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Biomedical subjects

M A Emanuele

Publications and source records attributed to M A Emanuele.

At least 19 recordsLinked to original sources
PubMed1992

The effect of acute in vivo ethanol exposure on follicle stimulating hormone transcription and translation.

The impact of ethanol (EtOH) on male rodent reproduction has been well characterized for luteinizing hormone (LH) with suppression of LH release from the pituitary being reported. We have previously reported that acute ethanol (EtOH) exposure in vivo results in rapid and marked suppression of beta-LH gene expression and protein release from the pituitary. This suppression of beta-LH gene expression was unaccompanied by a change in the common alpha-subunit mRNA. To further explore the impact of ethanol on male rodent reproduction, we have expanded our studies to follicle stimulating hormone (FSH) and hypothalamic luteinizing hormone releasing hormone (LHRH) as well as of pituitary protein kinase C (PKC). Previously castrated male rats were acutely exposed to EtOH and a dramatic reduction in both serum FSH and LH levels was noted at 1.5 and 3 hr after treatment. These levels returned to saline injected control values at 6 and 24 hr. Despite the fall in serum FSH, there was no change in intrapituitary FSH content at any time point; this lack of pituitary FSH depletion in the face of a fall in serum levels is suggestive of impaired FSH release. In contrast to the fall in beta-LH steady-state mRNA levels seen previously and confirmed in the present studies, there was no change in beta-FSH steady-state mRNA at any time point suggesting that EtOH has dichotomous effects on the expression of these two gonadotropins. Pituitary PKC levels were also assessed and found to be unaffected by EtOH at any time point.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcoholic Intoxication↗
PubMed1992

The effect of "binge" ethanol exposure on growth hormone and prolactin gene expression and secretion.

The effects of ethanol (EtOH) on GH and PRL have been previously explored, and a dicotomy in results noted. While serum GH levels appear to fall after EtOH exposure, PRL levels rise. We have attempted to expand these studies by examining the impact of acute or "binge" EtOH in vivo on GH and PRL synthesis and secretion. At 0.5, 1.5, and 3.0 h after one dose of ip EtOH, serum GH levels fell significantly compared with those seen in saline-injected controls. This correlated with a fall in GH mRNA levels, but no change in pituitary GH content. Conversely, serum PRL levels rose significantly, while the mRNA for PRL decreased by approximately 20%. There was no change in pituitary PRL content. Interestingly, the mRNA for pit-1 (GHF-1), a transcription factor important to both GH and PRL gene expression, was unchanged at any time point. Despite the fall in GH and PRL mRNA levels, the pituitary cAMP content was markedly elevated at 0.5 h, with no change at any other time point. In summary, acute EtOH exposure in vivo appears to dampen both GH and PRL synthesis, while serum levels behave dissimilarily. Possible explanations for these findings are discussed.

Alcoholism↗
PubMed1990

Effect of a hypoglycemic episode on neuropsychological functioning in diabetic children.

The present study investigated neuropsychological functioning in school-age children at various points in time surrounding a hypoglycemic episode using 13 tasks drawn from age-appropriate, standard neuropsychological tests. The results demonstrate the effects of a hypoglycemic episode on neuropsychological functioning even after detectable physical symptoms have subsided. Although we are unable to delineate clearly their temporal course, it appears that the impact of such episodes is transient. In general, the pattern exhibited by these children who have presumably recovered from their mild hypoglycemic episode involved reduced motor performance, attention, and memory. The observed prolonged recovery time of these functions presents important implications for the child in both school and social settings.

Adolescent↗
PubMed1990

The effect of in vitro ethanol exposure on LHRH release from perifused rat hypothalami.

A variety of indirect data suggest that the luteinizing hormone (LH) lowering effects of ethanol (ETOH) are mediated at a hypothalamic level decreasing the synthesis and/or release of LH-releasing hormone (LHRH). Little direct data support this concept, however. The current study was, therefore, designed utilizing a perifusion system with frequent sampling for LHRH with and without ethanol added to determine if ethanol had a direct effect on basal or stimulated LHRH release. A variety of secretagogues, including dopamine, norepinephrine, naloxone, prostaglandin E2, and a high dose of potassium were utilized. Ethanol at a dose of 300 mg% did not alter either basal or secretagogue-stimulated LHRH release from the hypothalami of ethanol-naive male rats. Thus, ethanol did not appear to have a direct effect on LHRH in this system. Alterations in LHRH release by ethanol may occur at a suprahypothalamic level, involving neurotransmitter-LHRH interactions. Alternatively, the well-described lowering effect of ethanol on LH may be secondary to a direct pituitary locus of action, or involve a metabolic breakdown product of ethanol rather than ethanol itself.

