Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Exposure of male rats to ozone for 24 hrs at 1 ppm caused a profound depression of the pituitary-thyroid axis as indicated by a highly significant reduction of circulating thyrotropin hormone (TSH), thyroid hormones (T4 and T3), and protein-bound iodine (PBI). The metabolic clearance of TSH was not altered during ozone exposure and the high TSH levels seen in thyroidectomized rats were also not affected. Circulating prolactin (PRL) levels were significantly elevated after exposure. Pituitary TSH and PRL content was considerably increased in ozone-exposed rats; however, only TSH was released significantly above control values in vitro. Thyroid weight was also significantly increased after exposure. The results suggest that the depression of the pituitary-thyroid axis may be an adaptive mechanism during ozone exposure by reducing hypothalamic stimulation via thyrotropin releasing hormone (TRH) and at the same time lifting the hypothalamic catecholamine inhibition on PRL release. Both may be necessary alterations in order to develop tolerance during ozone exposure.
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PMID:Changes in thyroid function after short-term ozone exposure in rats. 744 Nov 19

With goats and dwarf pigs two experiments were made with semi-synthetic rations. The influence of insufficient (0.05 resp. 0.06 ppm) and sufficient (0.42 resp. 0.56 ppm) supply with iodine on feed consumption and the development of the live weight during the growth period and gestation was investigated. While iodine deficiency resulted in diminished feed consumption and a growth depression of the goats, a negative influence on feed consumption and the live weight increase of the dwarf pigs could not be detected, feed expenditure per kg weight increase, however, was distinctly higher.
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PMID:[Investigation of iodine metabolism. 1. The influence of iodine deficiency of the feed consumption and the development of the live weight of goats and dwarf pigs]. 745 65

We developed an improved determination method of mitochondrial proton adenosine triphosphatase (ATPase) activity in the liver. The activity was measured fluorometrically with a 3,3'-dipropylthiodicarbocyanine iodide (diS-C3(5)), which is excited at 625 nm and emits fluorescence at 670 nm. This dye transmits the electric potential across the inner mitochondrial membrane. The fluorescence intensity of diS-C3(5) with mitochondria (100 microliters, 4-16 mg/ml protein) in a 2 ml potassium buffer (pH 7.4) was regarded as a standard electric potential. After confirming the activity of the mitochondrial electron transport chain by succinic acid (9 mumol), we inhibited the chain by antimycin A (1.25 micrograms). Fluorescence intensity decreased by adenosine 5'-triphosphate (ATP) (2 mumol) and oligomycin (25 micrograms) inhibited this depression. The value of mitochondrial proton ATPase activity was calculated as a percentage of the fluorescence intensity change by ATP per the standard electric potential. The activity of mitochondrial proton ATPase in the normal fresh rat livers was 50.3 +/- 2.2%. Good correlation (r2 = 0.807) between two methods for mitochondrial proton ATPase activity, our newly developed method and a conventional colorimetric method, was obtained in the rat livers with various conditions. This method has advantages that the proton ATPase activity can be measured in intact mitochondria, and all procedures can be completed within 40 min. It is suitable for the determination of mitochondrial viability of liver graft in the hepatic resections and transplantations.
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PMID:Rapid fluorometric assay for mitochondrial proton adenosine triphosphatase activity for assessment of viability of liver graft tissue. 786 82

