A simple method for the construction of electrode arrays

A simple method is described for the construction of electrode arrays consisting of insulated metal wires (33 μm diameter) spaced at small, equal distances (0.1 mm). No specialized instrumentation and techniques are needed, as only simple mechanical tools are sufficient. The electrode arrays are used for field potential recording from in vitro brain slice preparations

Development of an electret microphone in silicon

We describe a subminiature electret microphone, which has been realized in silicon using wafer processing techniques. The microphone consists of a rigid backplate fabricated in silicon and a 2.5 μm thick metallized Mylar foil (PETP) acting as the diaphragm. Between the diaphragm and the backplate a 20 μm thick air cavity and a 1.1 μm thick charged SiO2 layer are present. The SiO2 layer is used as the electret and generates an electric field in the air gap. The electret has been changed to 300 V using a corona-charging set-up. The time constant of the charge decay amounts to more than 100 years at ambient laboratory conditions.\ud \ud The microphone cartridge, which measures 3 × 3 × 0.3 mm, shows an open-circuit sensitivity of about 2.5 mV/μbar at 1 kHz

Generation and propagation of epileptiform activity in the hippocampal slice preparation

For the investigation of epileptiform events in the hippo-campal CA1 field, in-vitro slices of the guinea-pig were used. After adding 0.1 mmol 4-aminopyridine to the bathing medium, field potentials were recorded with an electrode array, consisting of 8 semi-microelectrodes at spacings of 0.1 ram. A comparison was made between the spontaneously occurring field potentials (SFP) in CA I and those evoked by different inputs to the CA1 pyramidal cells, namely alveus, str. oriens and Schaffer collaterals. For this purpose the electrode array was placed in CA l, parallel to the axes for the pyramidal cells. The regularly occurring SEP's presented a similar distribution as the potentials evoked by stimulation of str. oriens or alveus of CAI, but differed from those evoked by stimulation of the chaffer colaterals. This indicates that in CA1 SFP's are generated in a similar way as field potentials evoked by alveus or str. oriens stimulation. It was also found that SFP's are propagated from CA3 and CAI at a velocity of 0.16-0.30 m/sec. Therefore pathways in alveus and str. oriens, connecting CA3 and CA1, may be important in propagating epileptiform activity. This was supported by experiments in which different pathways were sectioned

Single fibre action potentials in skeletal muscle related to recording distances

Single muscle fibre action potentials (SFAPs) are considered to be functions of a bioelectrical source and electrical conductivity parameters of the medium. In most model studies SFAPs are computed as a convolution of the bioelectrical source with a transfer function. Calculated peak-to-peak amplitudes of SFAPs decrease with increasing recording distances. In this paper an experimental validation of model results is presented. Experiments were carried out on the m. extensor digitorum longus (EDL) of the rat. Using a method including fluorescent labelling of the active fibre, the distance between the active fibre and the recording electrode was derived. With another method, the decline of the peak-to-peak amplitude of SFAPs detected along a multi-electrode was obtained. With both experimental methods, in general peak-to-peak amplitudes of SFAPs decreased with increasing recording distances, as was found in model results with present volume conduction theory. However, this behaviour was not found in all experiments. The rate of decline of the peak-to-peak amplitudes with recording distance was always less than in models

CD34+ cells home, proliferate, and participate in capillary formation, and in combination with

