Effects of insulin and growth hormone on the flux rates of plasma glucose and plasma free fatty acids in man.
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Adult↗
Biomedical subjects
J S Cheng
Publications and source records attributed to J S Cheng.
Independence of growth hormone effects on nitrogen retention and free fatty acid mobilization.
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Animals↗
AM-404 elevates renal intracellular Ca(2+), questioning its selectivity as a pharmacological tool for investigating the anandamide transporter.
The effect of N-(4-hydroxyphenyl)-arachidonamide (AM-404), a drug commonly used to inhibit the anandamide transporter, on intracellular free Ca(2+) levels ([Ca(2+)](i)) was studied in Madin Darby canine kidney (MDCK) cells. [Ca(2+)](i) was measured using fura-2 as a Ca(2+) indicator. Between 2 and 40 microM, AM-404 increased [Ca(2+)](i) in a concentration-dependent fashion with an EC(50) value of 20 microM. Removal of extracellular Ca(2+) abolished the [Ca(2+)](i) signals. The [Ca(2+)](i) increase was nearly abrogated by 10 microM La(3+), but was insensitive to 50 microM Ni(2+) and 10 microM of nifedipine, nimodipine, nicardipine, and verapamil. At a concentration that did not increase [Ca(2+)](i), AM-404 (1 microM) did not alter the [Ca(2+)](i) increases induced by 10 microM ATP and 1 microM bradykinin. AM-404 (5 microM) also increased [Ca(2+)](i) in Chang liver cells, PC3 human prostate cancer cells, BFTC human bladder cancer cells, and MG63 human osteoblast-like cells. Together, this study shows for the first time that AM-404 at concentrations commonly used to inhibit the anandamide transporter in various systems induced an increase in [Ca(2+)](i) in different cell types. The [Ca(2+)](i) increase was solely due to extracellular Ca(2+) influx. Thus caution must be exercised in using AM-404 as a selective inhibitor of the anandamide transporter.
Adenosine Triphosphate↗
Haemodynamic effects of enalaprilat on portal hypertension in patients with HBsAg-positive cirrhosis.
It has been suggested that enalaprilat inhibits the renin-angiotensin-aldosterone system in plasma and tissue; it may therefore reduce portal vascular pressure owing to secondary hyperaldosteronism in patients with liver cirrhosis. In order to evaluate this concept, 20 patients with hepatitis B surface antigen (HBsAg)-positive liver cirrhosis and portal hypertension received an intravenous infusion of 2.5 mg of enalaprilat. Wedged hepatic venous pressure, free hepatic venous pressure and cardiac index were measured before, immediately after, and then 15 min, 30 min and 1 h after intravenous enalaprilat infusion. The mean pressure gradient between wedged hepatic venous pressure and free hepatic venous pressure was significantly decreased, by 13% immediately after, 18% at 15 min, 23% at 30 min and 13% at 1 h after infusion of enalaprilat. Thirteen patients experienced a decrease of hepatic venous pressure gradient (HVPG) greater than 5 mmHg, another three 3-5 mmHg and the remaining four patients exhibited no significant change in HVPG. Systemic haemodynamic indices, including pulmonary arterial pressure, pulmonary capillary wedge pressure and central venous pressure, decreased significantly at 15 and 30 min after enalaprilat infusion (P < 0.01). Liver function, renal function and blood routine before and after enalaprilat infusion showed no significant change. There were no adverse effects during or after enalaprilat infusion. We conclude that enalaprilat infusion can quickly and safely reduce the hepatic venous pressure gradient in patients with HBsAg-positive cirrhosis.
Aged↗
Effects of electro-acupuncture on C-FOS expression in gerbil hippocampus during transient global ischemia.
We studied the effects of electro-acupuncture (EA) on C-FOS expression as well as on the histological changes in various regions of hippocampus in the gerbil acute global ischemia model. EA was administered at points of 'Feng-fu' and 'Jin-suo' with a frequency of 7 Hz and an intensity of 6 mA for 30 minutes. EA can substantially potentiate the induction of C-FOS protein like immunoreactivity (CFPLI) in neurons of various regions in hippocampus following transient global ischemia, especially in the CA1 subfield. At the same time EA can prevent most of the CA1 cells from delayed degeneration after ischemia. These results indicate that EA has the protective effect on neurons of hippocampus after cerebral ischemia and C-FOS may be involved in this process.
Animals↗
Effect of electroacupuncture on the level of preproenkephalin mRNA in rat during penicillin-induced epilepsy.
