ALBERT

Description: Profundal lake sediment cores are often interpreted in line with diverse and detailed sedimentological processes to infer paleoenvironmental conditions. The effects of frozen lake surfaces on terrigenous sediment deposition and how climate changes on the Tibetan Plateau are reflected in these lakes, however, is seldom discussed. A lake sediment core from Hala Lake (590 km2), northeastern Tibetan Plateau spanning the time interval from the Last Glacial Maximum to the present was investigated using high-resolution grain-size composition of lacustrine deposits. Seismic analysis along a north–south profile across the lake was used to infer the sedimentary setting within the lake basin. Periods of freezing and melting processes on the lake surface were identified by MODIS (MOD10A1) satellite data. End-member modeling of the grain size distribution allowed the discrimination between lacustrine, eolian and fluvial sediments. The dominant clay sedimentation (slack water type) during the global Last Glacial Maximum (LGM) reflects ice interceptions in long cold periods, in contrast to abundant eolian input during abrupt cold events. Therefore, fluvial and slack water sedimentation processes can indicate changes in the local paleoclimate during periods of the lake being frozen, when eolian input was minor. Inferred warm (i.e., ∼22.7 and 19.5 cal. ka BP) and cold (i.e., ∼11–9 and 3–1.5 cal. ka BP) spells have significant environmental impacts, not only in the regional realm, but they are also coherent with global-scale climate events. The eolian input generally follows the trend of the mid-latitude westerly wind dynamics in winter, contributing medium-sized sand to the lake center, deposited within the ice cover during icing and melting phases. Enhanced input was dominant during the Younger Dryas, Heinrich Event 1 and at around 8.2 ka, equivalent to the well-known events of the North Atlantic realm.

Description: Insulin and insulin-like growth factor 1 (IGF-1) are evolutionarily conserved hormonal signalling molecules, which influence a wide array of physiological functions including metabolism, growth and development. Using genetic mouse studies, both insulin and IGF-1 have been shown to be anabolic agents in osteoblasts and bone development primarily through the activation of Akt and ERK signalling pathways. In this study, we examined the temporal signalling actions of insulin and IGF-1 on primary calvarial osteoblast growth and differentiation. First, we observed that the IGF-1 receptor expression decreases whereas insulin receptor expression increases during osteoblast differentiation. Subsequently, we show that although both insulin and IGF-1 promote osteoblast differentiation and mineralization in vitro , IGF-1, but not insulin, can induce osteoblast proliferation. The IGF-1-induced osteoblast proliferation was mediated via both MAPK and Akt pathways because the IGF-1-mediated cell proliferation was blocked by U0126, an MEK/MAPK inhibitor, or LY294002, a PI3-kinase inhibitor. Osteocalcin, an osteoblast-specific protein whose expression corresponds with osteoblast differentiation, was increased in a dose- and time-dependent manner after insulin treatment, whereas it was decreased with IGF-1 treatment. Moreover, insulin treatment dramatically induced osteocalcin promoter activity, whereas IGF-1 treatment significantly inhibited it, indicating direct effect of insulin on osteocalcin synthesis. Copyright © 2012 John Wiley & Sons, Ltd.

Description: Insulin and insulin-like growth factor 1 (IGF-1) are evolutionarily conserved hormonal signalling molecules, which influence a wide array of physiological functions including metabolism, growth and development. Using genetic mouse studies, both insulin and IGF-1 have been shown to be anabolic agents in osteoblasts and bone development primarily through the activation of Akt and ERK signalling pathways. In this study, we examined the temporal signalling actions of insulin and IGF-1 on primary calvarial osteoblast growth and differentiation. First, we observed that the IGF-1 receptor expression decreases whereas insulin receptor expression increases during osteoblast differentiation. Subsequently, we show that although both insulin and IGF-1 promote osteoblast differentiation and mineralization in vitro , IGF-1, but not insulin, can induce osteoblast proliferation. The IGF-1-induced osteoblast proliferation was mediated via both MAPK and Akt pathways because the IGF-1-mediated cell proliferation was blocked by U0126, an MEK/MAPK inhibitor, or LY294002, a PI3-kinase inhibitor. Osteocalcin, an osteoblast-specific protein whose expression corresponds with osteoblast differentiation, was increased in a dose- and time-dependent manner after insulin treatment, whereas it was decreased with IGF-1 treatment. Moreover, insulin treatment dramatically induced osteocalcin promoter activity, whereas IGF-1 treatment significantly inhibited it, indicating direct effect of insulin on osteocalcin synthesis. Copyright © 2012 John Wiley & Sons, Ltd.