2,030 research outputs found
Regulation of dopamine receptors in the MtT/W15 transplantable pituitary tumor by estrogen
We investigated the effects of estrogens on the regulation of dopamine receptors in the MtT/W15 transplantable rat pituitary tumor. Diethylstilbestrol (DES) and 17[beta]-estradiol treatment in female rats significantly decreased the number of dopamine binding sites (Bmax) from 85 +/- 3.9 fmol/mg protein in untreated rats to 9.2 +/- 1.2 and 8.2 +/- 2.8 fmol/mg protein in DES and 17[beta]-estradiol-treated rats, respectively, while the binding affinities (Kd) did not change significantly. Testosterone treatment did not change the Bmax, while ovariectomy resulted in a significant increase in the Bmax (146.3 +/- 6.7 fmol/mg protein). The effects of DES on the Bmax were reversible, since removal of the DES for one week before sacrificing the animals led to a marked increase in the Bmax (54.9 +/- 3.1 fmol/mg protein).Pituitaries from normal female rats treated with DES for 6 and 9 weeks had a significant decrease in the Bmax.These results show that the number of dopamine binding sites in the membranes of MtT/W15 tumors is decreased by estrogen treatment and that this effect is reversible after removal of the estrogenic stimulus.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/26273/1/0000358.pd
Calcitonin free oat-cell carcinoma of the thyroid gland
Two cases of primary oat-cell carcinoma of thyroid, in a 63-year-old woman and a 73-year-old man, are described. Case 1 was a compound tumour with the oat-cell component merging with a papillary component. Both tumours, in addition to histological features consistent with oat-cell carcinoma, showed immunohistochemical positivity with anti-chromagranin A and anti-synaptophysin antisera. Negative results were obtained when anti-calcitonin and anti-thyroglobulin antisera were employed. Using in situ hybridization, chromogranin A and B messenger RNAs were localized with biotinylated oligonucleotide probes. In contrast, with in situ hybridization, no localization for calcitonin messenger RNA was seen using radioactive and biotinylated probes. It is concluded that these calcitonin-free, small-cell carcinomas should be considered separately from medullary thyroid carcinomas and be regarded as a distinct entity, probably the thyroid equivalent of oat-cell carcinomas of the lung.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47516/1/428_2005_Article_BF01600144.pd
Metastatic carcinoma to the sphenoid sinus case report and review of the literature
Metastatic carcinoma to the sphenoid sinus is a rare event. A case of metastatic adenocarcinoma from the prostate gland to the sphenoid sinus and diagnosed with the aid of immunoperoxidase staining is presented. A concurrent review of the literature uncovered only 17 previously reported cases of carcinoma metastatic to the sphenoid sinus. Among these cases, adenocarcinoma from the large bowel and prostate gland predominated.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47269/1/405_2004_Article_BF00453691.pd
Idiopathic prolactin cell hyperplasia of the pituitary mimicking prolactin cell adenoma: a morphological study including immunocytochemistry, electron microscopy, and in situ hybridization
Prolactin cell adenoma is the most frequently found lesion in surgically removed pituitaries of patients with hyperprolactinemia. However, in several instances, instead of prolactin cell adenoma, other lesions are encountered by morphological investigation. We report here the morphological findings in a patient with hyperprolactinemia who underwent transsphenoidal pituitary surgery for suspected prolactin cell adenoma. A morphological diagnosis of tumor could not be confirmed and massive diffuse prolactin cell hyperplasia was identified. The aim of this publication is to describe the lesion by histology, immunocytochemistry, electron microscopy, and in situ hybridization and to call attention to primary prolactin cell hyperplasia which can mimic prolactin cell adenoma.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47231/1/401_2004_Article_BF00293958.pd
