Endothelial Dysfunction and Increased Carotid Intima-Media Thickness in the Patients with Slow Coronary Flow

Flow mediated brachial dilatation (FMD) and carotid intima-media thickness (IMT) have been a surrogate for early atherosclerosis. Slow coronary flow in a normal coronary angiogram is not a rare condition, but its pathogenesis remains unclear. A total of 85 patients with angina were evaluated of their brachial artery FMD, carotid IMT and conventional coronary angiography. Coronary flow was quantified using the corrected thrombosis in myocardial infarction (TIMI) frame count method. Group I was a control with normal coronary angiography (n = 41, 56.1 ± 8.0 yr) and group II was no significant coronary stenosis with slow flow (n = 44, 56.3 ± 10.0 yr). Diabetes was rare but dyslipidemia and family history were frequent in group II. Heart rate was higher in group II than in group I. White blood cells, especially monocytes and homocysteine were higher in group II. The FMD was significantly lower in group II than in group I. Elevated heart rate, dyslipidemia and low FMD were independently related with slow coronary flow in regression analysis. Therefore, endothelial dysfunction may be an earlier vascular phenomenon than increased carotid IMT in the patients with slow coronary flow

Autologous stem cells collected after debulking by high dose chemotherapy in late phase chronic myeloid leukemia may improve Imatinib efficacy

The current curative therapeutic option for the treatment of chronic myeloid leukemia (CML) in the chronic phase is still allogeneic stem cell transplantation (SCT). For the patients who are not candidates for allogeneic SCT, Imatinib is the treatment of choice. It was found that high dose chemotherapy with autologous stem cell rescue prolongs the disease-free survival and may also restore sensitivity to interferon. Here we report the results of Imatinib treatment in three late-phase CML patients who were submitted to autologous SCT following resistance to interferon. Complete cytogenetic response and major molecular response were achieved in the three cases. Imatinib has the potential to induce late molecular remissions during the course of treatment and its effect may be optimized by a previous autologous SCT in this type of patients. (c) 2006 Published by Elsevier Ltd

Roles of HMGA proteins in cancer.

The high mobility group A (HMGA) non-histone chromatin proteins alter chromatin structure and thereby regulate the transcription of several genes by either enhancing or suppressing transcription factors. This protein family is implicated, through different mechanisms, in both benign and malignant neoplasias. Rearrangements of HMGA genes are a feature of most benign human mesenchymal tumours. Conversely, unrearranged HMGA overexpression is a feature of malignant tumours and is also causally related to neoplastic cell transformation. Here, we focus on the role of the HMGA proteins in human neoplastic diseases, the mechanisms by which they contribute to carcinogenesis, and therapeutic strategies based on targeting HMGA proteins