Data were pooled from 11 studies evaluating supplemental fat sources differing primarily in degree of saturation (tallow, animal-vegetable fat, vegetable oil, and hydrogenated fats). Data were standardized as proportions of the respective controls to reduce variation among individual studies and were subjected to stepwise multiple regression against the iodine value of fats, the percentage increases of total fatty acids in diets above the respective controls, or the ratio of total C16 to C18 fatty acids in fats (only for hydrogenated fats). Increased iodine value (increasing unsaturation) of fats increased apparent fatty acid digestibility, especially as iodine value increased from 11 to 27. For partially hydrogenated fat sources, as the ratio of C16 to C18 fatty acids increased, digestibility also increased, especially with increasing iodine value (positive interaction). Beneficial effects of higher C16:C18 ratio were reduced as amount of added fat increased (negative interaction). Dry matter intake and FCM production decreased as iodine value increased, perhaps because of inhibition of fiber digestion or metabolic regulation of DMI. Milk protein percentage depression averaged .2 percentage units for most fats. However, as partially hydrogenated fat sources became more saturated, milk protein depression appeared to be less evident; increased ratio of C16:C18 of fatty acids appeared to increase milk protein percentage. Despite the lower apparent digestibility of fatty acids of hydrogenated fats, increased milk production and percentages of fat and protein appeared to make them more economical than more unsaturated fats.
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PMID:Assessment of the effects of iodine value on fatty acid digestibility, feed intake, and milk production. 796 57

RIA was used to study the quantitative content in the blood serum of thyrotropic (TTH), thyroid (total thyroxine (T4), free thyroxine, triiodothyronine (T3) hormones and thyroxine-binding capacity of blood plasma proteins in 30 patients with brain concussion from the first to the 12th day of disease. The patients' hormonal profile was characterized by normal characteristics of TTH, depression of the transport organic phase of thyroid metabolism with a decrease of the T4 concentration, a reduction of the thyroxine-binding capacity of plasma protein, and simultaneous activation of the peripheral stage of iodine metabolism with excess accumulation in the blood of active hormones--free thyroxine and T3. The data obtained deepen our understanding of the pathogenesis of craniocerebral injury (CCI). The neuroendocrine syndrome identified is specific for mild CCI. It can be used as a differential diagnostic criterion for expert medical evaluation purposes.
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PMID:[Thyroid function in brain concussion]. 804 5

The aims of this study were to clarify the mechanism of giant negative T waves (GNT) in patients with apical hypertrophic cardiomyopathy (AHCM), using myocardial SPECT with thallium-201 (201TI) and iodine-123 metaiodobenzylguanidine (123I-MIBG). Myocardial SPECT in 8 patients with AHCM, diagnosed with GNT in EKG and apical hypertrophy in echocardiogram, were compared with those in 7 normal subjects. The EKG in patients with AHCM showed tall R waves, GNT and ST segment depression in the left precordial leads. With the SPECT, the ratio of radioisotope activities apical ROI vs. other ROI (anterior, septal and lateral segments) were calculated. The ratio of 201TI was high in AHCM, compared with that of normal subjects, suggested the increase in apical myocardial blood flow. The ratio of 123I-MIBG tended to be low in AHCM. The 201TI/123I-MIBG ratio was high in the apical myocardium in AHCM, indicated low sympathetic nerve activities, though there was myocardial hypertrophy. We concluded that giant negative T waves in apical hypertrophic cardiomyopathy might be due to relatively low cardiac sympathetic nerve activities in apical myocardium with idiopathic hypertrophy.
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PMID:[The mechanism of giant negative T wave in electrocardiogram in patients with apical hypertrophic cardiomyopathy: evaluation with thallium-201 and iodine-123 metaiodobenzylguanidine myocardial scintigraphy]. 892 68

