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1.
The genus Fusarium contains many fungal species known to be pathogenic to animals and plants alike. One species complex within this genus, the Fusarium solani species complex (FSSC), is of particular concern due to its high numbers of pathogenic members. FSSC members are known to contribute significantly to plant, human and other animal fungal disease. One member of the FSSC, Fusarium keratoplasticum, is of particular ecological concern and has been implicated in low hatching success of endangered sea turtle eggs, as well as contribute to human and other animal Fusarium pathogenesis. Species-specific primers for molecular identification of F. keratoplasticum currently do not exist to our knowledge, making rapid identification, tracking and quantitation of this pathogenic fungus difficult. The objective of this study was to develop primers specific to F. keratoplasticum that could be applied to DNA from isolated cultures as well as total (mixed) DNA from environmental samples. RPB2 sequence from 109 Fusarium isolates was aligned and analysed to determine nucleotide polymorphisms specific to F. keratoplasticum useful for primer design. A set of primers were generated and found to be effective for identification of F. keratoplasticum from total DNA extracted from sand surrounding sea turtle nesting sites. 相似文献
2.
Henry C. Stevens Elaine M. Metz Percy Saboya Del Castillo Juan Díaz Alvn Mark T. Bowler 《Journal of Field Ornithology》2019,90(1):70-79
White‐sand forests are patchily distributed ecosystems covering just 5% of Amazonia that host many specialist species of birds not found elsewhere, and these forests are threatened due to their small size and human exploitation of sand for construction projects. As a result, many species of birds that are white‐sand specialists are at risk of extinction, and immediate conservation action is paramount for their survival. Our objective was to evaluate current survey methods and determine the relative effect of the size of patches of these forests on the presence or absence of white‐sand specialists. Using point counts and autonomous recorders, we surveyed avian assemblages occupying patches of white‐sand forest in the Peruvian Amazon in April 2018. Overall, we detected 126 species, including 21 white‐sand forest specialists. We detected significantly more species of birds per survey point with autonomous recorders than point counts. We also found a negative relationship between avian species richness and distance from the edge of patches of white‐sand forest, but a significant, positive relationship when only counting white‐sand specialists. Although we detected more species with autonomous recorders, point counts were more effective for detecting canopy‐dwelling passerines. Therefore, we recommend that investigators conducting surveys for rare and patchily distributed species in the tropics use a mixed‐method approach that incorporates both autonomous recorders and visual observation. Finally, our results suggest that conserving large, continuous patches of white‐sand forest may increase the likelihood of survival of species of birds that are white‐sand specialists. 相似文献
3.
Ivana Tonic Wan-Ni Yu Youngku Park Chia-Chen Chen Nissim Hay 《The Journal of biological chemistry》2010,285(31):23790-23798
Akt is perhaps the most frequently activated oncoprotein in human cancers. Overriding cell cycle checkpoint in combination with the inhibition of apoptosis are two principal requirements for predisposition to cancer. Here we show that the activation of Akt is sufficient to promote these two principal processes, by inhibiting Chk1 activation with concomitant inhibition of apoptosis. These activities of Akt cannot be recapitulated by the knockdown of Chk1 alone or by overexpression of Bcl2. Rather the combination of Chk1 knockdown and Bcl2 overexpression is required to recapitulate Akt activities. Akt was shown to directly phosphorylate Chk1. However, we found that Chk1 mutants in the Akt phosphorylation sites behave like wild-type Chk1 in mediating G2 arrest, suggesting that the phosphorylation of Chk1 by Akt is either dispensable for Chk1 activity or insufficient by itself to exert an effect on Chk1 activity. Here we report a new mechanism by which Akt affects G2 cell cycle arrest. We show that Akt inhibits BRCA1 function that induces G2 cell cycle arrest. Akt prevents the translocation of BRCA1 to DNA damage foci and, thereby, inhibiting the activation of Chk1 following DNA damage. 相似文献
4.
Benjamin C. Blum Weiwei Lin Matthew L. Lawton Qian Liu Julian Kwan Isabella Turcinovic Ryan Hekman Pingzhao Hu Andrew Emili 《Molecular & cellular proteomics : MCP》2022,21(1):100189
Metabolism is recognized as an important driver of cancer progression and other complex diseases, but global metabolite profiling remains a challenge. Protein expression profiling is often a poor proxy since existing pathway enrichment models provide an incomplete mapping between the proteome and metabolism. To overcome these gaps, we introduce multiomic metabolic enrichment network analysis (MOMENTA), an integrative multiomic data analysis framework for more accurately deducing metabolic pathway changes from proteomics data alone in a gene set analysis context by leveraging protein interaction networks to extend annotated metabolic models. We apply MOMENTA to proteomic data from diverse cancer cell lines and human tumors to demonstrate its utility at revealing variation in metabolic pathway activity across cancer types, which we verify using independent metabolomics measurements. The novel metabolic networks we uncover in breast cancer and other tumors are linked to clinical outcomes, underscoring the pathophysiological relevance of the findings. 相似文献
5.