Tendency to Maximum Complexity in a Non-Equilibrium Isolated System
The time evolution equations of a simplified isolated ideal gas, the
"tetrahe- dral" gas, are derived. The dynamical behavior of the LMC complexity
[R. Lopez-Ruiz, H. L. Mancini, and X. Calbet, Phys. Lett. A 209, 321 (1995)] is
studied in this system. In general, it is shown that the complexity remains
within the bounds of minimum and maximum complexity. We find that there are
certain restrictions when the isolated "tetrahedral" gas evolves towards
equilibrium. In addition to the well-known increase in entropy, the quantity
called disequilibrium decreases monotonically with time. Furthermore, the
trajectories of the system in phase space approach the maximum complexity.Comment: 22 pages, 0 figures. Published in Phys. Rev. E 63, 066116(9) (2001
MALIGNANT SOMATOSTATINOMA PRESENTING WITH DIABETIC KETOACIDOSIS
High circulating levels of somatostatin (SRIF) were detected in a patient with a metastatic tumour after development of diabetic ketoacidosis (DKA). Fasting insulin and C-peptide levels were markedly suppressed, but plasma glucagon was not suppressed below normal. Progressive cachexia ensued; at autopsy a poorly differentiated non-small cell neuroendocrine carcinoma metastatic to liver was found. Small gallstones were noted. Electron microscopy of tumour tissue showed neurosecretory granules and tonofilament bundles. Immunohis-tochemical staining of tumour cells was diffusely positive for carcinoembryonic antigen, bombesin-like immunoreactivity, and calcitonin with focal immuno-reactivity for SRIF, serotonin, neuron-specific enolase, chromogranin, and epithelial membrane antigen. Column chromatography of plasma and tumour extract revealed five or more peaks of material with SRIF-like immunoreactivity (SRIF-LI): predominantly SRIF-28 and intermediates in tumour extract, and SRIF-14 and an intermediate between SRIF-28 and SRIF-14 in plasma. DKA in this case of somatostatinoma syndrome may reflect differential effects of tumour production of larger molecular weight SRIF forms on insulin and glucagon secretion.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/75579/1/j.1365-2265.1987.tb00817.x.pd
Epigenomic and somatic mutations of pituitary tumors with clinical and pathological correlations in 111 patients
Objective To profile clinically non-aggressive and aggressive pituitary adenomas (PAs)/pituitary neuroendocrine tumours (PitNETs) and pituitary carcinomas for somatic mutations and epigenetic alterations of genes involved in cell proliferation/differentiation, microRNAs (miRNA)/long noncoding RNA (LncRNA)-post-transcriptional regulators and therapy targets. Design Retrospective observational study. Patients and Measurements A total of 64 non-aggressive and 41 aggressive PAs/PitNETs and 6 pituitary carcinomas treated by endoscopic surgery with >= 1-year follow-up were included. Somatic mutations of 17 genes and DNA methylation of 22 genes were assessed. Ten normal pituitaries were used as control. Results We found at least one mutation in 17 tumours, including 6/64 non-aggressive, 10/41 aggressive PAs/PitNETs, and 1/6 pituitary carcinoma. AIP (N = 6) was the most frequently mutated gene, followed by NOTCH (4), and TP53 (3). Hypermethylation of PARP15, LINC00599, ZAP70 was more common in aggressive than non-aggressive PAs/PITNETs (p < .05). Lower levels of methylation of AIP, GNAS and PDCD1 were detected in aggressive PAs/PITNETs than non-aggressive ones (p < .05). For X-linked genes, males presented higher level of methylation of FLNA, UXT and MAGE family (MAGEA11, MAGEA1, MAGEC2) genes in aggressive vs. non-aggressive PAs/PITNETs (p < .05). In pituitary carcinomas, methylation