Objective - Emerging evidence suggests that human blood contains bone marrow (BM)-derived endothelial progenitor cells that contribute to postnatal neovascularization. Clinical trials demonstrated that administration of BM-cells can enhance neovascularization. Most studies, however, used crude cell populations. Identifying the role of different cell populations is important for developing improved cellular therapies. Methods and Results - Effects of the hematopoietic stem cell-containing CD34+ cell population on migration, proliferation, differentiation, stimulation of, and participation in capillary-like tubule formation were assessed in an in vitro 3-dimensional matrix model using human microvascular endothelial cells. During movement over the endothelial monolayer, CD34+ cells remained stuck at sites of capillary tube formation and time- and dose-dependently formed cell clusters. Immunohistochemistry confirmed homing and proliferation of CD34+ cells in and around capillary sprouts. CD34+ cells were transduced with the LNGFR marker gene to allow tracing. LNGFR gene-transduced CD34 + cells integrated in the tubular structures and stained positive for CD31 and UEA-1. CD34+ cells alone stimulated neovascularization by 17%. Coculture with CD34- cells led to 68% enhancement of neovascularization, whereas CD34- cells displayed a variable response by themselves. Cell-cell contact between CD34+ and CD34- cells facilitated endothelial differentiation of CD34+ cells. Conclusions - Our data suggest that administration of CD34+-enriched cell populations may significantly improve neovascularization and point at an important supportive role for (endogenous or exogenous) CD34- cells. © 2005 American Heart Association, Inc. Chemicals / CAS: nitric oxide, 10102-43-9; Antigens, CD34; Biological Marker

Bragatston study protocol: a multicentre cohort study on automated quantification of cardiovascular calcifications on radiotherapy planning CT scans for cardiovascular risk prediction in patients with breast cancer

Introduction Cardiovascular disease (CVD) is an important cause of death in breast cancer survivors. Some breast cancer treatments including anthracyclines, trastuzumab and radiotherapy can increase the risk of CVD, especially for patients with pre-existing CVD risk factors. Early identification of patients at increased CVD risk may allow switching to less cardiotoxic treatments, active surveillance or treatment of CVD risk factors. One of the strongest independent CVD risk factors is the presence and extent of coronary artery calcifications (CAC). In clinical practice, CAC are generally quantified on ECGtriggered cardiac CT scans. Patients with breast cancer treated with radiotherapy routinely undergo radiotherapy planning CT scans of the chest, and those scans could provide the opportunity to routinely assess CAC before a potentially cardiotoxic treatment. The Bragatston study aims to investigate the association between calcifications in the coronary arteries, aorta and heart valves (hereinafter called ‘cardiovascular calcifications’) measured automatically on planning CT scans of patients with breast cancer and CVD risk. Methods and analysis In a first step, we will optimise and validate a deep learning algorithm for automated quantification of cardiovascular calcifications on planning CT scans of patients with breast cancer. Then, in a multicentre cohort study (University Medical Center Utrecht, Utrecht, Erasmus MC Cancer Institute, Rotterdam and Radboudumc, Nijmegen, The Netherlands), the association between cardiovascular calcifications measured on planning CT scans of patients with breast cancer (n≈16 000) and incident (non-)fatal CVD events will be evaluated. To assess the added predictive value of these calcifications over traditional CVD risk factors and treatment characteristics, a case-cohort analysis will be performed among all cohort members diagnosed with a CVD event during follow-up (n≈200) and a random sample of the baseline cohort (n≈600). Ethics and dissemination The Institutional Review Boards of the participating hospitals decided that the Medical R

Functional mechanisms underlying pleiotropic risk alleles at the 19p13.1 breast-ovarian cancer susceptibility locus

A locus at 19p13 is associated with breast cancer (BC) and ovarian cancer (OC) risk. Here we analyse 438 SNPs in this region in 46,451 BC and 15,438 OC cases, 15,252 BRCA1 mutation carriers and 73,444 controls and identify 13 candidate causal SNPs associated with serous OC (P=9.2 × 10-20), ER-negative BC (P=1.1 × 10-13), BRCA1-associated BC (P=7.7 × 10-16) and triple negative BC (P-diff=2 × 10-5). Genotype-gene expression associations are identified for candidate target genes ANKLE1 (P=2 × 10-3) and ABHD8 (P<2 × 10-3). Chromosome conformation capture identifies interactions between four candidate SNPs and ABHD8, and luciferase assays indicate six risk alleles increased transactivation of the ADHD8 promoter. Targeted deletion of a region containing risk SNP rs56069439 in a putative enhancer induces ANKLE1 downregulation; and mRNA stability assays indicate functional effects for an ANKLE1 3′-UTR SNP. Altogether, these data suggest that multiple SNPs at 19p13 regulate ABHD8 and perhaps ANKLE1 expression, and indicate common mechanisms underlying breast and ovarian cancer risk