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In the current article, two kindergarten teachers and two university researchers explain how 45 kindergarten students collaboratively engaged in a specific inquiry approach called Project-Based Inquiry (PBI) Global. PBI Global consists of five-phases: (a) ask a compelling question, (b) gather and analyse sources, (c) creatively synthesize claims and evidences, (d) critically evaluate and revise, and (e) share, publish, and act. The teachers were in a master's degree program that led to K-12 reading certification. The PBI Global was an assignment in the course, New Literacies and Media. Specifically, the teacher team addressed the question: How can teachers use inquiry and digital tools to teach global awareness with kindergarten students? Applying the PBI Global process, the teachers used the book, Same Same but Different (Kostecki-Shaw and Adam, 2015) as an anchor text to students' exploration of the five senses through different cultural artifacts. Additionally, the kindergarten students utilized Flipgrids to explain their findings for an authentic audience of parents and community members. The article concludes with lessons learned about implementing the process and implications for other kindergarten teachers who may be interested in inquiry-based learning. [ABSTRACT FROM AUTHOR]

Complex problems and emerging technologies challenge the public health system and create both opportunities and risks for population health. Risk governance is an appropriate tool with which public health practitioners can maximize benefit and minimize risk to the public's health. To date, there is no risk governance framework that is robust, rigorous, and applicable to population health. This article first explores existing risk governance frameworks and discusses their potential applicability to population health challenges. It then explains specifically how biobanks, which have great potential to improve the population's health, but threaten individual interests, could benefit from the application of a risk governance framework. [ABSTRACT FROM AUTHOR]

In the article, the authors discuss developments in the healthcare sector in the U.S. as of late June 2016, particularly in care delivery and payment in advanced primary care. Also cited are the move by the Centers for Medicare & Medicaid Services (CMS) to introduce alternative payment models that reward value and quality, and the objectives of the Affordable Care Act and the Medicare Access and CHIP Reauthorization Act of 2015.

Antibiotic persistence permits a subpopulation of susceptible bacteria to survive lethal concentrations of bactericidal antibiotics. This prolongs antibiotic therapy, promotes the evolution of antibiotic-resistant pathogen strains and can select for pathogen virulence within infected hosts. Here, we review the literature exploring antibiotic persistence in vivo , and describe the consequences of recalcitrant subpopulations, with a focus on studies using the model pathogen Salmonella Typhimurium. In vitro studies have established a concise set of features distinguishing true persisters from other forms of bacterial recalcitrance to bactericidal antibiotics. We discuss how animal infection models are useful for exploring these features in vivo, and describe how technical challenges can sometimes prevent the conclusive identification of true antibiotic persistence within infected hosts. We propose using two complementary working definitions for studying antibiotic persistence in vivo : the strict definition for studying the mechanisms of persister formation, and an operative definition for functional studies assessing the links between invasive virulence and persistence as well as the consequences for horizontal gene transfer, or the emergence of antibiotic-resistant mutants. This operative definition will enable further study of how antibiotic persisters arise in vivo , and of how surviving populations contribute to diverse downstream effects such as pathogen transmission, horizontal gene transfer and the evolution of virulence and antibiotic resistance. Ultimately, such studies will help to improve therapeutic control of antibiotic- recalcitrant populations. • Antibiotic persistence is well described in vitro, but challenging to study in vivo. • Salmonella Typhimurium is an ideal organism for studying antibiotic persistence. • Virulence factors shape intracellular niches, which permits persister formation. • Persister formation has consequences for antimicrobial therapy and pathogen evolution. • Characterising true antibiotic persistence in vivo is experimentally challenging. [ABSTRACT FROM AUTHOR]

Biological sex differences affect the course of HIV infection, with untreated women having lower viral loads compared to their male counterparts but, for a given viral load, women have a higher rate of progression to AIDS. However, the vast majority of data on viral evolution, a process that is clearly impacted by host immunity and could be impacted by sex differences, has been derived from men. We conducted an intensive analysis of HIV-1 gag and env-gp120 evolution taken over the first 6–11 years of infection from 8 Women’s Interagency HIV Study (WIHS) participants who had not received combination antiretroviral therapy (ART). This was compared to similar data previously collected from men, with both groups infected with HIV-1 subtype B. Early virus populations in men and women were generally homogenous with no differences in diversity between sexes. No differences in ensuing nucleotide substitution rates were found between the female and male cohorts studied herein. As previously reported for men, time to peak diversity in env-gp120 in women was positively associated with time to CD4+ cell count below 200 (P = 0.017), and the number of predicted N-linked glycosylation sites generally increased over time, followed by a plateau or decline, with the majority of changes localized to the V1-V2 region. These findings strongly suggest that the sex differences in HIV-1 disease progression attributed to immune system composition and sensitivities are not revealed by, nor do they impact, global patterns of viral evolution, the latter of which proceeds similarly in women and men. [ABSTRACT FROM AUTHOR]

