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hypertensive rats and human hypertensives (Liu et al.,2005; 2006). In this study, we investigate whether TRPC3 up-regulation in aorta from SHR is associated with angiotensin II receptor Arterial and Venous Endothelin-1 Content in Humans: Interactions with
(AT1R) mediate calcium influx. Methods: Blood pressure was measured using tail-cuff
Other Predictors of Hypertension
plethys-mography and a pressure transducer. Vasoconstriction of aortic rings was measured byorgan chamber. Aortic smooth muscle cells (VSMCs) was cultured. Cytosolic calcium Ralph E Watson, Cristiane N Pereira, Muhammad Pervaiz, Nandu Gourineni, Albert Q Pham, concentration was measured by the fluorescence technique. TRPC3 and AT1R expressions Dana Hougton, John D Talbott, Gregory D Fink; Michigan State Univ, East Lansing, MI were detected by western blotting. Results TRPC3 expression was significantly increased in
aorta form SHR compared to WKY (1.48Ϯ0.05 vs. 1.00Ϯ0.06, pϽ0.01). AT1R expression was
Introduction: Local production of endothelin-1 (ET-1) by vascular endothelial cells may
no significantly difference in aorta from SHR compared to WKY (pϾ0.05). Administration of Ang contribute to hypertension development by causing vascular constriction or hypertrophy. Most II significantly increased TRPC3 expression in VSMCs from SHR compared to SHR control studies have shown, however, that arterial content of ET-1 is not higher in patients with mild conditions (pϽ0.05). Administration of telmisartan, an AT1R blocker, significantly down to moderate essential hypertension. Nevertheless, such measurements are possibly con- regulated TRPC3 expression in cultured VSMCs (pϽ0.05). Immuno-fluorescence showed that founded by effects of hyperlipidemia, type II diabetes, and other factors on ET-1 content. In TRPC3 and AT1R coexisted in cultured VSMC. Ang II significantly increased mean arterial blood addition, ET-1 is a potent venoconstrictor, but relatively few studies report venous ET-1 pressure in SHR compared to WKY (53Ϯ3 vs. 22Ϯ4 mmHg, pϽ0.01). AngII-induced content. Hypothesis: We tested the hypothesis that arterial or venous ET-1 content can predict
vasoconstriction was significantly higher in aortic rings from SHR compared to WKY (82Ϯ3% hypertension when adjusted for these confounding variables. Methods: We determined ET-1
vs. 54Ϯ6%, pϽ0.01). After administration of telmisartan (5mg/kg/day) in SHR for 4 weeks content in internal mammary artery and saphenous veins of 57 subjects, who underwent systolic blood pressure was significantly reduced from 202Ϯ20 mmHg to 124Ϯ18 mmHg coronary artery bypass graft surgery for atherosclerotic disease. A chemiluminescent ELISA (nϭ6, pϽ0.01). Upregulation of TRPC3 by overexpressing TRPC3 gene in the cultured VSMCs was used to measure ET-1 content. Other patient data was obtained from medical records and significantly increased TRPC3 expression (pϽ0.01), and AngII-induced calcium influx was patient interviews. Univariate comparisons, correlation analyses and logistic regression significantly increased to 155Ϯ12% (nϭ6; pϽ0.01). After siRNA against TRPC3 significantly modeling were used to analyze the data. Results: No statistically significant differences in
reduced TRPC3 expression by 30Ϯ5% in the cultured VSMCs and Ang II-induced calcium influx arterial or venous ET-1 content were found when comparing patients according to blood was accompanied reduced (pϽ0.05). Conclusion This study for the first time highlights the
pressure, age, sex, smoking, lipids, fasting glucose levels, or type II diabetes status. Also no importance of AT1R mediated the calcium influx through TRPC3 channel in genetic differences were found in patients taking statins, ACE inhibitors, or beta-blockers. Arterial ET-1 hypertension (supported by 973 program 2006CB503804).
