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Biomedical subjects

Y Q Liu

Publications and source records attributed to Y Q Liu.

At least 19 recordsLinked to original sources
PubMed2000

beta-cell adaptation in 60% pancreatectomy rats that preserves normoinsulinemia and normoglycemia.

Islet beta-cells are the regulatory element of the glucose homeostasis system. When functioning normally, they precisely counterbalance changes in insulin sensitivity or beta-cell mass to preserve normoglycemia. This understanding seems counter to the dogma that beta-cells are regulated by glycemia. We studied 60% pancreatectomy rats (Px) 4 wk postsurgery to elucidate the beta-cell adaptive mechanisms. Nonfasting glycemia and insulinemia were identical in Px and sham-operated controls. There was partial regeneration of the excised beta-cells in the Px rats, but it was limited in scope, with the pancreas beta-cell mass reaching 55% of the shams (40% increase from the time of surgery). More consequential was a heightened glucose responsiveness of Px islets so that glucose utilization and insulin secretion per milligram of islet protein were both 80% augmented at normal levels of glycemia. Investigation of the biochemical basis showed a doubled glucokinase maximal velocity in Px islets, with no change in the glucokinase protein concentration after adjustment for the different beta-cell mass in Px and sham islets. Hexokinase activity measured in islet extracts was also minimally increased, but the glucose 6-phosphate concentration and basal glucose usage of Px islets were not different from those in islets from sham-operated rats. The dominant beta-cell adaptive response in the 60% Px rats was an increased catalytic activity of glucokinase. The remaining beta-cells thus sense, and respond to, perceived hyperglycemia despite glycemia actually being normal. beta-Cell mass and insulin secretion are both augmented so that whole pancreas insulin output, and consequently glycemia, are maintained at normal levels.

Adaptation, Physiological↗
PubMed1999

Glucose-fatty acid cycle to inhibit glucose utilization and oxidation is not operative in fatty acid-cultured islets.

The glucose-fatty acid cycle of Randle entails two elements: decreased pyruvate dehydrogenase (PDH) activity, which inhibits glucose oxidation, and inhibition of phosphofructokinase (PFK) by a rise in citrate so that glucose-6-phosphate (G-6-P) levels increase, thereby inhibiting hexokinase activity and hence glucose utilization. Chronic exposure of islets to long-chain fatty acids (FA) is reported to lower PDH activity, but the effect on glucose oxidation and glucose-induced insulin secretion is uncertain. We investigated rat islets that were cultured for 4 days with 0.25 mmol/l oleate/5.5 mmol/l glucose. Glucose oxidation was doubled at 2.8 mmol/l glucose and unchanged at 27.7 mmol/l glucose in the FA-cultured islets despite a 35% decrease in assayed PDH activity. Pyruvate content was increased 60%, which may well compensate for the decreased PDH activity and maintain flux through the citric acid cycle. However, a greater diversion of pyruvate metabolism through the pyruvate-malate shuttle is suggested by unchanged pyruvate carboxylase Vmax and a fourfold higher release of malate from isolated mitochondria. The FA-cultured islets also showed increased basal glucose usage and insulin secretion together with a lowered level of G-6-P and 50% reductions in citrate synthase Vmax and the citrate content. Thus, the effects of chronic FA exposure on islet glucose metabolism differ from the glucose-fatty acid interactions reported in some other tissues.

Animals↗
PubMed1999

Effects of dexamethasone, cyproheptadine, anisodamine, and dinoprostone on TNF alpha production in endotoxic shock.

AIM: To study the effects of dexamethasone (Dex), cyproheptadine (Cyp), anisodamine (Ani), and dinoprostone (Din) on lipopolysaccharides (LPS)-induced tumor necrosis factor alpha (TNF alpha) gene expression and antishock effects of inhibiting TNF alpha production. METHODS: Endotoxic shock in rats was produced by i.v. injection of LPS (E coli O111B4, 5 mg.kg-1). TNF alpha mRNA accumulation was assessed by Northern blot. Plasma TNF alpha contents were determined by radioimmunoassay. RESULTS: The TNF alpha mRNA levels in rat liver at 2 h after LPS challenge was increased obviously (autoradiograms analyzed by scanning were 38 +/- 10 vs saline control 11 +/- 8, P < 0.01). The plasma TNF alpha contents were markedly increased [(22 +/- 3) micrograms.L-1 vs saline control (2.2 +/- 1.0) micrograms.L-1, P < 0.01]. Dex 5, Cyp 5, Ani 10, or Din 2 mg.kg-1 immediately injected after i.v. LPS markedly decreased the TNF alpha mRNA levels in rat liver and plasma TNF alpha contents. The Dex, Cyp, Ani, and Din improved the mouse survival rate 24 h after LPS 20 mg.kg-1 challenge. CONCLUSION: Dex, Cyp, Ani, and Din strongly inhibit LPS-induced TNF alpha gene expression, and have a beneficial antishock effects.

