Vesterbuur3324

This project promotes a reduction incarbon footprint, a reduction in water waste, a sustainable organic food source,may lead to income generation, and provides a shared purpose and sense of pride among staff and dialysis patients.

Encompassing "environmental protection" practices into a hemodialysis unit can be done with relatively simple and practical steps.

Encompassing "environmental protection" practices into a hemodialysis unit can be done with relatively simple and practical steps.This paper aims at assessing and exploring socioeconomic inequalities in tobacco use in Kenya. Using the theory of fundamental causes, and concentration index, we investigate the determinants of tobacco use, and whether it disproportionately affects the poor. learn more All data used in this study emanated from the 2014 Global Adult Tobacco Survey implemented in Kenya on a nationally representative sample of men and women aged 15 years and older. Our results suggest a link between tobacco use and socioeconomic inequality. Overall, poorer households are more affected by tobacco use than richer households. This socioeconomic inequality is more evident among men and households living in urban areas. The decomposition of the concentration index indicates that the overall socioeconomic inequality for current tobacco smokers is explained by 69.11% of household wealth. To reduce the prevalence rate of smoking in Kenya, policymakers could design and implement tobacco control programs through the equity lens. Community health workers could be used to promote non-smoking behaviors among the poor.Rising drug spending has led to increased calls to curtail drug costs. However, it is unclear where to target policy solutions. We estimated excess returns (the extent to which a firm's profits are higher than expected given the risk associated with their investments) for manufacturers and middlemen in the pharmaceutical supply chain to determine who is making excessive profits. Excess returns were calculated as the difference between return on invested capital and the expected returns given risk, which is known as the weighted average cost of capital. We compared excess returns for manufacturers and middlemen to the average for S&P 500 companies. We find that both manufacturers and middlemen have higher excess returns in 2013-2018 compared with the S&P 500. However, if we treat research and development (R&D) as an investment rather than an expense, we find that excess returns for pharmaceutical manufacturers are lower than the S&P 500 (1.7% vs. 3.6%), but biotech manufacturers (9.6%), wholesalers (8.1%), and insurers/PBM/retailers (5.9%) continue to have significantly higher excess returns compared to the S&P 500. Our findings suggest public policies that promote competition in all areas of the pharmaceutical supply chain are important avenues for curtailing drug spending.Transient abnormal myelopoiesis (TAM) is a unique clonal myeloproliferation characterized by immature megakaryoblasts that occurs in 5-10% of neonates with Down syndrome (DS). Although TAM regresses spontaneously in most patients, approximately 20% of TAM cases result in early death, and approximately 20% of survivors develop acute megakaryoblastic leukemia (AMKL). We retrospectively reviewed records of 35 DS patients with TAM to determine the correlation between clinical characteristics and blast percentage. Thirteen of the 35 patients were classified as low blast percentage TAM (LBP-TAM), defined as TAM with a peak peripheral blast percentage ≤ 10%. Although no patient with LBP-TAM experienced systemic edema, disseminated intravascular coagulation, or early death, eight patients had elevated direct bilirubin levels (> 2 mg/dl) and one developed AMKL. All patients with LBP-TAM had serum markers of liver fibrosis that exceeded the normal limits, and two patients underwent liver biopsy to clarify the etiology of pathological jaundice. Taken together, our results suggest that patients with LBP-TAM may be at risk of liver fibrosis and liver failure, similarly to patients with classical TAM. Although these patients generally have a good prognosis, they should be carefully monitored for potential development of liver disease and leukemia.Improving exercise capacity during adolescence impacts positively on cognitive and motor functions. However, the neural mechanisms contributing to enhance physical performance during this sensitive period remain poorly understood. Such knowledge could help to optimize exercise programs and promote a healthy physical and cognitive development in youth athletes. The central dopamine system is of great interest because of its role in regulating motor behavior through the activation of D1 and D2 receptors. Thus, the aim of the present study is to determine whether D1 or D2 receptor signaling contributes to modulate the exercise capacity during adolescence and if this modulation takes place through the striatum. To test this, we used a rodent model of forced running wheel that we implemented recently to assess the exercise capacity. Briefly, rats were exposed to an 8-day period of habituation in the running wheel before assessing their locomotor performance in response to an incremental exercise test, in which the speed was gradually increased until exhaustion. We found that systemic administration of D1-like (SCH23390) and/or D2-like (raclopride) receptor antagonists prior to the incremental test reduced the duration of forced running in a dose-dependent manner. Similarly, locomotor activity in the open field was decreased by the dopamine antagonists. Interestingly, this was not the case following intrastriatal infusion of an effective dose of SCH23390, which decreased motor performance during the incremental test without disrupting the behavioral response in the open field. Surprisingly, intrastriatal delivery of raclopride failed to impact the