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Biomedical subjects

E M Allen

Publications and source records attributed to E M Allen.

At least 73 records · Page 4Linked to original sources

The effect of iodide ingestion on the development of spontaneous lymphocytic thyroiditis in the diabetes-prone BB/W rat.

It has been suggested that the incidence of Hashimoto's thyroiditis is increased in the presence of high iodide intake. The diabetes-prone BB/W rat develops spontaneous histological autoimmune lymphocytic thyroiditis (LT) without functional hypothyroidism between 60 and 120 days of age. Studies were carried out to determine whether iodine administration to BB/W rats would affect the incidence and severity of LT and induce hypothyroidism. Iodide (0.05% in water) or tap water (C) was administered ad libitum to 42 10-month-old BB/W rats and 71 30-day-old BB/W rats for 8 weeks. For control purposes, 0.05% iodide or tap water (C) was also administered ad libitum to 42 30-day-old nondiabetic and non-LT-prone BB/W genetically equivalent rats (W-line) for 12 weeks and 41 21-day-old Wistar rats for 7 weeks. In a separate experiment, weanling BB/W rats were fed a low iodine diet, a control iodine-sufficient (C) diet, or Purina chow (P) and tap water ad libitum for 8 weeks. In each experiment, blood was obtained at the time of death for the measurement of serum T4, T3, TSH, and antithyroglobulin antibody (anti-Tg Ab), and the thyroids were removed for histological evaluation (0 = no LT; 1-4 = LT). Iodide administration (0.05%) induced a significant increase in the incidence of LT in 30-day-old BB/W rats (I, 77%; C, 30%, P less than .001). Thyroid weight and serum T4, T3, and anti-Tg Ab concentrations were not affected by iodide administration. However, the presence of LT was associated with a significant increase in thyroid weight and anti-Tg Ab concentrations. BB/W rats subjected to a low iodine diet exhibited a significantly decreased incidence of LT (low I, 8.6%; C, 47.3%; P less than 0.01), but no statistically significant difference in anti-Tg Ab levels. Increased iodide intake did not significantly affect the incidence of LT in adult BB/W rats and did not induce LT or affect thyroid function in W-line or Wistar rats. These data show that iodine intake significantly affects the incidence of spontaneous LT in young, genetically predisposed rats.

Animals↗

The assessment of two methods for removing eye movement artefact from the EEG.

A quantitative assessment of both computerised correlation and analogue techniques for the removal of eye movement artefact from the electroencephalogram was undertaken. In both methods a fraction of the measured EOGs was subtracted from the measured EEG to leave the corrected EEG. In the correlation method the correction factors were computed from the cross-correlations of the EOGs and measured EEGs. In the analogue method the fraction subtracted was derived using a potential divider arrangement. The relative effectiveness of the two methods was determined by comparing the autocorrelation functions of the corrected EEGs at a lag of 2 sec. It was found that the computerised correlation technique was superior. A 3-channel EOG correlation correction procedure was found adequate in which two horizontal and one vertical EOGs were used. The analogue technique was very time consuming and possibly erroneous.

Electroencephalography↗

The effect of activated charcoal and hyoscine butylbromide alone and in combination on the absorption of mefenamic acid.

Mefenamic acid 500 mg orally was administered to nine healthy volunteers on four occasions 7 days apart. On two occasions allocated at random, activated charcoal (2.5 g of medicoal) was administered 1 h after the drug. Hyoscine butylbromide (20 mg intramuscularly) was given immediately after mefenamic acid on one of these occasions, and on one occasion after mefenamic acid without charcoal. Hyoscine significantly delayed the time to maximum mefenamic acid concentrations but did not affect the area under the plasma concentration-time curve. Charcoal reduced the area under the plasma concentration curve by 36% and charcoal and hyoscine reduced the area under the plasma concentration curve by 42% from their respective control values. We conclude that early charcoal administration in a ratio of 5 g to 1 g of drug effectively reduces the area under the plasma concentration-time curve after oral mefenamic acid administration. Early charcoal administration may be of value therefore in reducing the toxicity of mefenamic acid after deliberate or accidental overdosage.

