Academic literature on the topic 'Endothelin Axi'
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Journal articles on the topic "Endothelin Axi"
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Tyagi, Suresh C., Lane M. Smiley, and Vibhas S. Mujumdar. "Homocyst(e)ine impairs endocardial endothelial function." Canadian Journal of Physiology and Pharmacology 77, no. 12 (November 15, 1999): 950–57. http://dx.doi.org/10.1139/y99-102.
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Homocyst(e)ine injured vascular endothelium and modulated endothelial-dependent vascular function. Endothelium plays an analogous role in both the vessel and the endocardium. Therefore, we hypothesized that homocyst(e)ine modulated endocardial endothelium (EE) dependent cardiac function. The ex vivo cardiac rings from normal male Wistar-Kyoto rats were prepared. The contractile responses of left and right ventricular rings were measured in an isometric myobath, using different concentrations of CaCl2. The response was higher in the left ventricle than right ventricle and was elevated in endocardium without endothelium. The half effective concentration (EC50) and maximum tension generated by homocyst(e)ine were 106 and 5-fold lower than endothelin (ET) and angiotensin II (AII), respectively. However, in endothelial-denuded endocardium, homocyst(e)ine response was significantly increased (p < 0.005, compared with intact endothelium) and equal to the response to ET and AII. To determine the physiological significance of ET, AII, homocyst(e)ine, and endothelial nitric oxide in EE function, cardiac rings were pretreated with AII (10-10 M) or ET (10-13 M) and then treated with homocyst(e)ine (10-8 M). Results suggested that at these concentrations AII, ET, or homocyst(e)ine alone had no effect on cardiac contraction. However, in the presence of 10-10 M AII or 10-13 M ET, the cardiac contraction to homocyst(e)ine (10-8 M) was significantly enhanced (p < 0.01, compared with without pretreatment) and further increased in the endocardium without endothelium. The pretreatment of cardiac ring with the inhibitor of nitric oxide, Nω-nitro-L-arginine methyl ester (L-NAME), increased contractile response to homocyst(e)ine. These results suggested that homocyst(e)ine impaired EE-dependent cardiac function and acted synergistically with AII and ET in enhancing the cardiac contraction.Key words: endocardial remodeling, homocyst(e)ine, contraction, endothelin, angiotensin, endothelial-derived relaxing factor (EDRF), Nω-nitro-L-arginine methyl ester (L-NAME), endothelial dysfunction, ex vivo cardiac function, heart failure.
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O. R. Luchko. "A relation of the indices of systemic inflammation and endothelial dysfunction in patients with chronic pyelonephritis and arterial hypertension." Bukovinian Medical Herald 17, no. 1 (65) (February 2, 2013): 59–63. http://dx.doi.org/10.24061/2413-0737.xvii.1.65.2013.15.
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The dynamics of the indicators of systemic inflammation (C-reactive protein - CRP, tumor necrosis factoralpha – TNF-α, IL-1 – IL-1, IL-6 – IL-6, soluble cell-cell adhesion molecule – sICAM-1) and endothelial dysfunction (pulse blood pressure – PBP, aortic stiffness index – ASI, the thickness of intima-media complex – TIMC, the velocity of the pulse wave propagation – VPWP, CAVI, endothelium dependent vasodilatation – EDVD and endothelium independent vasodilatation – EIVD, endothelin-1 – ET-1) in 105 patients with chronic pyelonephritis (CPN) and arterial hypertension (AH), depending on the glomerular filtration rate (GFR). 91 (86,67 %) patients have demonstrated the signs of a systemic inflammation which intensify with decreased GFR <90 ml/min. Reduced resilient- elastic properties of the arteries with increased ASI, VPW, CAVI, the levels of endothelinemia and a decrease of EDVD and EIVD was noted in 87 (82,86 %) patients with CPN and AH. The authors have observed a correlation between the indicators of the systemic inflammatory response (CRP, TNF-α, IL-1β, IL-6, sICAM-1) and the markers of the endothelial dysfunction (EDVD, EIVD, CAVI) in the group mentioned above which increases with a decrease of the glomerular filtration rate which should be considered, when treating such patients.
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Hao, Ying, Zhuang Wang, Francis Frimpong, and Xingjuan Chen. "Calcium–Permeable Channels and Endothelial Dysfunction in Acute Lung Injury." Current Issues in Molecular Biology 44, no. 5 (May 16, 2022): 2217–29. http://dx.doi.org/10.3390/cimb44050150.
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The increased permeability of the lung microvascular endothelium is one critical initiation of acute lung injury (ALI). The disruption of vascular-endothelium integrity results in leakiness of the endothelial barrier and accumulation of protein-rich fluid in the alveoli. During ALI, increased endothelial-cell (EC) permeability is always companied by high frequency and amplitude of cytosolic Ca2+ oscillations. Mechanistically, cytosolic calcium oscillations include calcium release from internal stores and calcium entry via channels located in the cell membrane. Recently, numerous publications have shown substantial evidence that calcium-permeable channels play an important role in maintaining the integrity of the endothelium barrier function of the vessel wall in ALI. These novel endothelial signaling pathways are future targets for the treatment of lung injury. This short review focuses on the up-to-date research and provide insight into the contribution of calcium influx via ion channels to the disruption of lung microvascular endothelial-barrier function during ALI.
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Lam, Chen-Fuh, Yen-Chin Liu, Jen-Kuo Hsu, Pei-An Yeh, Ting-Ya Su, Chien-Chi Huang, Ming-Wei Lin, Ping-Ching Wu, Pei-Jung Chang, and Yu-Chuan Tsai. "Autologous Transplantation of Endothelial Progenitor Cells Attenuates Acute Lung Injury in Rabbits." Anesthesiology 108, no. 3 (March 1, 2008): 392–401. http://dx.doi.org/10.1097/aln.0b013e318164ca64.
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Background Acute lung injury (ALI) and end-stage acute respiratory distress syndrome (ARDS) are among the most common causes of death in intensive care units. Activation and damage of pulmonary endothelium is the hallmark of ALI/ARDS. Recent studies have demonstrated the importance of circulating endothelial progenitor cells (EPCs) in maintaining normal endothelial function as well as endothelial repairing after vascular injury. Here, the authors present the first study demonstrating the therapeutic potential of EPCs in a rabbit model of ALI/ARDS. Methods Circulating EPCs were obtained from rabbits using Ficoll centrifugation. One week after culturing, ALI was induced in rabbits by oleic acid (75 mg/kg, intravenous), and autologous EPCs were transplanted intravenously. Vasomotor function of isolated pulmonary artery and degrees of lung injury were assessed 2 days later. Results Endothelial dysfunction in the pulmonary artery was significantly attenuated in rabbits treated with EPCs, whereas the endothelium-independent relaxation responses were not different. Expression of inducible nitric oxide synthase was suppressed in the pulmonary artery of EPC-treated animals. Infiltration of leukocytes in the lung parenchyma was significantly reduced after EPC transplantation. EPCs also decreased water content, hyaline membrane formation, and hemorrhage in lungs. Conclusion The authors demonstrated that autologous transplantation of EPCs preserves pulmonary endothelial function and maintains the integrity of pulmonary alveolar-capillary barrier. Transplantation of EPCs can be a novel cell-based, endothelium-targeted therapeutic strategy for prevention and treatment of ALI/ARDS.
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Vorob’eva, Nadezda A., Alena I. Vorob’eva, and Anastasiya A. Marusiy. "Risk of Endothelial Dysfunction and Total Antioxidant Capacity in Seafarers During an Arctic Voyage." Journal of Medical and Biological Research, no. 2 (May 9, 2021): 192–200. http://dx.doi.org/10.37482/2687-1491-z057.
