514 research outputs found
Stendhal, Lucien Leuwen, éd. A.-M. Meininger
No full textArrous M. Stendhal, Lucien Leuwen, éd. A.-M. Meininger. In: Romantisme, 1984, n°43. Le livre et ses images. pp. 118-122
Post aus Australien - In den Fängen des starken Dollars [Mail from Australia - In the clutches of a strong dollar]
No full textMartin Hirche hat nach seinem Sudium der InternationalenWeinwirtschaft (B. Sc.) an der HochschuleRhein-Main, Fachbereich Geisenheim,berufliche Erfahrungen in einer Baden-BadenerWeinhandelsagentur und später in der Verkostungsabteilungdes MEININGER VERLAGS gesammelt.Mit einem Stipendium für ein Auslandsstudiumin der Tasche, durfte er sich im Frühjahr2011 nach Australien aufmachen, um dort seineStudien mit dem Master zu krönen. Wir batenihn, von Zeit zu Zeit über Neues aus AustraliensWeinwelt zu berichten. Lesen Sie hier seine ers ten Eindrück
Adenosine stimulates the rate of proliferation of aortic and microvascular endothelial cells
No full textTypescript (photocopy).The effect of adenosine and/or hypoxic growth conditions on the proliferation of bovine aortic and coronary microvascular endothelial cells was investigated. Endothelial cells growing at standard tissue culture conditions were stimulated to proliferate by the addition of adenosine (final concentrations 0.5 ��M and 5.0 ��M). Cell counts of adenosine-treated cultures were 18-188% greater for aortic cells and 19-52% greater for microvascular cells than cell counts of nontreated control cells. This response was not dose-dependent within a concentration range of 5 nM and 50 ��M. When culture medium conditioned by endothelial cells growing at 2% oxygen was added to endothelial cells growing at standard conditions, cell counts were 19-56% greater than controls with fresh nonconditioned medium. This suggests that hypoxia causes endothelial cells to release a factor(s) into the medium which stimulates cell proliferation. The addition of 10^-5M 8-phenyltheophyl-line eliminated the stimulation of proliferation caused by 5.0 ��M adenosine or 2% oxygen in both aortic and microvascular cultures. These results suggest that: (1) hypoxia causes the release of adenosine from the cells, and (2) adenosine mediates its stimulatory effect via an external membrane receptor. When adenosine analogues selective for A1 and A2 adenosine receptors were tested, no selectivity was evident; that is, equivalent stimulation was achieved with either analogue. This finding suggests that the mechanism for adenosine-mediated stimulation of cell proliferation might be independent of cyclic AMP. Alternatively, either type of adenosine receptor might be capable of triggering a response(s) that culminates in cell replication. A three hour pulse of adenosine was sufficient for triggering the stimulatory response supporting the idea that a cascade of responses is necessary. Addition of adenosine at the time of seeding or 24 hours after seeding did not affect the stimulatory response. This last finding indicates that the stimulatory response was not due to the fact that the cells were not attached to the dish at the time of adenosine addition
Mechanisms of a-adrenergic enhancement of the myogenic response
No full textVita.Mechanisms of interaction between ��-adrenergic and myogenic mechanisms were studied in the intact microcirculation of the rat cremaster muscle. Anesthetized rats were enclosed in an airtight box which could be pressurized to increase intravascular pressure in the cremaster. The vessel diameter, intravascular pressure and red cell velocity were measured in the first order arteriole (1A) (114 [plus or minus] 13 ��m, mean [plus or minus] SD) during box pressure increases of 10, 20 and 30 mmHg. The results indicate that activation of ��-adrenoceptors by norepinephrine (NE, 2x10^-7 M - 2x10^-6 M) results in significant enhancement of myogenic constriction. This NE-enhanced response was inhibited by the potential-operated Ca[^2+] channel (POC) antagonist nifedipine (10^-6 M or 10^-5 M), and potentiated by the POC agonist Bay K 8644 (5x10^-7 M). Bay K 8644 alone also potentiated the myogenic response. The involvement of the second messenger pathway leading to protein kinase C (PKC) activation was also investigated. G-protein