APC mutations.
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Adenomatous Polyposis Coli↗
Biomedical subjects
A Gordon
Publications and source records attributed to A Gordon.
Mechanisms of meat batter stabilization: a review.
Comminuted meat products are a complex mixture of muscle tissue, solubilized proteins, fat, salt, and water. The two theories that have been presented to explain meat batters stabilization are reviewed. The emulsion theory explains stabilization by the formation of a protein film around fat globules, whereas the physical entrapment theory emphasizes the role of the protein matrix in holding the fat in place during chopping and subsequent heating. However, some aspects of stabilization cannot be explained adequately by either one of these theories. In this article the role of meat proteins, aqueous phase, and lipid phase are examined in light of past and recent research findings.
Animals↗
The appearance in thyroidectomized mice of immunoglobulins that bind TSH and stimulate FRTL-5 thyrocytes.
The purpose of these studies was to examine whether thyroid stimulating antibodies in Graves' patients could arise as auto-antiidiotypic antibodies to endogenous anti-TSH antibodies. The model system chosen was the thyroidectomized mouse, exhibiting an elevated level of endogenous, circulating TSH. Mice were thyroidectomized by 131I administration. Sera samples were drawn 1 to 14 months later. The following activities were measured in the immunoglobulin (Ig) fractions prepared: (a) TSH binding by elisa techniques, (b) iodide pump activity (as measured by 99mTcO4 uptake) and (c) increased [3H]thymidine incorporation into the DNA of FRTL-5 cells. TSH binding Igs were detected in 29/98 mice thyroidectomized for 7-14 months. Stimulation of technetium uptake was observed in 59/110 mice and stimulated labeled thymidine uptake in 37/102 mice, beginning eight and nine months after thyroidectomy, respectively. Of the positive animals, 51 showed a single stimulating activity. The incidence and the serum titers of Igs that stimulate technetium uptake increased significantly with time. Indeed, in the group tested 14 months post-thyroidectomy, 75% of the sera were positive for this antibody with a mean titer eightfold higher than the controls. Hybridomas were prepared from the spleen lymphocytes of thyroidectomized mice. Of these, 18 produced 99mTcO4 uptake stimulating Igs, 12 [3H]thymidine-uptake stimulating Igs and 18 TSH binding Igs. Most of the hybridomas secreted Igs with a single bioactivity. One monoclonal antibody was isolated which neutralized the bioactivity of bTSH on FRTL-5 cells.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Glycosylated serum protein levels assayed with highly sensitive immunoradiometric assay accurately reflect glycemic control of diabetic patients.
OBJECTIVE: To develop a sensitive and reliable immunoreadiometric assay to measure glycosylated lysine residues on serum proteins (GSP) and to evaluate its efficacy in monitoring glycemic control. RESEARCH DESIGN: The effect of acute and chronic in vitro and in vivo changes in glucose levels on GSP concentration was evaluated. GSP determinations from insulin-dependent diabetic (IDDM) patients, non-insulin-dependent diabetic (NIDDM) patients, and control subjects were correlated with other indices of glycemic control. RESULTS: The GSP levels were unaffected by acute glucose changes after food or intravenous glucose administration but increased during storage at -20 degrees C due to in vitro glycosylation by endogenous glucose. Immediate acidification of the serum prevented this, permitting long-term storage despite high ambient glucose levels. In randomly selected diabetic patients, 96% of GSP values were greater than the mean +3SD of nondiabetic control subjects. In diabetic patients, GSP levels correlated with mean plasma glucose concentrations (Kendall correlation statistics 0.47, P less than 0.001), fasting plasma glucose levels (Kendall statistics 0.42, P less than 0.001), and glycosylated hemoglobin (GHb, Kendall statistics 0.30, P less than 0.005). Induction of near-normal glycemia in poorly controlled NIDDM patients reduced GSP levels with a slope consistent with a half time of disappearance of 4.7 +/- 0.4 days. GSP levels remained elevated in 6 of 10 well-controlled NIDDM patients, despite normal GHb concentrations. Chronic hypoglycemic states, like pregnancy and hyperinsulinemic hypoglycemia, were associated with significantly low GSP levels. CONCLUSION: We describe a reproducible and sensitive immunoradiometric assay for GSP that closely reflects the degree of glycemic control in diabetic patients. Further studies are needed to determine whether this assay may be useful in screening for glucose intolerance or gestational diabetes.
Blood Glucose↗
Nicotinic acetylcholine receptor desensitization is regulated by activation-induced extracellular adenosine accumulation.
