Paul B. Sears and the Ecological Society of America

Author Institution: College of Environmental Science & Forestry, State University of New YorkPaul B. Sears, perhaps more than any other person, epitomized American plant ecology. In a professional career spanning almost 7 decades, he made major contributions to vegetation mapping, paleoecology and Pleistocene history, vegetation studies, conservation, human ecology and our use of land; and particularly, the varied roles of scientists in modern society. He introduced his work in most of these subjects by presenting papers at the annual meetings of the Ecological Society of America (ESA). As a member or chair of numerous committees, Sears pushed the ESA to become involved in supporting the teaching of ecology in college curricula, conservation efforts, applied ecology, human ecology and outreach to government and the public. He also served the ESA as an editor, vice president and president. His influence is still felt in the ESA, although few realize where the ideas originated. Sears was named Eminent Ecologist by the ESA in 1965, a title as appropriate today as it was then

Molybdenum Complexes of Chiral C2-symmetric Picchxn-type Ligands: Synthesis, Characterization, and Structural Studies

A series of molybdenum complexes based on chiral C2-symmetric picchxn-type ligands (N4 ligands, defined as trans-N,N′-bis(heterocycl-2-ylmethyl)-1,2-diaminocyclohexanes) has been synthesized and characterized. Reported and novel picchxn-type ligands form (κ3-N4)Mo(CO)3, [(κ4-N4)Mo(NO)(CO)]PF6, and [(κ4-N4)Mo(NO)X]PF6 (X = Br, I) compounds. Multiple tridentate (κ3) and tetradentate (κ4) ligand configurations were observed, and the favored κ4 configuration was found to vary with N4 heterocycle identity. Heterocycle variation allowed for directed modification of the molybdenum electronic characteristics, but none of the studied {(κ4-N4)Mo(NO)}+ fragments was found to be a suitable π-base for dearomatization chemistry. The crystal structures of eight molybdenum complexes with picchxn-type ligands were determined

The effect of fo2 source on the solubility, diffusion, and speciation of tin in haplogranitic melt at 850°C and 2 kbar

International audienceDiffusion profiles of tin were produced in hydrous silicate melts adjacent to cassiterite crystals; the method of Harrison and Watson (1983) was adapted to produce Sn diffusion profiles in hydrous silicate melts adjacent to cassiterite crystals at 2 kbar, 850°C, and various redox conditions, from which information on the solubility, diffusion, and speciation of Sn in silicate liquids can be obtained. The use of diffusion profiles and a hydrous, yet slightly H2O-undersaturated melt composition were chosen, in order to avoid the loss of Sn to the noble-element capsule walls. Such losses occurred at reduced conditions in the previous experimental studies on the solubility or partitioning of Sn in silicate liquids (±fluid phase), which probably interfered with the redox or SnO2 activity control of those experiments. The redox conditions investigated in this study were controlled by the intrinsic or an imposed ƒH2 in rapid-quench cold-seal and internally heated pressure vessels, and were measured by either the hydrogen sensor or Shaw membrane techniques. Cassiterite solubilities at 850°C and 2 kbar range from 28,000 ppm SnO2 at FMQ−0.84 to approximately 800 ppm at FMQ+3.12, in a haplogranitic melt with a normative (anhydrous) composition of 37.2% quartz, 28.3% orthoclase, 34.1 % albite, 0.4% corundum, and 5.6 wt% H2O. For redox conditions higher than FMQ+1.5, SnO2 solubility is independent of ƒO2, indicating that cassiterite dissolved into the melt largely as Sn4+. By contrast at more reduced conditions, log SnO2 concentration vs. log ƒo2 define a slope of approximately −0.5, implying that Sn is dominantly in the 2+ valence, if γSnmelt2+. is constant. The solubilities obtained at reduced conditions in this study are an order of magnitude higher than previously published data (at a comparable P-T, composition and ƒH2 of the autoclave); the low values in the previous work are attributed to the loss of Sn to the capsule walls. The diffusion of Sn is also apparently related to ƒo2, ranging from approximately 10−8 cm2/s at FMQ-0.84 to 10−9 cm2/s at FMQ+3.12. This is consistent with Sn2+ behaving as a network modifier, whereas the diffusion of Sn4+ is slower, similar to other high field strength elements. The strong ƒO2 dependence of Sn solubility can be used to explain some magmatic tin deposits and also indicates that tin might prove useful as a marker of redox changes of a variety of magmatic systems

Analysis of Expression Pattern and Genetic Deletion of Netrin5 in the Developing Mouse

