Greenidea psidii (Hemiptera: Aphididae: Greenideinae) new invasive aphid in Costa Rica

P. 396-398The genus Greenidea comprises about 45 East Asian species of pear-shaped aphids with 6-segmented antennae, long hairy and pale reticulated siphunculi, rounded cauda with a median processus and 7.7.7 setae on first tarsal segments (Sugimoto 2008). The alatae viviparous females are more long-bodied and have longer siphunculi than the apterous ones. About half the species are included in subgenus Trichosiphum , in which the reticulation of the siphunculi is confined to the basal region. The genus occurs from Japan to Eastern Australia and from India to the Philippines (Blackman & Eastop 1994, 2006; Sugimoto 2008). They are mainly tree-living aphids and their biology is little known and sexual forms are generally unrecorded.S

Aphididae (Hemiptera: Sternorrhyncha) from Costa Rica, with new records for Central America

copyright 2010, Asociación Española de Entomología y los autores. Datos y artículo incluido por Lisela Moreira Carmona, CIBCM. disponible en repositorio BULERIA de la Universidad de León (España) https://buleria.unileon.es/handle/10612/5095Sixty-four aphid species (Hemiptera, Sternorrhyncha: Aphididae) were caught by the authors in Costa Rica during 2008. The Costa Rican aphid catalogue is presented from our data and the records in the literature; it consists of 88 species. Data on the species are given and the faunistic composition is discussed. Nine species are recorded for the first time in Central America and another 10 are recorded for the first time in Costa Rica. A list relationship of “host plant species / aphid species” is presented, 79 of which are new for the world and 97 are new for Costa Rica.Aphididae (Hemiptera: Sternorrhyncha) de Costa Rica, con nuevas citas para América Central. A partir de las capturas en Costa Rica de 64 especies durante 2008 y de los datos registrados se establece el catálogo de los áfidos (Hemiptera, Sternorrhyncha: Aphididae) de Costa Rica, que consta de 88 especies. Nueve especies se citan por primera vez en Centroamérica y otras 10 más por primera vez en Costa Rica. Se ofrecen datos sobre las especies citadas, se comenta la composición faunística y se presenta una lista de relaciones “especie de planta hospedadora / especie de pulgón”, con 79 nuevas relaciones para el Mundo y otras 97 para Costa Rica.Agencia Española de Cooperación Internacional para el Desarrollo (AECID) proyecto (D/010523/07) conjunto Universidad de León y Universidad de Costa RicaUCR::Vicerrectoría de Investigación::Unidades de Investigación::Ciencias Básicas::Centro de Investigación en Biología Celular y Molecular (CIBCM

Aphididae (Hemiptera: Sternorrhyncha) from Costa Rica, with new records for Central America

P. 145-182Aphididae (Hemiptera: Sternorrhyncha) de Costa Rica, con nuevas citas para América Central. A partir de las capturas en Costa Rica de 64 especies durante 2008 y de los datos registrados se establece el catálogo de los áfidos (Hemiptera, Sternorrhyncha: Aphididae) de Costa Rica, que consta de 88 especies. Nueve especies se citan por primera vez en Centroamérica y otras 10 más por primera vez en Costa Rica. Se ofrecen datos sobre las especies citadas, se comenta la composición faunística y se presenta una lista de relaciones “especie de planta hospedadora/especie de pulgón”, con 79 nuevas relaciones para el Mundo y otras 97 para Costa RicaS

Arginase Promotes Skeletal Muscle Arteriolar Endothelial Dysfunction in Diabetic Rats

Endothelial dysfunction is a characteristic feature in diabetes that contributes to the development of vascular disease. Recently, arginase has been implicated in triggering endothelial dysfunction in diabetic patients and animals by competing with endothelial nitric oxide synthase for substrate L-arginine. While most studies have focused on the coronary circulation and large conduit blood vessels, the role of arginase in mediating diabetic endothelial dysfunction in other vascular beds has not been fully investigated. In the present study, we determined whether arginase contributes to endothelial dysfunction in skeletal muscle arterioles of diabetic rats. Diabetes was induced in male Sprague Dawley rats by streptozotocin injection. Four weeks after streptozotocin administration, blood glucose, glycated hemoglobin, and vascular arginase activity were significantly increased. In addition, a significant increase in arginase I and II mRNA expression was detected in gracilis muscle arterioles of diabetic rats compared to age-matched, vehicle control animals. To examine endothelial function, first-order gracilis muscle arterioles were isolated, cannulated in a pressure myograph system, exposed to graded levels of luminal flow, and internal vessel diameter measured. Increases in luminal flow (0-50µL/min) caused progressive vasodilation in arterioles isolated from control, normoglycemic animals. However, flow-induced vasodilation was absent in arterioles obtained from streptozotocin-treated rats. Acute in-vitro pretreatment of blood vessels with the arginase inhibitors Nω-hydroxy-nor-L-arginine or S-(2-boronoethyl)-L-cysteine restored flow-induced responses in arterioles from diabetic rats and abolished differences between diabetic and control animals. Similarly, acute in-vitro pretreatment with L-arginine returned flow-mediated vasodilation in vessels from diabetic animals to that of control rats. In contrast, D-arginine failed to restore flow-induced dilation in arteri

