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Biomedical subjects

J Luo

Publications and source records attributed to J Luo.

At least 217 records · Page 12Linked to original sources
PubMed1998

Angiostatin upregulates E-selectin in proliferating endothelial cells.

Angiostatin, a 38 kilodalton fragment of plasminogen, is a potent inhibitor of angiogenesis. However, little is known about how angiostatin affects endothelial gene expression. To learn more about its effect on endothelial-specific genes implicated in angiogenesis, we examined E-selectin expression and function in bovine capillary endothelial cells treated with recombinant angiostatin. Angiostatin caused a four to five-fold increase in E-selection polypeptide levels in proliferating endothelial cells but little or no increase in confluent cells. P-selection polypeptide levels were unaffected by angiostatin in either proliferating or confluent cells. E-selectin mRNA and adhesion activity in proliferating endothelial cells were also increased by angiostatin. Angiostatin had little effect on the distribution of endothelial cells in G0/G1, S, and G2/M, indicating angiostatin does not alter cell cycle progression significantly. These data demonstrate that angiostatin selectively upregulates E-selectin in proliferating endothelial cells in vitro. This selectivity may provide insights into the mechanism by which angiostatin inhibits tumor growth in vivo without apparent effects on quiescent endothelium.

Angiostatins↗
PubMed1998

[Association between angiotensin II type I receptor gene and human essential hypertension].

OBJECTIVE: To determine whether the angiotensin II type I receptor gene might be implicated in human essential hypertension. METHODS: This was a case-control study on hypertension and normal blood pressure in Chinese DNA abstracted samples from 51 cases of essential hypertension and 74 normal controls were analysed by polymerase chain reaction,digestion of restriction enzyme and electrophesis. RESULTS: The genotype frequency of 1166A/1166C was 0. 196 (10/51) in the essential hypertension group, 0.081 (6/74) in the control group. The genotype frequency of 1166C/1166C was 0 in both groups. The gene frequency of 1166C was 0.098 in the essential hypertension group, 0.041 in the controls. There was a significant increase in allelic frequency of 1166C in hypertension. CONCLUSION: The results indicate that the increase in allelic frequency of 1166C is a risk factor and hence suggest that the change in the angiotensin II type I receptor gene is associated with essential hypertension.

Adolescent↗
PubMed1998

Masoprocol (nordihydroguaiaretic acid): a new antihyperglycemic agent isolated from the creosote bush (Larrea tridentata).

An ethnomedically-driven approach was used to evaluate the ability of a pure compound isolated from the creosote bush (Larrea tridentata) to lower plasma glucose concentration in two mouse models of type 2 diabetes. The results indicated that plasma glucose concentration fell approximately 8 mmol/l in male C57BL/ks-db/db or C57BL/6J-ob/ob mice following the oral administration of masoprocol (nordihydroguaiaretic acid), a well known lipoxygenase inhibitor. The decline in plasma glucose concentration following masoprocol treatment in the mice was achieved without any change in plasma insulin concentration. In addition, oral glucose tolerance improved and the ability of insulin to lower plasma glucose concentrations was accentuated in masoprocol-treated db/db mice. These data raise the possibility that masoprocol, or other lipoxygenase inhibitors, represents a new approach to the pharmacological treatment of Type 2 diabetes.

Animals↗
PubMed1998

Ethnobotanical-directed discovery of the antihyperglycemic properties of cryptolepine: its isolation from Cryptolepis sanguinolenta, synthesis, and in vitro and in vivo activities.

Using an ethnobotanical approach in combination with in vivo-guided fractionation as a means for lead discovery, cryptolepine was isolated as an antihyperglycemic component of Cryptolepis sanguinolenta. Two syntheses of cryptolepine, including an unambiguous synthesis, are reported. The hydroiodide, hydrochloride, and hydrotrifluoromethanesulfonate (hydrotriflate) salts of cryptolepine were synthesized, and a comparison of their spectral properties and their in vitro activities in a 3T3-L1 glucose transport assay is made. Cryptolepine and its salt forms lower blood glucose in rodent models of type II diabetes. While a number of bioactivities have been reported for cryptolepine, this is the first report that cryptolepine possesses antihyperglycemic properties.

