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Biomedical subjects

P Collins

Publications and source records attributed to P Collins.

At least 217 records · Page 12Linked to original sources
PubMed1993

Photodistributed nifedipine-induced facial telangiectasia.

Five months after starting nifedipine (Adalat), two patients developed photodistributed facial telangiectasia, which became more noticeable with time. Neither patient complained of photosensitivity or flushing. Both patients reported a significant cosmetic improvement after discontinuing the drug. One commenced the closely related drug amlodipine 3 years later, with recurrence of telangiectasia. The photodistribution of the telangiectasia suggests a significant drug/light interaction.

Adult↗
PubMed1993

Hyperinsulinaemia is associated with stimulation of cholesterol synthesis in both type 1 and type 2 diabetes.

The effect of hyperinsulinaemia and hyperglycaemia on cholesterol synthesis was examined in lymphocytes from diabetic subjects. The first part of the study involved the provocation of hyperinsulinaemia by consumption of a carbohydrate-rich meal, in obese patients with Type 2 diabetes mellitus. Cholesterol synthesis was measured before and 4 h after completing the meal. Results were compared to groups of obese non-diabetic patients and to control subjects. Analysis of the three groups demonstrated that the percentage change in cholesterol synthesis was directly proportional to the percentage rise in serum insulin (r = 0.49, p < 0.05). This physiological study demonstrated that postprandial hyperinsulinaemia promoted cholesterol synthesis; however, we could not estimate the effect of the meal on cholesterologenesis. To study hyperinsulinaemia in isolation, we examined the effects of varying insulin infusion rates for 4 h at either low or high levels of serum glucose using the glucose clamp technique in young Type 1 diabetic patients. Cholesterol synthesis in lymphocytes was again measured before and after the study period. Hyperinsulinaemia stimulated cholesterol synthesis (+28.6%, p < 0.05) but hyperglycaemia alone did not exhibit this effect (-1.7% NS). The combination of hyperinsulinaemia and hyperglycaemia produced the greatest increase in cholesterol synthesis (+51.4%, p < 0.05) but this increase was not significantly different from hyperinsulinaemia alone. The percentage increase in serum insulin levels was again proportional to the percentage change in cholesterol synthesis (r = 0.46, p < 0.05).

Acetates↗
PubMed1993

The regulation of post-prandial cellular cholesterol metabolism in type 2 diabetic and non-diabetic subjects.

The purpose of the study was to determine the effect of diabetes on the regulation of postprandial cholesterol metabolism. Four groups of patients (n = 8 for each group) were examined: Type 2 diabetic patients with and without hypercholesterolaemia and non-diabetic subjects with and without hypercholesterolaemia. Serum lipoproteins, lipoprotein composition, cellular cholesterol, and cellular cholesterol synthesis were measured before and 4 h after a high calorie meal. The BMI for the hypercholesterolaemic diabetic patients of 31.5 +/- 0.95 (SEM) was significantly higher than that for the control group of 26.2 +/- 1.0 (p < 0.01). Fasting triglyceride levels were significantly higher in the normocholesterolaemic and hypercholesterolaemic diabetic patients and in the hypercholesterolaemic non-diabetic subjects (1.45 +/- 0.22, 2.27 +/- 0.34, and 1.58 +/- 0.18 mmol l-1, respectively) compared with normocholesterolaemic non-diabetic subjects (0.75 +/- 0.12 mmol l-1: p < 0.01). The normocholesterolaemic and hypercholesterolaemic diabetic subjects had significantly lower fasting serum high density lipoprotein (HDL) (1.06 +/- 0.08 and 1.04 +/- 0.06 mmol l-1) compared to the corresponding non-diabetic groups (1.29 +/- 0.11 and 1.45 +/- 0.17 mmol l-1, p < 0.05). The esterified/free cholesterol ratio of very low density lipoprotein (including chylomicrons VLDL-C) decreased postprandially in all groups with an overall decrease of 1.33 to 0.83 (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Glucose↗
PubMed1993

Tuberculosis in wild seals and characterisation of the seal bacillus.