activation with AIF3 (2x10^-3 M NaF & 2x10^-5 M AICI3) caused 15% constriction of the 1A and facilitated myogenic constriction. The AIF3 vasoconstriction was inhibited by phospholipase C (PLC) inhibition with neomycin (10^-3 M) or 2-nitro-4-carboxyphenyl N,N-diphenylcarbamate (NCDC) (10^-4 M) and with the PKC inhibitor calphostin C (5x10^-7 M). These data suggest that G-protein activation potentiates myogenic responsiveness and involves activation of PKC. PLC inhibition with NCDC also significantly attenuated the NE-enhanced myogenic response, implicating the involvement of PLC. Inhibitors of PKC, staurosporine (10^-7 M) and calphostin C (10^-6 M), also significantly attenuated the NE-enhanced myogenic response. PKC activation with indolactam (10^-6 M) was found to increase vascular tone in the 1A (109 [plus or minus] 6 to 89 [plus or minus] 7 ��m) and to enhance myogenic responsiveness. These results suggest that NE acts in part through activation of PKC. Collectively, the results indicate that both POC and the intracellular signaling pathway involving PLC and PKC are involved in the ��-adrenergic enhancement of myogenic activity. These two mechanisms appear to represent overlap in the signaling pathways for ��-adrenergic and myogenic activation of vascular smooth muscle
Beneficial effects of dietary L-arginine supplementation to diabetic rats
No full textDiabetic rats exhibit decrease in plasma arginine, NO synthesis and tetrahydrobiopterin in endothelial cells (EC). Treatment with L-arginine may be beneficial for enhancing NO synthesis in diseases associated with endothelial dysfunction. However, little is known about the mechanism responsible for the stimulatory effect of arginine on endothelial NO synthesis. We hypothesized that dietary arginine supplementation increases BH4 for NO synthesis in EC of diabetic rats, thereby preventing endothelial dysfunction. In experiment I, streptozotocin (STZ) induced-diabetic male Sprague Dawley (SD) rats (a model of type-I diabetes) were individually pair-fed a casein-based diet on the basis of feed intake (per kg body weight) of non-diabetic SD rats. Addition of arginine-HCl or alanine to drinking water for the rats were adjusted daily to ensure isonitrogenous provision per kg body weight. In non-diabetic rats, arginine supplementation increased plasma arginine (144%), plasma insulin (44%), EC arginine (88%), EC BH4 (106%) and EC NO synthesis (80%), compared with alanine treatment. In diabetic rats, arginine supplementation reduced body weight loss (36%), and plasma glucose (54%), and increased plasma arginine (110%), plasma insulin (209%), EC arginine (173%), EC BH4 (128%) and EC NO synthesis (125%), compared with alanine treatment. In experiment II, male Zucker diabetic fatty (ZDF) rats (a model of type-II diabetes) were individually pair-fed a Purina 5008 diet on the basis of feed intake by alanine-treated diabetic rats (per kg body wt). Addition of arginine-HCl or alanine to drinking water for the rats was adjusted daily to ensure isonitrogenous provision per kg body weight. Arginine supplementation to ZDF rats did not affect plasma glucose and insulin, reduced epidididmal fat (30%), abdominal fat (43%) and body weight gain (18%), and increased plasma arginine (273%), EC arginine (197%), EC BH4 (120%) and EC NO synthesis (122%), compared with alanine-treated ZDF rats. These results show that dietary L-arginine supplementation increases BH4 and NO synthesis in EC of both STZ-diabetic and ZDF rats. Strikingly, arginine treatment prevented hyperglycemia in STZ-diabetic SD rats and reduced obesity in ZDF rats. Collectively, results demonstrate that oral administration of arginine is beneficial for both type-I and type-II diabetic rats
Amino acids, polyamines, and nitric oxide synthesis in the ovine conceptus