content did not predict hypertension when added to any logistic regression model; but the data
revealed a strong correlation between arterial ET-1 content and plasma triglyceride levels. The
only logistic model that strongly predicted (pϭ 0.0083) hypertension included sex and venous
ET-1 content as predictor variables. Conclusions: Two important conclusions are drawn from
these results. First, in confirmation of earlier work, arterial ET-1 content is not higher in
hypertension, but such measures may be confounded by an influence of plasma triglycerides
on arterial ET-1. Second, venous ET-1 may have a larger effect on hypertension development Effects of Recombinant Human Brain Natriuretic Peptide on a Porcine
Model of Acute Pulmonary Hypertension
Jun Pu, Ben He, Shanghai Renji Hosp, Sch of Medicine, Shanghai Jiaotong Univ, Shanghai, China; Pei-ren Shan, Zhi-qing Qiao, An-cai Yuan, Wei Song; Shanghai Renji Hosp, Sch of Regulation of Blood Pressure by Prostaglandin F
Med, Shanghai Jiaotong Univ, Shanghai, China 2a Receptor Gene (FP)
OBJECTIVES: The effects of brain natriuretic peptide (BNP) on the pulmonary hypertension
Ying Yu, Margaret Lucitt, Tom Price, Garret FitzGerald; ITMAT, Philadelphia, PA remains unknown. The aim of the present study was to evaluate the effects of recombinanthuman BNP (rhBNP) on pulmonary and systemic haemodynamics in a porcine model of Aspirin reduces renin and blood pressure in renovascular hypertension and there is a rebound thromboxane-induced acute pulmonary hypertension. METHODS: Acute pulmonary hyperten-
rise in renin after reversible inhibition of cyclooxygenases by salicylates in humans. It has been sion was induced with a continuous infusion of the thromboxane analogue, U46619. Fifteen assumed that these effects reflect modulation of prostacyclin (PGI2) a potent renin secretagoge.
adult swine were randomized into two groups. Group 1 (n ϭ 8) received an intravenous bolus However, recent development of novel methodology indicates that prostaglandin (PG) F2␣ is a rhBNP at 0.3 mg/kg/min, followed by an infusion at a rate of 0.015 mg/kg/min, and group 2 far more abundant prostaglandin in urine of mice and humans and little is known of its (n ϭ 7) received a saline solution instead of rhBNP. RESULTS: Acute pulmonary hypertension
cardiovascular function. Intravenous PGF2␣ results in a dose dependent elevation of blood was achieved in all animals. The administration of rhBNP reversed pulmonary hypertension, pressure in wild type mice. This response is lost in mice lacking the F prostanoid (FP) receptor, with a significant decrease in mean pulmonary artery pressure and pulmonary vascular while the hypertensive response to angiotensin II is augmented, consistent with increased resistance, a moderate decrease in systemic arterial pressure and a concomitant increase in expression of AT1a and AT1b receptors in large arteries. Deletion of the FP reduces blood cardiac output, but no marked changes in heart rate. CONCLUSIONS: The administration of
pressure retards atherogenesis in hyperlipidemic mice and also reduces blood pressure in rhBNP is associated with predominant pulmonary vasodilatation with moderate systemic normolipidemic mice on either a chow or a high fat diet. Curiously, expression of the FP, while vasodilatation in this porcine model of acute pulmonary hypertension. This study was supported evident in arterioles and the renal collecting ducts, is not detectable in the heart or large by Natural Science Foundation of China ( No. 30600242 and 30670880) arteries of mice. Deletion of the FP depressed plasma renin activity, angiotensin andaldosterone under basal conditions and following salt depletion. These findings demonstratethat PGF2␣ plays a critical role in maintenance of blood pressure homeostasis by regulating therenin - angiotensin system in the kidney of mice. Antagonism / deletion of the I prostanoidreceptor (IP) which accelerates atherogenesis. Pharmacological blockade of the FP mayrepresent a novel therapeutic strategy in syndromes of renin dependent hypertension with amore cardioprotective profile than suppressing synthesis or disrupting activation of the IP by HMG-CoA Reductase Inhibitor Ameliorates Aortic Stiffness in
