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Biomedical subjects

J Patrick

Publications and source records attributed to J Patrick.

At least 109 records · Page 6Linked to original sources
PubMed1988

Urethral and urachal urine output to the amniotic and allantoic sacs in fetal sheep.

A chronic fetal sheep preparation was developed to measure, without interruption in utero, urethral and urachal urine output to the amniotic and allantoic sacs, respectively. Fetal urethral, urachal and total urine output was measured during a 5 day post-operative period, in late gestation. Total fetal urine output increased from day 1 to a volume of 1216 +/- 115 ml/day (SEM) on day 5 post-operative. Urachal urine output increased significantly from 12 ml/day on day 1 to 467 ml/day on day 5 (P less than 0.05). Fetal arterial blood gases, pH and immunoreactive ACTH, cortisol and immunoreactive arginine vasopressin concentrations were stable throughout the 5-day recovery period. Fetal urachal urine output to the allantoic cavity and total fetal urine output appears to require 4-5 days to stabilize post-operatively. Fetal urine is a major source of amniotic and allantoic fluid in late gestation and the volume of these sacs may be influenced, in part, by the distribution of urethral and urachal urine output.

Adrenocorticotropic Hormone↗
PubMed1987

Phenytoin infusion in severe pre-eclampsia.

Intravenous phenytoin sodium was given as a high-dose infusion (10 X 8-18 mg/kg) for anticonvulsive prophylaxis to 2 eclamptic patients and to 24 patients with moderate to severe pre-eclampsia. There were no major maternal or neonatal side-effects. Plasma phenytoin levels were within the therapeutic range (7-20 mg/l) at 30 min and 6 h after the infusion in all patients, and remained at a therapeutic level in 21 patients after 12 h. After a second dose of phenytoin in 19 patients, drug levels were within the therapeutic range at 24 h.

Female↗
PubMed1987

Muscle acetylcholine receptor biosynthesis. Regulation by transcript availability.

The expression of the muscle nicotinic acetylcholine receptor (AChR) on the cell surface entails a complex biosynthetic pathway, involving the expression and assembly of four subunits. The amount of AChR on the cell surface changes throughout muscle development and upon muscle denervation. We have examined the regulatory role of transcript levels on surface AChR expression by RNA blot analysis. During myogenesis of the fusing mouse muscle cell line C2, which expresses an embryonic type of receptor, changes in the rate of appearance of cell surface AChR have been assayed by 125I-alpha-bungarotoxin binding. The maximal increase in the rate of appearance of cell surface AChR occurs upon cell fusion, closely following the maximal increase in transcript levels for the alpha-, beta-, gamma-, and delta-AChR subunits. AChR alpha-, beta-, gamma-, and delta-subunit gene transcript levels have also been examined in innervated and denervated rat and mouse muscle. Muscle denervation results in an increase of transcripts for all four subunits. However, the amount of beta-subunit transcript in innervated rat skeletal muscle is high relative to the other subunit transcripts, and increases less than the other subunit transcripts upon denervation. Our results indicate that, during myogenesis and upon denervation, the availability of AChR subunit transcripts for translation plays a regulatory role in surface AChR appearance.

Animals↗
PubMed1987

Members of a nicotinic acetylcholine receptor gene family are expressed in different regions of the mammalian central nervous system.

Nicotinic acetylcholine receptors found in the peripheral and central nervous system differ from those found at the neuromuscular junction. Recently we isolated a cDNA clone encoding the alpha subunit of a neuronal acetylcholine receptor expressed in both the peripheral and central nervous system. In this paper we report the isolation of a cDNA encoding the alpha subunit of a second acetylcholine receptor expressed in the central nervous system. Thus it is clear that there is a family of genes coding for proteins with sequence and structural homology to the alpha subunit of the muscle nicotinic acetylcholine receptor. Members of this gene family are expressed in different regions of the central nervous system and, presumably, code for subtypes of the nicotinic acetylcholine receptor.

Amino Acid Sequence↗
PubMed1987

External vibratory acoustic stimulation near term: fetal heart rate and heart rate variability responses.

