PubMed Health⌕ Search

Biomedical subjects

C Limas

Publications and source records attributed to C Limas.

At least 73 records · Page 4Linked to original sources
PubMed1987

Effect of a high carbohydrate diet on cardiac alpha-1 and beta adrenoceptors.

Short-term (2 weeks) administration of a high-fructose diet to euthyroid Sprague-Dawley rats results in a significant (18%) increase of cardiac beta-adrenoceptors without any change in their affinities or their distribution between the plasma membrane and a vesicular fraction. A much smaller increase occurs in the number of alpha 1-adrenoceptors (8% higher than in rats fed a regular diet). The high-carbohydrate diet induced a 39% increase in beta-adrenoceptor numbers/heart in hypothyroid animals and a 19% increase in the total number of alpha 1-adrenoceptors. These results strongly suggest that changes in cardiac performance after dietary manipulations may be mediated, in part, through enhancement of adrenergic pathways.

Animals↗
PubMed1987

Altered intracellular adrenoceptor distribution in myocardium of spontaneously hypertensive rats.

The number of membrane-bound beta-adrenoceptors is reduced in the myocardium of spontaneously hypertensive rats, and this decline may account for the decreased inotropic responsiveness to beta-agonists. It is not known, however, whether the total complement of cellular beta-receptors is lower in hypertensive animals. This issue was examined using two different approaches: acid elution of cell surface-bound beta-receptor ligands and comparison of the number of receptors in the plasma membrane and a postcytosolic vesicular fraction. Approximately 30% of the total beta-receptors were located intracellularly in Wistar-Kyoto rats compared with 42% for spontaneously hypertensive rats. Similarly, a decline in membrane-bound beta-receptors in hypertensive rats was balanced by a rise in receptors associated with the vesicular fraction. In contrast, alpha 1-adrenoceptors were higher in the membrane and lower in the vesicular fraction of hypertensive rats without a significant difference in total alpha-receptors compared with normotensive animals. Differences in adrenergic responsiveness in this, and perhaps other, models of cardiac hypertrophy reflect altered intracellular distribution of adrenoceptors, which may be under the control of the sympathetic nervous system.

Adrenergic beta-Agonists↗
PubMed1987

Influence of thyroid status on intracellular distribution of cardiac adrenoceptors.

Previous studies have suggested that thyroid hormones influence the number of membrane-bound cardiac adrenoceptors, but their effect on the intracellular distribution of adrenoceptors has not been examined. A plasma cell membrane and a vesicular fraction devoid of membrane markers were prepared from hearts of euthyroid and hyperthyroid rats and were used to compare beta- and alpha-adrenoceptors. During daily injection of l-thyroxine, cardiac hypertrophy developed within 4 days and remained unchanged thereafter. The number of membrane-bound beta-receptors increased progressively and plateaued within 2 weeks of thyroxine administration. Vesicular beta-receptors, on the other hand, increased more gradually and to a lesser extent so that after 2 weeks of l-thyroxine injection, they constituted a smaller proportion of the total beta-receptor population compared to normal rats. In contrast, the number of cardiac alpha 1-adrenoceptors declined rapidly to about 80% of that in euthyroid animals and did not change further for the duration of the study. Membrane-bound and vesicular alpha 1-adrenoceptors were affected to the same extent in hyperthyroidism. During regression of cardiac hypertrophy following cessation of thyroxine administration, alpha 1-adrenoceptors rose rapidly (within 2 days) to normal values while beta-receptors declined more gradually to normal levels within 2 weeks. In hypothyroid rats, there was a significant decline in the density of both alpha 1- and beta-adrenoceptors, with a shift away from the vesicular fraction. These results indicate that both the total numbers of cardiac adrenoceptors and their distribution between the plasma membrane and vesicular fraction are influenced by the thyroid status.

Animals↗
PubMed1986

Transitional cell carcinomas of the urinary bladder. Effects of preoperative irradiation on morphology.

The effects of preoperative irradiation on the morphology of transitional cell carcinomas (TCCs) were evaluated by studying the pretreatment biopsy and radical cystectomy specimens from 35 patients. Twenty-six of these patients had received 2000 rad within the week preceding surgery, and nine patients had received no preoperative treatment. The frequency of bladders without residual TCC was 23% for irradiated and 22% for nonirradiated cases. Of the TCCs classified as papillary in the biopsy specimens and irradiated, 79% lacked a papillary component at cystectomy, but in no case was the invasive component eliminated or regression from muscle invasion to superficial TCC noticed. Flat carcinoma in situ (CIS) did not respond to irradiation. At cystectomy nuclear pleomorphism was greater than at biopsy in 60% of the irradiated TCCs, whereas all nonirradiated cases retained the same grade as at biopsy. In addition, irradiation induced squamous differentiation in neoplastic cells only, without affecting the nonneoplastic urothelium.