Spontaneously Hypertensive Rats

Jae-Bin Seo, Eun-Ji Kim, Kwang-Il Kim, Young-Seok Cho, Tae-Jin Youn, In-Ho Chae, Cheol-Ho Kim, Dong-Ju Choi; Seoul National Univ, Seongnam, Republic of Korea Enhanced Nuclear Translocation of Nuclear Factor-B in Micro-G
Stimulated Cardiomyocyte Cells

Systemic hypertension is associated with elevated cardiovascular morbidity and mortality andis at least partly due to large artery stiffening. Cholesterol-lowering therapy has been Ohwon Kwon, Univ of Cincinnati, Cincinnati, OH; Michael Tranter, Univ of Cincinnati , efficacious in reducing arterial stiffness in patients with hypercholesterolemia, and thus may be Cincinnati, OH; W Keith Jones, Univ of Cincinnati, Cincinnati, OH; John M Sankovic, NASA beneficial in systemic hypertension. The present study was to examine whether HMG CoA Glenn Rsch Cntr, Cleveland, OH; Rupak K Banerjee; Univ of Cincinnati , Cincinnati, OH reductase inhibitor plays a role in the regulation of vascular stiffness. Pulse wave velocity (PWV)was determined as the time delay between the foot of pressure waves recorded simultaneously Introduction: Rotating Wall Vessel (RWV) bioreactors developed by NASA have been used in the
at the aortic arch and abdominal aorta (just above the bifurcation) in anesthetized Spontaneous laboratory to create suspension cell culture environments for simulating microgravity (MG) Hypertensive Rats (SHR). Eight-week-old SHRs were given standard chow or chow containing conditions on earth, and to study the effect of shear stress and gravity on the evolution, growth, rosuvastatin at a dose of 10 mg/kg or for 8 weeks: an untreated control group (CON, n ϭ12), and physiological changes of mammalian cells. Nuclear factor-kappa B (NF-␬B) is one of the and an HMG-CoA reductase inhibitor, rosuvastatin (ROS, nϭ12). PWV was measured at the most prevailing oxidation-sensitive transcription factors. The objective of this study is to same blood pressure (BP) level as in the control group, and the level of collagen content and investigate the activation of NF-␬B in the rat cardiac cells (H9c2) under MG. Method: H9c2
advanced glycated end products (AGE) was measured in aortic wall. PWV was improved after were cultured in the RWV under MG and unit-gravity dynamic control (DC) conditions. Western treatment (CON vs. ROS: 10736.53Ϯ 2531mm/sec vs. 8742.94Ϯ1593mm/sec, pϽ0.05).
blots and enzyme-linked immunosorbent assay (ELISA) were done using the nuclear extracts Aortic systolic blood pressure was not changed after rosuvastatin treatment (180Ϯ17 vs.
for the evaluation of differential NF-␬B p65 protein detection. Results: NF-␬B p65 protein
189.0Ϯ22 mm Hg, pϭns), as were mean (151.3Ϯ16 vs. 156.1Ϯ24 mm Hg, pϭns), diastolic revealed differential expression under MG and DC conditions. Mean activations of p65 protein blood pressures (137.0Ϯ16 vs. 139.6Ϯ17 mm Hg, p ϭns) and pulse pressure (42.9Ϯ8 vs.
were 69% for MG and 46% for DC as compared to positive control which were stimulated with 49.4Ϯ13 mm Hg, pϭns). Hydroxyproline content was significantly reduced by treatment (CON TNF-␣ for 30 min (* pϽ0.05, nϭ3, Figure). The results from western blots were confirmed by vs. ROS: 14.8Ϯ 5mg/g vs. 10.4Ϯ3, pϽ0.05), whereas AGE content was not changed ELISA which showed 66% for MG and 45% for DC. Conclusions: The present result showed
(315.89Ϯ 9076U/mg vs. 291.20Ϯ8861, pϭns). This study demonstrates that rosuvastatin significantly differential expression of NF-␬B p65, a pro-inflammatory transcription factor that reduces collagen content in the aortic wall and is also associated with a concomitant reduction is sensitive to oxidative stress, under MG as compared to DC. The study may be linked to in aortic PWV. This suggests that HMG CoA reductase inhibitor has effect modifying arterial explain the physiological changes such as muscle atrophy and further to identify the regulatory stiffness and improves vascular function in hypertension.
