Interactions between peptides and sera.

<p>A. SPRi kinetic curves of serum and peptides immobilized on the surface of a prism. Changes in % reflectivity were measured as a function of time. Each curve shows binding to one of the peptides. B. SPRi difference images of the prism surface at different times. Peptide solutions at 10 mg/mL were spotted on the biochip surface. Difference images show the surface at the start of injection, during the injection and at the stop of injection. C. Number of effective interactions between the 39 peptides covering the sequence of hnRNP B1 and sera from healthy donors, autoimmune hepatitis (AIH), systemic lupus erytheamtosus (SLE), rheumatoid arthritis (RA) patients.</p

Comparisons of apparent k_off (s^-1)values.

<p>A. Between groups of patients and donors. Each group of patients was compared with a group of healthy donors. Complexes between AIH (autoimmune hepatitis) sera and peptide P7 (AA_55-70) were more stable than with healthy control sera. Conversely, complexes between donor sera and peptides P14 (AA_118-133) and P30 (AA_262-277) were more stable than with SLE (systemic lupus erytheamtosus) sera. The same applied to peptide P17 (AA_145-160) and RA (rheumatoid arthritis) sera. B. Between groups of patients. Complexes between AIH sera, peptides P6 (AA_46-61) /P7 (AA_55-70) and P30 (AA_262-277) were more stable than those formed respectively by RA and SLE sera. SLE sera also formed complexes less stable than RA sera with peptides P14 (AA_118-133), P20 (AA_172-187), P39 (AA_340-353). </p

Anti IgM binding to material from serum retained at immobilised peptide P7 in the presence and absence of nucleases.

<p>Sera were passed across immobilised peptides and the resulting complexes were allowed to dissociate so that only the most stable complexes remained. Anti-IgM was then flowed across the surfaces. The experiment was repeated after pre-treatment with, and in the presence of, nucleases as described in Materials and Methods. A. P7 Binding curves for AIH (autoimmune hepatitis), RA (rheumatoid arthritis) and SLE (systemic lupus erytheamtosus) sera binding to immobilised P7 and subsequent binding of anti-IgM antibodies in the presence or absence of nucleases. B. P7 Binding curves for donor sera binding to immobilised P7 and subsequent binding of anti-IgM antibodies in the presence or absence of nucleases. </p

Oxidative Stress, Inflammatory Biomarkers and Matrix Metalloproteinases Status in Ovarian Cancer Patients.

<p>Oxidative Stress, Inflammatory Biomarkers and Matrix Metalloproteinases Status in Ovarian Cancer Patients.</p

Pearson's Correlation Coefficients of Different Variables in Ovarian Cancer Patients.

<p>Pearson's Correlation Coefficients of Different Variables in Ovarian Cancer Patients.</p

Prognostic variables of ovarian cancer.

<p>Prognostic variables of ovarian cancer.</p

Result of all the variables among CKD patients and control.

<p>Result of all the variables among CKD patients and control.</p

Pearson’s correlation coefficients of different variables in CKD associated with CVD.

<p>Pearson’s correlation coefficients of different variables in CKD associated with CVD.</p

Oxidative injury is enhanced by inflammatory mediators (interleukins and TNF-α) as it provokes the activity of NADPH oxidase.

<p>The resultant superoxide anion (O₂¯) not only in turn further activate monocytes to release inflammatory mediators but also react with nitric oxide (NO) to form peroxynitrite (ONOO¯) which induce lipid peroxidation and NO consumption, important in proper vascular functioning and this decrease in NO increases mainly IL-1. It generates free radicals which again stimulate monocytes. O₂¯ processing into hydrogen peroxide (H₂O₂) is decreased as it is mediated by superoxide dismutase (SOD) which is deficient in CKD. H₂O₂ can be converted into hypochlorite ion (OCl¯) by myeloperoxidase (MPO) and into water and oxygen by catalase which may be decreased in CKD. Reduced glutathione (GSH) not only decreases H₂O₂ processing but also reduces vitamin C which has three effects, firstly it increases inflammatory mediators, secondly raises OCl¯ and thirdly limits vitamin E (vit E) recycling. Raised OCl¯ free radicals attack albumin to produce advanced oxidative protein products (AOPPs) which promote NADPH oxidase activity thus aggravating oxidative insult. Reduction in vitamin E results not only in increased inflammatory mediators but also in raised asymmetrical dimethylarginine (ADMA) levels which competes L-arginine (also decreased in CKD) for nitric oxide synthase (NOS) thus reduces its levels and hampers NO formation leading to cardiovascular injury.</p