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BackgroundParents use apps to access information on child health, but there are no standards for providing evidence-based advice, support, and information. Well-developed apps that promote appropriate infant feeding and play can support healthy growth and development. A 2015 systematic assessment of smartphone apps in Australia about infant feeding and play found that most apps had minimal information, with poor readability and app quality. ObjectiveThis study aimed to systematically evaluate the information and quality of smartphone apps providing information on breastfeeding, formula feeding, introducing solids, or infant play for consumers. MethodsThe Google Play store and Apple App Store were searched for free and paid Android and iPhone Operating System (iOS) apps using keywords for infant feeding, breastfeeding, formula feeding, and tummy time. The apps were evaluated between September 2018 and January 2019 for information content based on Australian guidelines, app quality using the 5-point Mobile App Rating Scale, readability, and suitability of health information. ResultsA total of 2196 unique apps were found and screened. Overall, 47 apps were evaluated, totaling 59 evaluations for apps across both the Android and iOS platforms. In all, 11 apps had affiliations to universities and health services as app developers, writers, or editors. Furthermore, 33 apps were commercially developed. The information contained within the apps was poor: 64% (38/59) of the evaluations found no or low coverage of information found in the Australian guidelines on infant feeding and activity, and 53% (31/59) of the evaluations found incomplete or incorrect information with regard to the depth of information provided. Subjective app assessment by health care practitioners on whether they would use, purchase, or recommend the app ranged from poor to acceptable (median 2.50). Objective assessment of the apps’ engagement, functionality, aesthetics, and information was scored as acceptable (median 3.63). The median readability score for the apps was at the American Grade 8 reading level. The suitability of health information was rated superior or adequate for content, reading demand, layout, and interaction with the readers. ConclusionsThe quality of smartphone apps on infant feeding and activity was moderate based on the objective measurements of engagement, functionality, aesthetics, and information from a reliable source. The overall quality of information on infant feeding and activity was poor, indicated by low coverage of topics and incomplete or partially complete information. The key areas for improvement involved providing evidence-based information consistent with the Australian National Health and Medical Research Council’s Infant Feeding Guidelines. Apps supported and developed by health care professionals with adequate health service funding can ensure that parents are provided with credible and reliable resources.

Transgenic mice with Alzheimer presenilin 1 (PS-1) mutations have been shown to have accelerated neurodegeneration without amyloid plaque formation so the pathogenic role of the PS-1 mutation is upstream of the amyloid cascade. Careful quantitative studies on PS-1 transgenic mice were carried out. Without amyloid plaque formation, neurodegeneration was seen to be accelerated significantly in mice more than 13 months old and having familial Alzheimer disease mutant PS-1.

CD40 antibody has been found to evoke a cytotoxic T-cell response that eradicates lymphoma and bypasses T-cell help. In a study it has been seen that when antibody against CD40 is used to treat mice with syngeneic lymphoma, a rapid cytotoxic T-cell response independent of T-helper cells takes place, with expansion by a factor of 10 in CD8(super.+) T cells over 5 days.

Fc receptors ( Fc Rs) play a key role in regulating and coordinating responses from both innate and adaptive arms of the immune system. The inhibitory Fc gamma receptor II ( Fcγ RIIB; CD32) is central to this regulation with Fcγ RIIB−/− mice demonstrating augmented responses to m Ab immunotherapy, elevated incidence and severity of auto-immunity, and increased response to m Ab-mediated cancer therapy. To date, these observations have remained unexploited therapeutically, partly through a lack of specific m Ab reagents capable of exclusively binding mouse Fcγ RIIB. Thus almost all of the Fcγ RIIB-binding m Ab currently available, such as 2.4 G2, also bind Fcγ RIII ( CD16), and polyclonal reagents have limited availability and are of unproven specificity and avidity, making in vivo manipulation of Fcγ RIIB impossible. Following an extensive immunisation protocol using Fcγ RIIB−/− mice, we recently produced three unique m Ab that are suitable for this purpose. Here we characterise these novel reagents and demonstrate that they fall into two distinct categories; those which cause phosphorylation and subsequent activation of Fcγ RIIB (agonistic) and those that block receptor phosphorylation (antagonistic). These two types of mAb exhibit different characteristics in a range of biochemical, cellular, and functional assays relevant to Fcγ RIIB activity and m Ab therapy. [ABSTRACT FROM AUTHOR]

