Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ectopic acromegaly is a very rare clinical entity occurring in less than 1% of acromegalic patients. In most cases it is caused by GHRH or rarely GH-secreting neoplasms. Even rarer are ectopic pituitary adenomas located in the sphenoid sinus or nasopharynx that originate from pituitary remnants in the craniopharyngeal duct. This dissertation presents the difficulties in visualizing GH-secreting adenoma located in the sphenoid sinus. A 55-year-old man had somatic features of acromegaly for several years. MRI imaging revealed a slightly asymmetric pituitary gland (14 yen 4 mm) without focal lesions. Simultaneously, a spherical mass, 10 mm in diameter, corresponding with ectopic microadenoma was demonstrated on the upper wall of the sphenoid sinus. The serum GH level was 4.3 mg/l, IGF-1 = 615 mg/l, and a lack of GH suppression with oral glucose was proven. After preliminary treatment with a long-acting somatostatin analogue, transsphenoidal pituitary tumour removal was performed. Histopathological, electron microscopical and immunohistochemical analysis revealed densely granulated somatotropic pituitary adenoma: GH(+), PRL(-), ACTH(-), TSH(-), FSH(-), LH(-), MIB1 < 1%, SSTR3(+) and SSTR5(+). Post-surgical evaluation showed normal pituitary MRI scans, GH and IGF-1 levels 0.18 mug/l and 140 mg/l, respectively, as well as normal GH suppression with oral glucose. The careful analysis of possible pituitary embryonic malformations points out their significance for proper localization of extrapituitary adenomas.
Endokrynol Pol
PMID:Acromegaly in a patient with normal pituitary gland and somatotropic adenoma located in the sphenoid sinus. 1877 6

Autosomal dominant polycystic kidney disease (ADPKD) is one of the most common causes of end stage renal failure (ESRF). Nevertheless, until now the standard therapy of ADPKD consists merely of nephroprotection and treatment of complications. In the sixth decade of life in about 50% of patients renal replacement therapy is initiated. Surgery procedures such as nephrectomy and renal contraction therapy are performed in some patients. In 21st century numerous studies concerning patophysiology of the disease (role of polycystins, intracellular calcium, cAMP) were published and gave an impulse for searching new drugs that could slower progression of ADPKD. Somatostatin receptor agonists, vasopressin V2 receptor antagonists, rapamycin, and tyrosine kinase inhibitors are among medications that are thought to be effective. Although it is unclear if any of these drugs will be really effective there are strong theoretical backgrounds and promising results of experimental studies on animals. Nephrologists and their patients are waiting for the results of clinical trials that are performed now.
Pol Merkur Lekarski 2008 Oct
PMID:[Modern treatment of autosomal dominant polycystic kidney disease]. 1914 40

A 59-year-old woman presented to the Department of Gastroenterology complaining of progressing weight loss, unexplained diarrhoea, and, as revealed by abdominal ultrasound, numerous hyperechogenic foci in the liver. The immunohistochemical evaluations of the specimens from biopsy revealed well-differentiated hepatic neuroendocrine metastases. The biochemical marker levels, including serum chromogranin A (CGA) and urine 5-hydroxyindolacetic acid (5-HIAA) 24-hour excretion, were significantly elevated. Whole body somatostatin receptor scintigraphy showed tracer accumulation in the liver lesions, with no extrahepatic tumour, possibly the primary origin. Long-term somatostatin analog therapy was initiated and a peptide-receptor targeted radionuclide therapy decision was made parallel to this treatment. Therefore, a followed-up CT scan of the abdomen showed, as well as the metastatic changes within the liver, a wellvascularised jejunal tumour suspected to be the primary focus of the disseminated neuroendocrine neoplasm. Unexpectedly, the pathological examination revealed a positive cell reaction for CD 117, confirming the diagnosis of a rare jejunal stromal tumour. Two months later peptide-receptor therapy with 90Y/77Lu-DOTA-TATE was commenced.
Endokrynol Pol
PMID:A jejunal stromal tumour in a patient with metastatic neuroendocrine cancer of unknown origin; a rare coexistence, diagnostic and therapeutic challenge. 1956 23

