PubMed Health⌕ Search

Biomedical subjects

V Hafner

Publications and source records attributed to V Hafner.

5 recordsLinked to original sources
PubMed2006

[Safety of blood transfusion at the international level. The role of WHO].

Blood safety is an international public health challenge, particularly since the emergence of HIV AIDS. Recognizing the gross disparities between countries in the adequacy of national blood supplies and the risks arising from poorly organized services, particularly in developing countries, the World Health Organization has developed a global strategy for blood safety and availability. Dr N. Dhingra, coordinator, blood transfusion safety, WHO Headquarters, and Dr V. Hafner, focal point for blood safety in the WHO regional office for Europe, present the main features of this strategy: well-organized, nationally coordinated blood transfusion services with quality systems in all areas; the collection of blood only from voluntary non-remunerated blood donors from low-risk populations; the quality-assured testing of all donated blood; the safe and appropriate use of blood and blood products; and global collaboration for blood safety. WHO's programs, some difficulties encountered and outcomes are also described in this article.

Adult↗
PubMed1999

Aldose reductase functions as a detoxification system for lipid peroxidation products in vasculitis.

Giant cell arteritis (GCA) is a systemic vasculitis preferentially affecting large and medium-sized arteries. Inflammatory infiltrates in the arterial wall induce luminal occlusion with subsequent ischemia and degradation of the elastic membranes, allowing aneurysm formation. To identify pathways relevant to the disease process, differential display-PCR was used. The enzyme aldose reductase (AR), which is implicated in the regulation of tissue osmolarity, was found to be upregulated in the arteritic lesions. Upregulated AR expression was limited to areas of tissue destruction in inflamed arteries, where it was detected in T cells, macrophages, and smooth muscle cells. The production of AR was highly correlated with the presence of 4-hydroxynonenal (HNE), a toxic aldehyde and downstream product of lipid peroxidation. In vitro exposure of mononuclear cells to HNE was sufficient to induce AR production. The in vivo relationship of AR and HNE was explored by treating human GCA temporal artery-severe combined immunodeficiency (SCID) mouse chimeras with the AR inhibitors Sorbinil and Zopolrestat. Inhibition of AR increased HNE adducts twofold and the number of apoptotic cells in the arterial wall threefold. These data demonstrate that AR has a tissue-protective function by preventing damage from lipid peroxidation. We propose that AR is an oxidative defense mechanism able to neutralize the toxic effects of lipid peroxidation and has a role in limiting the arterial wall injury mediated by reactive oxygen species.

Aldehyde Reductase↗
PubMed1998

Giant cell arteritis--a molecular approach to the multiple facets of the syndrome.

Molecular studies of giant cell arteritis indicate that T cells are recruited to the wall of medium-sized and large arteries, are activated locally, produce IL-2 and IFN-gamma, and regulate the activity of tissue-infiltrating macrophages. Downstream effects of T cell activation include the production of proinflammatory cytokines, metalloproteinases, and growth factors. Growth factors are instrumental in the process of intimal hyperplasia, leading to luminal occlusion and tissue ischemia. The amounts of IL-2, IFN-gamma, and the growth factor PDGF in the vascular lesions varies among patients and are correlated with differences in patterns of clinical manifestations. Giant cell arteritis complicated by cranial ischemia, such as anterior optic neuropathy or stroke, is characterized by high levels of IFN-gamma and PDGF. If the IFN-gamma-PDGF loop is less developed, fever and wasting can dominate the disease. Dominant production of IL-2 is associated with polymyalgia rheumatica. The finding of different inflammatory pathways translating into different clinical phenotypes may reflect differences in the contribution of the arterial wall. Alternative hypotheses include a role of multiple disease-inducing antigens with different tissue distributions or tropisms.

Brain Ischemia↗
PubMedDate not supplied

[Temporary changes and permanent changes in the erythrocyte blood-group antigens in malignant hemopathies].

Samples of peripheral blood were taken from 11 patients (blood group A, B and O), suffering from acute myeloblastic leukemia (AML), acute lymphoblastic leukemia (ALL), myelodysplastic syndrome (MDS), before and after chemotherapy, compared to normal control samples. The RBC's typing was done by standard agglutination technique (with conventional human and murine anti-sera) and flow cytometry. While using different reagent dilutions, a lower expression of the A or B antigen was noticed in all patients, even if direct typing of the RBC's revealed an apparently normal pattern. The most important depletion of antigenic expression was found to correspond to the highest concentration of myeloblasts in the bone marrow, with hypoplastic erythrocytic series. The modified H reactivity, detected at admission, was still present after complete remission, as an expression of the residual disease. Studies of the H expression could eventually become a parameter of evaluating the moment of relapse of the myeloproliferative disease.

ABO Blood-Group System↗