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Among other areas of research, clinical medicine studies the adaptation mechanisms of the vascular endothelium to the extreme conditions of the Arctic. This paper dwells on the possible relationship of the development of endothelial dysfunction and the antioxidant system with modifiable risk factors during a short translatitudinal voyage in the Arctic. The study involved 32 crew members of the research vessel Mikhail Somov during the TransArctic–2019 research expedition. Venous blood sampling was carried out before the voyage at the zero point (Arkhangelsk, 64°33’N 40°32’E) and at the highest point of the expedition (Hayes Island, 80°34’N 57°41’E). Endothelin-1 concentration and serum total antioxidant capacity were determined using the enzyme-linked immunosorbent assay. We found statistically significant differences (Student’s t-test: t = –3.6532; df = 31; p < 0.001) in endothelin-1 concentration at the zero point (4.79 ± 2.10 pg/ml) and high point (7.02 ± 2.42 pg/ml), which indicates vasoconstriction, i.e. the first signs of the formation of vascular endothelium maladaptation. In 84.4 % of the crew members at the high point we detected high total antioxidant capacity, which can indicate compensation of antioxidant defence mechanisms. Noteworthy, serum total antioxidant capacity in smokers was statistically significantly higher than in non-smokers. Moreover, the predominance of high antioxidant activity among the crew members points to an increased oxidative load on the sailors’ body having to neutralize the excess amount of reactive oxygen species. For citation: Vorob’eva N.A., Vorob’eva A.I., Marusiy A.A. Risk of Endothelial Dysfunction and Total Antioxidant Capacity in Seafarers During an Arctic Voyage. Journal of Medical and Biological Research, 2021, vol. 9, no. 2, pp. 192–200. DOI: 10.37482/2687-1491-Z057
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Zaikina, T. S., P. G. Kravchun, D. V. Minukhina, D. V. Minukhin, D. O. Yevtushenko, and I. O. Kudrevych. "COMPREHENSIVE ASSESSMENT OF ENDOTHELIUM-DEPENDENT MEDIATORS IN PATIENTS WITH ACUTE MYOCARDIAL INFARCTION AND DIABETES MELLITUS TYPE 2." Problems of Endocrine Pathology 76, no. 2 (June 10, 2021): 14–18. http://dx.doi.org/10.21856/j-pep.2021.2.02.
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The aim of study is to evaluate the levels of endothelium-dependent mediators: endothelial nitric-oxide synthase (NOS), plasminogen activator inhibitor-1 (PAI-1) and circulating soluble CD40 ligand (sCD40L) in patients with acute myocardial infarction (AMI) and concomitant type 2 diabetes mellitus (DM). The study included 255 patients with AMI, who were divided into two groups depending on the presence of concomitant type 2 DM: 1 group — 143 patients with concomitant type 2 DM; 2 group — 112 patients without concomitant disturbances of carbohydrate metabolism. Studied endothelial-dependent indicators were investigated using enzyme-linked immunosorbent assay. Statistical data were processed using the Mann–Whitney U-test, quantitative variables were described by the following parameters: median (Me), 25th and 75th percentiles (Q1; Q3). Analyzing the studied indicators on admission of patients to the hospital, a statistically significant decrease in NOS levels (p < 0,01), as well as an increase in PAI-1 (p < 0,01) and sCD40L (p < 0,01) in the cohort of patients with AMI and concomitant type 2 DM compared with patients without disturbances of carbohydrate metabolism. This indicates a more significant violation of endothelium-dependent vasodilation, thrombin fibrinolysis and activation of intravascular inflammation caused by comorbidity. Over the next 10 days, an increase in NOS levels, a decrease in PAI-1 and sCD40L levels were observed in patients of both groups, indicating a gradual improvement of the endothelial function. However, in patients with AMI and concomitant type 2 DM, the levels of the studied endothelium-dependent mediators continued to differ statistically even on the 10th day after acute occlusion of the coronary artery. In our opinion, this tendency is caused by the negative impact of metabolicdisorders associated with type 2 DM on the endothelium of the coronary arteries in patients with insulin resistance and, apparently, may increase the risk of complications of AMI.
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Kolosova, Irina A., Tamara Mirzapoiazova, Liliana Moreno-Vinasco, Saad Sammani, Joe G. N. Garcia, and Alexander D. Verin. "Protective effect of purinergic agonist ATPγS against acute lung injury." American Journal of Physiology-Lung Cellular and Molecular Physiology 294, no. 2 (February 2008): L319—L324. http://dx.doi.org/10.1152/ajplung.00283.2007.
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Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are major causes of acute respiratory failure associated with high morbidity and mortality. Although ALI/ARDS pathogenesis is only partly understood, pulmonary endothelium plays a major role by regulating lung fluid balance and pulmonary edema formation. Consequently, endothelium-targeted therapies may have beneficial effects in ALI/ARDS. Recently, attention has been given to the therapeutic potential of purinergic agonists and antagonists for the treatment of cardiovascular and pulmonary diseases. Extracellular purines (adenosine, ADP, and ATP) and pyrimidines (UDP and UTP) are important signaling molecules that mediate diverse biological effects via cell-surface P2Y receptors. We previously described ATP-induced endothelial cell (EC) barrier enhancement via a complex cell signaling and hypothesized endothelial purinoreceptors activation to exert anti-inflammatory barrier-protective effects. To test this hypothesis, we used a murine model of ALI induced by intratracheal administration of endotoxin/lipopolysaccharide (LPS) and cultured pulmonary EC. The nonhydrolyzed ATP analog ATPγS (50–100 μM final blood concentration) attenuated inflammatory response with decreased accumulation of cells (48%, P < 0.01) and proteins (57%, P < 0.01) in bronchoalveolar lavage and reduced neutrophil infiltration and extravasation of Evans blue albumin dye into lung tissue. In cell culture model, ATPγS inhibited junctional permeability induced by LPS. These findings suggest that purinergic receptor stimulation exerts a protective role against ALI by preserving integrity of endothelial cell-cell junctions.
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Dube, Shataakshi, Tejasvi Matam, Jessica Yen, Henry E. Mang, Pierre C. Dagher, Takashi Hato, and Timothy A. Sutton. "Endothelial STAT3 Modulates Protective Mechanisms in a Mouse Ischemia-Reperfusion Model of Acute Kidney Injury." Journal of Immunology Research 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/4609502.
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STAT3 is a transcriptional regulator that plays an important role in coordinating inflammation and immunity. In addition, there is a growing appreciation of the role STAT3 signaling plays in response to organ injury following diverse insults. Acute kidney injury (AKI) from ischemia-reperfusion injury is a common clinical entity with devastating consequences, and the recognition that endothelial alterations contribute to kidney dysfunction in this setting is of growing interest. Consequently, we used a mouse with a genetic deletion of Stat3 restricted to the endothelium to examine the role of STAT3 signaling in the pathophysiology of ischemic AKI. In a mouse model of ischemic AKI, the loss of endothelial STAT3 signaling significantly exacerbated kidney dysfunction, morphologic injury, and proximal tubular oxidative stress. The increased severity of ischemic AKI was associated with more robust endothelial-leukocyte adhesion and increased tissue accumulation of F4/80+ macrophages. Moreover, important proximal tubular adaptive mechanisms to injury were diminished in association with decreased tissue mRNA levels of the epithelial cell survival cytokine IL-22. In aggregate, these findings suggest that the endothelial STAT3 signaling plays an important role in limiting kidney dysfunction in ischemic AKI and that selective pharmacologic activation of endothelial STAT3 signaling could serve as a potential therapeutic target.
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Gauthier, Kathryn M., David X. Zhang, Erik M. Edwards, Blythe Holmes, and William B. Campbell. "Angiotensin II Dilates Bovine Adrenal Cortical Arterioles: Role of Endothelial Nitric Oxide." Endocrinology 146, no. 8 (August 1, 2005): 3319–24. http://dx.doi.org/10.1210/en.2005-0129.