Animals↗
PubMed1990

Cross-reaction of albumin with polyclonal LH antibody on western blots.

When pituitary tissue was subjected to Western blot analysis utilizing polyclonal antibody NIDDK-rLH-S-10, bands at 17 and 19 Kd representing LH subunits were identified. In addition, a high molecular weight 66 Kd band was seen. Surprisingly this high molecular weight band was also seen in rat cerebral cortex, brain stem, hypothalamus, spinal cord, lung, liver, pancreas, spleen, kidney, testis, and serum. Antibody preabsorbed with iodination grade rat LH antigen no longer recognized the 17 and 19 Kd bands in pituitary, but recognized the 66 Kd bands in pituitary and the other tissues examined. Since 66 Kd is the molecular weight of albumin, we found that antisera to rat albumin recognized this same high molecular weight band in the tissues examined. Preabsorption of LH antibody with albumin reduced the ability of that antibody to recognize this 66 Kd. A monoclonal antibody to bovine LH beta-subunit recognized only the LH protein in anterior pituitary, but no high molecular weight band in either pituitary or the other tissues studied. Finally, 10, 100, and 1000 micrograms of rat albumin caused no substantial interference under conditions of RIA. We conclude that the polyclonal antibody, provided by the NIH, is excellent for conditions of RIA, but caution must be exercised when it is used for Western analysis where some lots of this antibody may recognize other unrelated proteins.

Animals↗
PubMed1990

Rat spleen lymphocytes contain an immunoactive and bioactive luteinizing hormone-releasing hormone.

An interaction between the immune and endocrine systems has been long known. This association is further strengthened by the finding that splenic lymphocytes have the capacity to produce molecules similar to if not the same as classical hormones, including several members of the opiate family, PRL, GH, and neuropeptide Y. Because of such findings and because of information from other laboratories suggesting that LHRH might have direct effects upon the immune system, we hypothesized that immune cells themselves might contain LHRH. Lymphocytes were purified from spleens of intact adult male Sprague-Dawley rats and the cells were lysed with sodium hydroxide. The concentration of immunoreactive LHRH was 403 +/- 184 pg/20 X 10(6) lymphocytes. Increasing amounts of lymphocyte lysate displaced [125-I]LHRH from LHRH antibody in a manner parallel to that produced by synthetic hypothalamic LHRH, suggesting immunologic similarity between lymphocyte and hypothalamic LHRH. Lymphocyte LHRH-like immunoactivity coeluted from Nova-Pak C18 columns with synthetic hypothalamic LHRH. When lymphocyte lysates were applied to rat anterior pituitary cells in monolayer culture, significant stimulation of LHRH secretion was seen, from 2,144 +/- 54 pg LH/ml.4 h to 15,364 +/- 587 pg LH/ml.4 h (P less than 0.001), a finding verified in five additional experiments. In other studies, this LH response evoked by lymphocyte lysates was found to be dose dependent and could be significantly inhibited by an LHRH-antagonist. Furthermore, when lymphocyte lysate and identically treated synthetic LHRH were HPLC fractionated, there was coelution of lysate and hypothalamic LHRH bioactivity. The lysate itself contained no substantial LH immunoreactivity. Thus, lymphocytes from spleens of adult male rats contain an immunoactive and bioactive LHRH, a finding further strengthening an association between the endocrine and immune systems.

Animals↗
PubMed1990

Acquired partial corticosterone methyl oxidase type II defect in diabetes mellitus. Case of hyperreninemic hypoaldosteronism.

The aim of this study was to investigate the pathogenesis of hypoaldosteronism in diabetes. Endogenous elevation of plasma renin activity and exogenous corticotropin were used to study steroidogenesis. Observations were made over 12 yr on the evolution and treatment of hyperkalemia in a diabetic subject. In 1977, potassium, baseline cortisol, aldosterone, and renin activity were normal; renin activity increased normally with posture; and cortisol responded normally to ACTH infusion. Nine yr later, persistent hyperkalemia was documented. Upright renin activity was elevated to 5.26 ng.L-1.s-1, with concomitant elevation of 18-hydroxycorticosterone (18-OHB) and a low-normal aldosterone level. One hour after administration of 0.25 mg i.m. cosyntropin, cortisol increased normally, aldosterone increased from 220 to 360 pM, and 18-OHB increased from 3700 to 4800 pM. During treatment with fludrocortisone, fludrocortisone with furosemide, and furosemide alone, improvement of hyperkalemia was noted. Endogenous hyperreninemia and basal elevations of 18-OHB, accompanied by limited aldosterone responsiveness to renin and ACTH, suggest the presence of a partial corticosterone methyl oxidase type II defect. Evolution of hyperkalemia between 1977 and 1986 suggests this defect was acquired.

