Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0432222 (
SEM
)
47,337
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Plasma of insulin-treated diabetics and of newborn infants of insulin-treated diabetic mothers contains insulin antibodies which invalidates the radioimmunoassay of insulin. Therefore, the endogenous insulin antibody complex must be splitted at a pH lower than 5 and the total IRI (TIRI) is separated by ethanol extraction. It was investigated the recovery rate in dependence upon plasma volume used for extraction. By reduction of used plasma volume from 500 to 200 mul per extraction the recovery rate was increased from 65.1 +/- 8.4 to 88.3 +/- 4.2% (mean +/-
SEM
). The low plasma volume of 200 mul for TIRI extraction made it possible to determine TIRI during glucose loads of newborn infants. To eliminate different conditions of incubation for standard and unknown plasma samples the TIRI levels were computed by means of so-called "extracted" standard curve, obtained with extracted insulin from standard insulin dilution in insulin-free pooled human plasma. Using the described method a temporary regeneration of insulin secretion of a newly diagnosed juvenile diabetic after insulin treatment could be shown. In contrast to newborn infants of healthy mothers a biphasic/insulin release was found during the intravenous glucose loads in newborn infants of insulin-treated diabetic mothers.
Endokrinologie 1975
Dec
PMID:Determination of total insulin (TIRI) in plasma of insulin-treated diabetics and newborn infants of insulin-treated diabetic mothers. 0 60
1. A Valsalva-like manoeuvre was used to elicit graded rises in total peripheral resistance (TPR) in conscious rabbits. The rises were reflex and mediated through sympathetic constrictors. Propranolol infused at different rates reaching plasma concentrations up to 240 (
SEM
33) ng/ml had no effect on this reflex but reduced mean arterial pressure. However, the response was attenuated by clonidine in a dose-dependent manner. 2. Valsalva manoeuvres were used to elicit graded sympathetically mediated rises in TPR index in twenty-nine subjects with mean arterial pressure ranging from 75 to 165 mmHg. Absolute sensitivity of the constrictor response increased with rising resting TPR index, resulting in some enhancement of constrictor responses in the hypertensive subjects. It seems likely that non-autonomic factors (e.g. vessel structure) rather than hyperactive neural constrictor effects are involved in the enhanced constrictor responses in essential hypertension.
Clin Sci Mol Med Suppl 1976
Dec
PMID:Valsalva vasoconstrictor reflex in human hypertension in after beta-adrenoreceptor blockade in conscious rabbits. 1 55
Aspirin alters the gastric mucosal barrier as measured by ionic flux and potential difference. The effect of cimetidine on aspirin-induced alterations in gastric mucosa was studied in five normal male volunteers. Aspirin effects were studied with and without previous treatment with cimetidine. Mean (+/-
SEM
) basal potential difference was -48 +/- 1 mV. After 600 mg of aspirin in 1 dl of isotonic saline, potential difference decreased in 10 min to -39 +/- 1 mV (P less than 0.001) and returned to baseline within 60 min. Control biopsies showed 2% damaged mucosal cells compared with 20% damaged at the time of maximal drop in potential difference (P less than 0.001) after aspirin. Recovery to 9% damage occurred by 60 min. In subjects pretreated with 300 mg cimetidine, potential difference rose during 1 h to -62 +/- 1 mV (P less than 0.001). After aspirin potential difference fell to -48 +/- 1 mV compared with -39 +/- 1 mV with aspirin alone (P less than 0.01) and returned to -62 +/- 1 mV at 60 min. The cimetidine-treated group showed 4% mucosal damage at the peak potential difference fall after aspirin, significantly less (P less than 0.02) than in the untreated subjects.
