Developing and Piloting a School-Based Online Adolescent Student-Athlete Concussion Surveillance System.

BACKGROUND: Despite increased awareness of concussions, epidemiologic surveillance efforts have been scarce, especially among adolescents. This project, which was developed with school stakeholders (certified athletic trainers [ATCs], nurses, athletic directors), piloted a public secondary school-based online surveillance tool for interscholastic and intramural sports and physical education-related concussions in New Jersey during 2014-2017 school years (SY). METHODS: Participating public high schools (5 within 4 districts) and career-technical-vocational education districts (2 with 5 campuses) completed forms anonymously online via PsychData within 5 days. RESULTS: There were 208 concussions reported, 115 in 2015-2016 SY and 93 in 2016-2017 SY. In fall 2015, 86 concussions were reported, including 16 from summer preseason. In fall 2016, 56 concussions were reported; 3 occurred during preseason. There were 7 concussions reported in winter 2016 and 16 in winter 2017. Twenty-two concussions were reported in spring of both 2016 and 2017. Most online forms were completed in <10 minutes, usually using either desktop computers or tablets/iPads. School nurses followed by ATCs were primary sources of data entered online, usually by ATCs. CONCLUSIONS: Cooperation of nurses and ATCs at participating schools suggested online surveillance was valued and viable. Data inform future concussion prevention education and ongoing injury surveillance.

An update on the pathogenesis and treatment of IgA nephropathy.

Over the past two decades significant progress has been made in unravelling the complex pathogenesis of immunoglobulin A nephropathy (IgAN). Excess amounts of poorly galactosylated immunoglobulin (Ig)A1 in the serum appear to be the trigger for generation of glycan-specific IgG and IgA autoantibodies, resulting in the formation of circulating IgA immune complexes, which are pivotal to the development of nephritis. It remains unclear why there is an increase in poorly galactosylated IgA1 molecules in the serum in IgAN. One intriguing possibility is that this IgA is derived from displaced mucosal B cells, which have mis-homed from their mucosal induction sites to systemic sites, where they secrete polymeric, poorly galactosylated IgA directly into the circulation rather than onto mucosal surfaces. Lack of a clear appreciation of the origins of poorly galactosylated IgA1 and an incomplete understanding of immune complex formation have hampered development of specific therapeutic strategies to prevent mesangial IgA deposition. Clinicians have therefore been left to manage patients with generic therapies, mainly by control of blood pressure and renin-angiotensin blockade. A paucity of high-quality clinical trials has meant that evaluation of additional therapies, particularly immunosuppressive regimens, has been difficult and there remains a great deal of confusion over the optimum treatment of patients at high risk of progressive chronic kidney disease.

Inherited IgA glycosylation pattern in IgA nephropathy and HSP nephritis: where do we go next?

New data from Kiryluk et al. show the importance of genetic factors in determining the profile of serum IgA1 O-glycoforms in IgA nephropathy and Henoch-Schönlein purpura nephritis. Elevated serum levels of poorly galactosylated IgA1 O-glycoforms do not, however, appear sufficient in themselves to cause nephritis in these two diseases, and a 'second hit' is necessary before changes in IgA1 glycosylation translate into clinical disease. The challenge now is to determine what these genetic factors are.

Immune complex formation in IgA nephropathy: CD89 a 'saint' or a 'sinner'?

New data suggest that a soluble form of the IgA receptor CD89 may be protective against development of progressive renal injury in IgA nephropathy (IgAN). Understanding how IgA triggers shedding of CD89 from myeloid cell surfaces could help clarify the process of immune complex formation in IgAN, and measurement of this soluble form of CD89 may in the future prove a useful prognostic indicator of end-stage renal disease in this common glomerulonephritis.

D-six4 plays a key role in patterning cell identities deriving from the Drosophila mesoderm.

Patterning of the Drosophila embryonic mesoderm requires the regulation of cell type-specific factors in response to dorsoventral and anteroposterior axis information. For the dorsoventral axis, the homeodomain gene, tinman, is a key patterning mediator for dorsal mesodermal fates like the heart. However, equivalent mediators for more ventral fates are unknown. We show that D-six4, which encodes a Six family transcription factor, is required for the appropriate development of most cell types deriving from the non-dorsal mesoderm - the fat body, somatic cells of the gonad, and a specific subset of somatic muscles. Misexpression analysis suggests that D-Six4 and its likely cofactor, Eyes absent, are sufficient to impose these fates on other mesodermal cells. At stage 10, the mesodermal expression patterns of D-six4 and tin are complementary, being restricted to the dorsal and non-dorsal regions respectively. Our data suggest that D-six4 is a key mesodermal patterning mediator at this stage that regulates a variety of cell-type-specific factors and hence plays an equivalent role to tin. At stage 9, however, D-six4 and tin are both expressed pan-mesodermally. At this stage, tin function is required for full D-six4 expression. This may explain the known requirement for tin in some non-dorsal cell types.