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Biomedical subjects

Z Ma

Publications and source records attributed to Z Ma.

At least 217 records · Page 12Linked to original sources
PubMed1996

Differential regulation of 5-hydroxytryptamine release by GABAA and GABAB receptors in midbrain raphe nuclei and forebrain of rats.

1. Extracellular 5-hydroxytryptamine (5-HT) was determined in dorsal raphe nucleus (DRN), median raphe nucleus (MRN) and nucleus accumbens by use of microdialysis in unanaesthetized rats. 2. Infusion of the gamma-aminobutyric acid (GABA)A receptor agonist muscimol into DRN and MRN resulted in decreased 5-HT in DRN and MRN, respectively. Muscimol infusion into nucleus accumbens had no effect on 5-HT. 3. Infusion of the GABAA receptor antagonist bicuculline into DRN resulted in increased DRN and nucleus accumbens 5-HT. Bicuculline infusion into MRN had no effect on 5-HT. This suggests that endogenous GABA had a tonic, GABAA receptor-mediated inhibitory effect on 5-HT in DRN, but not in MRN. 4. Infusion of the GABAB receptor agonist baclofen into DRN produced a decrease in DRN 5-HT. Baclofen infusion into nucleus accumbens resulted in decreased nucleus accumbens 5-HT. This suggests that GABAB receptors are present in the area of cell bodies and terminals of 5-hydroxytryptaminergic neurones. 5. Infusion of the GABAB receptor antagonists phaclofen and 2-hydroxysaclofen had no effect on midbrain raphe and forebrain 5-HT. This suggests that GABAB receptors did not contribute to tonic inhibition of 5-HT release. 6. In conclusion, 5-HT release is physiologically regulated by distinct subtypes of GABA receptors in presynaptic and postsynaptic sites.

5,7-Dihydroxytryptamine↗
PubMed1996

Serum leptin levels in women with anorexia nervosa.

Leptin is a protein encoded by the ob gene that is expressed in adipocytes and regulates eating behavior via central neuroendocrine mechanisms. Serum leptin levels have been shown to correlate with weight and percent body fat in normal and obese individuals; however, it is not known whether the regulation of leptin is normal below a critical threshold of body fat in chronic undernutrition. We investigated serum leptin levels in 22 women, aged 23 +/- 4 yr, with anorexia nervosa. Duration of disease, weight, BMI, percent body fat, and serum leptin levels were determined for each patient. Nutritional status was assessed further by caloric intake and measurement of insulin and insulin-like growth factor I (IGF-I) levels. Twenty-three healthy women, aged 23 +/- 4 yr, taking no medications, with normal menstrual function and body mass index (BMI) between 20-26 kg/m2 (mean, 23.7 +/- 1.7 kg/m2), served as a control population for comparison of leptin levels. Subjects with anorexia nervosa were low weight (BMI, 16.3 +/- 1.6 kg/m2; normal, 20-26 kg/m2) and exhibited a striking reduction in percent body fat (7 +/- 2%; normal, 20-30%). The mean serum leptin level was significantly decreased in subjects with anorexia nervosa compared with that in age- and sex-matched controls of normal body weight (5.6 +/- 3.7 vs. 19.1 +/- 8.1 ng/mL; P < 0.0001). Serum leptin levels were correlated highly with weight, as expressed either BMI (r = 0.66; P = 0.002) or percent ideal body weight (r = 0.68; P = 0.0005), body fat (r = 0.70; P = 0.0003), and IGF-I (r = 0.64; P = 0.001), but not with caloric intake or serum levels of estradiol or insulin in subjects with anorexia nervosa. The correlation between leptin and body fat was linear, with progressively lower, but detectable, leptin levels measured even in patients with less than 5% body fat, but was not significant when the effects of weight were taken into account. In contrast, the correlation between leptin and IGF-I remained significant when the effects of weight, body fat, and caloric intake were taken into account. In normal controls, leptin correlated with BMI (r = 0.55; P = 0.007) and IGF-I (r = 0.44; P < 0.05), but not with fat mass. These data demonstrate that serum leptin levels are reduced in association with low weight and percent body fat in subjects with anorexia nervosa compared to normal controls. Leptin levels correlate highly with weight, percent body fat, and IGF-I in subjects with anorexia nervosa, suggesting that the physiological regulation of leptin is maintained in relation to nutritional status even at an extreme of low weight and body fat.

