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Biomedical subjects

J Burden

Publications and source records attributed to J Burden.

18 recordsLinked to original sources
PubMed2000

Propofol and pain on induction: the effect of injectate temperature in children.

A prospective, randomized, double-blind study was conducted to determine whether cooled intravenous propofol reduces the incidence of pain on induction of anaesthesia in children. Seventy patients aged 3-10 years, ASA I or II, were randomized to receive 1% propofol plus 0.05% lidocaine either at room temperature (20-23 degrees C) or cooled to 4C. Pain was assessed by a blinded observer using a behavioural scale. Data from 69 patients were analysed. The incidence of pain was 9/34 (26%, 95% confidence intervals 11-41%) in the room temperature injectate group and 5/35 (14%, 95% confidence intervals 3-26%) in the cold injectate group. These differences were not statistically significant (P=0.21, chi-squared test). Pain scores were similar in both groups.

Anesthetics, Intravenous↗
PubMed1994

A case of successful use of reproductive technology for a couple with subfertility due to retrograde ejaculation, where artificial insemination had failed.

A case history of a couple where the infertility was due to retrograde ejaculation is presented; when conventional treatment with artificial insemination using sperm isolated from postejaculatory urine failed, IVF and GIFT technology was applied. This resulted in a pregnancy which unfortunately failed at 3 months, unrelated to the method of conception. This case report highlights the possible use of IVF/GIFT for yet another type of male subfertility.

Adult↗
PubMed1989

Systemic bacillus-Calmette Guerin infection after transurethral administration for superficial bladder carcinoma.

It is well known that intravesical bacillus Calmette-Guerin therapy is a safe and effective treatment for superficial bladder carcinoma with few serious complications. However, we report a case of pneumonitis, hepatitis, azotemia, fever and pancytopenia in a patient after transurethral administration of bacillus Calmette-Guerin. Even though severe systemic complications are rare, patients who have high fevers of signs of other systemic manifestations require documentation of the extent of the infection. Also, we address the use of prophylactic antituberculous drugs, not only to prevent these symptoms but also to raise the questions of diminishing the immunological effect of the treatment.

Administration, Intravesical↗
PubMed1987

Giant neurilemoma: unusual scrotal mass.

General physical examination of the male at whatever age is incomplete unless the scrotum and its contents are assessed. Since the scrotum consists of skin, fibrous connective tissue, smooth muscle, vessels, nerves, and a lining of simple squamous epithelium, a variety of tumors may arise in it. Scrotal tumors, however, are infrequent. Rare tumors are solitary neurilemomas. The English literature does not describe a giant neurilemoma of the scrotum.

Genital Neoplasms, Male↗
PubMed1976

Effect on various putative neurotransmitters on the secretion of corticotrophin-releasing hormone from the rat hypothalamus in vitro-a model of the neurotransmitters involved.

The effect of incubating the hypothalamus of adult male rats with various neurotransmitters upon the release of corticotrophin-releasing hormone (CRH) was studied. The CRH activity in the incubation medium was assayed in 48 h median eminence-lesioned rats and the corticosteroidogenesis of excised adrenals in vitro was used as the end-point. 5-Hydroxytryptamine (100 pg/ml-10ng/ml) caused a dose-dependent release of CRH which was antagonized by methysergide (30-100 ng/ml). The response to 5-hydroxytryptamine was also inhibited by hexamethonium and atropine which indicated that it was acting through a cholinergic interneurone. Melatonin (10 ng) did not alter the basal release of CRH but inhibited the action of both 5-hydroxytryptamine (10 ng) and acetylcholine (3 pg). Thus it appears that both 5-hydroxytryptamine and melatonin play a role in the control of CRH release. Noradrenaline blocked the release of CRH induced by both acetylcholine and 5-hydroxytryptamine and presumably this inhibition was caused by direct action on the CRH neurone. gamma-Aminobutyric acid (GABA) also inhibited the release of CRH and may also be involved in the regulation of CRH secretion. The inhibitory neurotransmitters, noradrenaline, GABA and melatonin, act via independent receptor mechanisms. A model based on the above data is presented.

Acetylcholine↗
PubMed1975

The effect of various putative neurotransmitters on the release of corticotrophin releasing hormone from the hypothalamus of the rat in vitro. I. The effect of acetylcholine and noradrenaline.

