The article presents a case of intravital diagnosis of a rare heart disease, isolated primary amyloidosis. The clinical onset of the disease was heart failure (HF) that was resistant to treatment; chemotherapy was ineffective and was poorly tolerated by the patient. The diagnostics was based on a combination of refractory HF and changes in echocardiography data (atrial dilatation, small size of the left ventricular cavity, interventricular septal hypertrophy with the presence of hyperechoic inclusions of the "granular fluorescence" type), and changes detected by contrast-enhanced cardiac magnetic resonance imaging.
View Article and Find Full Text PDFWe studied a role of the inducible heat shock protein 70 (Hsp70) in cellular response to radiosensitizing treatments with inhibitors of the heat shock protein 90 (Hsp90) chaperone activity. Cell lines derived from solid tumors of different origin were treated with the Hsp90 inhibitors (17AAG, geldanamycin, radicicol, NVP-AUY922) or/and γ-photon radiation. For comparison, human cells of the non-cancerous origin were subjected to the same treatments.
View Article and Find Full Text PDFProof of clinical equivalence of generic and original dugs - the way to lessen cost of therapy of patients while providing comparable clinical effects. We present in this paper results of 1 year follow-up of 115 patients receiving Egithromb or Plavics after coronary artery stenting. Comparable clinical efficacy and safety of Egithromb and Plavics has been established.
View Article and Find Full Text PDFUsing the Ehrlich ascite carcinoma cells, exposed to oxidative stress, heat shock, cytochalasin B, vinblastine, Triton X-100 and energy starvation, morphological changes, DNA degradation, and form of cell death were investigated. A rather clear specificity of cell morphology, characteristic of apoptosis, was revealed for the most of treatments, including membrane blebs, chromatin condensation and apoptotic body formation. Karyorhexis was not common for the examined cells.
View Article and Find Full Text PDFPreviously we have found that stationary Ehrlich ascites carcinoma (EAC) cells in vivo accumulated heat shock proteins (HSPs) and became resistant to necrotic death induced by prolonged energy deprivation of hyperthermia. Here we report that apoptotic death induced by nutrient starvation, transient ATP depletion, heat shock and a microtubule-disrupting drug, vinblastine, was also suppressed in stationary EAC cells comparing with exponential cells. When exponential (sensitive) cells were subjected to short-term heating with recovery to accumulate inducible form of HSP70, they also became resistant to all of the employed apoptosis-inducing exposures, and an inhibitor of cytosolic protein synthesis, cycloheximide, prevented acquisition of the resistance.
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