of autosomal genes PARP15, LINC00599, MIR193 and ZAP70 was higher than in PAs/PITNETs, while X-linked genes methylation level was lower. Conclusions Somatic mutations and methylation levels of genes involved in cell proliferation/differentiation, miRNA/LncRNA-post-transcriptional regulators and targets of antineoplastic therapies are different in non-aggressive and in aggressive PAs/PitNETs. Methylation profile also varies according to gender. Combined genetic-epigenetic analysis, in association with clinico-radiological-pathological data, may be of help in predicting PA/PitNET behaviour
Sites of synthesis of chromogranins A and B in the human brain
The sites of synthesis of the chromogranins A and B, and their potential processed peptides, were examined by quantitating the levels of chromogranin A and B mRNA in various regions of the human brain by Northern blot analysis. Chromogranin A and B mRNA expression in the brain is region-specific and confined to grey matter. In situ hybridization histochemistry detected chromogranin A and B mRNA in pyramidal neurons of human cerebral cortex. Cell-specific expression in subpopulations of cerebrocortical neurons suggest that chromogranin A and B gene products may play a role in central neuronal function.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/30124/1/0000500.pd
Carcinosarcoma of bladder Evaluation by electron microscopy and immunohistochemistry
A case of carcinosarcoma of the urinary bladder characterized by electron microscopy and immunohistochemistry is described. The use of these studies in poorly differentiated bladder neoplasms and in suspected cases of carcinosarcoma is encouraged. Increased accuracy in characterizing these tumors will permit a better understanding of their natural history and response to therapy.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/24686/1/0000105.pd
MEN I pancreas: A histological and immunohistochemical study
The spectrum and extent of islet cell histopathological findings in patients with multiple endocrine neoplasia, type I (MEN I) syndrome has never been clearly defined. Although some patients have discreet tumors causing clinically evident syndromes, others may have no symptoms until metastatic islet cell carcinoma is apparent. Whether diffuse islet cell disease occurs in all patients with grossly apparent tumors is not known. This study is an attempt to define both the functional and anatomical extent of islet cell disease and its relationship with the clinical course of patients with MEN I syndrome. The resected specimens of pancreas from 14 patients with MEN I syndrome were evaluated for hyperplasia, nesidioblastosis, multiple tumors, and evidence of malignancy. In 12 cases, specimens consisted of distal pancreas and, in 2 cases, the entire pancreas was available. Multiple sections were taken from each specimen. Immunoperoxidase staining was done for gastrin, pancreatic polypeptide, glucagon, serotonin, VIP, somatostatin, and neuron-specific enolase in sections of 24 tumors from 10 patients. Five of the 10 patients with Zollinger-Ellison syndrome underwent total gastrectomy and 3 others underwent only pancreatic procedures to control their acid hypersecretion. The following is concluded. All MEN I patients with pancreatic neoplasms have diffuse islet cell involvement consisting of nesidioblastosis, micro- and macronodular hyperplasia. Some tumors produce multiple hormones and these patients are at risk to develop new tumors, but complete excision of grossly apparent tumors may result in long-term control of the endocrinopathy present. This is particularly true for patients with insulinoma and hypoglycemia. Selected patients with gastrinoma may also be considered for excision of their islet cell tumor(s) without concomitant gastrectomy, especially if transhepatic venous sampling demonstrates a single site of excess gastrin production. However, if