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Biomedical subjects

J Patrick

Publications and source records attributed to J Patrick.

At least 199 records · Page 11Linked to original sources
PubMed1980

Linkage between the frequency of muscular weakness and loci that regulate immune responsiveness in murine experimental myasthenia gravis.

Mice immunized with acetylcholine receptor (AChR) purified from Torpedo californica form anti-AChR antibodies and often develop muscular weakness and flaccid paralysis closely resembling the human disease myasthenia gravis. This condition, termed experimental myasthenia gravis (EMG), is strain dependent in that the frequency of paralysis is much greater in some strains than in others. Differences in the frequency of EMG might result from differences in the immune system or the neuromuscular junction. In these studies, we have identified two loci, the major histocompatibility complex (H-2) region on chromosome 17 and the region that contains the structural genes for the constant region of immunoglobulin heavy chains (IgCH region) on chromosome 12, which significantly effect the probability with which a mouse immunized with T. californica AChR can be expected to become paralyzed. One genotype (H-2b, Ig-1b) correlated with high susceptibility to EMG in four strains with three dissimilar backgrounds. These studies demonstrate that susceptibility to EMG is a heritable trait determined by at least two distinct loci that are linked to regions of the mouse genome that regulate immune responsiveness.

Animals↗
PubMed1980

Nutritional oedema.

Explore the source record for details and available documents.

Cell Membrane Permeability↗
PubMed1980

A definition of human fetal apnea and the distribution of fetal apneic intervals during the last ten weeks of pregnancy.

Fetal breathing movements were studied over 24-hour observation periods for a total of 744 hours in 31 healthy pregnant women at 30 to 39 weeks' gestational age. An analysis of 165,786 breath-to-breath intervals in eight fetuses demonstrated that 97% of breath-to-breath intervals were less than 6 seconds in duration. It was concluded that a breath-to-breath interval of 6 seconds or more is a rational definition of fetal apnea during the last 10 weeks of pregnancy. An analysis of intervals during which time no fetal breathing activity occurred in the 31 fetuses demonstrated that prolonged episodes of apnea were distributed in a similar fashion at different gestational ages. The longest periods of apnea were 65 minutes at 30 to 31 weeks, 105 minutes at 34 to 35 weeks, and 120 minutes at 38 to 39 weeks. No periods of apnea of more than 45 minutes were measured during the second and third hours following maternal meals. A useful strategy for recognition of significant fetal apnea would be to make observations during the second and third hours following maternal meals when apneic lengths greater than 45 minutes were not observed in this highly selected group of normal fetuses.

Apnea↗
PubMed1980

Circadian rhythms in maternal plasma cortisol and estriol concentrations at 30 to 31, 34 to 35, and 38 to 39 weeks' gestational age.

In order to examine the relationship between circadian rhythms in different steroids, cortisol and estriol were measured by radioimmunoassay in maternal venous plasma taken at 30- to 60-minute intervals over 24 hours from nine healthy women at 30 to 31, 11 at 34 to 35, and 10 at 38 to 39 weeks' gestation. Maternal cortisol was maximal at 0730 to 0830 hours and fell significantly to its lowest concentration between 1830 and 0130 hours. At 30 to 31 and 34 to 35 weeks there was a significant circadian rhythm in estriol concentrations which was inversely related to the circadian rhythm in cortisol. At 38 to 39 weeks mean estriol concentrations were significantly higher than those at 30 to 31 and 34 to 35 weeks but there was no significant circadian pattern. We concluded that there is an inverse relationship between maternal cortisol and estriol at 30 to 31 and 34 to 35 weeks, which would be consistent with a maternal effect on fetal adrenal function. The increase in mean concentration and absence of circadian rhythm in maternal plasma estriol at term might suggest an additional positive stimulus to fetal adrenal function. The existence of patterns in maternal estriol concentrations must be taken into account in the u;se of sequential measurements of this hormone during the last 10 weeks of pregnancy.

Circadian Rhythm↗
PubMed1980

Binding properties of a neurotoxin from the venom of the green mamba, Dendroaspis viridis.