Adenosine modulation of nicotinic ACh receptor (nAChR) function was studied in primary cultures of rat skeletal muscle. Activation of the nAChR by carbachol increased extracellular adenosine concentration in a dose-dependent manner. Furthermore, carbachol activation of the nicotinic receptor resulted in a twofold increase in cAMP levels in the muscle cells. The carbachol-dependent increase in cAMP levels was inhibited by adenosine receptor antagonists as well as by nicotinic receptor antagonists. These results suggest that the increased cAMP levels were due to adenosine receptor activation by the extracellular adenosine accumulated on nAChR activation. Others have shown that desensitization of the nAChR by agonist is mediated, in part, by phosphorylation. Since we found that nicotinic cholinergic agonists also cause adenosine accumulation with concomitant cAMP increases, we determined whether the accumulated adenosine has a role in desensitization. We found that the adenosine receptor antagonist, BW1434U, significantly inhibited carbachol-induced nAChR desensitization, indicating that extracellular adenosine is involved in nAChR desensitization. Our data suggest that nAChR function is regulated via a feedback mechanism mediated by adenosine released from muscle on activation of the nAChR.
Adenosine↗
Panic disorder: a clinical perspective on acute treatment and future research needs.
Panic disorder is a common disorder for which there are highly effective treatments. Patients usually present for treatment in acute distress and initially have difficulty responding to cognitive behavioral therapies. In contrast there is a high response rate to pharmacologic treatments. Cognitive behavioral techniques can be helpful in facilitating the taper and eventual discontinuation of medication and may play a role in preventing relapse. The disorder appears to have a chronic course requiring maintenance medication for at least six months. Phobic avoidance appears to be primarily a learned response and is best treated with in vivo desensitization.
Acute Disease↗
An Irish out-patient based in-vitro fertilisation service.
The first year's activity of a fully out-patient based, self financing, in vitro fertilisation service is reported. 98 couples had superovulation regimes tailored to need. 138 cycles were started. 109 retrievals were attempted using the vaginal ultrasound probe under Fentanyl and Midazolam sedation. In 106, oocytes were successfully retrieved (average seven per patient). In 80, embryos were transferred (average three). 13 patients achieved clinical pregnancies giving an overall pregnancy rate of 9.4% per cycle, 12% per oocyte retrieval, 16.5% per embryo transfer and 13% per patient who embarked on the programme. One pregnancy was ectopic, two aborted, and 10 are ongoing; this includes seven singleton foetuses and three sets of twins. All pregnant patients were referred back to their unit of origin for antenatal care and delivery.
Adult↗
Ethanol increases tyrosine hydroxylase gene expression in N1E-115 neuroblastoma cells.
Catecholamines appear to be involved in behavioral responses to acute and chronic ethanol consumption. Since tyrosine hydroxylase (TH) is the rate-limiting enzyme for catecholamine biosynthesis and is regulated by second messenger systems known to be modulated by ethanol, we studied ethanol-induced changes in TH gene expression. In the N1E-115 neural cell line, Northern and Western blot analyses showed that treatment with 25-200 mM ethanol for 3 days caused a dose-dependent increase in TH mRNA and protein levels. N1E-115 cells were also stably transfected with pTH5'CAT, a plasmid containing 773 base pairs of the TH promoter fused to a chloramphenicol acetyltransferase (CAT) reporter gene. Subclones expressing pTH5'CAT showed ethanol-induced increases in CAT activity, suggesting that ethanol modulates TH gene transcription. Furthermore, simultaneous treatment of transfected cells with 100 mM ethanol and 1 nM to 1 microM prostaglandin E1 increased prostaglandin E1-mediated stimulation of TH-promoter activity. Similarly, simultaneous treatment of transfected cells with 100 mM ethanol and either 10 mM (-)-N6-(R-phenylisopropyl)adenosine or 0.5 mM 8-bromo-cAMP also resulted in increased TH-promoter activity compared to treatment with these agents without ethanol. These results suggest that ethanol treatment of N1E-115 cells has a prominent effect on both basal and cAMP-regulated TH expression. Ethanol-induced changes in TH expression may be a critical molecular event in adaptation of the central nervous system to ethanol.
8-Bromo Cyclic Adenosine Monophosphate↗
Longitudinal study of inmates of a prison for the psychiatrically disturbed: plasma concentrations of biogenic amine metabolites and amino acids.
