Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Amino acid balance and nitrogen balance during total parenteral nutrition (TPN) and continuous arteriovenous hemofiltration (CAVH) were investigated in 11 critically ill anuric patients during the first 7 days after onset of anuria. Nitrogen intake ranged from 0.115 +/- 0.013 (SEM) g/kg/day on day 1 to 0.291 +/- 0.029 (SEM) g/kg/day on day 7. After 7 days of TPN, 9 patients had a positive cumulative protein-N balance of 287.52 +/- 68.52 (SEM) mg/kg, 2 patients had a negative balance of 781.8 and 1,103.2 mg/kg, respectively. Mean amino acid loss in ultrafiltrate was 0.159 +/- 0.008 (SEM) g/kg/day. Four patients died without recovery of renal function.
 ...
PMID:Nitrogen and amino acid balance during total parenteral nutrition and continuous arteriovenous hemofiltration in critically ill anuric children. 175 24

Assay of free and total malondialdehyde (MDA) in human serum and plasma from healthy subjects and from patients with high risk of lipoperoxidation was performed as follows: (a) acidic (HClO4, pH 1, at 20 degrees C) or basic (NaOH, pH 13, at 60 degrees C) treatments for 30 min; (b) reaction of the protein-free extract (obtained by acid precipitation) with thiobarbituric acid (TBA); (c) HPLC separation on C18 columns with an eluting solution of methanol/phosphate buffer, 10 mmol/L, pH 5.8 (40/60, by vol), at a flow rate of 1.5 mL/min. Free MDA averaged 0.042 (SEM 0.008) and 0.043 (SEM 0.007) mumol/L, respectively, in serum and plasma from healthy subjects. Free (+/- SEM) MDA increased significantly in the plasma from cancer patients (0.270 +/- 0.047 mumol/L) and from hemodialyzed patients (0.214 +/- 0.035 mumol/L). In serum of hemodialyzed patients, analyses for total MDA were unsuitable because of interfering peaks. MDA bound to NH2 groups constituted 83.2% and 83.5% of total MDA in serum and plasma of healthy subjects, respectively, and only 58% in plasma of hemodialyzed patients.
 ...
PMID:Free and bound malondialdehyde measured as thiobarbituric acid adduct by HPLC in serum and plasma. 186 5

1. Oxytocin receptors in the uterus of the brushtail possum (T. vulpecula) were characterized by radioreceptor assay and compared with those of the sheep and rat uterus. 2. A single oxytocin binding site was found with an affinity (Kd) and receptor concentration (Ro) of 3.0 +/- 0.8 nmol/l and 200 +/- 60 fmol/mg protein, respectively (SEM; n = 5). The receptor was stable at -20 degrees C; divalent ions were required for optimum binding. 3. Competitive displacement curves with related peptides showed the following order of specificity: vasotocin greater than oxytocin greater than mesotocin = arginine-vasopressin = [Thr4, Gly7]-oxytocin greater than lysine-vasopressin = isotocin much greater than [d(CH2)5, D-Phe2, Ile4, Ala9-NH2]-AVP. 4. It was concluded that oxytocin receptors in the possum have similar characteristics to those of placental mammals.
 ...
PMID:Uterine oxytocin receptors in an Australian marsupial, the brushtail possum, Trichosurus vulpecula. 196 6

Radioligand binding studies of the cardiac arginine vasopressin (AVP) receptor, together with studies on the AVP-evoked alterations in the [Ca2+]i levels, were undertaken using primary cultures of neonatal rat cardiomyocytes. Rapid, reversible, specific, high-affinity and low-capacity binding sites were detected for the agonist, [3H]AVP, and the V1 selective antagonist, d(CH2)5 Tyr (Me)-[3H]AVP (V1 antagonist), radioligands. The V2 selective antagonist radioligand, d(CH2)5 D-Ile des-Gly NH2-[3H]AVP, showed very little binding even at very high concentrations. [3H]AVP and [3H]V1 antagonist specific binding attained equilibrium in 10 minutes at 37 degrees C. The Kd and Bmax values (mean +/- SEM) were [3H]AVP: Kd 1.44 +/- 0.18 nM; Bmax 5,253 +/- 590 sites/cell; [3H]V1 antagonist: Kd 0.96 +/- 0.10 nM; Bmax 6,869 +/- 485 sites/cell. Ki values for a series of AVP-related peptide analogues and antagonists determined by competitive inhibition of [3H]AVP binding were consistent with the saturation data. The results suggest that these cells possess a homogeneous population of V1 subtype AVP receptors. AVP increased [Ca2+]i in a concentration-dependent manner as judged by fura-2 fluorescence. This was completely attenuated by inclusion of the V1 antagonist. The maximal increase in [Ca2+]i evoked by AVP from a resting level of 60 +/- 5 nM was less (250 +/- 35 nM) in comparison to the maximal response evoked by angiotensin II (2,337 +/- 640 nM).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Vasopressin increases cytosolic free [Ca2+] in the neonatal rat cardiomyocyte. Evidence for V1 subtype receptors. 205 37

