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PubMed1987

Changes in protein kinase C activity are associated with the differentiation of Friend erythroleukemia cells.

We investigated the activity and cellular distribution of protein kinase C during the dimethylsulfoxide (DMSO) and hypoxanthine-induced differentiation of Friend murine erythroleukemia cells. Most of the cellular protein kinase C activity was found in the soluble fraction of unstimulated Friend cells. Within 15 min of the addition of DMSO or hypoxanthine, protein kinase C underwent a dramatic and prolonged reversal of this distribution which was accompanied by a gradual decline in total cellular protein kinase C activity over the ensuing 5 days. The loss of total activity was found to be dose dependent although maximal translocation from soluble to insoluble components occurred at even lower concentrations of the inducers tested. Two clones of Friend cells, selected for their failure to differentiate in response to DMSO, showed alterations in protein kinase C activity and/or distribution following DMSO addition when compared to wild-type Friend cells. These data show that different inducers of Friend cell differentiation have similar effects on cellular protein kinase C, that the protein kinase C changes accompanying this process are immediate but prolonged, and that changes in protein kinase C activity and distribution are associated with Friend cell differentiation.

Animals↗
PubMed2005

Childhood friends who smoke: do they influence adolescents to make smoking transitions?

This study investigated longitudinally the extent to which childhood friends who smoke influence adolescents' smoking transitions, and compared that influence with that of parents who smoke. In a sample of 4744 children, results showed that the probability, per close friend, that a smoking close friend influenced the adolescent to make the first transition to trying smoking was 38% (95% CI: 28%, 46%); to make the second transition from trying to monthly smoking, 10% (95% CI: 5%, 15%); and to make the third transition from monthly to daily smoking, 11% (95% CI: 5%, 17%). Compared to parents' smoking, close friends' smoking was 12% (p=0.03) more influential for the first transition, no different for the second transition (p=0.53), and 16% (p=0.01) less influential for the third transition. Results provide new evidence suggesting that childhood close friends who smoke influence not only initiation but also escalation of adolescents' smoking. Results also confirmed the important role of parents' smoking. Targeting both childhood close friends' and parents' smoking would be valuable in prevention research.

Adolescent↗
PubMed2006

Best friends and alcohol consumption in adolescence: a within-family analysis.

Although friends and siblings are considered to be important role models in adolescents' peer contexts, these peer influences on adolescent alcohol consumption over time are seldom examined simultaneously in a within-family design. The present study examined the relative impact of alcohol use of the best friend, adolescent sibling and sibling's best friend on the development of alcohol consumption during adolescence. Data reported in this study are part of an ongoing longitudinal questionnaire study among families with two adolescent siblings (N=416). Results from structural equation modeling showed a strong similarity in drinking between best friends and adolescents cross-sectionally. Over time, however, only marginal effects of friends alcohol use on drinking of the youngest sibling, and no effects for the oldest sibling were found. Robust evidence was found for peer-selection processes. In addition, we found a moderate to high relative similarity in drinking within sibling pairs, but no longitudinal effect of sibling's drinking. We also found no support for a possible additional influence of sibling's best friend's drinking on adolescent drinking. Therefore, we tested several potential moderating variables on peer influences, but found no effects of a set of relationship characteristics or individual characteristics on the links between peer and adolescent drinking over time.

Adolescent↗
PubMed2006

Shared targets for aggression by early adolescent friends.

Similarity in early adolescent friends' general aggressiveness is well known, but questions remain regarding the degree to which friends aggress against the same victims. The authors examined this by administering the newly created Dyadic Aggression and Victimization Inventory to 417 sixth- through eighth-grade boys and girls (53%). Friends were found to share more targets for aggression than nonfriends, even after general levels of aggression were controlled (all ps < .05). Moreover, greater sharing of targets with friends relative to nonfriends was more pronounced among aggressive youths than nonaggressive youths, especially among aggressive youths' best friends relative to their other friends. Generally, these findings were similar across boys and girls as well as among older and younger youths. Implications of these findings and directions for future research are discussed.