pathways and effector molecules under exposure to MG.
at UNIV OF CINCINNATI on October 9, 2010 2008 ATVB Poster Presentations
have shown that PPAR-␥ agonists reduce the progression of atherosclerotic lesions by directanti-atherogenic and anti-inflammatory actions with PPAR-␥ dependent or independentmechanisms. Oxidative stress and reactive oxygen species (ROS) underpin the pathogenesis ofcardiovascular diseases including atherosclerosis. NADPH oxidase is a predominant source ofROS and activation of this enzyme leads to intracellular signaling events causing endothelialdysfunction. We aimed to investigate the inhibition of PPAR-␥ agonists rosiglitazone (RGZ) and15-deoxy⌬12,14-prostaglandin J2 (15d-PGJ2) on TNF-␣ induced- NADPH oxidase mediated-oxidative stress in human aortic smooth muscle cells (AoSMC) by PPAR-␥ dependentmechanism. METHODS: AoSMC were treated with TNF-␣ (10ng/ml) for 12h and superoxideproduction was examined by lucigenin-enhanced chemiluminescence assay. AoSMC waspre-treated with RGZ (5␮M) or 15d-PGJ2 (10␮M) for 12h in the presence and absence ofselective PPAR␥ antagonist GW9662 (10␮M) and treated with TNF-␣ (10ng/ml) for 12h. DMSO(0.1%) was used as vehicle control. Real time RT-PCR analysis was performed to determine theNADPH oxidase subunit Nox4 gene expression level. RESULTS: Superoxide production was detected in AoSMC after treatment with TNF-␣ through up-regulation of Nox4 (nϭ4, PϽ0.05).
Nuclear Shp-2 Is One Important Negative Regulator of the Nuclear Export
Both RGZ and 15d-PGJ2 significantly inhibited TNF␣-induced superoxide production and this of Telomerase Reverse Transcriptase Induced by Oxidative Stress:
effect was reversed by selective PPAR␥ antagonist GW9962 (nϭ4, PϽ0.05). RGZ significantly Implication for Aging Processes and Vascular Diseases
inhibited TNF-␣-induced Nox4 gene up-regulation by nearly 50% whilst 15d-PGJ2 showedsignificant inhibition of more than 80%. The inhibitory effect of RGZ and 15d-PGJ2 was Sascha Jakob, Peter Schroeder, Diane Schmiegelt, Kerstin Kunze, Judith Haendeler; IUF, reversed by GW9662. (nϭ4, PϽ0.05). CONCLUSIONS: We demonstrated that TNF-␣ stress elicits elevated AoSMC superoxide and that TNF-␣ induced superoxide production is mediatedby Nox4. Our data reveals that, for the first time, both synthetic PPAR-␥ agonist RGZ and In the western society one major risk factor associated with aging are vascular diseases. The endogenous PPAR-␥ agonist 15d-PGJ2 inhibit TNF-␣ induced- Nox4 mediated-oxidative stress risk of heart attack and coronary diseases increases with aging. Therefore, it is important to in AoSMC by PPAR-␥ dependent mechanism.
understand aging on a cellular level. One factor of cell aging is the shortening of telomeres, theends of the chromosomes. The enzyme telomerase reverse transcriptase (TERT) counteracts this shortening. Therefore, TERT can exert the life span of different cell types. One importantregulatory mechanism of TERT is its localisation. In this context, we recently showed that in Novel Nox1-Mediated Mechanism of SSH1L Activation in VSMC: Role in Cell
endothelial cells oxidative stress induced Src kinase family-dependent tyrosine phosphorylation Migration
of TERT, which resulted in nuclear export of TERT and reduction of nuclear TERT activity. Thisled to accelerated senescence and enhanced apoptosis sensitivity of endothelial cells.