Ann Intern Med 1977
Dec
PMID:Protective effect of cimetidine on aspirin-induced gastric mucosal damage. 2 5
1. Haemodynamic responses to diazoxide (300 mg intravenously) were studied in 15 hypertensive patients before and after chronic beta-adrenoreceptor blockade by 320 mg of propranolol daily. After diazoxide alone, mean arterial pressure and total peripheral resistance were lowered by 24 +/- 3 and 35 +/- 5% (mean +/-
SEM
) respectively. Cardiac output and heart rate rose by 25 +/- 9 and 21 +/- 3%. During beta-adrenoreceptor blockade, the percentage changes of mean arterial pressure, heart rate, cardiac output and total peripheral resistance after vasodilatation were not significantly different from those after diazoxide alone. 2. Atropine, 0.04 mg/kg body weight, was given to 12 hypertensive patients chronically treated with beta-adrenoreceptor blockade, before acute vasodilatation by diazoxide. Diazoxide caused no increase in heart rate after combined beta-adrenoreceptor and parasympathetic blockade. However, cardiac output rose by 14 +/- 5%. 3. We conclude that withdrawal of parasympathetic tone is an important determinant of circulatory homeostasis after acute vasodilatation during beta-adrenoreceptor blockade.
Clin Sci Mol Med Suppl 1978
Dec
PMID:Sympathetic and parasympathetic components of reflex cardiostimulation during vasodilator treatment of hypertension. 3 8
A description of the different stages of Trypanosoma (M.) melophagium in different regions of the gut of the sheep ked (Melophagus ovinus) as observed by the
SEM
is presented. The extensive pile carpet or palisade colonization of the midgut and pylorus is described. The method of attachment and the relationship of the parasites to the microvilli in the midgut and the cuticle of the pylorus and ileum observed by other methods are confirmed. The micro-structure of the surfaces themselves in the regions of the gut to which parasites attach are described. The use of the technique for the study of other similar systems is discussed.
Acta Trop 1978
Dec
PMID:Trypanosoma (megatrypanum) melophagium in the sheep ked, Melophagus ovinus. A scanning electron microscope (SEM) study of the parasites and the insect gut wall surfaces. 3 51
Beta-endorphin-like immunoactivity was measured in the umbilical cord plasma of 45 term human fetuses. Mean concentration was 91 +/- 16 (
SEM
) pg/ml,an the normal adult level of 30.7 +/- 2.7 pg/ml. This immunoactivity was further characterized in 10 cases by Sephadex G-50 chromatography to separate beta-endorphin from beta-lipotropin (beta-LPH). Mean beta-endorphin and beta-LPH concentrations were 57 +/- 12.8 and 455 +/- 101 pg/ml, respectively. Both were higher (P less than 0.01) than the mean beta-endorphin and beta-LPH concentrations reported in the adult. The mean molar beta-endorphin to beta-LPH ratio was 0.35 in the fetus and 0.36 in the adult. In 17 fetuses whose umbilical arterial and venous concentrations were measured separately, mean beta-endorphin-like immunoactivity was higher in the artery than in the vein. A highly significant negative correlation (r = -0.831; P less than 0.001) was present between umbilical arteiral pH and beta-endorphin-like immunoactivity. A negative correlation (r = -0.611; P less than 0.005) with arterial pO2 was also noted. We conclude that high levels of beta-endorphin-like immunoactivity, composed of both beta-endorphin and beta-LPH, circulate in the human fetus at term, and that hypoxia and secondary acidosis may be major stimuli to the release of these peptides.
J Clin Endocrinol Metab 1979
Dec
PMID:Plasma beta-endorphin and beta-lipotropin in the human fetus at delivery: correlation with arterial pH and pO2. 4 46
Uroporphyrinogen I synthase [porphobilinogen ammonia-lyase (polymerizing), EC 4.3.1.8] from human erythrocytes was separated into two active protein peaks (A and B on DEAE-cellulose, by ammonium sulfate fractionation, on Sephadex G-100, and on DEAE-Sephadex A-50 with a NaCl gradient. The final purification was 613 and 743 times for A and B, respectively. The corresponding yields were 2.2 and 3.4% Fraction A was separated further into two (A1 and A2) active protein bands and fraction B into three (B1, B2, and B3) on analytical polyacrylamide disc gel electrophoresis. Bands A1 and A2 were identical with B1 and B2; B3 represented a third isoenzyme. Molecular weights (mean +/-
SEM
), measured by gel filtration and sodium dodecyl sulfate/polyacrylamide gel electrophoresis, were 38,000 +/- 1000 for B1 and 40,000 +/- 1000 for B2 and B3. Isoelectric focusing on 4% polyacrylamide gel separated both fractions A and B into three active protein bands. Maximal activity of the enzyme was found in gel cuts (5-mm) at pH 5.6 for both fractions A and B.
