Grandmother's Grandchild: My Crow Indian Life

Grandmother's Grandchild: My Crow Indian Life. Alma Hogan Snell and Becky Matthews. eds.; foreword by Peter Nabokov. Lincoln: University of Nebraska Press, 2000. 213 pp.     

They're All My Children: Foster Mothering in America

They're All My Children: Foster Mothering in America. Danielle F. Wozniak. New York: NYU Press, 2002. + 245 pp.     

I Am My Language: Discourses of Women and Children in the Borderlands.

. Am My Language: Discourses of Women and Children in the Borderlands. Norma González. Tucson: University of Arizona Press, 2001. 240 pp.     

Characterization of adult human marrow hematopoietic progenitors highly enriched by two-color cell sorting with My10 and major histocompatibility class II monoclonal antibodies

Monoclonal antibodies, My10 (HPCA-1) and major histocompatibility class II (HLA-DR), were used to enrich and phenotype normal human marrow colony-forming unit: granulocyte-macrophage (CFU-GM), burst-forming unit: erythroid (BFU-E), and multipotential colony-forming unit: granulocyte-erythroid-macrophage-megakaryocyte (CFU-GEMM) progenitor cells. Nonadherent low density T lymphocyte-depleted marrow cells were sorted on a Coulter Epics 753 dye laser flow cytometry system with the use of Texas Red-labeled anti-My10 and phycoerythrin conjugated anti-HLA-DR. Cells were separated into populations with nondetectable expression of antigens (DR-My10-) or with constant expression of one antigen and increasing densities of the other antigen. More than 98% of the CFU-GM, BFU-E, and CFU-GEMM were found in fractions containing cells expressing both HLA-DR and My10 antigens. The cloning efficiency (CE) of cells in the DR-My10- cell fraction was 0.01%. In the antigen-positive sorted fractions, the CE was highest (up to 47%) in the fractions of cells expressing high My10 and low DR (My10 DR+) antigens and was lowest (2.5%) in the fraction of cells expressing low My10 and low DR (My10+DR+) antigens. Populations of cells varying in the density of HLA-DR, but not My10, antigens varied in the proportion and types of progenitor cells present. When My10-positive cells were sorted for HLA-DR density expression, the CE for CFU-GM was similar in the DR+ and DR++ fractions, but most of the BFU-E and CFU-GEMM were found in the DR+ fraction. Within the CFU-GM compartment, most of the eosinophil progenitors were found in the DR+ fraction, whereas a greater proportion of macrophage progenitors were detected in the DR++ fraction. CFU-GM and BFU-E in the fractions of cells positive for DR and My10 were assessed for responsiveness to the effects of recombinant human tumor necrosis factor-alpha, recombinant human interferon-gamma, and prostaglandin E1. Colony formation from CFU-GM was suppressed by the three molecules, and colony formation by BFU-E was suppressed by recombinant human tumor necrosis factor-alpha and interferon-gamma and enhanced, in the presence of T lymphocyte-conditioned medium, by prostaglandin E1 in all antigen-positive fractions.(ABSTRACT TRUNCATED AT 400 WORDS)     

My experience with Bison hybrids

Ohne Zusammenfassung

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My experience with Bison hybrids

     

I Foresee My Life: The Ritual Performance of Autobiography in an Amazonian Community

I Foresee My Life: The Ritual Performance of Autobiography in an Amazonian Community . Suzanne Oakdale. Lincoln: University of Nebraska Press, 2006. 206 pp.     

Cloning and sequence analysis of the aminopeptidase My gene from Mycoplasma salivarium

Abstract The complete nucleotide sequence of a major component of aminopeptidase My purified from Mycoplasma salivarium was determined. The protein gene encoded a protein consisting of 520 amino acids with a molecular mass of 58079 Da. The protein contained two tryptophan residues, one of which was encoded by UGA. A computer-aided homology search suggested that aminopeptidase My had properties similar to those of leucine aminopeptidase (EC 3.4.11.1).     

