Retention and Attrition of Athletic Training Mothers in the National Collegiate Athletic Association Division II Setting

More women are entering the professional field of athletic training. Despite the growth of women in the profession, many are leaving the collegiate setting by the age of 30. While this trend has been studied extensively at the National Collegiate Athletic Association Division I (NCAA DI) setting, little research has been completed at the National Collegiate Athletic Association Division II (NCAA DII) setting. This study aims to gain insight and understanding into the factors that affect female certified athletic trainer retention and attrition in the NCAA DII setting. This is a qualitative phenomenological study using an advocacy lens. Participants included eleven female certified athletic trainers from ten NCAA DII institutions. Data was collected using semi-structured interviews, transcribed verbatim, and analyzed using spillover theory. Peer review and member checking were performed to establish trustworthiness. Results of the study revealed five themes that affect female certified athletic trainer attrition and retention. These themes included role overload/conflict, support networks, women as caretakers, the culture of athletics, and gender issues. The most significant factors influencing this group of female certified athletic trainers\u27 retention and attrition were role overload/conflict and support networks. The categories of women and caretakers, the culture of athletics, and gender issues fell to the patriarchal nature of athletics. The participants all indicated that it was an issue but did not believe that they alone could overcome the gender stereotypes in collegiate athletics

The Interplay of Defense Mechanisms Against Infectious Diseases

The total complex of immune expression is an interplay between nonspecific antimicrobial humoral systems plus specific antibodies and accessory factors. These systems are backstopped by the phagocytic functions of PMNs. If these fail, mononuclear phagocytes respond as a second line of defense to carry out chronic engagements. In addition to a direct activation process by substrate, macrophages may be activated and mobilized by a lymphocyte-mediated immunologic reaction which probably involves either a lymphotoxin and/or a specific antibody cytophilic for macrophages. Immunologically activated lymphocytes appear to be the primary effector cells of anti-tissue (transplantation) cellular immunity, whereas immunologically activated macrophages appear to be the primary effector cells of antibacterial cellular immunity

Alveolar macrophage priming by intravenous administration of chitin particles, polymers of N-acetyl-D-glucosamine, in mice

Intravenous (i.v.) administration of phagocytosable chitin particles (1 to 10 mm) in C57BL/6 mice and SCID mice primed alveolar macrophages (Mf) within 3 days to yield up to a 50-fold increase in their oxidative burst when elicited in vitro with phorbol myristate acetate (PMA). C57BL/6 mice pretreated with monoclonal antibodies (MAbs) against mouse gamma interferon (IFN-g) or NK1.1 showed a markedly decreased level of alveolar Mf priming following injection of chitin particles. To confirm IFN-g production in vitro, spleen cells isolated from normal C57BL/6 mice and SCID mice were cultured with chitin particles. Significant IFN-g production was observed following stimulation with chitin but not with chitosan or latex beads. When spleen cells were treated with anti-NK1.1 MAb, IFN-g production was significantly inhibited. Another set of experiments showed that when C57BL/6 mice were pretreated i.v. with a small dose IFN-g, a higher level of priming was induced with not only phagocytosable chitin particles but also phagocytosable chitosan and even latex beads. Likewise, the spleen cell cultures preconditioned with IFN-g provided an up-regulation of IFN-g production by these phagocytosable particles. Taken together, the in vivo and in vitro results suggest that (i) the alveolar Mf priming mechanism is due, at least in part, to direct activation of Mf by IFN-g, which is produced by NK1.11 CD42 cells; (ii) IFN-g would have an autocrine-like effect on Mf and make them more responsive to particle priming; and (iii) phagocytosis of particulates, probably by a postmembrane event such as interiorization, appears to be important for the up-regulation of alveolar Mf priming and IFN-g production. Originally published Infection and Immunity, Vol. 65, No. 5, May 199

How do whitefish exporters adapt to increased pressure for sustainable transportation of fish to the EU market?

