[Blood lipid changes at long-term antiretroviral treatment].

Unlabelled: The aim of study was to find the development trend of blood lipid concentration in a group of HIV positive patients treated by combination antiretroviral therapy (cART). We followed changes during the therapy and evaluated their aterogennic nature.

Methods: The group included 118 patients stepwise allocated to the AIDS Centre of the Faculty Hospital Brno, with the monitoring period being up to 1 month as the minimum and up to 17 years as the maximum.

[HIV lipodystrophy].

Combined antiretroviral therapy results in extraordinary decrease of morbidity and mortality of HIV-infected patients and in an essential change of the HIV/AIDS disease prognosis. However, long-term intake of antiretroviral medicaments is related to occurrence of metabolic and morphological abnormalities, of which some have been combined into a new syndrome--the so called HIV lipodystrophy. The HIV lipodystrophy syndrome covers metabolic and morphological changes.

[Kaposi's sarcoma].

Kaposi's sarcoma (KS) is an unusual form of tumor which in the era of HIV/AIDS pandemic is increasingly observed outside the original endemic areas. It was shown that the development of KS is in directly related to infection with human herpes virus 8 (HHV-8). The pathophysiology of KS is complex and is influenced by HIV co-infection and by global cytokine interactions.

[Dyslipidaemia inducted by antiretroviral agents].

The clinical course of HIV/AIDS has been substantially modified by up-to date therapy in the recent years. The progress of the disorder has changed--today it is a chronic disease of many years course. Already in 1997 and 1998 it turned out that adverse metabolic changes which significantly affect the subsequent progress of the disease were produced by long-term HAART (highly active antiretroviral therapy).

A proteomic analysis of protein variations during differentiation of v-myb-transformed monoblasts.

v-myb oncogene of avian myeloblastosis virus (AMV) transforms myelomonocytic cells in vitro and induces acute monoblastic leukemia in vivo. The transforming effect of the v-myb can be suppressed using phorbol ester (TPA) or histone deacetylase inhibitor trichostatin A (TSA), the inducers of cell differentiation that are in clinical trials. In this study, we used proteomics-based approach to identify proteins with variable expression in differentiated BM2 cells.