Relevant bibliographies by topics / S-NO-HSA

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Academic literature on the topic 'S-NO-HSA'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "S-NO-HSA"

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Tsiountsioura, Melina, Gerhard Cvirn, Axel Schlagenhauf, Harald Haidl, Kathrin Zischmeier, Nicole Janschitz, Martin Koestenberger, et al. "The Antiplatelet Action of S-Nitroso Human Serum Albumin in Whole Blood." Biomedicines 10, no. 3 (March 11, 2022): 649. http://dx.doi.org/10.3390/biomedicines10030649.

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Nitric oxide donors (NO-donors) have been shown to have therapeutic potential (e.g., ischemia/reperfusion injury). However, due to their release rate/antiplatelet properties, they may cause bleeding in patients. We therefore studied the antiplatelet effects of the two different NO-donors, i.e., S-NO-Human Serum Albumin (S-NO-HSA) and Diethylammonium (Z)-1-(N,N-diethylamino)diazen-1-ium-1,2-diolate (DEA-NONOate) in whole blood (WB) samples. WB samples were spiked with S-NO-HSA or DEA-NONOate (100 µmol/L or 200 µmol/L), and the NO release rate (nitrite/nitrate levels via HPLC) and antiplatelet efficacy (impedance aggregometry, platelet function analyzer, Cone-and-platelet analyzer, thrombelastometry) were assessed. S-NO-HSA had a significantly lower NO release compared to equimolar concentrations of DEA-NONOate. Virtually no antiplatelet action of S-NO-HSA was observed in WB samples, whereas DEA-NONOate significantly attenuated platelet function in WB. Impedance aggregometry measurements revealed that Amplitudes (slope: −0.04022 ± 0.01045 ohm/µmol/L, p = 0.008) and Lag times (slope: 0.6389 ± 0.2075 s/µmol/L, p = 0.0051) were dose-dependently decreased and prolonged by DEA-NONOate. Closure times (Cone-and-platelet analyzer) were dose-dependently prolonged (slope: 0.3738 ± 0.1403 s/µmol/L, p = 0.0174 with collagen/ADP coating; slope: −0.5340 ± 0.1473 s/µmol/L, p = 0.0019 with collagen/epinephrine coating) by DEA-NONOate. These results in WB further support the pharmacological potential of S-NO-HSA as an NO-donor due to its ability to presumably prevent bleeding events even at high concentrations up to 200 µmol/L.
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Jakubovics, Nicholas S., Steven W. Kerrigan, Angela H. Nobbs, Nicklas Strömberg, Craig J. van Dolleweerd, Dermot M. Cox, Charles G. Kelly, and Howard F. Jenkinson. "Functions of Cell Surface-Anchored Antigen I/II Family and Hsa Polypeptides in Interactions of Streptococcus gordonii with Host Receptors." Infection and Immunity 73, no. 10 (October 2005): 6629–38. http://dx.doi.org/10.1128/iai.73.10.6629-6638.2005.

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ABSTRACT Streptococcus gordonii colonizes multiple sites within the human oral cavity. This colonization depends upon the initial interactions of streptococcal adhesins with host receptors. The adhesins that bind salivary agglutinin glycoprotein (gp340) and human cell surface receptors include the antigen I/II (AgI/II) family polypeptides SspA and SspB and a sialic acid-binding surface protein designated Hsa or GspB. In this study we determined the relative functions of the AgI/II polypeptides and Hsa in interactions of S. gordonii DL1 (Challis) with host receptors. For an isogenic mutant with the sspA and sspB genes deleted the levels of adhesion to surface-immobilized gp340 were reduced 40%, while deletion of the hsa gene alone resulted in >80% inhibition of bacterial cell adhesion to gp340. Adhesion of S. gordonii DL1 cells to gp340 was sialidase sensitive, verifying that Hsa has a major role in mediating sialic acid-specific adhesion to gp340. Conversely, aggregation of S. gordonii cells by fluid-phase gp340 was not affected by deletion of hsa but was eliminated by deletion of the sspA and sspB genes. Deletion of the AgI/II polypeptide genes had no measurable effect on hsa mRNA levels or Hsa surface protein expression, and deletion of hsa did not affect AgI/II polypeptide expression. Further analysis of mutant phenotypes showed that the Hsa and AgI/II proteins mediated adhesion of S. gordonii DL1 to human HEp-2 epithelial cells. Hsa was also a principal streptococcal cell surface component promoting adhesion of human platelets to immobilized streptococci, but Hsa and AgI/II polypeptides acted in concert in mediating streptococcal cell-platelet aggregation. The results suggest that Hsa directs primary adhesion events for S. gordonii DL1 (Challis) with immobilized gp340, epithelial cells, and platelets. AgI/II polypeptides direct gp340-mediated aggregation, facilitate multimodal interactions necessary for platelet aggregation, and modulate S. gordonii-host engagements into biologically productive phenomena.
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Nakajima, G., K. Uchida, K. Hayashi, Y. Xi, K. Takasaki, and J. Ju. "Non-coding microRNA hsa-let-7g as a novel chemoresponse biomarker for S-1 in colon cancer." Journal of Clinical Oncology 24, no. 18_suppl (June 20, 2006): 13513. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.13513.

