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Biomedical subjects

I Blasko

Publications and source records attributed to I Blasko.

21 records · Page 2Linked to original sources
PubMed1989

[Mineralization status in bones in patients with femoral neck fractures].

The authors present the results of the evaluation of the state of the art of mineralization of the bone in 56 patients over 45 years of age with the fracture of the femoral neck. The state of the art of mineralization was evaluated by means of bone indices. In each patient there were determined 6 values of bone indices and thus they got a more objective picture of the state of the art of bone tissue. They found out that most cases of fractures occurred on the osteporous skeleton. For pathological values corresponding to osteoporosis they considered such values when the bone index according to Barnet-Nordin was less than 45, Garn index less than 67, Singh index equal to the values I, II, III and Kocian index corresponded to normograms. Lower cortico-diaphyseal index on the side of the fracture in comparison with the contralateral side they explain by timely demineralization after the fracture during immobilization. Proceeding from the results achieved they emphasize the necessity of a timely prevention and treatment of osteoporosis.

Aged↗
PubMedDate not supplied

The possible role of the immune system in Alzheimer's disease.

Currently, there is little doubt that the immune system plays a role in the neurodegenerative process in Alzheimer's disease (AD). Inflammatory proteins such as complement components, enzymes, eicosanoids, and cytokines are found in association with cerebral amyloid plaques and may exacerbate the fundamental pathology of AD, by stimulating Amyloid beta (A beta) production, supporting its aggregation and increasing its cytotoxicity. Activated microglia and astrocytes are the main source of these proteins, and A beta may trigger their release. Interestingly, there are also indications that the immune system may play a protective role against the development of AD. Microglial cells have been shown to degrade A beta, and recent evidence suggests that autoreactive A beta-specific T cells may be relevant to the elimination of the peptide. This mechanism seems, however, impaired in the majority of patients with AD. The immune system seems thus to represent a natural line of defense against the accumulation of dangerous amyloidogenic substances. Impairment of this specific immunological defense mechanism and the failure to eliminate a toxic metabolite can be the basis for a chronic nonspecific inflammatory process in the brain, as described above. AD is a good example how an immune response initially aiming at maintaining the integrity of the body may fail and consequently lead to tissue destruction and neuronal loss.

Alzheimer Disease↗