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Biomedical subjects

J L Botha

Publications and source records attributed to J L Botha.

At least 73 records · Page 4Linked to original sources
PubMed1985

What do pacemaker recipients think of their implantations? An exploratory study.

Interviews conducted with 94 pacemaker recipients were analysed to assess their knowledge and understanding of their disease and treatment, as well as to determine their self-assessment of the quality of life before and after implantation. Many patients knew little about their illness, the reason for having a pacemaker, or their prognosis. Eighteen patients claimed still to be in bad physical condition; 47 patients claimed to be physically handicapped, in 32 of whom the handicaps could be related to their cardiac condition. Fifty patients said that they were less active after implantation than before it. These findings suggest a lack of meaningful patient-doctor/doctor-patient communication. It is suggested that a team approach involving a social worker would improve continuity of care and communication, as well as the quality of patients' lives.

Adaptation, Physiological↗
PubMed1985

African vital statistics--a black hole?

An attempt was made to describe the disease patterns among blacks on the basis of registered deaths, which have been collected for the whole of the RSA since 1978. The pattern of cause-specific proportional mortality resembled that of an underdeveloped population. It was noticed that the data were not suitable for detailed descriptions because there was evidence of under-registration and misclassification, in particular in the national states. A large proportion (20% on average) of the deaths are classified as caused by symptoms, signs and ill-defined conditions. It is recommended that the process of registration be reviewed in order to improve the quality of the data so necessary for epidemiological and health care research.

Adolescent↗
PubMed1985

Mseleni joint disease in 1981: decreased prevalence rates, wider geographical location than before, and socioeconomic impact of an endemic osteoarthrosis in an underdeveloped community in South Africa.

Mseleni joint disease (MJD), an endemic osteoarthrosis, was first described in 1970, localized to Kwa Zulu, South Africa. In 1981 another survey was conducted (1) to see whether prevalence had changed, (2) to estimate the prevalence in areas not previously surveyed and (3) to estimate its socioeconomic impact. A 5% stratified random sample of homesteads was selected and five local interviewers surveyed 333 kraals, interviewing 333 individuals, obtaining information on 3368 live members of these homesteads. Overall prevalence rates were 7.4% in 1566 females and 3.0% in 1179 males (age or sex unknown in 623). The previously affected area still had the highest prevalence rates, but they were significantly lower than before, even if only residents of at least ten years' duration were considered. These consistently lower age-specific prevalence rates are compatible with a decline in incidence rate, possibly because of disappearance of an environmental causal agent. Prevalence rates for females in some areas not previously surveyed were between 5 and 10%, suggesting that a larger area than stated before is affected. The proportions of severely disabled individuals are the same as reported in 1973 but greater in number considering the larger area affected. Of these, an estimated 67% of males and 47% of females are not receiving disability grants. Fifty per cent of children (aged 6-25 years) of affected parents have had no schooling compared with 30% of children of unaffected parents. This study also highlighted several methodological problems unique to rural research. It is suggested that while aetiological research should continue, the existing prevalence of MJD has major social, economic and health care implications, for which solutions should be researched as a high priority.

Adolescent↗
PubMed1984

The causes of non-natural deaths in children over a 15-year period in greater Cape Town.

This study was undertaken to describe the causes of non-natural death in children aged under 15 years in the Cape Peninsula. Information was abstracted from the official death register kept at the South African Police Mortuary in Cape Town for the period of 1 July 1966-30 June 1981. During the 15-year period 3 248 medicolegal autopsies were performed on children under 15 years of age who had died of non-natural causes. There were significantly higher percentages of Coloureds and Blacks, males, and children aged under 6 years in the sample than in the general population aged under 15 years in the Cape Peninsula. The majority of deaths (54,4%) were caused by road traffic injuries. Other important causes of deaths were burns (12,8%), drowning (11,0%), assault/abuse (5,4%) and poisoning (3,3%). Special attention was paid to the causes of fatal head injuries--head injury alone was given as the cause of death in 819 autopsies (25,2%). The majority of fatal head injuries (72,4%) were also caused by road traffic accidents. This study demonstrates the alarming number of deaths from non-natural causes among children aged under 15 years in the Cape Peninsula. The finding that more than half of these deaths were due to road traffic accidents indicates the impact that successful intervention could have.

Accidents↗
PubMed1984

A retrospective study of head-injured children admitted to two hospitals in Cape Town.

A retrospective study was undertaken to describe the patterns of head injury in children in the Cape Peninsula. Information was abstracted from Groote Schuur Hospital and Red Cross War Memorial Children's Hospital records for all children aged under 15 years admitted with head injury between July 1966 and June 1981. Data were collected on 1 820 admissions. There were significantly higher percentages of Coloureds and Blacks, males and children aged under 6 years in the sample than in the corresponding population of the Cape Peninsula. In children under 1 year old, fails accounted for approximately 70% of head injuries in all three race groups. In the 1-5-year age group, transport-related injuries were the most common cause of admission in Blacks (63,1%) and Coloureds (46,5%), but in Whites falls were still most common (58,2%). In the 6-14-year age group, transport-related accidents accounted for approximately 64% of head injuries in all three race groups. Pedestrian accidents were the commonest cause of admissions due to transport-related head injury. Severe or very severe concussive injuries, multiple injuries or death occurred more commonly in transport-related injuries than among those caused by falls or assault/abuse. Transport, falls and assault/abuse together accounted for 88,4% of all causes of head injury.

