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Biomedical subjects

C Wen

Publications and source records attributed to C Wen.

51 records · Page 3Linked to original sources
PubMed1995

Characterization of the murine mu opioid receptor gene.

The analgesic and addictive properties of morphine and other opioid drugs are thought to result from their interaction with mu opioid receptors. Using a delta opioid receptor cDNA as a probe, we have isolated a murine mu opioid receptor cDNA clone (mMOR). Stable expression of mMOR in Chinese hamster ovary cells conferred high binding affinity for mu receptor ligands including morphine and [D-Ala2,N-methyl-Phe4,Gly5-ol]-enkephalin and low affinity for delta and kappa preferring ligands. Treatment of these cell lines with morphine and other mu agonists inhibited forskolin-induced cAMP accumulation, demonstrating a functional coupling of mMOR to the inhibition of adenylate cyclase. The predicted amino acid sequence of mMOR shares approximately 55% overall amino acid identity with the delta receptor and approximately 97% identity with the recently reported rat mu opioid receptor. Expression of the mu receptor in mouse brain as revealed by in situ hybridization parallels the reported pattern of distribution of mu-selective ligand binding sites. Chromosomal localization (to mouse chromosome 10) and Southern analysis are consistent with a single mu opioid receptor gene in the mouse genome, suggesting that the various pharmacologically distinct forms of the mu receptor arise from alternative splicing, post-translational events, or from a highly divergent gene(s).

Amino Acid Sequence↗
PubMed1995

Specific binding of avidin to biotin containing lipid lamella surfaces studied with monolayers and liposomes.

The interaction of avidin (from egg white) with phospholipid (monolayer and bilayer) model membranes containing biotin-conjugated phospholipids has been studied. In the first part, using surface sensitive techniques (ellipsometry and surface plasmon resonance) we demonstrated that the nonspecific adsorption of avidin to phospholipid lamella could be abolished by adding an amount of Ca2+, Mg2+ or Ba2+ that led to an electrostatic interaction. The specific binding of avidin to lipid mixtures containing biotin-conjugated phospholipids was obviously composition dependent. The ratio 1:12 of a B-DPPE/DPPE mixture was found to be the optimum molar ratio. When we compared the results from the surface sensitive techniques with those from the electron micrographs of a two dimensional crystal of avidin (obtained in our laboratory), the optimum ratio was found to be determined by the effect of lateral steric hindrance. In the second part, we observed the pattern of the layers of fluorescently labeled phospholipid and adsorbed proteins with a home-made micro fluorescence film balance. The fluorescence images showed that avidin was preferentially bound to the receptors that were in the fluid domains. Further, with a sensitive fluorescence assay method, the effect of the phase behavior of liposomes on the specific binding of avidin was measured. This showed that avidin interacted with biotinlipid more weakly in the gel state liposome than in the liquid state liposome. The major conclusion was that the binding of avidin to a membrane bound model receptor was significantly restricted by two factors: one was the lateral steric hindrance and the other was the fluidity of the model membrane.

Adsorption↗
PubMed1995

Long-term ouabain administration does not alter blood pressure in conscious Sprague-Dawley rats.

