Central neurocytoma--case report.

A 29-year-old male was admitted with chronic headache on February 26, 1987, when there were no neurological deficits or physical abnormalities. Computed tomographic (CT) scans showed a mixed-density mass with no evidence of calcification in the left lateral ventricle, which was irregularly enhanced by contrast medium. Under a diagnosis of an intraventricular glial tumor, surgery was performed via a left transcortical-transventricular approach on March 31. The highly vascular, nodular tumor, originated from the lateral wall of the left lateral ventricle near the foramen of Monro, was successfully removed. The postoperative course was uneventful and he was discharged 3 months after postoperative irradiation. Light microscopic examination revealed the tumor cells with the clear cytoplasm and perinuclear halos characteristic of an oligodendroglioma. However, electron microscopy showed neuronal elements identical with central neurocytoma as reported by Hassoun et al. in 1982. These included large numbers of dense-core or clear vesicles in the cell processes and synaptic structures.     

Simple method for determination of triazolam in human plasma by high-performance liquid chromatography/tandem mass spectrometry

Triazolam was analyzed from human plasma samples by high-performance liquid chromatography (HPLC)-tandem mass spectrometry (MS/MS) with an MSpak GF polymer column (50 mm x 4.6 mm i.d., particle size 6 microm), which enabled direct injection of crude biological samples. Separation of triazolam, and lorazepam as the internal standard (IS) was carried out using 10mM ammonium acetate (pH 3.56)-0.1% formic acid and an acetonitrile gradient elution. Both compounds formed base peaks due to [M + H]+ ions by HPLC/ESI-MS, and product ions were produced from each [M + H]+ ion as seen by HPLC-MS/MS. Quantification of triazolam and the IS in plasma samples was made by selective reaction monitoring using each base peak of product ions of HPLC-MS/MS. The recovery range of triazolam spiked into plasma was 86.4-92.7%. The regression equation for triazolam showed excellent linearity in the range of 0.25-20 ng/mL, and the detection limit was 0.1 ng/mL. Intra- and inter-day precisions for triazolam in plasma samples were not greater than 12.4%. Accuracy for the drug was in the range of 88.0-101.4%. Data obtained after oral administration of triazolam in male and female subjects are also presented.     

Mutant Escherichia coli enterotoxin as a mucosal adjuvant induces specific Th1 responses of CD4+ and CD8+ T cells to nasal killed-bacillus calmette-guerin in mice

On single nasal immunization of mice with killed-bacillus calmette-guerin (BCG) plus a mutant Escherichia coli enterotoxin, delayed-type hypersensitivity was induced and BCG-infection decreased. Spleen cells, particularly CD4+ T cells among them produced IL-2, IFNgamma and TNFalpha in response to the killed-BCG or purified protein derivatives. CD8+ T cells including cytotoxic T lymphocytes produced IFNgamma and TNFalpha. However, both types of T cells reacted a little to Ag85B. The mutant induces cellular immunity to nasal killed-BCG vaccine and decreases BCG-infection. CD4+ and CD8+ T cells produce cytokines effective for tuberculosis. Although killed-BCG loses some antigens like Ag85B, nasal killed-BCG plus the mutant is useful for tuberculosis.     

Fusion imaging of the 3D MR cisternography/angiography for the assessment of the intracranial major cerebral arterial stenosis

The fusion imaging of the 3D MR cisternography (MRC) and 3D MR angiography (MRA) was applied for the assessment of the major cerebral arterial stenosis. The outer wall configurations of the stenotic lesions of the intracranial major cerebral arteries within a cisternal space were depicted by 3D MRC. Flow-related vascular structures were shown by 3D MRA. Fusion imaging was created by compositing volumetric data of MRC and co-registered MRA by using a workstation with transparent perspective volume-rendering technique. Stenotic lesions of the intracranial cerebral arteries were assessed as a discrepancy of 3D MRC and 3D MRA findings on a fusion image. Fusion imaging of 3D MRC/MRA could visualize stenotic lesions of the intracranial major cerebral arteries caused by atherosclerotic plaques; and this may provide useful information in the management of acute and chronic ischemic stroke caused by atherosclerosis of the intracranial major cerebral arteries.     

Involvement of hepatocyte growth factor in the development of bone metastasis of a mouse mammary cancer cell line, BALB/c-MC