Tuberculosis was diagnosed in 3 otariid seals found dead on beaches at 3 locations on the south coast of Western Australian between May 1990 and March 1991. This confirms that tuberculosis is present in the 2 native seals (Neophoca cinerea and Arctocephalus forsteri) in Western Australian waters. Mycobacterium sp isolated from the lungs of 2 of the seals were studied to determine the similarity of the strains to each other, to the strains isolated during 1986 from Australian sea lions and New Zealand fur seals kept in captivity at a marine park near Perth, Western Australia, and to a strain isolated in 1988 from a seal trainer who worked with the infected captive seals for 3 years. After restriction endonuclease analysis (REA) with the endonucleases Bst EII, Bcl I and Pvu II, one of the wild seal strains appeared to have identical DNA fragment patterns to the strains from the captive seals and the seal trainer. The other wild seal isolate had identical REA profiles using Bst EII and Bcl I, but a minor difference was detected using Pvu II. Differences in these isolates were more clearly seen in restriction fragment length polymorphisms after hybridisation with two DNA probes. The secretory protein MPB70, present in M bovis, was not detected in wild seal isolates using sodium dodecyl sulphate polyacrylamide gel electrophoresis and Western blotting techniques. Analysis of protein and DNA fragment profiles indicated that seal tuberculosis isolates form a unique cluster within the M tuberculosis complex.

Animals↗
PubMed1993

Coronary flow reserve.

Explore the source record for details and available documents.

Angioplasty, Balloon, Coronary↗
PubMed1993

Endothelium dependent and independent responses in coronary artery disease measured at angioplasty.

OBJECTIVE--To investigate the effects of substance P and papaverine, two drugs that increase coronary blood flow by different mechanisms, on vasomotion in stenotic coronary arteries at percutaneous transluminal coronary angioplasty (PTCA). DESIGN--Coronary blood flow responses to substance P and papaverine were measured in stenotic coronary arteries at the time of PTCA with quantitative angiography and a Doppler flow probe. SETTING--A cardiothoracic referral centre. PATIENTS--15 patients undergoing elective PTCA of a discrete epicardial coronary artery stenosis. INTERVENTIONS--Pharmacological coronary flow reserve was determined with papaverine 5-10 minutes before and after successful PTCA. Endothelium dependent responses to 2 minute infusions of substance P (10-15 pmol.min-1) were assessed immediately before PTCA. MAIN OUTCOME MEASURES--Coronary blood flow responses and changes in epicardial coronary artery area at stenotic, proximal, and distal sites with papaverine and substance P. RESULTS--Stenotic sites dilated with papaverine before PTCA (17.7%(6.9%) (mean (SEM)) area increase, p < 0.05 v baseline). Substance P dilated stenotic sites (16.8%(5.7%) area increase, p < 0.05) and proximal (14.3%(5.4%), p < 0.05) and distal sites (41.7%(9.3%), p < 0.005). Coronary flow reserve increased but did not reach normal values after PTCA (2.3(0.4) before PTCA v 3.0(0.4) after PTCA, p < 0.05) and was associated with an increase in peak flow with papaverine. Angioplasty did not alter baseline flow. After PTCA papaverine caused significant vasoconstriction at the stenotic site (-13.6%(4.3%) area decrease, p < 0.05). There was a negative correlation (r = -0.68, p < 0.05) between the dilator response with papaverine before PTCA and the constrictor response after PTCA. CONCLUSIONS--Substance P causes endothelium dependent dilatation in atheromatous coronary arteries, even at sites of overt atheroma. The cause of the paradoxical constrictor response to papaverine after PTCA is uncertain, but unopposed flow mediated vasoconstriction (the myogenic response) after balloon induced endothelial denudation may be one of several contributory factors.

Angioplasty, Balloon, Coronary↗
PubMed1993

Coronary flow reserve in patients with chest pain and normal coronary arteries.