Aged↗
PubMed1986

T-antigen in normal and neoplastic urothelium.

The expression of the Thomsen-Friedenreich antigen (T-antigen) in normal and neoplastic urothelium was investigated using paraffin-processed and fresh frozen tissue sections obtained by biopsy from 56 patients. The T-antigen was detected through its binding to the peanut agglutinin (PNA) with two methods: a biotin-avidin-peroxidase system or a modified red cell adherence test. In vitro treatment of the tissue sections with neuraminidase induced PNA binding in the normal and neoplastic urothelium as well as the red blood cells and the vascular endothelium. Spontaneous PNA binding was absent in normal bladder epithelium, but was observed in 10% of the noninvasive and 65% of the invasive transitional cell carcinomas (TCC). The positive reactions were seen in the cytoplasm, cell surface, and mucin. These results were correlated with the light and electron microscopic findings and with the detectability of the A, B, H blood group antigens in the same tissues. Ultrastructurally, the PNA binding sites frequently corresponded to the Golgi apparatus and to secretory products which stained with Alcian blue. About 90% of TCCs with spontaneous PNA binding did not express the expected blood group antigen. The latter was also undetectable in 54% of TCCs lacking spontaneous PNA binding. It appears, therefore, that the expression of T-antigen occurs later in the evolution of aggressive TCCs, usually when they have advanced to invasive stages. The finding of spontaneous T-antigen unmasking correlates with the presence of invasion and a higher risk for metastatic involvement of regional lymph nodes.

ABO Blood-Group System↗
PubMed1986

Analysis of fixation effects on immunohistochemical localization of prostatic specific antigen in human prostate.

We studied human prostatic specific antigen (PSA) localization in human prostate to investigate the possibility that the previously reported variations in the intensity of antigen staining were due to fixation and embedding methods. We have evaluated the effects of physical and several chemical fixatives on prostate samples obtained immediately after prostatectomies and radical cystectomies. Our analysis of fixation effects and immunohistochemical staining of polyclonal antibody to PSA indicates that the formalin fixation and paraffin embedding methods used previously did provide optimum localization of the antigen and the variations in the intensity of PSA staining could not be attributed to the methodology. Although PSA staining was relatively uniform in the lower grade neoplastic tumors, the higher grade, moderately to poorly differentiated tumors showed intense-through-weak PSA localization or no PSA staining suggesting that PSA staining intensity was not uniformly related to tumor differentiation.

Adenocarcinoma↗
PubMed1986

Up-regulation of renal prostaglandin receptors in genetic salt-dependent hypertension.

Development of hypertension in Dahl salt-sensitive rats (DS) is accompanied by reduced renomedullary prostaglandin synthesis, which may be responsible for their lower natriuretic capacity. To examine the changes in renomedullary prostaglandin E2 synthesis, the effects of high (8.0%) and normal (0.6%) NaCl diets were examined in DS and in Dahl salt-resistant rats (DR). In response to an 8.0% NaCl diet, the number of prostaglandin E2 receptors in the renal outer medulla of DR increased (2.97 +/- 0.2 vs 2.18 +/- 0.2 pmol/mg on 0.6% NaCl diet) while no change was noted in their affinities (Kd, 9.5 +/- 0.2 vs 9.4 +/- 0.3 nM). Receptor number and affinity in the renal cortex, inner medulla, and liver of DR were not affected. In contrast, renomedullary receptors of DS had a lower affinity than those of age-matched DR (Kd, 13.9 +/- 0.2 nM on 0.6% NaCl diet and 14.0 +/- 0.3 nM on 8.0% NaCl diet) and did not increase in number after a high salt diet. This apparent inability of DS to modulate prostaglandin receptors may contribute to their susceptibility to salt-induced hypertension.

Adenylyl Cyclases↗
PubMed1986

Phorbol ester receptors in cardiac myocytes of salt-sensitive and salt-resistant Dahl rats.

A moderate degree of cardiac hypertrophy develops in salt-sensitive Dahl (DS) rats after 5 weeks on a high-salt (8% NaCl) diet. Cardiac hypertrophy is accompanied by a significant reduction in the number of phorbol ester receptors on enzymatically dissociated myocytes with no changes in their affinities. In contrast, the number and properties of these receptors are not influenced by variations of dietary salt intake in the salt-resistant Dahl (DR) rat. Since phorbol esters are closely related to protein kinase C, a potent stimulator of Ca2+ transport in the heart, these results suggest that loss of phorbol ester binding sites may limit the inotropic reserve of the hypertrophied myocardium.

