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Secrecy is a growing topic of interest in research, but little research has been done on adolescents keeping secrets from their friends. The purpose of this study was to find out if keeping secrets from friends was related to elevated depression and more behavior problems. The data in this study were obtained from 197 adolescents who were interviewed the summer after their 6th (n = 182, M age = 12.4, SD = 1.01) grade school year in southern Louisiana. This sample was 50.8% female, and the majority of the adolescents self-identified themselves as being white, non-Hispanic (47.7%) or African American (46.7%), while few self-identified themselves as being of other ethnicities (6.1%). Results showed that keeping secrets from friends is associated with higher levels of depression but not with more behavior problems. Keeping secrets from friends accounted for unique variance in depression after controlling for keeping secrets from parents. Secrets from friends accounted for the association between low friendship quality and depression. The link between secrets from friends, depression and behavior problem was not moderated by friendship quality and depression.

Zytotoxische T-Zellen (CD8+) spielen eine wichtige Rolle bei retroviralen Infektionen des Menschen, wie HIV und HTLV. Ihre molekulare Wirkweise war bisher aber nicht bekannt. Die Infektion von Mäusen mit dem retroviralen Friend Virus Komplex (FV) wurde daher als Modell verwendet, um die antiviralen Mechanismen gegen Retroviren aufzuklären. Als erstens wurde die Beteiligung von CD8+ T-Zellen bei der Kontrolle der FV Infektion in Depletion-Experimenten gezeigt. In akut FV infizierten Tieren konnten außerdem aktivierte Virus-spezifische CD8+ T-Effektorzellen nachgewiesen werden, welche zytotoxische Moleküle produzierten. Die Infektion von „knockout“ Mäusen ergab, dass die CD8+ T-Zellen hauptsächlich den Exozytoseweg benutzten, um FV-infizierte Zellen zu eliminieren. Die Anwesenheit eines der drei am Exozytoseweg beteiligten zytotoxischen Moleküle Perforin, Granzym A oder Granzym B war in der akuten Phase der Infektion ausreichend, um die Virusreplikation zu kontrollieren. Diese Ergebnisse weisen auf neue molekulare Mechanismen von Granzymen bei der Virusabwehr hin. In Gegensatz zur Abwehr des pathogenen FV Komplex benutzten CD8+ T-Zellen nicht den Exozytoseweg zur Abwehr von apathogenen Retroviren. Eine Infektion von Mäusen mit dem nicht-pathogenen F-MuLV induzierte keine Produktion von zytotoxischen Molekülen in CD8+ T-Zellen. Die Infektion von „knockout“ Mäusen zeigte, dass F-MuLV von CD8+ T-Zellen über den Fas/FasL Weg kontrolliert wurde. Das pathogene Potential von Retroviren scheint also einen Einfluß auf den jeweils verwendeten Abwehrmechanismus von zytotoxischen T-Zellen zu haben. Trotz der wichtigen Funktion von CD8+ T-Zellen bei der Kontrolle der akuten FV Infektion, spielten diese Zellen bei der persistierenden Infektion keine Rolle mehr. Die Untersuchungen von aktivierten CD8+ T-Zellen aus persistierend infizierten Mäusen zeigte, dass die Zellen agranulär waren und keine zytotoxischen Moleküle produzierten. Folglich hatten sie auch keine zytotoxische Aktivität in vitro. Der Exozytoseweg von Virus-spezifischen CD8+ T-Zellen war also in der persistierenden FV Infektion gestört. So entwickelten viele persistierend infizierte Tiere nach einer Reinfektion eine Splenomegalie, was zusätzlich beweist, dass die Funktion von Virus-spezifischen T-Zellen auch in vivo gestört war. Mäuse, die chronisch mit FV infiziert waren, wiesen also einen kompletten Funktionsverlust von CD8+ T-Zellen auf, der offensichtlich eine wichtige Voraussetzung für die Persistenz des Virus darstellt. Da die CD8+ T-Zellen nicht mehr funktionell waren, mussten vermutlich CD4+ T-Zellen über den Fas/FasL-Weg die Kontrolle über die chronische Infektion übernehmen. Das Verständnis der molekularen Mechanismen der CD8+ T-Zell Abwehr gegen Retroviren ermöglicht es neue Strategien der Immuntherapie gegen retroviralen Infektionen zu entwickeln. / Cytotoxic T-cells play an important role in the control of retroviral infections such as HIV and HTLV; however the molecular mechanisms used by these cells is not known. We used the infection of mice with the retroviral Friend Virus complex as model to investigate the antiviral mechanisms of CD8+ T-cells. The participation of CD8+ T-cells in the control FV infection was shown in depletion experiments. Activated virus-specific CD8+ T-cells were found in acutely FV infected animals and these cells produced cytotoxic molecules. The infection of knockout mice indicated that CD8+ T-cells eliminated infected cells via the exocytosis pathway. The presence of one of these three molecules involved in the exocytosis pathway (perforin, granzyme A or granzyme B) was sufficient to control virus-replication. These results suggest new molecular mechanisms of granzyme in the defence against retroviral infection. In contrast to the control of pathogenic FV complex, CD8+ T-cells do not need the exocytosis pathway to respond to non-pathogenic retroviruses. The infection of mice with non-pathogenic F-MuLV did not induce the production of cytotoxic molecules in CD8+ T-cells and knockout mice with defects in perforin, granzyme A and granzyme B were not susceptible to F-MuLV infection. In contrast, knockout mice with defect in the Fas/FasL pathway were unable to control virus-replication. These data indicate that CD8+ T-cells used the Fas/FasL pathway to control non-pathogenic retroviruses whereas the exocytosis pathway was crucial to keep pathogenic retroviruses in check. The establishment of chronic Friend virus infections is enabled by the induction of CD4+ regulatory T cells that impair CD8+ T-cell functions and allow the virus to escape (Dittmer et al., 2004). The current study characterizes this CD8+ T-cell dysfunction by analyzing the production and release of cytolytic molecules by virus-specific CD8+ T-cells. During acute infection, FV-specific CD8+ T cells produced the cytotoxic molecules perforin and granzyme B, and actively degranulated cytotxic granules. In contrast, CD8+ T cells of the same specificity from chronically infected mice neither produced any of these cytotoxic molecules nor showed evidence of degranulation. The defect in cytotoxine production in T cells from persistently infected mice did not occur at the level of transcription as both CD8+ T-cells from acutely and persistently infected animals had equal levels of mRNA for perforin and granzyme. CD8+ T-cells from persistently infected mice were unable to induce apoptosis in target cells. These results demonstrate a broad impairment of cytolytic CD8+ T-cell effector functions associated with chronic retroviral infection.