BACKGROUND: Many studies have shown that coronary flow reserve is reduced in patients with chest pain and angiographically normal coronary arteries. The methods used to assess coronary blood flow have varied, but in nearly all reports dipyridamole has been used to bring about vasodilatation. This study was designed to assess whether the apparent impairment of coronary flow reserve seen with dipyridamole could be reproduced with either papaverine or adenosine, which induce maximum coronary blood flow by different mechanisms. METHODS: 25 patients with chest pain and angiographically normal coronary arteries were studied with an intracoronary Doppler flow probe and quantitative angiography to determine epicardial coronary artery area, coronary blood flow velocity, coronary flow reserve, and coronary vascular resistance index (CVRI, the ratio of resistance after intervention to basal resistance). All patients received papaverine 8 mg. Eight patients with positive exercise tests received intracoronary papaverine (8 and 10 mg), intracoronary adenosine (6, 20, 60 micrograms), and high-dose intravenous dipyridamole (0.84 mg/kg). RESULTS: The velocity ratio (peak after intervention: baseline) (mean (SEM)) after 8 mg papaverine was 3.3 (0.2) (n = 25) and the coronary flow reserve was 4.1 (0.3) (n = 25). There were no differences between patients with a positive (n = 16) or negative (n = 9) exercise test. In eight patients coronary flow reserve was measured after increasing doses of papaverine, adenosine, and dipyridamole. Coronary flow reserve was 4.5 (0.3) with papaverine, 4.8 (0.3) with adenosine, and 3.5 (0.4) with dipyridamole (p = 0.08 v papaverine and adenosine). CVRI was 0.22 (0.01) with papaverine, 0.21 (0.02) with adenosine, and 0.29 (0.03) with dipyridamole (p < 0.05 v papaverine, p = 0.09 v adenosine). CONCLUSIONS: These results indicate that measurement of coronary flow reserve and CVRI in patients with chest pain and normal coronary arteries depends on the pharmacological stimulus. Normal values were obtained with papaverine in all patients, irrespective of the exercise test response. In patients with a positive exercise test significantly lower values were obtained with dipyridamole than with papaverine, or adenosine. The reported impairment of coronary flow reserve in patients with angina and normal coronary arteries may reflect the variability in response to different pharmacological agents. The mechanism underlying this variability is unknown, but may involve an abnormality of adenosine metabolism in the myocardium.

Adenosine↗
PubMed1993

Homozygous variegate porphyria: an evolving clinical syndrome.

Variegate porphyria is one of the most frequently encountered genetic conditions in South Africa. It is inherited as an autosomal dominant disease and in excess of 300 heterozygous cases have been studied by the Cape Town unit. Despite this, the homozygous condition has not previously been encountered in South Africa. We report two cases of homozygous variegate porphyria, one of whom represents the first South African case. We delineate a syndrome principally characterized by growth retardation, developmental delay, epileptic seizures, photosensitivity and an abnormal porphyrin excretion pattern. In addition we describe, in one case, two features not previously reported: skin disease in areas unexposed to light and a severe sensory neuropathy which may account at least in part for the hand deformities of this disorder.

Bone and Bones↗
PubMed1993

Hemoglobin inhibits endothelium-dependent relaxation to acetylcholine in human coronary arteries in vivo.

