Viewing affirmative mentions of gene expression of IL2 (H. sapiens) in heart

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Ide et al. (1989)IL-2heartIn conclusion impaired IL-2 production might be responsible for deficient lymphocyte function after open heart surgery.
Chu et al. (1995)IL-2heartWe monitored leukocyte count, lymphocyte subpopulation count, soluble IL- 2 receptor (sIL-2r) and serum IL-2 levels, and an immunosuppressive acidic protein (IAP) level before and on the 1st, 7th, and 14th day after open heart surgery.
Normann et al. (1996)interleukin-2heartCONCLUSIONS: Human, clinical heart rejection can occur in the absence of locally produced interleukin-2; the degree of immunosuppression achieved with cyclosporine A may explain the different results obtained in the canine withdrawal model versus human clinical allograft rejection.
Hisatomi et al. (1989)interleukin-2HeartHowever, interleukin-2 production remained depressed on day 3 in all patients with transfusion from random donors and remained significantly diminished even on day 7 in such patients in New York Heart Association classes III and IV.
Hisatomi et al. (1989)interleukin-2heartWe conclude that heart operations for which cardiopulmonary bypass is used are associated with depression of cellular immunity, including interleukin-2 production.
Mazzone et al. (1999)interleukin 2heartPlasma levels of interleukin 2, 6, 10 and phenotypic characterization of circulating T lymphocytes in ischemic heart disease.
van Emmerik et al. (1994)IL-2heartExpression of interleukins, IL-2, IL-4, IL-6 and IL-10 mRNA was studied in sequential endomyocardial biopsies (EMB) and in graft-infiltrating lymphocyte (GIL) cultures propagated from EMB taken after heart transplantation.
Simon et al. (2001)interleukin-2heartElevated plasma levels of interleukin-2 and soluble IL-2 receptor in ischemic heart disease.
van Gelder et al. (1998)IL-2heartBlockade of the interleukin (IL)-2/IL-2 receptor pathway with a monoclonal anti-IL-2 receptor antibody (BT563) does not prevent the development of acute heart allograft rejection in humans.
de Groot-Kruseman et al. (2002)interleukin 2heartIntragraft interleukin 2 mRNA expression during acute cellular rejection and left ventricular total wall thickness after heart transplantation.
Zhao et al. (1993)IL-2heartThe polymerase chain reaction (PCR) was used to detect the expression of IL-1, IL-2, IL-4, IL-5, IL-6, TNF-alpha, IFN-gamma, TGF-beta, TCR-beta chain and aFGF genes in 21 myocardial biopsies obtained from 9 heart transplant patients.
Li et al. (1996)IL-2heartOBJECTIVE: To analyse IL-2, IL-2R mRNA gene expression and protein production before, during, and after rejection of heart transplantation in vitro model.
Morris et al. (1993)IL-2heartEnhancement of IL-1, IL-2 production and IL-2 receptor generation in patients with acute rheumatic fever and active rheumatic heart disease; a prospective study.
Morris et al. (1993)IL-2heartIn a prospective study, patients with quiescent rheumatic heart disease (CRHD), streptococcal pharyngitis (SP) and healthy normal subjects produced comparable amounts of IL-1 and IL-2, but acute rheumatic fever (ARF) patients produced significantly elevated amounts of IL-1 and IL-2 at all intervals up to 48 weeks.
Hasatomi et al. (1992)IL-2heartWe administered 200U/kg/day of rEPO for 7 days in a patient with postoperative erythroderma after open heart surgery and the level of IL-2 production was found to also increase in patient according with recovery of symptom.
Miller et al. (1989)IL-2heartTonsillar cells from patients with rheumatic heart disease produced significantly less IL-1, TNF, IL-2, and Ig than control tonsillar cells.
Deng et al. (1995)interleukin-2heartIn 15 consecutive patients undergoing HTx we prospectively determined levels of interleukin-6 (IL-6), tumor-necrosis-factor-alpha (TNF-alpha), interleukin-2 (IL-2), and soluble-interleukin-2-receptor (sIL-2-R) at eight points in time during biopsy and right heart catheterization and within 12 hr of echocardiography during the first three months after HTx.
Ikeda et al. (1996)IL-2heartOn the other hand, plasma levels of TNF-alpha but not IL-1 beta, IL-2 or IL-6, were elevated in 4 of 9 patients with congestive heart failure complicated with cachexia and/or infection.
de Groot-Kruseman et al. (2002)IL-2 mRNAHeartRESULTS: Histological signs of acute rejection (International Society for Heart and Lung Transplantation (ISHLT) rejection grade > 2) were strongly associated with IL-2 mRNA expression (IL-2 mRNA was present in 12 of 20 endomyocardial biopsies (60%) with acute rejection and in 24 of 103 endomyocardial biopsies (23%) without acute rejection, p = 0.002).
Baan et al. (2007)IL-2heartAfter heart transplantation, the highest intragraft IL-21, IL-21R alpha-chain, and IL-2 mRNA expression levels were measured during acute rejection (P<0.001, P=0.01, P=0.03).
Narin et al. (2003)IL-2heartTo estimate the activity of the immunopathological process in patients with ARF, plasma nitric oxide metabolities (NOx) concentrations, IL-1alpha and IL-2 levels were investigated in 22 patients with ARF at the time on admission, and after 3 months, in children with chronic rheumatic heart disease (CRHD).
Saatvedt et al. (1995)IL-2heartC3 activation products, terminal complement complex (TCC), and cytokines including interleukins 6 and 2 (IL-6, IL-2) and tumour necrosis factor-alpha (TNF), and the soluble IL-2 and TNF receptors were determined serially during and up to 48 h after open heart surgery in children.
Tepliakov et al. (2004)IL-2heartA comparative randomized clinical study was conducted to evaluate the diagnostic and prognostic value of the activation of proinflammatory cytokines [tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1alpha, IL-2, IL-6, IL-8)] and the increased production of autoimmune complexes in the pathogenesis of chronic heart failure (CHF) in patients with coronary heart disease (CHD).
Li et al. (2008)IL-2heartThe levels of IFN-gamma, IL-2, and TNF-alpha were increased in the spleen, kidney, and heart throughout the study period.
Teplliakov et al. (2008)IL-2heartCONCLUSION: Immune disorders in the form of hyperactivation of proinflammatory cytokines (most of all TNFalpha, IL-1alpha, IL-2, IL-6), enhanced expression of CIC and autoAB to CL growing with severity of CCF and abnormal heart pump function play an important role in CCF pathogenesis in IHD patients with LCPR and can be markers of the disease progression.
Das (2000)IL-2heartN-3 fatty acids can inhibit the synthesis and release of pro-inflammatory cytokines such as tumor necrosis factoralpha (TNFalpha) and interleukin-1 (IL-1) and IL-2 that are released during the early course of ischemic heart disease.