Both tissue microenvironment and genetic changes are involved in development of cancer. We employed the Friend murine leukemia virus (F-MuLV)- induced erythroleukemia model to study the role of these parameters in induction of malignancy. The tissue microenvironment is composed of non-cellular and cellular components. In regards to the non-cellular part, we previously reported that vascular endothelial growth factor (VEGF), in combination with macrophage chemoattractant protein-5, contributes to leukemia progression in F-MuLV- infected mice. To study the influence of constitutively elevated VEGF levels on the progression of erythroleukemia, we inoculated VEGF hi/+ mice, which are heterozygous for a VEGF “hypermorphic” allele, with F-MuLV. Unexpectedly, a significant delay in erythroleukemia was observed in these mice when compared with wild-type controls. The VEGF hi/+ mice exhibited a higher natural killer (NK) cell activity, elevated B cells, and a decrease in T-cell number. Furthermore, higher erythroid progenitors (i.e. CD34+, CD36+, and TER119+ cells) were evident in the bone marrow, spleen, and peripheral blood of these mice. Also, the CFU-E levels were significantly elevated in VEGF hi/+ bone marrow cultures. We propose that a compensatory erythropoietic response combined with increased NK cell activity account for the extended survival of erythroleukemic, VEGF hi/+mice. In regards to the cellular component of tissue microenvironment we studied the role of B cells in response to F-MuLV. To test the hypothesis that virus- neutralizing antibodies are involved in providing sterilizing immunity to F-MuLV we inoculated adult female mice with F-MuLV so that their newborns are provided with anti-viral antibodies. F-MuLV challenge of these newborns did not lead to induction of erythroleukemia. Conversely, mice from a control group (newborns whose mother had not received viral inoculation) contracted erythroleukemia upon F-MuLV challenge, as shown by hepatosplenomegaly, anemia, and emergence of leukemic cells in the spleen. These results indicated the importance of anti-viral antibodies in immunity to F-MuLV and suggested that anti-F-MuLV antibodies were generated in mothers, transferred to their offspring and protected them from viral challenge. The key genetic event upon F-MuLV infection is viral integration at the Fli-1 locus. We set to identify F-MuLV integration sites in SCID mice following two observations that these mice show a delay in induction of leukemia and also they do not exhibit viral integration at the Fli-1 locus. We hypothesized that development of leukemia in these mice is due to F-MuLV integration at a region other than the Fli-1 locus. Using a GenomeWalking approach we identified a total of 15 viral integration sites in F-MuLV-infected SCID mice, with eight of them interrupting the following genes: Mex3d, Fam125b, Prdm16, Rhoq, Ahdc1, Zc3h4, Msh3, and Hcls1. Using PCR to amplify the virus- host DNA junction fragment we found that one of the viral insertion sites (chromosome 10; position 20,942,825) occurs with a frequency of 35 % and therefore is considered as a common integration site.