OBJECTIVE The aim of the study was to investigate whether pyridostigmine, a cholinesterase inhibitor which is thought to act at the hypothalamus to inhibit somatostatin secretion, would augment spontaneous or GHRH-stimulated serum GH levels in patients with GH-insufficiency. DESIGN Oral pyridostigmine 60 mg or placebo was administered at the start of a 9-h subcutaneous infusion of either GHRH (1-29)NH2 10 micrograms/kg/h or saline control. Studies were performed during the daytime (0900-1800 h) in five patients, and the night-time (2100-0600 h) in a further five. PATIENTS Ten short, pre-pubertal children (aged 6-11 years; eight boys) with growth hormone insufficiency were studied. MEASURES Blood for serum GH was sampled every 20 min, and analysed using the PULSAR program. RESULTS The subcutaneous infusion of GHRH 10 micrograms/kg/h increased mean serum GH levels (+/- SEM): by day 17.7(+/- 6.8) vs placebo 2.2(+/- 0.4) mU/l (P less than 0.01), and by night 26.9(+/- 3.3) vs 5.5(+/- 1.3) mU/l (P less than 0.05). There was a significant rise in mean 'baseline' GH concentration: by day 5.5(+/- 1.7) vs 1.0(+/- 0.0) mU/l (P less than 0.05); and night 8.2(+/- 2.7) vs 1.3(+/- 0.3) mU/l (P less than 0.05). Pyridostigmine failed to produce a significant overall increase in either spontaneous or GHRH-stimulated GH secretion by day or night, although there was a significant rise in mean GH levels during the 3 h following pyridostigmine administration in the morning: 4.4(+/- 1.1) vs 2.4(+/- 0.5) mU/l (P less than 0.001). GHRH or pyridostigmine given singly or in combination had no significant effect on the number of pulses. Side-effects attributable to pyridostigmine occurred in seven children. CONCLUSIONS Pyridostigmine, either on its own or as an adjuvant therapy in combination with GHRH, acts for only a brief time and does not offer any potential benefit in the management of children with short stature.
 ...
PMID:Pyridostigmine fails to increase either spontaneous or GHRH-stimulated GH secretion during day or night in growth hormone-insufficient children. 206 Jan 50

The acute GH release stimulated by the synthetic hexapeptide, His-DTrp-Ala-Trp-DPhe-Lys-NH2 [GH releasing peptide (GHRP)], was determined in 18 normal men and compared with the effects of GH-releasing hormone, GHRH-(1-44)-NH2. Specificity of effect was assessed by measurement of serum PRL, LH, TSH, and cortisol. GHRP was administered at doses of 0.1, 0.3, and 1.0 microgram/kg by iv bolus. GHRH at a dose of 1.0 microgram/kg was administered alone and together with various does of GHRP. No adverse clinical effects of laboratory abnormalities were observed in response to GHRP. A side-effect of mild facial flushing of 1- to 3-min duration occurred in 16 of the 18 subjects who received GHRH-(1-44)-NH2. Mean (+/- SEM) peak serum GH levels after injection of placebo and 0.1, 0.3, and 1.0 microgram/kg GHRP were 1.2 +/- 0.3, 7.6 +/- 2.5, 16.5 +/- 4.1, and 68.7 +/- 15.5 micrograms/L, respectively. The submaximal dosages of 0.1 and 0.3 microgram/kg GHRP plus 1 microgram/kg GHRH stimulated GH release synergistically. Serum PRL and cortisol levels rose about 2-fold above basal levels only at the 1 microgram/kg dose of GHRP, and there were no changes in serum LH and TSH over the first hour after administration of the peptide(s). GHRP is a potent secretagogue of GH in normal men. Since GHRP and GHRH together stimulate GH release synergistically, these results suggest that GHRP and GHRH act independently. This supports our hypothesis that the GH-releasing activity of GHRP reflects a new physiological system in need of further characterization in animals and man.
 ...
PMID:Growth hormone (GH)-releasing peptide stimulates GH release in normal men and acts synergistically with GH-releasing hormone. 210 87

Obese patients are characterised by several neuroendocrine abnormalities, including characteristically a decrease in growth hormone responsiveness to GH-releasing hormone. In normal subjects, the GH response to GHRH is enhanced by the acetylcholinesterase inhibitor, pyridostigmine. We have studied the effect of this drug on GH secretion in gross obesity. Twelve obese patients were studied (mean weight 156% of ideal) and compared with a group of 8 normal volunteers. Each subject was initially studied on two occasions, in random order, with GHRH (1-29) NH2 100 micrograms iv alone and following pretreatment with pyridostigmine 120 mg orally one hour prior to GHRH. In obese patients, the GH response to GHRH was significantly blunted when compared to controls (GH peak: 20 +/- 4 vs 44 +/- 16 micrograms/l; mean +/- SEM). After pyridostigmine, the response to GHRH was enhanced in the obese subjects, but remained significantly reduced compared to non-obese subjects treated with GHRH and pyridostigmine (GH peak: 30 +/- 5 vs 77 +/- 20 micrograms/l, respectively). In 6 subjects, higher doses of GHRH or pyridostigmine did not further increase GH responsiveness in obese patients. Our results suggest that obese patients have a disturbed cholinergic control of GH release, probably resulting from increased somatostatinergic tone. This disturbed regulation may be responsible, at least in part, for the blunted GH responses to provocative stimuli.
 ...
PMID:Pyridostigmine enhances, but does not normalise, the GH response to GH-releasing hormone in obese subjects. 210 45

