Patient-perceived barriers to surgical treatment of cleft lip and palate in Brazil: A multi-region study.

INTRODUCTION: Many patients worldwide are unable to access timely primary repair of cleft lip and palate. The aim of this study was to assess patient-perceived barriers to accessing timely cleft lip and palate repair across Brazil. METHODS: A 29-item questionnaire was applied to patients undergoing surgery for cleft lip and/or palate across five contrasting sites in Brazil from February 2016 to November 2017. Differences in patient timelines, demographics, and patient-reported barriers were compared by region. A multivariate logistic regression was used to determine predictors of delayed care. RESULTS: Of 181 patients, 42% of patients received timely primary surgical repair. The age of the patient at the interview was 82 months (standard deviation [SD] 107) and 52% were male. The majority of delays occurred between diagnosis and primary surgical repair. The mean number of barriers to accessing timely surgical care cited by each patient was 3.77. The most common barrier was perceived "lack of hospitals that provided the surgery in my area" (48% (n = 86)). Univariate logistic regression showed increased odds of receiving late care in the state of Amazonas (odds ratio [OR] 2.91; 95% confidence interval [CI] 1.07-7.96; P = 0.037) or Para (OR 4.46; 95% CI 1.09-19.70; P = 0.037). Multivariate logistic regression determined predictors of delayed care to be female sex (OR = 2.05; 95% CI 1.05-3.99; P = 0.035) and perceived poor availability of care (OR = 0.045; 95% CI 1.02-4.37; P = 0.045). CONCLUSION: The majority of patients in Brazil are not receiving timely primary repair of their clefts. Improvements in the coordination of care, patient education and patient empowerment are required.

Effects of remote ischemic preconditioning and topical hypothermia in renal ischemia-reperfusion injury in rats.

PURPOSE: To evaluate whether combining hypothermia and remote ischemic preconditioning (RIPC) results in protection from ischemia-reperfusion (IR). METHODS: Thirty-two Wistar rats underwent right nephrectomy and were randomly assigned to four experimental protocols on the left kidney: warm ischemia (group 1), cold ischemia (group 2), RIPC followed by warm ischemia (group 3), and RIPC followed by cold ischemia (group 4). After 240 minutes of reperfusion, histological changes in the left kidney, as well as lipid peroxidation and antioxidant enzyme activity, were analyzed. The right kidney was used as the control. Serum creatinine was collected before and after the procedures. RESULTS: RIPC combined with hypothermia during IR experiments revealed no differences on interventional groups regarding histological changes (p=0.722). Oxidative stress showed no significant variations among the groups. Lower serum creatinine at the end of the procedure was seen in animals exposed to hypothermia (p<0.001). CONCLUSIONS: Combination of RIPC and local hypothermia provides no renal protection in IR injury. Hypothermia preserves renal function during ischemic events. Furthermore, RIPC followed by warm IR did not show benefits compared to warm IR alone or controls in our experimental protocol.

Effects of remote ischemic preconditioning and topical hypothermia in renal ischemia-reperfusion injury in rats

Abstract Purpose: To evaluate whether combining hypothermia and remote ischemic preconditioning (RIPC) results in protection from ischemia-reperfusion (IR). Methods: Thirty-two Wistar rats underwent right nephrectomy and were randomly assigned to four experimental protocols on the left kidney: warm ischemia (group 1), cold ischemia (group 2), RIPC followed by warm ischemia (group 3), and RIPC followed by cold ischemia (group 4). After 240 minutes of reperfusion, histological changes in the left kidney, as well as lipid peroxidation and antioxidant enzyme activity, were analyzed. The right kidney was used as the control. Serum creatinine was collected before and after the procedures. Results: RIPC combined with hypothermia during IR experiments revealed no differences on interventional groups regarding histological changes (p=0.722). Oxidative stress showed no significant variations among the groups. Lower serum creatinine at the end of the procedure was seen in animals exposed to hypothermia (p<0.001). Conclusions: Combination of RIPC and local hypothermia provides no renal protection in IR injury. Hypothermia preserves renal function during ischemic events. Furthermore, RIPC followed by warm IR did not show benefits compared to warm IR alone or controls in our experimental protocol.

Increases of kinin B1 and B2 receptors binding sites after brain infusion of amyloid-beta 1-40 peptide in rats.

Although numerous inflammation pathways have been implicated in Alzheimer's disease, the involvement of the kallikrein-kinin system is still under investigation. We anatomically localized and quantified the density of kinin B(1) and B(2) receptors binding sites in the rat brain after the infusion of amyloid-beta (Abeta) peptide in the right lateral brain ventricle for 5 weeks. The conditioned avoidance test showed a significant reduction of memory consolidation in rats infused with Abeta (68.6+/-20.9%, P<0.05) when compared to control group (90.8+/-4.1%; infused with vehicle). Autoradiographic studies performed in brain samples of both groups using [(125)I]HPP-[des-Arg(10)]-Hoe-140 (150pM, 90min, 25 degrees C) showed a significant increase in density of B(1) receptor binding sites in the ventral hippocampal commissure (1.23+/-0.07fmol/mg), fimbria (1.31+/-0.05fmol/mg), CA1 and CA3 hippocampal areas (1.05+/-0.03 and 1.24+/-0.02fmol/mg, respectively), habenular nuclei (1.30+/-0.04fmol/mg), optical tract (1.30+/-0.05fmol/mg) and internal capsule (1.26+/-0.05fmol/mg) in Abeta group. For B(2) receptors ([(125)I]HPP-Hoe-140, 200pM, 90min, 25 degrees C), a significant increase in density of binding sites was observed in optical tract (2.04+/-0.08fmol/mg), basal nucleus of Meynert (1.84+/-0.18fmol/mg), lateral septal nucleus - dorsal and intermediary portions (1.66+/-0.29fmol/mg), internal capsule (1.74+/-0.19fmol/mg) and habenular nuclei (1.68+/-0.11fmol/mg). In control group, none of these nuclei showed [(125)I]HPP-Hoe-140 labeling. This significant increase in densities of kinin B(1) and B(2) receptors in animals submitted to Abeta infusion was observed mainly in brain regions related to cognitive behavior, suggesting the involvement of the kallikrein-kinin system in Alzheimer's disease in vivo.