18-Hydroxycorticosterone↗
PubMed1990

Mental efficiency and hypoglycemia.

Cognitive functioning after a mild hypoglycemic episode (MHE) was studied in 24 school-age children with insulin-dependent diabetes mellitus (IDDM). All children were administered a battery of neuropsychological tests which included digit spans, trailmaking tasks, Klove Mathews Maze test, and finger-tapping and handwriting tasks. The experimental group (n = 14) consisted of children who were tested initially after resolution of hypoglycemic symptoms following a documented MHE (Chemstrip bG less than or equal to 60 mg/dl with symptoms). The comparative group (n = 10) consisted of children who were initially evaluated after documentation of euglycemia. Comparison of the comparative group scores with test scores of the experimental group after recovery from the MHE demonstrated statistically significant differences (p less than 0.05 by dependent t-tests) in five of 12 tasks. No differences were noted when second trial scores of both groups were compared when they were retested after documentation of euglycemia. This study suggests that a discrepancy exists between the recovery rate of physical symptoms and cognitive function in children following a MHE.

Achievement↗
PubMed1990

Follicular cell predominance in the cytologic examination of dominant thyroid nodules indicates a sixty percent incidence of neoplasia.

The interpretation of aspiration cytologic smears that contain a predominance of follicular components often presents a dilemma to the clinician who is treating a patient who has a dominant thyroid nodule, especially when thyroid-stimulating hormone suppression does not produce any significant involution of the dominant nodule. We reviewed a consecutive series of 555 fine-needle aspiration cytologic examinations of dominant thyroid nodules. All specimens that contained colloid or follicular cells mixed with lymphocytes or Hürthle cells were excluded from this review. Additionally, nine aspirates contained degenerated follicular cells with insufficient material for cytologic diagnosis. The remaining 76 specimens contained a predominance of follicular cells: 27 specimens were interpreted as containing "normal" follicular cells, and the remaining 49 specimens were read as "atypical" follicular cells. Histopathologic examination of the resected specimens indicated a 60% incidence of neoplasia (30% carcinoma, 30% adenoma) in which the aspiration cytologic study was interpreted as "normal" follicular cells. On the other hand, a 63% incidence of neoplasia (27% carcinoma, 36% adenoma) occurred in which the cytologic study was read as "atypical." In conclusion, aspirates showing a predominance of follicular cells, whether "normal" or "atypical" indicate a 60% incidence of neoplasia in dominant thyroid nodules that do not decrease significantly in size with thyroid-stimulating hormone suppression.

Adenocarcinoma↗
PubMed1989

In-vivo effect of ethanol on release of LH-releasing hormone and LH in rats.

The effect of exposure to ethanol on hypothalamic LH-releasing hormone (LHRH) release in vivo was investigated in rats both acutely (i.p. injection) and after 3 days of administration, utilizing a permanent gastric cannula. In both designs, the animals were castrated before being given ethanol and, in both experiments, ethanol successfully lowered the post-castration LH rise compared with control castrated animals. In both the acutely and chronically treated groups, basal LHRH release was not impaired, despite the documented decrease in LH levels. Finally, stimulated LHRH release was investigated with depolarizing concentrations of potassium and, again, no change was noted between the hypothalamic release of this decapeptide in the ethanol-exposed compared with the ethanol-naive animals. Thus, ethanol failed to inhibit basal or stimulated LHRH secretion in the acutely and chronically treated animal. This lack of effect on LHRH occurred despite a concomitant lowering of serum concentrations of LH.

Animals↗
PubMed1989

In vitro effect of ethanol exposure on basal and GnRH-stimulated LH secretion from pituitary cells.