Adolescent↗
PubMed1984

Association between familial hypercholesterolaemia and church affiliation. Is this the result of sociocultural isolation of migrant farmers in 19th-century South Africa?

The family trees of 57 Afrikaans -speaking familial hypercholesterolaemia (FH) index cases were traced to look for founder surnames, for an association between FH and affiliation to the Gereformeerde Kerk (GK), and for consanguinity. Two possible founder surnames were identified. Each occurred in more than 5% of individuals and both were well known among the founders of the GK. Affiliation to the GK was much more common in our sample (45% of 994 individuals) than in the general population (5%), an overall odds ratio of 7,38. This association was stronger in older generations. There were 21 consanguineous marriages, the two suspected founder surnames and affiliation to the GK featuring prominently among them.

Consanguinity↗
PubMed1981

Serum lipid, uric acid and glucose levels in urban black males doing manual or clerical work.

Serum lipid, uric acid and glucose levels were measured in four groups of Black male factory workers 1 hour after an oral glucose load. These groups comprised non-obese manual, obese manual, non-obese clerical and obese clerical workers. Obese men had significantly higher serum uric acid, total cholesterol and triglyceride levels and lower high=density lipoprotein (HDL) cholesterol levels than non-obese men. Serum glucose and low-density lipoprotein (LDL) cholesterol values were also higher in obese than in non-obese men, but the differences were not significant. Clerical workers had higher levels than manual workers for most of the biochemical variables measured, but only in the case of uric acid was the difference significant. Possible reasons for the fact that the effect of occupation on the variables was slight are briefly discussed.

Adult↗
PubMed1978

Gastric inhibitory polypeptide in acquired pancreatic diabetes: effects of insulin treatment.

Oral glucose tolerance tests were done in eight insulin-requiring pancreatic diabetic patients to study the effect of withdrawal of insulin treatment on gut hormone release. Basal levels of gastric inhibitory polypeptide (GIP), glucagon-like immunoreactivity, and immunoreactive glucagon levels rose on insulin withdrawal, more so in patients on short-acting insulin, and were lowered by insulin treatment. Insulin treatment did not affect the GIP, glucagon-like immunoreactivity, or IRG responses to oral glucose. Improved glucose tolerance was greater in patients receiving soluble insulin than in those receiving lente insulin, and there was a significant positive linear correlation between basal plasma GIP and blood glucose levels in these patients. Therefore, it is suggested that insulin treatment lowers basal hormones levels, possibly via a metabolic effect, whereas the hormone responses to oral glucose may be controlled by several factors unrelated to insulin administration or changes in glucose homeostasis.

Adolescent↗
PubMed1977

The effect of somatostatin on epinephrine-induced free fatty acid release in normal man.

Epinephrine and saline or cyclic somatostatin were infused into normal persons to study the effect of somatostatin on free fatty acid (FFA) release. Somatostatin had no effect on epinephrine-induced hyperglycaemia. It enhanced basal and epinephrine-induced FFA release, while the release of both immunoreactive insulin (IRI) and immunoreactive glucagon (IRG) was inhibited. We suggest that the rise in FFA levels may be due to either inhibition of IRI or another effect of somatostatin on fatty acid metabolism.

Adult↗
PubMed1977

The effects of somatostatin on hormonal and metabolic responses in chronic pancreatitis.

Unmodified synthetic somatostatin, given as a 200-microgram intravenous bolus, plus 200 microgram infused over 3 hours, had no effect on basal plasma insulin and pancreatic glucagon-like immunoreactivity (GLI) levels, both in controls and in patients with chronic pancreatitis. Somatostatin inhibited insulin-hypoglycaemia-induced pancreatic GLI release in controls and in patients with pancreatitis, and prolonged the insulin-induced fall in blood glucose in the patients. Arginine, presumably via insulin release, caused a fall in free fatty acids (FFA) in controls, which was inhibited by somatostatin. Somatostatin abolished the rebound rise in plasma FFA in patients with pancreatitis after insulin-hypoglycaemia. This effect may be related to inhibition of pancreatic GLI release or may be a direct action of somatostatin on lipolysis.

Adult↗
PubMed1977

Pancreatic glucagon-like immunoreactivity in a pancreatectomized patient.

