Background: Cerebral radionecrosis, a subacute or late effect of radiotherapy, can be debilitating and difficult to treat. Steroids can reduce symptoms, but have significant long-term side effects. Bevacizumab has been shown to reduce edema and other radiologic features associated with radionecrosis and improve patient symptoms. We report our experience using bevacizumab for cerebral radionecrosis. Methods: We retrospectively reviewed the charts of all patients treated at our institution with bevacizumab for non-glioma-associated cerebral radionecrosis. We recorded change in symptoms, change in steroids, change in performance status, time to tumor progression, and time to death. We delineated the volume of necrosis pre- and post-bevacizumab on T1-post-gadolinium and fluid-attenuated inversion recovery (FLAIR) MRI scans. Results: We identified 15 patients, 8 with brain metastases, 6 with meningioma, and 1 with nasopharyngeal carcinoma. Most received four doses of bevacizumab, 7.5 mg/kg q 3 weeks × 4 doses. Neuroimaging demonstrated a reduced T1 gadolinium-enhancing volume and edema in 14/15 patients (the average reduction in T1-post-gadolinium volume was 3.0 cm3, and average reduction in FLAIR volume was 27.9 cm3). There was no appreciable change in patient performance status. Steroid doses decreased in five of nine patients. There was a high rate (26%) of adverse events, including pulmonary embolism, stroke, and wound dehiscence. The median progression-free survival was 6.5 months. Conclusion: Although bevacizumab is commonly prescribed for cerebral radionecrosis, in our retrospective cohort, the clinical benefits were modest and there was significant toxicity.

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IntroductionMicrochimeric cells have been studied for over a decade, with conflicting reports on their presence and role in autoimmune and other inflammatory diseases. To determine whether microchimeric cells were pathogenic or mediating tissue repair in inflammatory myopathies, we phenotyped and quantified microchimeric cells in juvenile idiopathic inflammatory myopathies (JIIM), muscular dystrophy (MD), and noninflammatory control muscle tissues.MethodFluorescence immunophenotyping for infiltrating cells with sequential fluorescence in situ hybridization was performed on muscle biopsies from ten patients with JIIM, nine with MD and ten controls.ResultsMicrochimeric cells were significantly increased in MD muscle (0.079 ± 0.024 microchimeric cells/mm2 tissue) compared to controls (0.019 ± 0.007 cells/mm2 tissue, p = 0.01), but not elevated in JIIM muscle (0.043 ± 0.015 cells/mm2). Significantly more CD4+ and CD8+ microchimeric cells were in the muscle of patients with MD compared with controls (mean 0.053 ± 0.020/mm2 versus 0 ± 0/mm2p = 0.003 and 0.043 ± 0.023/mm2 versus 0 ± 0/mm2p = 0.025, respectively). No differences in microchimeric cells between JIIM, MD, and noninflammatory controls were found for CD3+, Class II+, CD25+, CD45RA+, and CD123+ phenotypes, and no microchimeric cells were detected in CD20, CD83, or CD45RO populations. The locations of microchimeric cells were similar in all three conditions, with MD muscle having more microchimeric cells in perimysial regions than controls, and JIIM having fewer microchimeric muscle nuclei than MD. Microchimeric inflammatory cells were found, in most cases, at significantly lower proportions than autologous cells of the same phenotype.ConclusionsMicrochimeric cells are not specific to autoimmune disease, and may not be important in muscle inflammation or tissue repair in JIIM.

was expected to contain information for at least partial phylogenetic characterization that was useful to subclassify clinically important bacterial species (13 ). The variability of this interprimer region was not revealed clearly in conventional PCR because of the low-resolution capability of agarose gel electrophoresis. However, the intrinsic variability of real-time PCR products could be disclosed by high-resolution melting curve analysis, where T m could serve as a measure of DNA length and nucleotide composition (Table 1).We identified four subgroups of bacteria each with distinct T m s in a limited range. Similar to any broad-range PCR detection of bacterial DNA, the assay could not determine the viability of the organism, particularly during the treatment with antibiotics, or identify the bacterial species. However, because it detects a broad range of bacteria usually present in clinical specimens, this assay may complement the time-consuming blood culture test and supply timely information needed by physicians to determine whether bacterial infection has occurred and to plan treatment regimens. The unique feature of the method presented in this study (the classification information disclosed by the melting peak profiles) could be used in the design of multiplex PCR to confirm the identity of infectious bacterial species in a clinical or laboratory setting.In summary, the decontamination procedure and the broad-range real-time PCR method allow rapid detection, quantification, and classification of several clinically important bacteria and may facilitate rapid detection of local and systemic infection. Our laboratory and others have demonstrated the presence of microchimeric cells in the peripheral blood of nonpregnant patients with systemic sclerosis (SSc) (1-4 ). In addition, we have demonstrated the presence of ma- Detection of Microchimeric Cells in the Peripheral

Diffuse infiltrating gliomas are the most common malignant brain tumors in adults. The 2021 World Health Organization classification for central nervous system tumors (CNS5 WHO) has significantly altered the rules for classification and grading of diffuse gliomas. Clinicians, including neurology residents and neurologists, will have to consider the changes that include the introduction of new tumor types, allotting established tumor types to other groups, and substituting previously essential morphological features for additional molecular markers. For example, in the current classification, glioblastoma is defined as isocitrate dehydrogenase (IDH)-wildtype, grade 4. Whereas, a grade 4 IDH-mutated astrocytic glioma is referred to as astrocytoma, IDH-mutated, grade 4. Additionally, potential targeted treatments, based on the underlying molecular alterations, have become therapeutic options for diffuse gliomas. For clinicians, it is important to know the rationale for why these options are only available for specific tumors. Due to the emphasis of molecular markers in the CNS5 WHO classification, interpretation of a pathology report and understanding of its clinical implications can be challenging. This review describes the most important molecular alterations in glioma, summarizes the recent changes in the CNS5 WHO classification for glioma, and presents a stepwise approach for trainees and neurologist to decipher a glioma pathology report.