My 43, a monoclonal antibody that reacts with human myeloid cells inhibits monocyte IgA binding and triggers function

A mAb My 43 of the IgM isotype was obtained from a fusion of spleen cells immunized against human monocytes. This mAb inhibited monocyte binding of both soluble FITC-labeled IgA and IgA-coated E, whereas it did not inhibit IgG binding. The Ag recognized by My 43 was induced on HL-60 cells in parallel with IgA binding ability by 1-25 dihydroxy-vitamin D3 treatment. Phagocytosis of IgA-coated E by monocytes and 1-25 dihydroxyvitamin D3-treated HL-60 cells was inhibited by My 43. Furthermore, a heteroantibody of My 43 x F(ab)'2 anti-E promoted phagocytic uptake of E by monocytes. Production of superoxide anion by IFN-gamma treated U-937 cells was stimulated by My 43 but not by other IgM mAb recognizing myeloid cells. By these criteria My 43 recognized a molecule capable of triggering function. Moreover, its binding reactivity, ability to block binding of IgA and IgA-complexes, and its ability to induce activation of IgA receptor bearing myeloid cells, are consistent with the possibility that My 43 reacts with the IgA receptor on these cells.     

My primate studies

In this paper, I describe my 62 years in primatology focusing on some of the key findings from fieldwork conducted in Japan, India, and Africa. My first study on nonhuman primates described in detail the division of a troop of Japanese macaques at Takasakiyama. After that, I had an opportunity to work on Hanuman langurs at Dharwar, India. These langurs lived in one-male, multi-female groups. This type of group structure was maintained through takeovers by all-male parties. The adult male and all juvenile males were chased out of the group. By this process, the one-male, multi-female group system was maintained. The incoming adult male bit and killed all infants in the group. Mothers who lost their infants went into estrus and mated with the newly arrived male. For many years, scientists ignored these events or ruled them out as abnormal behavior. My work on Japanese macaques suggested that concentrated resources created by artificial feeding exaggerated dominance rank hierarchies among individuals, whereas it is comparatively relaxed in the natural environment. I also investigated the population dynamics of a troop and the life histories of individuals. From these studies, I documented the frequency of twin births, the carrying of dead infants by mothers, and the occurrence of physical malformations. These observations were made possible through artificial feeding, revealing the merits and demerits of this approach. I pointed out that authors and journal editors must be careful to acknowledge important elements of the environment where studies are conducted, and these should be described when reporting results in scientific articles. My studies of chimpanzees were conducted at Bossou, Guinea. I suggested that there are males who lived outside of bisexual groups. Chimpanzees in this population made and used many kinds of tools. Some of them were observed only at Bossou, and a few were only discovered 20 years after the establishment of Bossou as a research site. After decades of research on tool use in this species, I also suggested that there are cultural zones throughout the geographic distribution of chimpanzees.

     

Isolation and characterization of My23, a myeloid cell-derived antigen reactive with the monoclonal antibody AML-2-23

In this study, we describe the isolation and characterization of My23, a human myeloid antigen defined by the monoclonal antibody (MoAb) AML-2-23. Cells of the HL-60 human promyelocytic cell line, when cultured in the presence of 1,25-dihydroxyvitamin D3 (calcitriol), express a surface protein of approximately 50 to 55 kilodaltons (Kd) which was immunoprecipitated with the AML-2-23 MoAb. Furthermore, after 2 days of exposure to calcitriol, HL-60 cells began to release My23 into culture medium, as determined by the ability of culture supernatant from these cells to block the binding of AML-2-23 to myeloid cells. My23 release was almost totally inhibited by incubation of cells at 4 degrees C, and was partially blocked by treatment of cells with cycloheximide or tunicamycin. The culture supernatant blocking factor, soluble My23, was identified as a 45 to 50 Kd protein by Western blot/immune overlay, using AML-2-23 and an 125I-labeled second antibody. My23, which was affinity-purified from culture supernatant, retained the ability to block AML-2-23 binding to myeloid cells. The affinity-purified antigen migrated on SDS-PAGE as a diffuse band in the m.w. range of 44 to 52 Kd. On treatment with endoglycosidase, the apparent m.w. of My23 decreased to approximately 40,000, indicating the presence of carbohydrate residues on My23. Serum from mice immunized with the purified antigen reacted with the same spectrum of myeloid cells as AML-2-23 MoAb, reacted with the My23 soluble protein in immunoblots, and competed with AML-2-23 for binding to myeloid cells. Binding of this antiserum to myeloid cells was blocked by cell supernatant from both monocytes and calcitriol-treated HL-60 cells, suggesting, along with results from m.w. determinations of the two preparations, that the soluble and cell surface forms of My23 are similar. Moreover, based on our finding that human plasma specifically inhibits the binding of AML-2-23 to myeloid cells, My23 may also be released in vivo. The enhanced expression of My23 on activated and more mature myeloid cells and its shedding or secretion by these cells is consistent with a functional role for My23.     

