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Biomedical subjects

A Gordon

Publications and source records attributed to A Gordon.

At least 199 records · Page 11Linked to original sources
PubMed1987

Basal and adenosine receptor-stimulated levels of cAMP are reduced in lymphocytes from alcoholic patients.

Alcoholism causes serious neurologic disease that may be due, in part, to the ability of ethanol to interact with neural cell membranes and change neuronal function. Adenosine receptors are membrane-bound proteins that appear to mediate some of the effects of ethanol in the brain. Human lymphocytes also have adenosine receptors, and their activation causes increases in cAMP levels. To test the hypothesis that basal and adenosine receptor-stimulated cAMP levels in lymphocytes might be abnormal in alcoholism, we studied lymphocytes from 10 alcoholic subjects, 10 age- and sex-matched normal individuals, and 10 patients with nonalcoholic liver disease. Basal and adenosine receptor-stimulated cAMP levels were reduced 75% in lymphocytes from alcoholic subjects. Also, there was a 76% reduction in ethanol stimulation of cAMP accumulation in lymphocytes from alcoholics. Similar results were demonstrable in isolated T cells. Unlike other laboratory tests examined, these measurements appeared to distinguish alcoholics from normal subjects and from patients with nonalcoholic liver disease. Reduced basal and adenosine receptor-stimulated levels of cAMP in lymphocytes from alcoholics may reflect a change in cell membranes due either to chronic alcohol abuse or to a genetic predisposition unique to alcoholic subjects.

Adult↗
PubMed1987

T3 stimulation of 2-deoxy-D-glucose uptake in cultured chick embryo carcass derived cells, requires neosynthesis of proteins.

T3 stimulated, in a dose dependent manner, the uptake of 2-deoxy-D-glucose (2-DOG) into cultured chick embryo carcass derived cells. A significant increase in sugar uptake was seen already at a T3 concentration of 1 pmol/l. The stimulation of 2-DOG uptake increased with time during the 6 h of exposure to T3. The hormone also stimulated, within 45 min, the incorporation of [3H]leucine and [3H]uridine into the trichloroacetic acid precipitable material of these cells. Actinomycin-D (100 micrograms/l) and cycloheximide (1 mg/l) each were capable of blocking the stimulatory effect of 10(-8) mol/l T3 on sugar uptake and on uridine and leucine incorporation. Thus, T3 in these cultured chick embryo cells stimulated sugar transport through processes dependent on neosynthesis of proteins. In this respect the effect of T3 is different from that seen in cultured chick embryo cardiomyocytes.

Animals↗
PubMed1987

TSH binding proteins in rat and human serum.

When serum of hypothyroid rats was fractionated on a Sephadex G-100 column, most of the immunoreactive TSH was found as a front running peak, together with the high molecular weight serum proteins. Similarly, a rTSH preparation (10 mU), chromatographed in the presence of 1 ml of normal rat serum also migrated at the front, however, when a high load of TSH (4.4 U) was added to 1 ml of serum, two immunoreactive peaks were found, suggesting the saturation of the front running fraction. Immunoelectrophoresis and autoradiography of rat or human sera containing the respective 125I-labelled TSHs showed binding of the labelled TSH to IgG, alpha-2-macroglobulin, and to a third unidentified protein, migrating near the albumin line. In order to determine if the bound TSH is biologically active, the high molecular weight protein fraction was separated from hypothyroid rat serum by 45% ammonium sulphate precipitation. Immunoreactivity was determined by RIA and the biological activity was determined, in vitro, by the stimulation of 99Tc uptake by FRTL-5 cells. The 45% ammonium sulphate precipitate contained almost all of the immunoreactivity and the bioactivity of the TSH of whole serum. These results indicate that: a) The endogenous circulating TSH in the hypothyroid rat exists mainly in a protein-bound form and this protein-bound TSH contains most of the hormonal bioactivity of the serum. b) Exogenous TSH binds to serum proteins in euthyroid and hypothyroid rats and in humans. There are three protein fractions in these sera that bind TSH, one of which is an immunoglobulin. The occurrence of TSH binding immunoglobulins may involve autoimmune mechanisms.

Animals↗
PubMed1987

2'-nor-cGMP, a new cyclic derivative of 2'NDG, inhibits HSV-1 replication in vitro and in the mouse keratitis model.

