Inundation,Hydrodynamics and Vegetation Influence Carbon Dioxide Concentrations in Amazon Floodplain Lakes

Ecosystems - Extensive floodplains and numerous lakes in the Amazon basin are well suited to examine the role of floodable lands within the context of the sources and processing of carbon within...     

Potential feedback between coral presence and farmerfish collective behavior promotes coral recovery

Stable between‐group differences in collective behavior have been documented in a variety of social taxa. Here we evaluate the effects of such variation, often termed collective or colony‐level personality, on coral recovery in a tropical marine farmerfish system. Groups of the farmerfish Stegastes nigricans cultivate and defend gardens of palatable algae on coral reefs in the Indo‐Pacific. These gardens can promote the recruitment, growth, and survival of corals by providing a refuge from coral predation. Here we experimentally evaluate whether the collective response of farmerfish colonies is correlated across intruder feeding guilds – herbivores, corallivores and egg‐eating predators. Further, we evaluate if overall colony responsiveness or situation‐specific responsiveness (i.e. towards herbivores, corallivores, or egg‐eaters in particular) best predicts the growth of outplanted corals. Finally, we experimentally manipulated communities within S. nigricans gardens, adding either macroalgae or large colonies of coral, to assess if farmerfish behavior changes in response to the communities they occupy. Between‐group differences in collective responsiveness were repeatable across intruder guilds. Despite this consistency, responsiveness towards corallivores (porcupinefish and ornate butterflyfish) was a better predictor of outplanted coral growth than responsiveness towards herbivores or egg‐eaters. Adding large corals to farmerfish gardens increased farmerfish attacks towards intruders, pointing to possible positive feedback loops between their aggression towards intruders and the presence of corals whose growth they facilitate. These data provide evidence that among‐group behavioral variation could strongly influence the ecological properties of whole communities.     

Synthesis,biological evaluation,and molecular docking of new series of antitumor and apoptosis inducers designed as VEGFR-2 inhibitors

Based on quinazoline, quinoxaline, and nitrobenzene scaffolds and on pharmacophoric features of VEGFR-2 inhibitors, 17 novel compounds were designed and synthesised. VEGFR-2 IC₅₀ values ranged from 60.00 to 123.85 nM for the new derivatives compared to 54.00 nM for sorafenib. Compounds 15_a, 15_b, and 15_d showed IC₅₀ from 17.39 to 47.10 µM against human cancer cell lines; hepatocellular carcinoma (HepG2), prostate cancer (PC3), and breast cancer (MCF-7). Meanwhile, the first in terms of VEGFR-2 inhibition was compound 15_d which came second with regard to antitumor assay with IC₅₀ = 24.10, 40.90, and 33.40 µM against aforementioned cell lines, respectively. Furthermore, Compound 15_d increased apoptosis rate of HepG2 from 1.20 to 12.46% as it significantly increased levels of Caspase-3, BAX, and P53 from 49.6274, 40.62, and 42.84 to 561.427, 395.04, and 415.027 pg/mL, respectively. Moreover, 15_d showed IC₅₀ of 253 and 381 nM against HER2 and FGFR, respectively.     

Prenatal exposure to a 50 Hz magnetic field has no effect on spatial learning in adult mice

Male CD1 mice were exposed in utero to a 50 Hz sinusoidal magnetic field at 5 mT (rms) for the period of gestation and were raised subsequently without applied fields. At 82-84 days of age, they began a radial-arm-maze experiment that was designed to test for deficits in spatial learning in memory. Mice exposed in utero and sham-exposed mice exhibited no statistically significant differences in performances. © 1996 Wiley-Liss, Inc.     

Spatial distribution of fine root biomass in a remnant Eucalyptus tereticornis woodland in Eastern Australia

Plant Ecology - In forests, the majority of fine roots are located within the upper soil horizons, and fine root biomass decreases with depth. We evaluated spatial patterns in the distribution of...     