A toxin, alpha-mambatoxin, was purified from the venom of the green mamba Dendroaspis viridis using the procedures of Shipolini et al. (Shipolini, R. A., Bailey, G. S., Edwardson, J. A., and Banks, E. C. (1973) Eur. J. Biochem. 40, 337-344). The purified toxin blocks agonist-induced activation of acetylcholine receptors on muscle cells but, like alpha-bungarotoxin, it does not affect agonist-induced activation of receptors on a clonal sympathetic nerve cell line (PC12), an endothelial cell line, cultured chick ciliary ganglion neurons, or frog cardiac ganglion neurons. The toxin does block binding of alpha-bungarotoxin to cultures of muscle and nerve, and iodinated alpha-mambatoxin binds to cultures of muscle and nerve. The alpha-mambatoxin binding component on muscle was identified as acetylcholine receptor on the basis of sedimentation, immunoprecipitation, and rate of degradation. The alpha-mambatoxin binding component on PC12 cells, like the alpha-bungarotoxin binding component on these cells, is not recognized by anti-acetylcholine receptor antisera which do recognize acetylcholine receptor on these cells. The number of alpha-mambatoxin binding sites on both nerve and muscle when assayed in situ is twice that of alpha-bungarotoxin binding sites. However, when muscle cells are solubilized in nonionic detergents and then labeled with toxins, the number of alpha-mambatoxin binding sites is reduced and the two toxins bind in equal molar amounts. Finally, unlike alpha-bungarotoxin, which dissociates from complexes formed with nerve, alpha-mambatoxin forms complexes with nerve which dissociate only very slowly if at all.

Animals↗
PubMed1980

Experimental myasthenia gravis. A murine system.

Mice from eight inbred strains were immunized with acetylcholine receptor (AChR) purified from Torpedo californica. All mice developed high concentrations of serum antibodies (10(-6) M) against the immunogen and approximately 80% possessed antibodies reactive with mouse nicotinic AChR. 33% of the mice immunized (n = 236) developed muscular weakness and flaccid paralysis. Behavioral, electrophysiological, and pharmacological similarities were found between the experimentally induced muscular weakness and the disease myasthenia gravis. Susceptibility to experimental myasthenia was found to be strain dependent in that the frequency of paralysis was much greater in some strains than others. The occurrence of muscular weakness and flaccid paralysis did not correlate with the concentration of antibodies reactive with T. californica or mouse AChR. Anti-receptor antibodies which increased the rate of AChR degradation on the mouse muscle cell line, BC3H-1, were found in the serum of both myasthenic and nonmyasthenic mice. 40% of the mice tested possessed antibodies reactive with antigenic determinants present on mouse receptor but not T. californica receptor. The occurrence of antibodies unique to mouse receptor did not correlate with myasthenia. Thus, myasthenia in the mouse does not occur simply as a consequence of the presence of antibodies directed against cell surface antigenic determinants of AChR. If anti-AChR antibodies are both necessary and sufficient for the induction of myasthenia, then these studies suggest that populations of a particular structure and/or specificity are required. It is anticipated that the mouse model of myasthenia gravis will permit the regulation of the anti-receptor immune response to be studied in detail.

Acetylcholine↗
PubMed1980

Nerve growth factor mediates phosphorylation of specific proteins.

Nerve growth factor (NGF), epidermal growth factor (EGF), insulin, cholera toxin (CT) and cAMP all stimulate the phosphorylation of proteins in the PC12 nerve-like cell line. NGF, CT and cAMP enhance phosphorylation of the same set of proteins including tyrosine hydroxylase, ribosomal protein S6, histones H1 and H3, and the nonhistone chromosomal and cytoplasmic high mobility group (HMG) 17 protein, and reduce phosphorylation of H2A. EGF but not insulin enhances the phosphorylation of tyrosine hydroxylase. Insulin but not EGF enhances the phosphorylation of histone H3 and decreases the phosphorylation of H2A. EGFD and insulin each enhance phosphorylations of both ribosomal protein S6 and histone H1, but neither hormone induces phosphorylation of HMG 17. The extent of these effects depends upon the ligand concentration and is half-maximal at physiological concentrations of the hormones (beta-NGF, 2 ng/ml; EGF, 1 ng/ml. insulin, 0.5 microunits/ml). Maximal effects of NGF are seen within 15 min and persist even after 3 days of culture in the presence of NGF. When phosphorylation of ribosomal protein S6 is maximally stimulated by NGF, no further stimulation can be achieved by adding saturating quantities of either cAMP or CT. However, simultaneous addition of saturating quantities of NGF and either EGF or insulin results in an enhancement of phosphorylation that is equal to the sum of that achieved when the two ligands are added separately. These results suggest that the enhanced phosphorylation of S6 achieved by NGF or cAMP occurs through a common mechanism which differs from those which mediate EGF or insulin-enhanced phosphorylation. The data also provide strong evidence that the action of NGF included protein phosphorylation mediated by cAMP-dependent protein kinase. The phosphorylation of each of these proteins in response to NGF may play an important role in NGF action.

Animals↗
PubMed1980

Time series analysis of human foetal breathing activity at 30-39 weeks gestation.