Animals↗
PubMed1999

Velvet antler polypeptides promoted proliferation of chondrocytes and osteoblast precursors and fracture healing.

AIM: To study the effects of velvet antler (VA) total polypeptides (VATP) and VA polypeptides, VAP-A, VAP-B, and VAP-C on proliferation of chondrocytes and osteoblast precusors. METHODS: Chondrocytes (rabbit and human fetus) and osteoblast precusors (chick embryo) were incubated in the culture medium containing VATP or VAP-A, VAP-B, and VAP-C. [3H]TdR incorporation into DNA was measured. Fracture healing-promoting action of VATP was determined in rats. RESULTS: VATP 50-200 mg.L-1 and VAP-B 12.5, 25, and 50 mg.L-1 showed most marked proliferation-promoting activity for rabbit costed chondrocytes and increased incorporation of [3H]TdR from (73 +/- 9) Bq (control group) to (272 +/- 55), (327 +/- 38), and (415 +/- 32) Bq, respectively (P < 0.01). The activity of VAP-A was weaker than that of VAP-B, and VAP-C had no activity. VATP 10 and 20 mg.kg-1 by local injection into the cross-section fracture area accelerated healing of radial fracture. The healing rate of VATP-treated group was higher (75%) than that of control group (25%) (P < 0.05). CONCLUSION: VATP accelerated fracture healing by stimulating proliferation of chondrocytes and osteoblast precursors.

Animals↗
PubMed1998

Fatty acid-induced beta cell hypersensitivity to glucose. Increased phosphofructokinase activity and lowered glucose-6-phosphate content.

Diabetic states are characterized by a raised serum/islet level of long chain fatty acids and a lowered ED50 for glucose-induced insulin secretion. Prolonged culture (> 6 h) of islets with long chain fatty acids replicates the basal insulin hypersecretion. We examined this effect in rat islets cultured for 24 h with 0.25 mM oleate. Insulin secretion at 2.8 mM glucose was doubled in combination with a 60% lowered islet content of glucose-6-phosphate (G6P). Investigation of the lowered G6P showed: (a) increased glucose usage from 0.5 to 100 mM glucose with identical values measured by [2-3H]glucose and [5-3H]glucose, (c) indicating little glucose- 6-phosphatase activity, (b) unchanged low pentose phosphate shunt activity, (c) 50% increased phosphofructokinase (PFK) Vmax, (d) a normal ATP/ADP ratio, and (e) unchanged fructose 2,6 bisphosphate content. Triacsin C, an inhibitor of fatty acyl-CoA synthetase, prevented the increase in PFK activity and the lowered G6P content. These results suggest that long chain acyl-CoA mediates the rise in PFK activity, which in turn lowers the G6P level. We speculate that the inhibition of hexokinase by G6P is thus attenuated, thereby causing the basal insulin hypersecretion.

Allosteric Regulation↗
PubMed1998

Active antitumor immunotherapy, with or without B7-mediated costimulation, increases tumor progression in an immunogenic murine T cell lymphoma model.

BW-Sp3 is a BW-5147-derived T cell lymphoma with limited immunogenicity since, despite regression of the majority of subcutaneous tumors, an important fraction of the animals will die from metastases. In the present study, the BW-Sp3 cells were transfected with genes encoding B7-1 or B7-2, known to be involved in the induction of T cell responses. The resulting transfectants exhibited a reduced tumorigenicity and did not cause mortality in the syngeneic recipients. Furthermore, immunization with the B7-1 or B7-2 transfectants resulted in an increased generation of cytotoxic T lymphocytes (CTL) that lysed both the transfectants and the wild-type BW-Sp3 cells. Since the B7 transfectants were completely rejected in syngeneic recipients and induced potent CTL recognizing the wild-type BW-Sp3 cells, these engineered cells were considered as candidates for immunotherapy. Vaccinations with the B7-1 or B7-2 transfectants could completely protect the animals from metastatic disease when subsequently challenged with wild-type BW-Sp3 cells. Furthermore, immunization with the B7 transfectants could prolong the survival time of mice that had been challenged intravenously with BW-Sp3 cells. Surprisingly, however, when these transfectants, as well as the wild-type BW-Sp3 cells, were used for vaccination of tumor-bearing animals, the presence of the subcutaneous BW-Sp3 tumors clearly interfered with the outcome of immunotherapy, resulting in increased malignancy, as reflected by a higher incidence of progressing tumors and a reduced survival rate. Possible implications for immunotherapy in humans are discussed.

