Background-Tryptophan catabolism via the kynurenine pathway, mediated by indoleamine 2,3-dioxygenase (IDO), is a mechanism involved in tumor immuno-resistance. Positron emission tomography (PET) with α-[ 11 C]methyl-L-tryptophan (AMT) can quantify transport and metabolism of tryptophan in infiltrating gliomas and glio-neuronal tumors. In the present study, we investigated whether increased tryptophan metabolism in brain tumors measured by PET is related to expression of IDO in resected brain tumor specimens.
Background and Purpose— The increasing demand and shortage of experts to evaluate and treat acute stroke patients has led to the development of remote communication tools to aid stroke management. We aimed to evaluate the JOIN App smartphone system—a low-cost tool for rapid clinical and neuroimaging data sharing to expedite decision-making in stroke. Methods— Consecutive acute ischemic stroke patients treated at a University Hospital in Brazil from December 2014 to December 2015 were evaluated. The analysis included all patients presenting with acute ischemic stroke who underwent initial evaluation by neurology residents followed by JOIN teleconsultation with a stroke neurologist on call for management decisions. An expert panel of stroke neurologists and neuroradiologists revised all cases using a standard Picture Archiving and Communication System imaging workstation within 24 hours and analyzed the decision made with remote assistance during the emergency setting. Results— A total of 720 stroke codes were evaluated with 442 acute ischemic stroke qualifying. Seventy-eight (18%) patients were treated with intravenous thrombolysis. The main reasons for tPA (tissue-type plasminogen activator) exclusion were symptom onset >4.5 hours (n=295; 67%) and hypodense middle cerebral artery territory area >1/3 (n=31; 7%). The agreement rates between Picture Archiving and Communication System versus JOIN-based thrombolysis decisions were 100% for the stroke (unblinded) and 99.3% for the neuroradiologist (blinded) experts. The use of the application resulted in a significant reduction in the door-to-needle times across the pre- versus postimplementation periods (median, 90 [interquartile range, 75–106] versus 63 [interquartile range, 61–117] minutes; P =0.03). The rates of 90-day excellent outcomes (modified Rankin Scale, 0–1) were 51.3%; 90-day mortality, 2.6%; and symptomatic intracranial hemorrhage, 3.8%. Conclusions— The JOIN smartphone system allows rapid sharing of clinical and imaging data to facilitate decisions for stroke treatment. The remote application-based decisions seem to be as accurate as the physical presence of stroke experts and might lead to faster times to treatment. This system represents an easily implementable low-cost telemedicine solution for centers that cannot afford the full-time presence of stroke specialists.
Tuberous sclerosis complex (TSC) is a multisystem genetic disorder caused by mutations in the TSC1 and TSC2 genes. Over 80% of TSC patients are affected by epilepsy, but the molecular events contributing to seizures in TSC are not well understood. Recent reports have demonstrated that the brain is enriched with microRNA activity, and they are critical in neural development and function. However, little is known about the role of microRNAs in TSC. Here, we report the characterization of aberrant microRNA activity in cortical tubers resected from 5 TSC patients surgically treated for medically intractable epilepsy. By comparing epileptogenic tubers with adjacent nontuber tissue, we identified a set of 4 coordinately overexpressed microRNAs (miRs 23a, 34a, 34b*, 532-5p). We used quantitative liquid chromatography-tandem mass spectrometry (LC-MS/MS) proteomic profiling to investigate the combined effect of the 4 microRNAs on target proteins. The proportion of repressed proteins among the predicted targets was significantly greater than in the overall proteome and was highly enriched for proteins involved in synaptic signal transmission. Among the combinatorial targets were TSC1, coding for the protein hamartin, and several epilepsy risk genes. We found decreased levels of hamartin in epileptogenic tubers and confirmed targeting of the TSC1 3' UTR by miRs-23a and 34a.
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