte aging.

Anion Exchange Protein 1, Erythrocyte↗
PubMed1987

Trachoma grading: observer trials conducted in southern Malawi.

A variety of grading schemes have been proposed for the clinical classification of inflammatory trachoma. During a population based study of ocular disease conducted in southern Malawi we tested a simplified version of the current WHO grading scheme. Intraobserver agreement statistics were less than satisfactory for three of four graders. Interobserver agreement when compared against either a well experienced standard ophthalmologist or a consensus grade improved over time for two of the three graders. However, initial agreement for all three graders was only fair to moderate. Previous studies of trachoma grading schemes support these unsatisfactory results. A new system of classification is needed that is both accurate and reliable in a field setting.

Adult↗
PubMed1987

Prospectively randomized clinical trial of three intensive chemotherapy regimens for the treatment of advanced unfavorable histology non-Hodgkin's lymphoma.

Three hundred thirty-two eligible patients with advanced (Ann Arbor stage III or IV) non-Hodgkin's lymphoma of aggressive histologic subtype (Rappaport classification diffuse histiocytic [DH], diffuse poorly differentiated lymphocytic [DPDL], diffuse mixed [DM], or diffuse undifferentiated [DU]) were randomly assigned to receive induction chemotherapy with one of three intensive regimens in a clinical trial conducted by the Eastern Cooperative Oncology Group (ECOG) between 1978 and 1983. Chemotherapy regimens consisted of cyclophosphamide, vincristine, prednisone, and doxorubicin (Adriamycin; Adria Laboratories, Columbus, OH) (COPA) administered in 3-week cycles; cyclophosphamide plus doxorubicin plus prednisone beginning day 1, with vincristine plus bleomycin day 15 of each 3-week cycle (COPA + Bleo); or cyclophosphamide plus doxorubicin plus procarbazine beginning day 1, and bleomycin plus vincristine plus prednisone beginning day 15 of each 4-week cycle (CAP-BOP). The median patient follow-up from study entry for patients still alive is 5 years. The three regimens were not significantly different with respect to complete response (CR) rates (43% to 46%), time to progression of malignant disease (median, 1.0 to 1.7 years), or survival (5-year survival, 34% to 45%), although duration of complete remission appeared to be shorter in patients receiving COPA (P = .03). COPA + Bleo and CAP-BOP were significantly more toxic than the COPA regimen. This study did not demonstrate any substantial therapeutic advantage associated with the addition of a fifth or sixth chemotherapy drug, or with treatment administered on a more frequent administration schedule, compared with the COPA regimen in this population of patients with advanced diffuse non-Hodgkin's lymphoma. The relatively small proportion of long-term disease-free survivors treated with COPA underscores the need for prospective clinical trials of new and more effective treatments for patients with these potentially curable tumors.

Adult↗
PubMed1986

Von Hippel-Lindau disease in a Newfoundland kindred.

Von Hippel-Lindau disease, an autosomal dominant condition with complete penetrance, has been recognized in a large family that originated in Newfoundland but has some members who live in New Brunswick and Ontario. A collaborative investigation was begun in 1982 to document the number of affected members and the extent of their disease and to improve management of the disease. The condition has been documented in 38 members of the family, 28 living and 10 dead. The most common manifestations are retinal angioma (present in 60% of the gene carriers) and pheochromocytoma (present in 53%). Of the 28 living affected members 14 had been identified before the study began. Only 3 of the 14 patients in whom the disease was subsequently diagnosed presented with symptoms; in the remaining 11 the condition was detected by routine screening. Overall the mean age at the time of diagnosis was 23 years; in the 21 affected members of the fourth generation it was 18 years. The authors outline a regimen of regular screening for members at risk that has evolved as a result of their experience with this family.

Adolescent↗
PubMed1986

Prevalence and severity of xerophthalmia in southern Malawi.

The first population-based study of xerophthalmia in Africa was conducted in the Lower Shire River Valley of Malawi in the autumn of 1983. A total of 5,436 children under six years of age were examined by three survey teams over an eight-week period. The prevalence of active xerophthalmia was 3.9%. Rates for night blindness and active corneal disease were more than five times the World Health Organization criterion for a problem of public health importance. Xerophthalmic corneal scarring occurred at a rate of 5.9/1,000, more than 10 times the World Health Organization criterion. All cases of bilateral blindness in this age group were considered to be due to vitamin A deficiency. Given recent evidence from Asia linking even subclinical vitamin A deficiency to increased risk of mortality and morbidity, this disease is not only a leading cause of blindness in this area, but may have an important impact on child survival as well.

Child, Preschool↗
PubMed1986

The burden of genetically determined eye disease.

We determined the underlying aetiology of blindness for the registered blind population of the Province of Newfoundland and Labrador. In both 1981 and 1984 single-gene disorders accounted for 30% of total blindness and congenital defects for another 10-11%. Genetically determined conditions, diabetes, and senile macular degeneration (SMD) were the three leading causes of registration in each year, 1980-4. We calculated mean ages of registration and mean ages of death over the last four years for five major aetiological groups. Patients with genetic conditions were registered at a much younger age and had a correspondingly longer duration of blindness (21 years as compared with 5 years for either diabetes or SMD). Total 'person-years of blindness' was then calculated from the product of this duration of blindness and the total numbers registered in each group. This index shows that the overall individual and population impact of monogenic blindness is overwhelmingly greater than that of other causes (6849 person-years compared with 270 for diabetes and 430 for SMD). In view of this frequency and duration of monogenic blindness, and also of the substantial hereditary liability to relatively common causes of blindness such as glaucoma, diabetic retinopathy, and high myopia, we suggest that more attention needs to be paid to elucidating the genetic contribution to blindness.

Adult↗