The pig has been widely used as a model in cardiovascular research. A unique feature of the porcine extrinsic sympathetic cardiac nerves is that they arise from intermediate ganglia in the thoracic cavity. The localization and pattern of distribution of nerve cell bodies and fibers containing tyrosine hydroxylase (TH), dopamine B-hydroxylase (DBH), neuropeptide Y (NPY), vasoactive intestinal polypeptide (VIP), somatostatin (SOM), galanin (GAL), methionine-enkephalin (MET) as well as calcitonin gene-related peptide (CGRP), substance P (SP) and pituitary adenylate cyclase-activating peptide (PACAP) was studied with immunohistochemistry. Almost all the neurons showed immunoreactivity to TH. Immunoreactivity to NPY, VIP, SOM, GAL, MET and PACAP was displayed by nerve cell bodies while nerve fibers exhibited immunoreactivity to all the neuropeptides studied. Therefore, it seems that the chemical coding of neurons and especially nerve fibers in the porcine intermediate ganglion share general similarities (with certain neurochemical variability), with porcine prevertebral ganglia (e.g., celiacomesenteric and caudal mesenteric ganglia).
Pol J Vet Sci 2010
PMID:Analysis of the chemical coding of neurons in the intermediate thoracic ganglion of the pig. 2103 70

Stress is generally a natural phenomenon that affects behaviour, physiological processes, and neuroendocrine, neurochemical, neurological and immune responses. Many somatic and mental disorders are thought to result from chronic stress. Stress-induced gonadal dysfunction is not restricted to humans, but is observed in all higher animals. Stress-induced gonadal dysfunction comprises disturbances of the hypothalamic-pituitary-gonadal axis and of spermatogenesis. Various stressors induce changes in the secretion of neurotransmitters and hormones, such as CRH, ADH, beta-endorphins, somatostatin, VIP, PRL, GH, TSH, dopamine, serotonin, neuropeptide Y, melatonin, ACTH, glucocorticosteroids, catecholamines and androgens. In acute stress, testicular function is principally modified by cytokines and fluctuating concentrations of gonadotropins, while in chronic stress, hypogonadotropic hypogonadism and disruption of spermatogenesis of varying severity, including spermatogenetic arrest, are observed. In spite of the decades-long interest in the relationships between psychological stress and the function of male gonads, many questions in this area remain unanswered.
Endokrynol Pol 2012
PMID:Psychological stress and the function of male gonads. 2237 97

We present the diagnostic and therapeutic difficulties encountered in a patient with a clinically advanced pancreatic neuroendocrine tumour. The report concerns a 60-year-old female patient with the diagnosis of non-functioning pancreatic neuroendocrine tumour (NET G1) with liver, peripancreatic lymph node and mediastinal metastases. Due to the presence of advanced disease (inoperable pancreatic tumour, presence of multiple metastases) the patient was considered ineligible for surgical treatment on two occasions. Tissue samples for histopathology were collected during an exploratory laparotomy, which made it possible to establish the diagnosis. As somatostatin receptor scintigraphy was positive, the patient was started on somatostatin analogues and radionuclide therapy was initiated, resulting in satisfactory response in the form of complete remission of liver metastases and the decreased size of the primary tumour in the pancreas. The use of somatostatin analogues in the case of an inoperable neuroendocrine tumour which was assessed as clinically advanced, yet possessing a low proliferative potential, is a promising therapeutic option.
Endokrynol Pol 2012
PMID:A non-functioning pancreatic neuroendocrine tumour: a case report. 2237

Neuroendocrine neoplasms are a rare and heterogeneous group of diseases that account for only 2% of all gynecologic malignancies. The most common types are ovarian carcinoid tumor and small cell neuroendocrine carcinoma of the cervix. The tumors are staged according to FIGO clinical staging system. The diagnosis is usually made retrospectively after obtaining the results of histopathological evaluation of the primary tumor They rarely cause syndromes related to hormone overexpression. Neuroendocrine neoplasms are characterized by aggressive behaviour Even at an early stage there is high incidence of nodal and distant metastases. Survival is poor regardless of stage at diagnosis. The most important is to diagnose the neuroendocrine tumor accurately and treat it in multimodal, aggressive approach to control the disease better and reduce the incidence of reccurences. Apart from typical therapeutic approach, treatment may encompass isotope therapy using radiolabeled somatostatin analogs. This method should be reserved for patients with expression of somatostatin receptors detected by the somatostatin receptor scyntygraphy. Data concerning the management of neuroendocrin tumors are based mainly on retrospective studies and clinical case series. Lack of randomized trials makes it impossible to select the best treatment option. Better understanding of the biology of neuroendocrine tumors, especially the molecular genetics, will in the future help to determine the optimal treatment strategies for these tumors.
Ginekol Pol 2011 Sep
PMID:[Contemporary management of neuroendocrine neoplasms of the female genital organs]. 2237 29