Twenty-five pregnant women between 36 and 40 weeks' gestational age were studied to examine effects of a 5-second external vibratory acoustic stimulus on the fetal heart rate and fetal heart rate variability. There was an immediate significant increase in the basal heart rate, which persisted for 1 hour after the stimulus, compared to that of the control subjects. There was also a significant increase in the total time during which accelerations occurred for the first 20 minutes after the stimulus. There were no changes in computer-derived indices of fetal heart rate variability. Maternal blood pressure and heart rate were not altered following vibratory acoustic stimulus. We hypothesize that external vibratory acoustic stimulus causes a change from a state of sleep to a state of wakefulness in near term healthy fetuses.

Acoustic Stimulation↗
PubMed1987

Transcriptional regulation of nicotinic acetylcholine receptor genes: identification of control elements of a gamma-subunit gene.

The muscle nicotinic acetylcholine receptor undergoes profound changes in abundance and distribution in response to innervation and denervation. As a start towards understanding the detailed mechanisms of acetylcholine receptor gene regulation, we have identified transcriptional regulatory regions of a receptor subunit gene. A region of genomic DNA at the 5' end of the mouse acetylcholine receptor gamma-subunit gene has been shown to promote transcription of the bacterial chloramphenicol acetyltransferase gene in a cell-type specific manner. In addition, the transcriptional activity of this fragment is developmentally regulated in mouse muscle C2C12 cells. We propose that this fragment contains transcriptional control elements of the mouse muscle acetylcholine receptor gamma-subunit gene.

Acetyltransferases↗
PubMed1987

Patterns of human fetal heart rate accelerations from 26 weeks to term.

Computerized analysis of the distribution of 2598 fetal heart rate accelerations in 83 healthy fetuses at 26 to 40 weeks' gestation demonstrated that the currently used definition of an acceleration as greater than or equal to 15 beats/min for greater than or equal to 15 seconds is applicable only after 30 weeks' gestational age in fetuses with a basal fetal heart rate of less than or equal to 128 beats/min. A significant negative correlation was found between the mean hourly basal fetal heart rate and the mean amplitude of fetal heart rate accelerations from 30 weeks to term. There was also a significant maturational process in the pattern of fetal heart rate and fetal heart rate accelerations that occurred between 26 and 28 and between 30 and 32 weeks; this was characterized by a decrease in basal fetal heart rate, an increase in the amplitude of fetal heart rate accelerations, and an increase in long-term fetal heart rate variability.

Embryonic and Fetal Development↗
PubMed1987

Human fetal responses to vibratory acoustic stimulation from twenty-six weeks to term.

Eighty-three healthy pregnant women between 26 and 40 weeks' gestational age were studied to examine effects of a 5-second external vibratory acoustic stimulus on the fetal heart rate, fetal breathing, and gross fetal body movement patterns. There was an immediate fetal heart rate response, following stimulus, characterized by an increase in duration of fetal heart rate accelerations from 26 weeks to term with an increase in basal fetal heart rate after 30 weeks. There was also a delayed response after 33 weeks' gestation, which consisted of an increase in the number of fetal heart rate accelerations and the incidence of gross fetal body movements for up to 1 hour after a 5-second stimulus with the electronic artificial larynx. Term (36 to 40 weeks) fetuses made breathing movements more irregularly after vibratory acoustic stimulation. We suggest that human fetal responses to stimulation with the electronic artificial larynx may reflect a functional maturation of the fetal central nervous system.

Acoustic Stimulation↗
PubMed1987

Cerebral oxidative metabolism in fetal sheep with multiple-dose ethanol infusion.

Cerebral oxidative metabolism and cotylendonary blood flow were measured in 10 unanesthetized fetal sheep (127 to 132 days' gestation) during a control period, after the first, third, and fourth infusions of four doses of 0.5 gm of ethanol per kilogram of maternal body weight infused into the ewe during 5 hours, and 24 hours after ethanol infusion. Preductal arterial and sagittal vein blood samples were analyzed for oxygen content, blood gases, pH, and ethanol. Cerebral and cotylendonary blood flow were measured with a radioactive microsphere technique. Fetal blood gases and pH changed little with the ethanol infusions, although PaO2 and oxygen content decreased 24 hours after ethanol infusion. Cotylendonary blood flow, which was decreased after the third and fourth ethanol infusions, did not account for these delayed hypoxemic changes. Similarly, cerebral oxidative metabolism was decreased when measured after each of the ethanol infusions, with no dose response or tolerance evident. This noted fall in fetal cerebral oxidative metabolism appears to be a direct depressant effect that was maximal at rather low fetal ethanol levels, which, if prolonged, might well affect cerebral growth and development. Recovery of cerebral metabolic function appeared complete by 24 hours. However, relative fetal hypoxemia was evident at this time, the mechanism of which remains to be determined.