The present study examined the antiherpetic effect of 2'-nor-cGMP, a new cyclic phosphate derivative of 2'NDG, in vitro and in the mouse keratitis model. The 50% inhibitory dose (ID50) was determined with HSV-1 RE strain in Vero cell monolayers for 2'-nor-cGMP (6.9 mcg./ml), 2'NDG (.06 mcg/ml), and trifluridine (F3T) (.72 mcg/ml). Balb C mice underwent bilateral ocular inoculation with HSV-1 RE strain, and then were treated with different therapeutic regimens. The antiviral efficacy of each drug was evaluated by ocular virus titers, clinical grading of epithelial keratitis, and histological evaluation of stromal keratitis. 2'-nor-cGMP was the most effective drug (P = .0001) in reducing ocular viral titers. Both 2'-nor-cGMP and 2'NDG were significantly more effective (P = .0001) than F3T in reducing epithelial keratitis, and as effective as F3T in reducing stromal keratitis.

Acyclovir↗
PubMed1986

Regional brain 5-hydroxytryptamine levels are reduced in senile Down's syndrome as in Alzheimer's disease.

5-Hydroxytryptamine (5-HT) and choline acetyltransferase (ChAT) were assayed in amygdala, cingulate cortex and caudate nucleus of post-mortem brains from 7 cases of Down's syndrome (6 with the neuropathological features of Alzheimer's disease and one with no such features), 9 cases of Alzheimer's disease and 12 controls. 5-HT was markedly reduced in all 3 areas of the pathologically affected Down brains, unaltered in the Down brain with no Alzheimer pathology and reduced in the amygdala and cingulate cortex of the Alzheimer brains. ChAT showed a similar pattern of reduction. These results supply biochemical evidence that 5-hydroxytryptaminergic, as well as cholinergic, neurons are reduced in Down's syndrome with Alzheimer pathology.

Adult↗
PubMed1986

Autoantibodies to Alzheimer and normal brain structures from virus-transformed lymphocytes.

B-Lymphocytes from two patients with Alzheimer's disease and one healthy subject were transformed into lymphoblastoid cells by exposure to Epstein-Barr virus. In culture, more than 50% of these cells secreted sufficient IgM or IgG antibody (mainly IgM) to allow immunohistochemical screening against cryostat sections of normal and Alzheimer temporal cortex. More than 30% of the IgM antibodies from each subject recognised brain components, namely: neurons, astrocytes, nuclei, nucleoli, and Alzheimer plaques and neurofibrillary tangles. This methodology represents a major addition to the procedures currently available for the generation of antibodies towards normal and pathological structures in human brain.

Alzheimer Disease↗
PubMed1986

Adaptation during surgical stress. A reevaluation of the role of glucocorticoids.

Pharmacologic doses of glucocorticoids are administered to patients with adrenal insufficiency during operative procedures to prevent hemodynamic instability, cardiovascular collapse, and death. Since these supraphysiologic doses might not be necessary and might have adverse effects, we examined the effects of different doses of glucocorticoids on hemodynamic adaptation during surgical stress in adrenalectomized primates. Sham-adrenalectomized placebo-treated animals served as controls. Adrenalectomized monkeys were maintained for 4 mo on physiologic glucocorticoid and mineralocorticoid replacement. The adrenalectomized monkeys were then stratified into three groups receiving, respectively, subphysiological (one-tenth the normal cortisol production rate), physiological, or supraphysiological (10 times the normal cortisol production rate) cortisol (hydrocortisone) treatment. 4 d later a cholecystectomy was performed. The intraoperative hemodynamic and metabolic parameters, perioperative survival rates, and postoperative wound healing were compared. The subphysiologically treated group was hemodynamically unstable before, during, and after surgery and had a significantly higher mortality rate than control. In this group, arterial blood pressure was low, and the cardiac index, systemic vascular resistance index, and left ventricular stroke work index were all reduced, suggesting decreased cardiac contractility and blood vessel tone. In contrast, the physiologically replaced group was indistinguishable from either supraphysiologically treated animals or sham-operated controls. All groups had similar metabolic profiles and normal wound healing. These findings suggest that the permissive actions of physiologic glucocorticoid replacement are both necessary and sufficient for primates to tolerate surgical stress. Supraphysiological glucocorticoid treatment has no apparent advantage during this form of stress in the primate.

Adaptation, Physiological↗
PubMed1986

The stimulation of sugar transport in heart cells grown in a serum-free medium by picomolar concentrations of thyroid hormones: the effects of insulin and hydrocortisone.