Complete Genome Sequence of Pectobacterium carotovorum subsp. carotovorum Bacteriophage My1

Pectobacterium carotovorum subsp. carotovorum, a member of the Enterobacteriaceae family, is an important plant-pathogenic bacterium causing significant economic losses worldwide. P. carotovorum subsp. carotovorum bacteriophage My1 was isolated from a soil sample. Its genome was completely sequenced and analyzed for the development of an effective biological control agent. Sequence and morphological analyses revealed that phage My1 is a T5-like bacteriophage and belongs to the family Siphoviridae. To date, there is no report of a Pectobacterium-targeting siphovirus genome sequence. Here, we announce the complete genome sequence of phage My1 and report the results of our analysis.     

Deficient major histocompatibility complex-linked innate murine cytomegalovirus immunity in MA/My.L-H2b mice and viral downregulation of H-2k class I proteins

NK cells are key effectors of innate immunity and host survival during cytomegalovirus (CMV) infection. Innate murine CMV (MCMV) resistance in MA/My mice requires Ly49H/m157-independent H-2k-linked NK cell control. Here we show that replacement of MA/My H-2k with C57L H-2b susceptibility genes led to a remarkable loss of innate virus immunity, though NK gamma interferon was induced in H-2b and H-2k strains shortly after infection. Thus, H-2b genes expressed in C57L or MA/My.L-H2b are sufficient in alerting NK cells to intrusion but fail to support NK restraint of viral infection. In addition, novel H-2 recombinant strains were produced and utilized in a further refinement of a critical genetic interval controlling innate H-2k-linked MCMV resistance. Importantly, this analysis excluded the gene interval from Kk class I through class II. The responsible gene(s) therefore resides in an interval spanning Dk class Ia and more-distal major histocompatibility complex (MHC) nonclassical class Ib genes. Recently, the NK activation receptor Ly49P and MHC class I Dk proteins were genetically implicated in MCMV resistance, in part because Ly49P-expressing reporter T cells could specifically bind Dk molecules on MCMV-infected mouse embryonic fibroblasts (MEFs). However, as we found that H-2k innate resistance differs in the C57L or MA/My backgrounds and because MCMV very efficiently downregulates H-2k class I proteins in L929 cells and primary MEFs shortly after infection, a Ly49P/Dk model should not fully explain H-2k-linked MCMV resistance.     

Addition of aluminum oxide microparticles to Trichoderma viride My preculture enhances cellulase production and influences fungal morphology

Morphological engineering techniques have recently become popular, since they are used to increase the production of a variety of metabolites and enzymes when fungi are grown in submerged cultures. This study aimed to facilitate cellulase production by adding aluminum oxide to Trichoderma viride My precultures.

The results showed that the highest cellulase activity was achieved when aluminum oxide at 10 g/L was used, and the activities of cellulase for filter paper and endoglucanase activity assays increased from 519.11 to 607.35 U/mL by 17.1%, and from 810.08 U/mL to 917.59 U/mL by 13.3%, compared with the control, respectively. Addition of aluminum oxide decreased the size of T. viride My pellets and increased the final pH. The changes in pellet diameter after the addition of different concentrations of aluminum oxide were fitted using a modified exponential decay model, which could precisely predict the pellet size by controlling aluminum oxide concentration.