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Abstract Adrenal steroidogenesis is modulated by humoral and neuronal factors and blood flow. Angiotensin II (AII) stimulates adrenal cortical aldosterone and cortisol production and medullary catecholamine release. However, AII regulation of adrenal vascular tone has not been characterized. We examined the effect of AII on diameters of cannulated bovine adrenal cortical arteries. Cortical arteries (average internal diameter = 230 μm) were constricted with U46619 and concentration-diameter responses to AII (10−13 to 10−8 mol/liter) were measured. In endothelium-intact arteries, AII induced dilations at low concentrations (maximum dilation = 25 ± 6% at 10−10 mol/liter) and constrictions at high concentrations (maximum constriction = 25 ± 18% at 10−8 mol/liter). AII constrictions were blocked by the angiotensin type 1 (AT1) receptor antagonist, losartan (10−6 mol/liter). AII dilations were enhanced by losartan (maximal dilation = 48 ± 8%), abolished by endothelial cell removal or N-nitro-l-arginine (L-NA, 3 × 10−5 mol/liter) and inhibited by the angiotensin type 2 (AT2) receptor antagonist, PD123319 (10−6 mol/liter, maximal dilation = 18 ± 4%). In a 4,5-diaminofluorescein diacetate nitric oxide (NO) assay of isolated cortical arteries, AII stimulated NO production, which was abolished by PD123319, L-NA, or endothelial cell removal. Western immunoblot of arterial homogenates and endothelial and zona glomerulosa cell lysates revealed 48-kD and 50-kD bands corresponding to AT1 and AT2 receptors, respectively, in all three and a 140-kD band corresponding to endothelial NO synthase in endothelial cells and arteries. Our results demonstrate that AII stimulates adrenal cortical arterial dilation through endothelial cell AT2 receptor activation and NO release and AT1 receptor-dependent constriction.
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Stanojevic, Dragana, Svetlana Apostolovic, Sonja Salinger-Martinovic, Ruzica Jankovic-Tomasevic, Danijela Djordjevic-Radojkovic, Milan Pavlovic, Tomislav Kostic, Vladan Cosic, Tatjana Ristic, and Ivana Stojanovic. "Endothelin-1 and nitric oxide in 3-year prognosis after acute myocardial infarction." Vojnosanitetski pregled 74, no. 9 (2017): 862–70. http://dx.doi.org/10.2298/vsp151029278s.
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Background/Aim. Acute myocardial infarction (AMI) is an important cause of mortality/morbidity worldwide. Biomarkers improve diagnostic and prognostic accuracy in AMI. The aim of this study was to investigate an increase of markers of endothelial dysfunction in AMI, measured on the 3rd day after the initial event and to investigate their association with short- and long-term (3-year) prognosis (outcome). Methods. The prospective study included 108 patients with AMI in the experimental group and 50 apparently healthy subjects in the control group. Endothelin-1 (ET-1) and nitric oxide degradation products (NOx) were determined. Results. The average age of the participants in the experimental group was 62 ? 10 years and 59 ? 9 years in the control group; 74.1% of the patients in experimental group were males and 68.8% in the control group. In 74.1% of the patients, ST-elevation myocardial infarction (STEMI) was diagnosed, and 25.9% of the patients presented with non-ST-elevation myocardial infarction (NSTEMI). Thirteen (5.6%) patients died during 3 years and they had significantly higher ET-1 levels compared to survivors [4.02 (2.72?5.93) vs 3.06 (2.23?3.58) pg/mL; p = 0.015]. Endothelin- 1 in 46 (42.6%) patients with composite endpoint (3- year mortality and rehospitalization) was significantly increased compared to other patients [3.14 (2.54?4.41) vs 3.05 (2.18?3.56) pg/mL; p = 0.035]. Intrahospital complications were found in 41 (48%) patients. Participants with echocardiographically detected complications (ventricular dyskinesia, left ventricular thrombus and papillary muscle rupture) had higher ET-1 levels compared to other patients [4.02 (2.78?5.57) vs 3.06 (2.29?3.66) pg/mL; p = 0.012]. Endothelin- 1 concentration above the 75th percentile (> 3.77 pg/mL) was associated with the increased risk for composite endpoint [Log Rank (?2 = 13.44; p < 0.001)]. Patients who were rehospitalized had significantly lower NOx concentration [125.5 (111.4?143.6) vs 139.3 (116.79?165.2) ?mol/L; p = 0.04]. Endothelin-1 positively correlated with high sensitivity troponin I (hsTnI), brain natriuretic peptide (BNP) and a number of leukocytes. Conclusion. Endothelin- 1 and NOx were increased on the 3rd day after AMI, and they were predictors of worse short- and long-term (3- year) prognosis (outcome). Endothelin-1 positively correlated with conventional prognostic markers in AMI.
Dissertations / Theses on the topic "Endothelin Axi"
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SPINA, CECILIA. "Emerging Evidences for a Protumorigenic Role of the Endothelin Axis Uncover New Therapeutic Targets in Multiple Myeloma." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2017. http://hdl.handle.net/10281/144189.
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Multiple Myeloma (MM) is a monoclonal tumor of bone marrow (BM) plasma cell (PC), usually associated with a number of disease manifestations, including skeletal damage, anemia and immunosuppression. Despite recent therapeutic advances and an increased patient life expectancy, MM still remains an incurable malignancy.
MM PC is characterized by a strong BM niche dependence, acquiring an autonomous capacity of growth only in the latter stages of disease. The endothelin (ET) axis is mainly composed of Endothelin-1 (ET-1), and 2 G-protein coupled receptors, the ET receptor A (ETAR) and ET receptor B (ETBR). In the last decades it has been demonstrated that the ET axis is able to promote the development and progression of tumor cells in an autocrine and/or paracrine fashion. Accordingly, recent experimental and clinical data obtained in solid tumors have evidenced the possibility of interfering with ET receptors (ETRs) - via specific antagonists - for therapeutic purposes. On the basis of these premises, primary aim of this study was to assess whether the ET axis may have a protumorigenic role in MM, therefore becoming a therapeutic target. The experimental evidences we obtained demonstrated that MM cell lines, primary MM PCs and BM microenvironment cells express ET-1 transcript and release the corresponding protein. Interestingly, while ETAR was constitutively expressed by PCs from healthy donors, primary malignant PCs and MM cell lines, ETBR was detected only on malignant PCs of 54 of the 100 patients enrolled in the study and in 3/5 MM cell lines. Interestingly, B lymphocytes isolated from healthy donors BM or peripheral blood (PB) or from MM patients PB, did express ETAR but not ETBR. Based on the evidence that the expression of ETBR was strictly connected to the neoplastic transformation, we next demonstrated an altered methylation status of the ETBR promoter gene in malignant PCs from ETBR-expressing MM patients and MM cell lines. The possibility of interfering with ETRs in MM was investigated in vitro using RPMI-8226 and U266 MM cell lines through the use of ETAR and ETBR selective antagonists. Both ETAR and ETBR antagonists, used alone and/or in combination, decreased RPMI-8226 and U266 cell lines viability. Based on these data we next evaluated the potential therapeutic significance in MM of Bosentan, a dual ETRs antagonist already used in clinical practice for pulmonary arterial hypertension. In agreement with our in vitro experiments, Bosentan appeared to be effective in inhibiting the viability of RPMI-8226 and U266 cell lines by reducing p-p44/42 MAPK. Furthermore, this action appeared to be synergic to that of bortezomib, a proteasome inhibitor drug already used in first-line treatment of MM.
Overall our data demonstrate that the ET axis is a potential therapeutic target in MM. Further data are awaited in order to establish the prognostic significance of the aberrant expression of ETBR in MM.
