A new species of Mimosa (Leguminosae) from Coahuila,Mexico

Mimosaunipinnata from the Sierra de San Marcos in the Cuatro Ciénegas Basin of central Coahuila, Mexico, is described. It is unique among mimosas in having oncepinnate leaves.     

Skeletal involution by age-associated oxidative stress and its acceleration by loss of sex steroids

Both aging and loss of sex steroids have adverse effects on skeletal homeostasis, but whether and how they may influence each others negative impact on bone remains unknown. We report herein that both female and male C57BL/6 mice progressively lost strength (as determined by load-to-failure measurements) and bone mineral density in the spine and femur between the ages of 4 and 31 months. These changes were temporally associated with decreased rate of remodeling as evidenced by decreased osteoblast and osteoclast numbers and decreased bone formation rate; as well as increased osteoblast and osteocyte apoptosis, increased reactive oxygen species levels, and decreased glutathione reductase activity and a corresponding increase in the phosphorylation of p53 and p66(shc), two key components of a signaling cascade that are activated by reactive oxygen species and influences apoptosis and lifespan. Exactly the same changes in oxidative stress were acutely reproduced by gonadectomy in 5-month-old females or males and reversed by estrogens or androgens in vivo as well as in vitro.We conclude that the oxidative stress that underlies physiologic organismal aging in mice may be a pivotal pathogenetic mechanism of the age-related bone loss and strength. Loss of estrogens or androgens accelerates the effects of aging on bone by decreasing defense against oxidative stress.     

Quantitative real-time PCR to determine allele number for the astringency locus by analysis of a linked marker in Diospyros kaki Thunb

Persimmon (Diospyros kaki Thunb.) is a polyploidy fruit tree species of economic importance to East Asia. Natural astringency loss is an important trait in persimmon breeding programs. Quantitative real-time PCR was used to determine the number of AST/ast alleles for fruit astringency in persimmon (D. kaki Thunb.). To this end, the cultivar Jiro was transformed with one or two copies of a gene encoding NADP-dependent sorbitol-6-phosphate dehydrogenase (S6PDH), which was used as a standard for measuring the allele number of a sequenced marker tightly linked to the recessive ast locus for nonastringency. Primers for markers linked to the AST or ast allele were then used to measure the AST to ast ratio directly in the progeny of a full-sib cross. From determination of the AST to ast ratio and the results of the S6PDH copy number, the number of AST and ast alleles at the AST/ast locus was estimated. This research supported the hypothesis that D. kaki is a hexaploid with six AST and/or ast alleles. In addition to the determination of the allelic status of the AST locus, the application of real-time PCR for confirmation of the ploidy level and allelic composition of target genes in autopolyploids or allopolyploids was demonstrated.     

The heat-shock response co-inducer arimoclomol protects against retinal degeneration in rhodopsin retinitis pigmentosa

Retinitis pigmentosa (RP) is a group of inherited diseases that cause blindness due to the progressive death of rod and cone photoreceptors in the retina. There are currently no effective treatments for RP. Inherited mutations in rhodopsin, the light-sensing protein of rod photoreceptor cells, are the most common cause of autosomal-dominant RP. The majority of mutations in rhodopsin, including the common P23H substitution, lead to protein misfolding, which is a feature in many neurodegenerative disorders. Previous studies have shown that upregulating molecular chaperone expression can delay disease progression in models of neurodegeneration. Here, we have explored the potential of the heat-shock protein co-inducer arimoclomol to ameliorate rhodopsin RP. In a cell model of P23H rod opsin RP, arimoclomol reduced P23H rod opsin aggregation and improved viability of mutant rhodopsin-expressing cells. In P23H rhodopsin transgenic rat models, pharmacological potentiation of the stress response with arimoclomol improved electroretinogram responses and prolonged photoreceptor survival, as assessed by measuring outer nuclear layer thickness in the retina. Furthermore, treated animal retinae showed improved photoreceptor outer segment structure and reduced rhodopsin aggregation compared with vehicle-treated controls. The heat-shock response (HSR) was activated in P23H retinae, and this was enhanced with arimoclomol treatment. Furthermore, the unfolded protein response (UPR), which is induced in P23H transgenic rats, was also enhanced in the retinae of arimoclomol-treated animals, suggesting that arimoclomol can potentiate the UPR as well as the HSR. These data suggest that pharmacological enhancement of cellular stress responses may be a potential treatment for rhodopsin RP and that arimoclomol could benefit diseases where ER stress is a factor.     