Proc Natl Acad Sci U S A 1979
Dec
PMID:Uroporphyrinogen I synthase from human erythrocytes: separation, purification, and properties of isoenzymes. 4 11
Baboons anaesthetized with halothane and nitrous oxide in oxygen were given Althesin 0.05 ml kg-1 i.v. Cerebral blood flow (c.b.f.) was measured by an electromagnetic flowmeter and by xenon clearance whilst extracellular fluid (e.c.f.) pH of the parietal cortex was measured with a micro pH electrode. Carotid blood flow (carBF) began to decrease and carotid vascular resistance (carVR) to increase 2.0 s (
SEM
0.3) after the slowing of the e.e.g. produced by Althesin, while e.c.f. pH began to change to alkaline 10.5 s (
SEM
1.0) after the e.e.g. change. The first statistically significant increase in mean e.c.f. pH occurred 25 s after the Althesin-induced change in the e.e.g. The duration of the changes in carVR and e.c.f. pH were 7 and 5 min respectively. It is concluded that the change in e.c.f. pH cannot have initiated the increase in carVR which followed the cerebral matabolic depression produced by Althesin. The later alkaline shift in e.c.f. pH may, however, have maintained the increased carVR during the duration of cerebral metabolic depression produced by Althesin.
Br J Anaesth 1979
Dec
PMID:Relationship between cerebral blood flow changes and cortical extracellular fluid pH during cerebral metabolic depression induced by althesin. 4 61
30 patients on long-term lithium therapy have been studied. The results are presented of the urinary concentrating ability after water deprivation and the intranasal administration of vasopressin, of the simultaneous determination of glomerular filtration rate (GFR) and effective renal plasma flow (ERPF), of the minimal urine pH after an oral dose of ammonium chloride, and of the urinary beta-2-microglobulin excretion. Mean urine concentration (+/-
SEM
) after 22 hr water deprivation (= Uosm) amounted to 854 +/- 22 mOsm/kg H2O, mean GFR was 101 +/- 4 ml/min, mean ERPF 360 +/- 18 ml/min, and mean minimal urine pH 4.95 +/- 0.06. In 8 out of 30 patients there was polyuria. In these 8 patients the values were 778 +/- 51 mOsm/kg H2O, 113 +/- 6 ml/min, 415 +/- 33 ml/min and 4.99 +/- 0.08, respectively. Serum levels of beta-2-microglobulin and lysozyme and the urinary excretion of beta-2-microglobulin were normal in all patients. No correlation was established between Uosm and the serum lithium concentration during the test (0.8 +/- 0.05 mmoles/l) nor between Uosm and the average serum lithium level during treatment (0.79 +/- 0.03). GFR was only correlated with age. It was found that administration of indomethacin during the concentration test increased Uosm in these patients. The results suggest that, given proper dosage and surveillance, long-term treatment with lithium is not likely to cause disturbances in renal function.
Clin Nephrol 1979
Dec
PMID:A renal function study in 30 patients on long-term lithium therapy. 4 7
The effects of a 0.5 g/kg body weight arginine infusion on plasma inorganic phosphates and potassium were examined in nineteen normal subjects. Plasma phosphorus displayed a highly significant (p less than 0.001) fall with a maximum depression below baseline of 1.11 +/- 0.15 mg/100 ml or 33 +/- 3% (mean +/-
SEM
); there was a significant correlation (p less than 0.01) between this fall and the insulin peaks induced by arginine. Plasma potassium levels displayed a distinct and significant increase in eleven of the twelve subjects studied; the maximum increase above baseline was 1.02 +/- 0.14 mEq/1 or 27 +/- 4.5% (p less than 0.001). No change occurred in blood pH values determined in four subjects. In six normal subjects, the test was repeated with the addition of somatostatin (250 micrograms bolus, followed by 500 micrograms/hr), which abolished the insulin and growth hormone response to arginine. It also abolished the fall in plasma phosphorus but appeared (if anything) to augment the increase in potassium. These findings show that arginine is responsible for a fall in plasma phosphorus related to the insulin response, and for an increase in plasma potassium of clinical significance, the mechanism(s) of which, however, are still obscure.
Diabete Metab 1979
Dec
PMID:Arginine-induced hypophosphatemia and hyperkaliemia in man. 4 74
1
2
3
4
5
6
7
8
9
10
Next >>