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K Maas

Publications and source records attributed to K Maas.

8 recordsLinked to original sources
PubMed2004

A gene expression signature for recent onset rheumatoid arthritis in peripheral blood mononuclear cells.

BACKGROUND: In previous studies the presence of a distinct gene expression pattern has been shown in peripheral blood cells from patients with autoimmune disease. OBJECTIVE: To determine whether other specific signatures might be used to identify subsets of these autoimmune diseases and whether gene expression patterns in early disease might identify pathogenetic factors. METHODS: Peripheral blood mononuclear cells were acquired from patients with rheumatoid arthritis (RA) and analysed by microarrays containing over 4300 named human genes. Patients with RA for <2 years were compared with subjects with longstanding RA (average duration 10 years) and with patients with other immune or autoimmune diagnoses. RESULTS: Cluster analyses permitted separation of the patients with early RA (ERA) from those with longstanding disease. Comparison with other patient groups suggested that the ERA signature showed some overlap with that seen in the normal immune response to viral antigen as well as with a subset of patients with systemic lupus erythematosus. CONCLUSIONS: The ERA signature may reflect, in part, a response to an unknown infectious agent. Furthermore, shared features with some lupus patients suggest that common aetiological factors and pathogenetic pathways may be involved in these two autoimmune disorders.

Acute Disease↗
PubMed2000

Microvascular remodelling in chronic airway inflammation in mice.

1. Chronic inflammation is associated with blood vessel remodelling, including vessel proliferation and enlargement, and changes in vessel phenotype. We sought to characterize these changes in chronic airway inflammation and to determine whether corticosteroids that inhibit inflammation, such as dexamethasone, can also reduce microvascular remodelling. 2. Chronic airway inflammation was induced in C3H mice by infection with Mycoplasmapulmonis and the tracheal vessels treatment also decreased the immunoreactivity for P-selectin and the number of adherent leucocytes (595 +/- 203 vs 2,024 +/- 393 cells/ mm2 in treated and non-treated infected mice, respectively). 6. We conclude that microvascular enlargement and changes in vessel phenotype are features of some types of chronic inflammation and, furthermore, that dexamethasone reverses the microvascular enlargement, changes in vessel phenotype and leucocyte influx associated with chronic inflammatory airway disease.

Animals↗
PubMed1994

Selected indications for and applications of magnetic resonance angiography in children.

The purpose of this study was to investigate the efficacy and practicality of magnetic resonance angiography (MRA) in evaluating pediatric cerebrovascular disorders. A retrospective evaluation was performed of MR angiograms in 20 pediatric patients with cerebrovascular pathology. When appropriate, comparisons were made with duplex ultrasonography or conventional catheter angiography. MRA accurately assessed the patency of carotid reanastomoses in 8 babies who had previously undergone extracorporeal membrane oxygenation (ECMO). In 6 patients with moyamoya syndrome, MRA accurately evaluated stenotic intracranial carotid and circle of Willis arteries and progressive enlargement of the superficial temporal and middle cerebral arteries after revascularization procedures, and thus obviated the need for sequential angiograms. Thrombi and emboli were identified in 4 of 5 patients with symptoms and imaging evidence of an acute stroke. Two-dimensional time-of-flight MR venograms, acquired in both axial and coronal planes, were useful for preoperative venous mapping in a patient with an occipital encephalocele and detecting venoocclusive disease. MRA provided diagnostically useful information in a spectrum of pediatric cerebrovascular disorders. It can be used as the initial vascular imaging modality for patients with imaging evidence of acute cerebrovascular event, to evaluate progression of chronic vasoocclusive disease, to evaluate vessel patency following intracranial revascularization surgery, and for visualization of the venous circulation.

Adolescent↗
PubMed1993

Angiotensin II-induced vasopressin release is mediated through alpha-1 adrenoceptors and angiotensin II AT1 receptors in the supraoptic nucleus.

The central actions of angiotensin II (ANG II) include the release of vasopressin (AVP) from the supraoptic nucleus (SON) via the pituitary gland into the blood. In conscious rats, we investigated whether catecholamines in the SON are involved in this release process. It was found that i.c.v. injections of ANG II (100 ng) selectively increased the release of norepinephrine (NA) from the SON. Like the ANG II i.c.v.-induced AVP release, this effect was prevented by i.c.v. pretreatment with the ANG II AT1 receptor antagonist, losartan (5 micrograms). The alpha-1 adrenoceptor antagonist, prazosin (0.7 nmol), injected bilaterally into the SON, significantly reduced the ANG II 100-ng i.c.v.-induced AVP release. Pretreatment with the alpha-2, beta-1 and beta-2 adrenoceptor antagonists, idazoxan, atenolol and ICI 118551, respectively, had no effect. Injections of NA into the SON increased plasma AVP at doses up to 10 nmol but not at higher doses (30-100 nmol). The effects of NA were mimicked by the alpha-1 adrenoceptor agonist, methoxamine (1-5 nmol). Bilateral pretreatment of the SON with losartan (5 micrograms) markedly inhibited the i.c.v. ANG II 100 ng-induced AVP release. The increase in AVP release after ANG II injections into the SON was also inhibited by losartan pretreatment into the SON, whereas prazosin had no effect. These results demonstrate that the ANG II-induced release of AVP is initiated through periventricular ANG II AT1 receptors and involves postsynaptic alpha-1 adrenoceptor stimulation in the SON. In addition, ANG II AT1 receptors in the SON can contribute to AVP release after periventricular ANG II receptor stimulation.

Adrenergic alpha-1 Receptor Antagonists↗
PubMedDate not supplied

Ultramicro zone melting.

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Chemistry Techniques, Analytical↗