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Adner, Mikael. "Altered expression of contractile endothelin receptors in the vascular bed." Lund : Dept. of Internal Medicine, University of Lund, 1998. http://catalog.hathitrust.org/api/volumes/oclc/39103326.html.
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Irani, Soussan. "The Endothelin Axis and Angiogenesis in Papillary Thyroid Carcinoma." Thesis, Griffith University, 2014. http://hdl.handle.net/10072/366833.
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Papillary Thyroid Cancer (PTC) is the most common thyroid cancer accounting for 80% of all cases. The prognosis is good, with 5-year survival rates of 95%, but in some cases the tumour behaves in an aggressive manner characterized by local recurrence and/or metastasis, processes contributed to by angiogenesis.
Angiogenesis is an essential physiologic activity involved in normal tissue biology and several pathologic conditions such as cardiac failure, and cancer. During carcinogenesis, tumour cells secrete pro-angiogenic factors to initiate angiogenesis. Angiogenesis also causes the migration of endothelial cells from pre-existing vessels to improve nutrient and oxygen delivery to tumours, angiogenesis has a key role in tumour growth and metastasis.
Vascular endothelial growth factor (VEGF) has a pivotal role in the control of angiogenesis, aggressiveness in thyroid cancers. The endothelins (ETs) are a family of genes inducing DNA synthesis and cellular growth in different cells, affecting vascular tone and angiogenesis. ET-1 has a direct effect on neoplastic cells by inducing cellular proliferation, migration as well as invasion and inhibition of apoptosis. ET-1 induces VEGF expression by increasing hypoxia-inducible factor-1α (HIF-1α) stimulation.Thesis (PhD Doctorate)
School of Medical Science
Griffith Health
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Rabura, Sebastian. "Bedeutung der Endothelin-Plasmakonzentration für die Effektivität von inhalativem Stickstoffmonoxid im Modell des akuten Lungenversagens." Doctoral thesis, Universitätsbibliothek Leipzig, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-137313.
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Das akute Lungenversagen ist gekennzeichnet durch eine schwere Störung des Gasaustausches mit ausgeprägter arterieller Hypoxämie. Die inhalative Gabe von Stickstoffmonoxid (iNO) erfolgt in der Therapie zur Verbesserung der arteriellen Oxygenierung, der Effekt ist jedoch variabel. Bisher existieren nur wenige Studien zur Identifikation von Faktoren, die die Effektivität von iNO bestimmen. Die positive Wirkung von iNO auf den Gasaustausch lässt eine Vasokonstriktion in beatmeten Lungenarealen vermuten. Wir untersuchten eine mögliche Wechselwirkung zwischen dem endogenen Vasokonstriktor Endothelin-1 (ET-1) und iNO in einem tierexperimentellen Modell des akuten Lungenversagens.
Sechzehn Schweine wurden narkotisiert, invasiv beatmet und nach Induktion des akuten Lungenschadens (ALI) mittels repetitiver Surfactantauswaschung (Lavagemodell nach Lachmann) zwei Gruppen zugeteilt. Die NO-Gruppe (n=8) erhielt eine Inhalation von 30ppm NO, die Kontrolltiere (CTR-Gruppe, n=8) blieben ohne weitere Intervention. Während der nächsten vier Stunden wurden Messungen von Gasaustausch und ET-1 Konzentrationen im arteriellen Blut durchgeführt. Bei allen Tieren führte die Induktion des ALI zu einer signifikanten Verschlechterung des Gasaustausches. Die Gabe von iNO bewirkte in der NO-Gruppe eine signifikante Erhöhung des PaO2. Die ET-1 Plasmaspiegel stiegen im Verlauf an und waren nach drei Stunden in der NO-Gruppe signifikant niedriger als in der CTR-Gruppe. Dabei zeigte sich eine signifikante, moderate Korrelation zwischen den ET-1 Plasmaspiegeln und den durch iNO induzierten Änderungen in PaO2 und Shunt.
Damit konnte ET-1 als ein Einflussfaktor auf die durch iNO induzierte Verbesserung des Gasaustausches identifiziert werden.
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Borrull, Aurélie. "Obtention et caractérisation d’anticorps monoclonaux dirigés contre les récepteurs des endothélines, ETAR et ETBR, surexprimés dans de nombreux cancers et impliqués dans la progression tumorale." Thesis, Paris 11, 2015. http://www.theses.fr/2015PA114820/document.
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Il est admis que l’axe endothéline (endothélines ET-1, -2 et -3 et leurs RCPG ETAR et ETBR), participe à la progression tumorale. Alors qu’ETAR est par exemple surexprimé dans le cancer de l’ovaire, ETBR l’est dans le mélanome. Cette surexpression, ainsi que l’implication d’ETA/BR dans la carcinogenèse, font de ces RCPG une cible tumorale pertinente. En raison de leurs forte spécificité, actions cytotoxiques variées, possibilités de couplage, les anticorps monoclonaux (AcM) sont des outils de choix en diagnostic et thérapie anti-cancéreuse. Cependant, on déplore actuellement l’absence d’AcM ciblant des RCPG sur le marché. Par une technique d’immunisation génique, 4 AcM anti-ETAR et 24 anti-ETBR ont été produits. Les résultats préliminaires obtenus avec les anti-ETAR sont prometteurs puisque ces AcM lient avec une haute affinité ETAR surexprimé dans des cellules CHO, l’un d’eux inhibant fortement la liaison du ligand. Mon travail de thèse s’est cependant concentré sur la caractérisation d’un anti-ETBR. Cet AcM reconnaît de façon spécifique et avec une forte affinité la conformation native d’ETBR surexprimé à la surface de cellules de mélanomes, suggérant l’existence d’une forme tumorale du récepteur. Suite à sa liaison aux cellules UACC-257 (lignée de mélanome), l’AcM se trouve internalisé. Dans ces cellules, malgré son incapacité à inhiber la liaison de l’ET, cet AcM inhibe l’activation de la voie PLC induite par le ligand et est également un fort inhibiteur de la migration due à l’activation de l’axe endothéline. Ces travaux soulignent l’intérêt de cet AcM comme outil diagnostique et thérapeutique dans le cas du mélanomeIt has been admitted that endothelin axis (endothelins ET-1, -2 and -3 and related GPCRs ETAR and ETBR) is involved in tumor progression. For instance, while ETAR is overexpressed in ovarian cancer, ETBR is in melanoma. This overexpression, as well as ETA/BR involvement in carcinogenesis, make these GPCRs a relevant tumor target. Because of their high specificity, various cytotoxic actions, possibilities of coupling, the monoclonal antibodies (mAbs) are useful tools in diagnosis and anti-cancer therapy. However, the absence of mAbs targeting GPCRs on the market is regrettable. Thanks to DNA immunization, 4 anti-ETAR mAbs and 24 anti-ETBR mAbs were produced. Preliminary results obtained with anti-ETAR are promising since these mAbs bind ETAR overexpressed in CHO cells with high affinity, one of them being a potent inhibitor of ligand binding. However, the aim of my PhD research works focused on the characterization of one anti-ETBR. This mAb specifically recognizes with high affinity the native conformation of ETBR overexpressed on the surface of melanoma cells, suggesting the existence of a tumor-specific receptor. Following its binding on UACC-257 cells (melanoma cell line), the mAb is internalized. In these cells, despite its inability to inhibit ET binding, this mAb is able to inhibit the ligand-induced activation of PLC pathway and display a potent inhibition of endothelin axis-induced migration. This work highlights the interest of this mAb as a tool for diagnosis and therapy in melanoma
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Allard, Bertrand. "Production et caractérisation d’anticorps polyclonaux et monoclonaux ciblant les récepteurs des endothélines en vue d’une immunothérapie des cancers." Thesis, Paris 11, 2012. http://www.theses.fr/2012PA114803/document.
