Holistic Mission God’s Plan for God’s People

This volume on holistic mission addresses this challenge in a dynamic and multi-faceted way through a variety of voices from different contexts. Many should find the collection of materials it contains useful, stimulating and rewarding. Above all, as I commend it to you, may it stir greater response and engagement in the spread of the gospel of the kingdom of God throughout the world.https://scholar.csl.edu/edinburghcentenary/1008/thumbnail.jp

Linking African easterly wave activity with equatorial waves and the influence of Rossby waves from the Southern Hemisphere

A connection is found between African easterly waves (AEWs), equatorial westward-moving mixed Rossby-gravity (WMRG) waves and equivalent barotropic Rossby waves (RWs) from the Southern Hemisphere (SH). The amplitude and phase of equatorial waves is calculated by projection of broad-band filtered ERA-Interim data onto a horizontal structure basis obtained from equatorial wave theory. Mechanisms enabling interaction between the wave types are identified. AEWs are dominated by a vorticity wave which tilts eastwards below the African Easterly Jet and westwards above: the tilt necessary for baroclinic wave growth. However, a strong relationship is identified between amplifying vorticity centres within AEWs and equatorial WMRG waves. Although the waves do not phase-lock, positive vorticity centres amplify whenever the cross-equatorial motion of the WMRG wave lies at the same longitude in the upper troposphere (southwards flow) and east of this in the lower troposphere (northwards flow). Two mechanisms could explain the vorticity amplification: vortex stretching below the upper-tropospheric divergence and ascent associated with latent heating in convection in the lower-tropospheric moist northwards flow. In years of strong AEW activity, SH and equatorial upper-tropospheric zonal winds are more easterly. Stronger easterlies have two effects: i) they Doppler shift WMRG waves so that their period varies little with wavenumber (3-4 days) and ii) they enable westward-moving RWs to propagate into the tropical wave guide from the SH. RW phase speeds can match those of WMRG waves, enabling sustained excitation of WMRG. The WMRG waves have an eastwards group velocity with wave activity accumulating over Africa and invigorating AEWs at similar frequencies through the vorticity amplification mechanism

Effective science teaching

127 p. : il.; 26 cm

Lines of Sight : An Exhibition of Drawing by Six Artists of Prince Edward Island

Collected interviews, correspondence and statements trace the artists' relationship to the medium of drawing over the course of preparation for the exhibition. Biographical notes. 6 bibl. ref

The marine compound and elongation factor 1A1 inhibitor, didemnin B, provides benefit in western diet-induced non-alcoholic fatty liver disease

Inhibition of eukaryotic elongation factor 1A1 (EEF1A1) with the marine compound didemnin B decreases lipotoxic HepG2 cell death in vitro and improves early stage non-alcoholic fatty liver disease (NAFLD) in young genetically obese mice. However, the effects of didemnin B on NAFLD in a model of long-term diet-induced obesity are not known. We investigated the effects of didemnin B on NAFLD severity and metabolic parameters in western diet-induced obese mice, and on the cell types that contribute to liver inflammation and fibrosis in vitro. Male 129S6 mice were fed either standard chow or western diet for 26 weeks, followed by intervention with didemnin B (50 μg/kg) or vehicle by intraperitoneal (i.p.) injection once every 3 days for 14 days. Didemnin B decreased liver and plasma triglycerides, improved oral glucose tolerance, and decreased NAFLD severity. Moreover, didemnin B moderately increased hepatic expression of genes involved in ER stress response (Perk, Chop), and fatty acid oxidation (Fgf21, Cpt1a). In vitro, didemnin B decreased THP-1 monocyte proliferation, disrupted THP-1 monocyte-macrophage differentiation, decreased THP-1 macrophage IL-1β secretion, and decreased hepatic stellate cell (HSteC) proliferation and collagen secretion under both basal and lipotoxic (high fatty acid) conditions. Thus, didemnin B improves hepatic steatosis, glucose tolerance, and blood lipids in obesity, in association with moderate, possibly hormetic, upregulation of pathways involved in cell stress response and energy balance in the liver. Furthermore, it decreases the activity of the cell types implicated in liver inflammation and fibrosis in vitro. These findings highlight the therapeutic potential of partial protein synthesis inhibition in the treatment of NAFLD