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To investigate the prevalence of urolithiasis in cystic fibrosis (CF) and to summarize the available clinical features within this unique population.
Studies reporting the prevalence of urolithiasis in CF patients were identified by a systematic search of the literature from inception to July 31, 2020 on three databases Ovid Medline, Ovid Embase, and Web of Science. Data was extracted on a pre-determined standardized form by two independent authors.
A total of 596 publications were retrieved and screened, 15 of which met the eligibility criteria. The publications were published between 1993 and 2019 and were all observational in design. There were a total of 2,982 patients with CF included in this review. The overall prevalence of stone formation in the CF population was 4.6% (137/2,982). The mean age of diagnosis was 25.1 ± 9.6 and ranged from 0.25 - 47. Ultrasound was the most common imaging modality for kidney stone diagnosis. There was no apparent sex difference, with a female to male ratio of 11. Stion. Given the heterogeneity of the literature for urolithiasis in CF, larger population-based studies reporting the epidemiology, clinical features, and management strategies are required to further our understanding of urolithiasis in CF.Significance As the central metabolic organ, the liver is exposed to a variety of potentially cytotoxic, proinflammatory, profibrotic, and carcinogenic stimuli. To protect the organism from these deleterious effects, the liver has evolved a number of defense systems, which include antioxidant substrates and enzymes, anti-inflammatory tools, enzymatic biotransformation systems, and metabolic pathways. Recent Advances One of the pivotal systems that evolved during phylogenesis was the heme catabolic pathway. Comprising the important enzymes heme oxygenase and biliverdin reductase, this complex pathway has a number of key functions including enzymatic activities, but also cell signaling, and DNA transcription. It further generates two important bile pigments, biliverdin and bilirubin, as well as the gaseous molecule carbon monoxide. These heme degradation products have potent antioxidant, immunosuppressive, and cytoprotective effects. Recent data suggest that the pathway participates in the regulation of metabolic and hormonal processes implicated in the pathogenesis of hepatic and other diseases. Critical Issues This review discusses the impact of the heme catabolic pathway on major liver diseases, with particular focus on the involvement of cellular targeting and signaling in the pathogenesis of these conditions. Future Directions To utilize the biological consequences of the heme catabolic pathway, several unique therapeutic strategies have been developed. Research indicates that pharmaceutical, nutraceutical, and lifestyle modifications positively affect the pathway, delivering potentially long-term clinical benefits. Oltipraz clinical trial However, further well-designed studies are needed to confirm the clinical benefits of these approaches.
We sought to examine the intrarenal fluid and tissue temperature during dusting and fragmentation with the Thulium fiber laser (TFL) in an in vivo porcine kidney.
In two pigs, temperature was continuously measured within the upper, middle, and lower calyces and at the tip of the ureteroscope. Four experimental protocols were performed dual lumen ureteroscope with both warmed (37°C) and room temperature (20-22ºC) irrigation and single lumen ureteroscope with warmed and room temperature irrigation. In each pig, one kidney had a 14F ureteral access sheath (UAS), other kidney had no UAS. A 200µm TFL was fired at three settings dusting (0.5J, 80Hz, 40W) with continuous activation for 5 minutes or until a temperature reached 44⁰C; low power (1J, 10Hz, 10W) and high-power fragmentation (1.5J, 20Hz, 30W). For fragmentation, the laser was activated for 10 seconds with a 2 second intermission for 1 minute.
In the absence of an UAS, in all but one circumstance, temperatures exceeded 44ºC at all settings with the uperatures that could result in urothelial tissue injury.Background Near-infrared autofluorescence (NIRAF) imaging is known to reduce the incidence of post-thyroidectomy hypocalcemia. However, there are no studies on how much NIRAF imaging affects the serum parathyroid hormone (PTH) level after surgery. We investigated the changes of the serum PTH level and ionized calcium (iCa.) in patients undergoing total thyroidectomy with central neck dissection (CND). Materials and Methods This retrospective study with historical control enrolled 542 patients who underwent total thyroidectomy with CND. Patients were divided into two groups the NIRAF group (261 patients) and the control group (281 patients). PTH and iCa. levels were measured at the hospital stay, 1, 3, and 6 months after surgery. In addition, the number of identified parathyroid glands (PGs), autotransplanted PGs, and the inadvertent resection rate of PGs was evaluated. Results The incidence of postoperative hypoparathyroidism (PTH less then 15 pg/mL) was significantly lower in the NIRAF group during the hospitalization (88 patients 33.7% vs. 131 patients 46.6%; p = 0.002) and at 1 month postoperatively (23 patients 8.8% vs. 53 patients 18.9%; p = 0.001). There was no difference in the permanent hypoparathyroidism rate (6 months after surgery) between the NIRAF group and the control group (4.2% vs. 4.6%; p = 0.816). There was no difference in the incidence of hypocalcemia (iCa. less then 1.09 mmol/L) (during hospitalization 6.5% vs. 10.0%; 1 month 2.3% vs. 2.5%; 3 months 0.8% vs. 0.7%; 6 months after surgery 1.1% vs. 1.1%) between the two groups. The number of inadvertently resected PGs was significantly lower in the NIRAF group (186.9% vs. 3612.8%; p = 0.021). Conclusions These results suggest that NIRAF imaging may reduce temporary hypoparathyroidism and the risk of inadvertent resection of PGs in patients undergoing total thyroidectomy with CND.Tissue engineering in reconstructive surgery seeks to generate bioartificial tissue substitutes. The arteriovenous (AV) loop allows the generation of axially