Conantokin G (CTG), isolated from the venom of the marine cone snail Conus geographus, is an antagonist of N-methyl-d-aspartate receptors (NMDARs), the activation of which, especially those located on the central afferent terminals and dorsal horn neurons, leads to hypersensitivity and pain. Thus, CTG blocking of NMDARs, has an antinociceptive effect, particularly in the case of neurogenic pain treatment. As many urinary bladder disorders are caused by hyperactivity of sensory bladder innervation, it seems useful to estimate the influence of CTG on the plasticity of sensory neurons supplying the organ. Retrograde tracer Fast Blue (FB) was injected into the urinary bladder wall of six juvenile female pigs. Three weeks later, intramural bladder injections of CTG (120 microg per animal) were carried out in all animals. After a week, dorsal root ganglia of interest were harvested from all animals and neurochemical characterization of FB+ neurons was performed using a routine double-immunofluorescence labeling technique on 10-microm-thick cryostat sections. CTG injections led to a significant decrease in the number of FB+ neurons containing substance P (SP), pituitary adenylate cyclase activating polypeptide (PACAP), somatostatin (SOM), calbindin (CB) and nitric oxide synthase (NOS) when compared with healthy animals (20% vs. 45%, 13% vs. 26%, 1.3% vs. 3%, 1.2 vs. 4% and 0.9% vs. 6% respectively) and to an increase in the number of cells immunolabelled for galanin (GAL, 39% vs. 6.5%). These data demonstrated that CTG changed the chemical coding of bladder sensory neurons, thus indicating that CTG could eventually be used in the therapy of selected neurogenic bladder illnesses.
Pol J Vet Sci 2012
PMID:Conantokin G-induced changes in the chemical coding of dorsal root ganglion neurons supplying the porcine urinary bladder. 2270 64

Although resiniferatoxin (RTX) becomes more often used in experimental therapies of sensory system disorders, so far there is no data concerning the influence of RTX on the chemical coding of neurons in dorsal root ganglia (DRG) supplying the urinary bladder in the pig, an animal species considered as a reliable animal model for investigation dealing with human lower urinary tract disorders. Retrograde tracer Fast Blue (FB) was injected into the wall of the right half of the urinary bladder in six juvenile female pigs, and three weeks later, bladder instillation of RTX (500 nmol per animal) was carried out in all the animals. After a week, DRGs were harvested from all the pigs and the neurochemical characterization of FB+ neurons was performed using routine single-immunofluorescence labeling technique on 10-microm-thick cryostat sections. RTX instillation resulted in a distinct decrease in the numbers of FB+ cells containing calcitonin gene-related peptide (CGRP), nitric oxide synthase (NOS), somatostatin (SOM) and calbindin (CB) when compared with those found in the healthy animals (18% vs. 36%, 1% vs. 6%, 0.8% vs. 4% and 0.5% vs. 3%, respectively), and an increase in the number of pituitary adenylate cyclase-activating polypeptide (PACAP)- and galanin (GAL)-immunoreactive (IR) nerve cells (51% vs. 26% and 47% vs. 6.5%). The results obtained suggest that RTX could be taken into consideration when the neuroactive agents are planned to be used in experimental therapies of selected neurogenic bladder illnesses.
Pol J Vet Sci 2012
PMID:The influence of resiniferatoxin on the chemical coding of neurons in dorsal root ganglia supplying the urinary bladder in the female pig. 2270 68

Botulinum toxin type A (BTX) is a potent neurotoxin, which in recent years has been effectively applied in experimental treatments of many neurogenic disorders of the urinary bladder. BTX is a selective, presynaptically-acting blocking agent of acetylcholine release from nerve terminals what, in turn, leads to the cessation of somatic motor and/or parasympathetic transmission. However, application of this toxin in urological practice is still in the developmental stages and the full mechanism of its action remain elusive. Thus, the present study was aimed at investigating the neurochemical characterization of dorsal root ganglion (DRG) neurons supplying the porcine urinary bladder after BTX treatment. Retrograde tracer Fast Blue (FB) was injected into the urinary bladder wall in six juvenile female pigs and three weeks later, intramural bladder injections of BTX (100 IU per animal) were carried out in all the animals. After a week, DRG from L1 to Cql were harvested from the pigs and neurochemical characterization of FB+ neurons was performed using double- labeling immunofluorescence technique on 10-microm-thick cryostat sections. BTX injections led to a significant decrease in the number of FB+ neurons containing substance P (SP), calcitonin gene-related peptide (CGRP), calbindin (CB), somatostatin (SOM) and neuronal nitric oxide synthase (nNOS) when compared with that found in the healthy animals (19% vs. 45%, 18% vs. 36%, 0.6% vs. 3%, 0.4 vs. 4% and 0.1% vs. 6%, respectively) These data demonstrated that BTX changed the chemical coding of bladder sensory neurons, and therefore this drug should be taken into consideration when it planning experimental therapy of selected neurogenic bladder disorders.
Pol J Vet Sci 2012
PMID:Botulinum toxin type A-induced changes in the chemical coding of dorsal root ganglion neurons supplying the porcine urinary bladder. 2284 14


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