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Related Products of 3682-14-2, Catalysts function by providing an alternate reaction mechanism that has a lower activation energy than would be found in the absence of the catalyst. In some cases, the catalyzed mechanism may include additional steps.In a article, 3682-14-2, molcular formula is C8H7N3O2, introducing its new discovery.

Experimental evidence of the reciprocal oxidation of Bovine Serum Albumin and Linoleate in aqueous solution, initiated by HO? free radicals

An investigation of radiation-induced oxidation of aqueous bovine serum albumin (BSA) in the presence of linoleate (LH) at pH 10.5 has been carried out in order to better understand the respective oxidative processes involved in both lipid and protein phases. Solutions containing BSA (15 mumol L-1) and linoleate (15-600 mumol L-1) below the critical micellar concentration (cmc = 2000 mumol L-1), have been irradiated by gamma-rays (137Cs) at radiation doses ranging from 10 to 400 Gy (dose rate 9.5 Gy min-1). It can be noticed that, in the absence of BSA, the main hydroperoxides formed from HO?-induced linoleate oxidation below the cmc, do not exhibit a conjugated dienic structure. This was also verified in the presence of BSA. Selected chemical markers of oxidation have been monitored: non-conjugated dienic hydroperoxides and conjugated dienes (without hydroperoxide function) for linoleate oxidation, and carbonyl groups for BSA oxidation. We have shown that for the lowest linoleate concentration (15 mumol L-1) in the presence of BSA (15 mumol L-1), the formation of conjugated dienes was not observed, meaning that LH was not exposed to HO? radicals attack. However, non-conjugated dienic lipid hydroperoxides were simultaneously detected, indicating that LH was secondarily oxidised by BSA oxidised species. Moreover, the oxidation of linoleate was found to be enhanced by the presence of BSA. For the highest linoleate concentration (600 mumol L-1), the expected protection of BSA by LH was not observed, even if LH monomers were responsible for the total scavenging of HO? radicals. In this latter case, the formation of non-conjugated dienic lipid hydroperoxides was lower than expected. Those results showed that BSA was not oxidised by the direct action of HO? radicals but was undergoing a secondary oxidation by non-dienic lipid hydroperoxides and/or lipid radical intermediates, coming from the HO?-induced linoleate oxidation.

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Phthalazine – Wikipedia,
Phthalazine | C8H6N542 – PubChem

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Congenital heart block and immune mediated sensorineural hearing loss: Possible cross reactivity of immune response

Immune-mediated sensorineural hearing loss may complicate systemic autoimmune diseases. We have previously reported the presence of antibodies directed against inner ear antigens in patients with Cogan syndrome, a disease characterized by sudden hearing loss and interstitial keratitis. Such autoantibodies cross-react with an epitope of SSA/Ro60 protein. Anti-Ro/SSA antibodies in pregnant women cross the placenta and reach the fetal tissues inducing an immune-mediated damage of the cardiac conduction system. We wanted to evaluate whether mothers with anti-Ro/SSA antibodies who gave birth to children with congenital heart block have antibodies directed against inner ear antigens and whether these antibodies are connected with the presence of immune-mediated sensorineural hearing loss. We did not find anti-inner ear antibodies in the majority of the mothers. On the contrary a 13-year-old boy with congenital heart block and sensorineural hearing loss was positive for the presence of anti-inner ear antigens antibodies. Moreover his serum was positive for the presence of anti-Ro60 peptide antibodies but did not recognize the entire protein Ro60 (TROVE2), a behaviour similar to that of sera from patients with Cogan syndrome. In conclusion the data obtained so far show that anti-inner ear antibodies do not recognize the entire protein TROVE2 and do not support the hypothesis that such antibodies may be involved in the pathogenesis of congenital heart block.

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Phthalazine | C8H6N525 – PubChem

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Chapter 4 The immunochemical/photochemical interface

In this chapter we have seen that the immunochemical reaction and chemiluminescent reaction can be interfaced in a variety of ways though chiefly by coupling the chemiluminescent reactant itself (direct chemiluminescence labelling) to an immunoreactant, or by coupling another component of a chemiluminescent reaction other than the chemiluminescent molecule itself (indirect chemiluminescence labelling). It can be seen that the indirect labelling systems are incapable of achieving the level of simplicity offered by certain direct labelling systems, though some indirect labelling systems offer an equivalent level of sensitivity. The chemical techniques required to conjoin the chemiluminescent and immunochemical reactions are relatively well established though do not always permit substantial retention of light emission and immunoreactivity respectively. This is often dictated by the chemical properties of the species to be conjugated themselves. We have briefly considered the role of bioluminescent systems here even though they have yet to be widely accepted in the context of chemiluminescence immunoassay. Their true potential may yet be realized by the interface with genetic engineering techniques which will permit controlled biosynthesis of the appropriate enzymes.

