Fixation and embedding.
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Biomedical subjects
Publications and source records attributed to C Oliver.
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A gravida 3, para 1,32-year-old black female presented at 27 weeks gestation for routine prenatal serologic tests. She typed as group A, D positive, category DIII mosaic. IgGl anti-D, -hrB, and -E were identified in her serum Ultrasound revealed an apparently normal fetus with no evidence of hydrops or ascites. Amniocentesis, performed at 30,33, and 35 weeks, showed some evidence of hemolysis that did not increase over time. At 36 weeks of gestation, she delivered a full-term infant who was group A, D positive, E negative, with a 3+ direct antiglobulin test. The eluate revealed anti-D and -hrB, Treatment of the hemolytic disease of the newborn included phototherapy, intravenous fluids, and transfusion of 60 mL of mother's deglycerolized red blood cells.
To investigate the impact of changes in the level of the endogenous atrial natriuretic factor (ANF) on pituitary-adrenocortical activity, the secretion of corticotropin (ACTH) and corticosterone was studied under the conditions of enhanced and decreased circulating ANF levels in rats. Volume expansion (intravenous infusion of 5 ml of saline within 2 min) induced significant elevation in ANF levels 5 min after the infusion, whereas ACTH levels remained unchanged during the first 20 min and were elevated only at 40 min, i.e. at the time when ANF levels were again normal. Water deprivation for 48 h resulted in decreased ANF levels and increased corticosterone concentrations. ANF concentrations in peripheral blood obtained under thiopental anesthesia were lower than those in blood sampled in the same rats in conscious state. However, such changes were not observed in water deprived animals. In addition, ANF was found to be present in the hypophysial portal blood of anesthetized rats. In conscious sheep, portal ANF levels were significantly higher than those in peripheral blood. Our results support the suggestion of an inhibitory role of ANF in the control of ACTH release and indicate that this role of ANF is physiologically relevant.
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Report on a tonsillar parasitosis in a 5-year-old child living in the countryside from leeches of Hirudinea. He consulted because a feeling of foreing body in the throat and spitting of blood, since a fortnight. The AA. remark the low incidence of those cases in our environment.
During the stress hyporesponsive period (postnatal days 2-10), the stimulation of corticosterone secretion by ACTH is very low. In our study, we have observed that administration of ACTH during 3 consecutive days is followed by a striking increase in corticosterone response to an acute ACTH test. A comparable potentiation of corticosterone secretion was observed after a similar treatment with Lys gamma 3-MSH. The 3 day-treatment with each peptide induced an increase in adrenal weight. Similar data were obtained with alpha-MSH. However, corticosterone response to ACTH was not significantly altered following the same pattern of alpha-MSH administration.
Pancreastatin (PST), a novel COOH-terminally alpha-amidated peptide is a part of Chromogranin A molecule. Precursor processing implies also the final amidation step dependent on peptidylglycine alpha-amidating monooxygenase (PAM). High activity of PAM as well as Thyroliberin (TRH, another alpha-amidated peptide) concentration and biosynthesis were reported to be very high in neonatal rat pancreas. We followed the concentration of PST-like immunoreactivity in rat pancreas during ontogenesis. High perinatal PST concentration, resembling that of previously reported for PAM activity and TRH concentration was found. These findings suggest that perinatal PAM activation may affect a broader spectrum of pancreatic peptides.
This study was designed to assess the involvement of corticotropin-releasing factor (CRF) in the corticosterone response to the acute administration of the serotonergic indirect agonist D-fenfluramine in the rat. In addition to plasma corticosterone, D-fenfluramine-induced hyperglycemia (which is independent from the hypothalamo-pituitary-adrenal axis) was also analyzed. Acute i.v. injection of sheep anti-CRF antiserum (15 min beforehand) markedly diminished either stress-induced corticosterone release (but not ether stress-induced increases in plasma glucose levels), thereby indicating that passive immunization was efficient. Acute administration of D-fenfluramine (3 mg/kg i.v.) increased plasma corticosterone and glucose levels to similar extents in control rats (i.e. injected with normal sheep serum) and in anti-CRF antiserum-injected rats. These results indicate that, under our experimental conditions, D-fenfluramine-induced corticosterone elevation is of peripheral origin (through pituitary and/or adrenocortical pathways).
2H3 subline of rat basophilic leukemia (RBL-2H3) cells are mast cell analogs that lack responsiveness to nonimmunologic stimuli such as compound 48/80 and substance P. To determine if fibroblasts can influence this responsiveness, RBL-2H3 cells were cocultured with confluent monolayers of mouse 3T3 fibroblasts and assayed for secretagogue-induced histamine release. After 1 wk in coculture, RBL-2H3 cells began to respond to compound 48/80. Responsiveness reached a maximum at 2 wk in coculture and remained at this level for an additional 2 wk. Histamine release was specific, noncytotoxic, dose-dependent, and occurred even in the absence of extracellular Ca2+. No soluble factor from 3T3 cells was found that induced these alterations. Moreover, neither recombinant rat or mouse steel factor, at concentrations up to 250 ng/ml, was able to alter RBL-2H3 cell reactivity to compound 48/80. By 2 wk in coculture, RBL-2H3 cells also became responsive to substance P, although no changes in histamine content, Alcian blue+/safranin- staining or type of serine protease were detected. These results show that 3T3 fibroblasts cause an alteration in the functional repertoire of RBL-2H3 cells and that soluble steel factor cannot duplicate the effect.
Peptidylglycine alpha-amidating monooxygenase (PAM; EC 1.14.17.3) is a multifunctional protein containing two enzymes that act sequentially to catalyze the alpha-amidation of neuroendocrine peptides. Southern blot analysis of human placental DNA demonstrated that PAM is encoded by a single gene. The chromosomal localization of the PAM gene was established using in situ hybridization. A 2.2-kb human PAM cDNA hybridized to human metaphase chromosomes revealed a significant clustering of silver grains over chromosome 5 bands q14-q21. The gene encoding another enzyme important in the post-translational processing of neuroendocrine precursors, prohormone convertase 1 (PC1), is localized in the same region (5q15-q21).
Operant and biological theories of the cause of self-injurious behavior (SIB) in people with a mental handicap are often viewed as mutually exclusive. In this single case study, interactions between features of Rett syndrome and operant conditioning as determinants of SIB are examined. Functional analysis by analog methodology indicated different functions for two forms of SIB shown by the subject: automatic reinforcement by sensory stimulation and escape from social interactions. It is suggested that features of Rett syndrome established conditions under which operant conditioning of self-injurious responding was maximized. The implications of this interaction between features of syndromes and operant conditioning for the conceptualization of the cause of SIB are discussed and it is proposed that the notion of a unitary cause of SIB is inappropriate. It is more productive to consider operant conditioning as the process that maintains responding against a background of predisposing and mediating factors which may be biologically determined.