Effect of Hydrogen Sulfide on Essential Functions of Polymorphonuclear Leukocytes.

Impaired polymorphonuclear leukocyte (PMNL) functions contribute to increased infections and cardiovascular diseases in chronic kidney disease (CKD). Uremic toxins reduce hydrogen sulfide (H2S) levels and the anti-oxidant and anti-inflammatory effects of H2S. Its biosynthesis occurs as a side process of transsulfuration and in the disposal of adenosylhomocysteine, a transmethylation inhibitor and proposed uremic toxin. PMNL chemotaxis was measured by the under-agarose method, phagocytosis, and oxidative burst by flow cytometry in whole blood and apoptosis by determining DNA content by flow cytometry and morphological features by fluorescence microscopy. Sodium hydrogen sulfide (NaHS), diallyl trisulphide (DATS) and diallyl disulphide (DADS), cysteine, and GYY4137 were used as H2S-producing substances. Increased H2S concentrations did not affect chemotaxis and phagocytosis. NaHS primed PMNL oxidative burst activated by phorbol 12-myristate 13-acetate (PMA) or E. coli. Both DATS and cysteine significantly decreased E. coli-activated oxidative burst but had no effect on PMA stimulation. While NaHS, DADS, and cysteine attenuated PMNL apoptosis, GYY4137 decreased their viability. Experiments with signal transduction inhibitors suggest that the intrinsic apoptosis pathway is mainly involved in GYY4137-induced PMNL apoptosis and that GYY4137 and cysteine target signaling downstream of phosphoinositide 3-kinase.

Clinician and educator experiences of facilitating students' transition back to school following acquired brain injury: A qualitative systematic review.

OBJECTIVE: Transition back to school following paediatric acquired brain injury (ABI) is complex. It must be facilitated by healthcare and educational professionals, who need to work together to return affected students to learning. This qualitative systematic review synthesizes qualitative studies on clinicians' and educators' experiences of facilitating hospital-to-school transitions following ABI. METHODS: A search was conducted using seven electronic databases (CINAHL, Cochrane, EMBASE, ERIC, HealthSTAR, MEDLINE, PsycINFO) and key resources were manually reviewed. Publications selected for inclusion had a sample of clinicians and/or educators who worked with children/youth with ABI and focused on hospital-to-school transition processes from the professionals' perspectives. RESULTS: The initial search returned 4761 publications. Of those, 10 met the inclusion criteria. Six main themes emerged across those publications. Three related to transition barriers: (1) lack of training and education regarding transition processes; (2) lack of communication between stakeholders; and (3) lack of preparation for transition. The remaining three presented items that both facilitate and/or impede the transition process: (4) supports available; (5) linking agents; and (6) policies and procedures guiding transition. CONCLUSIONS: Clinicians and educators called for collaboration and communication to support students' transition back to school. Further inquiry into designated linking agents and policies that facilitate hospital-to-school transitions for students following ABI may address these lacking areas.