Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The results of adrenal scintiscans, venograms and venous aldosterone levels are compared with the histologic findings in 33 patients submitted to operations for primary aldosteronism. Standard and suppression scintiscans were performed 2-14 days following intravenous administration of 2mCi of 131I-19-iodocholesterol. The adrenal lesions were histologically classified into four categories: 25 patients had adenomas, 6 had macronodular hyperplasia, 1 had microscopic hyperplasia and 1 had an adenocarcinoma. Asymmetrical uptake between the two adrenals seen on standard scintiscans did not differentiate between a tumor or asymmetrical hyperplasia, unless the tumor was greater than 2 cm in diameter. During suppression scintiscans, unilateral uptake visible within five days of tracer injection was consistent with adenoma. Patients with nodular hyperplasia demonstrated early uptake in both adrenal glands during suppression scintiscans, while the patient with microscopic hyperplasia did not. The type of adrenal lesion was correctly identified in 20/26 (77%) of patients by suppression scintiscans; 21/28 (75% of patients by venograms and 12/16 (75%) of patients who had adrenal venous aldosterone measurements attempted. The majority of surgically correctible lesions could be identified on suppression adrenal scintiscans. Adrenal vein catheterization can be reserved for those patients in whom the results of suppression scintiscans are inconsistent with the clinical degree of aldosteronism.
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PMID:Adrenal imaging with 131I-19-iodocholesterol in the diagnostic evaluation of patients with aldosteronism. 124 93

A multimodality radioimmunological and clinicobiochemical study showed an increase in the hydrocortisone level and a decrease in the ACTH level in breast cancer patients. Stage I, following radical mastectomy (RM). A simultaneous increase in the hydrocortisone, ACTH and aldosterone level after RM, chemotherapy, hormone therapy was noted in all patients with breast cancer, Stages II and III, with initially lowered hydrocortisone and aldosterone levels and an elevated ACTH level. After RM and radiotherapy the level of hydrocortisone decreased, that of ACTH and aldosterone and renin activity increased. Scintigraphically in Stage I breast cancer the adrenals were enlarged, after RM in some cases they remained enlarged, in other cases they returned to normal. Enlarged adrenals with a lowered contrast and enhanced obscurity of the contours were observed in Stage II and III breast cancer. After therapy the adrenals remained asymmetrical with a low contrast.
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PMID:[Combined examination of the hypophysis-adrenal cortex system in breast cancer]. 402 50

Adrenal scintigraphy with 131I-19-iodo-cholesterol was performed in 13 hypertensive patients with biochemical disturbances suggesting an aldosterone-producing adenoma. The actual presence of an adenoma was subsequently confirmed in all cases. An asymmetrical tracer uptake (lateralization) was seen in 7 patients and in 6 of these the adenoma was located in the adrenal with the higher uptake. In one patient a large necrotic tumour was not visualized and a faint contralateral accumulation was wrongly taken to represent a tumour. In 6 patients the scintigram was non-lateralizing. In these highly selected patients a lateralizing scintigram had a high diagnostic specificity and at present adrenal scintigraphy should be the method of first choice in the preoperative side prediction. However, the sensitivity is low: a non-lateralizing scintigram does not exclude the presence of an aldosterone-producing adenoma.
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PMID:Adrenal scintigraphy in primary aldosteronism caused by an aldosterone producing adenoma. 720 37

