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L Kimball

Publications and source records attributed to L Kimball.

7 recordsLinked to original sources
PubMed2001

Activation of Kaposi's sarcoma-associated herpesvirus (human herpesvirus 8) lytic replication by human cytomegalovirus.

The majority of Kaposi's sarcoma-associated herpesvirus (KSHV)-infected cells identified in vivo contain latent KSHV, with lytic replication in only a few percent of cells, as is the case for the cells of Kaposi's sarcoma (KS) lesions. Factors that influence KSHV latent or lytic replication are not well defined. Because persons with KS are often immunosuppressed and susceptible to many infectious agents, including human cytomegalovirus (HCMV), we have investigated the potential for HCMV to influence the replication of KSHV. Important to this work was the construction of a recombinant KSHV, rKSHV.152, expressing the green fluorescent protein (GFP) and neo (conferring resistance to G418). The expression of GFP was a marker of KSHV infection in cells of both epithelial and endothelial origin. The rKSHV.152 virus was used to establish cells, including human fibroblasts (HF), containing only latent KSHV, as demonstrated by latency-associated nuclear antigen expression and Gardella gel analysis. HCMV infection of KSHV latently infected HF activated KSHV lytic replication with the production of infectious KSHV. Dual-color immunofluorescence detected both the KSHV lytic open reading frame 59 protein and the HCMV glycoprotein B in coinfected cells, and UV-inactivated HCMV did not activate the production of infectious KSHV-GFP. In addition, HCMV coinfection increased the production of KSHV from endothelial cells and activated lytic cycle gene expression in keratinocytes. These data demonstrate that HCMV can activate KSHV lytic replication and suggest that HCMV could influence KSHV pathogenesis.

Cytomegalovirus↗
PubMed1999

Recognition of major histocompatibility complex class II antigens by two anti-HLA-DR monoclonal antibodies on canine marrow cells correlates with effects on in vitro and in vivo hematopoiesis.

BACKGROUND: The role of major histocompatibility complex class II antigens in hematopoiesis is not well defined. We have shown that in vitro depletion of HLA-DR+ cells from canine marrow (e.g., by anti-HLA-DR monoclonal antibody [mAb] H81.9 and complement) prevents hematopoietic recovery. In vivo administration of the same mAb H81.9 after transplantation of unmanipulated autologous marrow results in graft failure. In vitro mAb H81.9 inhibited colony formation from short-term and long-term marrow cultures. METHODS AND RESULTS: We investigated the effect of another mAb, Ca1.41, which also recognizes nonpolymorphic determinants on human (HLA-DR) and canine major histocompatibility complex class II antigens but is reactive with a narrower spectrum of cells in both canine peripheral blood and marrow than mAb H81.9 (and other anti-HLA-DR mAbs). In contrast to all other anti-HLA-DR mAbs tested, Ca1.41 did not interfere with colony formation in short-term or long-term marrow cultures and spared a population of small mononuclear cells with low forward light scatter that was eliminated via apoptosis by exposure to mAb H81.9. These target cells included lymphocytes and CD34+ hemopoietic precursors that expressed MHC class II molecules as determined by mAb H81.9 but not by mAb Ca1.41. In addition, transmembrane signaling and up-regulation of interleukin-1beta mRNA occurred with mAb H81.9 but not with Ca1.41. Transplantation of autologous marrow treated in vitro cytolytically with mAb Ca1.41 allowed for complete hematopoietic reconstitution. Further, in vivo administration of Ca1.41 posttransplant did not lead to autologous graft failure as had been observed with mAb H81.9. CONCLUSIONS: These results support the notion that major histocompatibility complex class II is expressed on early hematopoietic precursor cells but recognition is dependent upon the mAb used. Preliminary studies show that mAb H81.9 triggered transmembrane signaling, resulting in up-regulation of interleukin-1beta and apoptosis, although mAb Ca1.41 did not. The fact that Ca1.41 binding was modified in the presence of exogenous invariant chain-derived peptide suggests that both binding and signaling are peptide dependent.

Animals↗
PubMed1995

Ultrastructural localization of stem cell factor in canine marrow-derived stromal cells.

Stromal cell lines derived from canine long-term bone marrow cultures (LTBMC) were characterized regarding the expression of growth factors and especially the localization of stem cell factor (SCF) (c-kit ligand). One cell line (DO64) was immortalized by transformation with a retroviral vector containing the open reading frames (ORFs) E6 and E7 of the human papilloma virus type 16 (HPV-16). Transfection did not change cellular characteristics but rendered the cell line more independent from culture conditions. The transformed line DO64 consisted mainly of fibroblast-like cells. In addition, some cells showed endothelial and some smooth-muscle cell features. Stromal cells expressed a broad spectrum of surface markers, including low levels of major histocompatibility-complex (MHC) class-II antigens. A new murine monoclonal antibody (MAb), RG7.6 (IgG1), specific for canine SCF, recognized the majority of fibroblast-like stromal cells. The staining pattern for SCF showed perinuclear and intracytoplasmic dense areas. Immunoelectron microscopy revealed the localization of SCF in secretory vesicles, the perivesicular cytoplasm, and bound to the cytoplasmatic membrane. RNA analysis showed that stromal cells transcribed, in addition to SCF, messages for granulocyte colony-stimulating factor (G-CSF), granulocyte-monocyte CSF (GM-CSF), interleukin-6 (IL-6), and transforming growth factor-beta (TGF-beta). In summary, we have established and characterized canine marrow-derived stromal cell lines, and using the new MAb RG7.6, we have localized SCF to cytoplasmatic vesicles as well as the membrane of stromal cells.

Animals↗
PubMedDate not supplied

Collaborative care: a quality improvement and cost reduction tool.

Collaborative care is a system of patient care delivery that focuses on the achievement of outcomes within effective and appropriate time frames and resources. It addresses the entire episode of illness, bridging all clinical settings in which the patient receives care. Through the collaborative efforts of multiple caregivers, a plan of medical care is mapped out that results in a clinical path. The clinical path can improve satisfaction levels for patients, nurses, rehabilitation staff, and physicians by establishing a method of reinforcement for everyone involved in efficient delivery of care.

Clinical Protocols↗