True or 'pancreatic' glucagon-like immunoreactivity (GLI) was found in the plasma of a pancreatectomized patient. In contrast with the regulation of pancreatic GLI in normal controls, there was paradoxical release after oral glucose, no response to arginine or insulin-hypoglycaemia and somatostatin did not suppress its release, but tolbutamide did. Similar to controls, this pancreatic GLI appeared to be under adrenergic beta-receptor control. There was no apparent effect on blood glucose regulation despite marked changes in pancreatic GLI levels during the various manipulations. On polyacrylamide gel electrophoresis, pancreatic GLI from our patient's plasma eluted as two equivalent peaks: one with the glucagon marker and the other in a more cathodal position. We therefore suggest that, although the extra-pancreatic 'pancreatic' GLI in our patient's plasma has immunologic similarities with pancreatic glucagon, the responses to stimulation and suppression are quite different from those in controls and the biologic activity does not appear to be that of pancreatic glucagon.

Antigens↗
PubMed1977

Inhibition of exaggerated gastrointestinal glucagon responses in chronic pancreatitis by somatostatin.

Oral glucose administration caused an exaggerated release of cross-reacting gastrointestinal glucagon-like immunoreactivity (GLI) and a slight early rise in immunoreactive glucagon (IRG) concentration in patients with chronic pancreatitis, who have impaired insulin release. Intravenous administration of 200 microgram of somatostatin, followed by infusion of 200 microgram over 2 1/2 h, abolished the GLI and insulin responses, but did not change glucose tolerance. This contrasts with the relatively minor effects of somatostatin on GLI responses in control subjects where the clear deterioration in glucose tolerance may relate to inhibition of insulin release.

Aged↗
PubMed1976

Kinetics of insulin secretion in chronic pancreatitis and mild maturity onset diabetes. (Evidence for "gut hormone" action beyond glucoreceptor and cyclic adenosine monophosphate mediated insulin release).

We studied insulin responses to glucose with and without cholecystokinin-pancreozymin and aminophyllin infusions in normal, chronic pancreatitic and genetic (maturity-onset) diabetic subjects. Glucose was given alone as separate 5 and 10 g boluses followed by infusion at 250 mg/min. and 500 mg/min., respectively. Chronic pancreatitis patients and genetic diabetic patients had decreased Imax values, indicating a decreased insulin reserve. Sensitivity to glucose was normal in pancreatitic subjects, but the diabetic subjects had a raised G50 value, compatible with glucoreceptor dysfunction. Infusions of aminophyllin enhanced insulin responses (Imax) to glucose injection in normal subjects and to a lesser degree in pancreatitic subjects, but decreased sensitivity to glucose (increase in G50) in both groups. Although the Imax value in pancreatitic subjects was significantly lower than in the control subjects during the glucose plus aminophyllin infusion, the blood glucose concentration in the pancreatitic subjects was nonetheless decreased. This suggests that pancreatitic subjects have increased endogenous insulin sensitivity. Aminophyllin had no effect in diabetic subjects. Crude cholecystokinin-pancreozymin changed the shape of the glucose/insulin dose response curve in normal, pancreatitic and diabetic subjects. These findings further suggest that the defect in insulin secretion in pancreatitic subjects is partly situated at the cyclic adenosine monophosphate stage of insulin release. Crude cholecystokin-pancreozymin seems to affect insulin release at a point beyond the cyclic adenosine monophosphate stage.

Adult↗
PubMed1976

Gastric inhibitory polypeptide (GIP) in chronic pancreatitis.

The plasma gastric inhibitory polypeptide (GIP), pancreatic glucagon-like immunoreactivity (PGLI), and gut glucagon-like immunoreactivity (GGLI) responses to oral glucose have been measured in five patients with chronic pancreatitis (with diabetic glucose tolerance tests) and in matched nondiabetic controls. Plasma GIP levels rise rapidly after glucose ingestion before changes in circulating glucose and insulin concentration. Patients with pancreatitis have a greater than normal GIP response to oral glucose, which may account for the relatively unimparied insulin response to oral glucose in these patients compared with that to iv glucose, as has been previously found. Patients with pancreatitis also have a paradoxical rise in PGLI and an exaggerated rise in GGLI concentration following oral glucose.

Adult↗
PubMed1976

The inexhaustible beta cell.

Repeated intensive pancreatic beta-cell stimulation was carried out in 42 subjects, comprising 22 normal controls, 10 mild to "severe" maturity-onset diabetics, and 10 chronic pancreatitis patients. Each subject received 75 gm. oral glucose twice and 1 mg. glucagon plus 0.5 gm. tolbutamide intravenously three times at short intervals. Each of the three combined stimuli caused almost equivalent marked spikes of insulin release in all experimental groups. The total calculated output of insulin was equivalent to the total daily insulin output in normal subjects. Pancreatitics and those with severe diabetes (fasting blood sugar greater than 120 mg./100 ml.) had qualitatively similar but a quantitatively smaller response. Those with mild diabetes were similar to the normal subjects but had an exaggerated response to the second oral glucose dose, suggesting overactivity of the enteroinsular axis. Despite the inordinate insulin levels, hypoglycemia did not occur.

Adult↗