Separating the climatic signal from tree-ring width and maximum latewood density records

We propose a technique for separating the climatic signal which is contained in two tree-ring parameters widely used in dendroclimatology. The method is based on the removal of the relationship between tree-ring width (TRW) and maximum latewood density (MXD) observed for narrow tree rings from high latitudes. The new technique is tested on data from three larch stands located along the northern timberline in Eurasia. Correlations were calculated between the temperatures of pentads (five consecutive days), TRW chronologies and MXD chronologies calculated according to the standard and proposed methods. The analysis confirms the great importance of summer temperature for tree radial growth and tree-ring formation. TRW is positively correlated with the temperature of four to eight pentads (depending on the region) at the beginning of the growth season, but MXD as obtained by the standard technique is correlated with temperature over a much longer period. For maximum density series from which the relationship between MXD and TRW has been removed (MXD′), there is a clear correlation with temperatures in the second part of the growing season. These results are consistent with the known dynamics of tree-ring growth in high latitudes and mechanisms of tree-ring formation.     

Cascade of autophosphorylation in the beta-subunit of the insulin receptor

Insulin stimulated autophosphorylation of the beta-subunit of the insulin receptor purified from Fao hepatoma cells or purified from Chinese hamster ovary (CHO/HIRC) or Swiss 3T3 (3T3/HIRC) cells transfected with the wild-type human insulin receptor cDNA. Autophosphorylation of the purified receptor occurred in at least two regions of the beta-subunit: the regulatory region containing Tyr-1146, Tyr-1150, and Tyr-1151, and the C-terminus containing Tyr-1316 and Tyr-1322. In the presence of antiphosphotyrosine antibody (alpha-PY), autophosphorylation of the purified receptor was inhibited nearly 80% during insulin stimulation. Tryptic peptide mapping showed that alpha-PY inhibited autophosphorylation of both tyrosyl residues in the C-terminus and one tyrosyl residue in the regulatory region, either Tyr-1150 or Tyr-1151. Thus, a bis-phosphorylated form of the regulatory region accumulated in the presence of alpha-PY, which contained Tyr(P)-1146 and either Tyr(P)-1150 or 1151. In intact Fao, CHO/HIRC, and 3T3/HIRC cells, insulin stimulated tyrosyl phosphorylation of the beta-subunit of the insulin receptor. Tryptic peptide mapping indicated that the regulatory region of the beta-subunit was mainly (greater than 80%) bis-phosphorylated; however, all three tyrosyl residues of the regulatory region were phosphorylated in about 20% of the receptors. As the phosphotransferase was activated by tris-phosphorylation but not bis-phosphorylation of the regulatory region of the beta-subunit (White et al.: Journal of Biological Chemistry 263:2969-2980, 1988), the extent of autophosphorylation in the regulatory region may play an important regulatory role during signal transmission in the intact cell.     

Multifunctional roles of the autoimmune disease-associated tyrosine phosphatase PTPN22 in regulating T cell homeostasis

The non-receptor tyrosine phosphatase PTPN22 has a vital function in inhibiting antigen-receptor signaling in T cells, while polymorphisms in the PTPN22 gene are important risk alleles in human autoimmune diseases. We recently reported that a key physiological function of PTPN22 was to prevent naïve T cell activation and effector cell responses in response to low affinity antigens. PTPN22 also has a more general role in limiting T cell receptor-induced proliferation. Here we present new data emphasizing this dual function for PTPN22 in T cells. Furthermore, we show that T cell activation modulates the expression of PTPN22 and additional inhibitory phosphatases. We discuss the implication of these findings for our understanding of the roles of PTPN22 in regulating T cell responses and in autoimmunity.     

SOCIAL SELECTION AND THE EVOLUTION OF ANIMAL SIGNALS

Social selection is presented here as a parallel theory to sexual selection and is defined as a selective force that occurs when individuals change their own social behaviors, responding to signals sent by conspecifics in a way to influence the other individuals' fitness. I analyze the joint evolution of a social signal and behavioral responsiveness to the signal by a quantitative-genetic model. The equilibria of average phenotypes maintained by a balance of social selection and natural selection and their stability are examined for two alternative assumptions on behavioral responsiveness, neutral and adaptive. When behavioral responsiveness is neutral on fitness, a rapid evolution by runaway selection occurs only with enough genetic covariance between the signal and responsiveness. The condition for rapid evolution also depends on natural selection and the number of interacting individuals. When signals convey some information on signalers (e.g., fighting ability), behavioral responsiveness is adaptive such that a receiver's fitness is also influenced by the signal. Here there is a single point of equilibrium. The equilibrium point and its stability do not depend on the genetic correlation. The condition needed for evolution is that the signal is beneficial for receivers, which results from reliability of the signal. Frequency-dependent selection on responsiveness has almost no influence on the equilibrium and the rate of evolution.     

Identification of Tumor Antigens in the HLA Peptidome of Patient-derived Xenograft Tumors in Mouse

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Highlights

• •Sufficient tumor tissues are often unavailable large HLA peptidome discovery.
• •Using patient derived xenograft (PDX) tumors can overcome this limitation.
• •The large PDX HLA peptidomes expand significantly those of the original biopsies.
• •The HLA peptidomes of the PDX tumors included many tumor antigens.

     

The opioid systems - Panacea and nemesis

This mini-review outlines the opioid systems and their roles primarily as related to reward and compulsive drug/alcohol intake. The central role is taken by the mu-opioid receptor, target for opiate analgesics and also a central target in compulsive alcohol abuse, alcoholism. The mu-opioid receptor and the cognate opioid neuropeptides from proenkephalin and proopiomelancortin are members of a superfamily of opioid systems, each with unique and still to be defined roles in the central nervous system.     

Structural and Functional Impact of SRP54 Mutations Causing Severe Congenital Neutropenia

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