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Query: UMLS:C0011570 (
depression
)
172,036
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Intermittent hyperthyreosis occurs under various forms of stress, especially heat stress. The clinician may diagnose such cases as masked or apathetic hyperthyroidism or "forme fruste" hyperthyreosis or thyroid autonomy. As most routine and standard tests may here yield inconsistent results, it is the patients' anamnesis which may provide the clue. Our Bioclimatology Unit has now seen over 100 cases in which thyroid hypersensitivity towards heat was the most prominent syndrome: 10-15% of weather-sensitive patients are affected. The patients complain before or during heat spells of such contradictory symptoms as insomnia, irritability, tension, tachycardia, palpitations, precordial pain, dyspnoe, flushes with sweating or chills, tremor, abdominal pain or diarrhea, polyuria or pollakisuria, weight loss in spite of ravenous appetite, fatigue, exhaustion,
depression
, adynamia, lack of concentration and confusion. Determination of urinary neurohormones allows a differential diagnosis, intermittent hyperthyreosis being characterized by three cardinal symptoms: 1. tachycardia -- every case with more than 80 pulse beats being suspect (not specific); 2. urinary histamine -- every case excreting more than 90 mug/day being suspect. Again the drawback of this test is its lack of specificity, as histamine may also be increased in cases of allergy and spondylitis; 3. urinary thyroxine -- every case excreting more than 20 mug/day T-4 being suspect. This is the only specific test. Therapy should make use of lithium carbonate and beta-blockers. Propyl thiouracil is rarely required.
Horm Metab Res 1975
Sep
PMID:Intermittent hyperthyreosis -- a heat stress syndrome. 5 84
Although the precise etiologic incitant of the minimal lesion idiopathic nephrotic syndrome of childhood is not known, it is likely that a host mechanism mediates the permeability alterations of the glomerular capillary wall resulting in massive proteinuria. As a first step in examining the possibility that local kinin release may account for the proteinuria in this disorder, two parameters of the plasma kinin-generating system, plasma prekallikrein and kallikrein inhibitor, were assayed during 27 nephrotic episodes in 21 corticosteroid-responsive children. Plasma kallikrein was assayed by means of its esterase activity on a synthetic arginine ester substrate, N-alpha-tosyl-L-arginine methyl ester (TAMe), after activation of Hageman factor by kaolin. This activity, after subtraction of spontaneous arginine esterase activity (i.e., TAMe esterase activity measured in plasma not exposed to kaolin) is derived from prekallikrein. Plasma prekallikrein activity in 11 normal children was 99.6 +/- 2.9 mumol TAMe hydrolyzed/ml plasma/hr (mean +/- SEM). Kallikrein inhibitor was quantified in arbitrary units. Kallifrein inhibitor activity in 11 normal children was 0.94 +/- 0.04 units. During the overt nephrotic syndrome, before initiation of intensive daily corticosteroid treatment, mean values were: prekallikrein, 58.5 +/- 7.24 mumol/ml/hr; and kallikrein inhibitor, 0.35 +/- 0.06 units. After corticosteroid-induced remission occurred, mean values were: plasma prekallikrein, 118.6 +/- 3.2 mumol/ml/hr; and kallikrein inhitor, 0.78 +/- 0.03 mumol/ml/hr. Both parameters were again assayed in 14 of the 21 children after complete cessation of corticosteroid treatment. Plasma prekallikrein was normal, 99.6 +/- 4.8 mumol/ml/hr; but kallikrein inhibitor was still somewhat depressed, 0.84 +/- 0.03 units. A subset of 9 patients had marked
depression
of plasma prekallikrein to levels less than 20 mumol/ml/hr and essentially undetectable inhibitor activity. Serum alpha-2 macroglobulin was elevated in nephrotic patients: mean value during relapse, 862 +/- 29 mg/100 ml; during corticosteroid-maintaining remission, 615 +/- 29 mg/100 ml. After cessation of corticosteroids, mean serum level was 481 +/- 20 mg/100 ml. The proportional reduction of plasma prekallikrein and kallikrein inhibitor suggested that an enzyme-inhibitor complex formed in vivo, perhaps at a local site of activation in proximity to the glomerular basement membrane. These data suggest that the plasma kinin-generating system may be the host effector mechanism subserving the increased glomerular capillary permeability in the minimal lesion nephrotic syndrome of childhood.
Pediatr Res 1975
Sep
PMID:A study of the plasma kinin-generating system in children with the minimal lesion, idiopathic nephrotic syndrome. 5 8
One patient with hepatitis-B surface antigen (HBsAg)-positive chronic aggressive hepatitis, and two chimpanzee carriers of HBsAg, were each given seven doses of 10(7) I.U. of human fibroblast interferon over two weeks. The main differnce observed after treatment was a
depression
of the nucleocapsid hepatitis-0 core antigen in the liver, indicating that hepatitis-B virus infection is sensitive to interferon. Except for a short febrile reaction, no undesirable effects were seen after the administration of human fibroblast interferon which has not been previously given to man.
