Search

Accidents due to 'fire and flames' are second only to “falls” as the most important cause of accidental death in the homes of elderly individuals throughout the United Kingdom. This study aims to ascertain whether older people are receiving fire accident advice appropriate to their needs. A questionnaire addressing the issues of risk perception, fire preventative action and access to fire safety information was distributed to 1100 randomly selected members of the 'Thousand Elders' (a nation-wide consumer group established by the Centre for Applied Gerontology at The University of Birmingham, comprising people above the age of 50 years). Eight hundred and four questionnaires were returned and were analysed using the Statistical Package for Social Sciences. Fire risk was perceived as far less of an immediate threat than the danger of a personal attack by an intruder in the home. Recognition of fire risk and the effectiveness of fire safety measures did not result directly in safety appliances being fitted. The majority of 'Elders' had received no fire-fighting training, yet more than half felt confident in tackling a small fire. Neither did experience of a fire in the home necessarily increase action towards safety precautions. The majority had not been exposed to a fire safety campaign in the past 12 months. On exposure to a campaign, the impact towards fire safety was positive. The educational process should aim to close the gap between the recognition of the need for fire safety precautions and the implementation of fire safety measures. The key to effective fire prevention amongst older people depends upon: Information, Training and Support, i.e., relevant information supported by practical help and subsequent practical training in-situ by trusted community figures.

P-aminophenol is considered a minor nephrotoxic metabolite of phenacetin and acetaminophen (paracetamol) in man. Our experiments show that p-aminophenol readily undergoes oxidative polymerization during incubation in human blood or plasma, to form melanin, as a component of soluble lipofuscin. Haemolysis accompanies this process in whole blood. Unmetabolized phenacetin and acetaminophen do not form soluble lipofuscins.Long-term excessive use of phenacetin or acetaminophen has been associated with chronic renal disease, haemolytic anaemia, and increased solid lipofuscin deposition in tissues. Excessive use of phenacetin has also been associated with cancer of renal pelvis and bladder. It appears to us that p-aminophenol and other o- and p- aminophenol metabolites of these drugs are intermediates not only in the etiology of chronic renal disease, but in the other developments as well.P-aminophenol and other ex(end)ogenous aminohydroxyphenyl, aminopolyhydroxyphenyl, polyhydroxyphenyl and polyaminophenyl compounds with these groups in ortho and para positions (such as 3-hydroxyanthranilic acid, 6-aminodopamine, dopamine, p-phenylenediamine, etc.) can undergo autoxidations and metal-catalyzed and enzymatic oxidations in man to produce toxic (semi)quinones(imines), (semi)quinonediimines and reactive oxygen species. After depletion of antioxidants these very reactive (semi)quinones(imines) and (semi)quinonediimine intermediates, many of which are precursors of plasma soluble lipofuscins and melanoproteins, react with essential proteins, DNA, other macromolecules and can cause or contribute to renal and other tissue toxicity, haemolytic anaemia, neoplasia, and granular lipofuscin formation. The reactive oxygen species can also deplete antioxidants, damage essential proteins, DNA, and other macromolecules, and thereby injure cells and extracellular matrix.

The soluble melanins of blood plasma form in vivo and in vitro from dopa, catecholamines, catechol, hydroquinone, homogentisic acid, 3-hydroxykynurenine, 3-hydroxyanthranilic acid, p-aminophenol, p-phenylenediamine and other structurally related end(ex)ogenous compounds by oxidative polymerization. The mean quantity of natural melanins in normal plasma is 1.61 < 0.10 (standard deviation) mg/ml, (n = 20) and in uraemic plasma 2.72 < 0.38 mg/ml, (n = 16). The plasma melanins (< 3%), are associated with proteins (< 85%), mucoproteins (< 0.25%), lipids (< 0.4%), as soluble lipofuscins, and probably are associated with proteins without lipids as soluble melanoproteins.Fluorescence, UV-VIS and IR spectroscopies and the melanin isolation method show the presence of soluble melanins in the urine of healthy people. Soluble melanins can also be formed in vitro in the urine by oxidative polymerization of the precursors. In most of the urine samples we studied, melanins were present in larger amounts than the urinary proteins, indicating that the kidneys can selectively excrete the melanin components of the lipofuscins, and that the solubility of melanins does not depend upon combination with proteins. The quantities of purified melanins precipitated with 6 N HC1 at 110°C during 72 h from urine samples collected during 24 h periods ranged from 0.1460 g to 3.7627 g (mean 1.1303 ± 1.1739 g, n = 8) and the plasma clearance rates ranged from 0.06 ml/min to 1.56 ml/min (mean 0.48 ± 0.48 ml/min, n = 8). From the individual 24 h urine samples we obtained from 9 to 216 mg/dl of precipitated melanins while the individual plasma samples contained from 145 to 175 mg/dl.