The pathogenicity of human immunodeficiency virus (HIV) type 1 Nef in CD4C/HIV transgenic mice is abolished by mutation of its SH3-binding domain, and disease development is delayed in the absence of Hck

The human immunodeficiency virus type 1 (HIV-1) Nef protein is an important determinant of AIDS pathogenesis. We have previously reported that HIV-1 Nef is responsible for the induction of a severe AIDS-like disease in CD4C/HIV transgenic (Tg) mice. To understand the molecular mechanisms of this Nef-induced disease, we generated Tg mice expressing a mutated Nef protein in which the SH3 ligand-binding domain (P(72)XXP(75)XXP(78)) was mutated to A(72)XXA(75)XXQ(78). This mutation completely abolished the pathogenic potential of Nef, although a partial downregulation of the CD4 cell surface expression was still observed in these Tg mice. We also studied whether Hck, one of the effectors previously found to bind to this PXXP motif of Nef, was involved in disease development. Breeding of Tg mice expressing wild-type Nef on an hck(-/-) (knockout) background did not abolish any of the pathological phenotypes. However, the latency of disease development was prolonged. These data indicate that an intact PXXP domain is essential for inducing an AIDS-like disease in CD4C/HIV Tg mice and suggest that interaction of a cellular effector(s) with this domain is required for the induction of this multiorgan disease. Our findings indicate that Hck is an important, but not an essential, effector of Nef and suggest that another factor(s), yet to be identified, may be more critical for disease development.     

Mitochondria at the Crossroad of Apoptotic Cell Death

In the past few years, it has become widely appreciated that apoptotic cell death generallyinvolves activation of a family of proteases, the caspases, which undermine the integrity ofthe cell by cleavage of critical intracellular substrates. Caspases, which are synthesized asinactive zymogens, are themselves caspase substrates and this cleavage leads to their activation.Hence, the potential exists for cascades of caspases leading to cell death. However, it has beenrecently recognized that another, perhaps more prominent route to caspase activation, involvesthe mitochondria. Upon receipt of apoptotic stimuli, either externally or internally generated,cells initiate signaling pathways which converge upon the mitochondria to promote release ofcytochrome C to the cytoplasm; cytochrome c, thus released, acts as a potent cofactor incaspase activation. Even cell surface death receptors such as Fas, which can trigger directcaspase activation (and potentially a caspase cascade), appear to utilize mitochondria as partof an amplification mechanism; it has been recently demonstrated that activated caspases cancleave key substrates to trigger mitochondrial release of cytochrome c, thereby inducing furthercaspase activation and amplifying the apoptotic signal. Therefore, mitochondria play a centralrole in apoptotic cell death, serving as a repository for cytochrome c.     

Telomere shortening exposes functions for the mouse Werner and Bloom syndrome genes

The Werner and Bloom syndromes are caused by loss-of-function mutations in WRN and BLM, respectively, which encode the RecQ family DNA helicases WRN and BLM, respectively. Persons with Werner syndrome displays premature aging of the skin, vasculature, reproductive system, and bone, and those with Bloom syndrome display more limited features of aging, including premature menopause; both syndromes involve genome instability and increased cancer. The proteins participate in recombinational repair of stalled replication forks or DNA breaks, but the precise functions of the proteins that prevent rapid aging are unknown. Accumulating evidence points to telomeres as targets of WRN and BLM, but the importance in vivo of the proteins in telomere biology has not been tested. We show that Wrn and Blm mutations each accentuate pathology in later-generation mice lacking the telomerase RNA template Terc, including acceleration of phenotypes characteristic of latest-generation Terc mutants. Furthermore, pathology not observed in Terc mutants but similar to that observed in Werner syndrome and Bloom syndrome, such as bone loss, was observed. The pathology was accompanied by enhanced telomere dysfunction, including end-to-end chromosome fusions and greater loss of telomere repeat DNA compared with Terc mutants. These findings indicate that telomere dysfunction may contribute to the pathogenesis of Werner syndrome and Bloom syndrome.