To determine whether differential response to growth hormone-releasing hormone (GHRH) could cause the developmental changes seen in growth hormone (GH) secretion, we administered 10 micrograms/kg GHRH (1-44 NH2) to a group of four unanesthetized, fasted, rhesus monkeys via acutely placed venous catheters at 1, 7, 14, and 28 d postnatal age. Serum GH was assayed by hGH RIA in sera collected at -60, -30, 0, 15, 30, 45, 60, and 90 min relative to the GHRH bolus. Serum cortisol was measured by ELISA in the 0-, 30-, and 60-min samples. Differences between age groups were analyzed by repeated measures analysis of variance and paired t tests. Mean basal GH levels were higher at 1 d (9.4 +/- 1.2 micrograms/L, mean +/- SEM) than at 7 (5.5 +/- 0.4), 14 (5.6 +/- 0.5), and 28 d (5.3 +/- 0.5) of age. There were no other significant differences in mean basal GH values between the age groups. Mean post-GHRH GH concentrations decreased significantly with each age after 1 d (22.6 +/- 1.6): 7 d (16.4 +/- 1.3); 14 d (11.3 +/- 1.0); and 28 d (7.9 +/- 0.9). Similarly, mean delta-GH values decreased with each increase in age from 1 d (15.0 +/- 1.9): 7 d (10.9 +/- 1.6); 14 d (5.9 +/- 1.1); and 28 d (2.7 +/- 0.8). Serum cortisol was not correlated with serum GH at any age. Our study demonstrates decreasing basal GH concentration and GH responses to GHRH with advancing age from 1 to 28 d in the rhesus monkey.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Longitudinal changes in growth hormone response to growth hormone-releasing hormone in neonatal rhesus monkeys. 211 88

Although corticosteroids (CS) cause nitrogen wasting in healthy humans, it is not known whether the salutary antiinflammatory and appetite-stimulating effects of CS in inflammatory diseases mitigate this effect. We measured nitrogen balance before, during, and after 3 d of high-dose methylprednisolone therapy in nine patients with flare-ups of rheumatoid arthritis. There was evidence of preexisting somatic protein and fat depletion in seven of nine subjects. Patients were allowed to eat freely on a metabolic ward. Nitrogen balances were -0.89 +/- 1.38 g/d (means +/- SEM) before CS therapy, -5.77 +/- 1.30 g/d during therapy (P less than 0.001), and -3.54 +/- 1.38 g/d after therapy (P less than 0.01) despite increased energy and nitrogen intake and clinical resolution of inflammation during and after the pulse therapy. We conclude that patients with rheumatoid arthritis are often cachectic and high-dose CS cause nitrogen wasting in these patients despite an antiinflammatory and appetite-stimulatory benefit.
 ...
PMID:Catabolic effects of high-dose corticosteroids persist despite therapeutic benefit in rheumatoid arthritis. 223 88

Human peripheral blood monocytes/macrophages derived from normal donors, patients of tuberculoid leprosy (BT/TT) and lepromatous leprosy (BL/LL) were assayed for stimulated phagocytic responses to the potent macrophage stimulator "Tuftsin" (NH2-Thr-Lys-Pro-Arg-OH) after varying periods (6 h to 14 days) of culture in vitro. The assays consisted of visual scoring of ingested Mycobacterium leprae and radiometric measurement of ingested 14C-acetate labelled Staphylococcus aureus and Mycobacterium tuberculosis (H37Ra). While normal and BT/TT macrophages showed a progressively increasing ability for tuftsin-stimulated phagocytosis with increasing age of culture in vitro, BL/LL macrophages showed the opposite response so that 14-day cultures were refractory to a stimulatory dose of up to 7.0 microM (10 to 20 times the optimal dose for normal and BT/TT macrophages). The 14-day BL/LL macrophage cultures were, however, responsive to 35 microM tuftsin (100 times the optimal dose for normal macrophages). Analysis of the dose-response curves also indicates that BT/TT cultures despite exhibiting an apparent similarity to normal macrophages demonstrate a rightward shift for a maximal stimulated phagocytosis. Finally SEM photo-micrographs of 14-day macrophage cultures of the three groups revealed that while normal and BT/TT cultures demonstrated an increase in membrane ruffling and filopodia on stimulation with 0.8 microM tuftsin, BL/LL cultures exhibited none of the features associated with stimulation. From the above findings, we conclude that lepromatous macrophages may display an aberrant differentiation profile leading to a terminal state of unresponsiveness and that the defect may possibly lie at the level of tuftsin receptor expression or transmembrane signal transduction.
 ...
PMID:Modulation of human lepromatous monocyte-macrophage functions in vitro by tuftsin. 229 63


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>