Met/HGF receptor modulates bcl-w expression and inhibits apoptosis in human colorectal cancers

The met proto-oncogene is the tyrosine kinase growth factor receptor for hepatocyte growth factor. In the present study, we investigated the role of met expression on the modulation of apoptosis in colorectal tumours. The gene expressions of c- met and the anti-apoptotic bcl -2 family, including bcl -2, bcl -x L and bcl-w, were analysed in human colorectal adenomas and adenocarcinomas by using a quantitative polymerase chain-reaction combined with reverse transcription. In seven of 12 adenomas and seven of 11 carcinomas, the c- met gene was overexpressed. The bcl -w, bcl -2 and bcl -x L genes were over-expressed in nine, five and six of 12 adenomas and in five, two and seven of 11 carcinomas, respectively. The c- met mRNA level in human colorectal adenomas and carcinomas was correlated with bcl -w but not with bcl -2 or with bcl -x L mRNA level. The administration of c- met -antisense oligonucleotides decreased Met protein levels in the LoVo human colon cancer cell line. In the case of c- met -antisense-treated cells, apoptotic cell death induced by serum deprivation was more prominent, compared to control or c- met -nonsense-treated cells. Treatment with c- met -antisense oligonucleotides inhibits the gene expression of bcl -w in LoVo cells. On the other hand, the gene expression of bcl -2 or bcl -x L was not affected by treatment with c- met -antisense oligonucleotides. These findings suggest that Met expression modulates apoptosis through bcl -w expression in colorectal tumours. © 2000 Cancer Research Campaig

Gallot-Tanno Theorem for closed incomplete pseudo-Riemannian manifolds and applications

We extend the Gallot-Tanno Theorem to closed pseudo-Riemannian manifolds. It is done by showing that if the cone over a manifold admits a parallel symmetric $(0,2)-$tensor then it is Riemannian. Applications of this result to the existence of metrics with distinct Levi-Civita connections but having the same unparametrized geodesics and to the projective Obata conjecture are given. We also apply our result to show that the holonomy group of a closed $(O(p+1,q),S^{p,q})$-manifold does not preserve any nondegenerate splitting of $\R^{p+1,q}$.Comment: minor correction

CALCIFICATION IN THE ARTICULATED CORALLINE ALGA CORALLINA-PILULIFERA, WITH SPECIAL REFERENCE TO THE EFFECT OF ELEVATED CO2 CONCENTRATION

Calcification in Corallina pilulifera Postels et Ruprecht displayed diurnal variations in aerated (350 ppm CO2) culture media, with faster rates during the light than during the dark period. Addition of CO2 (air + 1250 ppm) inhibited calcification. This was attributable to the decreased pH resulting from CO2 addition. Both photosynthesis and calcification were enhanced in seawater, with elevated dissolved inorganic carbon concentrations at a constant pH of 8.2

ENHANCED GROWTH OF THE RED ALGA PORPHYRA-YEZOENSIS UEDA IN HIGH CO2 CONCENTRATIONS

Leafy thalli of the red alga Porphyra yezoensis Ueda, initiated from conchospores released from free-living conchocelis, were cultured using aeration with high CO2. It was found that the higher the CO2 concentration, the faster the growth of the thalli. Aeration with elevated CO2 lowered pH in dark, but raised pH remarkably in light with the thalli, because the photosynthetic conversion of HCO3- to OH- and CO2 proceeded much faster than the dissociation of hydrated CO2 releasing H+. Photosynthesis of the alga was found to be enhanced in the seawater of elevated dissolved inorganic carbon (DIC, CO2 + HC O3- + CO3-). It is concluded that the increased pH in the light resulted in the increase of DIC in the culture media, thus enhancing photosynthesis and growth. The relevance of the results to removal of atmospheric CO2 by marine algae is discussed

Lipid-soluble smoke particles damage endothelial cells and reduce endothelium-dependent dilatation in rat and man

BACKGROUND: Cigarette smoking is a strong risk factor for vascular disease and known to cause dysfunction of the endothelium. However, the molecular mechanisms involved are still not fully understood. METHODS: In order to reveal the direct effects of lipid-soluble smoke particles on the endothelium, ring segments isolated from rat mesenteric arteries and human middle cerebral arteries (MCA) obtained at autopsy were incubated for 6 to 48 hrs in the presence of dimethylsulphoxide (DMSO)-soluble particles from cigarette smoke (DSP), i.e. lipid-soluble smoke particles. The endothelial microstructure was examined by transmission electron microscopy. The endothelial function was evaluated by acetylcholine (ACh)-induced endothelium-dependent vasodilatation, using a sensitive myograph. RESULTS: After DSP treatment, the arterial endothelium was swollen and loosing its attachment. In functional tests, the total ACh-induced dilatation, the nitric oxide (NO)-mediated and the endothelium-derived hyperpolarization factor (EDHF)-mediated dilatations were significantly decreased by DSP in a time- and concentration-dependent manner (p < 0.05). Nicotine, an important compound in cigarette smoke had, in an equivalent concentration as in DSP, no such effects (p > 0.05). Similar results were obtained in the human MCA. CONCLUSION: Thus, we demonstrate that the lipid-soluble smoke particles, but not nicotine, caused damage to arterial endothelium and reduced the endothelium-dependent dilatation in man and rat