Glioblastoma is the most common type of primary brain tumor in adults and is among the most lethal and least successfully treated solid tumors. Recently, research into the area of stem cells in brain tumors has gained momentum. However, due to the relatively new and novel hypothesis that a subpopulation of cancer cells in each malignancy has the potential for tumor initiation and repopulation, the data in this area of research are still in its infancy. This review article is aimed at attempting to bring together research carried out so far in order to build an understanding of glioblastoma stem cells (GSCs). Initially, we consider GSCs at a morphological and cellular level, and then discuss important cell markers, signaling pathways and genetics. Furthermore, we highlight the difficulties associated with what some of the evidence indicates and what collectively the studies contribute to further defining the interpretation of GSCs.
Sodium valproate is one of the most commonly used drugs to treat epilepsy. However, there is growing evidence that valproate can cause renal tubular injury in children, and there are increasing reports of valproate-induced Fanconi's syndrome where the renal tubules lose their ability to reabsorb electrolytes, urea, glucose and protein. In this review article we attempt to bring together all of the studies conducted to date on the effects of valproate on renal function in epileptic children. The research is generally considered in two themes; the first comprises studies which indicate subclinical tubular injury measured by renal enzymes such as N-acetyl-β-D-glucosaminidase (NAG), and the second comprises clinical reports where Fanconi's syndrome has occurred. This article goes on to analyse the current data and draws on recurring patterns to suggest that a specific subpopulation of severely disabled epileptic children may benefit hugely from the close monitoring of enzymes which are indicative of renal tubular injury, particularly NAG or in the very least periodical urinalysis.
Sporadic inclusion body myositis (IBM) is an acquired muscle disease and the most common idiopathic inflammatory myopathy over the age of 50. It is characterized by male predominance, with a prevalence rate between 1 and 71 cases per million, reaching 139 cases per million over the age of 50 globally. The diagnosis of IBM is based on clinical presentation and muscle biopsy findings. However, there is increasing evidence for the role of genetics and serum biomarkers in supporting a diagnosis. Antibodies against the cytosolic 59-nucleotidase 1A (Anti-CN1A), an enzyme catalyzing the conversion of adenosine monophosphate into adenosine and phosphate and is abundant in skeletal muscle, has been reported to be present in IBM and could be of crucial significance in the diagnosis of the disease. In this study, we investigated the diagnostic accuracy of anti-CN1A antibodies for sporadic IBM in comparison with other inflammatory myopathies, autoimmune disorders, motor neurone disease, using a hierarchical bivariate approach, and a Bayesian model taking into account the variable prevalence. The results of the present analysis show that anti-CN1A antibodies have moderate sensitivity, and despite having high specificity, they are not useful biomarkers for the diagnosis of IBM, polymyositis or dermatomyositis, other autoimmune conditions, or neuromuscular disorders. Neither the hierarchical bivariate nor the Bayesian analysis showed any significant usefulness of anti-CN1A antibodies in the diagnosis of IBM.
We present a case series of three patients with sodium valproate-induced Fanconi's syndrome, with ages ranging from 5 years to 12 years. The most important diagnostic features of this syndrome include hypophosphataemia, glycosuria and proteinuria, which are also noted in our series. Furthermore, also added is that clinical fractures representing an underlying osteopaenia may provide an opportunity for early intervention as it raises the suspicion of Fanconi's syndrome. Previous case reports suggest there is a subpopulation of individuals who are at risk of developing this condition. These individuals share similar characteristics, including being non-ambulatory, developmentally delayed and/or tube fed. Withdrawing sodium valproate therapy is the ultimate treatment for valproate-induced Fanconi's syndrome and from previous case series, normalised renal function occurs in approximately 6 months. Often, supplement support is also required for deranged electrolyte balance.
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