BACKGROUND: The endothelium can regulate vascular tone by releasing both endothelium-derived relaxing factor (EDRF or nitric oxide) and contracting factors. To date, there has only been circumstantial evidence to indicate EDRF activity in vivo in human coronary arteries. Using human hemoglobin as a specific inhibitor, the hypothesis that acetylcholine-induced coronary vasodilation is due to EDRF release was tested. METHODS AND RESULTS: We studied the response of normal coronary arteries to acetylcholine (an endothelium-dependent vasodilator) and isosorbide dinitrate (an endothelium-independent vasodilator) in seven patients. The specificity of any vasodilator response was assessed by the infusion of reduced free human hemoglobin. Hemoglobin 10(-5) M infusion alone had no effect on coronary artery diameter. Drugs were infused into the coronary artery, and the diameter changes were assessed by quantitative angiography. Acetylcholine 10(-7) M increased left anterior descending coronary artery diameter from control: 2.30 +/- 0.12 mm to 2.79 +/- 0.20 mm (mean +/- SEM, n = 7, p < 0.01). Hemoglobin both in a concentration of 10(-6) M and 10(-5) M reversed this vasodilator effect, causing constriction to 2.11 +/- 0.18 mm (p < 0.001 compared with acetylcholine 10(-7) M) and 2.29 +/- 0.14 mm (p < 0.05 compared with acetylcholine 10(-7) M). Isosorbide dinitrate in the presence of hemoglobin caused dilatation of the coronary artery in all cases to 3.04 +/- 0.24 mm (p < 0.001 compared with acetylcholine 10(-7) M and hemoglobin 10(-6) M). CONCLUSIONS: Using a specific inhibitor of nitric oxide, reduced free hemoglobin, we have demonstrated that basal EDRF release does not appear to play an important role in the maintenance of human epicardial coronary artery diameter in vivo but is responsible for the acetylcholine-induced dilatation.

Acetylcholine↗
PubMed1993

Photosensitivity associated with antibacterial agents.

Skin reactions following the interaction of photoactive drugs and ultraviolet or visible radiation are usually rapidly reversible after drug cessation. Within the antibacterial group, photosensitivity to sulphonamides, nalidixic acid, fluoroquinolones and tetracycline members have all been reported. In general such reactions are mild, although rarely some individuals have a severe response. Precise subcellular mechanisms are drug specific, appear complex, and as yet are ill understood. Measures such as drug dosage reduction, the wearing of photoprotective clothing and use of broad spectrum sunscreens can alleviate the problem.

Anti-Infective Agents↗
PubMed1993

Mechanisms of herpes virus resistance.

The introduction of virus-specific anti-herpes virus agents such as acyclovir, ganciclovir and Foscarnet has had a significant impact on the management of herpes virus infections. The use of specifically acting antimicrobial agents, however, raises the question of drug resistance. Exposure in cell culture of herpes virus to these agents results in the selection of drug-resistant variants, with resistance being due to alterations in the genes encoding the target enzymes involved in the mechanism of action of the drugs concerned, e.g. in the case of acyclovir resistance occurs as a result of deletions or alterations in the thymidine kinase (TK) or alterations in DNA polymerase genes. Pathogenicity studies reveal that drug-resistant variants are disadvantaged, in particular the TK deletion variants which are less pathogenic and unable to reactivate from latent infections. Extensive studies in cell culture and animal models with herpes viruses have provided an understanding of the mechanisms of resistance and more recently these findings have been correlated with the clinical experience. The incidence of virus resistance in immunocompetent patients is extremely rare, whereas resistance has infrequently been reported in immunocompromised individuals where exposure to drug is prolonged. However, the understanding of the mechanisms and consequences of virus resistance gained in cell culture and in animal models has led to the successful management of resistant episodes in the clinic, either by temporary removal of the selection pressure or by providing alternative therapies.

Acyclovir↗
PubMed1992

In situ transformation of striatal glia into cerebellar-like glia after brain transplantation.

Transplants of striatum from rabbit embryo were implanted into the colliculus posterior of newborn mice. After 4 weeks, astroglial cells derived from the transplant had migrated into the cerebellum of the host. Whenever they had settled in the cerebellum they presented forms similar to local glia. Some migrated glial cells were found to transform into forms of glia, such as radial-like glia, which are not present in the striatum. This observation confirms that glial precursor cells are highly plastic. It is an in vivo demonstration that local conditions alone define the morphology of glial cells. After grafting in an heterotopic location they take on forms that they were not destined to express in the region of origin.

Animals↗
PubMed1992

Progesterone induces endothelium-independent relaxation of rabbit coronary artery in vitro.

