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Biomedical subjects

G Hanson

Publications and source records attributed to G Hanson.

At least 55 records · Page 3Linked to original sources
PubMed1990

World Health Organization--basic radiographic system (WHO-BRS) unit: experimental clinical evaluation.

The basic radiographic system (BRS) is a simplified version of a standard radiographic unit designed by the World Health Organization and the Pan American Health Organization. The design of the BRS includes the requirement that it should be able to perform routine radiographic examinations with a minimum of operator training. This report describes the performance of a BRS manufactured by Siemens. The physical parameters of this BRS were very good and operation should require a minimum of training. A small number of BRS films were compared with films obtained using the standard equipment in the department. The BRS films were generally regarded as satisfactory. Radiation exposure to patients is equal to, and in some cases less than, exposures with conventional X-ray units.

Developing Countries↗
PubMed1990

Changing risk factor demographics in end-stage renal disease patients entering hemodialysis and the impact on long-term mortality.

Patient survival on hemodialysis has previously been shown to be associated with the presence of comorbid conditions on entrance. Significant comorbid conditions are atherosclerotic heart disease (ASHD), cerebral vascular disease (CVD), nonskin malignancies, chronic obstructive pulmonary disease, diabetes mellitus, and age on entrance to dialysis. Changes in annual mortality have been noted in the United States and at the Regional Kidney Disease Program. The increase in annual mortality was analyzed to determine the impact of risk factors during the time intervals 1976 to 1982 and 1983 to 1987. Patients with no major risk factors have longer survival rates and lower deaths per 1,000 treatment-months from 1983 to 1987 compared with 1976 to 1982. Diabetics have survival rates and deaths per 1,000 treatment-months that are comparable up to age 75. However, over age 75, diabetics have lower survival rates and higher death rates. The presence of comorbid conditions in the diabetic group is high and may account for the increased death rate. The percent of diabetics entering the program has increased from 29% to 48% over the intervals. Nondiabetics with comorbid conditions on entrance had higher deaths per 1,000 treatment-months from 1983 to 1987 compared with 1976 to 1982 across all age categories. Risk factor analysis shows that nondiabetics with major risks are entering with increasing numbers and continuation of comorbid conditions that impact death rates. Peripheral vascular disease, originally not significantly associated with death on dialysis, has dramatically increased from 18% to 60% in nondiabetics with comorbid conditions. In the patients over age 60 with comorbid conditions, 75% of patients now entering dialysis have peripheral vascular disease (PVD). In summary, major shifts in the hemodialysis population have occurred. Diabetics entering dialysis now account for almost 50% of all patients, with the older group having more comorbid conditions. This change alone would increase the annual mortality rate. Patients with comorbid conditions now enter with a higher prevalence of multiple comorbid conditions, which would increase the annual mortality rate. Nondiabetics without comorbid conditions now have better survival across all age categories compared with the previous data. PVD, with its current high prevalence, needs to be reevaluated as a significant risk factor for death on hemodialysis. Therefore, the increase in the annual gross mortality rate is highly predicted based on the change in the diabetic population and the increase in single and multiple comorbid conditions in the nondiabetic population.

Adolescent↗
PubMed1990

Body fluid spaces and blood pressure in hemodialysis patients during amelioration of anemia with erythropoietin.

Blood pressure (BP) may increase in hemodialysis patients during treatment of anemia with recombinant human erythropoietin (r-HuEPO). Since fluid volume is a determinant of BP in dialysis patients, changes in body fluid spaces during r-HuEPO therapy could affect BP. Thus, 51Cr-labeled red blood cell (RBC) volume, inulin extracellular fluid (ECF) volume, and urea total body water (TBW), as well as cardiac output, plasma renin activity (PRA), and plasma aldosterone concentration were determined postdialysis before and after r-HuEPO therapy in patients in whom changes in BP could be managed by ultrafiltration alone. Eleven patients entered the study: one had a renal transplant and two required addition of antihypertensive drug therapy and were excluded; eight, of whom two required antihypertensive drug therapy following the study, were included in the analyses. Results revealed an increase in predialysis hemoglobin from 67 to 113 g/L (6.7 to 11.3 g/dL) (P = 0.001) during 18 +/- 6 weeks of therapy. Predialysis diastolic BP increased from 80 to 85 mm Hg (P = 0.07), while postdialysis diastolic BP was unchanged at 73 mm Hg. 51Cr-RBC volume increased, from 0.7 to 1.3 L (P = 0.004). ECF tended to decrease, from 13.7 to 10.8 L (P = 0.064), while TBW decreased to a similar extent, but not significantly, 34.3 to 31.2 L (P = 0.16). Postdialysis ECF volume was positively correlated with mean arterial BP at baseline (r = 0.89, P = 0.007) and after therapy (r = 0.74, P = 0.035). However, the regression lines for this relationship were different (P = 0.022) before and after therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Molecular basis of complement activation in ischemic myocardium: identification of specific molecules of mitochondrial origin that bind human C1q and fix complement.

Mitochondria may be a source of molecules that activate complement during ischemic injury to myocardium, providing therewith a stimulus for infiltration of polymorphonuclear leukocytes. To identify specific molecules that activate the classical complement pathway, detergent lysates of canine cardiac mitochondria were fractionated by polyacrylamide gel electrophoresis and transferred electrophoretically to nitrocellulose paper (NCP). The NCP replicas of the gels were incubated with isolated C1q and fresh sera as a source of complement, washed briefly, and overlaid with sensitized sheep erythrocytes (RBC) in agarose. A cluster of four to six molecules between 45 and 53 kDa as well as four others, 34, 30, 26, and 23 kDa, consumed complement thereby preventing complement-mediated lysis of sensitized sheep RBC in the agarose overlay. Additional molecules reactive with C1 were identified by their ability to bind isolated human C1q and to serve as assembly sites for later acting complement components. Sites of localization of complement were demonstrated by incubating NCP replicas of fractionated mitochondria with antisera specific for C1q, C3, C5, and C9, followed by peroxidase-conjugated anti-immunoglobulin and substrate. A total of 12 C1q binding molecules ranging in size from 67 kDa to 23 kDa, which can fix later acting complement components, were identified. At least two of these reacted with antisera prepared against canine cardiac lymph collected in the first 3-4 hours after a 45-minute coronary artery occlusion. These studies present direct evidence that specific molecules, released from subcellular fractions of myocardial cells rich in mitochondria, can activate the complement cascade.

Animals↗