Biomedical subjects
Publications and source records attributed to D Schwartz.
The authors suggest a simple test for use in the comparison of several proportions. Its main advantage is that it may be used in the presence of low cell expectations. The price of this advantage is in having a sufficient number of proportions for the test to be valid. Other methods which have looked at this problem are examined.
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Vasopressin, its 1-deamino analog (dAVP), angiotensin II, and phenylephrine, administered intravenously, increased plasma atriopeptin immunoreactivity in chloral hydrate-anesthetized rats. A continuous one hour infusion of either dAVP or phenylephrine caused a sustained elevation in: a) systemic blood pressure; b) right atrial pressure; c) left ventricular end diastolic pressure; and d) plasma atriopeptin immunoreactivity. While continuous infusion of angiotensin II also produced a sustained elevation in left ventricular end diastolic pressure, the changes in right atrial pressure and plasma atriopeptin were only transient. These data suggest that plasma atriopeptin most closely correlates with right atrial pressure. Consistent with this hypothesis, we found that the release of atriopeptin directly correlated with changes in right atrial pressure in anesthetized, water-immersed rats.
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Administration of pharmacological doses of arginine-vasopressin, related peptides, and other pressor agents induced a profound release of atriopeptin immunoreactivity into the circulation. The stimulated release of atriopeptin apparently was related to increased arterial blood pressure. Neither the nonpressor vasopressin analog 1-deamino-D-Arg8-vasopressin nor arginine-vasopressin in the presence of a specific pressor antagonist caused atriopeptin to be released into the circulation. Urine output was correlated with the level of atriopeptin released. Physiological levels of arginine-vasopressin suppress diuresis and produced vasoconstriction. Pharmacological levels of the hormone stimulated the cardiac endocrine system to release atriopeptin, which may cause diuresis and vasodilation to physiologically antagonize the effects of vasopressin.
Vasopressin induces a concentration-dependent increase in atriopeptin immunoreactivity in plasma. Rat plasma, rat atrial extract, and synthetic atriopeptin III (APIII) produced parallel displacement curves of iodine-125-labeled APIII binding to specific antiserum. Fractionation of plasma atriopeptin immunoreactivity by reverse-phase high-performance liquid chromatography showed that the major portion consists of two species of low molecular weight peptides in a ratio of 10 to 1. Both peaks exhibited potent vasorelaxant activity, suggesting the presence of the carboxyl terminal Phe-Arg sequence of atriopeptin in each species. Sequence determination of the purified peptides indicated that the major peptide is Ser-Leu-Arg-Arg-APIII and the minor peptide APIII. It appears that the former is the major species of atrial peptide in the rat circulation and that it is the product of selective cleavage of the high molecular weight precursor.
The expression of epoxide hydrolases was studied in cultured rat hepatocytes and hepatoma cell lines. Styrene 7,8-oxide and benzo[a]pyrene 4,5-oxide were used as substrates for microsomal epoxide hydrolase and trans-stilbene oxide for the cytosolic form of this enzyme. In freshly isolated hepatocytes from control rats, microsomal epoxide hydrolase activity was 7.7 and 10.8 nmoles/mg cellular protein/min with benzo[a]pyrene 4,5-oxide and styrene 7,8-oxide as substrates respectively. This enzyme activity increased by more than 2-fold in hepatocytes after 24 hr in culture and remained elevated throughout 96 hr using both substrates. In cultured hepatocytes from rats pretreated in vivo with phenobarbital, trans-stilbene oxide, 2-acetylaminofluorene and N-hydroxy-2-acetylaminofluorene, both benzo[a]pyrene 4,5-oxide and styrene 7,8-oxide hydrolase activities were increased greater than 1.8 relative to controls. Hepatocytes from 2-acetylaminofluorene-pretreated animals at 24 hr in culture had approximately 9-fold higher activities than control hepatocytes. In marked contrast to microsomal epoxide hydrolase activity, the cytosolic enzyme showed an initial activity of 191 pmoles/mg cellular protein/min in freshly isolated hepatocytes, decreased by 75% after 24 hr in culture, and was barely detectable at 96 hr. A similar trend was apparent in hepatocytes from the pretreated animals. In vitro treatment of hepatocytes with trans-stilbene oxide and phenobarbital increased microsomal epoxide hydrolase, while this activity was refractory to 2-acetylaminofluorene treatment. Styrene 7,8-oxide hydrolase activity was increased in the McA-RH-7777 rat hepatoma cell line by phenobarbital, trans-stilbene oxide and 2-acetylaminofluorene treatment. Similarly, benzo[a]pyrene 4,5-oxide hydrolase activity was also increased in this cell line by treatment with phenobarbital and trans-stilbene oxide but not by 2-acetylaminofluorene. Microsomal epoxide hydrolase activity in rat H4-II-E hepatoma cells was refractory to induction, except by trans-stilbene oxide treatment, which caused a 70% increase in benzo[a]pyrene 4,5-oxide hydrolase activity.