3T3 Cells↗
PubMed1998

PPF-1, a post-floral-specific gene expressed in short-day-grown G2 pea, may be important for its never-senescing phenotype.

We cloned a developmentally regulated gene from a cDNA library constructed from short-day (SD) grown G2 pea tissue using cDNA representational difference analysis (cDNA RDA) and named it PPF-1 for the first Pisum sativum post-floral-specific gene. Sequence comparisons with various databases revealed that PPF-1 shares a substantial homology only at the deduced amino-acid level with the Bacillus subtilis gene SP3J, which is required for maintaining vegetative growth, and with other genes coding for bacterial inner membrane proteins. All five potential hydrophobic regions from the bacterial proteins were maintained in the PPF-1 sequence. A series of Northern blots showed that this gene was only expressed after floral initiation and was limited to the apical buds, with non-detectable levels in roots, stems and mature leaves. Under SD conditions, when G2 pea displays an unlimited growth habit, PPF-1 expression was sustained at a relatively high level long after floral initiation. Under long-day (LD) conditions, when G2 pea undergoes an apical senescence similar to wild-type plants with genotype sn hr, PPF-1 was only expressed very briefly after flower initiation. Interestingly, in day-neutral, wild-type Alaska pea, the PPF-1 level was hardly detectable under any growth conditions. Treatment of LD-grown G2 pea with gibberellin A3 (GA3) was able to stimulate PPF-1 expression unless it was applied at a very late growth stage, at which time the process of apical senescence cannot be reversed.

Amino Acid Sequence↗
PubMed1998

Cryptolepis sanguinolenta: an ethnobotanical approach to drug discovery and the isolation of a potentially useful new antihyperglycaemic agent.

Evidence has been published that a wide array of plant-derived active principles, representing numerous classes of chemical compounds, demonstrate activity consistent with their possible use in the treatment of patients with Type 2 diabetes mellitus (DM). Despite these interesting observations, to date, metformin is the only ethical drug approved for treatment of Type 2 DM derived from a medicinal plant. Why is this so, given the fact that higher plants are such a potential source of new drugs? The answer to this rhetorical question may lie in the reliance of most pharmaceutical companies on random, in vitro, mechanism-based, high throughput screening in the initial phases of plant drug research. In this article we describe an alternative pathway to discovery of drugs for the treatment of Type 2 DM: on based on an ethnomedical approach, involving ethnobotany and traditional medicine. In particular, we present evidence that cryptolepine, an indoloquinolone alkaloid isolated from Cryptolepis sanguinolenta, significantly lowers glucose when given orally to a mouse model of diabetes. The antihyperglycaemic effect of cryptolepine leads to a significant decline in plasma insulin concentration, associated with evidence of an enhancement in insulin-mediated glucose disposal. Finally, cryptolepine increases glucose uptake by 3T3-L1 cells. These data permit us to conclude that an ethnobotanical approach to drug discovery can identify a potentially useful drug for the treatment of Type 2 DM.

Adipose Tissue↗
PubMed1998

Corticosteroid therapy does not alter the threshold for contraction-induced injury in dystrophic (mdx) mouse diaphragm.

The effects of methylprednisolone therapy on the susceptibility of dystrophin-deficient myofibers to contraction-induced injury were evaluated in the mdx mouse diaphragm model of Duchenne dystrophy. Mdx myofibers were abnormally vulnerable to injury induced by high-stress eccentric contractions. However, methylprednisolone therapy did not significantly alter the degree of contraction-induced injury. These data suggest that beneficial effects of corticosteroid therapy in Duchenne dystrophy are unlikely to be related to a change in the threshold for contraction-induced myofiber damage.

Adrenal Cortex Hormones↗
PubMed1998

Effect of aprotinin on the red cell immunity in cardiopulmonary bypass.