Thirty-one healthy human fetuses were each observed with a real-time scanner continuously for 24 h. The percentage of time spent breathing was computed for each 5 min observation period during the 24 h which produced a time series of 288 observations for each fetus. Box-Jenkins modelling techniques and analysis of frequency spectrum distribution were used to quantify mathematically the human fetal breathing data. The data was described mathematically by a first-order auto-regression z(t)=0.7 z(t-1) + epsilon(t) which confirmed and quantified the episodic nature of foetal breathing activity. Evaluation of the spectral distribution of the fetal breathing movements identified a significant band of pseudo-periodic components with repeat periods ranging from 100 to 500 min (P less than 0.001). Results of this study indicated that the occurrence of fetal breathing movements were non-random and that Box-Jenkins modelling results and spectral power distribution may be useful in identification and description of any fetal breathing patterns which differ from normal patterns.

Female↗
PubMed1980

Zinc transport in normal human leucocytes: dependence upon media composition.

1. The transport of zinc has been studied in normal human leucocytes incubated in both a tissue culture medium and Krebs buffer. 2. 65Zn influx is characterized by an initial rapid phase followed by a slower influx. 65Zn influx is directly dependent upon the extracellular zinc concentration. 3. Net zinc influx could only be demonstrated in Krebs buffer at zinc concentrations in excess of 4.3 mumol/l and in tissue culture fluid at zinc concentrations in excess of 43.1 mumol/l. 4. A 65Zn efflux rate constant of approximately 1.0 per h was observed in both 4.3 and 15.4 mumol of zinc/l of Krebs buffer or tissue culture fluid. 5. In a zero external zinc Krebs buffer the 65Zn efflux rate constant fell to 0.57 per h and was accompanied by a small net zinc efflux.

Biological Transport↗
PubMed1980

Substance P enhances cholinergic receptor desensitization in a clonal nerve cell line.

Substance P inhibits carbamylcholine-induced 22Na+ uptake in the clonal cell line PC12. This inhibition is noncompetitive with agonist but competitive with Na+. Octahydrohistrionicotoxin (H8-HTX) also exhibits this same pattern of inhibition. Moreover, both substance P and H8-HTX are very effective in enhancing agonist-induced receptor desensitization. Local anesthetics, such as QX222, also cause inhibition that is competitive with Na+, but they have only marginal effects on desensitization. Because substance P and H8-HTX cannot by themselves cause desensitization, their action is dependent on and synergistic with the action of agonist. Furthermore, substance P and H8-HTX do not appear to compete for the same site as QX222, which is thought to bind to the ion channel. Finally, substance P can stabilize the desensitized state of the receptor even when added subsequent to the actual desensitization and removal of agonist. Thus, substance P does not require open ion channels for binding and may modulate the activity of the receptor-ionophore complex by binding to a distinct regulatory site.

Amphibian Venoms↗
PubMed1980

Leucocyte sodium transport and dietary zinc in protein energy malnutrition.

Zinc supplementation of children who were just completing a period of rapid "catch-up" growth during recovery from severe malnutrition was found to stimulate sodium transport in their leucocytes. These results suggest that zinc status should be studied in the large number of serious illnesses, now known or thought to be associated with impaired sodium transport.

Biological Transport↗
PubMed1980

Studies of liposome interactions with rat thymocytes.

1. The consequences of incubating liposomes with rat thymocytes have been studied using liposomes of dipalmitolyphosphatidylcholine and cholesterol or dipalmitoylphosphatidylcholine only. 2. Dipalmitoylphosphatidylcholine-cholesterol liposomes do not bind to the cells can be removed by washing. An increase in cellular cholesterol is observed. However dipalmitoylphosphatidylcholine liposomes bind rapidly to the cells and cannot be removed by repeated washing. Cholesterol is removed from the cells. 3. There are small changes in intracellular cations in the cholesterol-enriched cells, but no transport studies have been made. Cells depleted of cholesterol lose K+ with little change in intracellular Na+. Na+ influx is increased. The majority of this increase appears to be ouabain-sensitive, indicating in pump-mediated Na+ influx. K+ influx is reduced. 4. The significance of these results is discussed.

Animals↗
PubMed1980

A comparative study of scattered radiation levels from 80-kVp and 240-kVp x rays in the surgical intensive care unit.

The levels of scattered radiation from 80-kVp and 240-kVp mobile x-ray units were measured in the surgical intensive care unit (ICU). The intensity of scatter of the 240-kVp x rays does not decrease with distance as rapidly as with the 80-kVp beam. In an ICU with four beds, the weekly radiation exposure at the nurses' station approximated 0.05 mR (0.13 X 10(-7) C/kg) for the 80-kVp beam and 0.2 mR (0.52 X 10(-7) C/kg) for the 240-kVp beam. Thus, the annual exposure from either unit would be well below the Maximum Permissible Exposure for nonoccupational workers.

