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Biomedical subjects

L S Li

Publications and source records attributed to L S Li.

At least 55 records · Page 3Linked to original sources

[Role of substance P in pressor response of central amygdaloid nucleus to glutamate].

Substance P (SP)-immunoreactive cells and the axon terminals are widely distributed in the central amygdaloid nucleus (AC) and its important projection areas. The present study showed that (1) Excitation of the AC by glutamate (Glu) or injection of SP into the AC projection areas: locus coeruleus (LC), nucleus parabrachialis (NPB), periaqueductal gray matter (PAG) or lateral hypothalamus-perifornical region (LH/PF), all elicited pressor response. (2) Preinjection of DPDPDT (a SP antagonist) into bilateral LC, NPB, PAG or LH/PF could attenuate the AC pressor response to Glu. (3) Intra-RVLM (rostral ventrolateral medulla) preinjection of either phentolamine, propranolol or atropine (but not GDEE, a Glu antagonist) could also reduce the AC pressor response. Taken together with our previous findings that the alpha-, beta-, M-receptors in RVLM mediated the pressor response to LC excitation, alpha-receptors mediated the NPB pressor response, alpha- and beta-receptors mediated the PAG pressor response; these results indicate that the SPergic projections of the AC not only directly act upon the brainstem pressor areas (LC, NPB, PAG)-RVLM system, but also indirectly via the LH/PF act upon the brainstem pressor areas-RVLM system to induce the pressor response.

Amygdala↗

The number of stenotic coronary arteries and passive smoking exposure from husband in lifelong non-smoking women in Xi'an, China.

The relationship between the number of stenotic coronary arteries and passive smoking exposure from the husband was examined in a retrospective study of 78 cases with stenotic coronary arteries and 83 controls with normal coronary arteries. All the 161 subjects were examined by coronary arteriography and were Chinese women who had never smoked cigarettes (i.e. lifelong non-smokers). The Pearson's and Spearman's correlation coefficients between the number of stenotic coronary arteries and passive smoking exposure indices were 0.27-0.29 and 0.25-0.28 (all with P < 0.01), respectively. The linear prediction equations from multiple regression analysis showed that passive smoking exposure, after adjustment for other major risk factors, was a significant predictive variable for the number of stenotic coronary arteries. The multiple response logistic regression model was used to estimate the odds ratio of stenotic coronary arteries for passive smoking exposure categories. The crude and adjusted odds ratios showed that the number of stenotic arteries increased with the amount of exposure to passive smoking from the husband. These results provide new evidence to support that passive smoking is causally associated with coronary heart disease.

Adult↗

Genetic mapping and chromosome localization of the rat mitochondrial glycerol-3-phosphate dehydrogenase gene, a candidate for non-insulin-dependent diabetes mellitus.

The mitochondrial FAD-dependent glycerol-3-phosphate dehydrogenase (mtGPD) plays an important role in the regulation of insulin secretion and has been postulated as a candidate responsible for the pathogenesis of non-insulin-dependent diabetes mellitus (NIDDM) in humans as well as in rodent models of NIDDM. Recent molecular genetic studies of the Goto-Kakizaki (GK) rat model of NIDDM have identified loci linked to NIDDM. To elucidate whether rat mtGPD might play a role in the pathogenesis of NIDDM, the rat mtGPD gene (Gpd2) was cloned, and a genetic marker for Gpd2 was developed. The gene mapped to the region of rat chromosome 3 that contains a region linked to NIDDM in the GK rat. Fluorescence in situ hybridization was also carried out to verify the map position.

Animals↗

Phenotypic characterization of the Trp64Arg polymorphism in the beta 3-adrenergic receptor gene in normal weight and obese subjects.