To investigate the effects of aprotinin on red cell (RC) immune function in the patients undergoing cardiopulmonary bypass (CPB), 20 patients who received valve replacement procedure were prospectively studied. The patients were randomly assigned to aprotinin group and control group. Red blood cell C3b receptor ratio (RC3bRR), red blood cell immune-component ratio (RICR), plasma C3, C4, CH50 and IgG level were determined before operation, at the end of CPB and 1st, 3rd, 7th postoperative days. Our results showed that: (1) The blood requirement was reduced in aprotinin group. (2) After bypass, plasma C3, C4, CH50 was maintained in aprotinin group, while they declined in control group. (3) Plasma level IgG fell in both groups, but at 7th postoperative day it recovered in aprotinin group while the level stayed at low level in control group. (4) The RC3bRR and RICR was mildly inhibited in aprotinin group. It is concluded that the impairment of RC immune function caused by CPB can be mitigated by aprotinin, which may be related to the effects of aprotinin in blood sparing, restriction of complement activation, and reduction of blood requirement which could mitigate the non-specific inflammatory reaction.

Adjuvants, Immunologic↗
PubMed1998

Nongenetic mouse models of non-insulin-dependent diabetes mellitus.

The purpose of the study was to develop a mouse model of non-insulin-dependent diabetes mellitus (NIDDM) that closely simulates the metabolic abnormalities of the human disease and is also cost-effective compared with the genetic models currently available. For this purpose, insulin resistance was induced in male C57BL/6J or Institute of Cancer Research (ICR) mice by feeding diets enriched in either fructose or fat, and hyperglycemia was induced by injecting these mice with a dose of streptozotocin (STZ) that does not cause diabetes in chow-fed mice. In the case of C57BL/6J mice, insulin levels initially increased in response to the fructose- and fat-enriched diets and then decreased to levels comparable to or still higher than those in chow-fed mice following STZ injection. Associated with the decrease in insulin levels following STZ, fat-fed and fructose-fed C57BL/6J mice became significantly hyperglycemic, reaching values of 388 +/- 38 and 366 +/- 58 mg/dL, respectively. In contrast, neither plasma glucose nor insulin concentrations changed in chow-fed mice injected with an identical amount of STZ. Essentially identical findings were seen before and after STZ injection in fat-fed compared with chow-fed ICR mice. Although a direct comparison was not made, sensitivity to the diabetogenic effects of STZ appeared to be greater in fat-fed ICR compared with fat-fed C57BL/6J mice. Finally, plasma glucose decreased when mice with these experimental models of NIDDM were treated with either metformin or tolbutamide. Given these results, it seems reasonable to suggest that the combination of dietary-induced insulin resistance and relatively low-dose STZ results in mouse models that should be of use in studying the pathophysiology of NIDDM or in evaluating therapeutic compounds for the treatment of NIDDM.

Animals↗
PubMed1998

Effect of filler porosity on the abrasion resistance of nanoporous silica gel/polymer composites.

OBJECTIVES: This laboratory study was designed to investigate the effect of controlled nanoporosity on the wear resistance of polymeric composites reinforced with silica gel powders and to determine the mechanisms controlling the abrasive wear properties of these unique nanostructured materials. METHODS: Silica gels were prepared by hydrolysis and condensation of tetraethylorthosilicate (TEOS) using four different catalysts to modify the porous structure of the resulting polysilicate silanation, an organic monomer (TEGDMA) containing various initiators was introduced into the gel powders to form a paste. The various pastes were then polymerized inside a glass mold. A pin-on-disk apparatus was then used to record the specimen length and number of revolutions. Abrasive wear rates were determined by regression analysis and statistical differences were determined by analysis of variance and multiple comparisons. BET was used to characterize the filler pore structure and scanning electron microscopy was used used to visually examine the abraded surfaces. RESULTS: Significant differences (p < 0.05) in the wear rates of the experimental composites were noted. Within the range of filler porosities examined, wear resistance was found to be linearly dependent (R2 = 0.983) on filler pore volume. The wear rates decreased with increasing filler porosity. HCl-catalyzed gels having low porosity produced composites having relatively limited abrasion resistance. In contrast, high porosity HF-catalyzed gels produced more wear-resistant composites. The abrasive wear resistance of these nanocomposites was not significantly affected by the level of silane coupling used in these experiments. SEM evaluation suggested that better wear resistance was associated with fine-scale plastic deformation of the wear surface and the absence of filler particle pullout. SIGNIFICANCE: Porous particles prepared via sol-gel show some promise as fillers that improve the wear resistance of photopolymerized resins. The wear resistance of the fillers appears to be directly related to nanoporous structure of the gel particles. Unlike conventional dental composites, these materials rely primarily on nanomechanical coupling for improved wear resistance. This new principle should benefit subsequent investigations.