Adolescent↗
PubMed2005

Sibling relationship quality from birth to adolescence: the enduring contributions of friends.

The purpose of the present study was to examine continuity in sibling relationships across childhood and to evaluate the degree to which children's experiences with their friends and mothers prior to their sibling's birth predict the quality of the relationship they establish with their siblings in adolescence. Twenty-eight firstborn children, who were 48 months old at the time of their sibling's birth, were observed interacting with their siblings and friends at multiple time points. The level of positive social behaviors demonstrated in their early relationships with friends continued to predict sibling relationship quality in adolescence. Firstborn children who had more positive interactions with friends prior to their sibling's birth demonstrated more prosocial interactions with both their siblings and friends in adolescence and exhibited fewer externalizing behaviors. Longitudinal associations support the hypothesis that the social competencies that young children demonstrate in their early relationships with friends may have enduring significance for their social development.

Adaptation, Psychological↗
PubMed2002

Sf-Stk kinase activity and the Grb2 binding site are required for Epo-independent growth of primary erythroblasts infected with Friend virus.

During the initial stage of Friend virus-induced erythroleukemia in mice, interaction of the viral protein gp55 with the erythropoietin receptor, and other host factors, drives the expansion of erythroid precursor cells. Recently, we demonstrated that the Friend virus susceptibility locus, Fv2, which is required for the expansion of infected cells, encodes a naturally occurring, N-terminally truncated form of the Stk receptor tyrosine kinase (Sf-Stk). Here we show that in vitro expression of Sf-Stk confers Friend virus sensitivity to erythroid progenitor cells from Fv2(rr) mice. Furthermore, our data reveal that Sf-Stk kinase activity and Y436, but not Y429, are required for Epo-independent colony formation following Friend virus infection. Introduction of a mutation that results in failure to bind Grb2 abrogates the ability of Sf-Stk to induce colonies in response to Friend virus, while the Grb2 binding site from EGFR restores this response. Consistent with the ability of Grb2 to recruit SOS and Gab1, the Ras/MAPK and PI3K pathways are activated by Sf-Stk, and both of these pathways are required for gp55-mediated erythroblast proliferation. These data clearly demonstrate a requirement for signaling through Sf-Stk in the Epo-independent expansion of Friend virus-infected cells, and suggest a pivotal role for Grb2 in this response.

Adaptor Proteins, Signal Transducing↗
PubMed2006

GRB2-mediated recruitment of GAB2, but not GAB1, to SF-STK supports the expansion of Friend virus-infected erythroid progenitor cells.

Friend virus induces the development of erythroleukemia in mice through the interaction of a viral glycoprotein, gp55, with a truncated form of the Stk receptor tyrosine kinase, short form-Stk (Sf-Stk), and the EpoR. We have shown previously that the ability of Sf-Stk to participate in the transformation of Friend virus-infected cells requires the kinase activity and Grb2-binding site of Sf-Stk. Here we show that Grb2 heterozygous mice exhibit decreased susceptibility to Friend erythroleukemia and that expansion of erythroid progenitors in response to infection requires the C-terminal SH3 domain of Grb2. A fusion protein in which the Grb2-binding site in Sf-Stk is replaced by Gab2, supports the growth of progenitors from mice lacking Sf-Stk, whereas a Sf-Stk/Gab1 fusion protein does not. Gab2 is expressed in spleens from Friend virus-infected mice, co-immunoprecipitates with Sf-Stk and is tyrosine phosphorylated in the presence of Sf-Stk. Mice with a targeted deletion in Gab2 are less susceptible to Friend erythroleukemia and the expansion of erythroid progenitor cells in response to infection can be rescued by expression of Gab2, but not Gab1. Taken together, these data indicate that a Sf-Stk/Grb2/Gab2 complex mediates the growth of primary erythroid progenitor cells in response to Friend virus.

Adaptor Proteins, Signal Transducing↗
PubMed1975

Erythroid colony induction without erythropoietin by Friend leukemia virus in vitro.