Controversial data have been reported with regard to the diagnostic value of the positron emission tomographic (PET) measurement of striatal glucose consumption (rCMRGlc) in chorea-free subjects at risk of Huntington's disease (HD). For further clarification of this issue we measured striatal and cerebellar rCMRGlc in 27 chorea-free subjects at risk of HD, 20 patients with manifest HD and 20 control subjects, using PET and18F-fluorodeoxyglucose. In 6 of the at-risk subjects cerebellar ratios of striatal rCMRGlc were decreased below the corresponding 99% confidence limit determined in the controls. This indicates that the PET measurement of rCMRGlc may, indeed, be valuable in establishing the diagnosis of incipient HD in presymptomatic at-risk subjects.

Precipitates were obtained by 6 N HCl hydrolysis of human erythrocytes and subsequent extractions with ethanol-ether 1:1 and with tetrahydrofuran. The mean quantity of these precipitates (n=16) was 16.60 ± 1.60 (standard deviation) mg/ml, (15.09 ± 1.45 mg/g) and from saline washed erythrocyte samples (n = 8) 16.65 ± 0.73 mg/ml, (15.14 ± 0.67 mg/g). A large part of these precipitates (about 74%) is associated with haemoglobin (in average 12.34 mg/ml). Melanins account for the difference (16.60-12.34) = 4.26 mg/ml, approximately 8.7% of haemoglobin-free erythrocyte solids. Precipitates from red cells, and from haemoglobin produced similar UV-VIS and IR spectra. The precipitates from haemoglobin are mainly derivatives of haeme (about 97%); the remaining ∼ 3% are melanins from globin. The total melanins are about 1.3% of haeme-free solids of erythrocytes. Precipitation from the erythrocytes with 6 N HCl was also achieved in practically complete argon atmosphere, and similar quantities were obtained as those in air with the same UV-VIS and IR spectra. Since granules or solid particles are not found in the cytoplasm of normal human erythrocytes, we conclude that soluble melanins are present. Small amounts of melanins can be present in the membranes as well, since the precursors of melanins: norepinephrine, epinephrine are present in these membranes.

Abstract: Methods for the preparation and analysis of a new renal radiopharmaceutical,99mTc-thiodiglycolic acid (TDGA), are reported. The kit for Tc-TDGA contains a lypophilized acidic (pH 2.5) mixture of 5 mg TDGA and 0.05 mg SnCl2·2H2O. Acetate buffer has been found to be a suitable solvent for paper chromatography of99mTc-TDGA. The results of the quantitative organ distribution studies in rats and rabbits indicated the characteristics of99mTc-TDGA to be intermediate to the renal tubular agent131I-Hippuran and the GFR agent99mTc-DTPA.

In 39 healthy active people aged 17 to 79 who had not fallen, anteroposterior sway during quiet standing increased slightly with age; there was no increase with age in lateral sway. Sway increased on deprivation of visual information and altered proprioception due to foot pressure sensory change in all age groups, and especially when both forms of sensation were altered concurrently; but the increase of sway on pressure sensory change was no greater in the older than in the younger subjects.