Ceramics↗
PubMed1998

Growth factor-mediated neural proliferation: target of ethanol toxicity.

Ethanol exposure during development is teratogenic. The central nervous system (CNS) is particularly susceptible to ethanol toxicity. In fact, heavy gestational ethanol consumption is one of the leading known causes of mental retardation in the Western world. Ethanol exposure disrupts the proliferation of glia and neuronal precursors in the developing CNS. Depending upon cell population and blood ethanol concentration, ethanol can either inhibit or stimulate cell proliferation. Two features of cell proliferation that are affected by ethanol exposure are the growth fraction (the proportion of cells that is actively cycling) and the cell cycle kinetics, particularly in the length of the G1 phase of the cell cycle. Cell proliferation in the developing CNS reflects the action of positive (mitogenic growth factors) and negative (anti-proliferative factors) regulators. Increasing evidence shows that ethanol interferes with the action of growth factors. In vitro systems are a good model to investigate ethanol neurotoxicity, since the effects of ethanol on cultured cells parallel the effects of ethanol in the developing CNS. The inhibitory effects of ethanol on cell proliferation may result from interference with mitogenic growth factors (e.g., bFGF, EGF, PDGF, IGF-I). Conversely, the stimulatory effects of ethanol may result from the interference with growth inhibiting factors (e.g., TGFbeta1). Interestingly, both in vivo and in vitro studies show that proliferating neural cells display differential sensitivity to ethanol. This differential sensitivity correlates with their response to mitogenic growth factors; that is, cells that are actively regulated by mitogenic growth factors are much more susceptible to ethanol than cells that are less or unresponsive to such factors. Ethanol interference with growth factor action could occur at three levels: ligand production, receptor expression, and/or signal transduction. Thus, ethanol-induced alterations in the developing CNS that characterize fetal alcohol syndrome apparently result from alterations in the regulatory action of growth factors.

Animals↗
PubMed1998

The lesions of the pterygopalatine and infratemporal spaces: Computed tomography evaluation.

OBJECTIVE: The purpose of this study was to categorize the computed tomography features of lesions affecting the pterygopalatine fossa and infratemporal fossa and thus aid in the diagnosis of these lesions. DESIGN: Eighty-six patients with lesions of the pterygopalatine fossa and infratemporal fossa were examined with computed tomography; the lesions were confirmed by both surgery and biopsy. The patients were divided into three groups: group I consisted of patients in whom the lesions had originated in one or both fossae; group II, of patients in whom the lesions originated in other oral and maxillofacial regions but showed extension into the pterygopalatine and infratemporal fossae; and group III, of patients in whom the lesions had multicentric origins. RESULTS: Of the 11 cases in group I, demarcation was confined to both fossae in 4 patients, and involvement of the adjacent structures was shown on computed tomography images in 7 patients. Involved structures included the maxillary sinus (4 sides), nasal cavity (3 sides), mandibular ramus (6 sides), buccal space (2 sides), base of the skull (5 sides), palate (3 sides), and parapharyngeal space (5 sides). In the 70 cases in group II, computed tomography images showed that lesions had invaded both fossae via following routes: (1) 40 lesions in the maxillary sinus had infiltrated posterolaterally into 26 pterygopalatine and 39 infratemporal fossae; (2) two nasal cavity and three nasopharynx tumors had infiltrated laterally or lateroanteriorly into five pterygopalatine and one infratemporal fossae; (3) lesions originating in mandibular rami (9 lesions), buccal regions (4 lesions), parapharyngeal spaces (1 lesion) and parotid glands (1 lesion) had intruded medially into 15 infratemporal fossae; (4) two temporal bone tumors had encroached inferiorly on two infratemporal fossae; (5) four palate tumors had led to involvement of three pterygopalatine and four infratemporal fossae; and (6) four inflammatory diseases of the facial spaces involved two pterygopalatine and four infratemporal fossae. Group III lesions (5 cases) affecting one pterygopalatine and five infratemporal fossae were hemangiomas; one was a malignant lymphoma. CONCLUSION: Group I lesions may involve the adjacent anatomic structures of both pterygopalatine and infratemporal fossae in every direction. Group II lesions that correspond to the various origins of the maxillofacial region have different pathways of infiltration into the pterygopalatine or infratemporal fossae. Computed tomography examination is very important in the evaluation of lesions involving the pterygopalatine and infratemporal fossae.