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Le développement des anticorps monoclonaux thérapeutiques est en plein essor notamment à cause de leur bénéfice important pour le traitement des cancers. Cependant, à l’heure actuelle, aucun anticorps monoclonal sur le marché ou en phase III ne cible de RCPGs, en dépit de l’implication grandissante de ces récepteurs dans la carcinogenèse. Parmi les RCPGs les plus pertinents pour l’oncologie, souvent cités dans la littérature et dont certains inhibiteurs chimiques sont en phase clinique avancée, on trouve les deux sous-types de récepteurs des endothélines ETAR et ETBR. Dans ce contexte, mon projet de thèse a consisté à produire des anticorps monoclonaux capables de lier spécifiquement les récepteurs des endothélines, puis à les caractériser dans le but d’évaluer leur potentiel antitumoral. Grâce à une stratégie d’immunisation génique, un ensemble de 27 anticorps monoclonaux, tous spécifiques de la forme native d’ETBR, a été obtenu. Un de ces anticorps, nommé rendomab-B1, a fait l’objet d’une caractérisation précise et s’est révélé être un puissant inhibiteur allostérique d’ETBR. De plus, cette propriété antagoniste a permis de bloquer l’action autocrine antiapoptotique de l’ET-1 sur des cellules endothéliales vasculaires, suggérant ainsi que le rendomab-B1 pourrait être utilisé comme agent thérapeutique afin d’inhiber les effets tumorigènes liés à la suractivation de l’axe ET1/ETBR au niveau de l’endothélium vasculaire tumoral. Par ailleurs, le rendomab-B1 a également été testé sur des lignées de mélanomes humains ; l’absence de fixation de l’anticorps malgré la présence de récepteurs ETB fonctionnels à la surface de ces cellules suggère l’existence d’une forme moléculaire atypique du récepteur, potentiellement spécifique aux mélanomes. A la lumière de ces résultats, le rendomab-B1 apparaît comme un outil prometteur, à la fois pour l’étude structurale et fonctionnelle d’ETBR, mais aussi pour une éventuelle thérapie anticancéreuse. Enfin, les 26 autres anticorps monoclonaux anti-ETBR, actuellement en cours de caractérisation, constituent également des molécules potentiellement intéressantes pour un usage fondamental ou thérapeutique impliquant ETBR. Pour conclure, ces travaux ont démontré l’intérêt de la méthode d’immunisation génique pour la production d’anticorps monoclonaux anti-RCPGs à visée thérapeutiqueFor a decade, monoclonal antibodies have become increasingly important for the biotherapeutic management of cancer. However, none of the monoclonal antibodies currently on the market or in late stage clinical trial do target a G-protein coupled receptor in spite of the emerging role of these receptors in tumor progression. Among the therapeutically relevant GPCRs for oncology, the endothelin receptors (ETAR and ETBR) are particularly attractive considering their overexpression in a wide range of tumors and their involvement in various stages of tumorigenesis. In this context, my PhD project consisted in producing and characterizing monoclonal antibodies directed against endothelin receptors with a view to use them as anti-tumor agents. Using an original DNA immunization strategy, we produced a panel of 27 monoclonal antibodies which selectively recognized ETBR expressed at the surface of transfected cells. One of these antibodies, named rendomab-B1, was extensively characterized and proved to be a potent allosteric antagonist of ETBR. Moreover, rendomab-B1 was able to disrupt the autocrine ET1-mediated survival loop on vascular endothelial cells, suggesting that this antibody could be used to prevent the pro-tumorigenic effect due to ET-1 and ETBR upregulation in the tumor-surrounding endothelium. Furthermore, rendomab-B1 binding onto ETBR was also assessed on melanoma cell lines and revealed that a tumor-specific form of ETBR may exist, as illustrated by the poor fixation of rendomab-B1 on these cells in spite of the presence of functional ETB receptors. Together, these results present rendomab-B1 as promising agent, not only for the structural and functional study of ETBR, but also for its therapeutic modulation in the case of cancer for instance. Finally, the other 26 monoclonal antibodies, whose characterization is still ongoing, also constitute potential tools for fundamental or therapeutic applications involving ETBR. To conclude, this work has highlighted the relevance of the DNA immunization approach to generate monoclonal antibodies against the native form of GPCRs
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Miyoshi, Takashi. "The role of endothelial interleukin-8/NADPH oxidase 1 axis in sepsis." Kyoto University, 2011. http://hdl.handle.net/2433/142065.
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Sax, Michael John. "The CCL5-CCR5 Axis in Breast Cancer." Thesis, Griffith University, 2015. http://hdl.handle.net/10072/365646.
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Cancer is one of the leading underlying causes of death worldwide. Despite decades of research, cancer is predicted to be the leading cause of death by the year 2020. Anti angiogenic therapies that target the key signalling molecule, vascular endothelial growth factor (VEGF) have shown promise in the treatment of some solid tumours, resulting in increased progression-free survival times in patients. However, there are several significant problems with current anti-angiogenic therapies, such as the phenomenon of resistance. Tumours can be divided into those that are intrinsically nonresponsive to therapy, and those that do respond. However, for those tumours that do respond to therapy, an initial positive response (tumour regression) is followed by tumour re-vascularisation and rapid relapse. Secondly, anti-angiogenic therapies target normal physiological processes, including vascular homeostasis, wound healing and the immune system, leading to a range of potentially negative side effects, including death. Thus unravelling the biology of angiogenesis and developing new drug targets is a priority of current research. The C-C chemokine receptor 5 (CCR5) has been the subject of extensive research in the last few years. This is primarily because of its association with the pathology of disease, viral infection, and the immune response. However, while the main ligand for CCR5, C C chemokine ligand 5 (CCL5) is known to be upregulated in malignant breast cancer, little has been done to unravel the CCL5-CCR5 axis in breast cancer and its potential role as a driver of malignancy. Furthermore, while experimental evidence, including data from CCR5 knockout mouse, suggests a role for CCL5-CCR5 in neovascularisation, little has been done to study the potential role of CCL5-CCR5 in tumour angiogenesis, as well as implications CCL5-CCR5 signalling may have on clinical course in breast cancer.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Griffith Health
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Fang, Jennifer S., Brian G. Coon, Noelle Gillis, Zehua Chen, Jingyao Qiu, Thomas W. Chittenden, Janis M. Burt, Martin A. Schwartz, and Karen K. Hirschi. "Shear-induced Notch-Cx37-p27 axis arrests endothelial cell cycle to enable arterial specification." NATURE PUBLISHING GROUP, 2017. http://hdl.handle.net/10150/626459.
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Establishment of a functional vascular network is rate-limiting in embryonic development, tissue repair and engineering. During blood vessel formation, newly generated endothelial cells rapidly expand into primitive plexi that undergo vascular remodeling into circulatory networks, requiring coordinated growth inhibition and arterial-venous specification. Whether the mechanisms controlling endothelial cell cycle arrest and acquisition of specialized phenotypes are interdependent is unknown. Here we demonstrate that fluid shear stress, at arterial flow magnitudes, maximally activates NOTCH signaling, which upregulates GJA4 (commonly, Cx37) and downstream cell cycle inhibitor CDKN1B (p27). Blockade of any of these steps causes hyperproliferation and loss of arterial specification. Re-expression of GJA4 or CDKN1B, or chemical cell cycle inhibition, restores endothelial growth control and arterial gene expression. Thus, we elucidate a mechanochemical pathway in which arterial shear activates a NOTCH-GJA4-CDKN1B axis that promotes endothelial cell cycle arrest to enable arterial gene expression. These insights will guide vascular regeneration and engineering.
