Only mature B lymphocytes can enter the lymphoid follicles of spleen and lymph nodes and thus efficiently participate in the immune response. Mature, long-lived B lymphocytes derive from short-lived precursors generated in the bone marrow. We show that selection into the mature pool is an active process and takes place in the spleen. Two populations of splenic B cells were identified as precursors for mature B cells. Transitional B cells of type 1 (T1) are recent immigrants from the bone marrow. They develop into the transitional B cells of type 2 (T2), which are cycling and found exclusively in the primary follicles of the spleen. Mature B cells can be generated from T1 or T2 B cells.

C‐myb encodes a transcriptional activator that is essential for the development of the hematopoietic system but appears to lack major roles in non‐hematopoietic cells. The identification of two conserved myb‐related genes, designated A‐myb and B‐myb, has raised the possibility that these genes are functional equivalents of c‐myb in non‐hematopoietic cells. Here, we report the isolation and preliminary characterization of the mouse A‐myb gene. Mouse A‐myb maps to the proximal region of chromosome 1 and encodes a transcriptional activator with properties similar to those of the c‐myb and v‐myb proteins. During embryo‐genesis A‐myb is predominantly expressed in several regions of the developing central nervous system (CNS) and the urogenital ridge. Expression in the CNS is confined to the neural tube, the hindbrain, the neural retina and the olfactory epithelium, and coincides with the presence of proliferating immature neuronal precursor cells. In the adult mouse, A‐myb is expressed during the early stages of sperm cell differentiation and in B lymphocytes located in germinal centers of the spleen. Taken together, these results suggest a role for A‐myb in the proliferation and/or differentiation of neurogenic, spermatogenic and B‐lymphoid cells.

We have investigated the effect of the v-Myc oncoprotein on gene expression in myelomonocytic cells. We find that v-Myc dramatically down-regulates the expression of myelomonocytic-specific genes, such as the chicken mim-1 and lysozyme genes, both of which are known targets for C/EBP transcription factors. We present evidence that Myc downregulates these genes by inhibiting the function of C/EBP transcription factors. Detailed examination of the inhibitory mechanism shows that amino-terminal sequences of v-Myc, but not its DNA-binding domain, are required for the suppression of C/EBP-dependent transactivation. Our findings identify a new function for Myc and reveal a novel mechanism by which Myc affects the expression of other genes.Numerous studies have implicated the c-myc gene in a variety of cellular processes, such as proliferation, differentiation, and apoptosis, and have shown that mutant forms of the gene, such as transduced (v-myc) or rearranged myc alleles, are involved in tumorigenesis (1-6). It is now widely believed that c-myc plays a central role in a switch mechanism by which normal cells decide between the alternative fates of proliferation, differentiation, and apoptosis and that deregulation of c-myc causes an imbalance in this switch mechanism, resulting in the development of neoplasia.Structural and functional analyses have identified the c-myc protein product (c-Myc) as a transcription factor. The carboxyl terminus of c-Myc forms a basic region-helix-loop-helixleucine zipper (B-HLH-LZ) DNA-binding domain, heterodimerizes with the Max protein (7), and recognizes the consensus Myc binding site, CACGTG (8-10), whereas the amino terminus of c-Myc functions as a transcriptional activation domain (11)(12)(13)(14). Several genes whose expression is induced by c-Myc have been identified (15)(16)(17)(18)(19)(20). In addition, c-Myc also inhibits gene expression. The C/EBPa gene (21,22) and the adenovirus-2 major late promoter (22, 23) are downregulated by c-Myc. Interestingly, repression of these genes does not depend on Myc-specific DNA-binding sites but is mediated by so-called initiator elements located in the promoters of these genes (22, 23). Thus, increasing evidence suggests that c-Myc affects gene expression by several different mechanisms. Nevertheless, an unambiguous functional relationship to the physiological or malignant activities of myc has not been established for any of the putative target genes identified so far.We have studied the effect of v-Myc on gene expression in myelomonocytic cells. We have found that v-Myc inhibits the expression of several genes, including mim-1 and the lysozyme gene, both of which have been shown to be targets for C/EBP transcription factors (24,25). We have analyzed the mechanism by which Myc down-regulates these genes and have found that amino-terminal sequences of Myc interfere with the function of C/EBP transcription factors. Our findings identify a novel function for Myc and reveal a novel mechanism by which Myc affects the expression of othe...

Complex I is a proton-pumping multisubunit-complex involved in the respiratory electron transport chain, which provides the proton motive force essential for the synthesis of ATP. Homologs of this complex exist in bacteria, the mitochondria of eukaryotes, and the chloroplasts of plants. The bacterial and mitochondrial

Background: There is empirical evidence that the presence of a companion animal can have a positive impact on performance. The available evidence can be viewed in terms of differing hypotheses that attempt to explain the mechanisms behind the positive effects. Little attention has been given to motivation as a potential mode of action with regards to human-animal interactions. First we give an overview of evidence that animals might promote motivation. Second we present a study to examine the effect of a therapy dog on exercise performance in children with obesity.Methods: Twelve children, aged 8–12 years old, were randomly assigned to two groups in a crossover design: dog-group and human confederate group. Several types of physical activities via accelerometer and subjective ratings of wellbeing, satisfaction, and motivation were assessed. Data were analyzed using analysis of variance for repeated measures on one factor.Results: The main effect of condition was significant for all performance variables. There was less passive behavior and more physical activity for all performance variables in the presence of the dog than in that of the human confederate. Between dog- and human- condition there was no difference in the subjective rating of motivation, wellbeing, or satisfaction.Discussion: The results demonstrate that the presence of a therapy dog has the potential to increase physical activity in obese children. Task performance as a declarative measure was increased by the presence of the dog in comparison to a human confederate, but self-report measures of motivation, satisfaction or wellbeing did not differ between the two conditions. Therefore, it stands to reason that a dog could trigger implicit motives which enhance motivation for activity. The results of our study indicate the potentially beneficial effect of incorporating dogs into outpatient training for obese children.

Previous research has suggested that owners’ attitude to their family dogs may contribute to a variety of behaviour problems in the dog, and authors assume that dogs with separation-related disorder (SRD) attach differently to the owner than typical dogs do. Our previous research suggested that these dogs may have an insecure attachment style. In the present study we have investigated whether owners’ attachment style, personality traits and the personality of the dog influence the occurrence of SRD in the dog. In an internet-based survey 1508 (1185 German and 323 Hungarian) dog-owners filled in five questionnaires: Demographic questions, Separation Behaviour Questionnaire (to determine SRD), Human and Dog Big Five Inventory and Adult Attachment Scale. We found that with owners’ higher score on attachment avoidance the occurrence of SRD in the dog increases. Dogs scoring higher on the neuroticism scale were more prone to develop SRD. Our results suggest that owners’ attachment avoidance may facilitate the development of SRD in dogs. We assume that avoidant owners are less responsive to the dog’s needs and do not provide a secure base for the dog when needed. As a result dogs form an insecure attachment and may develop SRD. However, there may be alternative explanations of our findings that we also discuss.

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