The beta 3-adrenergic receptor, located mainly in fat cells of visceral adipose tissue, is involved in the regulation of lipolysis and thermogenesis. Recently, a mutation in the corresponding gene resulting in the replacement of tryptophan by arginine in position 64 (Trp64Arg) has been demonstrated, which associated with obesity and metabolic complications of obesity. We have investigated whether this polymorphism is associated with changes in beta 3-adrenergic receptor function or clinical characteristics in 40 non-obese and 43 obese non-diabetic subjects who underwent elective abdominal surgery. The beta-adrenergic receptor gene polymorphism was examined by restriction-enzyme cleavage conformation. Beta 3-adrenergic receptor function was investigated by measuring lipolysis in isolated visceral white fat cells incubated with noradrenaline (natural ligand) or (CGP) 12,177 (selective beta 3-agonist). No homozygotes for the mutation were found. The allelic frequency of Trp64Arg was similar in obese and non-obese subjects (9.4 and 12.5%, respectively). In obese and non-obese subjects there was no change in body mass index, body fat distribution, fat cell size, fasting circulating levels of insulin, glucose or lipids, blood pressure or adipocyte lipolysis induced by noradrenaline or CGP 12,177 when Trp64Arg heterozygotes were compared with Trp64A homozygotes. Our results suggest that the Trp64Arg mutation in its heterozygous form is not a major determinant of beta 3-adrenergic receptor function (when assessed by lipolysis in white adipose tissue) or of the pathophysiology of obesity.

Adipocytes↗

Genetic analysis of non-insulin dependent diabetes mellitus in the GK rat.

Non-insulin dependent diabetes mellitus (NIDDM) is a major public health problem, but its aetiology remains poorly understood. We have performed a comprehensive study of the genetic basis of diabetes in the Goto-Kakizaki (GK) rat, the most widely used animal model of non-obese NIDDM. The genetic dissection of NIDDM using this model has allowed us to map three independent loci involved in the disease. In addition, we identify a major factor affecting body weight, but not glucose tolerance, on chromosome 7 and map a further 10 regions that are suggestive for linkage. We conclude that NIDDM is polygenic and fasting hyperglycaemia and postprandial hyperglycaemia clearly have distinct genetic bases.

Animals↗

Effect of emodin on c-myc proto-oncongen expression in cultured rat mesangial cells.

AIM: To explore the possible molecular mechanism of emodin on the inhibition of glomerular mesangial cells (MC). METHODS: In rat MC culture, c-myc mRNA level was detected by dot-blotting as expressed by the dilutions of the total RNA on the visible dots. RESULTS: Low level c-myc mRNA was found in serum-free cultured quiescent MC. Addition of lipopolysaccharide (LPS 10 mg.L-1) induced a higher level expression of c-myc mRNA within 30 min, maximal expression at 2.5 h and persisted for 6 h. This over-expressing of c-myc mRNA was markedly suppressed by emodin (25 mg.L-1), the inhibition of emodin on c-myc mRNA expression was still seen at 6 h, and the greatest suppressive effect was at 2.5 h. CONCLUSION: Emodin participating in its down-regulatory effect of c-myc mRNA over-expression contributes to its inhibitory action on MC.

Animals↗

[Experimental study on effect of Cordyceps sinensis in ameliorating aminoglycoside induced nephrotoxicity].

In order to evaluate the effect of Cordyceps sinensis (CS) on aminoglycoside (AG) induced nephrotoxicity, gentamycin was imposed on the young and old rats with CS administration. The renal tubular injury was ameliorated as evidenced by less prominent increment of BUN, SCr, sodium excretion, urinary NAGase and less severity of histopathological changes as compared with control. In addition, the use of CS could promote an earlier recovery of renal oxygen consumption insulin clearance, and sodium absorption in isolated perfused kidney from CS treated intoxicated rat than that from control. Possible mechanisms of CS on drug-induced nephrotoxicity include: (1) Accelerating the regeneration of tubular cells; (2) Protecting the sodium pump activity of tubular cells; (3) Attenuating the tubular cell lysosome hyperfunction stimulated by phagocytosis of AG as well as decreasing the tubular cell lipoperoxidation in response to toxic injury; (4) Reducing the tissue Ca++ content.

Acute Kidney Injury↗

Regulation of human insulin receptor RNA splicing in HepG2 cells: effects of glucocorticoid and low glucose concentration.

Human insulin receptor RNA is expressed in two alternatively spliced forms (Ex. 11- and Ex. 11+) encoding protein isoforms with discrete functional differences. In vivo, the splicing varies between tissues and changes concomitantly with the control of glucose homeostasis. Recently, dexamethasone has been described to increase the relative expression of Ex. 11+ RNA molecules. In this study, we confirm that dexamethasone dose-dependently increases inclusion of exon 11, and demonstrate that low concentrations of glucose decrease inclusion. No effect was observed of either insulin or IGF1. These results suggest that hormonal as well as metabolic factors regulate the splicing of insulin receptor RNA in HepG2 cells.