Erythroid colonies could be produced without the addition of erythropeietin in plasma cultures seeded with bone marrow cells from normal C3Hf/Bi mice by exposure of the cells in vitro to medium from a cell line (IS) that continuously produces Friend leukemia virus in culture. The activity in the culture medium was viral rather than erythropoietin-like, since it was sedimentable by high-speed centrifugation and heat labile. Erythroid colonies did not develop when the bone marrow cells exposed to virus-containing medium were from mice genetically resistant to Friend virus. IS culture medium contained both Friend spleen focus-forming and XC-plaque-forming activities. No erythroid colonies were induced when genetically sensitive cells were exposed to a preparation from which the spleen focus-forming activity had been removed, but which contained XC plaque-forming activity in high concentration. Thus the spleen focus-forming component of Friend virus appeared to be responsible for inducing erythroid colony formation without erythropoietin in vitro. Some erythroid colonies were also found in control cultures to which neither virus nor erythropoietin had been added. Reduction in the concentration of fetal calf serum in the culture medium substantially decreased the number of these colonies but had only a minor effect on the number of virus-induced colonies. The number of erythroid colonies produced after 2 days of culture without erythropoietin or fetal calf serum was approximately proportional to the titer of Friend spleen focus-forming virus to whcih the bone marrow cells had been exposed. This system should prove useful for investigation in vitro of Friend virus--host cell interactions which lead to erythropoietin-independent erythropoiesis.

Animals↗
PubMed1978

Changes in genome composition of the Friend virus complex in erythroleukemia cells during the course of differentiation induced by dimethyl sulfoxide.

The Friend spleen focus-forming virus (SFFV) complex released by Friend virus-transformed erythroid cells has been analyzed with respect to changes in the genome composition that may occur during induction of erythropoiesis with dimethyl sulfoxide. It is shown that: (a) There are three types of virus particles, one with buoyant density 1.20 g/ml, one with density 1.17 g/ml (the density of the cloned lymphatic leukemia virus helper component of the complex), and a major fraction that has a density of 1.14 g/ml. (b) Three RNA subunits-35S, 32S, and 30S-have previously been shown to be detectable in the Friend virus complex. The 1.20-g/ml particles contain only 30S RNA, whilst the 1.14- to 1.17-g/ml particles contain a mixture consisting of predominantly 30S and 32S RNA and about 5-10% 35S RNA. (c) Induction of differentiation results in an increase in the 1.14-g/ml particles and 32S RNA. The amount of 30S RNA does not change. (d) Hybridization of the different genomic viral RNAs with full-length virus cDNA shows that the 30S RNA (of induced and uninduced Friend virus) is more closely related to the 32S RNA of the induced Friend virus than to the 32S RNA of the constitutively released Friend virus. (e) The 30S RNA contains SFFV-specific sequences. (f) A hypothesis is presented in which the induction of the new 32S RNA species is related to the increase of SFFV activity and to a specific function of the SFFV during induction of erythropoiesis.

Cell Differentiation↗
PubMed1983

Indirect induction of erythroid differentiation in mouse Friend cells: evidence for two intracellular reactions involved in the differentiation.

The mechanism of in vitro erythroid differentiation in mouse Friend cells was studied by employing cell fusion between two genetically marked Friend cells and other nonerythroid cells, including BHK (baby hamster kidney) and FM3A (mouse mammary gland) cells. We were able to induce erythroid differentiation indirectly by fusing Friend cells that had been exposed briefly to dimethyl sulfoxide prior to fusion with nonerythroid cells that had been treated with ultraviolet light (or other DNA-damaging agents). The results suggest that two distinct reactions are involved in erythroid differentiation in Friend cells in vitro. One reaction, originating from the damaged DNA (or inhibition of DNA replication as a consequence), exhibits an inducible nature, is nonspecific to Friend cells, and is trans-acting. The other reaction is specific to Friend cells and most likely is cis-acting. We also present evidence from the cell fusion experiments that a typical tumor promoter, 12-O-tetradecanoylphorbol 13-acetate, inhibits erythroid differentiation by affecting the latter reaction. The biological significance of these findings is discussed.

