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Friendship Chemistry: An Examination of Underlying Factors
Interpersonal chemistry refers to a connection between two individuals that exists upon first meeting. The goal of the current study is to identify beliefs about the underlying components of friendship chemistry. Individuals respond to an online Friendship Chemistry Questionnaire containing items that are derived from interdependence theory and the friendship formation literature. Participants are randomly divided into two subsamples. A principal axis factor analysis with promax rotation is performed on subsample 1 (n = 688) and produces 5 factors: Reciprocal candor, mutual interest, personableness, similarity, and physical attraction. A confirmatory factor analysis is conducted using subsample 2 (n = 715) and provides support for the 5-factor model. Participants with agreeable, open, and conscientious personalities more commonly report experiencing friendship chemistry, as do those who are female, young, and European/white. Responses from participants who have never experienced chemistry (n = 42) are qualitatively analyzed. Limitations and directions for future research are discussed
Nasal Acai Polysaccharides Potentiate Innate Immunity to Protect against Pulmonary Francisella tularensis and Burkholderia pseudomallei Infections
Pulmonary Francisella tularensis and Burkholderia pseudomallei infections are highly lethal in untreated patients, and current antibiotic regimens are not always effective. Activating the innate immune system provides an alternative means of treating infection and can also complement antibiotic therapies. Several natural agonists were screened for their ability to enhance host resistance to infection, and polysaccharides derived from the Acai berry (Acai PS) were found to have potent abilities as an immunotherapeutic to treat F. tularensis and B. pseudomallei infections. In vitro, Acai PS impaired replication of Francisella in primary human macrophages co-cultured with autologous NK cells via augmentation of NK cell IFN-Ξ³. Furthermore, Acai PS administered nasally before or after infection protected mice against type A F. tularensis aerosol challenge with survival rates up to 80%, and protection was still observed, albeit reduced, when mice were treated two days post-infection. Nasal Acai PS administration augmented intracellular expression of IFN-Ξ³ by NK cells in the lungs of F. tularensis-infected mice, and neutralization of IFN-Ξ³ ablated the protective effect of Acai PS. Likewise, nasal Acai PS treatment conferred protection against pulmonary infection with B. pseudomallei strain 1026b. Acai PS dramatically reduced the replication of B. pseudomallei in the lung and blocked bacterial dissemination to the spleen and liver. Nasal administration of Acai PS enhanced IFN-Ξ³ responses by NK and Ξ³Ξ΄ T cells in the lungs, while neutralization of IFN-Ξ³ totally abrogated the protective effect of Acai PS against pulmonary B. pseudomallei infection. Collectively, these results demonstrate Acai PS is a potent innate immune agonist that can resolve F. tularensis and B. pseudomallei infections, suggesting this innate immune agonist has broad-spectrum activity against virulent intracellular pathogens
Acai PS enhances the clearance of type A <i>F. tularensis</i> from RAW264.7 cells, but not murine BMDMs via NO.
<p>Cells were treated with Acai PS 16 hr prior to infection <i>F. tularensis</i> SchuS4 (MOIβΌ30), some wells were also pre-treated with 400 Β΅M L-NMA.</p>a<p>Log<sub>10</sub> CFU/well from three wells/treatment shown; standard deviation in parentheses; results are representative of two independent experiments.</p>*<p>p<0.05 as compared to the same cell type not treated with Acai PS at the same time point.</p>β§<p>p<0.05 as compared to the same cell type, with the same Acai treatment, treated with L-NMA at 20 hr post-infection. NDβ=βNot done.</p
Acai PS requires IFN-Ξ³ and NK cells for optimum protection against <i>B. pseudomallei</i> infection.
<p>Two days prior to infection, C57BL/6 mice received rat IgG, anti-IFN-Ξ³, or anti-NK1.1 mAb. Mice were treated i.n. with PBS (nβ=β5β10/group) or 1 mg of Acai PS (nβ=β10/group) one day prior to i.n. infection with 1Γ10<sup>4</sup> CFUs of <i>B. pseudomallei</i> 1026b. Survival was monitored over time. *P<0.05 as compared to animals receiving PBS and IgG. β§P<0.05 as compared to animals receiving Acai PS and anti-IFN-Ξ³.</p
Acai PS induces TNF-Ξ± and NO in type A <i>F. tularensis</i>-infected RAW264.7 cells, but not in murine BMDMs.
<p>Cells were treated and infected as in <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1002587#ppat-1002587-t001" target="_blank">Table 1</a>. 3/wells treatment at 20 hr post-infection shown; standard deviation in parentheses; results are representative of two independent experiments.</p>a<p>Mean NO (Β΅M) or</p>b<p>TNF-Ξ± (ng/ml) production.</p>*<p>p<0.05 as compared to the same cell type not treated with Acai PS.</p>β§<p>p<0.05 as compared to the same cell type, with the same Acai treatment, treated with L-NMA at 20 hr post-infection. NDβ=βnot done.</p
Nasal administration of Acai PS confers protection against pulmonary <i>B. pseudomallei</i> infection.