Adipose Tissue↗
PubMed1996

Radioimmunoassay of leptin in human plasma.

Recent studies suggest that leptin, the ob gene product absent in ob/ob mice, is a negative regulator of adiposity. We developed an RIA to measure human leptin in plasma or serum. The minimum detectable concentration by the assay is 0.5 microg/L leptin and the limit of linearity is 100 microg/L. Recovery of leptin added to serum was 99-104% over by the linear range of the assay. The RIA agreed reasonably well with rough quantification by Western blot (RIA = 0.90 blot + 3.7 microg/L, Sy/x = 10.9 microg/L). CVs within- and between-run ranged from 3.4% to 8.3% and from 3.6% to 6.2%, respectively. Variation in plasma leptin concentrations in specimens collected on consecutive mornings was large (CVs of 10.9% and 22.5%). After an overnight fast, leptin concentrations were similar to those 1-2 h after 1-2 meals. Plasma leptin concentrations in specimens from 83 lean and obese adults correlated directly with body mass index (BMI; kg/m2): r = 0.72, P <0.001. Correlations were significantly improved by separating results by gender (men r = 0.84, women r = 0.87; p <0.001). The increase in leptin concentrations with increasing BMI was greater in women than in men (slope 2.53 vs 0.97 microg/L per unit BMI, respectively). Leptin concentrations determined in lean subjects (BMI between 18 and 25) were higher in women (7.36 +/- 3.73 microg/L) than in men (3.84 +/- 1.79 microg/L) (P <0.001). Plasma leptin varied little with age and no significant difference was observed between whites and blacks. We conclude that: (a) plasma leptin concentrations are accurately and precisely measured by this new RIA; (b) leptin concentrations vary little due to short-term fasting, age, or race; but (c) plasma leptin concentrations are gender specific.

Adolescent↗
PubMed1996

[Long-term follow-up results of eleven cases after resection of hepatic metastases from colorectal cancer].

Eleven patients with hepatic metastases from colorectal cancer survived more than 5 years after the resection were reviewed. There were 3 (27.3%) disease-free survivors, the longest survival period was 7 years and 2 months. Compared with 41 survivors of less than 5-year duration after resection, it was shown that close follow-up after resection of the primary cancer, detecting early subclinical hepatic metastases, preoperative lower level of CEA, tumor less or equal to 5 cm in size, single metastatic nodule and radical resection were important factors influening long-term survival (P < 0.05). It is of the opinion that early diagnosis, early resection and re-resection after detecting subclinical local recurrence and metastases play important role in improving long-term response.

Adult↗
PubMed1996

[Video assisted thoracoscopic major lung resection].

We report the combined experience on video assisted thoracoscopic (VAT) anatomical lung resection from two hospitals in Hong King. 60 patients successfully underwent VAT anatomical lung resections: 55 lobectomies, 2 bi-lobectomies, 2 pneumonectomies and 1 segmectomy. There was no mortality. Intraopeative complication occurred in 1 patient due to malfunctioning of a vascular stapler. Postoperative complications were few. Average postoperative hospital stay was 7.2 days. Compared with the conventional thoracotomy approach, the VAT approach was associated with the conventional thoracotomy approach, the VAT approach was associated with significantly less analgesic requirement. We conclude that VAT anatomical lung resection is technically feasible. Specific complications, however, exist. The true role of this new approach in thoracic surgery awaits further study.