Animals↗
PubMed1980

Spontaneous regression of Friend virus-induced erythroleukemia. VI. Structural and antigenic differences between the regressing and conventional strains of virus.

The regressing and conventional strains of Friend virus were compared by neutralization assays, sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and tryptic peptide mapping of the individual viral components. Neutralization rates of the two viruses differed in the presence of monospecific anti-gp70 antiserum and sera from regressed or immunized mice. Neutralization of regressing Friend virus, but not conventional Friend virus, occurred when the viruses were incubated with anti-p15(E) and complement. Human serum inactivated conventional Friend virus more rapidly than regressing Friend virus, probably as a result of virolysis induced by the reaction of viral p15(E) with human complement component C1. Structural differences between the viruses were detected in their gp70 viral glycoproteins and p15(E) and p12 proteins. Analysis of different stocks and clonal isolates of the viruses showed that the differences between the gp70 and p15(E), but not the p12 proteins, were associated with the regressing phenotype of the regressing strain of Friend virus.

Animals↗
PubMed1987

Disease specificity of nondefective Friend and Moloney murine leukemia viruses is controlled by a small number of nucleotides.

Moloney murine leukemia virus induces T cell lymphomas after injection into NFS mice, whereas the nondefective Friend virus induces erythroleukemias. Previous studies showed that sequences encompassing the viral transcriptional signals in U3 are the primary determinant of this phenotype in recombinants between these two viruses. To more precisely identify the sequences responsible, we constructed additional recombinants, within U3, between Friend and Moloney viruses and assayed these recombinants for for their disease specificity. We found that a fragment 191 bases long that included the direct repeat (enhancer) region plus 22 nucleotides to its 3' side from Friend virus was sufficient to convert Moloney virus to a virus that induced only erythroleukemias. A 171-base-long fragment of Moloney virus, including just the direct repeat, converted Friend virus to a virus that induced primarily lymphomas (about 85% of mice injected). We also constructed Moloney and Friend virus variants with one rather than two copies of the enhancer element. These viruses retained their disease specificity, although they exhibited a marked increase in the latent period of disease induction. Together the results suggest that 25 or fewer nucleotide differences, lying within and also just 3' of the direct repeat, are the primary determinant of the distinct disease specificities of nondefective Friend and Moloney viruses.

Animals↗
PubMed2003

Effects of euthanasia on the bereaved family and friends: a cross sectional study.

OBJECTIVE: To assess how euthanasia in terminally ill cancer patients affects the grief response of bereaved family and friends. DESIGN: Cross sectional study. SETTING: Tertiary referral centre for oncology patients in Utrecht, the Netherlands. PARTICIPANTS: 189 bereaved family members and close friends of terminally ill cancer patients who died by euthanasia and 316 bereaved family members and close friends of comparable cancer patients who died a natural death between 1992 and 1999. MAIN OUTCOME MEASURES: Symptoms of traumatic grief assessed by the inventory of traumatic grief, current feelings of grief assessed by the Texas revised inventory of grief, and post-traumatic stress reactions assessed by the impact of event scale. RESULTS: The bereaved family and friends of cancer patients who died by euthanasia had less traumatic grief symptoms (adjusted difference -5.29 (95% confidence interval -8.44 to -2.15)), less current feeling of grief (adjusted difference 2.93 (0.85 to 5.01)); and less post-traumatic stress reactions (adjusted difference -2.79 (-5.33 to -0.25)) than the family and friends of patients who died of natural causes. These differences were independent of other risk factors. CONCLUSIONS: The bereaved family and friends of cancer patients who died by euthanasia coped better with respect to grief symptoms and post-traumatic stress reactions than the bereaved of comparable cancer patients who died a natural death. These results should not be interpreted as a plea for euthanasia, but as a plea for the same level of care and openness in all patients who are terminally ill.