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Lindberg, Lars. "Endothelial function during ischemia-reperfusion and effects of inhalation of nitric oxide." Lund : Dept. of Anesthesiology and Intensive Care, University of Lund, 1996. http://catalog.hathitrust.org/api/volumes/oclc/38164585.html.
Full textBooks on the topic "Endothelin Axi"
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McAuley, Danny F., and Thelma Rose Craig. Measurement of extravascular lung water in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0140.
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The accumulation of fluid in the interstitium and alveolar space is known as extravascular lung water (EVLW). EVLW is associated with increased morbidity and mortality in critically ill patients and is elevated in patients with cardiogenic pulmonary oedema, acute lung injury (ALI), and the acute respiratory distress syndrome (ARDS). Pulmonary oedema is a consequence of increased pulmonary capillary hydrostatic pressure and/or an increased capillary permeability. The quantity of pulmonary oedema fluid is dependent on the balance of fluid formation and clearance, and this contributes to the overall dynamic net lung fluid balance. Measurement of EVLW is therefore an indirect surrogate measurement of the alveolar epithelial and endothelial damage in ALI/ARDS. The single indicator transpulmonary thermodilution technique is an available bedside technique to measure EVLW.
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Goligorsky, Michael S., Julien Maizel, Radovan Vasko, May M. Rabadi, and Brian B. Ratliff. Pathophysiology of acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0221.
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In the intricate maze of proposed mechanisms, modifiers, modulators, and sensitizers for acute kidney injury (AKI) and diverse causes inducing it, this chapter focuses on several common and undisputable strands which do exist.Structurally, the loss of the brush border, desquamation of tubular epithelial cells, and obstruction of the tubular lumen are commonly observed, albeit to various degrees. These morphologic hallmarks of AKI are accompanied by functional defects, most consistently reflected in the decreased glomerular filtration rate and variable degree of reduction in renal blood flow, accompanied by changes in the microcirculation. Although all renal resident cells participate in AKI, the brunt falls on the epithelial and endothelial cells, the fact that underlies the development of tubular epithelial and vascular compromise.This chapter further summarizes the involvement of several cell organelles in AKI: mitochondrial involvement in perturbed energy metabolism, lysosomal involvement in degradation of misfolded proteins and damaged organelles, and peroxisomal involvement in the regulation of oxidative stress and metabolism, all of which become defective. Common molecular pathways are engaged in cellular stress response and their roles in cell death or survival. The diverse families of nephrotoxic medications and the respective mechanisms they induce AKI are discussed. The mechanisms of action of some nephrotoxins are analysed, and also of the preventive therapies of ischaemic or pharmacologic pre-conditioning.An emerging concept of the systemic inflammatory response triggered by AKI, which can potentially aggravate the local injury or tend to facilitate the repair of the kidney, is presented. Rational therapeutic strategies should be based on these well-established pathophysiological hallmarks of AKI.
Book chapters on the topic "Endothelin Axi"
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Gordon, John. "1992 NATO ASI Conference on “Vascular Endothelium: Physiological Basis of Clinical Problems II”." In Vascular Endothelium, 147–49. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2437-3_14.
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Becker, Richard C., and Frederick A. Spencer. "Vascular Biology, Thromboresistance, and Inflammation." In Fibrinolytic and Antithrombotic Therapy. Oxford University Press, 2006. http://dx.doi.org/10.1093/oso/9780195155648.003.0006.
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The delivery of vital substrate to metabolically active tissues and vital organs is achieved and maintained by the cardiovascular system including the heart, macrovasculature, and microvasculature. This life-sustaining process requires a normally functioning vascular endothelium—a multifunctional organ system composed of physiologically responsive cells responsible for vasomotion (vascular tone), thromboresistance, and inflammoresistance. Simply by virtue of its anatomic location, the vascular endothelium is functionally complex. It defines the intra- and extravascular components, serves as a selectively permeable barrier, and provides a continuous lining to the cardiovascular system. The location of the vascular endothelium is vital to its biologic interactions with cells found within the circulation and to the vessel wall itself. The surface activity is augmented in the microcirculation, also known as the resistance bed, where the ratio of endothelial surface to circulating blood is maximal. In most vertebrates, vascular endothelial cells form a single layer of squamous lining cells (0.1–0.5 μm in thickness) joined by intercellular junctions. The cells themselves are polygonal (varying between 10 and 50 μm) and are positioned in the long axis of the vessel, orienting the cellular longitudinal dimension in the direction of blood flow. The endothelial cell has three surfaces: luminal (nonthrombogenic), subluminal (adhesive), and cohesive. The luminal surface is devoid of electron-dense connective tissue. It does, however, possess an exterior coat (or glycocalyx), consisting primarily of starches and proteins secreted by the endothelial cells. Plasma proteins, including lipoprotein lipase, α2-macroglobulin, heparin cofactor II, antithrombin, and albumin, as well as small amounts of fibrinogen and fibrin are adsorbed to the luminal surface. The surface membrane itself adds significantly to thromboresistance by carrying a negative charge that repels similarly charged circulating blood cells. The subluminal (or abluminal) surface adheres to subendothelial connective tissues. Small processes penetrate through a series of internal layers to form myoendothelial junctions with subjacent smooth muscle cells. The cohesive component of the vascular endothelium connects individual endothelial cells to one another by cell junctions of two basic types: occluding (tight) junctions and communicating (gap) junctions. Occluding junctions represent a physical link between adjacent cells, sealing the intercellular space.
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Setyawati, Titik, Ricky Aditya, and Tinni Trihartini Maskoen. "Sepsis Associated Acute Kidney Injury." In Infectious Diseases and Sepsis [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97609.
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AKI is a syndrome consisting of several clinical conditions, due to sudden kidney dysfunction. Sepsis and septic shock are the causes of AKI and are known as Sepsis-Associated AKI (SA-AKI) and accounted for more than 50% of cases of AKI in the ICU, with poor prognosis. Acute Kidney Injury (AKI) is characterized by a sudden decline in kidney function for several hours/day, which results in the accumulation of creatinine, urea and other waste products. The most recent definition was formulated in the Kidney Disease consensus: Improving Global Outcome (KDIGO), published in 2012, where the AKI was established if the patient’s current clinical manifestation met several criteria: an increase in serum creatinine levels ≥0.3 mg/dL (26.5 μmol/L) within 48 hours, an increase in serum creatinine for at least 1.5 times the baseline value within the previous 7 days; or urine volume ≤ 0.5 ml/kg body weight for 6 hours. The AKI pathophysiology includes ischemic vasodilation, endothelial leakage, necrosis in nephrons and microtrombus in capillaries. The management of sepsis associated with AKI consisted of fluid therapy, vasopressors, antibiotics and nephrotoxic substances, Renal Replacement Therapy (RRT) and diuretics. In the analysis of the BEST Kidney trial subgroup, the likelihood of hospital death was 50% higher in AKI sepsis compared to non-sepsis AKI. Understanding of sepsis and endotoxins that can cause SA-AKI is not yet fully known. Some evidence suggests that renal microcirculation hypoperfusion, lack of energy for cells, mitochondrial dysfunction, endothelial injury and cycle cell arrest can cause SA-AKI. Rapid identification of SA-AKI events, antibiotics and appropriate fluid therapy are crucial in the management of SA-AKI.
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Ghosh, Samit. "Kidney Injuries in Sickle Cell Disease." In Sickle Cell Disease [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.102839.