No full textThe objective of this study was to determine concentrations of amino acids and polyamines as well as nitric oxide (NO) and polyamine synthesis in the ovine conceptus (embryo/fetal and associated placental membrane). Ewes were hysterectomized on Days 30, 40, 60, 80, 100, 120, or 140 of gestation to obtain allantoic and amniotic fluids, intercotyledonary placenta, placentomes and uterine endometrium for the analyses. Alanine, citrulline plus glutamine accounted for about 80% of total α-amino acids in allantoic fluid during early gestation. Serine (16.5 mM) contributed about 60% of total α-amino acids in allantoic fluid on Day 140 of gestation. Maximal ornithine decarboxylase (ODC) and arginase activities and highest rates of polyamine and NO synthesis occured in all tissues on Day 40 of gestation. In ovine allantoic and amniotic fluids, polyamines were most abundant during early (Days 40-60) and late (Days 100-140) gestation, respectively. Activity of guanosine 5??-triphosphate-cyclohydrolase I (GTP-CH), and concentrations of NOS cofactors, tetrahydrobiopterin (BH4) and NADPH (nicotinamide adenine dinucleotide), peaked on Day 40 of gestation in placental and endometrial tissues. In these tissues, NO synthesis was positively correlated with total NOS activity, GTP-CH activity, and concentrations of BH4 and NADPH. The physiological significance of these changes was manifested by undernutrition-induced intrauterine growth retardation (IUGR). Maternal undernutrition (50% of National Research Council nutrient requirements) reduced concentrations of total α-amino acids in fetal plasma and fluids, and retarded fetal growth at both mid (Day 78) and late (Day 135) gestation. Concentrations of polyamines in fetal fluids were lower in underfed ewes than in control-fed ewes. Realimentation of underfed ewes between Days 78 and 135 of gestation increased concentrations of total α-amino acids and polyamines in fetal plasma and fluids, when compared with non-realimented ewes. Results of these studies demonstrate metabolic coordination among the several integrated pathways to enable high rates of polyamine and NO synthesis in the placenta and endometrium during early pregnancy. Collectively, our findings may have important implications for both IUGR and fetal origins of adult disease
Breakdown of the crystalloid endoplasmic reticulum of UT-1 cells
No full textVita.The studies described focus on the sterol-regulated mechanism by which UT-1 cells dispose of an elaborate intracellular membrane system of smooth endoplasmic reticulum (ER) termed crystalloid ER (CER). The CER is formed in response to lipoprotein deprivation and competitive inhibition o f 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR). Under these conditions, UT-1 cells produce up to 500-fold more HMGR than parental CHO cells. HMGR has been shown to occupy the CER. Addition of sterols to the growth media of UT-1 cells has been shown to cause the degradation of HMGR and breakdown of the CER membrane system. It has also been shown that sterol-accelerated degradation of CER membranes occurs via a non-lysosomal pathway. Other possible mechanisms of CER elimination include intra- ER degradation and expulsion of CER membranes to the extracellular media. There were four specific aims included in these studies. First, indirect immunofluorescence microscopy and brefeldin A were used to determine the existence of an intra-ER degradative pathway for HMGR in UT-1 cells. Second, silver stain, 45ca2+, and 32p_(}TP overlay techniques were used on proteins separated by 2-D SDS-PAGE to determine changes in proteins during incubation of UT-1 cells in sterols. Third, immunoblotting of immunoprecipitated proteins was used to account for both intra- and extracellular disposition of CER membranes and proteins during CER breakdown. Lastly, a major constituent protein of the CER of UT-1 cells, CERp60, was purified and submitted for sequencing to determine if it was related to a multifiinctional ER protein, protein disulfide isomerase. The goals of these studies was to further define the location of HMGR degradation, to determine sterol-mediated changes in UT-1 proteins, in particular Ca^+- and GTP-binding proteins, and to determine if CERp60 was related to protein disulfide isomerase
Alterations in skeletal muscle arteriolar vasoreactivity during the progression of type 2 diabetes in the Zucker Diabetic Fatty rat
