Simultaneous MEG and EEG source analysis

A method is described to derive source and conductivity estimates in a simultaneous MEG and EEG source analysis. In addition the covariance matrix of the estimates is derived. Simulation studies with a concentric spheres model and a more realistic boundary element model indicate that this method has several advantages, even if only a few EEG sensors are added to a MEG configuration. First, a simultaneous analysis profits from the 'preferred' location directions of MEG and EEG. Second, deep sources can be estimated quite accurately, which is an advantage compared to MEG. Third, superficial sources profit from accurate MEG location and from accurate EEG moment. Fourth, the radial source component can be estimated, which is an advantage compared to MEG. Fifth, the conductivities can be estimated. It is shown that conductivity estimation gives a substantial increase in precision, even if the conductivities are not identified appropriately. An illustrative analysis of empirical data supports these findings.     

No cytogenetic evidence for involvement of gene(s) at 2p16 in sporadic cardiac myxomas: cytogenetic changes in ten sporadic cardiac myxomas

Cardiac myxomas are significant causes of cardiovascular morbidity and mortality. Their genetic background is presently unknown. Recently, linkage analysis in cardiac myxomas of Carney complex patients has indicated that 2p16 and 17q2 might carry genes responsible for the development of hereditary cardiac myxomas. Less is known about sporadic cardiac myxomas. To date, cytogenetic analysis has been performed on 13 sporadic cases, and no specific rearrangement has been deduced. We studied 15 sporadic cardiac myxomas and reviewed the literature. Ten of the present cases revealed abnormal karyotypes with clonal and nonclonal rearrangements including dicentric chromosomes and telomeric associations. No cytogenetic evidence was found for a role of 2p16 in the development of sporadic cases. Region 17q2 was involved in structural rearrangements, but to a lesser extent than other regions. Structural rearrangements involving regions 12p1 and 17p1 are more frequently present and might therefore harbor genes important for the development of sporadic cardiac myxomas.     

Abolition of (-)-CGP 12177-evoked cardiostimulation in double β1/β2-adrenoceptor knockout mice. Obligatory role of β1-adrenoceptors for putative β4-adrenoceptor pharmacology

Some beta1- and beta2-adrenoceptor-blocking agents, such as (-)-CGP 12177, cause cardiostimulant effects at concentrations considerably higher than those that antagonise the effects of catecholamines. The cardiostimulant effects of these non-conventional partial agonists are relatively resistant to blockade by (-)-propranolol and have been proposed to be mediated through putative beta4-adrenoceptors or through atypical states of either beta1- or beta2-adrenoceptors. We investigated the effects of (-)-CGP 12177 on sinoatrial rate and left atrial contractile force as well as the ventricular binding of (-)-[3H]CGP 12177 in tissues from wild-type, beta2-adrenoceptor knockout and beta1/beta2-adrenoceptor double knockout mice. The cardiostimulant effects of (-)-CGP 12177 were present in wild-type and beta2-adrenoceptor knockout mice but were absent in beta1/beta2-adrenoceptor double knockout mice. Thus, the presence of beta1-adrenoceptors is obligatory for the cardiostimulant effects of (-)-CGP 12177. It appears therefore that an atypical state of the beta1-adrenoceptor contributes to the mediation of the cardiostimulant effects induced by non-conventional partial agonists. Ventricular beta1- and beta2-adrenoceptors, labelled in wild-type with a K(D) approximately 0.5 nmol/l (approximately 16 fmol/mg protein), were absent in beta1/beta2-adrenoceptor double knockout mice. However, a high density binding site (approximately 154-391 fmol/mg protein) that did not saturate completely (K(D) approximately 80-200 nM) was labelled by (-)-[3H]CGP 12177 in the three groups of mice, being distinct from beta1- and beta2-adrenoceptors, as well as from the site mediating the agonist effects of (-)-CGP 12177.     

Analysis of Proliferation and Apoptosis in Brain Gliomas: Prognostic and Clinical Value