Vascular dementia (VAD) is currently considered to be the second most common cause of dementia in Europe and the USA, second to dementia of the Alzheimer's type (DAT). However, in Asia and many developing countries the incidence of VAD exceeds that of DAT. The positive clinical diagnostic workup for VAD requires six steps: (1) clear-cut quantitative assessment of cognitive deficits utilizing standard neuropsychological tests to establish and quantify the dementia syndrome and rule out pseudo-dementia OF depression; (2) ascertaining the presence of risk factors for stroke; (3) identifying cerebral vascular lesions by neuroimaging (MRI, Iodine or Xenon contrasted CT, PET and SPECT); (4) exclusion of other causes of dementia; (5) differential diagnosis of possible, probable or definite VAD versus DAT and ascertaining when there are mixtures of the two; and (6) temporal identification of causality between onset and progression of the dementia with identified cerebral vascular lesions. There are eight subtypes of VAD: (1) multi-infarct dementias. These are due to large cerebral emboli, and are usually readily identifiable; (2) strategically placed infarctions causing dementia; (3) multiple subcortical lacunar lesions. Patients with these develop VAD at least five to twenty-five times more frequently than those in age-matched general population samples; (4) Binswanger's disease (arteriosclerotic subcortical leuko-encephalopathy). This form is rare. Neuroimaging confirms the diagnosis during life but the diagnosis can not be made by neuroimaging alone; (5) mixtures of two or more of above VAD subtypes; (6) hemorrhagic lesions causing dementia; (7) subcortical dementias due to cerebral autosomally dominant arteriolopathy with subcortical infarcts and leuko-encephalopathy (CADASIL), or to familial amyloid angiopathies and coagulopathies all of which present with multiple subcortical lacunar lesions similar to Binswanger's disease; (8) mixtures of DAT and VAD. The clinical significance of leukoaraiosis and its suspected relationships to VAD remains to be better established. The presence of ischemic infarctions, single or multiple large or multiple small (lacunar) by neuroimaging are necessary for the diagnosis of VAD, but identifying their presence, by neuroimaging alone, does not permit the diagnosis of dementia which can only be established by neuropsychological assessments. VAD is a clinical entity, identifiable in at least 30-70% of patients after strokes but mechanisms responsible for the cognitive impairments are complex. Some of these mechanisms are incompletely understood but provide subjects for important future research.
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PMID:Vascular dementia: still a debatable entity? 898 Dec 95

Dementia of the Alzheimer-type (DAT) is characterized by progressive cognitive decline, variably combined with frontal lobe release signs, parkinsonian symptoms and myoclonus. The features of diffuse Lewy body disease (DLBD), the second most common cause of degenerative dementia, include progressive cognitive deterioration, often associated with levodopa-responsive parkinsonism, fluctuations of cognitive and motor functions, psychotic symptoms (visual and auditory hallucinations, depression), hypersensitivity to neuroleptics and orthostatic hypotension. A recent report suggests that positron emission tomography studies in patients with degenerative dementia may be useful in the differential diagnosis of DAT and DLBD. However, the diagnostic role of single-photon emission tomography (SPET) studies remains to be established. The aim of this study was therefore to evaluate regional cerebral perfusion [with either technetium-99m hexamethylpropylene amine oxime (99mTc-HMPAO) or 99mTc-ethyl cysteinate dimer (99mTc-ECD) SPET] and striatal dopamine transporter density [using iodine-123 2 beta-carboxymethoxy-3 beta-[4-iodophenyl]tropane (123I-beta-CIT) SPET] in patients with DAT and DLBD. Six patients with probable DAT and seven patients with probable DLBD were studied. Blinded qualitative assessment by four independent raters of 99mTc-HMPAO or 99mTc-ECD SPET studies revealed bilateral temporal and/or parietal hypoperfusion in all DAT patients. There was additional frontal hypoperfusion in two patients and occipital hypoperfusion in one patient. In the DLBD group, regional cerebral perfusion had a different pattern. In addition to temporoparietal hypoperfusion there was occipital hypoperfusion resembling a horseshoe defect in six of seven patients. In the DAT group, the mean 3-h striatal/cerebellar ratio of 123I-beta-CIT binding was 2.5 +/- 0.4, with an increase to 5.5 +/- 1.1 18 h after tracer injection. In comparison, in the DLBD patients the mean 3-h striatal/cerebellar ratio of 123I-beta-CIT binding was significantly reduced to 1.7 +/- 0.3, with a modest increase to 2.1 +/- 0.4 18 h after tracer injection (P < 0.05, Scheffe test, ANOVA). These results suggest that 99mTc-HMPAO or 99mTc-ECD and 123I-beta-CIT SPET may contribute to the differential diagnosis between DAT and DLBD, showing different perfusion patterns and more severe impairment of dopamine transporter function in DLBD than in DAT.
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PMID:Brain perfusion scintigraphy with 99mTc-HMPAO or 99mTc-ECD and 123I-beta-CIT single-photon emission tomography in dementia of the Alzheimer-type and diffuse Lewy body disease. 914 72

