Principal component analysis, trace elements, and blue crab shell disease.
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Biomedical subjects
Publications and source records attributed to J C Hamilton.
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Recently several papers have described the generalized rank annihilation method; however, in some cases complex eigenvalues and eigenvectors may appear when the generalized eigenproblem is solved. When complex eigenvalues and eigenvectors are encountered, the results cannot be used to estimate pure component profiles (e.g. spectra or chromatograms). In this paper, a similarity transformation is used to transform complex eigenvalues and eigenvectors into real eigenvalues and eigenvectors, thereby permitting spectra and profiles of pure constituents to be estimated. The modified GRAM method is illustrated with simulated and real data.
Plasma 25-hydroxy-vitamin D (25-OHD) concentrations and 25-OHD binding capacities were measured in 14 elderly patients and in 14 young controls. Both 25-OHD concentrations and 25-OHD binding capacities were reduced in the elderly. In neither group, however, was there a significant correlation between 25-OHD binding capacities and 25-OHD concentrations. Thus, although 25-OHD binding capacities are reduced in sick old people this does not account for the low 25-OHD concentrations often found in this group.
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Twelve elderly patients in a rehabilitation ward were given a four-week course of ultra-violet irradiation from a Vitalux lamp. They were compared with 12 controls selected from the same ward. Treatment produced a significant elevation in plasma 25-hydroxy-vitamin D (25OHD) by the end of the second week and concentrations continued to rise over the four-week period. Subject showing the greatest response were those starting with the lowest levels of plasma 25OHD. The findings suggest that ultra-violet irradiation is an effective means of treating vitamin D deficiency in old age and that patients with the greatest degree of deficiency show the greatest response.
Dietary intake, sunlight exposure and 25-hydroxy-vitamin D levels were estimated in 62 patients admitted to a geriatric assessment unit. There was a significant correlation between vitamin D intake and 25-hydroxy-vitamin D levels but none between sunlight exposure and these. This suggests that in old age dietary deficiency may be a more important cause of metabolic bone disease than limited sunlight exposure.
Tetracosactrin (Synacthen) tests were performed on 19 elderly women who had leucocyte ascorbic acid (LAA) levels of less than 15 microgram/108 WBC. 9 were then given a daily dose of 200 mg ascorbic acid orally for 2 weeks while the other 10 were left untreated. Following this, tetracosactrin tests were repeated in both groups. All initial plasm cortisol responses to tetracosactrin were within normal limits. Treatment with ascorbic acid produced no changes in these. This suggests that the low LAA levels often found in old people do not result in adrenal insufficiency.
Serial 25-hydroxy vitamin D (25-OHD) concentrations were measured in long-stay geriatric patients treated with vitamin D. Comparison between a treatment and a control group showed that a daily dose of 500 IU vitamin D produced a significant increase in 25-OHD levels by two months. The supplement had a striking effect when the initial 25-OHD level was low and very little effect when it was high. 25-OHD levels in subjects on 2000 IU vitamin D daily were only marginally higher than those in subjects on 500 IU. A dose of 500 IU vitamin D daily should therefore produce adequate blood 25-OHD concentrations in most old people, and probably prevent most cases of osteomalacia in the elderly--though a large-scale study is needed to confirm this.
1. Serial estimations of plasma (PAA) and leucocyte (LAA) ascorbic acid concentrations were made in geriatric patients in a stable phase of their illness, and compared with a similar ('unstable') group suffering from acute illness. 2. In the 'unstable' group, though PAA levels were unchanged, LAA levels were reduced. 3. The 'follow-up' period of 7-8 d there was much greater variation in both PAA and LAA levels in the 'unstable' group. 4. Acute illness was often accompanied by an increase and then a decrease in LAA levels. Recovery was associated with an increase in LAA levels.
Blood was obtained from 11 healthy voluteers, mixed with two standard types of anticoagulant used in blood transfusion centres and stored for 21-28 days at 4 degrees C. Leucocyte ascorbic acid (LAA) fell to deficient levels after 7 days in all cases. There were no corresponding changes in plasma ascorbic acid (PAA) levels. LAA and PAA were measured before, during and after surgery in 5 control patients who underwent definitive operations for benign peptic ulceration and in 4 patients under-going surgery for bleeding peptic ulceration. The average amount of blood administered to the latter group was 10 units. There was a fall in LAA and PAA in both groups of patients after operation. This fall had returned to normal by 7 days in the controls, but the LAA remained at a deficient level at 7 days in the patients who had bled. Deficient ascorbic acid in stored blood may contribute to low leucocyte ascorbic acid levels in patients after blood transfusion and may contribute to the increased complication rate when surgery is undertaken in these patients.
White-blood counts, polymorph counts, leucocyte ascorbic-acid and plasma ascorbic-acid levels were measured in 91 samples of blood obtained from patients admitted to a geriatric assessment unit. There was a correlation between both white-blood counts and polymorph counts and leucocyte ascorbic-acid levels. There was no correlation between white-blood counts and polymorph counts and plasma ascorbic-acid concentrations. It is suggested that this phenomenon represents migration of ascorbate-rich polymorphs to areas of infection and infarction.