Leiomyosarcoma of the inferior vena cava presenting as Budd-Chiari syndrome

A case of a 72-year-old male with a leiomyosarcoma of the inferior vena cava causing Budd-Chiari syndrome is described. Percutaneous decompression of the portal system was attempted but with no success. At autopsy, a large tumor arising from and completely obstructing the inferior vena cava was found, histologically proven to be a leiomyosarcoma. Over 50 cases of leiomyosarcoma of the inferior vena cava have been reported in the literature, the majority of which occurred in women and 1/3 of which were associated with the Budd-Chiari syndrome. Histologically up to two mitotic figures per 10 high power fields have been scored. This case indicates the unreliability of a low mitotic index as an indicator of benign behavior of smooth muscle neoplasms of the venous system.     

Identification and characterization of a high-affinity granulocyte- macrophage colony-stimulating factor receptor on primary rat oligodendrocytes

We previously showed the presence of receptors for granulocyte- macrophage colony-stimulating factor (GM-CSF) on tumor tissues and tumor cell lines that are derived from the neural crest. To determine whether normal neural cells express functional GM-CSF receptors, we isolated and analyzed primary rat brain cells, including microglia, astrocytes, and oligodendrocytes. Scatchard analysis of equilibrium binding of 125I-GM-CSF to primary rat oligodendrocytes showed an average of 1,110 GM-CSF binding sites per cell, with a kd of 20 pmol/L. In six separate experiments, no specific binding was detectable on the astrocyte population. Microglia were used in competitive binding experiments with oligodendrocytes, and addition of microglia did not increase the specific binding of labeled ligand to oligodendrocytes. In dose-response assays, we measured 3H-thymidine uptake in rat oligodendrocytes, microglia and control murine 32D cells stimulated with various concentrations of GM-CSF. Over concentration ranges of 0.025 to 1000 pmol/L, cell proliferation and peak 3H-thymidine incorporation was observed at approximately 30 pmol/L for both the control cells and the oligodendrocytes. However, the microglial cells did not proliferate in response to GM-CSF. These data indicate the presence of a functional receptor for GM-CSF on primary rat oligodendrocytes, and suggest that hematopoietic growth factors such as GM-CSF may play a role in nerve cell development, function, or response to injury.     

In vitro studies on cellular and molecular mechanisms of arsenic trioxide (As2O3) in the treatment of acute promyelocytic leukemia: As2O3 induces NB4 cell apoptosis with downregulation of Bcl-2 expression and modulation of PML-RAR alpha/PML proteins

It has been shown recently in China that arsenic trioxide (As2O3) is a very effective treatment for acute promyelocytic leukemia (APL). APL patients resistant to all-trans retinoic acid (ATRA) and conventional chemotherapy can still respond to AS2O3. In this study, we addressed the possible cellular and molecular mechanisms of this treatment by using NB4 cells as a model. The results show that: (1) As2O3 triggers relatively specific NB4 cell apoptosis at micromolar concentration, as proved by morphology, histogramic related nuclear DNA contents, and DNA gel eletrophoresis. (2) As2O3 does not influence bax, bcl-x, c-myc, and p53 gene expression, but downregulates bcl-2 gene expression at both mRNA and protein levels. (3) As2O3 induces a significant modulation of the PML staining pattern in NB4 cells and HL-60 cells. The micropunctates characteristic of PML-RAR alpha in NB4 cells dissappear after treatment with As2O3, whereas a diffuse PML staining occurs in the perinuclear cytoplasmic region. In addition, a low percentage of untreated NB4 cells exhibits an accumulation of PML positive particles in a compartment of cytoplasm. The percentage of these cells can be significantly increased after As2O3 treatment. A similar PML staining pattern is observed in apoptotic cells. (4) ATRA pretreatment does not influence As2O3-induced apoptosis. These results suggest that induction of cell apoptosis can be one of the mechanisms of the therapeutic effect of As2O3. Moreover, this apoptosis induction occurs independently of the retinoid pathway and may be mediated, at least partly, through the modulation of bcl-2, as well as PML-RAR alpha and/ or PML proteins.     

中药玉竹有效成分研究

自江苏海门产百合科植物玉竹[Polygonatum odoratum(Mill.)Druce]根茎的乙醇提取物中分得六个单体化合物,根据化学性质和光谱解析,鉴定其化学结构分别为β-谷甾醇(S-A)),β-谷甾醇-3-O-β-D-吡喃葡萄糖甙(S-B),25(R,S)螺甾-5-烯-3β-醇-3-O-β-D-吡喃葡萄糖基-(1→2)-[β-D-吡喃木糖基-(1→3)]-β-D-吡喃葡萄糖基(1→4)-β-吡喃半乳糖甙(POD-I),25(R)螺甾-5-烯-3β,14a-二醇-3-0-β-D-吡喃葡萄糖基-(1→2)-[β-D-吡喃木糖基-(1→3)]-β-D-吡喃葡萄糖基-(1→4)-β-D-吡喃半乳糖甙(POD-II),25(R,S)螺甾-5-烯-3β,14a-二醇-3-O-β-D-吡喃葡萄糖基-(1→2)-[β-D-吡喃葡萄糖基-(1→3)]-β-D-吡喃葡萄糖基(1→4)-β-D-吡喃半乳糖甙(POD-III)和25(R,S)螺甾-5-烯-3β-醇-3-O-β-D-吡喃葡萄糖基-(1-2)-[β-D-吡喃葡萄糖基-(1→3)]-β-D-吡喃哺葡萄糖基(1→4)-β-D-吡喃半乳糖甙(POD-IV)。POD-II为首次分离得到的25(R)构型的纯品,POD-III和POD-IV为首次从玉竹中得到。经初步药理实验显示,POD-II有诱生集落刺激因子(CSF)的作用,POD-III能协同ConA和Lps对淋巴细胞转化有促进作用。