Biomedical subjects
Publications and source records attributed to C West.
This spectrophotometric method for estimating carboxyhemoglobin is based on the production of a two-pigment mixture by reducing oxyhemoglobin and methemoglobin with sodium hydrosulfite . Absorbances of the pigment are measured at 420 and 432 nm. Protecting the solutions against exposure to air is unnecessary. Values are stable and reproducible when the solutions are buffered at pH 6.85.
Ophthalmologists do not consider pars planitis to occur on a familial basis. The development of pars planitis in nine members of four different families is reported. Affected family members include twin sisters, a mother and daughter, two brothers, and a sister and two brothers from the same family. This suggests that a common hereditary and/or environmental factor contributed to the disease in these patients.
The effects of 1 and 4 micrograms/kg/h somatostatin on pentagastrin-stimulated gastric mucosal blood flow and acid secretion were investigated in 12 normal subjects and in 12 patients with cirrhosis of the liver. Each dose of somatostatin was given intravenously to six normal subjects and to six patients. Gastric mucosal blood flow was measured by the neutral red clearance of the stomach. Pentagastrin at a dose of 0.67 micrograms/kg/h stimulated acid secretion less in patients with cirrhosis of the liver than in normal subjects. In normal subjects 1 micrograms/kg/h somatostatin induced a parallel decline of gastric mucosal blood flow and gastric secretion; with 4 micrograms/kg/h somatostatin mucosal blood flow was inhibited more than gastric secretion. In patients with cirrhosis of the liver gastric mucosal blood flow remained unaffected by both doses of somatostatin, while acid secretion was slightly decreased. It is concluded that somatostatin can affect gastric mucosal blood flow independently of acid secretion. Somatostatin may be ineffective in the treatment of gastric haemorrhage in patients with cirrhosis of the liver.
A child with hemolytic anemia was found to have severe erythrocyte adenylate kinase (AK) deficiency, but an equally enzyme-deficient sibling had no evidence of hemolysis. No residual enzyme activity was found in erythrocytes by spectrophotometric methods that could easily have detected 0.1% of normal activity. However, concentrated hemolysates were shown to have the capacity to generate small amounts of ATP and AMP from ADP after prolonged incubation. Hemolysates could also catalyze the transfer of labeled gamma-phosphate from ATP to ADP. Intact erythrocytes were able to transfer phosphate from the gamma-position of ATP to the beta-position, albeit at a rate substantially slower than normal. They could also incorporate 14C-labeled adenine into ADP and ATP. Thus, a small amount of residual AK-like activity representing about 1/2,000 of the activity normally present could be documented in the deficient erythrocytes. The residual activity was not inhibited by N-ethylmaleimide, which completely abolishes the activity of the normal AK1 isozyme of erythrocytes. The minute amount of residual activity in erythrocytes could represent a small amount of the AK2 isozyme, which has not been thought to be present in erythrocytes, or the activity of erythrocyte guanylate kinase with AMP substituting as substrate for GMP. Peripheral blood leukocytes, cultured skin fibroblasts, and transformed lymphoblasts from the deficient subject manifested about 17, 24, and 74%, respectively, of the activity of the concurrent controls. This residual activity is consistent with the existence of genetically independent AK isozyme, AK2, which is known to exist in these tissues. The cause of hemolysis in the proband was not identified. Possibilities include an unrelated enzyme deficiency or other erythrocyte enzyme defect and intraction of another unidentified defect with AK deficiency.
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CPD-A2 is a modified CPD blood preservative with adenine, containing 1 1/2 times as much glucose as CPD. Units (450 ml) of blood from 21 normal donors were collected in CPD-A2 in plastic bags and held at room temperature for 8 hr. An 80% red cell concentrate was prepared and this was stored for 42 or 49 days at 4 degrees C, with the containers in either a standing or lying position. Measurements of glucose consumption, red cell ATP, and 2,3-DPG and of plasma hemoglobin, pH, Na+, and K+ were performed on all samples. The size of the "fragile tail" of osmotically fragile red cells was estimated in 12 samples. The poststorage 24 hr viability of their own stored 51Cr-tagged red cells was documented in 19 of the volunteers. At least 4 months after the original donation, a second unit of blood was collected from eight of the donors to make possible intradonor comparison of the biochemical effects of storage position. After 42 days but not after 49 days of storage, red cells in concentrates stored in the lying position had consumed more glucose and had a higher poststorage pH than did cells stored in the standing position. The poststorage 24 hr viability of red cells stored for 42 days averaged 83.6%, with all units exceeding 70% viability. At 49 days the average viability was 69.1%. Although the average viability of cells stored in the lying position for 42 days was higher than that of concentrates stored standing, the difference was not statistically significant at the 5% level. The plasma hemoglobin level showed a weak correlation with viability of stored cells. Red cell ATP levels were correlated with viability only at 42 days' and not at 49 days' storage. Concentrates of red cell collected in CPD-A2 manifested fully satisfactory viability for 42 days. At 49 days storage the results of viability studies were borderline. High plasma hemoglobin values are observed at both 42 and 49 days' storage and may limit the usefulness of red cell concentrates stored for prolonged periods of time.