Lancet 1976
Sep
25
PMID:Administration of human fibroblast interferon in chronic hepatitis-B infection. 6 May 13
Sections of 150 seconds duration were taken on a random basis out of TV stored interviews of day 0, 10 and 20 of a double-blind antidepressive drug trial. Not identical sections were selected for the isolated audio and video channel and for the combined presentation in such a way that for each of the 20 patients three times three parts were presented for evaluation. It was the two rater's task to rank each patient's tapes in terms of the degree of
depression
. They were blind regarding the day of recording the interview (day 0, 10 or 20). The best results were reached with the combined presentation of the audio-video-channel while each channel taken seperately rendered less diagnostic information. The raters evaluated the material in two different modifications: a) Video, audio and than audio-video-channel or b) audio, video and audio-video-channel. The first version (a) was evaluated in a better way than the second one with respect to the content of diagnostic information. Furthemore we found that the evaluation of the visual information became less safe if the audio presentation preceded as in version b.
Pharmakopsychiatr Neuropsychopharmakol 1976
Sep
PMID:[New strategies in psychiatric diagnosis through the use of audio-visual technics. 2. Importance of verbal and non-verbal information for assessment of depressive patients]. 6 28
A combined familial study of multiple sclerosis (MS) in England and in the Rostock area of the GDR using the macrophage electrophoretic mobility (MEM)-LAD test embracing 132 relatives has revealed a closely similar pattern of distribution of "anomalous" LAD (Linoleic Acid
Depression
) values in relatives (77% type of reaction) to that originally reported in the British study. The anomaly in predominantly associated with females--all mothers of MS patients being affected, whilst daughters and sisters are also represented. In addition unusual full MS type of reaction (90% reduction) has been found in some children related to patients. There is clearly a genetic element in the development of MS probably mainfested in the inborn mishandling of unsaturated fatty acids suggested by Thompson; no recognizable pattern of inheritance is noticeable even within the combined material. There is evidence that the metabolic anomaly alone does not inevitably lead to MS, and the full abnormality may be present at an early age. A survey about the examinations and a selection of characteristic family trees of MS are given, illustrating the manner in which the 77% type anomaly is distributed with occasional omission of a generation.
J Neurol 1977
Sep
12
PMID:Anomalous lymphocyte-antigen reaction in relatives of multiple sclerosis patients. A study of a possible genetic factor in the disease. 7 3
(1) Extracellular multiunit recordings were made of the spontaneous activity in cerebellar Purkinje cells, nucleus interpositus, red nucleus and sensorimotor cortex in acute cat preparations. (2) Changes in this spontaneous neural activity produced by the administration of diphyenylhydantoin (DPH) were studied. DPH was infused i.v., generally at a concentration of 2.5 mg/ml and at a rate varying from 0.08 to 0.48 mg/kg/min. Two different patterns of infusion were used: fixed time, variable rate and variable time, fixed rate. Pulsed doses were also given at intervals of 5--10 min. (3) DPH at a level of 10--20 mg/kg produces a significative initial deceleration in all structures followed by a significative acceleration in the Purkinje cells, nucleus interpositus and red nucleus as a dose of 20--30 mg/kg is reached. Higher levels caused a profound
depression
of multiunit activity. (4) The activation produced by DPH is oscillatory (3--5/min) in character and is composed of 'trains' which occur at a rate of 20--30/sec with very rapid discharge frequencies (600--800 Hz). (5) A direct significant correlation was found between DPH serum levels and the intravenously administered dose. The activating DPH dose (20--30 mg/kg) corresponded to serum levels of 24--32 micrograms/ml. (6) The possibility is discussed whether the anticonvulsant action of DPH may be due in part to the production of rhythmic oscillatory activity in the cerebello-rubro-olivo-cerebellar ciruit and the
depression
of the cerebellothalamic-cortical pathway.
Electroencephalogr Clin Neurophysiol 1979
Sep
PMID:Effects of diphenylhydantoin on the spontaneous activity of Purkinje, nucleus interpositus, red nucleus and motor cortex cells. 9 Jun 5
A description is first given of the relevance of emotional factors to present-day pathological processes. Pain may be indicative of various causes: consecutive symptom of an organic process, expression of a functional disorder, emotionally conditioned symptom. The vicious circle of pain and emotion (anxiety, aggression,
depression
) is demonstrated as exemplified by nonarticular rheumatism. Tension revolt and suppressed aggression play a fundamental role in the cervicobrachial syndrome.