Boundary cap cells are a transient, neural-crest-derived population found at the motor exit point and dorsal root entry zone of the embryonic spinal cord. These cells contribute to the central/peripheral nervous system boundary, and in their absence neurons and glia from the CNS migrate into the PNS. We found Netrin5 (Ntn5), a previously unstudied member of the netrin gene family, to be robustly expressed in boundary cap cells. We generated Ntn5 knockout mice and examined neurodevelopmental and boundary-cap-cell-related phenotypes. No abnormalities in cranial nerve guidance, dorsal root organization, or sensory projections were found. However, Ntn5 mutant embryos did have ectopic motor neurons that migrated out of the ventral horn and into the motor roots. Previous studies have implicated semaphorin6A (Sema6A) in boundary cap cells signaling to plexinA2 (PlxnA2)/neuropilin2 (Nrp2) in motor neurons in restricting motor neuron cell bodies to the ventral horn, particularly in the caudal spinal cord. In Ntn5 mutants, ectopic motor neurons are likely to be a different population, as more ectopias were found rostrally. Furthermore, ectopic motor neurons in Ntn5 mutants were not immunoreactive for NRP2. The netrin receptor DCC is a potential receptor for NTN5 in motor neurons, as similar ectopic neurons were found in Dcc mutant mice, but not in mice deficient for other netrin receptors. Thus, Ntn5 is a novel netrin family member that is expressed in boundary cap cells, functioning to prevent motor neuron migration out of the CNS

p53-mediated neurodegeneration in the absence of the nuclear protein Akirin2.

Proper gene regulation is critical for both neuronal development and maintenance as the brain matures. We previously demonstrated that Akirin2, an essential nuclear protein that interacts with transcription factors and chromatin remodeling complexes, is required for the embryonic formation of the cerebral cortex. Here we show that Akirin2 plays a mechanistically distinct role in maintaining healthy neurons during cortical maturation. Restricting Akirin2 loss to excitatory cortical neurons resulted in progressive neurodegeneration via necroptosis and severe cortical atrophy with age. Comparing transcriptomes from Akirin2-null postnatal neurons and cortical progenitors revealed that targets of the tumor suppressor p53, a regulator of both proliferation and cell death encoded b

A Novel ENU-Induced

The fission and fusion of mitochondria are important processes for maintaining mitochondrial health. One of the proteins responsible for mediating mitochondrial fusion, mitofusin 2 (MFN2), has over 100 known mutations that cause Charcot–Marie–Tooth disease type 2A (CMT2A). This disease causes the nerves that control your muscles to degenerate, leading to muscle atrophy and weakness, problems walking, and other related symptoms. In this paper, we describe a mouse line with a recessive mutation in the Mfn2 gene (Leu643Pro) that causes a similar set of symptoms, including abnormal gait, weight loss, and decreased muscular endurance. However, further analysis of these mice revealed signs of skeletal muscle dysfunction (including smaller mitochondria) and bone abnormalities, with little evidence of axon degeneration typical of CMT2A. While this makes these mice a poor model for CMT2A, they are the first reported mouse line with a mutation in the transmembrane domain, a region critical for MFN2′s role in mitochondrial fusion. For this reason, we believe these mice will be a valuable tool for scientists interested in studying the biological functions of MFN2

Draft genome sequence of isolate Staphylococcus aureus LHSKBClinical, isolated from an infected hip

We report here the genome sequence of a clinical isolate of <i>Staphylococcus aureus</i> from an orthopedic infection. Phenotypically diverse <i>Staphylococcus aureus</i> strains are associated with orthopedic infections and subsequent implant failure, and some are highly resistant to antibiotics. This genome sequence will support further analyses of strains causing orthopedic infections

Inhibition of glycolysis and mitochondrial respiration promotes radiosensitisation of neuroblastoma and glioma cells

Background: Neuroblastoma accounts for 7% of paediatric malignancies but is responsible for 15% of all childhood cancer deaths. Despite rigorous treatment involving chemotherapy, surgery, radiotherapy and immunotherapy, the 5-year overall survival rate of high-risk disease remains < 40%, highlighting the need for improved therapy. Since neuroblastoma cells exhibit aberrant metabolism, we determined whether their sensitivity to radiotherapy could be enhanced by drugs affecting cancer cell metabolism. Methods: Using a panel of neuroblastoma and glioma cells, we determined the radiosensitising effects of inhibitors of glycolysis (2-DG) and mitochondrial function (metformin). Mechanisms underlying radiosensitisation were determined by metabolomic and bioenergetic profiling, flow cytometry and live cell imaging and by evaluating different treatment schedules. Results: The radiosensitising effects of 2-DG were greatly enhanced by combination with the antidiabetic biguanide, metformin. Metabolomic analysis and cellular bioenergetic profiling revealed this combination to elicit severe disruption of key glycolytic and mitochondrial metabolites, causing significant reductions in ATP generation and enhancing radiosensitivity. Combination treatment induced G2/M arrest that persisted for at least 24 h post-irradiation, promoting apoptotic cell death in a large proportion of cells. Conclusion: Our findings demonstrate that the radiosensitising effect of 2-DG was significantly enhanced by its combination with metformin. This clearly demonstrates that dual metabolic targeting has potential to improve clinical outcomes in children with high-risk neuroblastoma by overcoming radioresistance