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13513 Background: MicroRNAs (miRNAs) are small non-cording RNAs (∼ 22 nucleotide) that regulate gene expression by suppressing their target mRNAs at post-transcriptional level. Previous studies from our group have identified a number of dis-regulated miRNAs due to the loss of p53 tumor suppressor in cancer cell lines. As part of the efforts to further investigate the in vivo biological significance of these miRNAs, the expression of both hsa-let-7g and hsa-miR-200c were investigated using formalin-fixed paraffin embedded (FFPE) colon cancer specimens to evaluate the potential correlation with chemosensitivity and tumorigenesis. Methods: Forty-six patients with recurrent or residual colon cancer lesion assessable were treated with 5-FU based antimetabolite S-1. This includes twenty-one pair of tumor and normal samples. Total RNAs were isolated from these samples FFPE specimens (contains either > 90% normal or > 90% tumor tissue). cDNAs were synthesized using primers specific for hsa-let-7g, hsa-miR-200c and internal control 5S. The expression levels of each particular miRNAs were quantified using real time qRT-PCR analysis. The expression level of each miRNAs was quantified by measuring the difference of threshold cycle (CT) of candidate miRNAs and internal control 5S (Δ-CT). Results: The expression level of hsa-let-7g was significantly higher in tumor tissues compare to normal tissues (p=0.0026; Wilcoxon test). In the forty-six tumor tissues, the expression level of hsa-let-7g in disease response group (patients group of complete response, partial response and no change after chemotherapy) was significantly lower than the disease progression group (p=0.03; Mann-Whitney test). The expression of hsa-miR-200c was significantly over-expressed in tumor tissues compare to normal tissues (p=0.0001; Wilcoxon test). Although hsa-let-7g is strongly associated with patient’s response to S-1 treatment, it is not a prognostic factor for predicting survival. Conclusion: hsa-let-7g and hsa-miR-200c may be associated with tumorigenesis in colon cancer. In addition, hsa-let-7g may be a significant indicator for chemoresponse to S-1 based chemotherapy. No significant financial relationships to disclose.
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Rogóż, Wojciech, Jadwiga Pożycka, Aleksandra Owczarzy, Karolina Kulig, and Małgorzata Maciążek-Jurczyk. "Comparison of Losartan and Furosemide Interaction with HSA and Their Influence on HSA Antioxidant Potential." Pharmaceuticals 15, no. 5 (April 19, 2022): 499. http://dx.doi.org/10.3390/ph15050499.