Adolescent↗

Comparison of the effects of therapeutic doses of meptazinol and a dextropropoxyphene/paracetamol mixture alone and in combination with ethanol on ventilatory function and saccadic eye movements.

The respiratory and psychomotor effects of a single oral dose of meptazinol (200 mg) and dextropropoxyphene (65 mg)/paracetamol (650 mg) mixture, was compared alone and in combination with ethanol (0.8 g kg-1). Peak saccade velocity following meptazinol or the dextropropoxyphene/paracetamol mixture was not significantly different from placebo. When each of the treatments was followed by ethanol administration, a significant decrease in saccade velocity (P less than 0.01) was seen. Given alone, neither of the analgesic drugs produced a significant change in the slope of the ventilatory response to hypercapnia. Ethanol did not affect the ventilatory response to hypercapnia when given alone or in combination with meptazinol, but when given with the dextropropoxyphene/paracetamol mixture, a significant reduction in the slope of the ventilatory response to hypercapnia occurred at 1.5 h (P less than 0.05) and 2 h (P less than 0.01) after administration of the analgesic drug. No pharmacokinetic interaction was demonstrated between ethanol and meptazinol or the dextropropoxyphene/paracetamol mixture in the doses used. In contrast to meptazinol, the dextropropoxyphene/paracetamol mixture interacts with ethanol on the ventilatory function.

Acetaminophen↗

Hemolytic plaque inhibition by synthetic antigenic peptides of sperm whale myoglobin.

We have investigated the systemic antibody response to sperm whale myoglobin (SWMb) antigenic sites in three strains of inbred mice using an inhibition of plaque assay. Sperm whale myoglobin was attached to sheep red blood cells (SRBC) via rabbit anti-SRBC Fab' fragments. Inhibition of lysis was obtained with synthetic peptides representing the purported five antigenic sites but not with a peptide whose sequence was unrelated to SWMb and synthetic peptides of SWMb from outside the antigenic sites gave minimal or no inhibition. The results of our studies show that the pattern of response to the five antigenic sites differs in each strain, but that almost total inhibition is obtained in all strains with these five sites. The antigenic dominance of these sites supports the concept of discrete antigenic sites on soluble proteins. They also suggest a reason for contrary reports in the literature based on hybridoma technology.

Animals↗

Adaptive equipment for C6 quadriplegia: an approach to effective, simple, and inexpensive devices.

Three simple and inexpensive devices were developed by a man with complete C6 quadriplegia to increase his independence: a reacher that allows him to lift and move objects ranging in size from ballpoint pens to beverage cans; a wrist splint that permits him to open pop-top cans, dial a telephone, open a drawer, and page through a book; and an implement holder that stabilizes small devices.

Adult↗

Immunogenetics of BCG-induced anergy in mice: control by genes linked to the Igh complex.

The genetics of BCG-induced anergy was studied in mice by evaluating delayed hypersensitivity to sheep erythrocytes. Data obtained using congenic mice and by linkage analysis suggested that genes linked to the H-2 complex do not influence the development of anergy. However, studies in allotype-congenic partners (BALB/c; BALB.Igb) indicated that anergy was influenced by genes linked to the immunoglobulin heavy chain complex (Igh). Breeding studies indicated that the gene influencing anergy is recessive. These studies were extended by using BXD recombinant inbred mice, and verified that anergy is controlled by genes linked to the Igh complex. Because several markers and a tentative map has been constructed for the Igh complex on chromosome 12 in BXD mice, we suggest that the gene that controls BCG-induced anergy is located on the centrometric side of Igh-C approximately 18 to 28 recombination units.

Animals↗

Acute fatal pneumonia in calves due to respiratory syncytial virus.