MMW Munch Med Wochenschr 1979
Sep
14
PMID:[The psychosomatics of pain, particularly in the cervicobrachial region (author's transl)]. 9 Nov 4
Four patients without symptoms of episodic hyperkalemic weakness from two families with paramyotonia congenita (Eulenburg) are described. 1. Maximum voluntary muscle contraction of the upper and lower arm was studied under isometric conditions at different temperatures. If the temperature was lowered stepwise, distinct paresis occured at 32--31 degrees C which increased with the amount of muscular effort. The upper arm muscles, however, developed weakness gradually after cooling. 2. During cooling of the resting muscle, the EMG showed dense spontaneous activity of the fibrillary type, which decreased again at about 30 degrees C. It can be assumed that in paramyotonia congenita cooling produces muscle cell membrane depolarization which at a critical level causes the firing of action potentials and finally muscular paresis. 3. Increasing muscular stiffness can be interpreted as abnormally slow muscular relaxation after isometric contraction. In the forearm muscles the time to 3/4 relaxation after cooling was about six times normal, in the upper arm muscles only two times normal. As an additional parameter the mechanical resistance to passive stretching of a muscle has been studied. This passive muscular tension increased simultaneously with the onset of weakness. 4. The close relation between weakness and stiffness suggest that both symptoms are caused by the same basic defect which is probably located in the sarcolemma. It is suggested that a defect of the sodium channel causes a cooling-dependent increase in sodium conductance. Raised intracellular sodium causes in the first place membrane depolarization, and in the second place
depression
of calcium reuptake through competition by sodium for calcium binding sites. This would explain muscle stiffness and delayed relaxation as well.
J Neurol 1979
Sep
PMID:Influence of temperature on isometric contraction and passive muscular tension in paramyotonia congenita (Eulenburg). 9 68
Nondividing human diploid fibroblasts maintained in medium containing 0.5% calf serum do not survive when exposed to low doses of UV (254 nm). The extent of killing is dose and strain dependent. DNA excision repair-proficient cells are more resistant than excision repair-deficient cells. Results of measurements of the effect of UV on RNA and protein synthesis in repair-proficient and -deficient (XP12BE) cells are reported. UV causes an immediate and equal
depression
of the RNA synthesis rate in both kinds of cells. A recovery to control rates was observed only at low (5 J/m2) doses in repair-deficient cells and at higher doses (20 J/m2) in repair-proficient cells. No recovery was observed at doses that cause substantial reductions in survival (greater than 5 J/m2 for XP12BE; greater than 40 J/m2 for repair-proficient populations). No initial effect on rate of protein synthesis was detected at doses less than 20 J/m2. However, in XP12BE populations, a decreased rate first evident at 15-30 h post-UV and before any cell degeneration and loss was observed for doses as low at 7 J/m2. This delayed effect was not observed in repair-proficient populations. The results are consistent with the hypothesis that the lethal action of UV in nondividing cells is one on DNA that leads to an inhibition of required protein synthesis by preventing RNA transcription.
Biophys J 1979
Sep
PMID:An effect of ultraviolet light on RNA and protein synthesis in nondividing human diploid fibroblasts. 9 67
Intracoronary administration of contrast materials causes myocardial
depression
which is related to serveral physiochemical properties of the contrast solution. The role of variations in ambient calcium ions (Ca++) in mediating this effect was evaluated in 19 anesthetized dogs. Sodium meglumine diatrizoate caused decreases in left ventricular peak systolic pressure (LVPSP),-12.6 +/- 3.2%, and dp/dt at a left ventricular pressure (LVP) of 40 mm Hg, -14.3 +/- 4.1%. The total calcium (Cat) decreased from 10.2 +/- 0.2 to 6.5 +/- 0.2 mg%, while Ca++ decreased from 4.6 +/- 0.1 mg% to 2.3 +/- 0.7 mg%. In the presence of systemic hypocalcemia the myocardial depressant actions of this contrast materials were accentuated. Intracoronary administration of contrast material with added Ca++, calcium sodium meglumine metrizoate, caused no myocardial
depression
. Total calcium decreased only slightly (10.2 +/- 0.2 to 9.1 +/- 0.2 mg%), while Ca++ increased (4.8 +/- 0.1 to 5.1 +/- 0.2 mg%. During systemic hypocalcemia, the calcium metrizoate compound induced increases in LVPSP and dp/dt/LBP40. Thus, contrast materials caused myocardial
depression
which, at least in part, was related to reduction of ambient calcium through a dilutional and binding action. The addition of Ca++ to monomeric contrast materials reversed the myocardial depressant action and produced a transient rise in ambient Ca++.
Circulation 1978
Sep
PMID:Alterations in calcium levels of coronary sinus blood during coronary arteriography in the dog. 9 41
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