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Serum albumin (HSA) is the most important protein in human body. Due to the antioxidant activity, HSA influences homeostasis maintenance and transport of drugs as well as other substances. It is noteworthy that ligands, such as popular drugs, modulate the antioxidant activity of HSA. The aim of this study was to analyze the influence of losartan (LOS) and furosemide (FUR) on HSA antioxidant properties as well as the interaction between these drugs and protein using calorimetric and spectroscopic methods. LOS and FUR showed the high affinity for human serum albumin, and the binding reactions between them were spontaneous and exothermic. LOS and FUR, separately and together in the system, have no significant impact on the secondary HSA structure; however they have significant impact on the tertiary HSA structure. LOS and FUR mixed with HSA have the ability to scavenge free radicals, and the ligand(s)–HSA interactions were synergistic.
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Neumayer, C., A. Fügl, J. Nanobashvili, S. Hallström, H. Gasser, M. Prager, V. Brovkovych, P. Polterauer, T. Malinski, and I. Huk. "S-NITROSO HUMAN SERUM ALBUMIN (S-NO-HSA) REDUCES ISCHEMIA/REPERFUSION INJURY OF SKELETAL MUSCLE - HISTOMORPHOMETRIC ASPECTS." Shock 12, Supplement (November 1999): 58–59. http://dx.doi.org/10.1097/00024382-199911001-00182.

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Kerrigan, Steven W., Nick S. Jakubouvics, Gerardene Meade, Howard F. Jenkinson, and Dermot M. Cox. "A Novel GPIbα Binding Protein on Streptococcus Gordonii Induces Platelet Rolling at Low Shear." Blood 104, no. 11 (November 16, 2004): 3663. http://dx.doi.org/10.1182/blood.v104.11.3663.3663.

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Abstract Infective endocarditis is associated with considerable morbidity and mortality and oral Streptococci are the priniciple causative organism. Platelet adhesion and subsequent aggregation play a critical role in the pathogenesis and dissemination of the infective process. The mechanism by which S. gordonii interacts with and subsequently leads to platelet activation is currently unknown. Previously we described the ability of Streptococcus sanguis to induce platelet aggregation via the platelet vonWillebrand factor receptor, GPIbα, however identification of the bacterial protein involved was not established. Here we describe the novel interaction between a Streptococcal protein that triggers aggregation via platelet GPIbα, in a unique fashion. Wildtype S. sanguis (133–79) and S. gordonii (DL1) support platelet adhesion and induce αIIbβ3 dependent platelet aggregation. Pre-incubation of platelets with an anti-GPIbα antibody inhibited the adhesion (61±6%, p<0.001) and abolished platelet aggregation (0% of control, p<0.001) induced by S. gordonii. These results suggest that GPIbα is a key receptor for recognition of platelets by streptococci. Passing a mutanolysin cell wall extract of S. sanguis through a GPIb affinity column identified a highly glycosylated protein, Hsa, also present on S. gordonii. S. gordonii DL-1 deficient in the Hsa gene, was generated by allelic exchange with an antibiotic resistance cassette. Platelet adhesion to S. gordonii ΔHsa was reduced by 41±5%, (p<0.001), however aggregation was unaffected (49±7% vs 55±5% wt). To confirm that Hsa was binding to platelet GPIbα we immobilised soluble GPIbα (glycocalicin, 0.2μg/ml) on a 96 well plate. Wildtype S. gordonii bound to immobilised glycocalicin, however, the Hsa mutant adhered significantly less (9±3% of wildtype, p<0.001). Furthermore, wildtype S. gordonii induced αIIbβ3 dependent platelet aggregation in washed platelets in the absence of vWf, suggesting a direct interaction between Hsa and GPIbα. We further investigated the interaction between GPIbα and Hsa under shear. Experiments were recorded in real time for a period of 8 minutes. Upon commencement of shear (50s-1), platelets interacted with S. gordonii DL-1 with a rolling fashion followed by firm adhesion. This adhesion was completely inhibited by addition of an anti-GPIbα antibody. When platelets were sheared over immobilized S. gordonii ΔHsa no interaction was observed. In addition, S. gordonii DL-1 failed to interact with platelets at the higher shear rate of 500s-1. Collectively, these results identify a unique interaction between S. gordonii Hsa and platelet GPIbα. This interaction occurs at static and low shear but not at high shear, which is in direct contrast to the interaction between vwf and GPIbα. Furthermore, we propose that the platelet interaction with S. gordonii appears to be a 2 step process. Firstly, platelets roll across the S. gordonii via a GPIbα - Hsa interaction. Following this a second more stable interaction firmly immobilizes the platelet, thereby facilitating the intravascular colonization of a septic plaque.
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Mahata, Shibendu, Suman Kumar Saha, Rajib Kar, Durbadal Mandal, and Nilotpal Banerjee. "A Heuristic Approach to Design Discrete Fractional Order Integrators without Using s-to-z Transform." Solid State Phenomena 261 (August 2017): 386–93. http://dx.doi.org/10.4028/www.scientific.net/ssp.261.386.