The effect of various putative neurotransmitters upon the release of corticotrophin releasing hormone (CRH) was investigated using the hypothalamus of the rat in vitro. Acetylcholine (1-5 pg) caused a dose-dependent release of CRH which was antagonized by hexamethonium (1-10ng) and partially antagonized by atropine (300 pg). Neither noradrenaline, dopamine nor histamine had any effect on the basal secretion of CRH. Noradrenaline (10 ng), however, was able to inhibit the release of CRH in response to acetylcholine (3 pg) and this action of noradrenaline was reduced by phentolamine (100 ng), an alpha adrenergic blocking agent.

Acetylcholine↗
PubMed1974

Stimulation electrically and by acetylcholine of the rat hypothalamus in vitro.

1. The hypophysiotrophic area of the rat hypothalamus was studied in vitro. The preparation remained viable for at least 3 hr and showed oxygen consumption varying between 68.9-120 mumole/g.hr. The tissue potassium ion content (per unit wet weight) fell to about 50% of the in vivo concentration during this time compared with 15% in the presence of ouabain (10(-4) M). Histological examination of tissue incubated for 3 hr showed variable perineuronal oedema but the nuclei were of normal appearance and none showed the pyknotic changes that would be associated with cell degeneration.2. Corticotrophin releasing hormone (CRH) in the medium pooled from five to twenty hypothalami was assayed in five to twelve rats which were median-eminence lesioned 48 hr earlier. In vitro corticosterone production of quartered adrenals was used as the end point of the assay. Regression lines of the dose-response curves for ACTH, crude CRH and different volumes of medium from electrically stimulated hypothalami were parallel. CRH output was maximal at 75 Hz and 100 muA when the square-wave pulses lasted for 1 msec. No CRH activity was found on stimulation of cerebral cortex or thalamic tissue pieces of equivalent size.3. Hypothalami taken from rats, adrenalectomized 7-14 days previously, released several-fold more CRH into the medium during electrical stimulation than the initial content of the tissue, showing that the tissue was capable of synthesizing CRH in vitro. The hypothalami taken from intact rats released considerably less CRH into the medium than tissue taken from 12 to 14 day adrenalectomized rats. The hyper-secretion of CRH observed in hypothalami taken from adrenalectomized rats was abolished by pre-treatment with 5 mg/100 g s.c. of corticosterone 24 hr before removal of the tissue. It is therefore proposed that the delayed negative feed-back action of corticosterone at the hypothalamic level is by the suppression of CRH synthesis and that the effect of secretion is secondary to the effect on synthesis.4. The presence of Ca(2+) in the medium was essential for the release of CRH.5. CRH secretion increases linearly with doses of acetylcholine from 5.5 x 10(-15)-5.5 x 10(-14) M. Cerebral cortex incubated with acetylcholine showed no CRH activity. The effect of acetylcholine was reduced by atropine (3.5 x 10(-13) M). Median eminence-pituitary stalk fragments (which contain mainly terminal axons of neurones) incubated with acetylcholine showed no CRH stimulation in the doses that activate the release of CRH using the hypophysiotrophic hypothalamus. Acetylcholine may act as a neurotransmitter at the dendritic level in the CRH neurone.

Acetylcholine↗
PubMedDate not supplied

Circadian distribution of hematology variables in subjects with multiple sclerosis.

Hematology variables were measured in blood samples obtained every 3h (8/24h) from 10 multiple sclerosis (MS) patients and 34 healthy subjects and analyzed for circadian characteristics using the population multiple-components method. Red blood cell (RBC) and hemoglobin levels as well as hematocrits exhibited circadian rhythms with minimal amplitudes in healthy individuals and insignificant variability in the smaller group of MS patients. In contrast the total white blood cell (WBC) and platelet counts for MS patients and healthy individuals both showed significant circadian characteristics while the mean 24h WBC and platelet levels did not significantly differ between the two groups. When the different WBC subsets were examined independently, statistically significant circadian rhythms were seen for lymphocytes and eosinophils for both MS patients and healthy individuals and for neutrophils only in the latter. Moreover, the 24h mean levels of lymphocytes, basophils, and eosinophils were significantly higher for the healthy controls while those of monocytes were higher for the MS patients. However, of all the variables tested with significant circadian rhythms in both groups of individuals, only those of lymphocyte numbers exhibited different patterns with somewhat higher amplitude in healthy individuals and a peak level occurring over an hour after that of MS patients. These changes may be the reflection of a disturbance in the regulation of patterns of lymphocyte activity and migration in MS patients. In addition, the elevation in circulating monocytes in MS patients is consistent with the inflammatory nature of the disease.

Adult↗