Factors influencing weaning performance of beef calves in commercial and purebred herds in Tennessee

This study seeks to evaluate the influence of age of dam, sex of calf, age of calf, and month of birth on: 1. Birth weight 2. Average daily gain 3. Type score

The Natural Killer Cell Cytotoxic Function Is Modulated by HIV-1 Accessory Proteins

Natural killer (NK) cells’ major role in the control of viruses is to eliminate established infected cells. The capacity of NK cells to kill virus-infected cells is dependent on the interactions between ligands on the infected cell and receptors on the NK cell surface. Because of the importance of ligand-receptor interactions in modulating the NK cell cytotoxic response, HIV has developed strategies to regulate various NK cell ligands making the infected cell surprisingly refractory to NK cell lysis. This is perplexing because the HIV-1 accessory protein Vpr induces expression of ligands for the NK cell activating receptor, NKG2D. In addition, the accessory protein Nef removes the inhibitory ligands HLA-A and -B. The reason for the ineffective killing by NK cells despite the strong potential to eliminate infected cells is due to HIV-1 Vpu’s ability to down modulate the co-activation ligand, NTB-A, from the cell surface. Down modulation of NTB-A prevents efficient NK cell degranulation. This review will focus on the mechanisms through which the HIV-1 accessory proteins modulate their respective ligands, and its implication for NK cell killing of HIV-infected cells

CD155 on HIV-infected cells is not modulated by HIV-1 Vpu and Nef but synergizes with NKG2D ligands to trigger NK cell lysis of autologous primary HIV-infected cells

Activation of primary CD4(+) T cells induces the CD155, but not the CD112 ligands for the natural killer (NK) cell activation receptor (aNKR) CD226 [DNAX accessory molecule-1 (DNAM-1)]. We hypothesize that HIV productively infects activated CD4(+) T cells and makes itself vulnerable to NK cell-mediated lysis when CD155 on infected T cells engages DNAM-1. The primary objective of this study is to determine whether CD155 alone or together with NKG2D ligands triggers autologous NK cell lysis of HIV-infected T cells and whether HIV modulates CD155. To determine whether HIV modulates this activation ligand, we infected “activated” CD4(+) T cells with HIV in the absence or presence of Nef and/or Vpu and determined by flow cytometry whether they modulated CD155. To determine if CD155 alone, or together with NKG2D ligands, triggered NK cell lysis of autologous HIV-infected T cells, we treated purified NK cells with DNAM-1 and/or NKG2D blocking antibodies before the addition of purified autologous HIV-infected cells in cytolytic assays. Finally, we determined whether DNAM-1 works together with NKG2D as an NK cell coactivation receptor (caNKR) or whether they work independently as aNKRs to induce an NK cell lytic response. We demonstrate that HIV and specifically Nef and/or Vpu do not modulate CD155 on infected primary T cells; and both CD155 and NKG2D ligands synergize as aNKRs to trigger NK cell lysis of the infected cell

Book Reviews

Patent Law. by John Barker Waite, Professor of Law in the University of Michigan Law School. Princeton University Press, x92o

On Complete Sets of Polarization Observables

A new criterion is developed which provides a check as to whether a chosen set of polarization observables is complete with respect to the determination of all independent $T$-matrix elements of a reaction of the type $a+b\to c+d+...$. As an illustrative example, this criterion is applied to the longitudinal observables of deuteron electrodisintegration.Comment: 8 pages revtex, final version, accepted for Nucl. Phys.

Mother and father depression symptoms and child emotional difficulties: a Network model

INTRODUCTION: Enhancing understanding of depression symptom interactions between parents and associations with subsequent child emotional difficulties will inform targeted treatment of depression to prevent transmission within families. OBJECTIVES: To use a network approach to identify ‘bridge’ symptoms that reinforce mother and father depression, and whether bridge symptoms, as well as other symptoms, impact subsequent child emotional difficulties. METHODS: Symptoms were examined using two unregularized partial correlation network models. The study included 4,492 mother-father-child trios from a prospective, population-based cohort in the United Kingdom. Mother and father reports of depression symptoms were assessed when the child was twenty-one months old. Child emotional difficulties were reported by the mother at ages nine, eleven and thirteen years. RESULTS: Bridge symptoms mutually reinforcing mother and father depression symptoms were feelings of guilt and self-harm ideation, whereas anhedonia acted as a bridge from the father to the mother, but not vice-versa (fig.1, network 1). The symptom of feelings of guilt in mothers was the only bridge symptom which directly associated with child emotional difficulties. Other symptoms that directly associated with child emotional difficulties were feeling overwhelmed for fathers and anhedonia, sadness, and panic in mothers (fig.1, network 2). CONCLUSIONS: Specific symptom interactions are central to the co-occurrence of depression symptoms between parents. Of interest, only one of the bridge symptoms associated with later child emotional difficulties. In addition, specific symptom-to-child outcomes were identified, suggesting that different symptoms in mothers and fathers are central for increased vulnerability in children. DISCLOSURE: No significant relationships