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In this paper, a heuristic optimization technique called Harmony Search Algorithm (HSA) is efficiently employed to design Infinite Impulse Response (IIR) Discrete Fractional Order Integrators (DFOIs). Unlike the methods reported in the literature, no discretization (s-to-z transform) operator is necessary to obtain the DFOIs by using the proposed approach. To investigate the design efficiency, the HSA-based DFOIs have been evaluated against the designs based on Real coded Genetic Algorithm (RGA), Particle Swarm Optimization (PSO), and Differential Evolution (DE) using different frequency response error metrics. The reliability in the performance of the proposed DFOIs are extensively investigated by conducting various statistical tests. Comparison of fitness convergence demonstrates that HSA achieves the near global optimal solution in the least number of iterations. Thus, HSA exhibits superior computational efficiency in solving this multimodal optimization problem. The proposed DFOIs also outperform the reported designs.
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Bahlis, Nizar J., Carolyn J. Owen, Paola Neri, Adnan Mansoor, Kathy J. Gratton, Peter Duggan, Pietro Ravani, and Douglas A. Stewart. "A miRNA Risk Score for the Prediction of Response to Rituximab-CHOP Therapy and Survival of Patients with Diffuse Large B-Cell Lymphoma." Blood 116, no. 21 (November 19, 2010): 324. http://dx.doi.org/10.1182/blood.v116.21.324.324.