Alternative Splicing↗

Passive smoking at work as a risk factor for coronary heart disease in Chinese women who have never smoked.

OBJECTIVE: To study whether passive smoking at work is a risk factor for coronary heart disease. DESIGN: Case-control study. SETTING: Xi'an, China. SUBJECTS: 59 patients with coronary heart disease and 126 controls, all Chinese women with full time jobs, who had never smoked cigarettes. RESULTS: The crude odds ratio for passive smoking from husband was 2.12 (95% confidence interval 1.06 to 4.25) and at work was 2.45 (1.23 to 4.88). The final logistic regression model, with passive smoking from husband and at work as the base, included age, history of hypertension, type A personality, and total cholesterol and high density lipoprotein cholesterol concentrations; the adjusted odds ratios for passive smoking from husband and at work were 1.24 (0.56 to 2.72) and 1.85 (0.86 to 4.00) respectively. For passive smoking at work, statistically significant linear trends of increasing risks (for both crude and adjusted odds ratios) with increasing exposures (amount exposed daily, number of smokers, number of hours exposed daily, and cumulative exposure) were observed. When these exposure variables were analysed as continuous variables, the crude and adjusted odds ratios were also significant. CONCLUSION: Passive smoking at work is a risk factor for coronary heart disease. Urgent public health measures are needed to reduce smoking and to protect non-smokers from passive smoking in China.

Adult↗

[Effects of furyl-dihydropyridine I on coronary collateral circulation in myocardial infarction of dogs].

Effects of furyl-dihydropyridine I (FDP-1) on collateral circulation were observed in ischemic myocardium of dogs. FDP-1 (200 micrograms.kg-1) of intracoronary injection increased collateral flow, reduced systemic artery resistance, and coronary systolic pressure in infarcted region and the area of infarction decreased from 28.9 +/- 1.3% to 15.3 +/- 1.2% (P < 0.01, n = 6). The results indicated that FDP-1 could improve coronary collateral circulation, increase collateral flow in ischemic region, decrease collateral flow in ischemic region, decrease myocardial oxygen demand, and protect myocardial ischemia.

Animals↗

Role of transforming growth factor-beta in the growth inhibition of cultured rat mesangial cells in high glucose media.

The present study was designed to test the hypothesis that the inhibitory effect of elevated glucose levels on mesangial cell growth might be mediated by transforming growth factor beta (TGF beta). Increased glucose levels inhibited mesangial cell proliferation in a concentration dependent manner. The addition of a rabbit antipocine TGF beta 1 neutralizing antibody significantly enhanced the cell proliferation in both normal (5.5 mM) and high (50 mM) glucose media (12% and 30% respectively), and almost completely blocked the growth inhibition induced by high glucose media. TGF beta assay demonstrated mesangial cells produced more active than latent TGF beta after growth in high glucose media. We conclude that TGF beta functions as an autocrine cytokine in mesangial cells growth and the production of TGF beta is modulated by high glucose concentration. The growth inhibition induced by high glucose levels may be largely mediated by endogenous TGF beta.

Animals↗

Cloning, sequence determination, and regulation of the ribonucleotide reductase subunits from Plasmodium falciparum: a target for antimalarial therapy.

Malaria remains a leading cause of morbidity and mortality worldwide, accounting for more than one million deaths annually. We have focused on the reduction of ribonucleotides to 2'-deoxyribonucleotides, catalyzed by ribonucleotide reductase, which represents the rate-determining step in DNA replication as a target for antimalarial agents. We report the full-length DNA sequence corresponding to the large (PfR1) and small (PfR2) subunits of Plasmodium falciparum ribonucleotide reductase. The small subunit (PfR2) contains the major catalytic motif consisting of a tyrosyl radical and a dinuclear Fe site. Whereas PfR2 shares 59% amino acid identity with human R2, a striking sequence divergence between human R2 and PfR2 at the C terminus may provide a selective target for inhibition of the malarial enzyme. A synthetic oligopeptide corresponding to the C-terminal 7 residues of PfR2 inhibits mammalian ribonucleotide reductase at concentrations approximately 10-fold higher than that predicted to inhibit malarial R2. The gene encoding the large subunit (PfR1) contains a single intron. The cysteines thought to be involved in the reduction mechanism are conserved. In contrast to mammalian ribonucleotide reductase, the genes for PfR1 and PfR2 are located on the same chromosome and the accumulation of mRNAs for the two subunits follow different temporal patterns during the cell cycle.