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Although it is recognized that red cells lose membrane during storage, estimation of the osmotic fragility of erythrocytes has not previously proven to be a useful measurement of the storage lesion. Erythrocytes from blood stored in CPD-A2 were found to have a markedly increased osmotic fragility. A major portion of this increase was found to be due to accumulation of lactate, which is only slowly transported from within erythrocytes and which therefore exerts a strong osmotic effect in the usual osmotic fragility test. After an hour's incubation in a large volume of iso-osmotic buffer, the osmotic fragility curve of stored erythrocytes was much more nearly normal. Such cells were found to have a volume 5%--8% greater than that of normal cells, indicating that even after removal of lactate more osmotically active material was present in the stored erythrocytes than in fresh cells. Most of this differences can be accounted for by substitution of chloride ion for 2,3-DPG, since chloride exerts approximately 3.7 times the osmotic effect of 2,3-DPG per unit charge. In addition to the shift in osmotic fragility produced by the increased intracellular osmotically active material, a "fragile tail" of red cells was also present. Stored erythrocytes were labeled with 51Cr and reinfused into the volunteer donors. The osmotic fragility of the reinfused cells was estimated using a technique of sequential osmotic hemolysis that permitted accurate estimation of osmotic fragility of transfused cells using very small amounts of 51Cr. The osmotic fragility of the reinfused cells became less than those of fresh cells after 24 hr and was exactly the same as those of fresh cells after 4 days. The fragile tail disappeared at a rate that approximated the rate of loss of nonviable erythrocytes from the circulation as measured by 51Cr. These findings are consistent with the preferential destruction of a subpopulation of red cells with a diminished surface area.
We have compared the actions of ADM and mAMSA in Chinese hamster V79 cells in vitro, using cell survival and sister-chromatid exchange as end-points. Equimolar concentrations of ADM and mAMSA show similar toxicities to exponentially growing cells, and both drugs are less effective in killing chronically hypoxic and plateau-phase cells. Cytotoxicity to thermotolerant cells (41 degrees C for 16 h previously) shows little difference from that for exponential cells. Pre-treating cells with misonidazole under hypoxic conditions reduces the toxicity of both ADM and mAMSA. In addition, an ADM-resistant Chinese hamster cell line, 77A-177, was cross-resistant to mAMSA. Finally, low equimolar sub-toxic doses of both drugs were found to cause similar increases in the levels of sister-chromatid exchanges in V79 cells. These results reveal no major difference in activity between ADM and mAMSA in vitro.
Cultured skin fibroblasts from three unrelated patients with idiopathic hemochromatosis and two normal controls were cultured in media containing iron concentrations ranging from 383 to 963 ng/ml. The amount of ferritin accumulating in fibroblasts was related to the iron concentrations, but there was no significant difference in the fibroblasts of patients with hemochromatosis and the normal controls.
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The serum lipid profile (total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides) has been studied in 98 men and 158 women before and 6 months after introducing an employee fitness programme. Over this period, the sample sorted itself into 4 sub-groups (non-participants, drop-outs, high adherents, and low adherents). The high-adherents attended 2--3 30-min physical activity classes per week over the 6-month study, progressing to 15--17 min of aerobic activity per session, with significant gains of predicted maximum oxygen intake, and reductions of body fat. Nevertheless, there were few "favourable" changes of lipids that could be related to the physical activity sessions. A decrease of total cholesterol (mainly in the women) was unrelated to the changes of maximum oxygen intake, and occurred equally in non-participants and high adherents. High adherent women showed a decrease of LDL cholesterol, but this also was almost matched by changes in non-participants, while the main response of HDL cholesterol was a decrease in non-participants and drop-outs rather than an increase in high-adherents. It is concluded that if data are collected while subjects are in energy balance and persisting with their activity, a programme of the intensity practical in an employee fitness class has little impact upon blood lipids.
Life-style variables (perceived fitness, excess body mass, percent fat, lean mass, predicted maximum oxygen intake, cigarette consumption, alcohol consumption, use of contraceptive medication) have been related to the lipid profile (serum triglycerides, total cholesterol, HDL and LDL cholesterol) in a sizeable volunteer population of Toronto office-workers. Multivariate analysis demonstrates an independent positive association of age with total cholesterol, HDL and LDL cholesterol, and (in women only) a weak negative association with triglycerides. Much of the fitness effect is related to body fat, which is positively correlated with triglycerides and (in the men only) with total and LDL cholesterol, but is negatively related to HDL cholesterol. However, maximum oxygen intake per unit of body mass shows a small independent association with triglycerides, total cholesterol (women only) and LDL cholesterol. Cigarette smoking bears an independent relationship to triglycerides, HDL cholesterol and (in women only) LDL cholesterol. Alcohol consumption is independently related to high values for total and LDL cholesterol, but is also related to high HDL cholesterol readings. While multivariate analysis allows for the inter-relationship of smoking habits, alcohol consumption, and the various fitness measurements, it cannot prove cause and effect. Nevertheless, the potential improvement of lipid profile associated with (i) abstinence from cigarettes, (ii) a 4% reduction of body fat, and (iii) avoidance of contraceptive medication is sufficient to warrant experimental trial of such a change in life-style.
A dominantly inherited abnormality of the red blood cells is described. It is characterized by the presence of a small population of markedly distorted red blood cells resembling keratocytes. In addition, many of the red cells show minor deformities resembling the beginning stages of formation of echinocytes. Red cell lifespan is normal, and the severely deformed cells appear to represent the senescent population. Inappropriate increases in activities of some, but not all, age-dependent red cell enzymes were observed. The anomaly appeared to be entirely benign; no abnormal clinical findings were associated with this defect. It has been designated the Woronets trait.