ALBERT

Description: The Turkana rifted zone in northern Kenya is a long-lived and polyphased rift system where the lack of well-marked rift morphology makes it difficult to identify the zone of active deformation. A high-density river network is exceptionally well developed over the study area and shows evidence of drainage anomalies that suggest recent fault-induced movements at various scales. Correlation of surface drainage anomalies with Landsat remote sensing and deep seismic reflection data permits to characterize the deep geometry of the inferred fault structures. Seismic stratigraphy further allows distinction between the inherited (Oligocene-Pliocene) and the newly formed (〈3.7 Ma) origin of the recent deformation. Evidence for neotectonics are observed (1) along a large-scale transverse (EW) fault rooted at depth along a steep basement discontinuity (Turkwell), (2) along a rift-parallel (NS) fault zone probably emplaced during the Pliocene-Pleistocene and currently bounding the Napedet volcanic plateau to the west and (3) over a round-shaped uplifted zone caused by positive inversion tectonics (Kalabata). The major contribution of this work is the recognition of a broad (80 km wide) zone of recent/active extensional deformation in the Turkana Rift in contrast with the narrow (20 km wide) N10°E-trending axial trough forming the Suguta valley to the south, and the Chew Bahir faulted basin to the north. These along-strike variations in structural style are partly controlled by the occurrence of rejuvenated Oligocene-Miocene rift faults and long-lived transverse discontinuities in the Turkana Rift area. More generally, this study has implications for the use of river drainage network about recent/active extensional domains with subdued topography and slow deformation rate. © 2004 Blackwell Publishing Ltd.

Description: Our laboratory has purified an 18 kDa cell surface sialoglycopeptide growth inhibitor (CeReS-18) from intact bovine cerebral cortex cells. Evidence presented here demonstrates that sensitivity to CeReS-18-induced growth inhibition in BALB-c 3T3 cells is influenced by calcium, such that a decrease in the calcium concentration in the growth medium results in an increase in sensitivity to CeReS-18. Calcium did not alter CeReS-18 binding to its cell surface receptor and CeReS-18 does not bind calcium directly. Addition of calcium, but not magnesium, to CeReS-18-inhibited 3T3 cells results in reentry into the cell cycle. A greater than 3-hour exposure to increased calcium is required for escape from CeReS-18-induced growth inhibition. The calcium ionophore ionomycin could partially mimic the effect of increasing extracellular calcium, but thapsigargin was ineffective in inducing escape from growth inhibition. Increasing extracellular calcium 10-fold resulted in an approximately 7-fold increase in total cell-associated 45Ca+2, while free intracellular calcium only increased approximately 30%. However, addition of CeReS-18 did not affect total cell-associated calcium or the increase in total cell-associated calcium observed with an increase in extracellular calcium. Serum addition induced mobilization of intracellular calcium and influx across the plasma membrane in 3T3 cells, and pretreatment of 3T3 cells with CeReS-18 appeared to inhibit these calcium mobilization events. These results suggest that a calcium-sensitive step exists in the recovery from CeReS-18-induced growth inhibition. CeReS-18 may inhibit cell proliferation through a novel mechanism involving altering the intracellular calcium mobilization/regulation necessary for cell cycle progression.

Description: Previous attempts to physically separate the cell cycle inhibitory and protease activities in preparations of a purified cell regulatory sialoglycopeptide (CeReS) inhibitor were largely unsuccessful. Gradient elution of the inhibitor preparation from a DEAE HPLC column separated the cell growth inhibitor from the protease, and the two activities have been shown to be distinct and non-overlapping. The additional purification increased the specific biological activity of the CeReS preparation by approximately two-fold. The major inhibitory fraction that eluted from the DEAE column was further analyzed by tricine-SDS-PAGE and microbore reverse phase HPLC and shown to be homogeneous in nature. Two other fractions separated by DEAE HPLC, also devoid of protease activity, were shown to be inhibitory to cell proliferation and most likely represented modified relatives of the CeReS inhibitor. The highly purified CeReS was chemically characterized for amino acid and carbohydrate composition and the role of the carbohydrate in cell proliferation inhibition, stability, and protease resistance was assessed.