The physicochemical properties of water enable it to act as a solvent for electrolytes, and to influence the molecular configuration and hence the function--enzymatic in particular--of polypeptide chains in biological systems. The association of water with electrolytes determines the osmotic regulation of cell volume and allows the establishment of the transmembrane ion concentration gradients that underlie nerve excitation and impulse conduction. Fluid in the central nervous system is distributed in the intracellular and extracellular spaces (ICS, ECS) of the brain parenchyma, the cerebrospinal fluid, and the vascular compartment--the brain capillaries and small arteries and veins. Regulated exchange of fluid between these various compartments occurs at the blood-brain barrier (BBB), and at the ventricular ependyma and choroid plexus, and, on the brain surface, at the pia mater. The normal BBB is relatively permeable to water, but considerably less so to ions, including the principal electrolytes Brain fluid regulation takes place within the context of systemic fluid volume control, which depends on the mutual interaction of osmo-, volume-, and pressure-receptors in the hypothalamus, heart and kidney, hormones such as vasopressin, renin-angiotensin, aldosterone, atriopeptins, and digitalis-like immunoreactive substance, and their respective sites of action. Evidence for specific transport capabilities of the cerebral capillary endothelium, for example high Na+K(+)-ATPase activity and the presence at the abluminal surface of a Na(+)--H+ antiporter, suggests that cerebral microvessels play a more active part in brain volume regulation and ion homoeostasis than do capillaries in other vascular beds. The normal brain ECS amounts to 12-19% of brain volume, and is markedly reduced in anoxia, ischaemia, metabolic poisoning, spreading depression, and conventional procedures for histological fixation. The asymmetrical distributions of Na+ K+ and Ca2+ between ICS and ECS underlie the roles of these cations in nerve excitation and conduction, and in signal transduction. The relatively large volume of the CSF, and extensive diffusional exchange of many substances between brain ECS and CSF, augment the ion-homeostasing capacity of the ECS. The choroid plexus, in addition to secreting CSF principally by biochemical mechanisms (there is an additional small component from the extracellular fluid), actively transports some substances from the blood (e.g. nucleotides and ascorbic acid), and actively removes others from the CSF. In contrast with CSF secretion, CSF reabsorption is principally a biomechanical process, passively dependent on the CSF-dural sinus pressure gradient. Pathological increases in intracranial water content imply development of an intracranial mass lesion. The additional water may be distributed diffusely within the brain parenchyma as brain oedema, as a cyst, or as increase in ventricular volume due to hydrocephalus. Brain oedema is classified on the basis of pathophysiology into four categories, vasogenic, cytotoxic, osmotic and hydrostatic. The clinical conditions in which brain oedema presents the greatest problems are tumour, ischaemia, and head injury. Peritumoural oedema is predominantly vasogenic and related to BBB dysfunction. Ischaemic oedema is initially cytotoxic, with a shift of Na+ and CI- ions from ECS to ICS, followed by osmotically obliged water, this shift can be detected by diffusion-weighted MRI. Later in the evolution of an ischaemic lesion the oedema becomes vasogenic, with disruption of the BBB. Recent imaging studies in patients with head injury suggest that the development of traumatic brain oedema may follow a biphasic time course similar to that of ischaemic oedema. Hydrocephalus is associated in the great majority of cases with an obstruction to the circulation or drainage of CSF, or, occasionally, with overproduction of CSF by a choroid plexus papilloma. In either case, the consequence is a ris
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PMID:The normal and pathological physiology of brain water. 907 71

The brain aminopeptidases that participate in the enzymatic cascade of the renin-angiotensin system play a major role in blood pressure (BP) control, and their study offers new perspectives for the understanding of central BP control and the treatment of hypertension. In this system, angiotensin II is converted to angiotensin III (Ang III) by glutamyl aminopeptidase (GluAP) and Ang III is further metabolised to angiotensin IV by alanyl aminopeptidase or arginine-aminopeptidase. It is now clear that Ang III is the key active form of the central angiotensins, exerting tonic stimulatory control over BP. Therefore, the development of GluAP inhibitors as potential antihypertensive agents offers new perspectives for therapy. Brain aspartyl aminopeptidase, which converts angiotensin I to angiotensin 2-10, is also a possible target for antihypertensive therapy because of its potential role in BP control. Finally, since changes in BP levels, that paralleled changes in brain and plasma aminopeptidase activities, were observed after unilateral lesions of the nigrostriatal system, brain asymmetry, aminopeptidase activities and BP control appear to be related, resulting their interplay in an asymmetrical neuroendocrine response that differentially affect BP control. The study of this interaction may contribute to our understanding of how the brain controls BP.
J Renin Angiotensin Aldosterone Syst 2006 Sep
PMID:Brain aminopeptidases and hypertension. 1709 48