Neutrophils potently kill tumour cells in the presence of anti-tumour antibodies in vitro. However, for in vivo targeting, the neutrophils need to extravasate from the circulation by passing through endothelial barriers. To study neutrophil migration in the presence of endothelial cells in vitro, we established a three-dimensional collagen culture in which SK- BR-3 tumour colonies were grown in the presence or absence of an endothelial barrier. We demonstrated that - in contrast to targeting Fcγ R on neutrophils with m Abs - targeting the immunoglobulin A Fc receptor ( Fcα RI) instead triggered neutrophil migration and degranulation leading to tumour destruction, which coincided with release of the pro-inflammatory cytokines interleukin ( IL)-1β and tumour necrosis factor ( TNF)-α. Interestingly, neutrophil migration was enhanced in the presence of endothelial cells, which coincided with production of significant levels of the neutrophil chemokine IL-8. This supports the idea that stimulation of neutrophil Fcα RI, but not Fcγ R, initiates cross-talk between neutrophils and endothelial cells, leading to enhanced neutrophil migration towards tumour colonies and subsequent tumour killing. [ABSTRACT FROM AUTHOR]

Rheumatoid arthritis (RA) T cells respond poorly to conventional mitogens. We have examined the proliferative and cytokine responses of T cells to a synthetic trispecific antibody (Tsab) directed against CD2, CD3, and CD28. In 11 subjects RA T cells proliferated more, and secreted significantly more IL-2, in response to Tsab than did control peripheral blood (PB) cells. Very high levels of IL-2 were produced by 2 patients with aggressive disease. Measurement of intracellular IL-2, IFN-gamma, IL-4, and IL-5 by flow cytometry showed a Th1 pattern of cytokine production in 13 RA and 9 control subjects. We conclude that RA T cells are not irreversibly inactivated, and that spatial arrangement of stimulating molecules may be important in eliciting maximal responses. [ABSTRACT FROM AUTHOR]

The CD70/CD27 pathway plays a significant role in the control of immunity and tolerance, and previous studies demonstrated that targeting murine CD27 (mCD27) with agonist mAbs can mediate antitumor efficacy. We sought to exploit the potential of this pathway for immunotherapy by developing 1F5, a fully human IgG1 mAb to human CD27 (hCD27) with agonist activity. We developed transgenic mice expressing hCD27 under control of its native promoter for in vivo testing of the Ab. The expression and regulation of hCD27 in hCD27-transgenic (hCD27-Tg) mice were consistent with the understood biology of CD27 in humans. In vitro, 1F5 effectively induced proliferation and cytokine production from hCD27-Tg-derived T cells when combined with TCR stimulation. Administration of 1F5 to hCD27-Tg mice enhanced Ag-specific CD8+ T cell responses to protein vaccination comparably to an agonist anti-mCD27 mAb. In syngeneic mouse tumor models, 1F5 showed potent antitumor efficacy and induction of protective immunity, which was dependent on CD4+ and CD8+ T cells. The requirement of FcR engagement for the agonistic and antitumor activities of 1F5 was demonstrated using an aglycosylated version of the 1F5 mAb. These data with regard to the targeting of hCD27 are consistent with previous reports on targeting mCD27 and provide a rationale for the clinical development of the 1F5 mAb, for which studies in advanced cancer patients have been initiated under the name CDX-1127. [ABSTRACT FROM AUTHOR]

Poly-gamma-D-glutamic acid from Bacillus licheniformis is a water-soluble, nontoxic, nonimmunogenic exopolymer. Using synthetic linkers, the alpha-carboxylate side chains of PGA were conjugated to an exposed thiol side chain of an antibody F(ab') fragment, Mc109F4. Analysis of the PGA-Mc109F4 conjugate by gel filtration HPLC revealed a mixture of multivalent conjugates. The PGA-Mc109F4 conjugate retained biological activity, but showed a lower binding affinity to target BCL3B3 cells than free Mc109F4 F(ab')(2) by flow cytometry, and a lower efficacy for BCL3B3 growth inhibition than free Mc109F4 F(ab')(2). PGA was also conjugated with the free amino group of glycopeptide antibiotic vancomycin. The PGA-vancomycin conjugate showed slightly lower antibacterial activity than free vancomycin versus susceptible Bacillus subtilis, but slightly higher activity versus intrinsically resistant Leuconostoc mesenteroides.