Alejandra San Martin, Moo Y Lee, Kathy K Griendling; Emory Univ, Atlanta, GA Therefore, the aim of this study was to investigate the mechanism inhibiting nuclear export ofTERT. One potential “inhibitor” is the tyrosine phosphatase Shp-2, which can reduce the Platelet-derived growth factor (PDGF) activates a Nox1-based NADPH oxidase and contributes activity of the Src kinase family. For inhibiting the nuclear export of TERT the nuclear to atherosclerosis and restenosis by stimulating VSMC migration in a hydrogen peroxide localisation of Shp-2 is necessary. Thus, we first demonstrated that endogenous Shp-2 was (H2O2)-dependent manner. Migration requires rapid turnover of actin filaments, which is located in the nucleus and in the cytosol. Next, we showed that oxidative stress reduced Shp-2 partially controlled by cofilin. Cofilin is activated by dephosphorylation by the Slingshot protein levels and activity. Nuclear Shp-2 associated with TERT and overexpression of Shp-2 phosphatase1L (SSH1L). We recently demonstrated that SSH1L activity is required for wildtype inhibited H2O2-induced nuclear export of TERT. This inhibition was dependent on PDGF-induced cofilin activation and migration in VSMC. However, the mechanism leading to Shp-2 phosphatase activity, since a dominant negative Shp-2 mutant (Shp-2C459S) reduced SSH1L activation is mostly unknown. We hypothesize that Nox1-derived H2O2 participates in nuclear TERT protein and activity already under basal conditions. For identification of the SSH1L activation. We found that in VSMC exposed to H2O2, cofilin is dephosphorylated and member of the Src kinase family, which is responsible for the export of TERT, we used mouse SSH1L activity is increased (2124Ϯ132 vs 3489Ϯ880 pmoles PO4/300 ␮g) after 30 min.
embryonic fibroblasts deficient in the Src kinase family members Src, Fyn and Yes. In these Moreover, VSMC derived from Nox1 KO animals have impaired PDGF-induced migration cells the oxidative stress-induced nuclear export of TERT was completely abolished. Taken (150Ϯ28 vs 49Ϯ13 cells/field pϭ0.03) and SSH1L activation (205 Ϯ26 vs 151 Ϯ14), and this together, these data demonstrate for the first time that a function for nuclear Shp-2 exists in is accompanied by a decrease amount of active cofilin. Of relevance, PDGF-induced migration inhibiting nuclear export of TERT. Thus, increasing the amount of nuclear Shp-2 may a useful in Nox1 KO cells is recovered following transfection with a constitutively active form of cofilin therapeutic to delay/inhibit vascular aging processes.
(49 Ϯ13 vs 135 Ϯ27 cells/field pϭ0.04). In addition, we observed that Nox1 KO cellscompletely failed to activate Rac1 after 5 min of PDGF stimulation while wild type do robustly(182 Ϯ32 % percent control). One proposed mechanism of SSH1L regulation involves the release from an inhibitory complex with 14 –3–3 proteins in a Rac1-dependent manner. Indeed,SSH1L and 14 –3–3 coimmunoprecipitate in VSMC. Since 14 –3–3 protein has potential The Role of Nrf2 and Unfolded Protein Response in the Induction of
redox-sensitive cysteines, we hypothesized that in addition to its effects on Rac, Nox1 may also Antioxidant Enzymes by Oxidized Phospholipids
regulate SSH1L by oxidizing its interacting partners. We found that both H2O2 and PDGFcompletely oxidize 14 –3–3 at 30 min, suggesting that 14 –3–3 contains redox-sensitive SH Henna-Kaisa Jyrkka¨nen, Emilia Kansanen, Matias Inkala, Hanna Hurttila, Suvi E Heinonen, groups. Taken together, these data show that SSH1L activation is mediated by Nox1-produced Satu Tiainen, Harri Makkonen, Univ of Kuopio, Kuopio, Finland; Olga Oskolkova, Taras H2O2 and suggest that the activation mechanism involves Rac1 activation and oxidation of Afonyushkin, Valery N Bochkov, Med Univ of Vienna, Vienna, Austria; Masayuki Yamamoto, 14 –3–3. These findings suggest new therapeutic targets for vascular pathologies such as Tohoku Univ Graduate Sch of Medicine, Tohoku, Japan; Seppo Yla¨-Herttuala, Anna-Liisa restenosis and atherosclerosis in which migration is a significant component.