vascularized tissue constructs. Cellular mechanisms of this vascularization process are largely unclear. In this study, we developed two different chamber models for intravital microscopy and imaging of the AV loop in the rat. Multiple design variations were implanted and the stability of the chamber and AV loop patency was tested in vivo. Our novel chamber facilitates repetitive observation of the AV loop using fluorescence-enhanced intravital microscopy. This technique can be used for daily evaluation of leukocyte-endothelial cell interactions, vascularization, and tissue formation in the AV loop model on 14 consecutive days. Therefore, our newly developed model for intravital microscopy will provide better understanding of cellular and molecular processes in tissue engineering in the AV loop. Moreover, it supports initiation of the novel approaches for therapeutic applications. Impact statement In the Arteriovenous (AV) loop, axially vascularized tissue can be generated and modified using different tissue engineering approaches. Cellular mechanisms of this vascularization process are largely unclear. We managed to develop an intravital microscopy model for long-term observation of intravascular and perivascular events in the AV loop. Leukocyte-endothelial cell interactions, vascularization, and tissue formation in the AV loop can now be evaluated on a day-to-day basis. This will provide better understanding of cellular and molecular processes happening during tissue engineering within the AV loop.This study is the first to examine cognitive outcomes after pediatric mild TBI using the National Institutes of Health Toolbox Cognition Battery (NIHTB-CB), a computerized cognitive test battery. The NIHTB-CB includes two complex measures of attention and executive function that allow differentiation of accuracy and response speed. We compared performance on the NIHTB-CB among children 8-16 years of age with mild TBI (n = 143) versus children with orthopedic injuries (OIs; n = 74) recruited in emergency departments and followed for 6 months post-injury. Mixed-model analyses showed that the mild TBI group showed significantly lower Fluid Cognition composite scores than the OI group at 10 days (group intercept, p = 0.018); the magnitude of group differences declined modestly over time (group × time interaction, p = 0.055). Effect sizes were d = 0.34 at 10 days post-injury, d = 0.27 at 3 months, and d = 0.10 at 6 months. No significant effects of group or time were found for the Crystallized Cognition composite. Analyses of Fluid Cognition subtests indicated that children with mild TBI displayed deficits for as long as 3 months on measures of attention and executive function (e.g., cognitive flexibility, inhibitory control), but not on measures of explicit memory, working memory, or processing speed. The poorer performance of the mild TBI group on measures of attention and executive function was attributable largely to slowed reaction time, not decreased accuracy. The findings suggest that children with mild TBI demonstrate persistent deficits in fluid cognition that are most apparent on tasks that combine demands for both speed and executive function.Aims This study aims to explore the efficacy of punicalagin (PG) on diabetic cardiomyopathy (DCM), with a specific focus on the mechanisms underlying the effects of PG on mitochondrial fusion/fission dynamics. Results Cardiac structural and functional abnormalities were ameliorated in diabetic rats receiving PG administration as evidenced by increased ejection fraction, and attenuated myocardial fibrosis and hypertrophy. PG enhanced mitochondrial function and inhibited mitochondria-derived oxidative stress by promoting Opa1-mediated mitochondrial fusion. The benefits of PG could be abrogated by knockdown of Opa1 in vivo and in vitro. Inhibitor screening and chromatin immunoprecipitation analysis showed that Stat3 directly regulated the transcriptional expression of Opa1 by binding to its promoter and was responsible for PG-induced Opa1-mediated mitochondrial fusion. Moreover, pharmmapper screening and molecular docking studies revealed that PG embedded into the activity pocket of PTP1B and inhibited the activity of PTP1B. Overexpression of PTP1B blocked the promoting effect of PG on Stat3 phosphorylation and Opa1-mediated mitochondrial fusion, whereas knockdown of PTP1B mimicked the benefits of PG in high-glucose-treated cardiomyocytes. Innovation Our study is the first to identify PG as a novel mitochondrial fusion promoter against hyperglycemia-induced mitochondrial oxidative injury and cardiomyopathy by upregulating Opa1 via regulating PTP1B-Stat3 pathway. Conclusion PG protects against DCM by promoting Opa1-mediated mitochondrial fusion, a process in which PG interacts with PTP1B and inhibits its activity, which in turn increases Stat3 phosphorylation and then enhances the transcriptional expression of Opa1. These results suggest that PG might be a promising new therapeutic approach against diabetic cardiac complication.
This study aimed to examine neighborhood effects on the physical and socioemotional health of children from immigrant families, after controlling for parents' demographic characteristics, socioeconomic status, acculturation, and health care issues.
Pooled cross-sectional data were merged with community profiles.
The United States in 2013, 2014, and 2015.
10,399 children from immigrant families in the 2013-2015 National Health Interview Surveys and the U.S. Census Data.
Both objective and subjective measures of neighborhood environments were assessed, including neighborhood physical disorder, socioeconomic status, demographic composition, community resources, and social trust.
Descriptive statistics, logistic regression models.
About half of the sampled children were male (51%); 68% were white; 56% were of Hispanic; and 34% were school-aged. Three neighborhood factors-neighborhood trust, area-level poverty rate, and the presence of primary care physician-were identified as significant predictors for child health outcomes.
Homepage: https://www.selleckchem.com/products/oltipraz.html
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