Animals↗
PubMed1998

Triterpenoid saponins from Ilex latifolia.

Three new triterpenoid saponins, latifolosides F, G, H were isolated from the leaves of Ilex latifolia. Their structures were elucidated on the basis of chemical and spectral evidence. Latifoloside F was determined to be 3-O-[alpha-L-rhamnopyranosyl(1-2)]-[beta-D-glucopyranosyl(1-3)-]- alpha-L-arabinopyranosyl ilexgenin B 28-O-[alpha-L-rhamnopyranosyl(1-2)]-beta-D-glucopyranoside. Latifoloside G was 3-O-[alpha-L-rhamnopyranosyl(1-2)]-[beta-D-glucopyranosyl(1-3)-]- alpha-L-arabinopyranosyl pomolic acid 28-O-[alpha-L-rhamnopyranosyl(1-2)]-beta-D-glucopyranoside. Latifolioside H(3) was 3-O-[alpha-L-rhamnopyranosyl(1-2)]-[beta-D-glucopyranosyl(1-3)-]- alpha-L-arabinopyranosyl siaresinolic acid 28-O-[alpha-L-rhamnopyranosyl(1-2)]-beta-D-glucopyranoside.

Carbohydrate Conformation↗
PubMed1998

Growth inhibition of chronic myelogenous leukemia cells by ODN-1, an aptameric inhibitor of p210bcr-abl tyrosine kinase activity.

p210bcr-abl-Related tyrosine kinase activity has been shown to cause chronic myelogenous leukemia (CML), a disease of bone marrow stem cells. Having previously demonstrated that the aptameric oligonucleotide, ODN-1, could inhibit p210bcr-abl kinase activity, the current study sought to determine if ODN-1 could selectively inhibit the growth of CML cells relative to that of normal bone marrow. ODN-1, when introduced by electroporation into peripheral blood mononuclear cells (PBMC) from patients with CML, decreased the number of committed progenitors (CML CFU-GM) by an average of 67%+/-19% (mean+/-SEM, range 28-98%). Treatment of CML PBMC with ODN-1 was also shown to decrease the number of more primitive cobblestone area-forming cells (CAFC) by 35%-87%. In contrast, there was little suppressive effect by the combination of electroporation and ODN-1 on either CFU-GM or CAFC numbers from normal donor bone marrow. These studies suggest that inhibition of p210bcr-abl protein-tyrosine kinase (PTK) activity by ODN-1 is associated with some degree of selective growth inhibition of p210bcr-abl-transformed cells. p210bcr-abl kinase inhibitory agents may be useful for the ex vivo purging of bone marrow or peripheral blood progenitor/stem cells in the setting of autologous transplantation for CML.

Animals↗
PubMed1998

Shared biochemical properties of glucotoxicity and lipotoxicity in islets decrease citrate synthase activity and increase phosphofructokinase activity.

Diabetic states are characterized by a raised serum/islet level of triglycerides and a lowered EC50 (concentration at half-maximal stimulation) for glucose-induced insulin secretion. Culturing islets with long-chain fatty acids (FAs) replicates the basal insulin hypersecretion. In a previous study, we showed that the mechanism involved deinhibition of hexokinase by a 60% decrease in glucose-6-phosphate (G-6-P). The key event was proposed to be an increased phosphofructokinase (PFK) Vmax secondary to an upregulatory effect of the FA metabolite, long-chain acyl-coenzyme A (LC-CoA). We now show another contributory factor, a lowered content of the PFK inhibitor citrate. Citrate synthase Vmax and citrate levels were lowered 45% in rat islets cultured with 250 micromol/l oleate for 24 h. Both effects were reversed by triacsin C, an inhibitor of fatty acyl-CoA synthetase, the enzyme that generates LC-CoA. Culturing islets with high doses of glucose (16.7 mmol/l) for 48 h should also raise cytosolic LC-CoA. As predicted, citrate synthase Vmax was lowered and PFK Vmax was increased, both in a triacsin C-reversible fashion. These results show shared selected functional and biochemical properties in beta-cells of so-called glucotoxicity and lipotoxicity.