duration of forced running. Altogether, these results indicate that the level of locomotor response to incremental loads of forced running in adolescent rats is dopamine dependent and mechanistically linked to the activation of striatal D1 and extra-striatal D2 receptors.Astrocytes are the first responders to noxious stimuli by undergoing cellular and functional transition referred as reactive gliosis. Every acute or chronic disorder is accompanied by reactive gliosis, which could be categorized as detrimental (A1) of beneficial (A2) for nervous tissue. Another signature of pathological astrocyte activation is disturbed Ca2+ homeostasis, a common denominator of neurodegenerative diseases. Deregulation of Ca+ signaling further contributes to production of pro-inflammatory cytokines and reactive oxygen species. Trimethyltin (TMT) intoxication is a widely used model of hippocampal degeneration, sharing behavioral and molecular hallmarks of Alzheimer's disease (AD), thus representing a useful model of AD-like pathology. However, the role of astrocyte in the etiopathology of TMT-induced degeneration as well as in AD is not fully understood. In an effort to elucidate the role of astrocytes in such pathological processes, we examined in vitro effects of TMT on primary cortical astrocytes. The application of a range of TMT concentrations (5, 10, 50, and 100 μM) revealed changes in [Ca2+]i in a dose-dependent manner. Specifically, TMT-induced Ca2+ transients were due to L-type voltage-gated calcium channels (VGCC). Additionally, TMT induced mitochondrial depolarization independent of extracellular Ca2+ and disturbed antioxidative defense of astrocyte in several time points (4, 6, and 24 h) after 10 μM TMT intoxication, inducing oxidative and nitrosative stress. Chronic exposure (24 h) to 10 μM TMT induced strong upregulation of main pro-inflammatory factors, components of signaling pathways in astrocyte activation, A1 markers, and VGCC. Taken together, our results provide an insight into cellular and molecular events of astrocyte activation in chronic neuroinflammation.Spinocerebellar ataxia type 1 (SCA1) is a fatal neurodegenerative disease caused by an abnormal expansion of CAG repeats in the Ataxin1 (ATXN1) gene. SCA1 is characterized by motor deficits, cerebellar neurodegeneration, and gliosis and gene expression changes. Expression of brain-derived neurotrophic factor (BDNF), growth factor important for the survival and function of cerebellar neurons, is decreased in ATXN1[82Q] mice, the Purkinje neuron specific transgenic mouse model of SCA1. As this decrease in BDNF expression may contribute to cerebellar neurodegeneration, we tested whether delivery of extrinsic human BDNF via osmotic ALZET pumps has a beneficial effect on disease severity in this mouse model of SCA1. Additionally, to test the effects of BDNF on established and progressing cerebellar pathogenesis and motor deficits, we delivered BDNF post-symptomatically. We have found that post-symptomatic delivery of extrinsic BDNF ameliorated motor deficits and cerebellar pathology (i.e., dendritic atrophy of Purkinje cells, and astrogliosis) indicating therapeutic potential of BDNF even after the onset of symptoms in SCA1. However, BDNF did not alter Purkinje cell gene expression changes indicating that certain aspects of disease pathogenesis cannot be ameliorated/slowed down with BDNF and that combinational therapies may be needed.Condyloma acuminatum, in the form of genital warts, usually results from an infection by human papillomavirus, one of the most common causes of sexually transmitted diseases. It develops after an incubation period of 3 weeks to 8 months after infection; flat lesions are significantly rare. Condyloma acuminatum is prevalent in the genitals, particularly in the anus of immunodeficient patients. This also occurs in women during menstrual period and pregnancy. Although a common treatment option for rectal and anal lesions, surgical resection is highly invasive and results in a high rate of recurrence. Recently, endoscopic submucosal dissection has been performed for anorectal lesions, but data on its long-term follow-up are not available. We report the case of an immunocompromised patient due to pregnancy who remained recurrence-free 27 months after en-bloc resection by endoscopic submucosal dissection, with adequate visualisation of the flat lesion's safety margin, combined with magnifying narrow-band imaging.Inflammatory bowel diseases (IBD) are chronic and progressive conditions that can increase the risk of thromboembolism, including that of portal vein thrombosis (PVT). Overall, PVT is a serious complication with a significant associated mortality. PVTs are exclusively described in cases with confirmed IBD diagnosis. This report highlights a case of PVT as an initial manifestation of Crohn's disease.Aberrant right hepatic arteries are sometimes involved in pancreatic head tumors or accidentally damaged during surgical procedures, which could result in postoperative complications. The risk of such injury has been discussed in patients undergoing pancreatoduodenectomy; however, no reports describe the influence of this anomaly in distal pancreatectomy. We report a patient with pancreatic body cancer with an accessory right hepatic artery following a very unique route. A 77-year-old man was referred to our hospital for the treatment of pancreatic cancer. Computed tomography revealed an anomaly in the hepatic artery, with an accessory right hepatic artery encased in the extensive tumor, which also involved the stomach, left gastric artery, and portal vein. Curative resection was achieved by distal pancreatectomy with wedge resection of the stomach and portal vein reconstruction. Both the accessory right hepatic artery and the left gastric artery were sacrificed after confirming intrahepatic arterial flow by intraoperative Doppler ultrasonography.