Our previous studies have shown that seizure induced by injecting penicillin (0.24 mg/2 microliters) into hippocampus could be inhibited by electroacupuncture (EA) probably via decreasing enkephalin content in hippocampus. To determine whether this change reflected the peptide synthesis, preproenkephalin (PPE) mRNA was detected in hippocampus and some other limbic structures during seizure and after EA treatment by in situ hybridization. Four hours after injecting penicillin into hippocampus, PPE mRNA levels were significantly increased by 10 folds in entorhinal cortex, subiculum, CA1 area of hippocampus, amygdaloid nucleus and piriform cortex, whereas EA treatment apparently attenuated the seizure-induced increase of PPE mRNA in the areas mentioned above. The results indicated that EA may regulate the biosynthesis of PPE in hippocampus during seizure by an alteration in gene transcription.
Animals↗
Impact of bacterial eradication on the cell proliferation and p53 protein accumulation in Helicobacter pylori-associated gastritis.
BACKGROUND: This study investigates the cell proliferation and the expression of p53 protein in Helicobacter pylori (H. pylori)-associated gastritis and assesses the effect of bacterial eradication on these epithelial factors. MATERIAL AND METHODS: Seventy-nine patients with H. pylori-associated gastritis were randomized into the control group (n = 38) and anti-H. pylori group (n = 41). Each patient received endoscopic examinations with gastric biopsy before and 8 weeks after the treatment. The specimens from gastric antrum were immunostained for monoclonal antibodies against the proliferating cell nuclear antigen (PCNA) and p53 protein. RESULTS: In the control group, the total labeling index (L.I.) of PCNA and the positive index (P.I.) of p53 in the whole foveolar epithelium were unchanged after treatment. In the anti-H. pylori group, 35 of 41 cases (85.3%) achieved eradication of H. pylori. Amongst the H. pylori-eradicated cases, the total L.I. of PCNA in the whole foveolar epithelium did not meaningfully alter after H. pylori elimination (p > 0.05). However, a significant reduction of L.I. was observed in the middle compartments of the gastric pits (before vs. after treatment: 14.0 vs. 7.3, p < 0.05). With regard to the p53 expression, the P.I.s were significantly decreased in the whole foveolar epithelium (before vs. after treatment: 0.57 vs. 0.17, p < 0.05) and in each compartment of the gastric pits (before vs. after treatment: [upper compartment]: 0.34 vs. 0.15, p < 0.05; [middle compartment]: 0.67 vs. 0.23, p < 0.05; [lower compartment]: 0.71 vs. 0.20, p < 0.05) after eradication of H. pylori. CONCLUSIONS: Bacterial eradication reverses the hyperproliferating status of the foveolar epithelium in patients with H. pylori gastritis and leads to a decrease in p53 accumulation in the epithelial cells.
2-Pyridinylmethylsulfinylbenzimidazoles↗
Implications of serum basic fibroblast growth factor levels in chronic liver diseases and hepatocellular carcinoma.
Angiogenesis occurs in response to tissue damage, and is of vital importance for tumor growth and metastasis. Basic fibroblast growth factor (bFGF), a well-known angiogenic factor, has been suggested to be a useful diagnostic marker in certain hypervascular tumors. However, the relevance of its detection has not been well evaluated in patients with hepatocellular carcinoma (HCC) and benign chronic liver diseases. In the current study, immunoassay of bFGF was performed on serum samples from 39 patients with HCC, 21 with liver cirrhosis, 22 with chronic hepatitis and 40 normal subjects. The serum bFGF level was significantly increased in patients with liver cirrhosis and HCC when compared with those with chronic hepatitis or normal subjects (all p-values < 0.001). However, no difference was observed between the groups with liver cirrhosis and HCC (p > 0.05). If we set 9.6 pg/ml (mean + 3 standard deviations of bFGF in the control group) as the upper limit of normal serum level of bFGF, elevated bFGF concentrations were noted in 9.1%, 42.9% and 51.3% of patients with chronic hepatitis, liver cirrhosis and HCC respectively. In non-cancer patients, the coexistence of acute illness (p = 0.000) was an independent factor related to the elevation of serum bFGF. On the other hand, a multivariate analysis demonstrated that both advanced stage of cancer (p = 0.026) and coexistence of acute illness (p = 0.000) influence the serum level of bFGF in patients with HCC. We conclude that serum bFGF levels are significantly higher in patients with HCC and are positively correlated with advanced tumor stage. Nevertheless, elevation of serum bFGF may also be observed in a significant number of patients with liver cirrhosis. Therefore, measurement of serum bFGF alone cannot be satisfactory as a tumor marker for diagnosis of HCC. In addition, it is important to point out that coexistence of acute illness may be a crucial confounding factor in the diagnosis or monitoring of any cancer by the estimation of serum bFGF.
Adult↗