Amplitude Changes of the Electrically Evoked Compound Action Potential in Children with Cochlear Implants: Preliminary Results

Objective

Use of electrical instead of acoustical stimulation has made much objective electrophysiological evaluation possible. This is useful for management process of young children before and after the cochlear implant. These evaluations have been used for assessment of neuronal survival before cochlear implant and for monitoring of prosthesis function during and after the surgery. Electrically evoked compound action potential is one of these tests which makes a valid and reliable objective evaluation possible. The aim of this study was to evaluate the potential''s amplitude changes three months after receiving the device in pediatric cochlear implant recipients.

Methods

In this longitudinal study, changes of the potential''s amplitude in four given electrodes in four sessions after receiving the device are evaluated by approximately one month intervals in children implanted in Amir Alam and Hazrat-e-Rasoul hospitals, Tehran in July to December 2007.

Findings

The mean amplitude of the electrodes did not significantly change in different sessions, while there was significant difference between the first and the other electrodes’ responses in every session (P<0.05).

Conclusion

Due to high reliability of the responses, the clinician can fit the speech processor for a long time. Better responses in apical electrodes may lead to develop an effective coding strategy.     

Parkinson��s disease-linked LRRK2 is expressed in circulating and tissue immune cells and upregulated following recognition of microbial structures

Sequence variants at or near the leucine-rich repeat kinase 2 (LRRK2) locus have been associated with susceptibility to three human conditions: Parkinson's disease (PD), Crohn's disease and leprosy. As all three disorders represent complex diseases with evidence of inflammation, we hypothesized a role for LRRK2 in immune cell functions. Here, we report that full-length Lrrk2 is a relatively common constituent of human peripheral blood mononuclear cells (PBMC) including affinity isolated, CD14(+) monocytes, CD19(+) B cells, and CD4(+) as well as CD8(+) T cells. Up to 26% of PBMC from healthy donors and up to 43% of CD14(+) monocytes were stained by anti-Lrrk2 antibodies using cell sorting. PBMC lysates contained full-length (>260 kDa) and higher molecular weight Lrrk2 species. The expression of LRRK2 in circulating leukocytes was confirmed by microscopy of human blood smears and in sections from normal midbrain and distal ileum. Lrrk2 reactivity was also detected in mesenteric lymph nodes and spleen (including in dendritic cells), but was absent in splenic mononuclear cells from lrrk2-null mice, as expected. In cultured bone marrow-derived macrophages from mice we made three observations: (i) a predominance of higher molecular weight lrrk2; (ii) the reduction of autophagy marker LC3-II in (R1441C)lrrk2-mutant cells (<31%); and (iii) a significant up-regulation of lrrk2 mRNA (>fourfold) and protein after exposure to several microbial structures including bacterial lipopolysaccharide and lentiviral particles. We conclude that Lrrk2 is a constituent of many cell types in the immune system. Following the recognition of microbial structures, stimulated macrophages respond with altered lrrk2 gene expression. In the same cells, lrrk2 appears to co-regulate autophagy. A pattern recognition receptor-type function for LRRK2 could explain its locus' association with Crohn's disease and leprosy risk. We speculate that the role of Lrrk2 in immune cells may also be relevant to the susceptibility of developing PD or its progression.     

α-Synuclein in human cerebrospinal fluid is principally derived from neurons of the central nervous system

The source of Parkinson disease-linked α-synuclein (aSyn) in human cerebrospinal fluid (CSF) remains unknown. We decided to measure the concentration of aSyn and its gradient in human CSF specimens and compared it with serum to explore its origin. We correlated aSyn concentrations in CSF versus serum (Q(aSyn)) to the albumin quotient (Q(albumin)) to evaluate its relation to blood-CSF barrier function. We also compared aSyn with several other CSF constituents of either central or peripheral sources (or both) including albumin, neuron-specific enolase, β-trace protein and total protein content. Finally, we examined whether aSyn is present within the structures of the choroid plexus (CP). We observed that Q(aSyn) did not rise or fall with Q(albumin) values, a relative measure of blood-CSF barrier integrity. In our CSF gradient analyses, aSyn levels decreased slightly from rostral to caudal fractions, in parallel to the recorded changes for neuron-specific enolase; the opposite trend was recorded for total protein, albumin and β-trace protein. The latter showed higher concentrations in caudal CSF fractions due to the diffusion-mediated transfer of proteins from blood and leptomeninges into CSF in the lower regions of the spine. In postmortem sections of human brain, we detected highly variable aSyn reactivity within the epithelial cell layer of CP in patients diagnosed with a range of neurological diseases; however, in sections of mice that express only human SNCA alleles (and in those without any Snca gene expression), we detected no aSyn signal in the epithelial cells of the CP. We conclude from these complementary results that despite its higher levels in peripheral blood products, neurons of the brain and spinal cord represent the principal source of aSyn in human CSF.     

Religiousness and preoperative anxiety: a correlational study

Background  

Major life changes are among factors that cause anxiety, and one of these changes is surgery. Emotional reactions to surgery have specific effects on the intensity and velocity as well as the process of physical disease. In addition, they can cause delay in patients recovery. This study is aimed at determining the relationship between religious beliefs and preoperative anxiety.     