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Abstract Abstract 324 Background: Diffuse large B-cell lymphoma (DLBCL) may be curable with current immuno-chemotherapy, however nearly 30% of patients fail to benefit from this therapeutic approach. Gene expression profiling studies identified lymphocyte as well as stroma-based mRNA signatures that are predictive of response to R-CHOP; however the need for optimally cryopreserved samples has limited their clinical applicability. MicroRNAs (miRNA) are highly preserved non-coding RNAs that act post-transcriptionally to regulate gene expression by binding to the 3′UTR of mRNAs. To date multiple studies have reported selective miRNAs expression at different lymphocyte differentiation stages, distinct expression in mRNA-defined DLBCL subgroups and have correlated the expression of “selected” miRNAs with disease outcomes. Herein, we have conducted a comprehensive profiling of miRNA expression in R-CHOP treated DLBCL patients and established a miRNA-based risk score that is predictive of response to therapy. Methods and results: We have postulated that a miRNA signature in DLBCL is predictive of survival post R-CHOP chemotherapy. To test this hypothesis, we analyzed the miRNA and mRNA signatures of R-CHOP sensitive “S” and resistant “R” DLBCLs (n=20). miRNAs were hybridized to the miRNA Affymetrix gene-chip (847 hsa-miRNA probes) and raw miRNA expression values were log2 transformed and normalized (miRNA-QC tool, Affymetrix). Comparison of normalized miRNAs expression in “S” versus “R” patients (Anova testing) identified 59 differentially expressed miRNAs (Fold change < -1.5 or > 1.5 with a p value and FDR <0.05). In order to establish a risk score based on the expression of these 59 miRNAs, column-dendrogram branches were then sorted left to right based on each patient's difference between the average log2-scale expression of the 37 up-regulated and the 12 down-regulated miRNAs: this difference is interpreted as an up-/down-regulated mean ratio (ie, geometric mean) on the log2 scale [Log2 Geometric mean ratio [GMR] up-/down-regulated miRNA = Log2 [(2^ΣupregulatedümiRNA/ni)/(2^ΣdownregulatedümiRNA/nii)] where ni and nii represent the number of up-regulated and down-regulated miRNAs. This univariate summary (ie, GMR) of the 59-miRNA expression profiles for each patient enabled accurate prediction of all S versus R patients. Patients with log2 GMR > 0 had a 6-years PFS rate of 100%, while all patients with log2 GMR < 0 relapsed (HR=0.293 [95% CI 0.132–0.647]). Cox regression was then used to model relapse free survival times from treatment as a function of miRNA expression. Separate regression models were also built looking at fit measures, proportionality assumption, and discrimination ability (Harrell C statistics) and only miRNA with a discrimination ability (Harrell C) of > 85% (n=12 miRNA) were used to calculate the log2 GMR of up-/down-regulated miRNAs. A simplified model based on 12 miRNAs (Sensitive vs Resistant: upregulated: hsa-let-7i; hsa-miR-130a; hsa-miR-199a-3p; hsa-199b-3p; hsa-miR-223; hsa-miR22; hsa-miR-24; hsa-miR-26b; hsa-miR-27a; hsa-miR-331-5p; downregulated: hsa-miR-1288) accurately predicted sensitivity or resistance to R-CHOP. With this 12 miRNAs model, only 1 patient in each group (S and R) was misclassified (Fig 1). In addition we have validated the differential expression of these miRNA by short-stem loop RT-PCR and found a strong correlation between the gene-chip and qRT-PCR results (correlation coefficient 0.717). mRNA profiling (U133A Plus2 array chip) was