Plasma concentrations of eight large and neutral amino acids and 10 acidic metabolites of biogenic amines in seven inmates incarcerated in the Regional Psychiatric Centre (Praries), Correctional Service of Canada, were assessed each week day for 4 weeks (i.e., 20 samples each). Measures of central tendency and dispersion of the variables were calculated. The measures are distinctively different in their variability and their normality of distribution. The large and neutral amino acid (LNAA) measures are somewhat less variable, but also less likely to be normally distributed than most acid metabolites. Acid metabolites tend to show consistent interindividual differences that persist over time, with the notable exception of 5-hydroxyindoleacetic acid. LNAA measures tend to show differences across time but not between individuals. The distributional properties of LNAA measures are largely accounted for by the observation of a downward convergence of values of these variables over the 4 weeks of the study.
Adult↗
HIV-1 associated cognitive/motor complex in an injecting drug user.
The clinical and social consequences of AIDS dementia complex/HIV-1 associated cognitive/motor complex (ADC/HACC) in drug users have not been well documented. The value of prospective serial neuropsychological, neuroradiological and neurophysiological measurements to assist diagnosis of ADC/HACC in patients with premorbid personality disorder and intercurrent drug use is demonstrated. The psychosocial problems resulting from ADC/HACC with respect to community care and the location of hospitalization is considered. The relevance of the 1984 Mental Health Act (Scotland) with regard to drug users with ADC/HACC is discussed.
AIDS Dementia Complex↗
The role of adenosine and adenosine transport in ethanol-induced cellular tolerance and dependence. Possible biologic and genetic markers of alcoholism.
Acute exposure to ethanol in culture inhibits adenosine uptake into cells, thereby increasing the concentration of extracellular adenosine. Extracellular adenosine then reacts with adenosine A2 receptors to stimulate intracellular cAMP production. During prolonged exposure to ethanol, the increase in cAMP is followed by the development of heterologous desensitization of receptors coupled to adenylyl cyclase via Gs, the stimulatory GTP-binding protein. Ethanol-induced heterologous desensitization appears to be due to a reduction in mRNA and protein for G alpha s, a subunit of Gs. This is an example of cellular dependence on ethanol. The important implication of these findings is that a selective inhibitory effect of ethanol on adenosine uptake can lead to desensitization of diverse receptors coupled to cAMP production. Such changes could contribute to the pleiotropic effects of ethanol in the brain and other organs. Prolonged exposure to ethanol also alters the nucleoside transport system. While ethanol inhibits adenosine uptake into naive cells, ethanol no longer inhibits adenosine uptake into cells that have adapted to ethanol. This resistance to ethanol inhibition appears to be a form of cellular tolerance to ethanol. Thus, there appears to be a synergism between ethanol-induced heterologous desensitization of receptor-stimulated cAMP production (cellular dependence) and resistance to ethanol inhibition of adenosine uptake (cellular tolerance), because both lead to reduced intracellular levels of cAMP. Our studies on cAMP signal transduction in cell culture are directly relevant to the pathophysiology of human alcoholism. Heterologous desensitization of cAMP production is demonstrable in lymphocytes taken from actively drinking alcoholics; this measurement appears to be a biologic marker of active alcohol consumption. In addition, regulation of adenosine receptor-dependent cAMP production may be altered in patients at risk to develop alcoholism because of genetic factors. Thus, lymphocytes from alcoholics cultured many generations in the absence of ethanol show increased adenosine receptor-dependent cAMP production and increased sensitivity to ethanol-induced heterologous desensitization. These persistent phenotypic abnormalities in cell culture could be used as genetic markers for alcoholism. Studies are under way to test this possibility.
Adenosine↗
Long-term postthoracotomy pain.
We used a pain questionnaire to evaluate the prevalence and functional significance of long-term postthoracotomy pain. Data on 56 patients who were at least 2 months postsurgery were analyzed. Thirty patients (54 percent) with a median follow-up of 19.5 months had persistent pain; 26 others were pain free at a median of 30.5 months postthoracotomy. Pain was reported in 24 of 44 patients (55 percent) who were more than one year after surgery, 13 of 29 patients (45 percent) more than two years, six of 16 (38 percent) more than three years, and three of ten patients (30 percent) greater than four years postthoracotomy. Pain intensity was low, but 13 patients stated that pain "slightly" or "moderately" interfered with their lives. Five of 56 patients had sufficiently severe chronic pain to require either daily analgesic use, nerve blocks, relaxation therapy, acupuncture, or referral to a pain clinic. We conclude that long-term chest wall pain is common postthoracotomy. It is generally not severe, but a small proportion of patients may experience persistent, moderately disabling pain.