Intensive Care Units↗
PubMed1980

Measurement of human fetal breathing movements in healthy pregnancies using a real-time scanner.

Real-time scanners have permitted investigators to measure fetal breathing movements during pregnancy in humans. It has been demonstrated that fetal breathing movements are episodic and occur about 30% of the time during the last 10 wk of pregnancy. Design of studies must account for the episodic nature of fetal breathing movements. It will be important to account for the relationship of fetal breathing movements to maternal meals, time of day, and gestational age of fetuses. Furthermore, cigarette smoking, alcohol, and drugs may alter fetal breathing measurements. Finally, fetal breathing movements are absent during accelerated labor and may normally be diminished during the last 3 days prior to spontaneous term labor. Measurement of fetal breathing movements using real-time scanners has helped to understand circadian rhythms in fetal life and may ultimately be of use in the assessment of fetal health. It is important that much more information be obtained concerning factors that normally influence fetal breathing movements before proper strategies can be suggested for the use of these measurements in the clinical assessment of fetal health.

Alcohol Drinking↗
PubMed1980

Patterns of human fetal breathing during the last 10 weeks of pregnancy.

Continuous measurements of human fetal breathing movements and gross fetal body movements were made with an ultrasonic real-time scanner for periods of 24 houro 31 weeks' gestation, a significant increase in fetal breathing movements occurred during the second and third hours after meals; this pattern apparently followed an increase in maternal plasma glucose concentrations. At 38 to 39 weeks' gestation, fetal breathing movements increased during the second and third hours after breakfast, but the troughs seen before lunch and supper at 30 to 31 weeks' gestation were not present. Fetal breathing movements diminished over the day and reached a minimum between 1900 and 2400 hours. Fetal breathing activity increased in both groups between 0400 and 0700 hours while mothers were asleep; this was not related to an increase in maternal glucose concentrations. Absence of fetal breathing movements was observed for up to 122 minutes in this analysis of 480 hours in 20 patients. These data show that much more information must be obtained on factors that normally influence fetal breathing activity. Only then can research strategies be suggested for clinical evaluation of the usefulness of fetal breathing movements in the assessment of fetal health.

Blood Glucose↗
PubMed1979

Circadian rhythms in maternal plasma cortisol, estrone, estradiol, and estriol at 34 to 35 weeks' gestation.

In order to examine the relationship between circadian rhythms in different steroids, cortisol (F), estrone E1), estradiol (E2), and estriol (E3) were measured by radioimmunoassay in maternal venous plasma taken at 30 to 60-minute intervals over 24 hours from 11 healthy women at 34 to 35 weeks' gestation. Maternal F was maximal at 0730 hours and fell significantly to its lowest concentration at 0230 hours. Maretnal E3 was lowest between 1000 and 1130 hours and rose significantly to maximal values between 2230 and 0030 hours. Maternal E1 was maximal between 1000 and 1130 hours and showed a significant decrease to reach its lowest concentration at 0430 to 0630 hours. No significant circadian change was measured in uncorrected concentrations of E2. We conclude that there is an inverse relationship between maternal F and E3, which would be consistent with a maternal effect on fetal adrenal function, and the existence of circadian rhythms in F, E1, E2, and E3 must be taken into account in clinical investigations of these hormones during pregnancy.

Circadian Rhythm↗
PubMed1979

Concanavalin A inhibition of alpha-bungarotoxin binding to a nonfusing muscle cell line.

Incubation of a nonfusing muscle cell line, BC3H1, with concanavalin A (Con A) results in a maximum decrease of 35% in the cell's ability to bind alpha-bungarotoxin (alpha-BuTx). The Con A-induced inhibition of 125I-alpha-BuTx binding is reversible and the degree of inhibition parallels the degree of saturation of Con A binding sites on the cell surface. The maximum level of Con A-induced inhibition of 125I-alpha-BuTx binding is not affected by increasing the time of incubation in Con A, using higher concentrations of Con A or by increasing the time of incubation in the presence of 125I-alpha-BuTx. In addition, all BC3H1 cells in culture are sensitive to the Con A-induced inhibition of 125I-alpha-BuTx binding. A comparison of the pseudo-first order rate constants for 125I-alpha-BuTx binding to untreated (8.6 x 10(4) M-1 S-1) and Con A-treated (5.4 x 10(4) M-1 S-1) BC3H1 cells, however, shows that those acetylcholine receptors in Con A-treated cells which bind 125I-alpha-BuTx do so with a lowered apparent affinity. Partial inhibition of toxin-binding capacity is not a consequence of two classes of acetylcholine receptors on the cell surface. Furthermore, individual receptors experience partial inhibition of their binding capacity by Con A, resulting in receptors with at least one binding site blocked and at least one site available for alpha-BuTx binding.

Acetylcholine↗