Animals↗
PubMed1986

Detection of urothelial Lewis antigens with monoclonal antibodies.

The detectability of Lewis a and b antigens (Lea, Leb) was examined in the normal urothelium of 28 human subjects whose red blood cells (RBCs) were also tested for Lea and Leb. Mouse monoclonal antibodies as well as goat and human antisera were used on paraffin-processed and fresh-frozen tissues. Multiple biopsy specimens from the same individual were studied in order to evaluate temporal as well as topographic consistency of the results. In addition, the expression of the Lewis antigens in the appendiceal mucosa was investigated in 9 of these patients. The antibodies against Lea reacted with the urothelium of all patients with either Lea+b- or Lea-b+ RBC phenotype. None of the 5 patients with Lea-b- RBCs had Lea urothelial reactivity. The antibodies against Leb reacted with the urothelium of all patients with Lea+b- or Lea-b+ RBCs and with 2 of the 5 patients with Lea-b- RBCs. The mucin in the goblet cells of the appendiceal mucosa was positive only for the Lewis antigen that was also detectable of the individual's RBCs. These findings indicate that the expression of Lewis antigens in nonsecretory epithelia may not follow the same principles as in the blood and secretions.

Antibodies, Monoclonal↗
PubMed1985

Carbachol induces desensitization of cardiac beta-adrenergic receptors through muscarinic M1 receptors.

Incubation of enzymatically dissociated cardiac myocytes with carbachol leads to a time- and concentration-dependent loss of beta-receptors assayable with [3H]CGP-12177. This loss is due to a redistribution of beta-receptors from the plasma membrane to a cytosol-derived vesicular fraction, consistent with an internalization process. The carbachol effects are not influenced by gallamine or oxotremorine which interact with the high-affinity (M2) muscarinic receptors. These results suggest that carbachol-induced desensitization is secondary to activation of protein kinase C by diacylglycerols generated through M1 receptor-linked phosphoinositide hydrolysis.

Animals↗
PubMed1985

Simultaneous presentation of relapsing Hodgkin's disease and treatment-related non-Hodgkin's lymphoma.

A 55-year-old white man was diagnosed in 1975 with Hodgkin's disease stage IIA, mixed cellularity. He was treated with 4,500 rads to an inverted-Y field followed by six cycles of MOPP and remained in complete remission. In 1983 a right axillary lymph node biopsy showed recurrent Hodgkin's disease, mixed cellularity. While receiving his initial chemotherapy he developed persistent epigastric distress. Endoscopic gastric biopsy demonstrated a diffuse large-cell non-Hodgkin's lymphoma. Surface marker studies confirmed the separate identity of these two malignant lymphoproliferative processes. This represents the first reported simultaneous occurrence of relapsing Hodgkin's disease with treatment-related non-Hodgkin's lymphoma.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1985

Renomedullary phospholipases in salt-sensitive and salt-resistant Dahl rats.

Renomedullary prostaglandin synthesis is lower in salt-sensitive (S) Dahl rats than in age-matched salt-resistant (R) rats on either 0.6% or 8.0% NaCl. The possible role of substrate availability to the cyclooxygenase in determining these differences was examined. S and R rats were started on diets with variable salt content (0.6%, 4.0% or 8.0% NaCl) at five weeks and were sacrified at either 11 or 16 weeks of age for comparisons of renomedullary phospholipase A1 and A2 activities (EC 3.1.1.4. and 3.1.1.32) and arachidonate incorporation into the lipids of renal medulla. Both phospholipase activities were higher in R rats at the two ages examined and for all levels of salt intake. These differences could not be accounted for by variable amounts of endogenous phospholipid substrate. High salt intake did not influence the in vitro A2 deacylating activities per mg protein. Arachidonate incorporation into renomedullary triglycerides remained constant with age in both strains while phospholipid labeling declined with age in S rats only so that, at 16 weeks of age, S rats had significantly lower incorporation into membrane phospholipids. This age-related decline in phospholipid labeling in S rats was prevented by 4.0% NaCl. These results suggest that low renomedullary phospholipase activities in S rats may restrict the release of substrate for prostaglandin synthesis and may also be related to reduced rates of fatty acid incorporation into membrane phospholipids.

Age Factors↗
PubMed1985

Phorbol ester- and diacylglycerol-mediated desensitization of cardiac beta-adrenergic receptors.