Antisera to atriopeptin III and to a cyanogen bromide fragment of the precursor molecule atriopeptigen were prepared and used to examine the distribution of atriopeptin-like immunoreactive material in the heart and brain of the rat. Granules of this material were seen in myocytes throughout the right and left atria and were densest in the perinuclear region. The distribution of atriopeptin-like immunoreactive material in the heart is consistent with previous reports of atrial secretory granules. In the brain neurons containing the material were observed in the hypothalamus and the pontine tegmentum. Atriopeptin in the brain may serve as a neurotransmitter in neural systems controlling blood volume and composition, the same physiological functions regulated by blood-borne atriopeptin.
To examine the biochemical effects of 10-30 mg/day L-deprenyl, measurement of 24-hr urinary output of phenylethylamine (PEA), 3-methoxy 4-hydroxy phenylethyleneglycol (MHPG), and L-deprenyl's amphetamine metabolites were carried out before and during the treatment of atypical depressives. Platelet monoamine oxidase (MAO) activity was also assessed. With L-deprenyl 10-30 mg/day, the expected MAO B inhibition occurred, as indicated by significant increase in urinary PEA excretion and virtual disappearance of platelet MAO activity. Twenty-five to 33% of the daily dose of L-deprenyl was recovered as urinary methamphetamine or amphetamine. Excretion of MHPG was significantly decreased with L-deprenyl 10-20 mg/day. Overall, the results suggest that L-deprenyl's antidepressant effects are mediated by some mechanism other than, or in addition to, MAO B inhibition.
An analysis has been made of the general reproductive characteristics of mothers, including the temperature curves of preconception and conception cycles, in a prospective study which ended in the birth of 22 malformed infants and 894 normal infants. The differences observed have shown that the mothers of malformed infants had their first menstrual period at a later age (13.4 vs 12.8 years), their menstrual cycles were more often irregular (77% vs 40%) and lasted longer (32.9 vs 30.1 days). Moreover, they had a longer hypothermic phase during both their preconception cycle (21.7 vs 17.6 days) and during their conception cycle (24.0 vs 18.1 days), as well as a longer temperature rise during their conception cycle (3.7 vs 3.0 days). By taking into account the relation between these variables, we have been able to show that increased risk of malformation is associated with increase in the length of the hypothermic phase and the temperature rise of the conception cycle.
Studies of the effect of surgery on growth failure in adolescents with Crohn's disease have revealed conflicting data. To better determine the role of surgery for growth delay, growth data from 26 patients with Crohn's disease with intestinal resections and/or ileostomies were reviewed, 3 of whom had surgery twice. Operations were performed on 14 Tanner Stage I, 1 Tanner II, 1 Tanner III, and 13 Tanner IV or V patients. In the prepubertal group, 13 of the 14 had growth impairment, only one of whom had surgery primarily for that growth failure. One year after operation, 11 of 13 Tanner I growth failure patients experienced an increase in height velocity of 5.38 +/- 1.18 cm/yr (mean +/- SE;P less than 0.01); 9/11 achieved normal height velocity for Tanner I. Two attained their preillness height percentiles at one year follow-up, while 5 patients attained their preillness height percentiles 2.5 to 10 years following surgery. Of the four who failed to achieve normal height velocity, 3 had early recurrence of active disease. The Tanner Stage II and III patients both had growth failure, and both had a growth spurt following surgery. Of those who were Tanner Stage IV or V at the time of surgery, 5 of 13 had growth failure. Following surgery, none had an increase in height velocity. These data suggest that when patients with Crohn's disease and growth failure are prepubertal and surgery is performed primarily because of failure of medical therapy and/or other complications, a postoperative growth spurt may be expected within one year.