Adolescent↗
PubMed2005

Role of erythropoietin receptor signaling in Friend virus-induced erythroblastosis and polycythemia.

Friend virus is an acutely oncogenic retrovirus that causes erythroblastosis and polycythemia in mice. Previous studies suggested that the Friend virus oncoprotein, gp55, constitutively activates the erythropoietin receptor (EPOR), causing uncontrolled erythroid proliferation. Those studies showed that gp55 confers growth factor independence on an interleukin-3 (IL-3)-dependent cell line (Ba/F3) when the EPOR is coexpressed. Subsequently, we showed that a truncated form of the stem-cell kinase receptor (sf-STK) is required for susceptibility to Friend disease. Given the requirement for sf-STK, we sought to establish the in vivo significance of gp55-mediated activation of the EPOR. We found that the cytoplasmic tyrosine residues of the EPOR, and signal transducer and activator of transcription-5 (STAT5), which acts through these sites, are not required for Friend virus-induced erythroblastosis. The EPOR itself was required for the development of erythroblastosis but not for gp55-mediated erythroid proliferation. Interestingly, the murine EPOR, which is required for gp55-mediated Ba/F3-cell proliferation, was dispensable for erythroblastosis in vivo. Finally, gp55-mediated activation of the EPOR and STAT5 are required for Friend virus-induced polycythemia. These results suggest that Friend virus activates both sf-STK and the EPOR to cause deregulated erythroid proliferation and differentiation.

Animals↗
PubMed2003

Friends and social support in dementia caregiving. Assessment and intervention.

The purpose of this article is to explore the topic of friends as a spontaneously occurring response in open-ended interviews with dementia caregivers and to propose guidelines for assessment and intervention based on current knowledge. The sample includes 176 open-ended baseline interviews with dementia caregivers drawn from the National Caregivers Training Study, a 4-year multi-site, randomized, community-based, psycho-educational intervention study. References to friends were present in 60 of the 176 baseline transcripts. More than 50% of the references were positive, 63% referred to the present, 80% of the content scores were greater than 1, and 66% were categorized as emotional support or social integration for caregivers. Meaningful categories exist and can be helpful in structuring the assessment of support from friends. Data support prior research suggesting that friends are providers and facilitators of emotional support and social integration. Although further research is needed on the concept of social support in general and social network providers in particular (e.g., friends), current knowledge allows for preliminary recommendations for assessment and intervention of friends and social support.

Aged↗
PubMed1992

Friend virus induced murine erythroleukaemia: the p53 locus.

The development of Friend virus induced murine erythroleukaemia is associated with specific genetic events. One of these events is loss of wild type p53 expression, which can occur by internal deletion or proviral insertion in the p53 gene and by single point mutations in the coding sequence. In all cases, the corresponding wild type allele is absent. The high frequency of observed p53 mutations strongly suggests that inactivation of p53 may be an obligatory step in the development of Friend disease. Further evidence that abrogation of normal p53 expression contributes to the development of malignant clones was provided by in vitro reconstitution experiments in Friend cell lines: whereas exogenous mutant p53 was stably expressed in p53 negative FCLs, long term wild type p53 expression was not detected. Friend erythroleukaemia arises as a late consequence of infection of susceptible mice with Friend virus. In addition to p53 gene mutations, proviral insertions occur frequently adjacent to one of two cellular genes, Spi-1/PU.1 or Fli-1. Aberrant expression of these genes may therefore be involved in virus induced erythroleukaemia. Interaction of SFFV env gp55 with the EPO-R also appears to be important in providing a mitogenic signal to infected cells. The order in which these events occur and whether the order is relevant to the progression of the disease are not known. Investigation of the stepwise appearance of these events could provide information on the possible interactions of the gene products involved. Abrogation of normal p53 expression is not restricted to Friend erythroleukaemia: the observation of p53 mutations and allele loss in human breast, lung, colon and hepatocellular carcinomas and in leukaemia suggests that mutation of p53 may be the most common genetic abnormality detected in human cancer (reviewed in this issue). Studies of p53 expression in FCLs provided an early indication that p53 was a tumour suppressor gene. Further studies of the mechanisms by which wild type and mutant p53 affect the growth of p53 negative FCLs may reveal important biochemical properties of p53 in relation to cell cycle control and differentiation of erythroid cells.

