Perls Prussian blue stain (PPB) for hemosiderin, a marker of vascular injury is often employed as an adjunct in the diagnosis of vasculitic neuropathies. However, inflammation/vascular injury is also seen in leprosy, immune mediated, paraproteinemic, diabetic neuropathies, etc. The frequency of detection of hemosiderin in these neuropathies and its utility in diagnosis of vasculitis has not been explored. We evaluated 208 peripheral nerve biopsies for hemosiderin deposits by PPB stain in vasculitis (78) and compared with inflammatory/immune neuropathies [leprous neuritis-32, chronic inflammatory demyelinating polyneuropathy (CIDP)-15, paraproteinemic neuropathies (POEMS)-12, diabetic neuropathy-37] and nonimmune neuropathies [Charcot-Marie-Tooth (CMT) disease-15, vitamin B12 deficiency-7, and ischemic neuropathy in aged-12)]. Hemosiderin deposits were most frequent in vasculitis (48.72%) [59.2% in systemic; 43.1% in nonsystemic vasculitides] and enhanced the sensitivity of diagnosis in "probable" vasculosis of vasculitic neuropathy with high specificity but low sensitivity. Telomerase reverse transcriptase promoter (pTERT) mutation is a dominant altered telomere maintenance mechanism in primary glioblastomas (GBMs). The aim of this study was to correlate pTERT mutations with clinico-histological features and other molecular markers (p53 protein-expression, ATRX protein-expression, IDH mutations, EGFR gene amplification and MGMT methylation) in adult GBMs. Evaluated for histological patterns, p53 and ATRX protein expression by immunohistochemistry (IHC), IDH mutations by IHC followed by sequencing in IHC negative cases, EGFR gene amplification by fluorescence in situ hybridization, MGMT promoter methylation by methylation-specific PCR and pTERT mutation by sequencing. A total of 155 adult supratentorial GBMs [age-range 20-80 years] formed study cohort. Selleckchem NSC 74859 15.6% were IDH1R132 mutated, none were IDH2R172 mutated and 27% were EGFR amplified. 43% were MGMT methylated and were more common with IDH-mutation (mIDH) than EGFR amplification. 90% of mIDH (but no EGFR amplified) cases showed ATRX-loss. 43.5% were pTERT mutated (C228T was the commonest type) and were mutually exclusive with ATRX-loss. 14% of mIDH and 42% of EGFR amplified cases showed pTERT mutation, the latter was more commonly pMGMT unmethylated (63.6%). 43.5% of the GBMs showed pTERT mutation (C228T was commonest; 72%). pTERT mutations were mutually exclusive with ATRX protein loss, more commonly associated with IDH wild type and EGFR amplified GBMs.43.5% of the GBMs showed pTERT mutation (C228T was commonest; 72%). pTERT mutations were mutually exclusive with ATRX protein loss, more commonly associated with IDH wild type and EGFR amplified GBMs. Preliminary study of magnetic resonance (MR) diffusion kurtosis imaging (DKI) assessing the pathological glial fibrillary acidic protein (GFAP), TopoIIα, and O 6-methylguanine-DNA methyltransferase (MGMT) expression in astrocytomas. This study was approved by the local ethics committee, and informed consent was obtained from all participants. Sixty-six cases with pathologically proven astrocytomas were enrolled in this study; of which, 34 were high grade and remaining 32 were low grade. They patients underwent conventional MRI head scan, DKI scan, and enhanced scan under the same conditions. Fractional anisotropy (FA) and mean kurtosis (MK) calculated from DKI, as well as GFAP, TopoIIα, and MGMT expression level were compared prospectively between high and low-grade astrocytomas. Spearman rank correlation analysis was used for comparing values of DKI and GFAP, TopoIIα, and MGMT expression level in the two groups. The MK values were significantly higher in high-grade astrocytomas than those in low-grade y, invasion and metastasis, and can guide individual treatment.MK, the DKI parameter values of astrocytomas, was significantly correlated to the expression of GFAP and TopoIIα. To a certain extent, applying DKI may provide the biological behavior of tumor cell differentiation, proliferation activity, invasion and metastasis, and can guide individual treatment. A host of microRNAs have been reported to suppress tumor growth, invasion, and metastasis and play roles in neurodegeneration disorders. Moreover, microRNA changes are found in the peripheral blood, cerebrospinal fluid (CSF), and brain tissues of central nervous system diseases, including glioma, Alzheimer's disease (AD), Parkinson's disease (PD), multiple sclerosis, and depression. Compared with other body fluids, CSF can reflect the brain pathological processes more accurately. To understand whether microRNA expression may be misregulated in patients with PD, and further discover potential diagnostic biomarkers and promising therapeutic targets for PD. Here, through real-time reverse-transcription polymerase chain reaction (RT-PCR), we compared CSF microRNA from 15 PD patients, 11 AD patients, and 16 controls with other neurologic disorders, such as encephalitis and Guillain-Barre syndrome. Finally, we identified hsa-miR-626 changes in the CSF of PD patients. The mean expression level of hsa-miR-626 was significantly reduced in the CSF of PD patients compared with AD patients and controls. Our approach provides a preliminary research for identifying biomarkers in the CSF that could be used for the detection, diagnosis, and monitoring of PD.Our approach provides a preliminary research for identifying biomarkers in the CSF that could be used for the detection, diagnosis, and monitoring of PD. Information regarding the clinical presentation and outcome of Guillain-Barré Syndrome (GBS) in adults from Latin America is limited. To identify clinical characteristics and short-term outcome predictors in adult Mexican patients with GBS. We included adult patients with clinical and electrophysiological data with confirmed GBS, admitted to a tertiary hospital in Western Mexico, from January 2002 to February 2011. A good outcome at hospital discharge was considered if patients had a Hughes score of 0-2 and at 3 and 6 months, a Hughes score of 0-1. A total of 115 patients were analyzed (68% men, mean age 44 years old, range 18-84). Previous infection occurred in 63% of cases. Descendent pattern of weakness was observed in 40 (35%) patients. GBS subtypes were acute motor axonal neuropathy in 31%, acute inflammatory demyelinating polyneuropathy in 29%, sensory axonal neuropathy (AMSAN) in 18%, and equivocal in 22%. A total of 73 (63%) patients received induction therapy 50 (68%) received plasmapheresis and 13 (18%) received intravenous immunoglobulin (IVIG).