The effect of progesterone on isolated rabbit coronary arteries and its possible mechanism was investigated by measuring changes of isometric tension. Progesterone (1, 3, 10 and 30 microM) induced significant coronary relaxation in K+ (30 mM)-, prostaglandin F2 alpha (3 microM)- or Bay K 8644 (1 microM plus 15 mM K+)- precontracted arteries. There was no difference between endothelium-intact and -denuded coronary arteries from both male and female rabbits, precontracted with these three agents. Haemoglobin, indomethacin, methylene blue, glibenclamide or barium chloride did not affect the relaxation. In endothelium-denuded rabbit coronary arteries, progesterone shifted calcium concentration-dependent constrictor-response curves to the right, the maximal contraction was also reduced. The -log ED50s were 3.6 in control, and 3.3 and 2.9 after incubation with progesterone (3 and 30 microM), respectively. Similar results were obtained in rat aorta. We conclude that progesterone induces significant endothelium-independent relaxation in rabbit coronary arteries in vitro, possibly by affecting calcium influx.

Animals↗
PubMed1992

Surveillance of nosocomial infection in private psychiatric hospitals: an exploratory study.

BACKGROUND: The vast majority of work published about infection control programs, procedures, and practices addresses general acute care facilities. Consequently, infection-control coordinators at psychiatric hospitals have few established norms or models to use in adapting available standards to the unique needs of psychiatric hospitals and their patients. This descriptive study explored practices for the surveillance of nosocomial infections in private psychiatric hospitals. METHODS: A survey was mailed to the infection control coordinator of the 284 hospitals belonging to the National Association of Private Psychiatric Hospitals. Questionnaire data were collected anonymously. Surveys were returned by 103 (36%) of the hospitals. RESULTS: The most frequent criteria used to define the presence of nosocomial infections were the Center for Disease Control guidelines and clinical judgment, used by 38% and 39% of the respondents, respectively. Most (64%) of the respondents indicated that they did calculate a nosocomial infection rate. The most frequent method used to calculate infection rates was based on patient discharges. Sixty-five hospitals (63%) reported their most recent yearly infection rate, which ranged from 0.00 to 0.35, with a median rate of 0.05 (mean, 0.06; SD, 0.07). CONCLUSIONS: Overall, the findings reflected much variability in respondents' practices in defining nosocomial infections and calculating infection rates. We therefore suggest that both the method used to calculate the rate and facilities' definitions of nosocomial infection be considered when comparing infection rates across facilities.

Cross Infection↗
PubMed1992

Impairment of endothelium dependent responses in a rat model of chronic heart failure: effects of an exercise training protocol.

OBJECTIVE: The aim was to document the response of aortic rings from a rat model of heart failure to endothelium dependent and endothelium independent vasodilating agents. The effects of an exercise training schedule upon these responses was studied. METHODS: Heart failure was produced in one group of female Wistar rats by coronary artery occlusion, and sham operations were performed in a matched group. The rats were allowed to recover for six weeks, following which half the rats with heart failure were started on a treadmill exercise schedule for a further six weeks. After this time the rats were killed, and rings of aorta were studied in an organ bath to measure the response to both endothelium dependent and endothelium independent vasoactive agents. RESULTS: The presence of heart failure was confirmed in both the non-trained (NT, n = 5) and trained rats (TR, n = 5), but not in the sham operated animals (SH, n = 6). The constrictor response to prostaglandin F2 alpha was similar in aortic rings from all the animals. The relaxation response to the endothelium dependent vasodilator acetylcholine (10(-7) and 10(-6) M) was impaired in the rats with heart failure compared to the sham operated animals (10% v 33% with 10(-7) M acetylcholine, p < 0.005). The dilator response in the trained rats was not significantly greater than in the non-trained rats (TR 35% v NT 24% with 10(-6) M acetylcholine). There was no difference in the response to sodium nitroprusside (10(-7) and 10(-6) M) between the three groups. CONCLUSIONS: Chronic heart failure impairs the response of aortic rings to the endothelium dependent vasodilator acetylcholine in a rat model of heart failure. The response to sodium nitroprusside, an endothelium independent relaxing agent, is not impaired by heart failure. These findings may help to explain the raised systemic vascular resistance and the failure of vasodilatation in skeletal muscle vasculature which limits exercise capacity in subjects with heart failure.

Acetylcholine↗