Variability in the carbon isotopic composition of foliage carbon pools (soluble carbohydrates, waxes) and respiration fluxes in southeastern U.S. pine forests

Author Posting. © American Geophysical Union, 2012. This article is posted here by permission of American Geophysical Union for personal use, not for redistribution. The definitive version was published in Journal of Geophysical Research 117 (2012): G02009, doi:10.1029/2011JG001867.We measured the δ13C of assimilated carbon (foliage organic matter (δCOM), soluble carbohydrates (δCSC), and waxes (δCW)) and respiratory carbon (foliage (δCFR), soil (δCSR) and ecosystem 13CO2 (δCER)) for two years at adjacent ecosystems in the southeastern U.S.: a regenerated 32 m tall mature Pinus palustris forest, and a mid-rotation 13 m tall Pinus elliottii stand. Carbon pools and foliage respiration in P. palustris were isotopically enriched by 2‰ relative to P. elliottii. Despite this enrichment, mean δCER values of the two sites were nearly identical. No temporal trends were apparent in δCSC, δCFR, δCSR and δCER. In contrast, δCOM and δCW at both sites declined by approximately 2‰ over the study. This appears to reflect the adjustment in the δ13C of carbon storage reserves used for biosynthesis as the trees recovered from a severe drought prior to our study. Unexpectedly, the rate of δ13C decrease in the secondary C32–36 n-alkanoic acid wax molecular cluster was twice that observed for δCOM and the predominant C22–26 compound cluster, and provides new evidence for parallel but separate wax chain elongation systems utilizing different carbon precursor pools in these species. δCFR and δCER were consistently enriched relative to assimilated carbon but, in contrast to previous studies, showed limited variations in response to changes in vapor pressure deficit (D). This limited variability in respiratory fluxes and δCSC may be due to the shallow water table as well as the deep taproots of pines, which limit fluctuations in photosynthetic discrimination arising from changes in D.This work was supported by a NSF grants DEB-0343604, DEB-0344562 and DEB-0552202, and DOE grant DE-FC02-06ER64156/06-SC-NICCR-1063.2012-10-1

Transfusion-transmitted infections

Although the risk of transfusion-transmitted infections today is lower than ever, the supply of safe blood products remains subject to contamination with known and yet to be identified human pathogens. Only continuous improvement and implementation of donor selection, sensitive screening tests and effective inactivation procedures can ensure the elimination, or at least reduction, of the risk of acquiring transfusion transmitted infections. In addition, ongoing education and up-to-date information regarding infectious agents that are potentially transmitted via blood components is necessary to promote the reporting of adverse events, an important component of transfusion transmitted disease surveillance. Thus, the collaboration of all parties involved in transfusion medicine, including national haemovigilance systems, is crucial for protecting a secure blood product supply from known and emerging blood-borne pathogens

Immunological surveillance of tumors in the context of major histocompatibility complex restriction of T cell function.

The immunological surveillance hypothesis was formulated prior to the realization of the fact that an individual\u27s effector T cells generally only see neoantigen if it is appropriately presented in the context of self MHC glycoproteins. The biological consequence of this mechanism is that T lymphocytes are focused onto modified cell-surface rather than onto free antigen. The discovery of MHC-restricted T cell recognition, and the realization that T cell-mediated immunity is of prime importance in promoting recovery from infectious processes, has thus changed the whole emphasis of the surveillance argument. Though the immunological surveillance hypothesis generated considerable discussion and many good experiments, there is no point in continuing the debate in the intellectual context that seemed reasonable in 1970. It is now much more sensible to think of natural surveillance: and T cell surveillance,: without excluding the probability that these two systems have elements in common. We can now see that T cell surveillance probably operates well in some situations, but is quite ineffective in many others. Part of the reason for this may be that the host response selects tumor clones that are modified so as to be no longer recognized by cytotoxic T cells. The possibility that this reflects changes in MHC phenotype has been investigated, and found to be the case, for some experimental tumors. In this regard, it is worth remembering that many mutations: in MHC genes that completely change the spectrum of T cell recognition are serologically silent. The availability of molecular probes for investigating the status of MHC genes in tumor cells, together with the capacity to develop cloned T cell lines, monoclonal antibodies to putative tumor antigens, and cell lines transfected with genes coding for these molecules, indicates how T cell surveillance may profitably be explored further in both experimental and human situations

H-2Kb mutations limit the CTL response to SV40 TASA.

The cytotoxic T lymphocyte (CTL) responses directe towards SV40 tumor-associated specific antigen (TASA) in nine strains of spontaneously arising Kb mutant mice were analyzed. All nine mutants generated normal levels of H-2Db-restricted response, but the K-end-restricted CTL response varied. B6.C-H-2bm1 (bm1) did not produce K-end-restricted SV40 TASA-specific CTL upon immunization, and SV40-transformed bm1 cells were not lysed by intra-H-2 recombinant Kb [B10.A(5R)] CTL. Nonreciprocal cross-reactive lysis was seen between B6-H-2bm8 (bm8) and B10.A(5R). Strain B6-H-2bm8 mice produce highly specific Kbm8-restricted CTL that lyse SV40-transformed bm8 cells (Kbm8SV) but not B10.A(5R) target cells (K5RSV), although Kbm8SV targets can be partially lysed by B10.A(5R) CTL. The other seven Kb mutants cross-react with B10.A(5R). These experiments definitively show that genes mapping to the K and/or D region directly control the H-2-restricted CTL response to SV40 TASA