Animals↗
PubMed1997

A genome-based resource for molecular cardiovascular medicine: toward a compendium of cardiovascular genes.

BACKGROUND: Large-scale partial sequencing of cDNA libraries to generate expressed sequence tags (ESTs) is an effective means of discovering novel genes and characterizing transcription patterns in different tissues. To catalogue the identities and expression levels of genes in the cardiovascular system, we initiated large-scale sequencing and analysis of human cardiac cDNA libraries. METHODS AND RESULTS: Using automated DNA sequencing, we generated 43,285 ESTs from human heart cDNA libraries. An additional 41,619 ESTs were retrieved from public databases, for a total of 84,904 ESTs representing more than 26 million nucleotides of raw cDNA sequence data from 13 independent cardiovascular system-based cDNA libraries. Of these, 55% matched to known genes in the Genbank/EMBL/DDBJ databases, 33% matched only to other ESTs, and 12% did not match to any known sequences (designated cardiovascular system-based ESTs, or CVbESTs). ESTs that matched to known genes were classified according to function, allowing for detection of differences in general transcription patterns between various tissues and developmental stages of the cardiovascular system. In silico Northern analysis of known gene matches identified widely expressed cardiovascular genes as well as genes putatively exhibiting greater tissue specificity or developmental stage specificity. More detailed analysis identified 48 genes potentially overexpressed in cardiac hypertrophy, at least 10 of which were previously documented as differentially expressed. Computer-based chromosomal localizations of 1048 cardiac ESTs were performed to further assist in the search for disease-related genes. CONCLUSIONS: These data represent the most extensive compilation of cardiovascular gene expression information to date. They further demonstrate the untapped potential of genome research for investigating questions related to cardiovascular biology and represent a first-generation genome-based resource for molecular cardiovascular medicine.

Blotting, Northern↗
PubMed1997

Does the increase of 8-hydroxydeoxyguanosine lead to poor sperm quality?

Several studies have suggested a population-wide decline in the quality of human semen during the past three decades, but the mechanism remains unclear. It was proved that damage to the DNA of germ cells would lead to mutation, and 8-hydroxydeoxyguanosine (8-OHdG), one of the major products of oxidative damage to DNA, may serve as one of the important factors to affect the sperm quality. In the present paper, 67 semen samples were collected to analyze the sperm quality (density, sperm number, motility, normal head, etc.), and 8-OHdG was measured in DNA isolated from the same sperm samples. The results showed that a significant inverse correlation exists between 8-OHdG/dG(deoxyguanosine) and sperm density (r = -0.358, p = 0.004), and between 8-OHdG/dG and sperm number (r = -0.389, p = 0.01). The results indicate that endogenous oxidative DNA damage could affect sperm quality and subsequently increase the risk of genetic defects.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1997

Path test reactions to the Chinese Standard Screening Allergens in 1,135 patients investigated for allergic contact dermatitis.

BACKGROUND: The patch test has become the standard method of investigating patients with allergic contact dermatitis. Many countries have developed standard screening allergens to make patch testing more efficient. A series of the Chinese Standard Screening Allergens were studied and modified. OBJECTIVE: This study investigated the frequency of contact allergies in suspected allergic contact dermatitis and tested the practicality of the Chinese Standard Screening Patch Test Allergens. METHODS: A total of 1,135 patients suspected of having allergic contact dermatitis were patch tested. Three hundred twelve (27.5%) were men, and their age ranged from 2 to 75 years old (mean age, 34.3 years), 823 (72.5%) were women, and their age ranged from 2 to 76 years old (mean age, 33.0 years). Nanjing Medical University supplied the Chinese Standard Screening Allergens and Finn-Chamber. All patients were patch tested according to the Chinese Standard Screening Patch Test Allergens with Finn-Chamber the protocol as established by the International Contact Dermatitis Research Group (ICDRG). RESULTS: From the 1,135 patients suspected to have allergic contact dermatitis, 650 (57.3%) had at least one positive reaction. Nineteen (95%) of the Chinese Standard Screening Patch Test Allergens had positive reactions higher than 1%. Of 485 patients with negative reaction to the Standard Allergens, 106 patients were tested with other suspected contactants according to history. Thirty-nine (36.8%) had positive reactions to the contactants they provided. The total positive rate therefore increased by 3.4%. CONCLUSIONS: Our study results indicate that the Chinese Standard Screening Patch Test Allergens are suitable for use in routine clinic in China.