One hundred and twenty-five people aged 65 and over in the Birmingham area who fell at home were followed up for one year after the fall had been reported by the general practitioner. They were compared with 125 control subjects matched for age and sex and drawn from the same doctors' lists. Two months after the fall, one control and 11 fallers had died. One year after the fall, eight controls and 32 fallers had died. The main factor associated with increased mortality was impaired mobility before the index fall.

A description is given of the gait and balance laboratory of the Department of Geriatric Medicine of the University of Birmingham, and of the program of tests devised for use in elderly persons. These can be undertaken without discomfort or anxiety to the subjects. They are yielding data that should assist in the management of disorders of gait and balance in the elderly.

Two studied commercial human serum albumin solutions had developed yellow colors during storage. These yellow materials were isolated and shown to be soluble lipofuscin. Aqueous solutions of this lipofuscin exhibited fluorescence spectra with 355 nm excitation and 432 nm emission maxima. After acid hydrolysis of this lipofuscin a nonhydrolysable lipid-melanin fraction was obtained. Ethanol-ether extraction yielded a lipid-containing solution. When evaporated and mixed with water, a solution-suspension was obtained that produced very similar fluorescence spectra to those described above, with 368 nm excitation and 432 nm emission maxima. The separated melanin component was not fluorescent. The isolated lipofuscin exhibited a weak electron paramagnetic resonance spectrum and its g-value has been found to be 2.0069 and its line width 9.8 G. The albumin solution contained approximately 0.23 g of melanin precipitate per 9.31 g of soluble lipofuscin isolated from 25 g of albumin. The deleterious cardiac, pulmonary, renal and clotting changes associated with the use of albumin solution might be due to this lipofuscin.

Homogentisic acid (HGA) spontaneously starts to undergo oxidation and polymerization soon after the beginning of incubation in human blood or plasma at 37°C, and forms plasma soluble melanins (PSM). Haemolysis accompanies this process in blood. The addition of equimolar quantities of antioxidants delays this oxidation significantly (isoascorbic acid by 2: 30-4: 00 h; glutathione by 3: 20-4: 05 h; D-penicillamine by 5: 00-5: 45 h).HGA is a phenylalanine and tyrosine metabolite, related structurally to the catecholamines and other precursors of melanins. HGA is normally metabolized by the enzyme homogentisic acid oxidase. When this enzyme is genetically missing, part of HGA is excreted in the urine, another part polymerizes darkens many tissues (ochronosis), and produces widespread degenerative changes in cartilage and other connective tissues, joints, blood vessels, heart valves, kidneys and in other tissues. Collectively this disorder is known as alcaptonuria, for which no satisfactory treatment is known.The causes of both alcaptonuric arthritis and rheumatoid arthritis are thought to involve increased oxidative stress. Inflammation of joints and connective tissue damage are involved in both diseases. Oxygen radicals are suspected to cause inflammation and cellular damage. Hydroxyl radicals degrade hyaluronic acid (the viscous synovial fluid of joints). High levels of products of free radical reactions, with fluorescence excitation (ex) and emission (em) maxima in the wavelength ranges of those of PSM (ex 320-400 and em 400-470) were reported in the blood sera and synovial fluids of patients with rheumatoid arthritis.Many chemical reactivities of other melanin precursors (such as the catecholamines, 3-hydroxykynurenine, 3-hydroxyanthranilic acid, catechol) produced in normal metabolic processes are so similar to those of HGA that it seems certain that the unrecognized activities of the other precursors of soluble melanins produce similar degenerative processes in normal aging and particularly in chronic renal failure. Plasma levels of soluble melanins or lipofuscins rise in chronic renal failure and degenerative cardiovascular disease is a major cause of death in chronic renal failure, as in alcaptonuria. The uncommon disorder alcaptonuria, therefore, calls attention to the broadly adverse influence of the soluble melanins and their precursors. These adverse effects are apparently oxidative in nature and emphasize the significance of antioxidant protection in normal human metabolism and in illness and aging.