Chick embryo heart cells were propagated in a defined serum-free medium. They formed a confluent, synchronously contracting monolayer that is not different from myocytes grown in serum containing media. The uptake of 2-deoxy-D-[1-3H]glucose in these cells was stimulated by exposure to physiological concentrations of T3 (1 pM) and T4 (10 pM). Actinomycin-D and puromycin did not block the stimulation of 2-deoxy-D-[1-3H]glucose uptake when given with T3 throughout a 6-h incubation period. Cells grown in the absence of both insulin and hydrocortisone were unresponsive to T3. Insulin at 200 nM restored the sensitivity of the cells to 0.1 pM T3. Addition of 10 nM hydrocortisone to the growth medium enhanced the effects of T3 synergistically. The T3-stimulated sugar uptake was completely blocked by 5 X 10(-6) M cytochalasin B, suggesting that T3 acts, like insulin, by the translocation of glucose transporters to the plasma membrane.

Animals↗
PubMed1986

Report of a randomised pilot study of the treatment of patients with supratentorial gliomas using neutron irradiation.

A randomised pilot study is reported of d(15)+Be neutrons compared with 4 MV photons in the treatment of patients with astrocytoma. Sixteen patients were treated by photons and 18 by neutrons. Both treatments were well tolerated by patients. The median survival after photons was 11 months and after neutrons, 7 months. It was demonstrated that four of nine patients treated by neutrons had evidence at autopsy of radiation-induced brain damage. All had residual cancer. No patient treated by photons had signs of radiation-related morbidity. The trial was, therefore, discontinued prematurely.

Adolescent↗
PubMed1986

The results of a randomised trial of mixed-schedule (neutron/photon) irradiation in the treatment of supratentorial Grade III and Grade IV astrocytoma.

A randomised trial is reported of mixed-schedule (neutron/photon) irradiation compared with photon therapy for patients with Grade III or Grade IV astrocytoma. Thirty-one patients were allocated to be treated by the neutron/photon regime and 30 patients by photons. The median survival was 4 months in the mixed-schedule group and 8 months in the photon group. The survival rates were not significantly different. All patients who died had evidence of residual brain tumour. None had signs of radiation-related morbidity.

Adolescent↗
PubMed1986

A phase I study of mixed (neutron and photon) irradiation using two fractions per day in the treatment of high-grade astrocytomas.

A Phase I study of the treatment of 50 patients with high-grade astrocytomas by mixed schedule (neutron and photon) irradiation given in 12 fractions over 4 weeks is reported. The neutron and photon fractions were separated each day by 2-3 h. A total neutron dose of 6.36 Gy (8% gamma) and 20.40 Gy of photons was prescribed. Treatment was well tolerated and there was no clinical evidence of radiation-related morbidity in the brain. The median survival was 6.9 months, similar to that expected after photon irradiation alone. A multivariate analysis of prognostic variables in presented.

Brain Neoplasms↗
PubMed1985

The community residential treatment service: developing a continuum of prosthetic environments for the chronically disabled.

Among the many issues regarding the care of chronic mental patients, none is more pressing than the need for administrative and clinical models designed to organize and systematize the efforts of diverse community service providers. This paper describes the functioning of the Community Residential Treatment Service of the South Beach Psychiatric Center, a large-scale project of a state facility created to respond to this tissue. By blending sophisticated clinical and administrative technology, programs operated by the state, voluntary, and proprietary health care sectors have been integrated to form a balanced service delivery system. This system provides a broad continuum of inpatient and outpatient residential settings developed in accordance with social learning principles. The components of the system, with the Community Residential Treatment Service as the major integrative force, are linked together by detailed contracts as well as common behavioral clinical and behavioral administrative language. The treatment successes f this system have been significant enough to suggest that a positive synergistic effect is generated by this programming combination.

Community Mental Health Services↗
PubMed1985

Biochemical studies on rabbits with aluminium induced neurofilament accumulations.