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Phthalazine – Wikipedia,
Phthalazine | C8H6N669 – PubChem

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Blastomyces dermatitidis serine protease dipeptidyl peptidase IVA (DppIVA) cleaves ELR+CXC chemokines altering their effects on neutrophils

Blastomycosis elicits a pyogranulomatous inflammatory response that involves a prominent recruitment of neutrophils to the site of infection. Although neutrophils are efficiently recruited to the site of infection, this event is paradoxically coupled with the host’s inability to control infection by Blastomyces dermatitidis, the causative agent. The mechanisms underlying this characteristic pyogranulomatous response and inability of neutrophils to kill the yeast are poorly understood. We recently reported that the fungal protease dipeptidyl peptidase IVA (DppIVA) promotes B.?dermatitidis virulence by cleaving a dipeptide from the N-terminus of C?C chemokines and granulocyte/macrophage-colony stimulating factor, thereby inactivating them. Herein, we present evidence that DppIVA can also truncate the N-terminus of members of the ELR+CXC chemokine family, which are known to modulate neutrophil function. We show that the DppIVA cleaved form of human (h) CXCL-2, for example, hCXCL-2 (3-73), is a more potent neutrophil chemoattractant than its intact counterpart, but hCXCL-2 (3-73) is conversely impaired in its ability to prime the reactive oxygen species response of neutrophils. Thus, DppIVA action on ELR+CXC chemokines may promote the pyogranulomatous response that is typical of blastomycosis, while also explaining the inability of neutrophils to control infection.

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Oregonin reduces lipid accumulation and proinflammatory responses in primary human macrophages

Inflammation in the vascular wall is important for the development of atherosclerosis. We have previously shown that inflammatory macrophages are more abundant in human atherosclerotic lesions than in healthy arteries. Activated macrophages produce reactive oxygen species (ROS) that promote local inflammation in atherosclerotic lesions. Here, we investigated the role of oregonin, a diarylheptanoid, on proinflammatory responses in primary human macrophages and found that oregonin decreased cellular lipid accumulation and proinflammatory cytokine secretion. We also found that oregonin decreased ROS production in macrophages. Additionally, we observed that treatment of lipopolysaccharide-exposed macrophages with oregonin significantly induced the expression of antioxidant-related genes, including Heme oxygenase-1 and NADPH dehydrogenase quinone 1. In summary, we have shown that oregonin reduces lipid accumulation, inflammation and ROS production in primary human macrophages, indicating that oregonin has anti-inflammatory bioactivities.

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Phthalazine – Wikipedia,
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Nitroxide Tempol down-regulates kinase activities associated with NADPH oxidase function in phagocytic cells and potentially decreases their fungicidal response

Aims The identification of novel targets to control inflammation in humans is probably the primary challenge that impairs the development of new anti-inflammatory drugs. Therefore, the modulation of intracellular signaling pathways in phagocytes may be an interesting means of achieving this goal. However, this change to signaling can compromise the host’s susceptibility to invading pathogens. We investigated whether the antioxidant nitroxide Tempol regulates the activity of kinases associated with the production of oxidants in neutrophils, which affects the fungicidal capability of these cells. Main methods The effects of Tempol on PMA- or fMLP-activated neutrophils were examined by oxygen consumption as an index of the oxidative burst, a release of extracellular and total Reactive Oxygen Species (ROS) by chemiluminescence, kinase activities through analysis of ATP consumption during enzyme activities and the dot blot immunoassay and, finally, by neutrophil capacity of killing Candida albicans. Key findings Tempol significantly inhibited the neutrophil oxidative burst in a concentration-dependent manner and decreased oxygen consumption (IC50 = 45 muM) and extracellular/total ROS formation with an increase on the lag period response. In addition, Tempol inhibited neutrophil kinase activities (i.e., a decrease in protein phosphorylation) elicited through different biochemical pathways and consequently impaired the fungicidal activity of these cells. Significance Although Tempol has potential anti-inflammatory activity that acts on different intracellular pathways (such as those involving kinases), researchers should be cautious, since this nitroxide down-regulated oxidants production and the fungicidal response of neutrophils.

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Chapter 2 Chemiluminescence: the phenomenon

In this chapter a brief description of some photochemical and photophysical processes has been given in general terms. From this has developed an appreciation of the processes which give rise to luminescence emission. An introduction to chemiluminescence has been given from a phenomenological viewpoint. Reaction mechanisms and specific examples of chemiluminescent reactions have been presented for the more extensively studied systems together with a brief description of methods for monitoring and quantifying the emission from such reactions.