There are specific phorbol ester receptors on cardiac myocytes which may be identical with the calcium/phospholipid-dependent protein kinase (protein kinase C). Incubation of enzymatically dissociated rat cardiac myocytes with biologically active phorbol esters (such as 4 beta-phorbol-12, 13-dibutyrate and 12-O-tetradecanoyl phorbol-13-acetate) leads to a time- and concentration-dependent loss of beta-adrenergic receptors detectable with the hydrophilic ligand [3H]-CGP-12177. This loss is attributable to a reduction in both maximal beta-receptor numbers and their affinities. The synthetic diacylglycerol, 1-oleyl-2-acetyldiglycerol, which is known to activate protein kinase C, also induces desensitization of beta-receptors. Both phorbol dibutyrate and 1-oleyl-2-acetyldiglycerol have additive effects to isoproterenol, suggesting a separate site of action in promoting beta-receptor desensitization. The effects of phorbol dibutyrate and 1-oleyl-2-acetyldiglycerol are prevented by colchicine (but not its inactive analog, trimethylcolchicinic acid), indicating a microtubule dependence. The loss of membrane-bound beta-receptors after phorbol dibutyrate- or 1-oleyl-2-acetyldiglycerol preincubation is accompanied by an increase in beta-receptors associated with a cytosol-derived vesicular fraction devoid of plasma membrane markers, a finding consistent with an internalization process. These results suggest that protein kinase C activation by diacylglycerols derived from receptor-linked phosphoinositide hydrolysis may be a novel mechanism of cardiac beta-receptor desensitization.

Animals↗
PubMed1985

Transplantation of human renal carcinomas into athymic mice.

Thirty-one primary human renal carcinomas were transplanted into athymic mice of which ten produced tumors in the mouse host. Only tumors with a nuclear grade of 3 or 4 were successfully transplanted. The nuclear grades of the human tumor and transplant were similar; however, the cellular histology often varied. Patient prognosis appeared to be inversely related to successful tumor transplantation. In the transplant group, the 1-year survival was 30% in contrast to a 1-year survival of 83% among patients with renal cancers of similar stage and grade which did not produce tumors in the mice.

Animals↗
PubMed1985

Lewis antigens in normal and neoplastic urothelium.

The Lewis (Lea and Leb) antigens are closely related to the A, B, H blood group antigens and have been demonstrated in several secretory epithelia, but their expression in nonsecretory cells has not been studied systematically. This report provides detailed data on the expression of Lea and Leb in normal and neoplastic urothelium. The authors have examined multiple biopsy specimens of normal bladder mucosa and transitional cell carcinomas (TCCs) from 74 patients whose red blood cells (RBCs) were also typed for A, B, H, Lea, and Leb antigens and have correlated tissue antigen detectability with the RBC phenotype and the cytologic grade of malignancy. Antisera of human and animal sources were used in a modified red cell adherence test (RCA), and multiple controls were employed for determination of the specificity of the reactions. Both fresh-frozen and paraffin-processed tissues were examined from each patient. Paraffin processing as well as treatment with ethanol significantly suppressed the tissue reactions. Ninety-four percent of normal mucosa specimens and 73% of TCCs gave positive reactions with both anti-Lea and anti-Leb sera. Abnormal patterns of Lewis reactivity were observed in 43% of Grade III or IV and in 14% of Grade I or II TCCs. Although there was no direct correlation between A, B, H reactivity and Lewis reactivity, all TCCs which had abnormally low reactivity for both the expected Le and A, B, or H antigens were of high grade and invasive.

ABO Blood-Group System↗
PubMed1984

Prostaglandin receptors in rat kidney.

The physiological effects of prostaglandins (PGs) are mediated through their interactions with specific binding sites (receptors) on effector cells. Since such receptors potentially regulate the action of PGs on the kidney, the distribution and properties of renal PG receptors in the rat were examined. The distribution of PGE2, PGE1, and PGF2 alpha receptors along the nephron was not uniform; the outer medulla had by far the greatest density of sites, followed by the inner medulla and cortex. Receptors were found exclusively in the particulate fractions, of which the 40,000g pellet had the highest specific activity. In the outer medulla, receptor density calculated from Scatchard plots was 2.12 pmol/mg for PGE2, 1.12 for PGE1, and 0.44 for PGF2 alpha; the KD's were similar for all prostaglandins. The conditions for optimal in vitro binding of PGE2 and PGF2 alpha by outer medullary membranes were investigated. In vivo administration of 16,16'-dimethyl-PGE2 resulted in a dose-dependent "down" regulation of PGE2 binding to outer medullary membranes due to changes in both the number and affinities of receptors. Changes in the numbers and/or properties of PG receptors may be an important mechanism for regulating the effects of PGs and renal function under normal and pathologic conditions.

Alprostadil↗