Fluorescence spectrophotometry demonstrates that the levels of plasma soluble lipofuscins (SL) in patients with end-stage renal failure, undergoing continuous ambulatory peritoneal dialysis (CAPD) or haemodialysis (HD), remain significantly higher than in normal subjects. Plasma samples from these patients show the presence of SL generated from 3-hydroxy-anthranilic acid [excitation (ex) at ∼ 324 nm and emission (em) at ∼ 413 nm] and of other SL generated from dopa, catecholamines, 3-hydroxykynurenine and from structurally related precursors (ex at ∼ 345 nm, em at ∼ 445 nm.) These precursors form the melanin components, which are ∼ 3 wt % of SL. The fluorescence of SL appears to originate mainly from the melanin components.Peaks and shoulders at these wavelengths are found in the spectra of all dialysates. Based on intensity measurements at 413 nm and 445 nm, the weekly clearance rates with HD are in general greater than those with CAPD. The saponified cellulose ester membrane used in HD passes only lower-molecular-weight SL and/or components of SL. After HD, the greatest reductions in plasma intensities are found at ∼ 324 nm and ∼ 413 nm. The clearance rates (1/week) are always greater at 413 nm [means HD: 18.47 ± 4.44 standard deviation (SD), n = 8; CAPD: 12.50 ± 2.47, n = 4] than at 445 nm (HD: 10.94 ±3.86; CAPD: 7.95 ± 1.75) both with HD and CAPD. In CAPD, the membrane also permits the passage of large amounts of albumin and other high-molecular-weight substances. Gravimetric melanin measurements demonstrate that CAPD removes more melanins in g/week (means 43.14 ±7.32) than HD (13.90 ± 5.55), with higher weekly clearance rates for melanins in 1 (CAPD: 21.51 ±4.13; HD: 6.42± 1.85), probably due to the removal of higher molecular weight melanins which are less fluorescent and/or non-fluorescent. Dextrose in the dialysis solutions is essential for melanin removal by HD and increased osmolality (dextrose) of the dialysis fluids increases melanin removal by CAPD in most cases.

Background.: Inflammation-induced disease as seen with trauma and infection can lead to increased lung oxidant activity resulting in cell membrane lipid peroxidation. Acute zymosan-induced peritonitis in rats produces lung inflammation, edema, and lipid peroxidation. We determined whether administered @a-tocopherol (vitamin E), the key antioxidant protection against cell membrane lipid peroxidation, would improve this process. Methods.: Male Wistar rats were given 0.75 mg/kg of intraperitoneal zymosan, volume resuscitated, monitored, and killed at 4 or 24 hours. Lung histologic changes and levels of conjugated dienes, a marker of lipid peroxidation, were used to monitor injury. The levels of vitamin E, vitamin C, and catalase were used to monitor antioxidant defenses. The effect of administering @a-tocopherol (50 mg/kg) by gavage immediately after zymosan on the degree of the lung injury was then determined. Results.: Twenty-four hours after zymosan was administered, the vitamin E levels in plasma were significantly decreased, but lung tissue vitamin E levels were maintained, whereas tissue catalase and vitamin E levels decreased. Lung tissue-conjugated diene levels, alveolar edema, and neutrophil count were significantly increased. @a-Tocopherol treatment increased the postzymosan plasma vitamin E levels by 50%. Lung tissue vitamin E levels did not increase; however, the degree of lung injury and lipid peroxidation was significantly attenuated. Tissue catalase levels were also maintained. Conclusions.: We conclude that @a-tocopherol given at the onset of a progressing in flammatory injury can protect the lung from oxidant damage and attenuate the degree of lung injury.

An attempt has been made in this paper to describe the velocity structure of a transpired turbulent boundary layer. The analysis makes use of a “wall-plus-wake” concept and derives a universal representation of the velocity structure of the turbulent boundary layer with uniform injection, “blow-off” or suction. The results of the analysis agree reasonably well with those obtained using an implicit finite difference technique advanced by Patankar and Spalding. The results also show a good correlation with the experimental data of Mickley, et al., and Simpson, et al. Predicted shear stress distributions compare well with the experimental data of Wooldridge, et al.