Phasic and tonic motor neurons of crustaceans differ strikingly in their junctional synaptic physiology. Tonic neurons generally produce small excitatory postsynaptic potentials (EPSPs) that facilitate strongly as stimulation frequency is increased, and normally show no synaptic depression. In contrast, phasic neurons produce relatively large EPSPs with weak frequency facilitation and pronounced depression. We addressed the hypothesis that mitochondrial function is an important determinant of the features of synaptic transmission in these neurons. Mitochondrial fluorescence was measured with confocal microscopy in phasic and tonic axons and terminals of abdominal and leg muscles after exposure to supravital mitochondrial fluorochromes, rhodamine-123 (Rh123) and 4-diethylaminostyryl-N-methylpyridinium iodide (4-Di-2-Asp). Mitochondria of tonic axons and neuromuscular junctions had significantly higher mean Rh123 and 4-Di-2-Asp fluorescence than in phasic neurons, indicating more accumulation of the fluorochromes. Mitochondrial membrane potential, which is responsible for Rh123 uptake and is related to mitochondrial oxidative activity (the production of ATP by oxidation of metabolic substrates), is likely higher in tonic axons. Electron microscopy showed that tonic axons contain approximately fivefold more mitochondria per microm2 cross-sectional area than phasic axons. Neuromuscular junctions of tonic axons also have a much higher mitochondrial content than those of phasic axons. We tested the hypothesis that synaptic fatigue resistance is dependent on mitochondrial function in crayfish motor axons. Impairment of mitochondrial function by uncouplers of oxidative phosphorylation, dinitrophenol or carbonyl cyanide m-chlorophenylhydrazone, or by the electron transport inhibitor sodium azide, led to marked synaptic depression of a tonic axon and accelerated depression of a phasic axon during maintained stimulation. Iodoacetate, an inhibitor of glycolysis, and chloramphenicol, a mitochondrial protein synthesis inhibitor, had no significant effects on either mitochondrial fluorescence or synaptic depression in tonic or phasic axons. Collectively, the results provide evidence that mitochondrial oxidative metabolism is important for sustaining synaptic transmission during maintained stimulation of tonic and phasic motor neurons. Tonic neurons have a higher mitochondrial content and greater oxidative activity; these features are correlated with their greater resistance to synaptic depression. Conversely, phasic neurons have a lower mitochondrial content, less oxidative activity, and greater synaptic fatigability.
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PMID:Synaptic physiology and mitochondrial function in crayfish tonic and phasic motor neurons. 924 80

To evaluate the effects of complex spa therapy (swimming training in a hot spring pool + fango therapy + inhalation of iodine salt solution) on psychological factors, three psychological examinations; CMI (Cornell Medical Index), SDS (Self-Rating Depression Scale) and CAI (Comprehensive Asthma Inventory); were given 25 patients with bronchial asthma (10 male, 15 female, mean age 60 years), and the results of these examinations were compared before and after spa therapy. 1. Physical symptoms, respiratory system and CIJ symptoms by CMI were significantly improved after spa therapy, however the improvement of psychical symptoms was not significant. 2. In SDS, 11 of 25 patients showed more than 40 points, indicating depressive state. The number of such patients decreased from 11 to 2 and the mean SDS score significantly improved from 38.7 to 34.2 after spa therapy. 3. Conditioning, suggestion, fear of expectation, frustration, flight into illness, negative attitudes towards prognosis, and decreased motivation towards therapy by CAI were significantly reduced after spa therapy, with the reduction in negative attitudes towards prognosis and decreased motivation towards therapy being relatively large. Furthermore, CAI score, which is the average of the categories in CAI, was also significantly decreased from 37.9 to 28.4 after spa therapy. These results suggested that complex spa therapy improves psychological factors in patients with bronchial asthma.
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PMID:[Psychological investigation on spa therapy in patients with bronchial asthma]. 927 2


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