Pediatric emergency care in a low-income country: Characteristics and outcomes of presentations to a tertiary-care emergency department in Mozambique.

BACKGROUND: An effective pediatric emergency care (PEC) system is key to reduce pediatric mortality in low-income countries. While data on pediatric emergencies from these countries can drive the development and adjustment of such a system, they are very scant, especially from Africa. We aimed to describe the characteristics and outcomes of presentations to a tertiary-care Pediatric Emergency Department (PED) in Mozambique. METHODS: We retrospectively reviewed PED presentations to the "Hospital Central da Beira" between April 2017 and March 2018. Multivariable logistic regression was used to identify predictors of hospitalization and death. RESULTS: We retrieved 24,844 presentations. The median age was 3 years (IQR 1-7 years), and 92% lived in the urban area. Complaints were injury-related in 33% of cases and medical in 67%. Data on presenting complaints (retrieved from hospital paper-based registries) were available for 14,204 (57.2%) records. Of these, respiratory diseases (29.3%), fever (26.7%), and gastrointestinal disorders (14.2%) were the most common. Overall, 4,997 (20.1%) encounters resulted in hospitalization. Mortality in the PED was 1.6% (62% ≤4 hours from arrival) and was the highest in neonates (16%; 89% ≤4 hours from arrival). A younger age, especially younger than 28 days, living in the extra-urban area and being referred to the PED by a health care provider were all significantly associated with both hospitalization and death in the PED at the multivariable analysis. CONCLUSIONS: Injuries were a common presentation to a referral PED in Mozambique. Hospitalization rate and mortality in the PED were high, with neonates being the most vulnerable. Optimization of data registration will be key to obtain more accurate data to learn from and guide the development of PEC in Mozambique. Our data can help build an effective PEC system tailored to the local needs.

MiR-155 modulates the inflammatory phenotype of intestinal myofibroblasts by targeting SOCS1 in ulcerative colitis

Abnormal levels of microRNA (miR)-155, which regulate inflammation and immune responses, have been demonstrated in the colonic mucosa of patients with inflammatory bowel diseases (IBD), although its role in disease pathophysiology is unknown. We investigated the role of miR-155 in the acquisition and maintenance of an activated phenotype by intestinal myofibroblasts (IMF), a key cell population contributing to mucosal damage in IBD. IMF were isolated from colonic biopsies of healthy controls, ulcerative colitis (UC) and Crohn's disease (CD) patients. MiR-155 in IMF was quantified by quantitative reverse transcription-PCR in basal condition and following exposure to TNF-alpha, interleukin (IL)-1beta, lipopolysaccharide (LPS) or TGF-beta1. The effects of miR-155 mimic or inhibitor transfection on cytokine release and suppressor of cytokine signaling 1 (SOCS1) expression were assessed by enzyme-linked immunosorbent assay and western blot, respectively. Regulation of the target gene SOCS1 expression by miR-155 was assessed using luciferase reporter construct. We found that miR-155 was significantly upregulated in UC as compared with control- and CD-derived IMF. Moreover, TNF-alpha and LPS, but not TGF-beta1 and IL-1beta, significantly increased miR-155 expression in IMF. Ectopic expression of miR-155 in control IMF augmented cytokines release, whereas it downregulated SOCS1 expression. MiR-155 knockdown in UC-IMF reduced cytokine production and enhanced SOCS1 expression. Luciferase reporter assay demonstrated that miR-155 directly targets SOCS1. Moreover, silencing of SOCS1 in control IMF significantly increased IL-6 and IL-8 release. In all, our data suggest that inflammatory mediators induce miR-155 expression in IMF of patients with UC. By downregulating the expression of SOCS1, miR-155 wires IMF inflammatory phenotype.

MiR-155 modulates the inflammatory phenotype of intestinal myofibroblasts by targeting SOCS1 in ulcerative colitis

Abnormal levels of microRNA (miR)-155, which regulate inflammation and immune responses, have been demonstrated in the colonic mucosa of patients with inflammatory bowel diseases (IBD), although its role in disease pathophysiology is unknown. We investigated the role of miR-155 in the acquisition and maintenance of an activated phenotype by intestinal myofibroblasts (IMF), a key cell population contributing to mucosal damage in IBD. IMF were isolated from colonic biopsies of healthy controls, ulcerative colitis (UC) and Crohn's disease (CD) patients. MiR-155 in IMF was quantified by quantitative reverse transcription-PCR in basal condition and following exposure to TNF-alpha, interleukin (IL)-1beta, lipopolysaccharide (LPS) or TGF-beta1. The effects of miR-155 mimic or inhibitor transfection on cytokine release and suppressor of cytokine signaling 1 (SOCS1) expression were assessed by enzyme-linked immunosorbent assay and western blot, respectively. Regulation of the target gene SOCS1 expression by miR-155 was assessed using luciferase reporter construct. We found that miR-155 was significantly upregulated in UC as compared with control- and CD-derived IMF. Moreover, TNF-alpha and LPS, but not TGF-beta1 and IL-1beta, significantly increased miR-155 expression in IMF. Ectopic expression of miR-155 in control IMF augmented cytokines release, whereas it downregulated SOCS1 expression. MiR-155 knockdown in UC-IMF reduced cytokine production and enhanced SOCS1 expression. Luciferase reporter assay demonstrated that miR-155 directly targets SOCS1. Moreover, silencing of SOCS1 in control IMF significantly increased IL-6 and IL-8 release. In all, our data suggest that inflammatory mediators induce miR-155 expression in IMF of patients with UC. By downregulating the expression of SOCS1, miR-155 wires IMF inflammatory phenotype.