No full textAltered vasoreactivity and mechanical properties of skeletal muscle arterioles could impact peripheral insulin resistance and hypertension observed in type 2 diabetes. The purpose was to determine if increased vasoconstrictor reactivity, decreased vasodilator reactivity and alterations in the structural properties of 1A arterioles from both high-oxidative and low-oxidative glycolytic skeletal muscles is present during prediabetes as well as acute and chronic diabetes, and to determine if this dysfunction precedes the development of elevated arterial pressure in type 2 diabetes. Zucker Diabetic Fatty (ZDF) rats and lean age-matched controls were studied at 7 (prediabetes), 13 (acute diabetes) and 20 (chronic diabetes) weeks of age. Following measurement of arterial pressure, vasoconstrictor responsiveness to norepinephrine (NE), potassium chloride (KCl), and increasing intraluminal pressure (MYO), vasodilator responsiveness to acetylcholine (ACh), sodium nitroprusside (SNP) and intraluminal flow and passive mechanical properties were examined in arterioles from soleus and gastrocnemius muscles. Vasoconstriction to NE was enhanced in gastrocnemius muscle arterioles during prediabetes and preceded elevated arterial pressure. Alterations in the passive mechanical properties of arterioles from both muscles were observed throughout the progression of diabetes. Flow-induced vasodilation was decreased in the high-oxidative muscle arterioles during acute diabetes, and was coincident with the emergence of elevated arterial pressure. During chronic diabetes, vasodilation to ACh and flow were reduced in soleus muscle arterioles. The reduced vasodilation to ACh was the result of a loss of NO. Although the vasodilator capacity of low-oxidative glycolytic skeletal muscle arterioles was not diminished throughout the progression of diabetes, the contribution of NO to AChinduced dilation was lost in the prediabetic and acute diabetic rats. The data demonstrate that alterations in both the vasoconstrictor and passive properties of low-oxidative glycolytic skeletal muscle arterioles are present during prediabetes, and precede the development of type 2 diabetes, and that although endothelial dysfunction does not become manifest in these skeletal muscle arterioles, alterations in the signaling mechanisms to achieve that vasodilation are present in prediabetes. Moreover, overt type 2 diabetes results in endothelial dysfunction and altered mechanical properties in high-oxidative skeletal muscle arterioles
Detection of integrins using surface enhanced raman spectroscopy
No full textIntegrins are transmembrane heterodimer protein receptors that mediate adherence to both the intracellular cytoskeleton and extracellular matrix. They play a major role in cellular adhesion and the breadth of their importance in biology is only recently being understood. The ability to detect concentrations of integrins on the cell surface, spatially resolve them, and study the dynamics of their behavior would be a significant advance in this field. Ultimately, the ability to detect dynamic changes of integrins on the surface of a cell maybe possible by developing a combined device such as an atomic force microscope (AFM) and surface enhanced Raman spectroscopy (SERS) system. However, the focus of this research is to first determine if integrins can be detected using SERS. Surface enhanced Raman spectroscopy (SERS) is technique used to detect the presence of analytes at the nanomolar level or below, through detection of inelastically scattered light. This thesis discusses the detection of integrins employing SERS as the detection modality. Integrins have been detected, in solution, using two silver colloids as the enhancing surface. Two silver colloid preparation methods are compared by ease of formulation and degree of enhancement in this thesis. Citrate and hydroxylamine hydrochloride (HA-HCl) reduced silver colloids were prepared through wet chemistry,compared using UV-Vis light spectroscopy, and tested for surface enhancement using adenine (a strong SERS active molecule), and two different integrins, (alpha)V(beta)3 and (alpha)5(beta)1. Results indicated that both colloids demonstrate SERS activity for varying concentrations of adenine as compared to standard non-enhanced Raman, however, only the citrate reduced colloid showed significant enhancement effect for the integrins
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