Combining an experiential learning model and interprofessional peer-mentoring to improve maternal and neonatal health: Lessons learned from Indonesia.

Background: High maternal-neonatal mortality rate in the East Nusa Tenggara Timur Province, Indonesia, has raised a concern about improving quality health care and prevention. A task force team consisting of the district health office and the corresponding hospital implemented an interprofessional peer mentoring for improving maternal-neonatal health initiative involving various health professionals and community members. This study assesses the effectiveness of the interprofessional peer-mentoring program in improving health-care workers' capacity and community members' awareness of maternal-neonatal health in the primary care setting.

Reactive oxygen species and IRF1 stimulate IFNα production by proximal tubules during ischemic AKI.

We previously reported that expression of the transcription factor interferon regulatory factor 1 (IRF1) is an early, critical maladaptive signal expressed by renal tubules during murine ischemic acute kidney injury (AKI). We now show that IRF1 mediates signals from reactive oxygen species (ROS) generated during ischemic AKI and that these signals ultimately result in production of α-subtypes of type I interferons (IFNαs). We found that genetic knockout of the common type I IFN receptor (IFNARI-/-) improved kidney function and histology during AKI.

Early interleukin 6 production by leukocytes during ischemic acute kidney injury is regulated by TLR4.

Although leukocytes infiltrate the kidney during ischemic acute kidney injury (AKI) and release interleukin 6 (IL6), their mechanism of activation is unknown. Here, we tested whether Toll-like receptor 4 (TLR4) on leukocytes mediated this activation by interacting with high-mobility group protein B1 (HMGB1) released by renal cells as a consequence of ischemic kidney injury. We constructed radiation-induced bone marrow chimeras using C3H/HeJ and C57BL/10ScNJ strains of TLR4 (-/-) mice and their respective TLR4 (+/+) wild-type counterparts and studied them at 4 h after an ischemic insult.

Bardoxolone methyl (BARD) ameliorates ischemic AKI and increases expression of protective genes Nrf2, PPARγ, and HO-1.

Ischemic acute kidney injury (AKI) triggers expression of adaptive (protective) and maladaptive genes. Agents that increase expression of protective genes should provide a therapeutic benefit. We now report that bardoxolone methyl (BARD) ameliorates ischemic murine AKI as assessed by both renal function and pathology.

Toll-like receptor 4 regulates early endothelial activation during ischemic acute kidney injury.

Ischemic acute kidney injury (AKI) triggers an inflammatory response which exacerbates injury that requires increased expression of endothelial adhesion molecules. To study this further, we used in situ hybridization, immunohistology, and isolated endothelial cells, and found increased Toll-like receptor 4 (TLR4) expression on endothelial cells of the vasa rectae of the inner stripe of the outer medulla of the kidney 4 h after reperfusion. This increase was probably due to reactive oxygen species, known to be generated early during ischemic AKI, because the addition of hydrogen peroxide increased TLR4 expression in MS1 microvascular endothelial cells in vitro.

Successful renal re-transplantation in the presence of pre-existing anti-DQ5 antibodies when there was zero mismatch at class I human leukocyte antigen A, B, & C: a case report.

Introduction: Hyperacute rejection may be prevented by avoiding the transplantation of kidneys into patients with pre-existing anti-donor Class I human leukocyte antigen antibodies. However, the role of anti-donor-Class II-human leukocyte antigen-DQ antibodies is not established. The question is ever more relevant as more sensitive cross-matching techniques detect many additional antibodies during the final crossmatch.

The inflammatory response to ischemic acute kidney injury: a result of the 'right stuff' in the 'wrong place'?

Purpose Of Review: Ischemic acute kidney injury may be exacerbated by an inflammatory response. How injury elicits inflammation remains a major question in understanding acute kidney injury. The present review examines the hypothesis that molecules released by injured cells elicit inflammation.

Bc3h1 myogenic cells produce an infectious ecotropic murine leukemia virus.

cDNAs representing an endogenous C-type ecotropic murine leukemia virus were isolated from a cDNA library constructed to represent mRNAs present in BC3H1 myogenic cells but not in C2C12 myogenic cells. RNA blot hybridization analysis using the cDNA inserts as probes revealed that BC3H1 cells produce MuLV-related transcirpts of at least three different size classes. A polymerase chain reaction enhanced assay for reverse transcriptase activity revealed the presence of reverse transcriptase in a viral pellet from medium conditioned by BC3H1 cells.