Adolescent↗
PubMed1997

Construction of a human heart cDNA library and identification of cardiovascular based genes (CVBest).

The availability of high quality cDNA libraries is often crucial to the successful identification and characterization of genes. The concepts and potential pitfalls of constructing cDNA libraries are presented. Various applications requiring high quality cDNA libraries are outlined, including large-scale single pass sequencing of cDNA clones to generate expressed sequence tags (ESTs) and differential screening of cDNA libraries. The usefulness of combining such approaches for the discovery of novel disease-related and cardiovascular-based ESTs (CVBest) is discussed.

Base Sequence↗
PubMed1996

A mechanism of regulation of hepatic Fru 2,6-P2 concentration upon refeeding: involvement of xylulose 5-P and cyclic-AMP.

In order to determine the mechanism for delayed increase in Fructose 2,6-P2 in livers of refed rats, the time course of changes in various metabolites upon refeeding NIH or high sucrose diet was investigated. Kinetics of increase in Fructose 2,6-P2 and Xylulose 5-P were similar but different from hexose 6-P or glycogen in the livers of 48 h starved rats refed with NIH diet. The increase in the Fructose 2,6-P2 level was a result of a combination of changes in Fructose 6-P,2-kinase and Fructose 2,6-bisphosphatase activity ratios, indicating dephosphorylation of the bifunctional enzyme and decreased cAMP. A similar correlation between Fructose 2,6-P2 and Xylulose 5-P and dephosphorylation was observed with refeeding high sucrose diet and also with 16 h starved rats. These kinetic results are consistent with the idea that a specific protein phosphatase 2A, activated by Xylulose 5-P, dephosphorylates Fructose 6-P,2-kinase:Fructose 2,6-bisphosphatase and also decreased protein kinase A activity, resulting in increased hepatic Fructose 2,6-P2.

Animals↗
PubMed1996

A mechanism for fatty acid inhibition of glucose utilization in liver. Role of xylulose 5-P.

The glucose-stimulated rise in Fru-2,6-P2 in liver results from xylulose 5-P activation of a specific protein phosphatase 2A which dephosphorylates Fru-6-P,2-kinase:Fru-2,6-bisphosphatase (Nishimura, M., and Uyeda, K. (1994) J. Biol. Chem. 269, 26100-26106). In order to determine the role of xylulose 5-P in regulating Fru-2, 6-P2 in liver, the effect of fatty acids, various hexoses, and hormones was examined in perfused rat liver and in intact rats. When 24-h starved rat livers were perfused with acetate, butyrate, or propionate, Fru-2,6-P2 and xylulose 5-P decreased to the same extent and at similar rates. The activity ratios of the kinase and the phosphatase changed in a reciprocal manner, indicating that the phosphorylated form of the enzyme was increased by the fatty acids perfusion. The fatty acids caused the similar changes in the metabolites and the phosphorylation state of the bifunctional enzyme in livers of fed animals. Fructose, galactose, or mannose perfusion in starved rat liver increased both Fru-2,6-P2 and xylulose 5-P and converted the bifunctional enzyme to the dephospho form. Both the Fru-2,6-P2 and xylulose 5-P levels in rats fed a high fat diet decreased over 50% compared to that in control rats. These results indicated a close correlation between Fru-2,6-P2 and xylulose 5-P levels and the phosphorylation state of fructose 6-P, 2-kinase:fructose 2,6-bisphosphatase. Fatty acid inhibition of glucose metabolism can be explained by a decrease in xylulose 5-P, which lowers xylulose 5-P-activated protein phosphatase 2A activity, resulting in more phosphorylated form of the bifunctional enzyme and consequently lower Fru-2,6-P2.

Animals↗
PubMed1995

Dammarane saponins from Panax ginseng.

From the dried roots of Panax ginseng two new minor dammarane saponins named koryoginsenoside-R1 and -R2 were isolated, along with fourteen known saponins. On the basis of spectral and chemical evidence, the structure of the new saponins were elucidated as 6-O-[trans butenoyl-(1-->6)-beta-D-glucopyranosyl]-20-O-beta-D- glucopyranosyl dammar-24-en-3 beta,6 alpha,12 beta,20(S)-tetrol and 3-O-[beta-D-glucopyranosyl-(1-->2)-beta-D-glucopyranosyl]-20-O-[beta-D- glucopyranosyl-(1-->6)-beta-D-glucopyranosyl] dammar-22-en-3 beta,12 beta, 20(S),- 25-tetrol, respectively.

Carbohydrate Sequence↗