Animals↗
PubMed1987

Disposition of acute, multiple-dose ethanol in the near-term pregnant ewe.

The disposition of ethanol and its proximate metabolite, acetaldehyde, was determined in seven conscious instrumented pregnant ewes (127 to 132 days of gestation; term, 147 days) for intravenous infusion of four dosages of 0.5 gm ethanol/kg maternal body weight, administered over 5 hours to the mother. The maternal and fetal blood had ethanol concentrations that were maximal at 5 hours and were virtually identical during the 24-hour study. There was delayed transfer of ethanol into the amniotic and allantoic fluids during the dosing period, followed by higher ethanol concentrations in these fluids during the elimination phase compared with fetal blood. The ethanol elimination rate was similar for the four biologic fluids. Acetaldehyde concentrations in the four fluids were a thousandfold less than the respective ethanol concentrations. The maternal blood acetaldehyde concentration was greater than that in fetal blood. The data indicate that for a binge-type drinking episode during near-term pregnancy, there is unimpeded bidirectional placental transfer of ethanol between the mother and the fetus; the amniotic fluid surrounding the fetus is a reservoir for ethanol in utero; elimination of ethanol from the maternal-fetal unit is regulated by maternal hepatic biotransformation of ethanol; and there is appreciable acetaldehyde-oxidizing capacity in the maternal liver and at extrahepatic sites.

Acetaldehyde↗
PubMed1987

Permanent enteral feeding in cystic fibrosis: advantages of a replaceable jejunostomy tube.

A feeding jejunostomy constructed by the Witzel technique has been used to supplement 12 wasted patients with cystic fibrosis during 260 patient months. None of the patients has stopped the nocturnal feeding once started on the program. The preferred tube was the Entriflex enteral feeding tube, which, when placed without internal fixation, could be easily changed as necessary. There have been no major complications. Minor complications include tube blockage, dislodgement, local infection, and leakage around the tube causing granuloma formation. We have not lost the use of any of the jejunostomies because of inability to replace the tube when it has been dislodged.

Adolescent↗
PubMed1987

Functional expression of two neuronal nicotinic acetylcholine receptors from cDNA clones identifies a gene family.

A family of genes coding for proteins homologous to the alpha subunit of the muscle nicotinic acetylcholine receptor has been identified in the rat genome. These genes are transcribed in the central and peripheral nervous systems in areas known to contain functional nicotinic receptors. In this paper, we demonstrate that three of these genes, which we call alpha 3, alpha 4, and beta 2, encode proteins that form functional nicotinic acetylcholine receptors when expressed in Xenopus oocytes. Oocytes expressing either alpha 3 or alpha 4 protein in combination with the beta 2 protein produced a strong response to acetylcholine. Oocytes expressing only the alpha 4 protein gave a weak response to acetylcholine. These receptors are activated by acetylcholine and nicotine and are blocked by Bungarus toxin 3.1. They are not blocked by alpha-bungarotoxin, which blocks the muscle nicotinic acetylcholine receptor. Thus, the receptors formed by the alpha 3, alpha 4, and beta 2 subunits are pharmacologically similar to the ganglionic-type neuronal nicotinic acetylcholine receptor. These results indicate that the alpha 3, alpha 4, and beta 2 genes encode functional nicotinic acetylcholine receptor subunits that are expressed in the brain and peripheral nervous system.

Amino Acid Sequence↗
PubMed1987

A monoclonal antibody against neuron-specific enolase. Immunohistochemical comparison with a polyclonal antiserum.