Some cancers frequently affect the skeleton, and the bone microenvironment supports growth of certain cancer cells. After tumors metastasize to bone, they stimulate osteoclastogenesis and expand in the bone tissue. Hepatocyte growth factor (HGF), which was originally identified as a potent mitogen for hepatocytes, promotes tumor growth, invasion and metastasis. HGF is mainly produced by cells of mesenchymal origin, and osteoblasts/osteocytes and bone marrow stromal cells originate from mesenchymal cells. However, it is not clear what effect HGF has on tumor progression in bone metastasis. In the present study, we investigated the roles of HGF in bone metastasis using the mouse mammary cancer cell line BALB/c-MC. Cancer cells injected into hearts of mice metastasized to bone in their hind limbs. HGF immunoreactivity was detected in the stroma surrounding the tumor nests, and blood vessels expressing CD31 (a marker of endothelial cells) were observed in the HGF-positive area. To identify the cells producing HGF, we measured concentration of HGF in culture media. HGF concentration was elevated in osteoblast cultures (3.13+/-0.25 ng/ml), whereas HGF was undetectable (<0.4 ng/ml) in BALB/c-MC and bone marrow cell cultures. HGF concentration in osteoblast cultures increased 2.5-fold in response to 10(-6) M PGE(2). Addition of HGF to BALB/c-MC cultures caused doubling of the cell number. Moreover, Western blot analysis revealed expression of c-Met/HGF receptor by BALB/c-MC. In the Matrigel invasion chamber assay, addition of HGF to the bottom well increased the rate at which BALB/c-MC invaded the bottom well through the membrane. Furthermore, when osteoblasts were cultured in the bottom well, the number of BALB/c-MC cells that invaded the bottom well through the membrane increased 3.7-fold, compared to assays without osteoblasts. Addition of NK4, an inhibitor of HGF, completely abolished the enhancement of the invasive potential of the BALB/c-MC cells in the presence of osteoblasts. These findings suggest that HGF produced by osteoblasts induces migration of cancer cells from sinusoidal capillaries to bone marrow space and stimulates growth of cancer cells in the bone microenvironment. Thus, osteoblasts appear to promote bone metastasis of some cancers via HGF-c-Met signaling.     

Haemostatic and fibrinolytic parameters in septic patients with leukopenia or leukocytosis

Abstract: Induction of leukocytopenia by cytotoxic drugs protects against the generalized Shwartzman reaction induced by endotoxin. To elucidate the relationship between leukocyte number and in haemostatic and fibrinolytic disturbances in human sepsis, we studied 32 septic patients with abnormal leukocyte counts. Twenty patients had sepsis in the setting of leukopenia after chemotherapy for haematological malignancies. Twelve patients with leukocytosis developed sepsis associated with benign disorders. Concentrations of thrombin-antithrombin III complex (TAT), plasminogen activator inhibitor-1 (PAI-1) and plasma thrombomodulin (TM) in the leukocytosis group of (12.0 ± 11.0, 40.2 ± 27.0 and 5.5 ± 2.3 ng/ml, respectively) were significantly elevated compared to the leukopenia group of (3.8 ± 2.3, 18.0 ± 15.0 and 3.1 ± 1.0 ng/ml, respectively) and controls (3.3 ± 0.4, 10.5 ± 5.3, 3.0 ± 0.5 ng/ml, respectively). On the other hand, there were no significant differences in these values between leukopenia group and controls. Thus leucocytes may play important roles in thrombin generation, PAI-1 release and injury to endothelial cells.     

Oxylipins arabidopsides C and D from Arabidopsis thaliana

Two new oxylipins, arabidopsides C (1) and D (2), were isolated from the aerial parts of Arabidopsis thaliana, and the structures of 1 and 2 were elucidated using spectroscopic data, primarily NMR and MS, and chemical means. Arabidopsides C (1) and D (2) are rare digalactosyl diacylglycerides containing 12-oxophytodienoic acid and/or dinor-oxophytodienoic acid. Arabidopside D (2) and arabidopsides A (3) and B (4), which were also isolated from this plant, exhibited inhibitory effects on the growth of the root of cress (Lepidium sativum) seedlings at 5 x 10(-5) mol/L.     

Free radical scavenging and hepatoprotective actions of the medicinal herb, Crassocephalum crepidioides from the Okinawa Islands

Free radical scavenging and protective actions against chemically induced hepatotoxicity of Crassocephalum crepidioides were investigated. A water extract of C. crepidioides strongly scavenged superoxide anion, hydroxyl radical and also stable radical 1,1-diphenyl-2-picrylhydrazyl. Galactosamine (GalN, 400 mg/kg) and lipopolysaccharide (LPS, 0.5 microg/kg) induced hepatotoxicity of rats as seen by an elevation of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and of lipid peroxidation in liver homogenates was significantly depressed when the herbal extract was given intraperitoneally 1 and 15 h before GalN and LPS treatment. Similarly, carbon tetrachloride (CCl4) induced liver injury as evidenced by an increase in AST and ALT activities in serum was also inhibited by the extract pretreatment. Isochlorogenic acids, quercetin and kaempferol glycosides were identified as active components of C. crepidioides with strong free radical scavenging action. These results demonstrate that C. crepidioides is a potent antioxidant and protective against GalN plus LPS- or CCl4-induced hepatotoxicity.     

Inhibition of cultured bovine aortic smooth muscle cell proliferation by colominic acid

Colominic acid (CA) is an alpha2,8-linked polymer of sialic acid, originally isolated from capsular Escherichia coli K1. Since inhibition of arterial smooth muscle cell hyperplasia is one of the effective strategies to prevent atherosclerosis, we investigated the effect of CA, purified as an alpha2,8-linked homopolymer of N-acetylneuraminic acid, on the proliferation of bovine aortic smooth muscle cells in culture. The results demonstrate that CA inhibits the proliferation of the cells without nonspecific cell damage. Sulfation did not modify the inhibitory effect of CA. Specifically, the inhibitory effect of sulfated CA was almost equal to that of CA in vascular smooth muscle cell proliferation. On the other hand, it was suggested that the inhibition of the proliferation by CA is in a degree similar to that by heparin but weaker than that by sodium/calcium-spirulans, known sulfated polysaccharides as the potent inhibitor of vascular smooth muscle cells. The present data suggest that CA with or without sulfate groups can be an origin of beneficial agents that prevents atherosclerosis through a moderate inhibition of arterial smooth muscle cell proliferation.