YC-1 Stimulates the Expression of Gaseous Monoxide-Generating Enzymes in Vascular Smooth Muscle Cells

The benzylindazole derivative 3-(5′-hydroxymethyl-2′-furyl)-1-benzyl indazole (YC-1) is an allosteric stimulator of soluble guanylate cyclase (sGC) that sensitizes the enzyme to the gaseous ligands carbon monoxide (CO) and nitric oxide (NO). In this study, we examined whether YC-1 also promotes the production of these gaseous monoxides by stimulating the expression of the inducible isoforms of heme oxygenase (HO-1) and NO synthase (iNOS) in vascular smooth muscle cells (SMCs). YC-1 increased HO-1 mRNA, protein, and promoter activity and potentiated cytokine-mediated expression of iNOS protein and NO synthesis by SMCs. The induction of HO-1 by YC-1 was unchanged by the sGC inhibitor, 1H-(1,2,4)oxadiazolo[4,3-α]quinozalin-1-one (ODQ) or by the protein kinase G inhibitors (8R,9S,11S)-(-)-2-methyl-9-methoxyl-9-methoxycarbonyl-8-methyl-2,3,9,10-tetrahydro-8,11-epoxy-1H,8H,11H-2,7b,11a-triazadibenzo(a,g)cyclocta9(cde)trinen-1-one (KT 5823) and YGRKKRRQRRRPPLRKKKKKH-amide (DT-2) and was not duplicated by 8-bromo-cGMP or the NO-independent sGC stimulator 5-cyclopropyl-2[1-(2-fluorobenzyl)-1H-pyrazolo [3,4-b] pyridine-3-yl] pyrimidin-4-ylamine (BAY 41-2272). However, the YC-1-mediated induction of HO-1 was inhibited by the phosphatidylinositol-3-kinase (PI3K) inhibitors wortmannin and 2-(4-morpholinyl)-8-phenyl-1(4H)-benzopyran-4-one hydrochloride (LY294002). In contrast, the enhancement of cytokine-stimulated iNOS expression and NO production by YC-1 was prevented by ODQ and the protein kinase A inhibitor (9S,10S, 12R)-2,3,9,10,11,12-hexahydro-10-hydroxy-9-methyl-1-oxo-9, 12-epoxy-1H-diindolo(1,2,3-fg:3′,2′,1′-kl)pyrrolo(3,4-i)(1,6)-benzodiazocine-10-carboxylic acid hexyl ester (KT 5720) and was mimicked by 8-bromo-cGMP and BAY 41-2272. In conclusion, these studies demonstrate that YC-1 stimulates the expression of HO-1 and iNOS in vascular SMCs via the PI3K and sGC-cGMP-protein kinase A pathway, respectively. The ability of YC-1 to sensitize sGC to gaseous monoxides and simultaneously stimulate their production through the induction of HO-1 and iNOS provides a potent mechanism by which the cGMP-dependent and -independent biological actions of this agent are amplified. Originally published Molecular Pharmacology, Vol. 75, No. 1, Jan 200

Bilirubin Inhibits Neointima Formation and Vascular Smooth Muscle Cell Proliferation and Migration

Bilirubin is a heme metabolite generated by the concerted action of the enzymes heme oxygenase and biliverdin reductase. Although long considered a toxic byproduct of heme catabolism, recent preclinical, and clinical studies indicate the bilirubin exerts beneficial effects in the circulation. In the present study, we determined whether local administration of bilirubin attenuates neointima formation following injury of rat carotid arteries. In addition, the ability of bilirubin to regulate the proliferation and migration of human arterial smooth muscle cells (SMCs) was investigated. Local perivascular administration of bilirubin immediately following balloon injury of rat carotid arteries significantly attenuated neointima formation. Bilirubin-mediated inhibition of neointimal thickening was associated with a significant decrease in ERK activity and cyclin D1 and A protein expression, and an increase in p21 and p53 protein expression in injured blood vessels. Treatment of human aortic SMCs with bilirubin inhibited proliferation and migration in a concentration-dependent manner without affecting cell viability. In addition, bilirubin resulted in a concentration-dependent increase in the percentage of cells in the G0/G1 phase of the cell cycle and this was paralleled by a decrease in the fraction of cells in the S and G2M phases of the cell cycle. Finally, bilirubin had no effect on mitochondrial function and ATP content of vascular SMCs. In conclusion, these studies demonstrate that bilirubin inhibits neointima formation after arterial injury and this is associated with alterations in the expression of cell cycle regulatory proteins. Furthermore, bilirubin blocks proliferation and migration of human arterial SMCs and arrests SMCs in the G0/G1 phase of the cell cycle. Bilirubin represents an attractive therapeutic agent in treating occlusive vascular disease