EPHA2-dependent outcompetition of KRASG12D mutant cells by wild-type neighbors in the adult pancreas

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Nitrogen inputs and outputs for New Zealand in 2001 at national and regional scales

The Nanjing Declaration on Nitrogen Management, signed in Nanjing in October 2004, calls for national governments to optimize N management by several strategies including assessment of N cycles. Here we develop a first N budget for New Zealand (267,000 km²), at both national and regional scales. The national inputs are estimated to be 36.5 kg/ha, mainly from biological N fixation, but also increasingly from fertilizer application and atmospheric deposition. The outputs are estimated at 40.5 kg/ha. Biological N fixation from legumes in pasture was the most important input in most regions. Exceptions were Auckland, with a large urban population, and the West Coast of the South Island, with large tracts of rain forest. Outputs were distributed in the order leaching > ammonia volatilisation > erosion = produce = denitrification. These outputs are very different from global averages because of the large numbers of grazing animals on pasture. A large loss occurs between the subsoil and the oceans, and further research is needed to identify these pathways. Riverine export of N was generally well correlated with inputs.     

Leucoanthocyanidin dioxygenase gene (PpLDOX): a potential functional marker for cold storage browning in peach

Enzymatic browning of the peach fruit mesocarp is a major component of the postharvest physiological disorder commonly called chilling injury or internal breakdown (IB). Previously, we detected a major quantitative trait locus (QTL; qP-Brn5.1^m) affecting browning in peach using two related progeny populations (Pop-DG and Pop-G). In this report, a gene encoding the leucoanthocanidin dioxygenase (PpLDOX) enzyme was identified as the gene potentially responsible for this QTL. PpLDOX has a high similarity with the LDOX gene of the anthocyanin biosynthesis pathway of Arabidopsis thaliana. It was co-located with qP-Brn5.1^m via the bin mapping technique with the Prunus reference T×E map. A silent SNP within the PpLDOX coding sequence was used to locate the gene more precisely on the Pop-DG map and confirm its bin assignment. These results demonstrate both the utility of comparative mapping within Prunus using the T×E reference map and the power of the bin mapping approach for easily mapping genes in the Prunus genome. An SSR polymorphism was observed in the intron of PpLDOX gene sequence. The SSR co-segregated with the SNP and was used to assess association of PpLDOX with browning in 27 peach and nectarine cultivars. Cumulative evidence obtained indicates that PpLDOX partially explains genetic variation for cold storage browning susceptibility in peach and nectarine. This functional gene has potential use in marker-assisted breeding of new cultivars with lower IB susceptibility and for genotyping current cultivars for possible differential handling during storage to reduce symptom incidence.     

Biopersistence of PEGylated Carbon Nanotubes Promotes a Delayed Antioxidant Response after Infusion into the Rat Hippocampus

Carbon nanotubes are promising nanomaterials for the diagnosis and treatment of brain disorders. However, the ability of these nanomaterials to cross cell membranes and interact with neural cells brings the need for the assessment of their potential adverse effects on the nervous system. This study aimed to investigate the biopersistence of single-walled carbon nanotubes functionalized with polyethylene glycol (SWCNT-PEG) directly infused into the rat hippocampus. Contextual fear conditioning, Y-maze and open field tasks were performed to evaluate the effects of SWCNT-PEG on memory and locomotor activity. The effects of SWCNT-PEG on oxidative stress and morphology of the hippocampus were assessed 1 and 7 days after infusion of the dispersions at 0.5, 1.0 and 2.1 mg/mL. Raman analysis of the hippocampal homogenates indicates the biopersistence of SWCNT-PEG in the hippocampus 7 days post-injection. The infusion of the dispersions had no effect on the acquisition or persistence of the contextual fear memory; likewise, the spatial recognition memory and locomotor activity were not affected by SWCNT-PEG. Histological examination revealed no remarkable morphological alterations after nanomaterial exposure. One day after the infusion, SWCNT-PEG dispersions at 0.5 and 1.0 mg/mL were able to decrease total antioxidant capacity without modifying the levels of reactive oxygen species or lipid hydroperoxides in the hippocampus. Moreover, SWCNT-PEG dispersions at all concentrations induced antioxidant defenses and reduced reactive oxygen species production in the hippocampus at 7 days post-injection. In this work, we found a time-dependent change in antioxidant defenses after the exposure to SWCNT-PEG. We hypothesized that the persistence of the nanomaterial in the tissue can induce an antioxidant response that might have provided resistance to an initial insult. Such antioxidant delayed response may constitute an adaptive response to the biopersistence of SWCNT-PEG in the hippocampus.