The optimum concentration of microparticles, and therefore pellet size, could significantly improve cellulase production, which is an encouraging step towards commercial cellulase production.

     

My Journey to DNA Repair

I completed my medical studies at the Karolinska Institute in Stockholm but have always been devoted to basic research. My longstanding interest is to understand fundamental DNA repair mechanisms in the fields of cancer therapy, inherited human genetic disorders and ancient DNA. I initially measured DNA decay, including rates of base loss and cytosine deamination. I have discovered several important DNA repair proteins and determined their mechanisms of action. The discovery of uracil-DNA glycosylase defined a new category of repair enzymes with each specialized for different types of DNA damage. The base excision repair pathway was first reconstituted with human proteins in my group. Cell-free analysis for mammalian nucleotide excision repair of DNA was also developed in my laboratory. I found multiple distinct DNA ligases in mammalian cells, and led the first genetic and biochemical work on DNA ligases Ⅰ, and Ⅳ. I discovered the mammalian exonucleases DNase Ⅲ (TREX1) and IV (FEN1). Interestingly, expression of TREX1 was altered in some human autoimmune diseases. I also showed that the mutagenic DNA adduct O6-methylguanine (O6 mG) is repaired without removing the guanine from DNA, identifying a surprising mechanism by which the methyl group is transferred to a residue in the repair protein itself. A further novel process of DNA repair discovered by my research group is the action of AlkB as an iron-dependent enzyme carrying out oxidative demethylation.     

Development of a polymerase chain reaction assay for Mycoplasma salivarium by using the nucleotide sequence within aminopeptidase My gene

A polymerase chain reaction assay for a 278-nucleotide DNA fragment within aminopeptidase My gene of Mycoplasma salivarium was developed. The assay amplified M. salivarium DNA, but did not amplify DNAs of other mollicutes, bacteria and mammalian cells. The detection limit of the assay was 10 fg of DNA, approximately equivalent to 10 organisms.     

Requisite H2k role in NK cell-mediated resistance in acute murine cytomegalovirus-infected MA/My mice

Human CMV infections are a major health risk in patients with dysfunctional or compromised immunity, especially in patients with NK cell deficiencies, as these are frequently associated with high morbidity and mortality. In experimental murine CMV (MCMV) infections, Ly49H activation receptors on C57BL/6 (B6) NK cells engage m157 viral ligands on MCMV-infected cells and initiate dominant virus control. In this study, we report that MCMV resistance in MA/My relies on Ly49H-independent NK cell-mediated control of MCMV infection as NK cells in these mice do not bind anti-Ly49H mAb or soluble m157 viral ligands. We genetically compared MA/My resistance with MCMV susceptibility in genealogically and NK gene complex-Ly49 haplotype-related C57L mice. We found that MCMV resistance strongly associated with polymorphic H2k-linked genes, including MHC and non-MHC locations by analysis of backcross and intercross progeny. The H2b haplotype most frequently, but not absolutely, correlated with MCMV susceptibility, thus confirming a role for non-MHC genes in MCMV control. We also demonstrate a definite role for NK cells in H2k-type MCMV resistance because their removal from C57L.M-H2k mice before MCMV infection diminished immunity. NK gene complex-linked polymorphisms, however, did not significantly influence MCMV control. Taken together, effective NK cell-mediated MCMV control in this genetic system required polymorphic H2k genes without need of Ly49H-m157 interactions.     