There is skepticism about the value of antisera to neuron-specific enolase (NSE) for immunohistochemical identification of neural and neuroendocrine differentiation in neoplasms, because of reports of detection of NSE, in a large percentage of nonneuroendocrine neoplasms. By immunohistochemical methods, the authors compared a monoclonal antibody to NSE (Mab NSE) with a heterologous antiserum to NSE (Het NSE) on 348 samples of tumors of diverse histogenesis. They studied 93 neural and neuroendocrine tumors and 255 nonneuroendocrine, nonneural tumors. The Mab NSE was slightly less sensitive but clearly more specific than the Het NSE in recognizing neural and neuroendocrine differentiation. Only 2% of the nonneuroendocrine, nonneural tumors reacted positively with Mab NSE; in contrast, 20% of the same tumors were positive with the Het NSE. Moreover, intense nonspecific staining was frequent with Het NSE, which often rendered interpretation difficult. Because of its superior specificity, the Mab NSE used in this study is more valuable than the heterologous antiserum as a diagnostic reagent in tumor diagnosis.

Antibodies, Monoclonal↗
PubMed1987

Pharmacologic, metabolic, and toxicologic profile of spirapril (SCH 33844), a new angiotensin converting inhibitor.

Spirapril (SCH 33844; 7-N-[1(S)-ethoxycarbonyl-3-phenylpropyl]-(S)-alanyl-1,4-dithia- 7-azaspiro[4,4]-nonane-8(S)-carboxylic acid) is a new angiotensin-converting enzyme (ACE) inhibitor. SCH 33844 diacid inhibited hydrolysis of hip-his-leu by rabbit lung ACE in a potent (Ki = 0.74 nM), selective, and noncompetitive fashion. SCH 33844 (0.03-1 mg/kg p.o.) produced dose-related inhibition of angiotensin I (AI) pressor responses in conscious rats with a duration of 24 h at the higher dose. SCH 33844 (0.3-30 mg/kg p.o.) reduced blood pressure in a dose-related manner in conscious SHR with a 24-h duration. Antihypertensive activity was enhanced in the presence of hydrochlorothiazide. The drug (1-10 mg/kg p.o.) also lowered blood pressure in conscious hydrochlorothiazide-treated normotensive dogs. In anesthetized dogs, SCH 33844 (1 mg/kg i.v.) reduced blood pressure and total peripheral vascular resistance and slightly increased cardiac output and stroke volume. These results suggest that peripheral vasodilation is the primary mechanism of the antihypertensive action. The metabolic profile of SCH 33844 was evaluated in dogs and rats. The compound was absorbed in a dose-proportional manner and excreted primarily as the diacid form. In contrast to captopril and enalapril, most of the drug (67%) was excreted into the feces following i.v. dosing. Chronic toxicological evaluation in dogs and rats demonstrated that the drug was relatively devoid of toxicity at oral doses as high as 400 and 450 mg/kg/day, respectively. Slight decreases in heart weight (rats) and increases in granularity of the juxtaglomerular apparatus were observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1987

Expression of the high-affinity purine nucleobase transporter in mutant mouse S49 cells does not require a functional wild-type nucleoside-nucleobase transporter.

A novel type of somatic mutation that causes the expression of a high-affinity purine base permease (B. Aronow, D. Toll, J. Patrick, P. Hollingsworth, K. McCartan, and B. Ullmann, Mol. Cell Biol. 6:2957-2962, 1986) has been inserted into nucleoside transport-deficient S49 cells. Two classes of mutants expressing this nucleobase permease were generated. The first, as exemplified by the AE1HADPAB2 cell line, possessed an augmented capacity to transport low concentrations of the three purine bases, hypoxanthine, guanine, and adenine. The second class of mutants, as typified by the AE1HADPAB5 clone, possessed an augmented capability to translocate low levels of hypoxanthine and guanine, but not adenine. Neither the AE1HADPAB2 nor the AE1HADPAB5 cells could transport nucleosides, suggesting that the expression of the high-affinity base transporter did not reverse the mutation in the nucleoside transport system. The transport of purine bases by both AE1HADPAB2 and AE1HADPAB5 cells was much less sensitive than that by wild-type cells to inhibition by dipyridamole, 4-nitrobenzylthionosine, and N-ethylmaleimide, potent inhibitors of nucleoside and nucleobase transport in wild-type S49 cells. Fusion of the AE1HADPAB2 and AE1HADPAB5 cell lines with wild-type cells indicated that the expression of the high-affinity base transporter behaved in a dominant fashion, while the nucleoside transport deficiency was a recessive trait. These data suggest that the high-affinity purine base transporter of mutant cells and the nucleoside transport function of wild-type cells are products of different genes and that expression of the former probably requires the unmasking or alteration of a specific genetic locus that is silent or different in wild-type cells.

Adenine↗