also performed on the whole lymph node sections; 176 genes were identified as differentially expressed between S and R patients with many of these genes belonging to the “stroma-1 and -2” DLBCL signature. Using the TargetScan miRNA target mRNA prediction tool, combinatory analysis of miRNA and mRNA expression profiles of DLBCL patients identified positive and negative correlations (P <0.05) between differentially expressed miRNA and mRNAs. Lastly in a multivariate Cox regression analysis that included the IPI and the 12 miRNA based GMR risk score, both variables were independent predictors of survival post R-CHOP therapy. Conclusion: We believe that this log2 GMR score based on the 12 identified miRNA provides a robust method of predicting sensitivity to R-CHOP in DLBCL patients and it is currently being tested in a larger independent validation cohort. Disclosures: No relevant conflicts of interest to declare.
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Rungatscher, A., S. Hallström, D. Linardi, H. Suzuki, B. Podesser, H. Gasser, A. Mazzucco, and G. Faggian. "595 Cardioprotective Effects of S-Nitroso Human Serum Albumin (S-NO-HSA) during Cardioplegic Arrest and Cold Storage in a Working Heart Heterotopic Transplant Model." Journal of Heart and Lung Transplantation 30, no. 4 (April 2011): S199—S200. http://dx.doi.org/10.1016/j.healun.2011.01.607.

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Lodi, Tiziana, Barbara Neglia, and Claudia Donnini. "Secretion of Human Serum Albumin by Kluyveromyces lactis Overexpressing KlPDI1 and KlERO1." Applied and Environmental Microbiology 71, no. 8 (August 2005): 4359–63. http://dx.doi.org/10.1128/aem.71.8.4359-4363.2005.

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ABSTRACT The control of protein conformation during translocation through the endoplasmic reticulum is often a bottleneck for heterologous protein production. The core pathway of the oxidative folding machinery includes two conserved proteins: Pdi1p and Ero1p. We increased the dosage of the genes encoding these proteins in the yeast Kluyveromyces lactis and evaluated the secretion of heterologous proteins. KlERO1, an orthologue of Saccharomyces cerevisiae ERO1, was cloned by functional complementation of the ts phenotype of an Scero1 mutant. The expression of KlERO1 was induced by treatment of the cells with dithiothreitol and by overexpression of human serum albumin (HSA), a disulfide bond-rich protein. Duplication of either PDI1 or ERO1 led to a similar increase in HSA yield. Duplication of both genes accelerated the secretion of HSA and improved cell growth rate and yield. Increasing the dosage of KlERO1 did not affect the production of human interleukin 1β, a protein that has no disulfide bridges. The results confirm that the ERO1 genes of S. cerevisiae and K. lactis are functionally similar even though portions of their coding sequence are quite different and the phenotypes of mutants overexpressing the genes differ. The marked effects of KlERO1 copy number on the expression of heterologous proteins with a high number of disulfide bridges suggests that control of KlERO1 and KlPDI1 is important for the production of high levels of heterologous proteins of this type.
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Dissertations / Theses on the topic "S-NO-HSA"

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RUNGATSCHER, Alessio. "Cardioprotective role of S-Nitroso Human Serum Albuminduring regional myocardial ischemia-reperfusion." Doctoral thesis, 2010. http://hdl.handle.net/11562/344722.