Adolescent↗
PubMed1998

Adenovirus-mediated dystrophin minigene transfer improves muscle strength in adult dystrophic (MDX) mice.

Duchenne muscular dystrophy (DMD) and murine X-linked muscular dystrophy (mdx) are both due to absence of the subsarcolemmal protein dystrophin. Recombinant adenovirus vectors (AdV) are considered a promising means for delivering a functional dystrophin gene to muscle. However, the usefulness of AdV for this purpose is limited by vector toxicity as well as immune-mediated elimination of infected fibers. In addition, studies to date of AdV-mediated dystrophin gene transfer have either failed to examine effects on muscle strength or been performed in immunologically immature neonatal animals with little baseline abnormality of force-generating capacity. In the present study, AdV-mediated dystrophin gene transfer was performed in adult mdx mice with pre-existent dystrophic pathology and muscle weakness. The main findings are as follows: (1) acute myofiber toxicity and gene transfer efficiency are both AdV dose-dependent, such that the therapeutic margin of safety is fairly narrow; (2) immunosuppressive therapy (FK506) prevents immune-mediated elimination of dystrophin-positive fibers but not the dose-dependent toxic effects; (3) at the optimal vector dosage and with effective immunosuppression, AdV-mediated dystrophin minigene transfer is capable of alleviating the loss of force-generating capacity as well as histopathological evidence of disease progression normally seen in adult mdx muscles over a 2-month period. These findings have important implications for the eventual application of AdV-mediated dystrophin gene transfer in DMD patients.

Adenoviridae↗
PubMed1998

Transforming growth factor beta1 regulates the expression of cyclooxygenase in cultured cortical astrocytes and neurons.

The hypothesis that transforming growth factor beta1 (TGFbeta1) regulates the synthesis of prostaglandins by CNS tissue was tested by using purified cultures of cortical astrocytes or neurons that were obtained from rat pups on postnatal day 4 or 5 or fetuses on gestational day 16, respectively. The cells were exposed to TGFbeta1 for 2 days. The synthesis of prostaglandins depends upon the production and conversion of arachidonic acid, steps that are catalyzed by phospholipase A2 (PLA2) and cyclooxygenase (COX), respectively. Prostaglandin E2 (PGE2) concentration was determined by radioimmunoassay. The expression of cytosolic PLA2 and COX (the constitutive COX1 and the inducible COX2) was assessed by using immunohistochemical and quantitative immunoblotting procedures. Astrocytes produced much more PGE2 than neurons, suggesting that glial cells are an important source of PGE2 in the CNS. TGFbeta1 increased the production of PGE2 by astrocytes and neurons in a concentration-dependent manner. Furthermore, TGFbeta1 enhanced COX activity; the inhibitor indomethacin completely blocked TGFbeta1-mediated PGE2 synthesis. Cultured astrocytes and neurons expressed the three enzymes: cytosolic PLA2, COX1, and COX2. Cytosolic PLA2 expression was unaffected by TGFbeta1 treatment. In contrast, COX expression was altered by TGFbeta1 treatment in a concentration-dependent fashion. COX1 was increased by TGFbeta1, but only in astrocytes. TGFbeta1 increased COX2 expression in astrocytes and neurons. Thus, TGFbeta1-induced increases in PGE2 concentration are regulated by COX. This study suggests that TGFbeta1 is an important regulator of immune and inflammatory processes in the CNS.

