1,037 research outputs found

    Soft-Rot Capabilities of the Major Microfungi, Isolated from Douglas-Fir Poles in the Northeast

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    Four hundred seventeen fungi were isolated from 144 of the 163 Douglas-fir poles (ages 7 to 17 years and treatments CCA, penta and oil, or CellonÂź) sampled from transmission lines or storage piles in New York and Pennsylvania. Microfungi predominated and comprised nearly 85% of all isolates. They were isolated primarily from treated zones and were most abundant in older CCA-treated poles in transmission lines. Antrodia carbonica and Postia placenta were the principal basidiomycete decayers and isolated primarily from untreated zones in CCA-treated poles. A limited number of white-rot fungi were isolated from the treated and untreated zones of several poles.Seven of the 12 principal microfungi were established to have soft-rot capabilities. Soft rot was detected anatomically in 23 of the 144 poles in transmission lines. In most cases it was superficial and limited to several outer annual rings; however, it was severe in older CCA-treated poles and involved all of the treated zone and extended several centimeters radially into the untreated zone. Also, soft rot was detected anatomically and soft-rot fungi culturally, in 8 of 12 13-year-old CCA-treated poles that had been fumigated with Vapam 5 or 6 years previously. None was detected in the fumigated penta-treated poles.These data suggest that soft-rot fungi play an important role in decay development in the treated groundline zone of utility poles and should be considered in decay detection programs (culturally) and decisions on the timing of remedial treatments

    Fungi Associated with Decay in Treated Southern Pine Utility Poles in the Eastern United States

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    Approximately 1,320 fungi were isolated and studied from 246 creosote- or pentachlorophenol-treated southern pine poles in service in the eastern United States. The fungi identified were Basidiomycete decayers, soft rotters, and microfungi. White rot fungi predominated in the 262 Basidiomycete decayers isolated from 180 poles. The major Basidiomycetes isolated by radial position from poles of varying service ages appeared to develop initially in the outer treated zones and were often associated with seasoning checks. Some decay origins, however, appeared to be cases of preinvasion and escapes of preservative treatment. Five species of soft rot fungi comprised nearly 85% of 211 isolates obtained from 131 poles. They were isolated primarily from creosote-treated poles in outer treated zones at the groundline. Dissection analysis of 92 poles indicated that six developmental decay patterns and certain fungi were associated commonly with a pattern. The pole mycoflora isolated was relatively uniform in distribution in the eastern United States. The soft rotters and white rot group of Basidiomycete decayers appear to be a more important component of the treated southern pine pole mycoflora than has been recognized previously

    The novel chemokine receptor CXCR7 regulates trans-endothelial migration of cancer cells

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    <p>Abstract</p> <p>Background</p> <p>Migration of metastatic tumor cells from the bloodstream into lymph nodes is thought to be facilitated by expression of the chemokine receptors CCR7, CXCR4 and, for B cell-derived tumors, CXCR5. Expression of their respective chemokine ligands (CCL19, CCL21, CXCL12 and CXCL13) by endothelial cells inside the lymph nodes facilitates the trans-endothelial migration (TEM) of these cells through high endothelial venules into the lymph node parenchyma. It is known that CXCR7, a second CXCL12 receptor, regulates TEM of CXCR4+CXCR7+ tumor cells towards a CXCL12 source. In this study, we set out to assess the potential stimulation by CXCL12 of tumor cell TEM towards other chemokines and whether CXCR7 might be able to regulate such effects.</p> <p>Methods</p> <p>The human Burkitt's lymphoma cell line NC-37, which expresses CXCR4, CXCR5, CXCR7 and CCR7, was selected as a model system. TEM of these cells through a human HUVEC endothelial cell monolayer was used as the main model system for these studies. Regulation of their TEM behavior by various concentrations of the various cognate chemokines for the above-mentioned receptors, placed in either the source or target wells of modified Boyden chamber migration plates, was assessed by quantifying the number of cells migrated under each experimental condition.</p> <p>Results</p> <p>Exposure of CXCR4<sup>+</sup>CXCR7<sup>+ </sup>cancer cells to CXCL12 greatly potentiated their TEM towards the chemokines CCL19 and CXCL13. This CXCL12-potentiated TEM was inhibited by the second CXCR7 chemokine ligand, CXCL11, as well as CXCR7-specific small molecule antagonists and antibodies. In contrast, the CXCR4 antagonist AMD3100 was less effective at inhibiting CXCL12-potentiated TEM. Thus, CXCR7 antagonists may be effective therapeutic agents for blocking CXCL12-mediated migration of CXCR4<sup>+</sup>CXCR7<sup>+ </sup>tumor cells into lymph nodes, regardless of whether the cancer cells follow a CXCL12 gradient or whether serum CXCL12 stimulates their migration towards CCR7 and CXCR5 chemokines in the lymph nodes.</p

    Itinerant and Localized Magnetization Dynamics in Antiferromagnetic Ho

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    Using femtosecond time-resolved resonant magnetic x-ray diffraction at the Ho L 3 absorption edge, we investigate the demagnetization dynamics in antiferromagnetically ordered metallic Ho after femtosecond optical excitation. Tuning the x-ray energy to the electric dipole ( E 1 , 2 p → 5 d ) or quadrupole ( E 2 , 2 p → 4 f ) transition allows us to selectively and independently study the spin dynamics of the itinerant 5 d and localized 4 f electronic subsystems via the suppression of the magnetic (2 1 3 − τ ) satellite peak. We find demagnetization time scales very similar to ferromagnetic 4 f systems, suggesting that the loss of magnetic order occurs via a similar spin-flip process in both cases. The simultaneous demagnetization of both subsystems demonstrates strong intra-atomic 4 f − 5 d exchange coupling. In addition, an ultrafast lattice contraction due to the release of magneto-striction leads to a transient shift of the magnetic satellite peak

    Wolcott-Rallison Syndrome

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    Wolcott-Rallison syndrome (WRS) is a rare autosomal-recessive disorder characterized by the association of permanent neonatal or early-infancy insulin-dependent diabetes, multiple epiphyseal dysplasia and growth retardation, and other variable multisystemic clinical manifestations. Based on genetic studies of two inbred families, we previously identified the gene responsible for this disorder as EIF2AK3, the pancreatic eukaryotic initiation factor 2α (eIF2α) kinase. Here, we have studied 12 families with WRS, totalling 18 cases. With the exception of one case, all patients carried EIF2AK3 mutations resulting in truncated or missense versions of the protein. Exclusion of EIF2AK3 mutations in the one patient case was confirmed by both linkage and sequence data. The activities of missense versions of EIF2AK3 were characterized in vivo and in vitro and found to have a complete lack of activity in four mutant proteins and residual kinase activity in one. Remarkably, the onset of diabetes was relatively late (30 months) in the patient expressing the partially defective EIF2AK3 mutant and in the patient with no EIF2AK3 involvement (18 months) compared with other patients (&lt;6 months). The patient with no EIF2AK3 involvement did not have any of the other variable clinical manifestations associated with WRS, which supports the idea that the genetic heterogeneity between this variant form of WRS and EIF2AK3 WRS correlates with some clinical heterogeneity
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