Adenocarcinoma↗
PubMed1996

[The experimental study on expression of BMP3 gene during fracture healing].

The role of BMP3 in fracture repair and its basic mechanisms at the molecular aspect has been studied. Fourty-eight New Zealand white rabbits with the fractures in the middle of bilateral radial shafts were used as animal models, and divided randomly into six groups for calluses at the 1st, 2nd, 3rd, 4th, 6th and 8th week after the onset of fracture. The levels and the cellular localizations of expression of BMP3 mRNA were investigated with the nucleotide hybridization techniques. The results revealed that BMP3 gene expression was highly increased in the early phase of fracture repair, and reached its peak at the second week (about 3.4-fold of that of the normal control). The strong expression of BMP3 gene was localized in mesenchymal cells, chondroblasts and osteoblasts. The results suggest that BMP3 plays an important role of bone-induction in the early stage of fracture repair and it works by the way of autocrine or/and paracrine pathway.

Animals↗
PubMed1996

[Treatment of central retinal artery occlusion with thrombolysis via superselective ophthalmic artery catheterization].

OBJECTIVE: To investigate the therapeutic effect of thrombolysis via superselective ophthalmic artery catheterization for treatment of central retinal artery occlusion (CRAO). METHOD: Urokinase was directly infused via ophthalmic artery (OA) or common carotid artery by catheterization after angiography into 4 eyes of 4 patients with CRAO, The times of onset ranging from 7 to 14 days. RESULTS: The visual acuity was significantly improved in 2 eyes. No visual change was found in 2 eyes in which the beginning part of internal carotid artery (ICA) or OA was occluded. There was no complications. CONCLUSIONS: Good results were obtained in the eyes in which thrombolysis was launched early in the course of the disease and urokinase was successfully infused into the OA. It seems that there is no effect for the eyes complicated with occlusion in ICA and OA.

Adult↗
PubMed1996

[Studies on some characteristics of a strain of mink infectious enteritis virus].

A strain of mink infectious enteritis virus that was isolated from the east district of China can be bred on FK cell. Concentrated viruses were purified by using Sepharose-4B chromatography. The size of the virus was about 20-22 nm by electron microscope. Viral nucleic acid was extracted from pure virus by using SDS-protease K-Phenol. Tests with diphenylamine, acridine orange and the curve of thermal dentuation, etc. showed that the virus had a single-stranded DNA. The molecular weight of the ssDNA was from 1.5 x 10(6) to 2.0 x 10(6) determined by length of the virul nucleic acid.

DNA, Single-Stranded↗
PubMed1996

Urokinase mutant with better fibrin-specificity.

A 150-156 amino acids-deleted single-chain urokinase-type plasminogen activator (dscu-PA) and its recombinant wild-type counterpart (rscu-PA) were both expressed in Escherichia coli. After denaturation and renaturation in vitro, the expressed products were both purified to a single silver-stained band by means of IgG affinity chromatography. After activation by plasmin, similar enzymatic constants based on the hydrolysis of synthetic substrate S2444 by the two-chain molecular forms of dscu-PA and rscu-PA, or native tcu-PA were observed, suggesting that no impairment had been exerted on the catalytic active site of dtcu-PA by the 150-156 amino acids deletion. In both in vitro fibrin-clot and 125I-fibrin sepharose lysis tests, dtcu-PA showed a significantly higher fibrinolytic activity than rtcu-PA or rscu-PA. Hardly any effect on the concentration of fibrinogen in plasma was found in dtcu-PA. It was concluded that dtcu-PA had a higher fibrin specificity and that tcu-PA could be provided with better fibrin specificity by means of mutation.

Amino Acid Sequence↗
PubMed1995

A peptidomimetic inhibitor of farnesyl:protein transferase blocks the anchorage-dependent and -independent growth of human tumor cell lines.