Alleles↗
PubMed1985

New U1 RNA species found in Friend SFFV (spleen focus forming virus)-transformed mouse cells.

The U1 RNA species in 10 mouse cell lines were examined by two-dimensional polyacrylamide gel electrophoresis. Seven cell lines that were not infected by Friend spleen focus forming virus gave only one (I) or two (I and II) U1 RNA-containing spots. However, two Friend cell lines (FVTCT and Friend 745a cells) gave three spots (I, II, and III) and another Friend cell line, K-1 cells, gave four spots (I, II, III, and IV). As a result of further separation and fingerprinting analysis of each spot, FVTCT and Friend 745a cells were found to contain U1a-1, U1b-1, -2, and -6 RNAs whereas K-1 cells were found to contain several U1 RNAs, which we call U1a-1 and -2, U1b-4, -5, and -6 RNAs. We determined the sequences of these seven U1 RNAs and found that mouse U1 RNAs had two basic sequences (U1a and -b). The nucleotide sequence of U1a-1 RNA was identical to that of rat U1a RNA, while U1a-2 RNA was one base different from U1a-1 RNA. Relative to U1a-1 RNA all of the U1b RNAs had five base substitutions and one additional base and were under-methylated in the center. U1b-6 RNA contained two base substitutions and one base addition in the 3'-terminal portion of U1b-1 RNA. U1b-2, -4, and -5 RNAs, which were observed only in Friend cells, each had an additional base substitution in the 5'-half of U1b-1 RNA.

Animals↗
PubMed1985

Abnormalities in myelopoietic regulatory interactions with acidic isoferritins and lactoferrin in mice infected with Friend virus complex: association with altered expression of Ia antigens on effector and responding cells.

The regulation of myelopoiesis was evaluated in B6D2F1 mice inoculated with Friend virus complex (spleen focus-forming virus plus helper virus) or helper virus alone by analyzing acidic isoferritin (AIF) and lactoferrin (LF) interactions with target cells. Under normal conditions, AIF suppresses colony and cluster formation by an Ia-antigen-positive cycling subpopulation of mouse granulocyte-macrophage progenitor cells (CFU-GM). Under the same conditions, the release of AIF-inhibitory activity and granulocyte-macrophage colony stimulatory factors (GM-CSF) from an Ia-antigen-positive subpopulation of monocytes and macrophages is suppressed by LF. Within one to two days after inoculation in vivo with Friend virus complex or helper virus, mouse CFU-GM become insensitive in vitro to suppression by purified human AIF as well as crude mouse AIF, and by four days, bone marrow, spleen, and thymus cells of these mice release much greater quantities of AIF-inhibitory activity than the cells from mice injected with control medium. The Friend virus complex itself has no influence in vitro on CFU-GM from normal mice. In addition, the release of AIF-inhibitory activity from bone marrow, spleen, and resident peritoneal cells and the release of GM-CSF from resident peritoneal cells of mice infected with Friend virus complex are not suppressed by LF. The inability of AIF to suppress colony formation by bone marrow and spleen CFU-GM from mice infected with Friend virus complex is associated with the loss of Ia (I-A subregion) antigens from CFU-GM, even though CFU-GM are in cycle. The nonresponsiveness of bone marrow, spleen, and peritoneal cells from these mice to LF suppression of AIF release and the inability of LF to influence GM-CSF release from peritoneal cells is associated with loss of Ia antigens from these cells. The above abnormalities are similar to the defects noted using cells from patients with leukemia. These results suggest that mice infected with Friend virus complex can serve as a model for investigating abnormalities in cell regulation and their relationships to disease progression.

Animals↗