12-Molybdophosphoric acid anchored on aminopropylsilanized magnetic graphene oxide nanosheets (Fe3O4/GrOSi(CH2)3–NH2/H3PMo12O40): a novel magnetically recoverable solid catalyst for H2O2-mediated oxidation of benzylic alcohols under solvent-free conditions

In this work, 12-molybdophosphoric acid (H₃PMo₁₂O₄₀, HPMo) was chemically anchored onto the surface of aminosilanized magnetic graphene oxide (Fe₃O₄/GrOSi(CH₂)₃–NH₂) and was characterized using different physicochemical techniques, such as powder X-ray diffraction (XRD), Fourier transform infrared spectroscopy (FT-IR), Raman spectroscopy, energy-dispersive X-ray analysis (EDX), scanning electron microscopy (SEM), BET specific surface area analysis and magnetic measurements. The results demonstrated the successful loading of HPMo (∼31.5 wt%) on the surface of magnetic aminosilanized graphene oxide. XRD patterns, N₂ adsorption–desorption isotherms and SEM images confirm the mesostructure of the sample. FT-IR and EDX spectra indicate the presence of the PMo₁₂O₄₀³⁻ polyanions in the nanocomposite. The as-prepared Fe₃O₄/GrOSi(CH₂)₃–NH₂/HPMo nanocomposite has a specific surface area of 76.36 m² g⁻¹ that is much higher than that of pure HPMo. The selective oxidation of benzyl alcohol to benzaldehyde was initially studied as a benchmark reaction to evaluate the catalytic performance of the Fe₃O₄/GrOSi(CH₂)₃–NH₂/HPMo catalyst. Then, the oxidation of a variety of substituted primary and secondary activated benzylic alcohols was evaluated with H₂O₂ under solvent-free conditions. Under the optimized conditions, all alcohols were converted into the corresponding aldehydes and ketones with very high selectivity (≥99%) in moderate to excellent yields (60–96%). The high catalytic performance of the nanocomposite was ascribed to its higher specific surface area and more efficient electron transfer, probably due to the presence of GrO nanosheets. The nanocomposite catalyst is readily recovered from the reaction mixture by a usual magnet and reused at least four times without any observable change in structure and catalytic activity.

12-Molybdophosphoric acid was anchored on magnetic aminopropylsilanized graphene oxide nanosheets and used as a magnetically recoverable catalyst for solvent-free selective oxidation of benzylic alcohols into the carbonyl compounds with H₂O₂.     

Diminution of the NMDA receptor NR2B subunit in cortical and subcortical areas of WAG/Rij rats

Modulation of glutamatergic NMDA receptors affects the synchronization of spike discharges in in WAG/Rij rats, a valid genetic animal model of absence epilepsy. In this study, we describe the alteration of NR_2B subunit of NMDA receptors expression in WAG/Rij rats in different somatosensory cortical layers and in hippocampal CA1 area. Experimental groups were divided into four groups of six rats of both WAG/Rij and Wistar strains with 2 and 6 months of age. The distribution of NR_2B receptors was assessed by immunohistochemical staining in WAG/Rij and compared with age‐matched Wistar rats. The expression of NR_2B subunit was significantly decreased in different somatosensory cortical layers in 2‐ and 6‐month‐old WAG/Rij rats. In addition, the distribution of NR_2B in hippocampal CA1 area was lower in 6‐month‐old WAG/Rij compared with age‐matched Wistar rats. The reduction of NR_2B receptors in different brain areas points to disturbance of glutamate receptors expression in cortical and subcortical areas in WAG/Rij rats. An altered subunit assembly of NMDA receptors may underlie cortical hyperexcitability in absence epilepsy. Synapse 67:839–846, 2013 . © 2013 Wiley Periodicals, Inc.     

Impact of Vitamin A Supplementation on RAR Gene Expression in Multiple Sclerosis Patients

Vitamin A and its derivatives have been shown to modulate the immune system via retinoic acid receptor (RAR). This study explored the impact of retinyl palmitate supplementation on RAR subtype gene expression in peripheral blood mononuclear cells (PBMCs) in multiple sclerosis (MS) patients. The study designed as a double-blind randomized clinical trial in which relapsing remitting multiple sclerosis patients were evaluated. Both groups received one capsule 50,000 IU vitamin D3 per 2 weeks and one intramuscular injection interferon beta-1a per week. The intervention group received one 25,000 IU retinyl palmitate capsule daily for 6 months and the placebo group received one placebo capsule daily. The PBMCs were isolated from participants and the expression level changes of RAR-α and RAR-γ genes were determined by real-time PCR. After supplementation, in the intervention group, the RAR-α gene expression level was significantly decreased compared to the placebo group (p?=?0.03); however, the expression of RAR-γ gene did not significantly change (p?=?0.10). These results show that vitamin A supplementation can significantly downregulate the expression of RAR-α gene in PBMCs of MS patients that suggest the presence of in vivo regulatory mechanisms for the action of vitamin A on the immune system.