421 research outputs found

    2-Hy­droxy-N′-(5-hy­droxy-2-nitro­benzyl­idene)-3-methyl­benzohydrazide

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    The title compound, C15H13N3O5, was prepared by condensing 5-hy­droxy-2-nitro­benzaldehyde and 2-hy­droxy-3-methyl­benzohydrazide in methanol. The two benzene rings make a dihedral angle of 3.9 (3)°. An intra­molecular O—H⋯O hydrogen bond is observed. The crystal structure is stabilized by inter­molecular O—H⋯O and N—H⋯O hydrogen bonds, and C—H⋯O and π–π inter­actions [centroid–centroid distances = 3.5658 (17)–3.9287 (19) Å]

    Inhibition of cell growth and invasion by epidermal growth factor-targeted phagemid particles carrying siRNA against focal adhesion kinase in the presence of hydroxycamptothecin

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    <p>Abstract</p> <p>Background</p> <p>Previous studies demonstrated the EGF-targeted phagemid particles carrying siRNA against Akt could be expressed efficiently in the presence of hydroxycamptothecin (HCPT). However, no significant cell growth inhibition was obtained. This study was to further investigate whether the EGF-targeted phagemid particles carrying siRNA would be a promising tool for anti-cancer siRNA delivery.</p> <p>Results</p> <p>We found that pSi4.1-siFAK phagemid particles could significantly inhibit the expression of focal adhesion kinase in the HCPT-treated cells. Moreover, we also observed that the particles could potently suppress cell growth and cell invasion.</p> <p>Conclusion</p> <p>These results indicated that EGF-targeted phagemid particles might be a promising tool for anti-cancer siRNA delivery in the presence of HCPT.</p

    2-Hy­droxy-N′-(4-hy­droxy­benzyl­idene)-3-methyl­benzohydrazide

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    The title compound, C15H14N2O3, was prepared by condensing 4-hy­droxy­benzaldehyde and 2-hy­droxy-3-methyl­benzo­hydra­zide in methanol. The two benzene rings make a dihedral angle of 19.03 (11)°. An intra­molecular O—H⋯O hydrogen bond is observed. The crystal structure is stabilized by inter­molecular O—H⋯O and N—H⋯O hydrogen bonds and C—H⋯O inter­actions, which lead to the formation of a three-dimensional network

    Interleukin-11-induced capillary leak syndrome in primary hepatic carcinoma patients with thrombocytopenia

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    <p>Abstract</p> <p>Background</p> <p>Capillary leak syndrome (CLS) is a rare condition characterized by recurrent episodes of generalized edema and severe hypotension associated with hypoproteinemia. Interleukin-11 (IL-11) is a promising therapeutic agent for thrombocytopenia. A direct correlation between IL-11 and CLS has never been reported previously, particularly in patients with hepatic carcinoma.</p> <p>Case presentation</p> <p>We describe two cases of CLS after IL-11 administration in two males with thrombocytopenia. Case 1 was a 46-year-old man with recurrence of hepatic carcinoma who was treated with IL-11 (3 mg per day). After four days of therapy, hypotension and hypoproteinemia were detected. The chest X-ray and B ultrasound of the abdomen showed pleural effusion and ascites. IL-11 was then discontinued, fluid resuscitation was performed, and fresh frozen plasma and packed red blood cells were transfused into this patient. The patient had recovered after 19 days of treatment.</p> <p>Case 2 was a 66-year-old man who had undergone radiofrequency ablation (RFA) for hepatic carcinoma. He was treated with IL-11 (3 mg per day) for thrombocytopenia. After two days of therapy, this patient complained of dyspnea with bilateral edema of the hands. Laboratory values showed hypoproteinemia. IL-11 was stopped and human albumin was transfused at a rate of 10 g per day. On the 4<sup>th </sup>day, fluid resuscitation was performed. The patient had recovered after treatment for two weeks.</p> <p>Conclusions</p> <p>The detection of IL-11-induced CLS supports the hypothesis that CLS could be a severe side effect of IL-11 treatment in some patients. These two case reports also demonstrate that patients with hepatic carcinoma who experience this rare form of CLS after treatment with IL-11 seem to respond to a therapeutic regimen that involves hydroxyethyl starch, albumin, and diuretic therapy. Liver cancer patients might be more susceptible to CLS because of poor liver function and hypersplenia. In addition, bleeding after RFA might be a further inducer of CLS.</p

    N′-(3-Eth­oxy-2-hy­droxy­benzyl­idene)-2-hy­droxy-3-methyl­benzohydrazide

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    The title compound, C17H18N2O4, crystallizes with two independent mol­ecules in the asymmetric unit. The two benzene rings in each mol­ecule make dihedral angles of 7.6 (3) and 3.9 (3)°. Intra­molecular O—H⋯N and O—H⋯O hydrogen bonds are present in each mol­ecule. In the crystal, N—H⋯O hydrogen bonds link the mol­ecules into chains propagating in [010]. The are also a number of C—H⋯O and π–π inter­actions present [centroid–centroid distances = 3.874 (4) and 3.904 (3) Å], that result in the formation of a three-dimensional network

    N′-(4-Diethyl­amino-2-hy­droxy­benzyl­idene)-4-methyl­benzohydrazide

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    The title compound, C19H23N3O2, was prepared by condensing 4-diethyl­amino-2-hy­droxy­benzaldehyde and 4-methyl­benzo­hydrazide in methanol. The asymmetric unit contains two independent mol­ecules in which the two benzene rings make dihedral angles of 30.3 (3) and 18.9 (3)°. Intra­molecular O—H⋯N hydrogen bonds are observed in both mol­ecules. The crystal structure is stabilized by N—H⋯O hydrogen bonds, which form chains along the a axis

    8-Thia-1,6-diaza­bicyclo­[4.3.0]nonane-7,9-dione

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    There are two independent mol­ecules, A and B, in the asymmetric unit of the title compound, C6H8N2O2S. In the crystal, pairs of inter­molecular S⋯O contacts [3.286 (1) Å] link the B mol­ecules into inversion dimers

    Impact of the tissue factor pathway inhibitor gene on apoptosis in human vascular smooth muscle cells

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    Tissue factor pathway inhibitor (TFPI) plays a vitally important role in the blood coagulation pathway. Recent studies indicated that TFPI induces apoptosis in vascular smooth-muscle cells (VSMCs) in animals. The present study investigated whether the TFPI gene could also induce apoptosis in human vascular smooth-muscle cells (hVSMCs). Such cells were isolated from human umbilical arteries and subsequently transfected with pIRES-TFPI plasmid (2 μg/mL). MTT assaying and cell counting were applied to measure cell viability and proliferation, RT-PCR was utilized to analyze TFPI gene expression in the cells. Apoptosis was analyzed by fluorescence activated cell sorting (FACS). Several key proteins involved in apoptosis were examined through Western blotting. It was shown that TFPI gene transfer led to its increased cellular expression, with a subsequent reduction in hVSMC proliferation. Further investigation demonstrated that TFPI gene expression resulted in lesser amounts of procaspase-3, procaspase-8 and procascase-9, and an increased release of mitochondrial cytochrome c (cyt-c) into cytoplasm, thereby implying the involvement of both extrinsic and intrinsic pathways in TFPI gene-induced apoptosis in hVSMCs
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