Besides their well-characterized proinflammatory and proatherogenic effects, oxidized phos- pholipids (oxPLs), such as oxPAPC (oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero- Gene Transfer of Angiotensin-Converting Enzyme-2 Reverses Angiotensin
phosphocholine) have been shown to have beneficial responses in vascular cells via induction II- and IV-Induced Expression of Macrophage Migration Inhibitory Factor in
of antioxidant enzymes such as heme oxygenase-1 (HO-1). We therefore hypothesized that Insulin Resistance of Endothelial Cells
oxPAPC could evoke a general cytoprotective response via activation of antioxidativetranscription factor Nrf2. Here we show that oxPAPC increases nuclear accumulation of Nrf2.
Xi-Yong Yu, Jiu-Chang Zhong, Qiu-Xiong Lin, Zhi-Xin Shan, Xiao-Hong Li, Xiao-Zhong Using the siRNA approach, we demonstrate that Nrf2 is critical in mediating the induction of Huang, Shu-Guang Lin; Guangdong Provincial People’s Hosp, Guangzhou, China glutamate-cysteine ligase modifier subunit (GCLM) and NAD(P)H quinone oxidoreductase-1(NQO1) by oxPAPC in human endothelial cells, whereas the contribution to the induction of Insulin resistance is a proinflammatory state associated with enhanced oxidative stress, which HO-1 was less significant. The induction of GCLM and NQO1 was attenuated by reduction of has been closely linked to abnormalities in the renin-angiotensin system (RAS) . As electrophilic groups with sodium borohydrate as well as treatment with thiol antioxidants, predominant effectors of RAS, angiotensin (Ang) II and its fragment Ang IV exert various suggesting that the thiol reactivity of oxPAPCs is largely mediating its effect on Nrf2-responsive deleterious effects by promoting the productions of proinflammatory cytokines. Macrophage genes. The PERK-mediated unfolded protein response (UPR) induced by endoplasmic reticulum migration inhibitory factor (MIF) is now known as a proinflammatory cytokine that was recently stress was shown to be important for the induction of these genes by Nrf2. Finally, the associated with insulin resistance and exhibited previously to be induced by angiotensin (Ang) oxPAPC-inducible expression of HO-1, GCLM, and NQO1 is lower in Nrf2-null than wild type II. Our aim was to investigate whether Ang II, its fragment Ang IV and related enzyme mice carotid arteries in vivo. We suggest that the activation of Nrf2 by oxPLs provides a angiotensin-coverting enzyme 2 (ACE2) could modulate the expression of MIF and insulin mechanism by which their deleterious effects are limited in the vasculature.
signaling in cultured human endothelial cells. A recombinant plasmid encompassing humanACE2 cDNA was constructed and transfected into these cells. The mRNA, phosphorylation andprotein levels of p22phox, MIF and Akt in cells were determined by real-time polymerase chain reaction and Western blotting, respectively. The results showed that exposure of endothelial Inhibition of PPAR-Agonists on TNF--Induced Oxidative Stress in
cells to Ang II and Ang IV resulted in a time-dependent increase in MIF mRNA and protein Human Aortic Smooth Muscle Cells by PPAR--Dependent Mechanism
expressions, respectively. ACE2 gene transfer strikingly suppresses the expressions of p22phoxand MIF induced by Ang II and IV in endothelial cells. In addition, Ang II diminished Kyaw-Thu Moe, Philip Wong, Tian-Hai Koh, Meng Cheong Wong; National Heart Cntr, insulin-stimulated phosphorylation of Akt at serine 473 and eNOS at serine 1177 and NO generation, which were reversed by ACE2 gene transfer and anti-MIF treatment in endothelialcells. Our findings reveal that gene transfer of ACE2 regulates Ang II-mediated impairment of BACKGROUND AND PURPOSE: Peroxisome proliferator-activated receptors are members of the insulin signaling involving Akt-eNOS phosphorylation pathway. These beneficial effects of ACE2 nuclear hormone receptor superfamily of ligand-activated transcription factors. Recent studies overexpression are thought to result mainly from blocking MIF expression in endothelial cells, at UNIV OF CINCINNATI on October 9, 2010


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