Search PubMed⌕ Search

Biomedical subjects

J Patrick

Publications and source records attributed to J Patrick.

At least 181 records · Page 10Linked to original sources
PubMed1982

Effects of intravenous glucose injections on human fetal breathing movements and gross fetal body movements at 38 to 40 weeks' gestational age.

Fetal breathing movements and gross fetal body movements were studied subsequent to the intravenous injection of either 25 gm of glucose or an equal volume of normal saline solution in 10 healthy women with uncomplicated pregnancies at 38 to 40 weeks' gestation. The incidence of fetal breathing increased from 17.5% during the control period to 54.9% after glucose injection. Neither glucose nor saline solution had any effect on the incidence of gross fetal body movements. All fetuses made some breathing movements during any 15-minute interval between 30 and 75 minutes after glucose injection. These data suggest a useful strategy for clinical measurement of fetal breathing activity near term.

Apgar Score↗
PubMed1982

Patterns of gross fetal body movements over 24-hour observation intervals during the last 10 weeks of pregnancy.

Continuous measurements of gross fetal body movements were made with an ultrasonic real-time scanner for periods of 24 hours in 31 women. Fetuses made 0 to 130 gross fetal body movements per hour which accounted for 0% to 50% of the time. At 38 to 39 weeks' gestational age, fetuses demonstrated a peak in activity between 2100 and 0100 hours. The longest period of complete absence of gross fetal body movements was 75 minutes. Maternal meals and glucose concentrations did not influence gross fetal body movements.

Activity Cycles↗
PubMed1982

Molecular cloning of cDNA coding for the gamma subunit of Torpedo acetylcholine receptor.

From the electric organ of Torpedo californica, we purified mRNA that, when translated in vitro, produces polypeptides immunoprecipitable by antibodies against purified acetylcholine receptor. A novel cloning system [Okayama, H. & Berg, P. (1982) Mol. Cell. Biol. 2, 161-170] was used to produce a cDNA library from this mRNA. This library contained clones with receptor sequences identified by differential hybridization and hybridization-selection. We describe a clone of 2,030 base pairs with sequences appropriate for the amino-terminal amino acids of the gamma subunit of acetylcholine receptor. This clone contains 82 bases 5' of the codon for the amino-terminal amino acid of the mature protein. A portion of this sequence codes for a methionine followed by a 16-amino acid polypeptide that is contiguous to the amino-terminal amino acid of the mature protein and that has the characteristics of a leader peptide. The cDNA insert hybridizes to a 2,100-base RNA present in electric organ but not in the brain of T. californica.

Animals↗
PubMed1981

The nonstress test: how long is enough?

Longer observation intervals might increase the positive predictive value of a nonreactive nonstress test (NST). One thousand one hundred and one NSTs were performed on 343 fetuses in 333 high-risk hospitalized patients. Recordings were terminated when five fetal heart rate (FHR) accelerations with movement occurred in any 20-minute period or after 120 minutes. The conclusion drawn was that the positive predictive value for morbidity and mortality of a nonreactive NST was 85.7% if conducted over 120 minutes, and that the negative predictive value for a reactive NST was 98.5%. A reactive NST was predictive of good fetal health regardless of the length of observation time necessary to demonstrate reactivity up to 120 minutes.

Apgar Score↗
PubMed1981

Effects of synthetic glucocorticoid administration on human fetal breathing movements at 34 to 35 weeks' gestational age.

Fetal breathing movements were measured in six women who had received exogenous glucocorticoids throughout pregnancy and in whom the endogenous circadian rhythm in cortisol was absent or had been suppressed. Studies were performed for 24-hour observation periods while women received prednisone and then one week later on the same women after equivalent doses of dexamethasone. Fetal breathing movements occurred 29.9% +/- 1.9% of the time in the prednisone-treated group and this was not changed in the same fetuses after dexamethasone treatment. There was a significant increase in the percentage of time spent making breathing movements during the second and third hours following breakfast, lunch, and dinner (P less than 0.001). A fourth peak in fetal breathing activity occurred in the late evening and seemed to be related to the time of the evening glucocorticoid medication. These data were compatible with the hypothesis that maternal glucocorticoid concentrations may influence patterns of fetal breathing movements at 34 to 35 weeks' gestational age.

Blood Glucose↗
PubMed1981

Loss of diurnal rhythm in plasma estrone, estradiol, and estriol in women treated with synthetic glucocorticoids at 34 to 35 weeks' gestation.

In order to examine the effect of endogenous rhythms in fetal and/or maternal adrenal activity on diurnal changes in plasma estrone (E1), estradiol (E2), estriol (E3), and progesterone (P) in women at 34 to 35 weeks' gestation, we measured these steroids in a group of six women in whom the endogenous circadian rhythm in cortisol was absent or had been suppressed by treatment with exogenous synthetic glucocorticoids. All steroids were suppressed, and no diurnal rhythms in E1, E2, E3 or P were found. Suppression of cortisol and estrogens was greater after dexamethasone (Dx) than after a glucocorticoid-equivalent dosage of prednisone (Pd). Loss of the maternal estrogen rhythms seen in normal patients is consistent with the suggestion that such rhythms may be attributable to diurnal changes in maternal and/or fetal adrenal output of potential precursors. The differences in cortisol and estrogen concentrations after Dx and Pd may indicate dissociation of the glucocorticoid (hyperglycemic) and adrenocorticotropic hormone-suppressing activities of these compounds.