Andrew Leask 《Journal of cell communication and signaling》2010,4(1):71-72
Connective tissue growth factor (CTGF/CCN2) is overexpressed in diabetes. Diabetic rats possess myocardial and cardiomyocyte
hypertrophy. In a recent report, Wang and colleagues (Am J Physiol Cell Physiol. 2009 Jul 22. [Epub ahead of print]) show
that CCN2 directly mediates cardiomyocyte hypertrophy as well as that induced by high glucose and fatty acid. CCN2 acted via
the TrkA receptor. These data are the subject of this commentary, and emphasize that CCN2 may be an excellent target for therapy
in diabetes. 相似文献
6.
The l-thyroxine binding site in human serum thyroxine-binding globulin was investigated by affinity labeling with N-bromoacetyl-l-thyroxine (BrAcT4). Competitive binding studies showed that, in the presence of 100 molar excess of BrAcT4, binding of thyroxine to thyroxine-binding globulin was nearly totally abolished. The reaction of BrAcT4 to form covalent binding was inhibited in the presence of thyroxine and the affinity-labeled thyroxinebinding globulin lost its ability to bind thyroxine. These results indicate BrAcT4 and thyroxine competed for the same binding site. Affinity labeling with 2 mol of BrAcT4/mol of thyroxine-binding globulin resulted in the covalent attachment of 0.7 mol of ligand. By amino acid analysis and high voltage paper electrophoresis, methionine was identified as the major residue labeled (75%). Lysine, tyrosine, and histidine were also found to be labeled to the extent of 8, 8, and 5%, respectively. 相似文献
7.
BackgroundNeuroblastoma, the most common extracranial solid tumor in children, contributes disproportionately to childhood cancer mortality and few risk factors have been identified. Our objective was to evaluate associations between parental and infant characteristics and neuroblastoma incidence.MethodsChildren born in Texas between January 1995 and December 2011 were eligible for the present study. Cases (N = 637) were diagnosed with neuroblastoma in Texas during the same period; controls (N = 6370) matched on year of birth were randomly selected from birth certificates that did not link to a record in the Texas Cancer Registry. We obtained data on birth and parental demographic/reproductive characteristics from birth certificates, and estimated odds ratios (OR) and 95% confidence intervals (CIs) for neuroblastoma using logistic regression.ResultsGestational age 34–36 weeks at birth was associated with neuroblastoma (OR 1.45, CI 1.09–1.90), whereas female sex was inversely associated (OR 0.68, CI 0.58–0.81). Relative to children of non-Hispanic White women, children of Hispanic (OR 0.53, CI 0.43–0.64) or non-Hispanic Black (OR 0.52, CI 0.38–0.71) women were at reduced odds of neuroblastoma. When maternal and paternal race/ethnicity were evaluated jointly, similar patterns were observed (two non-Hispanic Black parents: OR 0.55, 95%CI 0.36–0.79; two Hispanic parents: OR 0.53, 95%CI 0.41–0.67). Older maternal age was also positively associated with neuroblastoma (OR 1.41, CI 1.04–1.90 for 35–39 years; OR 1.62, CI 0.87–2.81 for ≥40 years, relative to 25–29 years).ConclusionsFindings provide further evidence of racial/ethnic disparities in neuroblastoma incidence, determinants of which are unknown. In contrast to most published studies, we observed an association between maternal age and neuroblastoma. Further studies with more robust control for confounding are warranted. 相似文献
8.
《Cell》2021,184(22):5670-5685.e23
9.
A simple method is described for picomole determinations of fatty acid metal salts. Fatty acid salts are directly labeled with 4-bromomethyl-7-methoxycoumarin in the presence of excess ethylenediaminetetraacetic acid tripotassium salt without any solvent extractions. The fluorescence derivatives of fatty acids are separated by reverse-phase high-performance liquid chromatography followed by fluorometric detection. The response of each fatty acid (C8-C18) calcium salt is linear from 1 to 50 micrograms/ml of samples. The detection limit is about 7 pmol. Good recoveries are obtained for the calcium salts of myrystic acid and soap (C8-C18, C18:1,2). The new method is successfully applied to the study on biodegradation of fatty acids in river water. 相似文献
10.
Masaru Kubota Ying-Wei Lin Keigo Hamahata Machiko Sawada Seiji Koishi Haruyo Hirota Yoshihiro Wakazono 《Mutation Research - Genetic Toxicology and Environmental Mutagenesis》2000,470(2):21
The occurrence of a second neoplasm is one of the major obstacles in cancer chemotherapy. The elucidation of the genotoxic effects induced by anti-cancer drugs is considered to be helpful in identifying the degree of cancer risk. Numerous investigations on cancer patients after chemotherapy have demonstrated: (i) an increase in the in vivo somatic cell mutant frequency (Mf) at three genetic loci, including hypoxanthine–guanine phosphoribosyl-transferase (hprt), glycophorin A (GPA), and the T-cell receptor (TCR), and (ii) alterations in the mutational spectra of hprt mutants. However, the time required for and the degree of such changes are quite variable among patients even if they have received the same chemotherapy, suggesting the existence of underlying genetic factor(s). Accordingly, some cancer patients prior to chemotherapy as well as patients with cancer-prone syndrome have been found to show an elevated Mf. Based on the information obtained from somatic cell mutation assays, an individualized chemotherapy should be considered in order to minimize the risk of a second neoplasm. 相似文献