The activities of acid phosphatase, hexosaminidase, beta-galactosidase, Mg2+-stimulated Na+K+ATPase, fumarase and ATP:citrate lyase were measured in grey matter of rabbit spinal cord 7-8 days after intra-ventricular or intra-cisternal injection of aluminium. RNA, DNA, and water content were measured in whole spinal cords. Choline acetyltransferase (CAT) and acetylcholinesterase were assayed in dorsal grey matter of the cord, which contained no aluminium-induced neurofilament accumulations (NFAs), and ventral grey matter, which had large numbers of such NFAs. CAT was also assayed in the hypoglossal nerve. None of these measures were consistently altered in the aluminium treated rabbits, although the activity of beta-galactosidase was increased in the NFA-free caudate nucleus of rabbits given aluminium intra-ventricularly, possibly due to the presence of phagocytes on the ventricular surface of the caudate. It is concluded that neither aluminium nor its induced NFAs has a gross effect on neuronal metabolism within 7-8 days.

ATP Citrate (pro-S)-Lyase↗
PubMed1985

Increased proteins in post-mortem brain in a case of Pick's disease and in Huntington's disease.

Soluble proteins from temporal cortex and caudate nucleus from a case of Pick's disease, 5 cases of Huntington's disease and 5 controls were analysed by SDS-polyacrylamide gel electrophoresis. Acidic proteins of molecular weight 39 000-42 000, which showed glial fibrillary acidic protein immunoreactivity, were increased in temporal cortex of the Pick's case. Proteins of these molecular weights were also increased in caudate nucleus of the Huntington's cases. Our results show that the astrocytic gliosis observed in temporal cortex in Pick's disease and in caudate nucleus in Huntington's disease is associated with qualitatively similar increased amounts of soluble glial fibrillary acidic protein.

Aged↗
PubMed1985

Reductions in soluble brain proteins in older subjects with Down's syndrome.

Soluble proteins from temporal cortex and caudate nucleus from 6 cases of Down's syndrome (5 aged over 50 and 1 aged 27 years) and 7 controls were analysed by sodium dodecyl sulphate-polyacrylamide gel electrophoresis. In older Down's syndrome cases, reductions in tubulin and 5 other proteins were observed in cortex which had the neuropathology of Alzheimer's disease but not in caudate nucleus. No protein changes or neuropathological features of Alzheimer's disease were found in the youngest Down's syndrome case. The protein changes appear to be associated with the neuropathological features of Alzheimer's disease and not with Down's syndrome itself.

Adult↗
PubMed1985

Neurotensin immunoreactivity in post-mortem brain is increased in Down's syndrome but not in Alzheimer-type dementia.

Neurotensin immunoreactivity and choline acetyltransferase (ChAT) activity were measured in post-mortem brain from 10 cases of Down's syndrome (7 aged 53-63 years, one aged 27 years, one aged 16 months and one aged 10 months), 6 cases of Alzheimer-type dementia (ATD) and 19 control subjects (13 aged 40-88 years and 6 aged 9-18 months). Neurotensin concentrations in anterior and basal hypothalamus, amygdala, septal area, caudate nucleus and temporal cortex were unaltered in ATD. The concentrations of neurotensin were significantly increased in the caudate nucleus, temporal cortex and frontal cortex in the cases of Down's syndrome aged 53-63 years with the neuropathological features of ATD, and were also increased in the cerebral cortex of the 27-year-old, which did not have the neuropathological features of ATD, and in two infant Down's cases. ChAT activity was reduced in the ATD and the 53-63-year-old cases of Down's syndrome, but not in the 27-year or 10-month-old Down's cases. The increased neurotensin concentrations appear to be a feature of Down's syndrome not related to the presence of plaques and neurofibrillary tangles or to a deficit in ChAT activity.

Adult↗
PubMed1985

Reduced proteins in temporal cortex in Alzheimer's disease: an electrophoretic study.

Cytoplasmic and pellet fractions from post-mortem temporal cortex from eight cases of neuropathologically confirmed Alzheimer's disease, one case of cerebrovascular dementia, and five controls were examined by sodium dodecylsulphate-polyacrylamide gel electrophoresis. No differences were observed in the cytoplasmic proteins from the five controls and the case of cerebrovascular dementia. In five cases of Alzheimer's disease with neurone loss, there was a major loss of a cytoplasmic 55,000-dalton protein identified as tubulin and variable reductions in cytoplasmic proteins of molecular weights of 28,000, 30,000, 92,000, and 200,000 daltons. Three cases of Alzheimer's disease had no detectable neurone loss; two of these cases had protein patterns indistinguishable from the controls and one showed some reduction in soluble tubulin only. These results indicate that decreases of particular proteins in the temporal cortex in Alzheimer's disease may be associated with neurone loss.

Adult↗