Adrenal Glands↗
PubMed1981

Effects of external physical stimulation on fetuses near term.

Measurements were made in 17 healthy pregnant women between 36 and 42 weeks' gestational age 90 minutes before and after a standard physical stimulus. The mean fetal heart rate was 138 +/- 0.4 bpm; the median value of the 5-minute standard deviation of successive heartbeat intervals was 30.3 msec, and the percentage of time spent making gross fetal body movements was 11.1% +/- 0.4%. These measurements did not change following stimulation of fetuses. Fetal breathing movements diminished over the 180-minute observation period but did not appear to be changed by fetal stimulation. During studies, periodic increases separated by periodic decreases in fetal heart rate, fetal heart rate variability, gross fetal body movements, and fetal breathing movements were measured, and these changes did not seem to be related to external stimulation of fetuses. Periodic changes in these measurements may have been related to underlying patterns of fetal behavior but were not usually influenced by external physical stimulation of fetuses.

Female↗
PubMed1981

The effects of alterations in the external sodium concentration on human leucocyte sodium and potassium transport in vitro.

Human leucocytes incubated in tissue culture fluid of low-sodium concentration (2 mM; iso-osmolarity maintained with choline chloride) reached a new equilibrium within 1 hour and lost approximately 25% of intracellular potassium and 70% of intracellular sodium. The rate constant for ouabain-sensitive sodium efflux fell by more than 50% and the ouabain-insensitive rate constant increased nearly threefold in the low-sodium medium. Total sodium efflux fell in proportion to internal sodium whereas ouabain-insensitive sodium efflux remained unchanged. A reduction in external sodium from 140 to 2 mM was associated with a 75% fall in sodium influx. In the low-sodium medium ouabain-sensitive potassium influx exceeded ouabain-sensitive sodium efflux and no ouabain-sensitive potassium efflux could be demonstrated. Ouabain-insensitive potassium influx and that portion of potassium efflux which is dependent on external potassium fell in parallel in low-sodium cells, suggesting reduced activity of a ouabain-insensitive K:K exchange system.

Biological Transport↗
PubMed1981

Effect of extracellular potassium on the transport of sodium and potassium in rat thymocytes.

1. The effect of extracellular potassium on the transport of sodium and potassium in rat thymocytes has been studied in vitro. 2. A significant increase in the rate constant for total and ouabain-sensitive sodium efflux was demonstrated at an extracellular potassium concentration of 1 mmol/l as compared with that at either 0 or 2 mmol/l. 3. At potassium concentrations below 3 mmol/l ouabain-sensitive sodium influx was observed suggesting sodium-sodium exchange catalysed by the sodium pump. 4. Both total and ouabain-insensitive potassium efflux rose with external potassium. A small ouabain-sensitive potassium efflux was observed at all levels of external potassium studied. 5. Total and ouabain-insensitive potassium influx increased with external potassium, but did not appear to saturate. Ouabain-sensitive potassium influx reached a maximum at an external potassium concentration of 2 mmol/l then decreased with increasing external potassium.

Animals↗
PubMed1981

Increased sodium content and altered sodium transport in thymocytes of spontaneously hypertensive rats.

1. The intracellular sodium content and the sodium efflux rate constant have been determined in vitro in thymocytes derived from the Okamato-Aoki strain of spontaneously hypertensive rats. 2. A strong positive correlation between the systolic blood pressure and the sodium content of thymocytes was observed (r = 0.59, n = 39, P less than 0.001). 3. The rate constant for total sodium efflux was negatively correlated with systolic blood pressure (r = -0.43, n = 45, P less than 0.005) and this was due to a fall in the ouabain-sensitive component of sodium efflux. 4. Sodium efflux, influx and the thymocyte potassium content were not related to the blood pressure.

Animals↗
PubMed1981

Factors affecting the susceptibility of different strains of mice to experimental myasthenia gravis.

Mice immunized with purified AChR (T. californica) invariably form anti-AChR antibodies and often develop a condition of extreme muscular weakness and flaccid paralysis. Pharmacological, physiological, and ultrastructural studies indicate that the pathophysiology of EMG in the mouse closely resembles that of human MG. The single episode of muscular weakness typically found in mouse EMG differs from the acute phase of rat EMG in that macrophages and other phagocytes do not appear to play an active role in the destruction of the neuromuscular junction. The frequency of paralysis in mice immunized with AChR is highly strain dependent and is not attributable to polymorphisms with respect to susceptibility to cholinergic blockade. The incidence of paralysis does not correlate with the magnitude of the humoral response to either T. californica or mouse AChR. Because both paralyzed and nonparalyzed mice form antibodies which are able to increase the rate of both junctional and extrajunctional AChR degradation, the mere presence of antibodies reactive with cell surface antigenic determinants of AChR is not sufficient for the induction of paralysis. While it is still possible that antibody-induced degradation of AChR may be necessary for the induction of paralysis, these studies rule out the possibility that antigenic modulation of AChR is sufficient to account for the induction of paralysis in mouse EMG. In the present studies alleles of the two loci were identified which significantly effect the probability with which mice immunized with AChR can be expected to become paralyzed, the MHC and the IgCH region. Because one genotype, H-2b, Ig-1b segregated with high susceptibility to EMG in four strains derived from three dissimilar backgrounds, these studies strongly suggest that susceptibility to the development of paralysis is a heritable trait determined by regions of the mouse genome which regulate immune responsiveness.

Animals↗