We examined the serum levels of IL-6, IL-8, TNF, IL-6R, TNF-R1, and CRP and the dynamics of changes in these levels according to age. The study included healthy individuals of 20–90 years of age. Participants were divided into subgroups based on their decade of life, and into subgroups of ≥65 or <65 years. Serum cytokine levels were assayed by ELISA, and CRP using an immunoturbidimetric method. Serum CRP levels were within the normal range for all subgroups. The 60- to 70-year age group showed higher CRP than the 20- to 30- (p = 0.003), 30- to 40- (p = 0.009), and 40- to 50- (p = 0.030) year age groups. Serum cytokine levels were low. It was greater in the 60- to 70-year age group than in the 20- to 30- (p = 0.008) and 30- to 40- (p = 0.040) year groups, and was greater in the 70- to 90-year group than the 20- to 30-year group (p = 0.043). Serum TNF-R1 level in the 70- to 90-year group was greater than in all other age groups (p = 0.000 for all comparisons). Other measured parameters did not differ between groups. Serum levels of IL-6, CRP, and TNF-R1 were greater in participants ≥65 than <65 years of age. Healthy older people showed low serum levels of CRP and pro-inflammatory cytokines, but higher than in younger population. Therefore, the adjustment of normal ranges in the elderly should be considered. Serum levels of pro-inflammatory cytokines elevated beyond normal ranges indicate particular diseases.

Inflammatory activity of PCAT is greater than in other fat locations, in CAD is greater than in non-CAD controls, and is independently associated with coronary stenosis. In overweight patients, PCAT SUV correlates with the extent of CAD.

Using the Berline-Vergne integration formula for equivariant cohomology for torus actions, we prove that integrals over Grassmannians (classical, Lagrangian or orthogonal ones) of characteristic classes of the tautological bundle can be expressed as iterated residues at infinity of some holomorphic functions of several variables. The results obtained for these cases can be expressed as special cases of one formula involving the Weyl group action on the characters of the natural representation of the torus. MSC:14M15

IgA nephropathy (IgAN), membranous nephropathy (MN), and lupus nephritis (LN) represent important causes of chronic kidney disease. They belong to the immune-mediated glomerulonephritis (GNs), and have distinct pathogenesis, distinct clinical courses, and variable responses to treatment. Therefore, specific diagnostic procedures are necessary for more effective patient management. Recently, a role for oxidative stress has been proposed in various renal disorders. Thus, molecules related to oxidative stress, such as 2-Cys-peroxiredoxins (PRDXs), may represent plausible candidates for biomarkers in renal pathologies. The aim of this study was to assess whether there are differences between individual GNs and healthy controls in the context of PRDXs serum concentration. We enrolled 108 patients with biopsy-proven IgAN (47), MN (26), LN (35) and 30 healthy age- and sex-matched controls. The serum concentrations of PRDX 1–5 were measured with ELISA assays and correlated with demographic and clinical data. The PRDXs’ concentration varied depending on the GN type. We also observed an association of PRDXs with lower estimated glomerular filtration rates, complement, hemoglobin, and body mass index. Our study indicates that individual PRDX can play roles in pathophysiology of selected GNs and that their serum concentrations may become useful as a new supplementary diagnostic markers in IgAN, MN as well as LN. The results of this study open a new avenue for prospective research on PRDXs in renal diseases.

In [GK96] Guillemin and Kalkman proved how the nonabelian localization theorem of Jeffrey and Kirwan ([JK95]) can be rephrased in terms of certain iterated residue maps, in the case of torus actions. In [Zie14] we describe the push-forward in equivariant cohomology of homogeneous spaces of classical Lie groups, with the action of the maximal torus, in terms of iterated residues at infinity of certain complex variable functions. The aim of this paper is to show how, in the special case of classical Grassmannians, the residue formulas obtained in [Zie14] can be deduced from the ones described in [JK95] and [GK96].

We study residue formulas for push-forward in the equivariant K-theory of homogeneous spaces. For the classical Grassmannian, the residue formula can be obtained from the cohomological formula by a substitution. We also give another proof using symplectic reduction and the method involving the localization theorem of Jeffrey-Kirwan. We review formulas for other classical groups, and we derive them from the formulas for the classical Grassmannian. Next, we consider the homogeneous spaces for the exceptional group G 2. One of them, G 2 /P 2 corresponding to the shorter root, embeds in the Grassmannian Gr(2, 7). We find its fundamental class in the equivariant K-theory K T (Gr(2, 7)). This allows to derive a residue formula for the push-forward. It has significantly different character compared to the classical groups case. The factor involving the fundamental class of G 2 /P 2 depends on the equivariant variables. To perform computations more efficiently, we apply the basis of K-theory consisting of Grothendieck polynomials. The residue formula for push-forward remains valid for the homogeneous space G 2 /B as well.

Background and AimsDuring chronic hepatitis C virus (HCV) infection, CD8+ T-cells become functionally exhausted, undergoing progressive phenotypic changes, i.e., overexpression of “inhibitory” molecules such as PD-1 (programmed cell death protein 1) and/or Tim-3 (T-cell immunoglobulin and mucin domain-containing molecule-3). The extreme intrahost genetic diversity of HCV is a major mechanism of immune system evasion, facilitating epitope escape. The aim of the present study was to determine whether T-cell exhaustion phenotype in chronic HCV infection is related to the sequence repertoire of NS3 viral immunodominant epitopes.MethodsThe study population was ninety prospective patients with chronic HCV genotype 1b infection. Populations of peripheral blood CD8+ T-cells expressing PD-1/Tim-3 were assessed by multiparametric flow cytometry, including HCV-specific T-cells after magnetic-based enrichment using MHC-pentamer. Autologous epitope sequences were inferred from next-generation sequencing. The correction of sequencing errors and genetic variants reconstruction was performed using Quasirecomb.ResultsThere was an interplay between the analyzed epitopes sequences and exhaustion phenotype of CD8+ T-cells. A predominance of NS31406 epitope sequence, representing neither prototype KLSGLGLNAV nor cross-reactive variants (KLSSLGLNAV, KLSGLGINAV or KLSALGLNAV), was associated with higher percentage of HCV-specific CD8+PD-1+Tim-3+ T-cells, P=0.0102. Variability (at least two variants) of NS31406 epitope sequence was associated with increased frequencies of global CD8+PD-1+Tim-3+ T-cells (P=0.0197) and lower frequencies of CD8+PD-1−Tim-3− T-cells (P=0.0079). In contrast, infection with NS31073 dominant variant epitope (other than prototype CVNGVCWTV) was associated with lower frequency of global CD8+PD-1+Tim-3+ T-cells (P=0.0054).ConclusionsOur results indicate that PD-1/Tim-3 receptor expression is largely determined by viral epitope sequence and is evident for both HCV-specific and global CD8+ T-cells, pointing to the importance of evaluating autologous viral epitope sequences in the investigation of CD8+ T-cell exhaustion in HCV infection.

In this paper we show examples of computations achieved using the formulas of our previous paper, which express the push-forwards in equivariant cohomology as iterated residues at infinity. We consider the equivariant cohomology of the complex Lagrangian Grassmannian LG(n) and the orthogonal Grassmannian with the action of the maximal torus. In particular, we show how to obtain some well-known results due to P. Pragacz and J. Ratajski on integrals of Schur polynomials over the Lagrangian Grassmannian LG(n) and the orthogonal Grassmannian OG(n).