The Northern Home Front During the Civil War

Reviewer Antointette G. van Zelm writes that The Northern Home Front During the Civil War is engagingly written and chock full of American voices. Both the diversity and dissension that characterized the Northern populace come through prominently

B-cell Development and Primary Antibody Deficiencies

B lymphocytes are generated throughout life from hematopoietic stem cells in bone marrow, and contribute to the immune system by the production of antigen-specific antibodies (immunoglobulins; Ig). Two distinct phase of B-cell development can be distinguished: 1) antigen-independent precursor-B-cell differentiation in bone marrow, and 2) antigendependent B-cell maturation in peripheral lymphoid organs. The aim of precursor-B-cell differentiation is to generate a functional Ig receptor by V(D)J recombination of the genes encoding the Ig heavy (IgH) and Ig light (Ig. or Ig.) chains. When a precursor-B-cell succeeds in creating a functional Ig receptor, it will migrate to the periphery and become part of the naive B-cell pool. Because every precursor-B-cell creates a unique Ig receptor, the peripheral B-cell pool bears a diverse repertoire of specific receptors for antigen. Naive B lymphocytes are short-lived cells and because new cells are continuously generated, there is a high turnover. However, once a naive mature B-lymphocyte recognizes antigen with its specific Ig receptor, it will undergo clonal proliferation and differentiation, thereby generating a large number of plasma cells that produce and secrete antigen-specific Igs. During this response, the B-cell initiates additional molecular mechanisms to adapt and optimize the antigen-binding affinity and the effector function of its Ig molecule. Generation of a large repertoire of B lymphocytes and the response of one of these B lymphocytes to antigen is a multi-step process for which multiple proteins are required. The lack of one of these proteins leads to a problem with the humoral immunity of the individual, which is seen in patients with primary antibody deficiency diseases. These children or young adults carry rare inherited disorders and are subject to multiple, recurrent (mainly) bacterial infections. Several genetic defects have been identified in patients with a primary antibody deficiency. In many patients, however, the B-cell defect is not well understood. The studies in this thesis address several aspects of B-cell development and defects that lead to primary antibody deficiency diseases

Intersections of loci of admissible covers with tautological classes

For a finite group $G$, let \H_{g,G,\xi} be the stack of admissible $G$-covers $C\to D$ of stable curves with ramification data $\xi$, $g(C)=g$ and $g(D)=g'$. There are source and target morphisms \phi\colon \H_{g,G,\xi}\to \M_{g,r} and \delta\colon \H_{g,G,\xi}\to \M_{g',b}, remembering the curves $C$ and $D$ together with the ramification or branch points of the cover respectively. In this paper we study admissible cover cycles, i.e. cycles of the form \phi_* [\H_{g,G,\xi}]. Examples include the fundamental classes of the loci of hyperelliptic or bielliptic curves $C$ with marked ramification points. The two main results of this paper are as follows: Firstly, for the gluing morphism \xi_A\colon \M_A\to \M_{g,r} associated to to a stable graph $A$ we give a combinatorial formula for the pullback \xi^*_A \phi_*[\H_{g,G,\xi}] in terms of spaces of admissible $G$-covers and $\psi$ classes. This allows us to describe the intersection of the cycles \phi_*[\H_{g,G,\xi}] with tautological classes. Secondly, the pull-push $\delta_*\phi^*$ sends tautological classes to tautological classes and we also give a combinatorial description of this map in terms of standard generators of the tautological rings. We show how to use the pullbacks to algorithmically compute tautological expressions for cycles of the form \phi_* [\H_{g,G,\xi}]. In particular, we compute the classes [\Hyp_5] and [\Hyp_6] of the hyperelliptic loci in \M_5 and \M_6 and the class [\B_4] of the bielliptic locus in \M_4

Intersections of loci of admissible covers with tautological classes

For a finite group G, let Hg,G,ξ be the stack of admissible G-covers C → D of stable curves with ramification data ξ , g(C) = g and g(D) = g . There are source and target morphisms φ : Hg,G,ξ →Mg,r and δ : Hg,G,ξ →Mg ,b, remembering the curves C and D together with the ramification or branch points of the cover respectively. In this paper we study admissible cover cycles, i.e. cycles of the form φ∗[Hg,G,ξ ]. Examples include the fundamental classes of the loci of hyperelliptic or bielliptic curves C with marked ramification points. The two main results of this paper are as follows: firstly, for the gluing morphism ξA : MA →Mg,r associated to a stable graph A we give a combinatorial formula for the pullback ξ∗ Aφ∗[Hg,G,ξ ] in terms of spaces of admissible G-covers and ψ classes. This allows us to describe the intersection of the cycles φ∗[Hg,G,ξ ] with tautological classes. Secondly, the pull–push δ∗φ ∗ sends tautological classes to tautological classes and we give an explicit combinatorial description of this map. We show how to use the pullbacks to algorithmically compute tautological expressions for cycles of the form φ∗[Hg,G,ξ ]. In particular, we compute the classes [H5] and [H6] of the hyperelliptic loci in M5 and M6 and the class [B4] of the bielliptic locus inM4.Rheinische Friedrich-Wilhelms-Universität Bonn (1040)Peer Reviewe

Pullbacks of universal Brill-Noether classes via Abel-Jacobi morphisms

Following Mumford and Chiodo, we compute the Chern character of the derived pushforward $\textrm{ch} (R^\bullet\pi_\ast\mathscr{O}(\mathsf{D}))$, for $\mathsf D$ an arbitrary element of the Picard group of the universal curve over the moduli stack of stable marked curves. This allows us to express the pullback of universal Brill-Noether classes via Abel-Jacobi sections to the compactified universal Jacobians, for all compactifications such that the section is a well-defined morphism

Clathrin Heavy Chain subunits coordinate endo- and exocytic traffic and affect stomatal movement

The current model for vesicular traffic to and from the plasma membrane is accepted but the molecular requirements for this coordination are not well defined. We have identified the has1 mutant, which has a stomatal function defect, as a clathrin heavy chain 1 (CHC1) mutant allele and show that it has a decreased rate of endocytosis and growth defects that are shared with other chc1 mutant alleles. We used chc1 alleles and the related chc2 mutant as tools to investigate the effects clathrin defects have on secretion pathways and plant growth. We show that secretion and endocytosis at the plasma membrane is sensitive to CHC1 and CHC2 function in seedling roots, and that chc mutants have physiological defects in stomatal function and plant growth that have not been previously described. These findings suggest that clathrin supports specific functions of multiple cell types. Stomata movement and gas exchange is altered in chc mutants, indicating clathrin is important for stomatal regulation. The aberrant function of chc mutant stomata is consistent with the growth phenotypes observed under different water and light conditions, which are also similar to those of the secretory SNARE mutant, syp121. The syp121 and chc mutants have impaired endo- and exocytosis compared to wild type, indicating a link between SYP121-dependent secretion and clathrin-dependent endocytosis at the plasma membrane. Our findings provide evidence that clathrin and SYP121 functions are important for the coordination of endo- and exocytosis, and have an impact on stomatal function, gas exchange, and vegetative growth in Arabidopsis

ID2 (Inhibitor Of DNA Binding 2, Dominant Negative Helix-Loop-Helix Protein)

Review on ID2 (Inhibitor Of DNA Binding 2, Dominant Negative Helix-Loop-Helix Protein), with data on DNA, on the protein encoded, and where the gene is implicated