<p>Female C57BL/6 mice (nβ=β5/group) were treated i.n. with PBS or with 100β1000 Β΅g of Acai PS one day prior to, or immediately after, intranasal infection with 3Γ10<sup>3</sup> CFUs of <i>B. pseudomallei</i> 1026b. A) Body weights and B) clinical scores were recorded daily, and C) on day 3, CFU determinations were performed in the lungs, spleens, and livers. Error bars depict SEM. *P<0.05 as compared to PBS group. **** indicates that *P<0.05 for all Acai PS-treated groups in relation to PBS-treated group at this time point. Data depicted in AβB) are representative of two independent experiments. The dashed line in C) indicates the limit of bacterial CFU detection.</p
Acai PS enhances LVS clearance from in human primary macrophages and enhances NK cell IFN-Ξ³ mRNA.
<p>Human primary macrophages (1Γ10<sup>4</sup>cells/well, 3 wells/treatment) were derived from PBMCS and infected with LVS (MOIβΌ300). One day prior to macrophage infection, autologous NK cells were also isolated via magnetic sorting. Macrophages and NK cells were treated separately with varying amounts of Acai PS 16 h prior to macrophage infection. After infection of the macrophages, fresh media with or without Acai PS or fresh media containing NK cells (βΌ20 NK cells/macrophage) with or without Acai PS were then added to the macrophage containing wells. A) Twenty h after infection, NK cells (non-adherent) were removed, macrophages were lysed, and intracellular bacteria enumerated. Error bars represent standard error. *P<0.05, as compared to untreated macrophages. B) Total RNA was extracted from NK cells co-cultured with LVS-infected macrophages (with or without Acai PS), and RT-PCR was performed for Ξ²-actin (control) and IFN-Ξ³, TNF-Ξ±, IL-17A, IL-21, granzyme B, perforin, and TRAIL. Results are representative of independent experiments from five different blood donors.</p
Acai PS enhances IFN-Ξ³ by innate leukocytes during pulmonary type A <i>F. tularensis</i> infection.
<p>C57BL/6 mice (nβ=β5/group) were treated i.n. with 1 mg of Acai PS one day prior to i.n. infection with 50 CFUs of <i>F. tularensis</i> SchuS4. Some mice were also depleted of IFN-Ξ³ two days prior to infection. A) Intracellular expression of IFN-Ξ³ was determined for lung NK cells by flow cytometry, and two days after infection, and B) lung and splenic bacterial burdens were determined. Data are representative of two independent experiments. Error bars depict SEM. *P<0.05 as compared to PBS-treated animals receiving the same antibody treatment.</p
Nasal administration of Acai PS confers prophylactic and therapeutic protection against pulmonary Type A <i>F. tularensis</i> infection.
<p>Female C57BL/6 mice (5/group) were treated with PBS or with 10, 100, 1000 Β΅g of Acai PS by the intranasal (i.n.) route one day prior to aerosol infection with <i>F. tularensis</i> SchuS4. A) Mice were monitored for morbidity and mortality twice daily for a period of 14β28 days, at which time survivors were euthanized, and B) body weights were monitored. C) Female C57BL/6 mice (nβ=β15β20/group) were i.n. treated with PBS or with 100 Β΅g of Acai PS immediately after, one day after, or two days after aerosol infection with <i>F. tularensis</i> SchuS4. Mice were monitored for morbidity and mortality. *P<0.05 as compared to PBS group. Error bars depict S.D. Data depicted in C) are pooled from two independent experiments.</p
Acai PS reduces type A <i>F. tularensis</i> from primary human macrophages co-cultured with NK cells via IFN-Ξ³.
<p>A) and B) Primary human macrophages (10<sup>5</sup>/well, 3 wells/treatment) and NK cells were isolated and treated separately with 100 Β΅g/ml Acai PS 16 h prior to infection with <i>F. tularensis</i> SchuS4 (MOIβΌ30). Neutralizing anti-IFN-Ξ³ mAb, and/or autologous NK cells (βΌ5 NK cells/macrophage) were also added to some wells. Either immediately after (0 hr) or twenty h after infection, NK cells (non-adherent) were removed and A) macrophages were lysed and intracellular bacteria enumerated. Error bars represent standard deviation. *P<0.05 as compared to untreated macrophages. B) β§P<0.05 as compared to Acai PS stimulated co-cultures neutralized of IFN-Ξ³. Results are representative of independent experiments from three different blood donors. Similar results were obtained in macrophages infected with LVS (data not shown). NDβ=βnot determined.</p