transhepatic venous sampling demonstrates diffuse sources of hypergastrinemia, a local pancreatic procedure will invariably be unsuccessful. Total pancreatectomy in MEN I patients with disease localized to the pancreas is the only curative surgical procedure but is rarely indicated. L'histopathologie des cellules insulaires pancrĂ©atiques des malades qui prĂ©sentent un syndrome MEN I n'a jamais Ă©tĂ© parfaitement dĂ©finie. Si certains parmi eux sont porteurs de petites tumeurs qui se manifestent par des syndromes cliniques patents, d'autres n'accusent aucun symptĂ´me avant que des mĂ©tastases nĂ©oplasiques ne se manifestent. En particulier, on ne sait pas si les altĂ©rations des cellules insulaires sont diffuses quand les malades prĂ©sentent des tumeurs Ă©videntes. Cette Ă©tude a pour but de dĂ©finir Ă la fois l'importance anatomique et l'importance fonctionnelle de la maladie insulaire par rapport Ă son expression clinique chez les sujets concernĂ©s par ce syndrome. Pour ce faire, des spĂ©cimens provenant de 14 malades atteints du syndrome MEN I ont Ă©tĂ© Ă©tudiĂ©s eu Ă©gard Ă l'hyperplasie, Ă la nĂ©sidioblastose, Ă la multiplicitĂ© des Ă®lots tumoraux, Ă la malignitĂ©. Dans 12 cas, les spĂ©cimens rĂ©pondaient au pancrĂ©as distal, dans 2 cas Ă la totalitĂ© du pancrĂ©as. De multiples coupes furent pratiquĂ©es au niveau de chaque pièce soumise Ă l'examen. L'imprĂ©gnation Ă l'immunoperoxidase concerna les coupes de 24 tumeurs provenant de 10 patients. Cinq des 10 malades qui prĂ©sentaient un syndrome de Zollinger-Ellison avaient subi une gastrectomie totale et 3 une intervention pancrĂ©atique pour contrĂ´ler leur hypersĂ©crĂ©tion acide. Les conclusions tirĂ©es de cette Ă©tude furent les suivantes: tous les malades accusant un syndrome MEN I et porteurs d'un nĂ©opolasme pancrĂ©atique prĂ©sentaient des lĂ©sions insulaires diffuses rĂ©pondant Ă une nĂ©sidioblastose, Ă une hyperplasie micronodulaire et macronodulaire. Quelques tumeurs produisaient de multiples hormones: gastrine, polypeptide pancrĂ©atique, glucagon, sĂ©rotonine, V.I.P., somatostatine, testĂ©es par la mĂ©thode. Il rĂ©sulte de ces constatations que les risques de rĂ©cidive tumorale après exĂ©rèse complète des tumeurs Ă©videntes ne sont pas Ă Ă©carter, encore que l'exĂ©rèse permette de contrĂ´ler longtemps l'endocrinopathie. Ceci est particulièrement vrai pour les insulinomes hypoglycĂ©miants. En ce qui concerne les gastrinomes, leur exĂ©rèse peut ĂŞtre suffisante, en particulier lorsque les prĂ©lèvements veineux Ă©tagĂ©s montrent qu'ils sont uniques; la gastrectomie concomitante est alors inutile. En revanche, lorsque la gastrine est trouvĂ©e en excès au niveau de multiples Ă©chantillons veineux, l'exĂ©rèse tumorale est insuffisante et la pancrĂ©atectomie totale reprĂ©sente l'intervention indispensable; en fait, son indication est rare. La variedad del espectro de la histopatologĂa de las cĂ©lulas insulares en pacientes con sindrome de neoplasias endocrinas mĂşltiples tipo I (NEM I) todavĂa no ha sido claramente definido. AĂşn cuando algunos pacientes poseen tumores discretos que causan sĂndromes clĂnicamente evidentes, otros pueden no exhibir sintomatologĂa alguna hasta cuando se hace evidente un carcinoma metastásico de cĂ©lulas insulares. No se sabe si hay enfermedad difusa de las cĂ©lulas insulares en todo paciente con tumores macroscĂłpicamente aparentes, ni además se conoce con quĂ© frecuencia se desarrollan nuevos tumores en pacientes con sĂndrome NEM I despuĂ©s de resecciĂłn local o de pancreatectomĂa parcial para tumores primarios de cĂ©lulas insulares. El presente estudio intenta definir la extensiĂłn funcional y anatĂłmica de la enfermedad de las cĂ©lulas insulares y su relaciĂłn con la evoluciĂłn clĂnica en pacientes con el sĂndrome NEM I.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/41313/1/268_2005_Article_BF01654938.pd
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