The question of whether ethanol's (ETOH's) known suppressive effect on serum luteinizing hormone (LH) could be mediated directly at the anterior pituitary level was addressed by examining the effects of ETOH in vitro on release of LH from cultured male rat pituitary cells. The impact of added ethanol concentrations ranging from 50 to 400 mg% on LH release was examined in the basal state and after stimulation by gonadotropin-releasing hormone (GnRH) at a dose of 5 x 10(-10) M. While ETOH did not significantly suppress basal LH release, secretion stimulated with GnRH was noted to be attenuated with higher doses of ETOH (greater than or equal to 100 mg%) compared to stimulated control cells. It is concluded that ETOH exposure in vitro alters stimulated LH secretion by acting directly on pituitary gonadotropes.

Animals↗
PubMed1989

Adult nesidioblastosis. An unusual cause of fasting hypoglycemia.

Laidlaw coined the term nesidioblastosis in 1938 to characterize the neodifferentiation of the islet cells of Langerhans from pancreatic duct epithelium. It is well recognized in the pediatric population as a frequent cause of persistent neonatal hypoglycemia. However, its occurrence in adults is presumed to be rare and, therefore, it is not appreciated as a cause of hyperinsulinism. Three women, aged 29, 42, and 63, with adult onset hyperinsulinism secondary to nesidioblastosis are reported. All three patients required near-total pancreatectomy. The preoperative findings were consistent with hyperinsulinemic hypoglycemia as with insulinomas. Results of pancreatic imaging studies were normal in two patients and one patient had a pancreatic examination by computerized tomography and magnetic resonance imaging, with false-positive results. Two of the three patients had previously undergone a 50 per cent distal pancreatectomy in which the resected specimens were interpreted as normal in one patient and consistent with nesidioblastosis in the second. Both patients subsequently developed recurrent symptomatic hyperinsulinemic hypoglycemia that persisted despite dosage adjustments in diazoxide therapy. The oldest patient underwent a 95 per cent pancreatectomy at the initial surgical exploration because an insulinoma could not be identified. The other patients underwent a completion 95 per cent pancreatectomy. In both, histochemical examination of each specimen disclosed nesidioblastosis, characterized by clusters of islet cells interspersed throughout the exocrine tissue.

Adult↗
PubMed1988

Synthesis and secretion of insulin-like growth factor II by a leiomyosarcoma with associated hypoglycemia.

We describe a case of recurrent hypoglycemia apparently caused by secretion of insulin-like growth factor II (IGF-II) by a leiomyosarcoma. A 67-year-old woman presented with recurrent severe hypoglycemia and a large mass in the thorax. During hypoglycemia, plasma cortisol was elevated, but insulin and growth hormone levels were low. After resection of a large leiomyosarcoma, the hypoglycemia resolved. After an eight-year remission, both the tumor and symptomatic hypoglycemia recurred. During a second operation a second large tumor was removed, with relief of the patient's hypoglycemia. The tumor contained high concentrations of IGF-II mRNA and 2100 ng of IGF-II immunoreactive peptide per gram. Filtration through a BioGel P-60 gel column established that 77 percent of the IGF-II was present as a larger molecule, demonstrating incomplete processing of the pro-IGF-II peptides. A similar fraction of high-molecular-weight IGF-II was present in the serum, indicating that the tumor was the chief source of IGF-II. The high-molecular-weight IGF-II found in both the tumor and serum was fully reactive with the IGF-II receptor. Radioimmunoassay showed that the concentrations of insulin-like growth factor I (IGF-I) in tumor and serum were low, suggesting feedback inhibition of growth hormone secretion by IGF-II. Eight months after reoperation, plasma concentrations of IGF-I and IGF-II were normal, and high-molecular-weight IGF-II was virtually undetectable. We conclude that the most likely cause of this patient's recurrent hypoglycemia was IGF-II produced by the leiomyosarcoma.

Aged↗
PubMed1988

User attitudes toward end-user literature searching.

A survey to determine attitudes toward end-user searching was made at Loyola University's Medical Center Library using MEDIS, an online full-text and bibliographic medical retrieval system. One hundred forty-one completed questionnaires were analyzed for this report. Information was collected on user familiarity with computers, end-user training, system use, mechanics of searching, and attitudes toward future use. Computer familiarity was highest among the faculty users. Ninety percent of the respondents saw librarians as a crucial agent in training and in providing end-user assistance. Respondents identified five major reasons for using the system: helpfulness, convenience, time savings, rapid feedback, and presentation of needed information. Searching the MEDLINE database rather than the full-text database was the search method of choice. Continued use of both mediated and end-user searching was intended by most of the respondents. Survey results support a perceived need for end-user searching and confirmed recommendations of the Association of American Medical Colleges on medical information science skills.

Attitude of Health Personnel↗