Amino Acid Sequence↗

High level expression of the large subunit of mouse ribonucleotide reductase in a baculovirus system.

The large subunit of ribonucleotide reductase from mouse has been overexpressed in Spodoptera frugiperda cells infected with recombinant baculovirus. The expressed protein was purified by affinity chromatography to apparent homogeneity as determined by SDS-PAGE. The homogeneous protein is recognized in Western blot analysis by a monoclonal antibody raised to the large subunit of ribonucleotide reductase from calf thymus, has the correct N-terminal sequence, and, in the presence of the small subunit of mouse ribonucleotide reductase and nucleoside triphosphate effectors, catalyzes the reduction of both purine and pyrimidine nucleoside diphosphates.

Animals↗

Localization and characterization of a parotid Ca(2+)-dependent ecto-ATPase.

Parotid acini were isolated and tested to further establish the presence of ecto-ATPase in the intact cells. Inhibitors were used to determine if the inhibitor profile of the ATPase was similar to that of a Ca(2+)-ATPase from parotid membranes identified previously as an ecto-ATPase. The Ca(2+)-ATPase of intact cells was insensitive to oligomycin (10 micrograms/ml), N-ethylmaleimide (NEM) (0.1 mM), ruthenium red (0.1 mM), sodium azide (1 mM), and was inhibited approximately 22% by sodium orthovanadate (Na3VO4) (1 mM). This profile was similar to the Ca(2+)-ATPase of intact cells. Trifluoperazine (TFP) (0.1 mM) inhibited the enzyme in intact cells by approximately 32%. The nucleotide substrate specificity of the enzyme also reflected very closely the pattern seen in isolated membranes.

Adenosine Triphosphatases↗

Permanent hepatic artery embolization with dextran microspheres in 131 patients with unresectable hepatocellular carcinoma.

One hundred thirty-one patients with hepatocellular carcinoma were subjected to permanent hepatic artery embolization with dextran microspheres (G-25, 50-150 mu). Dextran hepatic artery embolization is indicated for massive, nodular or multinodular hepatocellular carcinoma with total bilirubin less than 3 mg/dl, serum albumin greater than 3.0 g/dl, tumor involvement area less than 50% or without involvement of the main portal vein. Following hepatic angiography a catheter was inserted superselectively into the hepatic artery feeding the tumor. Adriamycin (60-80 mg) or cisplatin (60-100 mg) was infused immediately before embolization. Under fluoroscopic guidance, 0.3-0.5 g of dextran microsphere embolizer permeated with 10 mg of mitomycin C was infused into the feeding artery through the catheter. Dextran microspheres caused marked homogeneous and distal micro-arterial embolization, especially in the arteriole with a caliber of about 100 mu. Dextran microspheres were not resorbed in a period of 16 weeks in humans, thus reducing or preventing the formation of intrahepatic and extrahepatic collaterals after hepatic artery embolization. Dextran hepatic artery embolization was very effective for not only main tumor but also daughter foci or metastatic nodules, as was confirmed histologically in 8 cases. The 1-year, 2-year and 3-year survival rates were 57.0%, 31.4% and 24.2% respectively.

Adult↗

[Effects of Rheum on renal hypertrophy and hyperfiltration of experimental diabetes in rat].

Renal hypertrophy and elevated glomerular filtration rate (GFR) appeared in early stage of diabetic nephropathy (DN). In order to investigate the effect of Rheum officinale (RO) on the renal hypertrophy, streptozotocin induced diabetic rats with moderate hyperglycemia were divided into two groups, receiving RO (RO-DN) or not (DN), and one group of non-diabetic control (C) was set up. At the 28th day, DN group exhibited heavier kidney weight (+61%), more protein (+133%) and DNA (+94%) contents in the kidney and higher GFR (+94%) than the control. RO-DN rats showed much less above mentioned changes. In addition, lipid abnormalities were ameliorated in RO-DN group. This result suggest that RO is beneficial to the diabetes in terms of renal hypertrophy and GFR changes at early stage and is recommended in the treatment of diabetic nephropathy.

Animals↗