Bioenergy production and forest landscape change in the southeastern United States

Production of woody biomass for bioenergy, whether wood pellets or liquid biofuels, has the potential to cause substantial landscape change and concomitant effects on forest ecosystems, but the landscape effects of alternative production scenarios have not been fully assessed. We simulated landscape change from 2010 to 2050 under five scenarios of woody biomass production for wood pellets and liquid biofuels in North Carolina, in the southeastern United States, a region that is a substantial producer of wood biomass for bioenergy and contains high biodiversity. Modeled scenarios varied biomass feedstocks, incorporating harvest of ‘conventional’ forests, which include naturally regenerating as well as planted forests that exist on the landscape even without bioenergy production, as well as purpose‐grown woody crops grown on marginal lands. Results reveal trade‐offs among scenarios in terms of overall forest area and the characteristics of the remaining forest in 2050. Meeting demand for biomass from conventional forests resulted in more total forest land compared with a baseline, business‐as‐usual scenario. However, the remaining forest was composed of more intensively managed forest and less of the bottomland hardwood and longleaf pine habitats that support biodiversity. Converting marginal forest to purpose‐grown crops reduced forest area, but the remaining forest contained more of the critical habitats for biodiversity. Conversion of marginal agricultural lands to purpose‐grown crops resulted in smaller differences from the baseline scenario in terms of forest area and the characteristics of remaining forest habitats. Each scenario affected the dominant type of land‐use change in some regions, especially in the coastal plain that harbors high levels of biodiversity. Our results demonstrate the complex landscape effects of alternative bioenergy scenarios, highlight that the regions most likely to be affected by bioenergy production are also critical for biodiversity, and point to the challenges associated with evaluating bioenergy sustainability.     

Plant regeneration from leaf explants of Glycine clandestina Wendl

Fully fertile plants with the expected chromosome number 2n=40 were regenerated from excised leaf sections of Glycine clandestina. Shoots formed directly on the explants through organogenesis. Utilizing the same media and procedures fully fertile plants were also regenerated from cotyledon and hypocotyl tissue of the same G. clandestina accession. We were not successful in regenerating plants from root tissue of G. clandestina.Abbreviations 6-BA 6-Benzyladenine - FAA Formalin - NAA Naphthalenacetic acid - IAA Indoleacetic acid - Na₂EDTA Disodium salt Ethylenediamine tetraacetic acid - Fe-NaEDTA Ferric-Sodium salt Ethylenediamine tetraacetic acid     

Thyroarytenoid muscle activity during loaded and nonloaded breathing in adult humans

Previous fiber-optic studies in humans have demonstrated narrowing of the glottic aperture in expiration during application of expiratory resistive loads. Nine healthy subjects were studied to determine the effect of expiratory resistive loads on the electromyographic activity of the thyroarytenoid (TA) muscle, a vocal cord adductor. Four of the nine subjects also underwent the application of inspiratory resistive loads and voluntary prolongation of either inspiratory (TI) or expiratory (TE) time. TA activity was recorded by intramuscular hooked-wire electrodes. During quiet breathing in all subjects, the TA was phasically active on expiration and often tonically active throughout the respiratory cycle. TA expiratory activity progressively increased with increasing levels of expiratory load. Inspiratory loads resulted in increased TA "inspiratory" activity. Voluntary prolongation of TE to times similar to those reached during loaded breathing induced increases in TA expiratory activity similar to those reached during the loaded state. Voluntary prolongation of TI was associated with an increase in TA inspiratory activity. Similar increases in TI during inspiratory loading or voluntary conditions were associated with comparable increases in TA inspiratory activity in three of the four subjects. In conclusion, increased activation of TA during the application of expiratory resistive loads implies that the reported narrowing of glottic aperture during expiratory loading is an active phenomenon. Changes in activation of the TA with resistive loads appear to be related to changes in respiratory pattern.     

The role of seed coats in seed viability

The seed coat is the seed’s primary defense against adverse environmental conditions. A hard seed coat protects the seed not only from mechanical stress but also from microorganism invasion and from temperature and humidity fluctuations during storage. Phenolic compounds in the seed coat contribute to seed hardness and inhibition of microorganism growth. During germination, the seed coat protects the seed from hydration stress and electrolyte leakage.     

The immunomodulatory protein SV-IV protects serum-deprived cells against apoptosis but not against G0/G1 arrest: possible implications for the survival of implanting embryo

Serum deprivation induced in human lymphoblastoid Raji cells oxidative stress-associated apoptotic death and G0/G1 cell cycle arrest. Addition into culture medium of the immunomodulatory protein Seminal vesicle protein 4 (SV-IV) protected these cells against apoptosis but not against cycle arrest. The antiapoptotic activity was related to: (1) decrease of endocellular reactive Oxygen species (ROS) (2) increase of mRNAs encoding anti-oxidant enzymes (catalase, G6PD) and antiapoptotic proteins (survivin, cox-1, Hsp70, c-Fos); (3) decrease of mRNAs encoding proapoptotic proteins (c-myc, Bax, caspase-3, Apaf-1). The biochemical changes underlaying these effects were probably induced by a protein tyrosine kinase (PTK) activity triggered by the binding of SV-IV to its putative plasma membrane receptors. The ineffectiveness of SV-IV to abrogate the cycle arrest was accounted for by its downregulating effects on D1,3/E G1-cyclins and CdK2/4 gene expression, ppRb/pRb ratio, and intracellular ROS concentration. In conclusion, these experiments: (1) prove that SV-IV acts as a cell survival factor; (2) suggest the involvement of a PTK in SV-IV signaling; (3) point to cell cycle-linked enzyme inhibition as responsible for cycle arrest; (4) provide a model to dissect the cycle arrest and apoptosis induced by serum withdrawal; (5) imply a possible role of SV-IV in the survival of hemiallogenic implanting embryos.     

COQ4 Mutations Cause a Broad Spectrum of Mitochondrial Disorders Associated with CoQ10 Deficiency

Primary coenzyme Q10 (CoQ₁₀) deficiencies are rare, clinically heterogeneous disorders caused by mutations in several genes encoding proteins involved in CoQ₁₀ biosynthesis. CoQ₁₀ is an essential component of the electron transport chain (ETC), where it shuttles electrons from complex I or II to complex III. By whole-exome sequencing, we identified five individuals carrying biallelic mutations in COQ4. The precise function of human COQ4 is not known, but it seems to play a structural role in stabilizing a multiheteromeric complex that contains most of the CoQ₁₀ biosynthetic enzymes. The clinical phenotypes of the five subjects varied widely, but four had a prenatal or perinatal onset with early fatal outcome. Two unrelated individuals presented with severe hypotonia, bradycardia, respiratory insufficiency, and heart failure; two sisters showed antenatal cerebellar hypoplasia, neonatal respiratory-distress syndrome, and epileptic encephalopathy. The fifth subject had an early-onset but slowly progressive clinical course dominated by neurological deterioration with hardly any involvement of other organs. All available specimens from affected subjects showed reduced amounts of CoQ₁₀ and often displayed a decrease in CoQ₁₀-dependent ETC complex activities. The pathogenic role of all identified mutations was experimentally validated in a recombinant yeast model; oxidative growth, strongly impaired in strains lacking COQ4, was corrected by expression of human wild-type COQ4 cDNA but failed to be corrected by expression of COQ4 cDNAs with any of the mutations identified in affected subjects. COQ4 mutations are responsible for early-onset mitochondrial diseases with heterogeneous clinical presentations and associated with CoQ10 deficiency.