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Phthalazine – Wikipedia,
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Chemiluminescence characteristics of N-(4-substituted benzyl)isoluminol

We synthesized N-(4-substituted benzyl)isoluminol which has 4-bromo-, 4-methyl-, 4-methoxy-, 4-nitro-groups. These compounds produced chemiluminescence by the reaction with the oxidizing agent, potassium hexacyanoferrate and hydrogen peroxide, in an alkaline medium. The chemiluminescence intensities of these compounds were 0.03-4.7 times that of isoluminol. We used Hamett substituent constants as a parameter for the electronic substituent effects. The relationship between the amino-H chemical shift value and the Hamett substituent constants showed a good linear correlation. The relationship between the chemiluminescence intensities and the Hamett substituent constants showed a good linear correlation. The relationship between the fluorescence intensities and the Hamett substituent constants also showed a good linear correlation. These results suggest that the change in the electron density around the amino group strongly influences the fluorescence intensities and corresponding chemiluminescence intensities of these derivatives.

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Phthalazine – Wikipedia,
Phthalazine | C8H6N644 – PubChem

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Chemiluminescent detection of enzymatically produced hydrogen sulfide: Substrate hydrogen bonding influences selectivity for H2S over biological thiols

Hydrogen sulfide (H2S) is now recognized as an important biological regulator and signaling agent that is active in many physiological processes and diseases. Understanding the important roles of this emerging signaling molecule has remained challenging, in part due to the limited methods available for detecting endogenous H2S. Here we report two reaction-based ChemiLuminescent Sulfide Sensors, CLSS-1 and CLSS-2, with strong luminescence responses toward H2S (128- and 48-fold, respectively) and H2S detection limits (0.7 ¡À 0.3, 4.6 ¡À 2.0 muM, respectively) compatible with biological H2S levels. CLSS-2 is highly selective for H2S over other reactive sulfur, nitrogen, and oxygen species (RSONS) including GSH, Cys, Hcy, S2O3 2-, NO2-, HNO, ONOO-, and NO. Despite its similar chemical structure, CLSS-1 displays lower selectivity toward amino acid-derived thiols than CLSS-2. The origin of this differential selectivity was investigated using both computational DFT studies and NMR experiments. Our results suggest a model in which amino acid binding to the hydrazide moiety of the luminol-derived probes provides differential access to the reactive azide in CLSS-1 and CLSS-2, thus eroding the selectivity of CLSS-1 for H2S over Cys and GSH. On the basis of its high selectivity for H2S, we used CLSS-2 to detect enzymatically produced H2S from isolated cystathionine gamma-lyase (CSE) enzymes (p < 0.001) and also from C6 cells expressing CSE (p < 0.001). CLSS-2 can readily differentiate between H2S production in active CSE and CSE inhibited with beta-cyanoalanine (BCA) in both isolated CSE enzymes (p < 0.005) and in C6 cells (p < 0.005). In addition to providing a highly sensitive and selective reaction-based tool for chemiluminescent H2S detection and quantification, the insights into substrate-probe interactions controlling the selectivity for H2S over biologically relevant thiols may guide the design of other selective H2S detection scaffolds. If you are interested in 3682-14-2, you can contact me at any time and look forward to more communication. category: phthalazine

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Phthalazine – Wikipedia,
Phthalazine | C8H6N523 – PubChem

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Histidine-Rich Glycoprotein Prevents Septic Lethality through Regulation of Immunothrombosis and Inflammation

Sepsis is a major cause of death worldwide. We show that a plasma protein histidine-rich glycoprotein (HRG) was decreased significantly in septic mice with cecal ligation and puncture (CLP) and supplementary treatment of septic mice with exogenous HRG improved survival, with strong inhibition of tight attachment of neutrophils to pulmonary vasculatures, subsequent immunothrombosis, DIC state, lung inflammation, hypercytokinemia, and activation of vascular endothelial cells (VECs). In contrast, knockdown of HRG by siRNA exacerbated lethality. Purified human HRG reversibly induced morphological changes in human neutrophils in vitro; induction of spherical shape with reduced microvilli and adhesiveness to VECs. HRG maintained the passage of neutrophils through microcapillaries and abolished production of reactive oxygen species. These results suggested that the supplementary therapy with HRG may provide a novel strategy for the treatment of sepsis through suppression of excessive systemic inflammation and immunothrombosis by keeping circulating neutrophils quiescent and preventing uncontrolled activation of VECs.

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Phthalazine – Wikipedia,
Phthalazine | C8H6N650 – PubChem