Farnesyl protein transferase (FPTase) catalyzes the first of a series of posttranslational modifications of Ras required for full biological activity. Peptidomimetic inhibitors of FPTase have been designed that selectively block farnesylation in vivo and in vitro. These inhibitors prevent Ras processing and membrane localization and are effective in reversing the transformed phenotype of Rat1-v-ras cells but not that of cells transformed by v-raf or v-mos. We have tested the effect of the FPTase inhibitor L-744,832 (FTI) on the anchorage-dependent and -independent growth of human tumor cell lines. The growth of over 70% of all tumor cell lines tested was inhibited by 2-20 microM of the FTI, whereas the anchorage-dependent growth of nontransformed epithelial cells was less sensitive to the effects of the compound. No correlation was observed between response to drug and the origin of the tumor cell or whether it contained mutationally activated ras. In fact, cell lines with wild-type ras and active protein tyrosine kinases in which the transformed phenotype may depend on upstream activation of the ras pathway were especially sensitive to the drug. To define the important targets of FTI action, the mechanism of cellular drug resistance was examined. It was not a function of altered drug accumulation or of FPTase insensitivity since, in all cell lines tested, FPTase activity was readily inhibited within 1 h of treatment with the inhibitor. Furthermore, the general pattern of inhibition of cellular protein farnesylation and the specific inhibition of lamin B processing were the same in sensitive and resistant cells. In addition, functional activation of Ras was inhibited to the same degree in sensitive and resistant cell lines. However, the FTI inhibited the epidermal growth factor-induced activation of mitogen-activated protein kinases in sensitive cells but not in two resistant cell lines. These data suggest that the drug does inhibit ras function and that resistance in some cells is associated with the presence of Ras-independent pathways for mitogen-activated protein kinase activation by tyrosine kinases. We conclude that FPTase inhibitors are potent antitumor agents with activity against many types of human cancer cell lines, including those with wild-type ras.

Alkyl and Aryl Transferases↗
PubMed1995

Cloning and expression of the cDNA of chicken cation-independent mannose-6-phosphate receptor.

We cloned and sequenced the 8767-bp full-length cDNA for the chicken cation-independent mannose-6-phosphate receptor (CI-MPR), of interest because, unlike its mammalian homologs, it does not bind insulin-like growth factor II (IGF-II). The cDNA encodes a protein of 2470 aa that includes a putative signal sequence, an extracytoplasmic domain consisting of 15 homologous repeat sequences, a 23-residue transmembrane sequence, and a 161-residue cytoplasmic sequence. Overall, it shows 60% sequence identity with human and bovine CI-MPR homologs, and all but two of 122 cysteine residues are conserved. However, it shows much less homology in the N-terminal signal sequence, in repeat 11, which is proposed to contain the IGF-II-binding site in mammalian CI-MPR homologs, and in the 14-aa residue segment in the cytoplasmic sequence that has been proposed to mediate G-protein-coupled signal transduction in response to IGF-II binding by the human CI-MPR. Transient expression in COS-7 cells produced a functional CI-MPR which exhibited mannose-6-phosphate-inhibitable binding and mediated endocytosis of recombinant human beta-glucuronidase. Expression of the functional chicken CI-MPR in mice lacking the mammalian CI-MPR should clarify the controversy over the physiological role of the IGF-II-binding site in mammalian CI-MPR homologs.

Amino Acid Sequence↗
PubMed1995

Herbimycin A induces the 20 S proteasome- and ubiquitin-dependent degradation of receptor tyrosine kinases.