Both tissue microenvironment and genetic changes are involved in development of cancer. We employed the Friend murine leukemia virus (F-MuLV)- induced erythroleukemia model to study the role of these parameters in induction of malignancy. The tissue microenvironment is composed of non-cellular and cellular components. In regards to the non-cellular part, we previously reported that vascular endothelial growth factor (VEGF), in combination with macrophage chemoattractant protein-5, contributes to leukemia progression in F-MuLV- infected mice. To study the influence of constitutively elevated VEGF levels on the progression of erythroleukemia, we inoculated VEGF hi/+ mice, which are heterozygous for a VEGF “hypermorphic” allele, with F-MuLV. Unexpectedly, a significant delay in erythroleukemia was observed in these mice when compared with wild-type controls. The VEGF hi/+ mice exhibited a higher natural killer (NK) cell activity, elevated B cells, and a decrease in T-cell number. Furthermore, higher erythroid progenitors (i.e. CD34+, CD36+, and TER119+ cells) were evident in the bone marrow, spleen, and peripheral blood of these mice. Also, the CFU-E levels were significantly elevated in VEGF hi/+ bone marrow cultures. We propose that a compensatory erythropoietic response combined with increased NK cell activity account for the extended survival of erythroleukemic, VEGF hi/+mice. In regards to the cellular component of tissue microenvironment we studied the role of B cells in response to F-MuLV. To test the hypothesis that virus- neutralizing antibodies are involved in providing sterilizing immunity to F-MuLV we inoculated adult female mice with F-MuLV so that their newborns are provided with anti-viral antibodies. F-MuLV challenge of these newborns did not lead to induction of erythroleukemia. Conversely, mice from a control group (newborns whose mother had not received viral inoculation) contracted erythroleukemia upon F-MuLV challenge, as shown by hepatosplenomegaly, anemia, and emergence of leukemic cells in the spleen. These results indicated the importance of anti-viral antibodies in immunity to F-MuLV and suggested that anti-F-MuLV antibodies were generated in mothers, transferred to their offspring and protected them from viral challenge. The key genetic event upon F-MuLV infection is viral integration at the Fli-1 locus. We set to identify F-MuLV integration sites in SCID mice following two observations that these mice show a delay in induction of leukemia and also they do not exhibit viral integration at the Fli-1 locus. We hypothesized that development of leukemia in these mice is due to F-MuLV integration at a region other than the Fli-1 locus. Using a GenomeWalking approach we identified a total of 15 viral integration sites in F-MuLV-infected SCID mice, with eight of them interrupting the following genes: Mex3d, Fam125b, Prdm16, Rhoq, Ahdc1, Zc3h4, Msh3, and Hcls1. Using PCR to amplify the virus- host DNA junction fragment we found that one of the viral insertion sites (chromosome 10; position 20,942,825) occurs with a frequency of 35 % and therefore is considered as a common integration site.

Friend lists allow Facebook users to group their friends and may be used to share certain information only with those in a specific list. This function has been around for several years, but has never gained any particular popularity among users, most of whom probably did not know it even existed a couple of years ago. In the fall of 2011, however, the function was updated and made more visible on the site. There are several possible uses of friend lists, such as privacy control, filtering of the news feed, self-presentation and targeted information sharing. This paper aims to investigate the extent to which friend lists are used by students today, as well as why students actually use their lists, i.e. for what purposes. Judging from the results of this study in comparison with earlier research, there seems to have been a somewhat recent increase in the awareness of the fact that friend lists actually do exist, but still most users tend not to utilize them. Moreover, the results indicate that friend lists quite rarely are used for privacy control, or anything else for that matter, probably due to a number of drawbacks that they possess as of today.

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