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BACKGROUND: The early period of reperfusion after myocardial ischemia is critical for endothelial dysfunction and the impairment of nitric oxide synthesis plays a critical role. We investigated the cardioprotective effect of S-NO-HSA in a regional myocardial ischemia/reperfusion rat model reproducing clinical scenarios. METHODS AND RESULTS: Male Wistar rats (n: 120) underwent reversible occlusion of the left anterior descending artery for 30 minutes and subsequent reperfusion for 24 hours. The animals were randomly treated with S-NO-HSA (0.3 μmol/kg/h) or human serum albumin (HSA) infusion. The infusion started 15 minutes before the beginning of ischemia in a group (Pre-I) whereas it starter 15 min after the initiation of ischemia in the other group (Post-I). The infusion continued until the first 30 minutes of reperfusion in both groups. Ventricular systolic and diastolic function was evaluated during early and late reperfusion (120 min and 24 h) in vivo at different preloads by a Millar microtip P-V conductance catheter. Hearts were excised after reperfusion to determine infarct size (IS) and area at risk (AR). Biopsies were obtained to measure high-energy phosphates, the expression of endothelial nitric oxide synthase (eNOS) and inducile nitric oxide synthase (iNOS) and the production of NFkB. Treatment with S-NO-HSA had a significative effect in reducing IS (42.2% +/-3.5 vs. 65.3 +/-4.2; p<0.05), the maximum effect is produced when the drug is administered before ischemia. S-NO-HSA effect on LV systolic function is evident considering the preload independent contractility parameters: maximal slope of the systolic pressure increment end diastolic volume relationship (dP/dtMAX-EDV), the slope EMAX of the end-systolic P-V relationship and the preload recruitable stroke work (PRSW) were significantly increased during reperfusion in all treated animals and after ischemia only in the pre-treated group (Pre-I). The LV diastolic function was improved by S-NO-HSA treatment. Tau-Weiss (index of ventricular relaxation), LV end-diastolic pressure (LVEDP) and end-diastolic P-V relationship (EDPVR) (indexes of ventricular stiffness) were significantly decreased with S-NO-HSA both in Pre-I and Post-I group after ischemia and during the 24 h reperfusion. NO supplementation by S-NO-HSA led to partial and in Pre-I group to total preservation of high energy phosphates. Phosphocreatine (CrP) content was preserved in Pre-I group (5.25 +/- 1.65 vs. 1.53 +/- 1.29 μmol/g protein; p < 0.05) and in Post-I group (3.85 +/- 1.12 vs. 1.53 +/- 1.29 μmol/g protein; p < 0.05) after 24 h reperfusion. Indeed energy charge was significantly higher only in the Pre-I group (0.62 +/- 0.07 vs 0.30 +/- 0.07). S-NO-HSA did not change the constitutive eNOS expression (measured by immunohistochemistry), instead it prevent the NFkB activation (quantified by EMSA) and therefore the iNOS mRNA expression (measured by Northern Blot). CONCLUSIONS: S-NO-HSA limits the infarct size, improves diastolic and systolic function and the energetic reserve of the heart after regional myocardial ischemia/reperfusion. These results suggest that S- NO-HSA might be an interesting option for patients undergoing regional myocardial ischemia reperfusion.
BACKGROUND: The early period of reperfusion after myocardial ischemia is critical for endothelial dysfunction and the impairment of nitric oxide synthesis plays a critical role. We investigated the cardioprotective effect of S-NO-HSA in a regional myocardial ischemia/reperfusion rat model reproducing clinical scenarios. METHODS AND RESULTS: Male Wistar rats (n: 120) underwent reversible occlusion of the left anterior descending artery for 30 minutes and subsequent reperfusion for 24 hours. The animals were randomly treated with S-NO-HSA (0.3 μmol/kg/h) or human serum albumin (HSA) infusion. The infusion started 15 minutes before the beginning of ischemia in a group (Pre-I) whereas it starter 15 min after the initiation of ischemia in the other group (Post-I). The infusion continued until the first 30 minutes of reperfusion in both groups. Ventricular systolic and diastolic function was evaluated during early and late reperfusion (120 min and 24 h) in vivo at different preloads by a Millar microtip P-V conductance catheter. Hearts were excised after reperfusion to determine infarct size (IS) and area at risk (AR). Biopsies were obtained to measure high-energy phosphates, the expression of endothelial nitric oxide synthase (eNOS) and inducile nitric oxide synthase (iNOS) and the production of NFkB. Treatment with S-NO-HSA had a significative effect in reducing IS (42.2% +/-3.5 vs. 65.3 +/-4.2; p<0.05), the maximum effect is produced when the drug is administered before ischemia. S-NO-HSA effect on LV systolic function is evident considering the preload independent contractility parameters: maximal slope of the systolic pressure increment end diastolic volume relationship (dP/dtMAX-EDV), the slope EMAX of the end-systolic P-V relationship and the preload recruitable stroke work (PRSW) were significantly increased during reperfusion in all treated animals and after ischemia only in the pre-treated group (Pre-I). The LV diastolic function was improved by S-NO-HSA treatment. Tau-Weiss (index of ventricular relaxation), LV end-diastolic pressure (LVEDP) and end-diastolic P-V relationship (EDPVR) (indexes of ventricular stiffness) were significantly decreased with S-NO-HSA both in Pre-I and Post-I group after ischemia and during the 24 h reperfusion. NO supplementation by S-NO-HSA led to partial and in Pre-I group to total preservation of high energy phosphates. Phosphocreatine (CrP) content was preserved in Pre-I group (5.25 +/- 1.65 vs. 1.53 +/- 1.29 μmol/g protein; p < 0.05) and in Post-I group (3.85 +/- 1.12 vs. 1.53 +/- 1.29 μmol/g protein; p < 0.05) after 24 h reperfusion. Indeed energy charge was significantly higher only in the Pre-I group (0.62 +/- 0.07 vs 0.30 +/- 0.07). S-NO-HSA did not change the constitutive eNOS expression (measured by immunohistochemistry), instead it prevent the NFkB activation (quantified by EMSA) and therefore the iNOS mRNA expression (measured by Northern Blot). CONCLUSIONS: S-NO-HSA limits the infarct size, improves diastolic and systolic function and the energetic reserve of the heart after regional myocardial ischemia/reperfusion. These results suggest that S- NO-HSA might be an interesting option for patients undergoing regional myocardial ischemia reperfusion.
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Book chapters on the topic "S-NO-HSA"