Herbimycin A is an ansamycin antibiotic isolated as an agent that reverses morphological transformation induced by v-src. Although herbimycin A is widely used as a tool for inhibiting multiple tyrosine protein kinases and tyrosine kinase-activated signal transduction, its mechanism of action is not well defined and includes a decrease in both tyrosine kinase protein levels and activity (Uehara, Y., Murakami, Y., Sugimoto, Y., and Mizuno, S. (1989) Cancer Res. 49, 780-785). We now show that herbimycin A induces a profound decrease in the total cellular activity of transmembrane tyrosine kinase receptors, such as insulin-like growth factor, insulin, and epidermal growth factor receptors. A substantial proportion of the in vivo inhibition could be explained by an increase in the rate of degradation. The enhanced degradation of insulin-like growth factor-insulin receptor was prevented by inhibitors of the 20S proteasome, whereas neither lysosomotropic agents nor general serine- and cysteine-protease inhibitors were active in preventing receptor degradation induced by herbimycin A. Moreover, in a temperature-sensitive mutant cell line defective in the E1-catalyzed activation of ubiquitin, herbimycin A treatment at the restrictive temperature did not result in the degradation of insulin receptor. These results suggest that herbimycin A represents a novel class of drug that targets the degradation of tyrosine kinases by the 20S proteasome. The ubiquitin dependence of this process indicates that this degradation of tyrosine kinases might involve the 20S proteasome as the proteolytic core of the ubiquitin-dependent 26S protease.

Amino Acid Sequence↗
PubMed1995

[Lumbar spinal stenosis syndrome: classification, pathology and operative consideration].

A total of 168 cases of lumbar spinal stenosis syndrome were operated on in recent 6 years. They included 13 cases of developmental spinal stenosis and 155 cases of acquired spinal stenosis. All patients were followed up for an average of 2 years and 7 months, ranging from 3 months to 5 years and 10 months. The results of treatment were not satisfactory in developmental spinal stenosis (excellent 46.2%, good 30.7%, fair 15.4%, poor 7.7%), but good in acquired spinal stenosis (excellent 72.2%, good 22.6%, fair 5.2%, poor 0). Moreover, with different classification and pathology, acquired spinal stenosis had different results. The authors stressed that it is very important to consider the methods and the range of operation according to the pathological characteristics of myelography and CTM of lumbar spinal stenosis.

Adult↗
PubMed1995

Cardiac plasma membrane physical properties and beta-adrenergic receptor function are unaltered in portal-hypertensive rats.

We have previously demonstrated that impairment of cardiac contractility in a rat model of cirrhosis may be secondary to altered cardiac plasma membrane physical properties affecting beta-adrenergic receptor function. It is unclear whether this is caused by the cirrhosis or by the portal hypertension in this model, so we studied cardiomyocyte plasma membrane physical properties, lipid composition, and beta-adrenergic receptor function in a rat model of prehepatic portal hypertension without cirrhosis. Portal hypertension was induced by graded portal vein stenosis, whereas controls had a sham operation. Cardiac sarcolemmal plasma membrane physical properties were studied by fluorescent polarization methods using diphenylhexatriene and a series of anthroyloxy-stearic acids to estimate, respectively, the static and dynamic components of membrane fluidity. beta-Adrenergic receptor density and binding affinity were measured using 3H-dihydroalprenolol as a radioligand. Isoproterenol-stimulated adenylyl cyclase activity was measured by radioimmunoassay. Neither the static nor the dynamic components of membrane fluidity were significantly different in portal-hypertensive rats compared with the controls. The membrane cholesterol, phospholipid content, and the cholesterol/phospholipid ratio did not differ between the two groups. beta-Adrenergic receptor density and binding affinity in the portal-hypertensive rats (respectively, 1.65 +/- 0.06 pmol/mg protein and 6.78 +/- 0.80 nmol/L) were not different from controls (1.76 +/- 0.17 pmol/mg protein and 7.25 +/- 1.48 nmol/L). Isoproterenol-stimulated adenylyl cyclase activity in membranes from portal-hypertensive rats did not significantly differ from controls. We conclude that cardiac plasma membrane physical properties and beta-adrenoceptor function in portal hypertensive rats remains unimpaired, suggesting that the cardiomyopathy of cirrhosis is not caused by portal hypertension per se.

Adenylyl Cyclases↗