52 research outputs found
Immunogenetica en ziekte : waar is dat goed voor?
HLA klasse II-peptide-TCR interacties en immunopathologische ziekte
Human leucocyte antigens (HLA) in neonates with an inadequate response to hepatitis B vaccination [1]
7-Nitro indazole, an inhibitor of neuronal nitric oxide synthase, attenuates pilocarpine-induced seizures
7-Nitro indazole (25–100 mg/kg i.p.), an inhibitor of neuronal nitric oxide (NO) synthase, attenuated the severity of pilocarpine (300 mg/kg i.p.)-induced seizures in mice. This indicates that the decreased neuroexcitability of the central nervous system (CNS) following administration of 7-nitro indazole may be due to inhibition of neuronal NO synthase, implying that NO acts as an excitatory and proconvulsant factor in the CNS
Bradykinin potentiation by angiotensin-(1-7) and ACE inhibitors correlates with ACE C- and N-domain blockade
ACE inhibitors block B(2) receptor desensitization, thereby potentiating
bradykinin beyond blocking its hydrolysis. Angiotensin (Ang)-(1-7) also
acts as an ACE inhibitor and, in addition, may stimulate bradykinin
release via angiotensin II type 2 receptors. In this study we compared the
bradykinin-potentiating effects of Ang-(1-7), quinaprilat, and captopril.
Porcine coronary arteries, obtained from 32 pigs, were mounted in organ
baths, preconstricted with prostaglandin F(2alpha), and exposed to
quinaprilat, captopril, Ang-(1-7), and/or bradykinin. Bradykinin induced
complete relaxation (pEC(50)=8.11+/-0.07, mean+/-SEM), whereas
quinaprilat, captopril, and Ang-(1-7) alone were without effect.
Quinaprilat shifted the bradykinin curve to the left in a biphasic manner:
a 5-fold shift at concentrations that specifically block the C-domain (0.1
to 1 nmol/L) and a 10-fold shift at concentrations that block both
domains. Captopril and Ang-(1-7) monophasically shifted the bradykinin
curve to the left, by a factor of 10 and 5, respectively. A 5-fold shift
was also observed when Ang-(1-7) was combined with 0.1 nmol/L quinaprilat.
Repeated exposure of porcine coronary arteries to 0.1 micromol/L
bradykinin induced B(2) receptor desensitization. The addition of 10
micromol/L quinaprilat or Ang-(1-7) to the bath, at a time when bradykinin
alone was no longer able to induce relaxation, fully restored the relaxant
effects of bradykinin. Angiotensin II type 1 or 2 receptor blockade did
not affect any of the observed effects of Ang-(1-7). In conclusion,
Ang-(1-7), like quinaprilat and captopril, po
AT(2) receptor-mediated vasodilation in the heart: effect of myocardial infarction
To investigate the functional consequences of postinfarct cardiac
angiotensin (ANG) type 2 (AT(2)) receptor upregulation, rats underwent
coronary artery ligation or sham operation and were infused with ANG II
3-4 wk later, when scar formation is complete. ANG II increased mean
arterial pressure (MAP) more modestly in infarcted animals than in sham
animals. The AT(1) receptor antagonist ir
Evaluación de las subpoblaciones de linfocitos T en pacientes tuberculosos empleand la modulación con teofilina
Genetics of ACPA-positive rheumatoid arthritis: the beginning of the end?
Heritability is a measure for the contribution of genetic variation to the variation in liability to disease and for rheumatoid arthritis (RA) had previously been estimated to be about 60%. This has been recently confirmed and could show that the heritability of anti-citrullinated protein autoantibody (ACPA)-positive and ACPA-negative RA is similar. Apart from gender, the main known genetic factor is HLA, and its contribution to genetic variation has previously been estimated as 37% but recent studies indicate that this figure may be too high. HLA-linked genes, and in particular the HLA-DRB1 SE alleles, predispose much more strongly to ACPA-positive than to ACPA-negative RA. The same is true for the protective effect of DERAA-positive DRB1 alleles. It has been calculated that the contribution of the protective and predisposing HLA alleles to genetic variance is about 40% for ACPA-positive and 2% for ACPA-negative RA. A meta-analysis indicated that the protective effect may be confined to the HLA-DRB1*1301 allele. The search for non-HLA genes contributing to the genetic variation in RA susceptibility has implicated about 30 other loci/genes. The OR of the associations with these non-HLA polymorphisms is considerably lower than the ORs of sex and HLA as is their contribution to the genetic variation-namely, altogether only about 5%. This means that known genetic factors do not explain much more than 50% of the genetic variance of ACPA-positive RA. Until recently, the only established non-genetic factor contributing to RA susceptibility was smoking. It has recently been shown that non-inherited maternal HLA-DRB1 DERAA-positive antigens (NIMA) should be added to the environmental factors affecting RA susceptibility.Stemcel biology/Regenerative medicine (incl. bloodtransfusion
Genetic risk factors for autoimmune diseases
In most autoimmune diseases multigenic factors play a significant role in pathogenesis. Progress in identifying these genetic factors, many of which are located outside the major histocompatibility complex, was the subject of a recent meeting. Chemicals/CAS: Interleukin-10, 130068-27-8; Transforming Growth Factor beta; Tumor Necrosis Factor-alph
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