Animals↗
PubMed1998

Dietary amylose-amylopectin starch content affects glucose and lipid metabolism in adipocytes of normal and diabetic rats.

The aim of this study was to evaluate the effects of the chronic consumption of two starches, characterized by different glycemic indices and amylose-amylopectin content, on glucose metabolism in rat epididymal adipocytes. The two chosen starches were from mung bean (32% amylose) and cornstarch (0.5% amylose). The alpha-amylase digestibility was higher for the waxy cornstarch than that of the mung bean starch (60 +/- 4 vs. 45 +/- 3%, mean +/- SEM, respectively). The glycemic index of the waxy cornstarch diet (575 g starch /kg diet) was higher than that of the mung bean starch diet (107 +/- 7 vs. 67 +/- 5%, P < 0.01) when measured in vivo in two groups of normal rats (n = 9). In a subsequent study, normal and diabetic (streptozotocin-injected on d 2 of life) male Sprague-Dawley rats (18 per group) consumed a diet containing 575 g starch/kg diet as either waxy cornstarch or mung bean starch. After 3 wk, food intake, epididymal fat pad weights, and plasma glucose, insulin and triglyceride concentrations did not differ between diet groups. Adipocyte diameter was smaller in rats that consumed mung bean starch compared with those that consumed the waxy cornstarch diet (P < 0.01). The mung bean diet increased maximal insulin-stimulated 14C-glucose oxidation (% of basal values, P < 0. 05). In contrast, incorporation of 14C-glucose into total lipids was significantly lower in rats that consumed the mung bean diet (P < 0. 05). We conclude that in both normal and diabetic rats, the chronic replacement of a high glycemic index starch by a low glycemic index one in a mixed diet increases insulin-stimulated glucose oxidation, decreases glucose incorporation into total lipids and decreases epididymal adipocyte diameter. Thus, the type of starch mixed into the diet has important metabolic consequences at the cellular level in both normal and diabetic rats.

Adipocytes↗
PubMed1998

A high glycemic index starch diet affects lipid storage-related enzymes in normal and to a lesser extent in diabetic rats.

The of this study was to evaluate the chronic effects of a high (waxy corn) vs. a low (mung beans) glycemic index starch diet on the lipogenic enzymes, fatty acid synthase (FAS) and lipoprotein lipase (LPL). Normal and diabetic (streptozotocin-injected on d 2 of life) male Sprague-Dawley rats consumed a diet containing 575 g/kg carbohydrates either as waxy cornstarch (WCS) or as mung bean starch (MBS). After 3 wk, neither body weights nor relative epididymal fat pad weights differed. In diabetic rats, the WCS diet induced high basal plasma insulin levels. Plasma triglycerides were not significantly affected by diet in either normal or diabetic rats. Adipose tissue and liver LPL activities were not modified by the type of starch in the diet. In normal rats, FAS activity and gene expression in epididymal adipose tissue but not in liver were greater in rats consuming the WCS diet than in those consuming MBS. To evaluate the implication of insulin in this regulation, two genes regulated by insulin [GLUT4 and phosphoenolpyruvate carboxykinase (PEPCK)] were also studied. The high glycemic index WCS diet compared with the low glycemic index MBS diet resulted in lower hepatic PEPCK mRNA in both normal and diabetic rats. Normal, but not diabetic rats fed WCS had greater GLUT4 gene expression in adipocytes than did those fed MBS. We conclude that the total replacement of 575 g/kg low glycemic index starch by a high glycemic index starch for 3 wk caused the following in normal rats: 1) high FAS activity and mRNA in adipose tissue but not in liver and 2) high GLUT4 gene expression in adipose tissue. In both normal and diabetic rats this same diet resulted in lower hepatic PEPCK mRNA. Therefore, high glycemic index starch diet is implicated in stimulating FAS activity and lipogenesis and might have undesirable long-term metabolic effects.

Adipose Tissue↗