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Sickle cell disease (SCD), characterized by the presence of unstable sickle hemoglobin in the homozygous state (HbSS), results in progressive organ damage and early mortality with the median age of death in the 40s. The kidney is one of the most severely affected organs in SCD. Kidney diseases gradually develop in individuals with SCD. Microalbuminuria is evident in childhood, progressing to apparent proteinuria, deteriorating glomerular filtration rate (GFR) in early adulthood. While CKD becomes prevalent in adults. Moreover, among SCD patients, exacerbation of anemia is an independent risk factor for acute kidney injury (AKI) which is a predisposing factor for CKD and End Stage Renal Diseases (ESRD), altogether contributing to 16–18% mortality among this patients’ population. The pathogenesis of renal diseases in SCD is not completely understood. While epidemiological studies have shown a strong association between rate of hemolysis, severity of anemia and CKD, intrinsic inflammatory, oxidative and hypercoagulative stress that contribute to the characteristic endothelial dysfunction also promotes development of renal diseases in SCD. This chapter will elaborately discuss current research on the pathogenesis of AKI, AKI-to-CKD transition and future research perspectives for development of novel therapeutic strategies.
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B. Oien, Derek, Jeremy Chien, Julian Molina, and Viji Shridhar. "Emerging Drug Therapies for Mesothelioma." In Mesothelioma. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.91752.
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The systemic chemotherapy combination of cisplatin and pemetrexed has been the mesothelioma standard of care for well over a decade. This regimen has only achieved a disappointing overall median survival of about 1 year. Improved survival has been reported when systemic chemotherapy is combined with surgery and radiotherapy, and for using localized chemotherapy in some cases. The choice of mesothelioma treatment often depends on the anatomical location, histologic subtype, and disease progression. Several experimental drugs have also been investigated in mesothelioma, often with limited positive results that maintain the reputation of mesothelioma as a graveyard for drug development. This chapter will review the use of drug treatment in mesothelioma and highlight emerging experimental drug therapies in clinical trials. Experimental drugs for mesothelioma include inhibitors for checkpoints, epidermal growth factor, AXL, focal adhesion kinase, vascular endothelial growth factor, poly-ADP-ribose-polymerase, and hippo signaling.
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Vicinanza, Roberto, Giuseppe Coppotelli, Carolina Malacrino, Tiziana Nardo, Barbara Buchetti, Luisa Lenti, Francesco Saverio Celi, and Susanna Scarpa. "Role of LDL Oxidation on Non-Genomic Thyroid Hormone Action in Human Endothelial Cells." In BASIC - Hypothalamic-Pituitary-Thyroid Axis: Thyroid Hormone Metabolism, Cellular Uptake & Action, P1–664—P1–664. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part2.p16.p1-664.
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Sharma, Yogita, Neeraj Kumar, and Devyani Thakur. "Interleukin 6 in Patients with Rheumatoid Arthritis." In Interleukins - The Immune and Non-Immune Systems’ Related Cytokines. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96887.
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Rheumatoid Arthritis is a widespread disease causing varying degrees of disability. It is characterised by flares and remissions and since ancient times, every culture has tried to get the better of it. Even now, research is aimed at finding novel serum biomarkers as surrogates for disease activity and newer targets to sharpen therapy. One such target is IL-6.It mediates neutrophil migration, osteoclast maturation and pannus formation through vascular endothelial growth factor (VEGF) stimulation causing synovitis and joint destruction.IL-6 leads to various systemic manifestations like hepcidin production causing anemia hypothalamo-pituitary–adrenal (HPA) axis activation causing fatigue and mood changes and osteoclast activation causes osteoporosis while increase in acute phase reactants (ESR and CRP). The literature we reviewed and our research, enrolling 40 patients of RA as well describes the role of IL-6 in pathogenesis and various manifestations of RA including articular, extra-articular and other comorbid states. It supports that Serum IL-6 levels correlate with disease activity (DAS-28ESR and BRAF-MDQ) and that IL-6 remains a viable target for drug therapy.
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Li, Sinian, Yiming Shao, Kanglan Li, Changmei HuangFu, Wenjie Wang, Zhou Liu, Zhiyou Cai, and Bin Zhao. "Vascular Cognitive Impairment and the Gut Microbiota." In Advances in Alzheimer’s Disease. IOS Press, 2022. http://dx.doi.org/10.3233/aiad220026.
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Vascular cognitive impairment (VCI), the second most common cause of dementia in elderly people, is a term that refers to all forms of cognitive disorders that can be attributed to cerebrovascular disease such as manifestations of discrete infarctions, brain hemorrhages, and white matter lesions. The gut microbiota (GM) has emerged recently as an essential player in the development of VCI. The GM may affect the brain’s physiological, behavioral, and cognitive functions through the brain-gut axis via neural, immune, endocrine, and metabolic pathways. Therefore, microbiota dysbiosis may mediate or affect atherosclerosis, cerebrovascular disease, and endothelial dysfunction, which are the predominant risk factors for VCI. Moreover, the composition of the GM includes the bacterial component lipopolysaccharides and their metabolic products including trimethylamine-N-oxide and short-chain fatty acids. These products may increase the permeability of the intestinal epithelium, leading to systemic immune responses, low-grade inflammation, and altered signaling pathways that are associated with the pathogenesis of VCI. In this review, we discuss the proposed mechanisms of the GM in the maintenance of VCI and how it is implicated in acquired metabolic diseases, particularly in VCI regulation.
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Fairley, Andrea, Christopher J. Stewart, Aedín Cassidy, Jayne V. Woodside, and Claire T. McEvoy. "Diet Patterns, the Gut Microbiome, and Alzheimer’s Disease." In Advances in Alzheimer’s Disease. IOS Press, 2022. http://dx.doi.org/10.3233/aiad220011.
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Given the complex bidirectional communication system that exists between the gut microbiome and the brain, there is growing interest in the gut microbiome as a novel and potentially modifiable risk factor for Alzheimer’s disease (AD). Gut dysbiosis has been implicated in the pathogenesis and progression of AD by initiating and prolonging neuroinflammatory processes. The metabolites of gut microbiota appear to be critical in the mechanism of the gut-brain axis. Gut microbiota metabolites, such as trimethylamine-n-oxide, lipopolysaccharide, and short chain fatty acids, are suggested to mediate systemic inflammation and intracerebral amyloidosis via endothelial dysfunction. Emerging data suggest that the fungal microbiota (mycobiome) may also influence AD pathology. Importantly, 60% of variation in the gut microbiome is attributable to diet, therefore modulating the gut microbiome through dietary means could be an effective approach to reduce AD risk. Given that people do not eat isolated nutrients and instead consume a diverse range of foods and combinations of nutrients that are likely to be interactive, studying the effects of whole diets provides the opportunity to account for the interactions between different nutrients. Thus, dietary patterns may be more predictive of a real-life effect on gut microbiome and AD risk than foods or nutrients in isolation. Accumulating evidence from experimental and animal studies also show potential effects of gut microbiome on AD pathogenesis. However, data from human dietary interventions are lacking. Well-designed intervention studies are needed in diverse populations to determine the influence of diet on gut microbiome and inform the development of effective dietary strategies for prevention of AD.
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Wang, Nan. "Tube Shunt Related Complications of the Cornea." In Complications of Glaucoma Surgery. Oxford University Press, 2013. http://dx.doi.org/10.1093/oso/9780195382365.003.0065.