Introduction Understanding the mechanisms by which some individuals are able to naturally control HIV- 1 infection is an important goal of AIDS research. We here describe the case of an HIV-1+ woman, CASE1, who has spontaneously controlled her viremia for the last 14 of her 20 years of infection. Methods CASE1 has been clinically monitored since 1993. Detailed immunological, virological and histological analyses were performed on samples obtained between 2009 and 2011. Results As for other Elite Controllers, CASE1 is characterized by low to undetectable levels of plasma HIV-1 RNA, peripheral blood mononuclear cell (PBMC) associated HIV-1 DNA a reduced in vitro susceptibility of target cells to HIV-1 infection. Furthermore, a slow rate of virus evolution was demonstrated in spite the lack of assumption of any antiretroviral agent. CASE1 failed to transmit HIV-1 to either her sexual male partner or to her child born by vaginal delivery. Normal values and ratios of T and B cells were observed, along with normal histology of the intestinal mucosa. Attempts to isolate HIV-1 from her PBMC and gut-derived cells were unsuccessful, despite expression of normal cell surface levels of CD4, CCRC5 and CXCR4. CASE1 did not produce detectable anti-HIV neutralizing antibodies in her serum or genital mucosal fluid although she displayed potent T cell responses against HIV-1 Gag and Nef. CASE1 also possessed multiple genetic polymorphisms, including HLA alleles (B*14, B*57, C*06 and C*08.02) and HLA-C single nucleotide polymorphisms (SNPs, rs9264942 C/C and rs67384697 del/del), that have been previously individually associated with spontaneous control of plasma viremia, maintenance of high CD4+ T cell counts and delayed disease progression Conclusions CASE1 has controlled her HIV-1 viremia below the limit of detection in the absence of antiretroviral therapy for more than 14 years and has not shown any sign of immunologic deterioration or disease progression. Co-expression of multiple protective HLA alleles, HLA-C SNPs and strong T cell responses against HIV-1 proteins are the most likely explanation of this very benign case of spontaneous control of HIV-1 disease progression. [ABSTRACT FROM AUTHOR]

The article presents a case study of a 35-year-old female diagnosed with renal disease caused by pre-eclampsia after receiving deceased donor kidney. The rarity of myeloid sarcoma in kidney without bone marrow disease development and donor transmitted malignancy in solid organ transplant is demonstrated. Possible explanations for the isolated involvement of the patient's kidney are also outlined.

Introduction: Understanding the mechanisms by which some individuals are able to naturally control HIV-1 infection is an important goal of AIDS research. We here describe the case of an HIV-1(+) woman, CASE1, who has spontaneously controlled her viremia for the last 14 of her 20 years of infection.Methods: CASE1 has been clinically monitored since 1993. Detailed immunological, virological and histological analyses were performed on samples obtained between 2009 and 2011.Results: As for other Elite Controllers, CASE1 is characterized by low to undetectable levels of plasma HIV-1 RNA, peripheral blood mononuclear cell (PBMC) associated HIV-1 DNA and reduced in vitro susceptibility of target cells to HIV-1 infection. Furthermore, a slow rate of virus evolution was demonstrated in spite the lack of assumption of any antiretroviral agent. CASE1 failed to transmit HIV-1 to either her sexual male partner or to her child born by vaginal delivery. Normal values and ratios of T and B cells were observed, along with normal histology of the intestinal mucosa. Attempts to isolate HIV-1 from her PBMC and gut-derived cells were unsuccessful, despite expression of normal cell surface levels of CD4, CCRC5 and CXCR4. CASE1 did not produce detectable anti-HIV neutralizing antibodies in her serum or genital mucosal fluid although she displayed potent T cell responses against HIV-1 Gag and Nef. CASE1 also possessed multiple genetic polymorphisms, including HLA alleles (B*14, B*57, C*06 and C*08.02) and HLA-C single nucleotide polymorphisms (SNPs, rs9264942 C/C and rs67384697 del/del), that have been previously individually associated with spontaneous control of plasma viremia, maintenance of high CD4(+) T cell counts and delayed disease progression.Conclusions: CASE1 has controlled her HIV-1 viremia below the limit of detection in the absence of antiretroviral therapy for more than 14 years and has not shown any sign of immunologic deterioration or disease progression. Co-expression of multiple protective HLA alleles, HLA-C SNPs and strong T cell responses against HIV-1 proteins are the most likely explanation of this very benign case of spontaneous control of HIV-1 disease progression. [ABSTRACT FROM AUTHOR]