An acute pneumonia developed in 28 calves which had been housed together from one to two weeks of age. The clinical signs included pyrexia, tachypnoea, respiratory distress and coughing. Some of the calves died. The pneumonia was characterised by an alveolitis with multinucleated syncytia, alveolar epithelial hyperplasia and bronchiolitis. Interstitial emphysema was also present. Fifteen of 19 calves examined serologically had rising neutralising antibody titres to respiratory syncytial virus; in nine calves the rise was fourfold or greater. Respiratory syncytial virus was not isolated from the calves. There was no evidence of parainfluenza type 3 virus involvement. The adult cows being sucked by the calves remained clinically normal throughout the incident. Six calves examined six weeks after the outbreak started had a chronic cuffing pneumonia characterised by lymphocytic bronchiolitis; some of the calves also had bronchiolitis obliterans. Mycoplasma dispar was found in two of them.

Acute Disease↗

Genetic basis of BCG-induced suppression of delayed hypersensitivity.

BCG can either act as an adjuvant to potentiate immunological responses or, in some cases, can induce suppression. The reasons for these differential activities are not clear but may include routes and doses of administration, as well as variable host reactivity to the agent. In this study, we have used killed BCG administered intravenously to produce chronic granulomatous inflammation (CGI) in the lungs and spleen of inbred mice. We report that strains which develop CGI were usually anergic, as evaluated by the development of delayed hypersensitivity (DH) to sheep erythrocytes (SRBC). Studies on the genetics of BCG-induced anergy indicated that it was unigenic, recessive and linked (approximately 28 recombination units) to the immunoglobulin heavy-chain allotype (Igh). There was no influence by genes linked to the major histocompatibility complex. The study indicates that anergy associated with CGI is under genetic control, which may explain the variability of anergy in patients with granulomatous diseases. The implication of linkage to the Igh complex is not clear, but it may be associated with VH receptors on T lymphocytes, which in turn act on macrophages to mediate suppression.

Animals↗

Strain variation in BCG-induced chronic pulmonary inflammation in mice: control by a cyclophosphamide-sensitive thymus-derived suppressor cell.

We previously reported that only certain strains of inbred mice develop intense chronic granulomatous inflammation (CGI) in the lungs and spleen in response to an i.v. injection of killed BCG in an oil-in-saline emulsion (BCG-E). The capacity to respond did not appear to be controlled by genes within the H-2 complex; subsequent studies have shown that genes linked to the Igh allotype complex influence the development of CGI. In other systems, unresponsiveness to certain antigens has been shown to be because of cyclophosphamide- (Cy) sensitive suppressor cells. We therefore used Cy as a probe to study mechanisms of unresponsiveness in low-responder (LR) CBA mice. The results indicate that LR mice could be converted into high responders (HR) by treatment with 100 mg of Cy per kilogram of body weight 2 days before injection with BCG-E. In addition, the effects of Cy were inhibited by the provision of syngeneic whole or purified spleen T cells from mice injected 7 days previously with BCG-E. Cells responsible for abolition of the Cy effect were sensitive to anti-Thy-1 serum + C. Thus, the intensity of BCG-E-induced CGI in mouse lungs is controlled by a population of Cy-sensitive T lymphocytes.

Animals↗

Methohexitone-induced convulsions in epileptics.

The risk of precipitating a convulsion in epileptic patients with methohexitone has been judged to vary widely. This article reports such complications arising during methohexitone-activated E.E.G. recording in a series of 48 epileptic patients from whom anticonvulsant medication was withheld. Two patients developed grand mal convulsions during induction with methohexitone 1-0%. Two others exhibited status epilepticus of the petit mal type and one of the myoclonic type, after stopping an infusion of 0-09% methohexitone. The specificity for methohexitone-induced convulsions in epileptics or crypto-epileptics is supported by a review of the literature.

Adolescent↗