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Tube shunts can be placed in the anterior chamber, the ciliary sulcus, or the pars plana. However, if the eye is phakic, the choice is limited to the anterior chamber; ciliary sulcus placement is likely to result in cataract formation, and pars plana placement will likely complicate removal of the cataract that will likely develop. Most corneal complications of tube shunt surgery result from tubes that are too anterior. Loss of vision may result due to these complications. If the tube is inadvertently inserted too close to the cornea, a loss of endothelial cells will result in edema and require transplantation to restore vision. Reported rates of corneal complications range from 2% to 33% and consist mostly of corneal edema/decompensation and corneal graft failure. In a cohort of patients implanted with the Ahmed™ Glaucoma Valve (New World Medical, Inc., Rancho Cucamonga, California), postoperative corneal abrasions occurred in 5 of 60 (8%) eyes. Another study reported the rate of corneal drying/dellen later in the postoperative course (8 of 59 eyes; 13.6%). Contact between the tube and the cornea has been noted at a rate of up to 5%. As the rate of tube shunt implantation has increased, the incidence of corneal edema in patients with tube shunts has also increased. Some of these cases develop corneal opacification with decreased vision and may require corneal transplantation to clear the visual axis. One large study of patients with Ahmed tube shunts (159 eyes total) reported corneal graft failure resulting in repeat penetrating keratoplasty (PKP) in 11 of 31 (35%) eyes with corneal grafts. Improper anterior chamber tube entry may damage the cornea. If the entry angle is not parallel to the iris and aims anteriorly, the needle used to create the tunnel may tear or detach Descemet’s membrane. Entry through the cornea (rather than the sclera) may also predispose to epithelial downgrowth or tube extrusion. To avoid such a complication, fullthickness entry into the anterior chamber should be as far posterior as possible.
Conference papers on the topic "Endothelin Axi"
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Kim, Mark S., Hyun Jin Choi, Ho-Jeong Lee, Junqin He, Qiuyu We, Robert R. Langley, Sin-Jin Kim, and Isaiah J. Fidler. "Abstract 5463: Role of the endothelin axis in astrocyte and endothelial cell mediated chemoprotection of cancer cells." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-5463.
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Said, Neveen A., and Dan Theodorescu. "Abstract 2280: Endothelin axis in bladder cancer metastasis." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-2280.
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Gupta, Suprit, Satyanarayana Rachagani, Sushil Kumar, Kavita Mallya, Surinder Kumar Batra, and Maneesh Jain. "Abstract 4191: Alterations in endothelin axis during pancreatic acinar to ductal metaplasia." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-4191.
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Bhagwani, A. R., M. Ali, E. A. Goncharova, and L. Farkas. "Endothelial Loss of P53 Promotes Endothelial Dysfunction via Impaired TLR3-BMP Axis in Pulmonary Arterial Hypertension." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a3652.
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Rizzi, Simone C., Charlotte Mermier, Sophie Crettaz, Valeria Blumer-Nesca, and Céline Gandar. "Abstract 5098: In vitro designer microenvironments for modeling the endothelin axis in brain cancer." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-5098.
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Yu, Hyun Kyung, Ho Jeong Lee, Fahao Zhang, Qiuyu Wu, Isaiah J. Fidler, and Sun Jin Kim. "Abstract 2943: Hypoxia induced resistance to chemotherapy is regulated by the endothelin receptor axis." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2943.
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Gupta, Suprit, Satyanarayana Rachagani, Sushil Kumar, Surinder Kumar Batra, and Maneesh Jain. "Abstract 2691: Cigarette smoke induced upregulation of endothelin axis in the initiation of pancreatic cancer." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2691.
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Kim, Seung Wook, Sun Jin Kim, Hyun Jin Choi, Ho-Jeong Lee, Junqin He, Qiuyu Wu, Erica J. Lawson, and Isaiah J. Fidler. "Abstract 4951: The role of endothelin axis signaling pathway in astrocyte mediated chemoprotection of tumor cells." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-4951.
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Lou, Jian, Songmin Ying, Zhihua Chen, Wen Li, Daxin Chen, Anthony Dorling, and Huahao Shen. "Late Breaking Abstract - Endothelial Cell-Specific Anticoagulation Reduces Inflammation in a Mouse Model of ALI." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa338.
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Ichihara, A., T. Toyama, T. Kudryashova, S. Lenna, A. Looney, Y. Shen, T. Avolio, et al. "Endothelial GATA6 Coordinates Cross-Talk Between BMP and Oxidative Stress Axis in Pulmonary Arterial Hypertension." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a6363.
Full textReports on the topic "Endothelin Axi"
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Wolfenson, David, William W. Thatcher, and James E. Kinder. Regulation of LH Secretion in the Periovulatory Period as a Strategy to Enhance Ovarian Function and Fertility in Dairy and Beef Cows. United States Department of Agriculture, December 2003. http://dx.doi.org/10.32747/2003.7586458.bard.
Full textAbstract:
The general research objective was to increase herd pregnancy rates by enhancing corpus luteum (CL) function and optimizing follicle development, in order to increase conception rate and embryo survival. The specific objectives were: to determine the effect of the duration of the preovulatory LH surge on CL function; to determine the function of LH during the postovulatory period on CL development; to optimize CL differentiation and follicle development by means of a biodegradable GnRH implant; to test whether optimization of CL development and follicle dynamics in timed- insemination protocols would improve fertility in high-yielding dairy cows. Low fertility in cattle results in losses of hundreds of millions of dollars in the USA and Israel. Two major causes of low fertility are formation of a functionally impaired CL, and subsequent enhanced ovarian follicle development. A functionally impaired CL may result from suboptimal LH secretion. The two major causes of low fertility in dairy cattle in US and Israel are negative energy status and summer heat stress; in both situations, low fertility is associated with reductions in LH secretion and impaired development of the ovulatory follicle and of the CL. In Florida, the use of 450-mg deslorelin (GnRH analogue) implants to induce ovulation, under the Ovsynch protocol resulted in a higher pregnancy rates than use of 750-mg implants, and pregnancy losses tended to decrease compared to controls, due probably to decrease in follicular development and estradiol secretion at the time of conceptus signaling to maintain the CL. An alternative strategy to enhance progesterone concentrations involved induction of an accessory CL by injection of hCG on day 5 after the cows were inseminated. Treatment with hCG resulted in 86% of the cows having two CLs, compared with 23% of the control cows. Conception rates were higher among the hCG-treated cows than among the controls. Another approach was to replace the second injection of GnRH analogue, in a timed-insemination protocol, with estradiol cypionate (ECP) injected 24 h after the injection of PGF₂ₐ Pregnancy rates were comparable with those obtained under the regular Ovsynch (timed- AI) program. Use of ECP induced estrus, and cows inseminated at detected estrus are indeed more fertile than those not in estrus at the time of insemination. Collectively, the BARD-supported programs at the University of Florida have improved timed insemination programs. In Ohio, the importance of the frequency of LH episodes during the early stages of the estrous cycle of cattle, when the corpus luteum is developing, was studied in an in vivo experiment in which cows were subjected to various episodic exposures to exogenous bovine LH. Results indicate that the frequent LH episodes immediately following the time of ovulation are important in development of the corpus luteum, from the points of view of both size and functionality. In another study, rates of cell proliferation and numbers of endothelial cells were examined in vitro in CLs collected from cows that received post-ovulation pulsatile LH treatment at various frequencies. The results indicate that the corpora lutea growth that results from luteal cell proliferation is enhanced by the episodes of LH release that occur immediately after the time of ovulation in cattle. The results also show that luteal endothelial cell numbers did not differ among cows treated with different LH doses. In Israel. a longer duration of the preovulatory LH surge stimulated the steroidogenic capacity of granulosa-derived luteal cells, and might, thereby, contribute to a higher progesterone output from the bovine corpus luteum. In an in vivo study, a subgroup of high-yielding dairy cows with extended estrus to ovulation interval was identified. Associated with this extended interval were: low plasma progesterone and estradiol concentrations and a low preovulatory LH surge prior to ovulation, as well as low post- ovulation progesterone concentration. In experiments based on the above results, we found that injection of GnRH at the onset of estrus increased the LHpeak, prevented late ovulation, decreased the variability between cows and elicited high and uniform progesterone levels after ovulation. GnRH at estrus onset increased conception rates, especially in the summer, and among primiparous cows and those with low body condition. Another study compared ovarian functions in multiparous lactating cows with those in nulliparous non-lactating heifers. The results revealed differences in ovarian follicular dynamics, and in plasma concentrations of steroids and gonadotropins that may account for the differences in fertility between heifers and cows.