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"t lo wnegn -t tieertmhicnecnrteuarsyei ( nFp ig re u c re ip i 2 ta .6 ti ) o , n , btuhtebpe ro ca buasbe il it oyfoafm ev o id deenl ce priosjn ec ottioynest conclusive. Some coupled climate ddirfofu er gehntt , f m or eatshueretdwo in paeb ri sood lu s. teArasiinm fa illlaraim nc oruen as ts e , iinst im opbae ct on drought in in sdoim ca e te patrh ts atofatnheaw nt ohrrlodpiosg li ekneilcyA ra u in sfta ra ll l ia f o in rtahegl iven state of evident in the twenty-first century. This can 1996b). ast twenty-five EyN ea S rs O ( N is ic hsoelelnseotvaelr . p ar aitstee rn fr somd ire cchtalnyge fo s rc iend th beyacthm an ogsepsheirn ic gcrierecnuh la otu io sne fou Inndf the N gases and other pollutants, possible changes in the affect th oertcro op hoerrtehntAm tl ualn ti tic, new evidence has been behaviour of ENSO (for which the evidence is Allen 1997). P ic o a te lnatn ia dlem xt arn at nruoaplicvaalrioac ti e ons in SS echanisms for asnuc ( hSu va tt roTn that iati aonndsd co ir netcrtadiincftloureyncaetporfesweanrtm ), in ogrm on er etlhye be su ca rf uasceeowfattheerN are orb th ei nAgtf la onutn ic d ( s G ea r ot szunre fa rceeta te l. m1p9e9r8a ) tu . rVe ar biin at vioolnvsinignr in al is ceraenac , gse. In th iv ein in graanine latter situation, given no or little Arctic regions have also long been su ifnaclrl, eassuemdm te enrdseoniclymtooisdtruoruegdhetf . icFir ts o m ca nam in o tr d ig euh in as gbeeveindefnocuendofthaatchoausplse ig dnioscpeeacnt -ed. Recently, ‘meteorological drought’ perspective, comb ficant aptom te onstp ia hletroeseyxspteecm te a d ti cianlc ly re raesd es u c in e p th oepu ra la in ti f o al n l , dseufc ic hiecnhcayng in eesdcw ou it lhda sc ff a e le cst ( t D he e lw cl o im rth at eeto al f . E 19 urope on multidecadal time at which society becomes stressed by the atshsroecsihao te ld dvCahra ia ntg io et al. (1997) have 9 id 7 e ) n . tIin fi e th dedtercoapdiaclaltiAmte la sncta ic le , p ag o r li itciuclatlutreanl si aonnds ( hRyodd ro dlaog1i9c9a5l ). droughts, leading to n so o m rt ehancnsodn in tr soautdhipto ro le pio ca flSA ST tl aann ti ocm , aallitehsoubg et hwteheenrethies pro Fgirna ally, the pr oversy about this dipole (Enfield and framew mom rk enh ec aessa sa m ev o io nugsliy ts m ob ejn ec ti t o iv neesdanWiM nte O r na CtL io InPaSldMeacyaedral1v9a9 ri 7 a ) ti . onSsuicnh ra vianrfiaaltlio in nsboctohulndor be linked to information and pr rey to th Africa and to the d dic t e io nnh . anTcheesaendacptr iv oim tie ostewcillilm li antke nor O th neaasgtlBorbaazlils , caallteh , o th uegrhetihseallsaottaemraprleeneovt id setn ro cnegt . hat V se O rv SeTsewvreoruaglhAtfm ric oanni to co ri unngtrc ie esn . tr T es hea lr IeRaIdyan se dtP up R O to ­ sdyesctaedmalcaanndsloom ng eetr im -sc easle co v n ar fioaubn ility in the climate more tho i u ll gahltsoiswboerikngtogw iv aerndtto hese objectives. Much climate s d the interannual climate data information and isnetaesgornaatli ng p re h d is itcotriiocnaslW tro apridca ( l1w9 ig 9n7a ) l . id Feonrtiifnystaanscte ro , nFgo lland et al. (1991) and within the context of how drought forecasts could be may be lin eksetdAtforivcaarniarta io in nfsaliln . T th h m ey u lt sipdeeccualdaatl signal in used, especially in developing countries (Frederick H. circu e global ther e m th oahtaltihniesM of . th Seesmeaizszsiu , epsearrseonda is lccuosm se mdu in nidceatta io il n f , o1r9n9o7r ) t . hSA ev f e ri rcaallsaotm io enlah ti aosn of the oceans. The thermohaline circu­ in Hulme et al. (1992a and 1992b). Here clima­ the Soouftthhtee he rnNpoortHtehnetrinalH to e m change the temperature of tologists, hydrologists, economists, and sociologists ti emisphere is opch ea e n re soocne an msurle ti la dteicvaedtaolscoacm ie e t al toig ss eutehserthtaotm id aeyntairfiysesoonmceero ea f so th nea bl cyom sk p il lfeuxlienvmeer scales (Sc cre , as leasr ge in -s ca hlesinge tr loe po asnpthhrraonpdogReanm ic anekfufte ty 1994). H eric aerosols, m cts o st rleyl at iend ow to ­ drought forecasts become possible. Northern the the A se dviasrciu at." In Droughts, 66. Routledge, 2016. http://dx.doi.org/10.4324/9781315830896-46.

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