Chronic Disease↗
Balb/C mice immunized with either xenogeneic or syngeneic TSH produce immunoglobulins with anti-TSH and thyroid-stimulating activities.
Balb/C mice were immunized with bTSH (xenogeneic TSH) or extracts of Balb/C pituitaries (containing syngeneic TSH), either intracutaneously with Freund's adjuvant or intrasplenically. After bTSH, all blood samples contained anti-TSH antibodies. Thyroid-stimulating activity was assayed on FRTL-5 cells. Of 80 sera from immunized mice, 33 induced an increase in 99mTcO4 uptake, and 31/79 induced an increase in thyroidal 3[H]thymidine uptake by thyrocytes. With syngeneic TSH, anti-TSH antibodies were found in 10/19 mice. Immunoglobulins increasing thyrocyte technetium uptake were found in 14/19 mice, and immunoglobulins that stimulated thymidine uptake in thyrocyte DNA were detected in 12/19 sera. After immunization with both types of TSH, sera of some mice showed only one of the two bioactivities. Hybridomas were prepared with splenic lymphocytes of the mice immunized with either of the TSH preparations. These secreted TSH-binding immunoglobulins or immunoglobulins which stimulated thymidine or technetium uptake by the thyrocytes. One of the hybridomas from mice immunized with pituitary extract secreted a monoclonal antibody which stimulated thyroidal thymidine uptake, but inhibited bTSH-induced 99mTcO4 uptake. These findings might suggest that the anti-idiotypic network acting on TSH as an antigen could be involved in the pathogenesis of stimulatory antibodies in thyroid disease.
Animals↗
Helicobacter pylori (Campylobacter pylori) and duodenal ulcer.
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Campylobacter↗
Avoidable mortality risks and cultural identification among urban Native American youths.
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Child↗
5-Hydroxytryptamine and dopamine in pre-senile and senile Alzheimer-type dementia.
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Age Factors↗
Variability of ultrasonic pachometry.
We evaluated the intraobserver, interobserver, and intersession variability of the Humphrey model 580 ultrasonic pachometer. Twenty eyes (10 subjects) were measured in the intraobserver study. Forty-two eyes (21 subjects) were measured in the interobserver and intersession studies. Multiple analysis of variance revealed no statistical differences between observers or between right and left eyes. A marginally significant time (intersession) effect was found, with greater corneal thicknesses measured in the afternoon. The intraobserver variability averaged 6 microns, whereas the interobserver and intersession variabilities were approximately 11 microns and 14 microns, respectively. The relative simplicity, objectivity, and repeatability of ultrasonic pachometry should enable corneal thickness changes to be monitored in clinical practice on a more routine basis.
Adult↗
Enzyme activities in relation to pH and lactate in postmortem brain in Alzheimer-type and other dementias.
Phosphate-activated glutaminase, glutamic acid decarboxylase, pyruvate dehydrogenase, succinic dehydrogenase, pH, and lactate were measured in frontal cortex and caudate nucleus of postmortem brains from cases of Alzheimer-type dementia (ATD), Down's syndrome, Huntington's disease, and one case of Pick's disease, as well as from sudden death and agonal controls. Lactate levels were higher and pH, phosphate-activated glutaminase, and glutamic acid decarboxylase levels were lower in the agonal controls than in the sudden death controls. Phosphate-activated glutaminase and glutamic acid decarboxylase were correlated with tissue pH and lactate, and also were reduced by in vitro acidification, suggesting that the low activities of these enzymes in agonal controls were related to decreased pH consequent upon lactate accumulation. Compared with control tissues at the same pH, phosphate-activated glutaminase and glutamic acid decarboxylase were unaltered in ATD and Down's frontal cortex and reduced in Huntington's caudate nucleus, and glutamic acid decarboxylase was reduced in Huntington's frontal cortex. These data suggest that GABAergic neurons are not affected in ATD and confirm the GABAergic defect in Huntington's disease. Pyruvate dehydrogenase and succinic dehydrogenase activities were the same in agonal controls and sudden death controls and were unaffected by acid pH and lactate in vitro, and pyruvate dehydrogenase was not correlated with pH or lactate. Reduced pyruvate dehydrogenase in frontal cortex of individual ATD, Down's, and Pick's cases, and in the caudate nucleus of Huntington's and Down's cases, was accompanied by gliosis/neuron loss. We conclude that decreased pyruvate dehydrogenase reflects neuronal loss.
Alzheimer Disease↗