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The coexistence of carcinoma in situ in flat epithelium adjacent to tumors is prognostically significant and is associated with an increased incidence of tumor recurrence and invasion. Recent investigations have been aimed at finding markers that will help identify flat areas of dysplasia or low-grade papillary transitional cell carcinomas that have a high potential to evolve into invasive tumors. Both DNA and karyotype analyses, as well as cell surface markers, have been examined in some detail and could have clinical value in certain settings. The tumor DNA index as measured by flow cytometry of nuclei retrieved from deparaffined sections may be particularly useful as a predictor of tumor recurrences and, possibly, tumor invasion as well. The diagnosis of superficial disease rests on urine cytology and the histopathologic assessment of tissue biopsies; however, intra- and inter-observer reproducibility of tissue and cytologic diagnoses by pathologists is a significant problem. The application of new technologies, such as flow cytometric analysis of deparaffined nuclei, may reduce the subjectivity involved in the light microscopic assessment of pathology specimens.
A patient with erythema multiforme developed septicemia with two strains of Staphylococcus aureus. Six blood cultures, obtained during 14 days, yielded a mixture of both strains. The strains differed in the ability to hemolyze human erythrocytes, in the production of beta-lactamase and in the susceptibility to antibiotics and bacteriophages. Following therapy with gentamicin, a Dwarf colony variant auxotrophic for vitamin K, tryptophan and p-aminobenzoic acid appeared in some of the blood cultures. This variant was apparently derived from one of the offending strains (phage Type 55/71). From other blood cultures, a different type of Dwarf colony variant was obtained; this variant was of the same phage type as the other offending S. aureus strain (Type 85). The metabolic deficiencies of this strain were not unraveled. Both events, the double infection with distinct S. aureus strains, and the emergence of Dwarf variants during antibiotic therapy, are unusual in clinical practice, and will be detected only if laboratory staff pays particular attention to the possible occurrence of such events.
Phosphatidylglycerol determination has been used as an additional parameter in the evaluation of fetal lung maturity. Meconium was added to aliquot samples of amniotic fluid after phosphatidylglycerol determination. On those amniotic fluid samples without phosphatidylglycerol, phosphatidylglycerol standard and meconium were added. Two-dimensional thin-layer chromatography was performed to detect the phosphatidylglycerol spot. Our results show that lightly stained meconium contamination of amniotic fluid does not hinder the detection of the phosphatidylglycerol spot on the chromatographic plate.
Anger/hostility and Type A behavior have been implicated in elevated cardiovascular reactivity and disease. In the present experiment systolic blood pressure (SBP), diastolic blood pressure (DBP), and heart rate (HR) were monitored during conditions of competition alone or in conjunction with goal blocking or harassment. Cardiovascular reactivity was examined as a function of conditions, Type A or B pattern, and various measures of anger/hostility. Harassment elicited significantly elevated SBP and HR changes relative to goal-blocking and control conditions. Type As reliably exceeded Type Bs in magnitude of SBP change during the harassment condition only. However, exploratory analyses correlating anger/hostility measures and cardiovascular reactivity indicated that only subjects scoring high on the Buss-Durkee Hostility Inventory showed significantly elevated SBP reactivity as a function of Type A behavior pattern, rated hostility during the A-B interview, or outward expression of anger assessed by the Framingham Anger-In vs Anger-Out Scale.