Greenidea psidii (Hemiptera: Aphididae: Greenideinae) New Invasive Aphid in Costa Rica

Copyright 2009, The Florida Entomologists (FLORIDA ENTOMOLOGICAL SOCIETY) and www.bioone.org. Datos incluidos por Lisela Moreira Carmona, responsable de depósitos del área de Patógenos y Plagas de Plantas (CIBCM-UCR).Greenidea (Trichosiphum) psidii van der Goot 1916 is recorded for the first time in Costa Rica and Central America. The species has been recorded on Psidium guajava, Psidium friedrichst halianum and Myrciaria cauliflora and seems to be widely distributed in all parts of the country and probably in all Central America.Universidad de Costa Rica/[801-A8-528]/UCR/Costa RicaUniversidad de Costa Rica/[801-A1-801]/UCR/Costa RicaAgencia Española de Cooperación Internacional para el Desarrollo/[D/010523/07]/AECID/EspañaUCR::Vicerrectoría de Investigación::Unidades de Investigación::Ciencias Básicas::Centro de Investigación en Biología Celular y Molecular (CIBCM

Arginase Promotes Neointima Formation in Rat Injured Carotid Arteries

Objective—Arginase stimulates the proliferation of cultured vascular smooth muscle cells (VSMCs); however, the influence of arginase on VSMC growth in vivo is not known. This study investigated the impact of arginase on cell cycle progression and neointima formation following experimental arterial injury. Methods and Results—Balloon injury of rat carotid arteries resulted in a sustained increase in arginase activity in the vessel wall and the induction of arginase I protein in both the media and neointima of injured vessels. Furthermore, local perivascular application of the potent and selective arginase inhibitors S-(2-boronoethyl)-L-cysteine (BEC) or NG-hydroxy-nor-L-arginine (L-OHNA) immediately after injury markedly attenuated medial and neointimal DNA synthesis and neointima formation. Substantial arginase I protein and arginase activity was also detected in rat cultured aortic VSMCs. Moreover, treatment of VSMCs with BEC or L-OHNA, or knockdown of arginase I protein, arrested cells in the G0/G1 phase of the cell cycle and induced the expression of the cyclin-dependent protein kinase inhibitor, p21. Conclusion—This study demonstrates that arginase is essential for VSMCs to enter the cell cycle and that arginase I contributes to the remodeling response following arterial injury. Arginase I represents a potentially new therapeutic target for the treatment of vasculoproliferative disorders.Originally published Arteriosclerosis, Thrombosis, and Vascular Biology, Vol. 29, No. 4, Apr 200

The cyclic GMP modulators YC-1 and zaprinast reduce vessel remodeling through anti-proliferative and pro-apoptotic effects

Guanosine-specific cyclic nucleotide signaling is suggested to serve protective actions in the vasculature; however, the influence of selective pharmacologic modulation of cyclic guanosine monophosphate (GMP)-synthesizing soluble guanylate cyclase (sGC) or cyclic GMP-degrading phosphodiesterase (PDE) on vessel remodeling has not been thoroughly examined. In this study, rat carotid artery balloon injury was performed and the growth-modulating effects of the sGC stimulator YC-1 or the cGMP-dependent PDE-V inhibitor zaprinast were examined. YC-1 or zaprinast elevated vessel cyclic GMP content, reduced medial wall and neointimal cell proliferation, stimulated medial and neointimal cellular apoptosis, and markedly attenuated neointimal remodeling in comparable fashion. Interestingly, sGC inhibition by ODQ failed to noticeably alter neointimal growth, and concomitant zaprinast with YC-1 did not modify any parameter compared to individual treatments. These results provide novel in vivo evidence that YC-1 and zaprinast inhibit injury-induced vascular remodeling through anti-mitogenic and pro-apoptotic actions and may offer promising therapeutic approaches against vasoproliferative disorders. Originally published J Cardiovasc Pharmacol Ther, Vol. 14, No. 2, June 200