Master of Science in Business (Siviløkonom) - Nord universitet 202

AAPT Diagnostic Criteria for Chronic Sickle Cell Disease Pain

Pain in sickle cell disease (SCD) is associated with increased morbidity, mortality, and high health care costs. Although episodic acute pain is the hallmark of this disorder, there is an increasing awareness that chronic pain is part of the pain experience of many older adolescents and adults. A common set of criteria for classifying chronic pain associated with SCD would enhance SCD pain research efforts in epidemiology, pain mechanisms, and clinical trials of pain management interventions, and ultimately improve clinical assessment and management. As part of the collaborative effort between the Analgesic, Anesthetic, and Addiction Clinical Trial Translations Innovations Opportunities and Networks public-private partnership with the U.S. Food and Drug Administration and the American Pain Society, the Analgesic, Anesthetic, and Addiction Clinical Trial Translations Innovations Opportunities and Networks-American Pain Society Pain Taxonomy initiative developed the outline of an optimal diagnostic system for chronic pain conditions. Subsequently, a working group of experts in SCD pain was convened to generate core diagnostic criteria for chronic pain associated with SCD. The working group synthesized available literature to provide evidence for the dimensions of this disease-specific pain taxonomy. A single pain condition labeled chronic SCD pain was derived with 3 modifiers reflecting different clinical features. Future systematic research is needed to evaluate the feasibility, validity, and reliability of these criteria. Perspective: An evidence-based classification system for chronic SCD pain was constructed for the Analgesic, Anesthetic, and Addiction Clinical Trial Translations Innovations Opportunities and Networks-American Pain Society Pain Taxonomy initiative. Applying this taxonomy may improve assessment and management of SCD pain and accelerate research on epidemiology, mechanisms, and treatments for chronic SCD pain

Phagosomal Rupture by Mycobacterium tuberculosis Results in Toxicity and Host Cell Death

Survival within macrophages is a central feature of Mycobacterium tuberculosis pathogenesis. Despite significant advances in identifying new immunological parameters associated with mycobacterial disease, some basic questions on the intracellular fate of the causative agent of human tuberculosis in antigen-presenting cells are still under debate. To get novel insights into this matter, we used a single-cell fluorescence resonance energy transfer (FRET)-based method to investigate the potential cytosolic access of M. tuberculosis and the resulting cellular consequences in an unbiased, quantitative way. Analysis of thousands of THP-1 macrophages infected with selected wild-type or mutant strains of the M. tuberculosis complex unambiguously showed that M. tuberculosis induced a change in the FRET signal after 3 to 4 days of infection, indicating phagolysosomal rupture and cytosolic access. These effects were not seen for the strains M. tuberculosisΔRD1 or BCG, both lacking the ESX-1 secreted protein ESAT-6, which reportedly shows membrane-lysing properties. Complementation of these strains with the ESX-1 secretion system of M. tuberculosis restored the ability to cause phagolysosomal rupture. In addition, control experiments with the fish pathogen Mycobacterium marinum showed phagolysosomal translocation only for ESX-1 intact strains, further validating our experimental approach. Most importantly, for M. tuberculosis as well as for M. marinum we observed that phagolysosomal rupture was followed by necrotic cell death of the infected macrophages, whereas ESX-1 deletion- or truncation-mutants that remained enclosed within phagolysosomal compartments did not induce such cytotoxicity. Hence, we provide a novel mechanism how ESX-1 competent, virulent M. tuberculosis and M. marinum strains induce host cell death and thereby escape innate host defenses and favor their spread to new cells. In this respect, our results also open new research directions in relation with the extracellular localization of M. tuberculosis inside necrotic lesions that can now be tackled from a completely new perspective

Pathogenic Mechanisms and Host Interactions in Staphylococcus epidermidis Device-Related Infection

Staphylococcus epidermidis is a permanent member of the normal human microbiota, commonly found on skin and mucous membranes. By adhering to tissue surface moieties of the host via specific adhesins, S. epidermidis is capable of establishing a lifelong commensal relationship with humans that begins early in life. In its role as a commensal organism, S. epidermidis is thought to provide benefits to human host, including out-competing more virulent pathogens. However, largely due to its capacity to form biofilm on implanted foreign bodies, S. epidermidis has emerged as an important opportunistic pathogen in patients receiving medical devices. S. epidermidis causes approximately 20% of all orthopedic device-related infections (ODRIs), increasing up to 50%in late-developing infections. Despite this prevalence, it remains underrepresented in the scientific literature, in particular lagging behind the study of the S. aureus. This review aims to provide an overview of the interactions of S. epidermidis with the human host, both as a commensal and as a pathogen. The mechanisms retained by S. epidermidis that enable colonization of human skin as well as invasive infection, will be described, with a particular focus upon biofilm formation. The host immune responses to these infections are also described, including how S. epidermidis seems to trigger low levels of pro-inflammatory cytokines and high levels of interleukin-10, which may contribute to the sub-acute and persistent nature often associated with these infections. The adaptive immune response to S. epidermidis remains poorly described, and represents an area which may provide significant new discoveries in the coming years