1. We tested the ability of ouabain to cause chronic hypertension by continuously infusing ouabain for 28 days (miniosmotic pump implantation; i.p.). The blood pressure and metabolic effects of sham (150 mmol/L NaCl; n = 12) or ouabain infusion (10 micrograms/kg per day; n = 14; 100 micrograms/kg per day; n = 14) were examined in conscious Sprague-Dawley rats. 2. Plasma ouabain concentrations measured after 28 days of ouabain infusion were as follows: sham, not detectable (n = 11); ouabain 10 micrograms/kg per day, 0.60 +/- 0.07 nmol/L (n = 14); and ouabain 100 micrograms/kg per day, 7.17 +/- 0.57 nmol/L (n = 14; P < 0.001). 3. Sham or ouabain infusion did not alter food intake, bodyweight, water intake or urine output in conscious rats. 4. Blood pressure was not altered by sham treatment. Ouabain at 10 micrograms/kg per day or 100 micrograms/kg per day did not produce consistent rises in blood pressure. Ouabain at 10 micrograms/kg per day increased blood pressure on treatment day 12 only (+6 mmHg; P < 0.05), while at 100 micrograms/kg per day blood pressure increased on treatment days 16 (+9 mmHg; P < 0.05) and day 18 (+8 mmHg; P < 0.05) only. There was no significant difference in blood pressure between sham and ouabain groups. 5. Renal blood flow was decreased in rats infused with ouabain at 10 micrograms/kg per day (2.0 +/- 0.3 mL/min per 100 g bodyweight; n = 5; P < 0.01) and 100 micrograms/kg per day (2.2 +/- 0.4 mL/min per 100 g bodyweight; n = 7; P < 0.05) compared with sham treatment (3.5 +/- 0.2 mL/min per 100 g bodyweight; n = 6). Renal vascular resistance was increased in rats treated with ouabain at 10 micrograms/kg per day (65.5 +/- 12.6 mmHg/mL per min per 100 g bodyweight; n = 5; P < 0.01) and 100 micrograms/kg per day (66.0 +/- 15.6 mmHg/mL per min per 100 g bodyweight; n = 7; P < 0.05) compared with sham treatment (32.6 +/- 2.5 mmHg/mL per min per 100 g bodyweight; n = 6). 6. High plasma concentrations of ouabain do not cause consistent increases in blood pressure in conscious Sprague-Dawley rats.

Animals↗
PubMed1993

Blood levels of sex hormone in lupus nephritis and their relationship to lupus activity.

One hundred and fifty-nine patients (140 females, 19 males) with lupus nephritis (LN) were studied. Renal biopsy was performed for each patient with light microscopy, immunofluorescence and electronic microscopic studies. 27 normal subjects were selected as controls. Blood levels of sex hormone including follicle-stimulating hormone (FSH), luteinizing hormone (LH), estradiol (E2) and testosterone (T) were measured by radioimmunoassay (RIA), and some clinical, laboratory and histological parameters were collected for analysis of lupus activity. It was found that serum FSH, LH and plasma E2 of all patients were much higher than normal (P < 0.01) while plasma T was much lower in female patients (P < 0.01) but normal in male patients. The lupus activity was proved to be closely related to plasma E2 and T (P < 0.05). There was no definite relationship between abnormal plasma E2 or T and serum IgG, C3 C4, ANA, A-dsDNA or A-Sm. The levels of sex hormones among every histological type of LN were not significantly different. It was concluded that: 1. The increment of plasma E2 is associated with lupus activity in both male and female patients. 2. The decrement of plasma T only in female patients is also related to lupus activity. 3. No relationship could be found among FSH, LH, E2 and T.

Adolescent↗
PubMedDate not supplied

Hypotensive effects of peptide T in conscious rats.

1. The present study investigated the effects of peptide T on mean arterial blood pressure (MAP) in conscious normotensive Sprague-Dawley (SD) rats, spontaneously hypertensive rats (SHR) and two-kidney one-clip (2K1C) hypertensive rats. 2. Peptide T was infused via the left jugular vein at a rate of 1 mg/kg per h in SD, SHR and 2K1C rats and then at doses of 0.1, 0.25, 0.5, 1 and 5 mg/kg per h in SHR, with 0.9% saline as a sham control in SHR and 2K1C. Mean arterial pressure was measured directly before, during and after infusion. 3. Peptide T (1 mg/kg per h) decreased blood pressure in both SHR (P < 0.01) and 2K1C (P < 0.05). In normotensive SD rats the fall in MAP approached statistical significance (P = 0.06). The effect of peptide T was not significantly different in normotensive compared with hypertensive rats. Saline infusion had no effect. The blood pressure lowering effect of peptide T appeared to be dose-dependent in SHR.

Animals↗