Monoclonal antibodies against seven sites on the head and tail of Dictyostelium myosin

Ten monoclonal antibodies (My1-10) against Dictyostelium discoideum myosin were prepared and characterized. Nine bound to the 210-kD heavy chain and one (My8) bound to the 18-kD light chain. They defined six topographically distinct antigenic sites of the heavy chain. Five binding sites (the My1, My5, My10 site, and the My2, My3, My4, and My9 sites) are located on the rod portion of the myosin molecule. The position of the sixth site (the My6 and My7 site) is less certain, but it appears to be near the junction of the globular heads and the rod. Three of the antibodies (My2, My3, and My6) bound to myosin filaments in solution and could be sedimented in stoichiometric amounts with the filamentous myosin. In contrast, My4, which recognized a site on the rod, inhibited the polymerization of monomeric myosin into filaments. A single antibody (My6) affected the actin-activated ATPase of myosin. The nature of the effect depended on the valency of the antibody and the myosin. Bivalent IgG and F(ab')2 fragments of My6 inhibited the actin-activated ATPase of filamentous myosin by 50% whereas univalent Fab' fragments increased the activity by 50%. The actin-activated ATPase activity of the soluble chymotryptic fragment of myosin was increased 80-90% by both F(ab')2 and Fab' of My6.     

Natural Selection on the Phase-Separation Properties of FUS during 160 My of Mammalian Evolution

Protein phase separation can help explain the formation of many nonmembranous organelles. However, we know little about its ability to change in evolution. Here we studied the evolution of the mammalian RNA-binding protein Fused in Sarcoma (FUS), a protein whose prion-like domain (PLD) contributes to the formation of stress granules through liquid–liquid phase separation. Although the PLD evolves three times as rapidly as the remainder of FUS, it harbors absolutely conserved tyrosine residues that are crucial for phase separation. Ancestral reconstruction shows that the phosphorylation sites within the PLD are subject to stabilizing selection. They toggle among a small number of amino acid states. One exception to this pattern is primates, where the number of such phosphosites has increased through positive selection. In addition, we find frequent glutamine to proline changes that help maintain the unstructured state of FUS that is necessary for phase separation. Our work provides evidence that natural selection has stabilized the liquid forming potential of FUS and minimized the propensity of cytotoxic liquid-to-solid phase transitions during 160 My of mammalian evolution.     

Making it transparent. On naming,framing and administrating biobank research on native people

Despite more than 50 years of genetic research on Sámi people in Sweden, there has been very little engagement with the ethical issues related to this research. My aim is to investigate the ethical challenges in biobank research on Sámi people, to identify ethical challenges that have been overlooked and to find ethical solutions. In my historical research inquiry of published material and interviews with people that have participated in this research, my research questions have been: How are blood samples from Sámi people collected, codified, governed and analyzed? What ethical strategies have been utilized? My main findings are: Sweden acquired biobank collections from Sámi people that are not registered or cannot be traced through the biobank register at the Swedish National Board of Health and Welfare. These collections entail ethical challenges concerning how the donors are identified, how the material is categorized, the regional ethical committees, governance and Sámi representation. My suggestions focus on transparency and traceability, competence and native peoples' rights and representation in biobank-related activities.     

The Color of My Skin: A Measure to Assess Children's Perceptions of Their Skin Color

The Color of My Skin is an instrument developed to assess children's internalized idea (abstraction) of the color of their skin; their satisfaction with that color; the desire, if any, to change the color of their skin; and their affect regarding their skin color. The assessment is part of a questionnaire utilized in a 3-year longitudinal study that examines psychosocial development, physical health, and behavioral adjustment of Puerto Rican children (N = 257) reared in the Greater Boston area. The results demonstrate that children's internalized representation of their skin color is a construct that can be reliably and validly measured. The children's ratings of their skin color were not associated with their sex, school grade, ethnic identity, the child's or the parent's nativity, or the racial or ethnic compositions of 3 social contexts: their neighborhood, their classmates, and their closest friends. Puerto Rican children did not show a preference for light-colored skin. Moreover, there were no significant differences in self-esteem based on the child's self-reported skin color. The lack of association between self-esteem and skin color was interpreted in light of a developmental tendency prevalent in early to middle childhood to place a positive value on different aspects of one's self. Whereas almost all children (96%) reported being happy or very happy with their color, 16% of the children would like to change their skin color if they could (51% to a lighter and 46% to a darker color).