With the introduction of new (immuno-)histochemical techniques it is now possible to assess rates of proliferation and apoptosis in brain gliomas using archival paraffin embedded material. As proliferation and apoptosis are related to tumour growth rate quantification of these processes has prognostic value and is related to tumour grading. In this study we assessed the proliferation rate by measuring the Ki-67 labelling index using the MIB-1 antibody (MIB-LI) and the apoptotic rate using the in situ labelling of DNA strand breaks with TUNEL (TUNEL-LI) in 315 supratentorial gliomas. MIB-LI and TUNEL-LI in astrocytomas (A) where significantly lower compared to anaplastic astrocytomas (AA), glioblastomas (GBM) and oligodendroglial tumours [oligodendrogliomas (O) and anaplastic oligodendrogliomas (AO)]. MIB-LI and TUNEL-LI were significantly lower in AA compared to GBM. In astrocytic tumours MIB-LI and TUNEL-LI appeared to be correlated.As the distinction between A and AA is of clinical value but can be difficult histomorphologically we analysed the prognostic value of MIB-LI and TUNEL-LI in gliomas with particular emphasis on A and AA. MIB-LI below 10% was of prognostic value in A and AA, O and AO but not in GBM on univariate survival analysis. TUNEL-LI was of no prognostic value. With multivariate survival analysis MIB-LI lost prognostic significance in O and AO. Astrocytomas with a gemistocytic component (AG) are similar to A with respect to survival and MIB-LI and TUNEL-LI. MIB-LI is of independent prognostic value in A and AA. Assessment of MIB-LI in A and AA can be used as an aid in distinguishing A and AA.     

Detection of canine intestinal allograft rejection by in vivo electrophysiologic monitoring

The aim of this study was to evaluate the significance of in vivo measurements of electrophysiologic parameters for the detection of canine small bowel (SB) allograft rejection. In dogs of group I (n = 17) a heterotopic SB autotransplantation was performed. Dogs of group II (n = 8) received a heterotopic SB allograft in a fully mismatched donor-recipient combination. No immunosuppression was given. All grafts were monitored regularly by in vivo measurements of transepithelial potential differences (PDs) and by biopsies of the grafts. The overall technical failure rate was 36% caused by thrombosis at the vascular anastomosis in most cases. All successful autografts survived the experimental period and showed physiologic PD responses after stimulation by both a theophylline solution and a glucose solution. The successful allografts survived 5.5 +/- 0.2 days (mean +/- SEM); the transepithelial PDs showed normal responses at postoperative day 3, but showed decreased responses at day 5 (P less than 0.05) and reversed responses at day 6 (P less than 0.05). The diminished PD responses correlated well with the onset of histologic alterations characteristic of rejection. This study demonstrates that serial monitoring of transepithelial PD responses is a noninvasive method to detect acute SB allograft rejection.     

Developmental aspects of gastroschisis

The development of gastroschisis was studied experimentally as well as clinically, particularly concerning the characteristic fibrous coating of the protruding bowel loops, associated intestinal atresia, and postoperative hypoperistalsis without intestinal obstruction. Experimental investigation was carried out in the chicken embryo. The clinical study was a joint one, involving a total of 50 patients with gastroschisis seen at the Sophia Children's Hospital, Rotterdam, and the Royal Hospital for Sick Children, Glasgow, between 1972 and 1985. Some patients were followed antenatally. The results, correlating with previous experiments, were compared with data from the literature. The fibrous coating of the protruding bowel loops appeared to be a late occurrence and directly related to changes of the amniotic fluid secondary to the onset of renal function. Associated intestinal atresia and postoperative hypoperistalsis in the absence of an obstruction both appeared to be due to another late gestational event, consisting of ischemic changes of the bowel wall secondary to the compression of bowel loops and mesentery in the small abdominal wall defect.     

Routinegastrostomie in der Behandlung der Ösophagusatresie — notwendig oder nicht?

Ohne Zusammenfassung     

Differential regulation of beta-1 and beta-2 adrenoceptors in guinea pig atrioventricular conducting system after chronic (-)-isoproterenol infusion

Quantitative autoradiography was used to determine the effects of chronic administration of (-)-isoproterenol (400 micrograms/kg/hr, 7 days) on the distribution and density of beta-1 and beta-2 adrenoceptors in guinea pig atrioventricular conducting system and surrounding regions. X-ray film was exposed to sections of heart labeled with (-)-[125I]-cyanopindolol in the absence or presence of ICI 118,551 (70 nM) to block beta-2 adrenoceptors, CGP 20712A (100 nM) to block beta-1 adrenoceptors or (-)-propranolol (1 microM) to define nonspecific binding. Quantitative autoradiography was performed using computer-assisted image processing and the AVID system. The proportions of beta-1 and beta-2 adrenoceptors were determined by the extent of inhibition of (-)-[125I]cyanopindolol binding by CGP 20712A (100 nM) together with equations which take into account the differing affinities of ligands for beta-1 and beta-2 adrenoceptors. In vehicle (1 mM HCl)-treated animals there was a higher density and proportion of beta-2 adrenoceptors in the atrioventricular node, bundle of His and right and left bundle branches than in myocardium. Chronic administration of (-)-isoproterenol produced marked loss of beta-2 adrenoceptor binding in all regions of the atrioventricular conducting system, surrounding myocardium, cardiac valves and the smooth muscle of the aorta accompanied by less pronounced effects on beta-1 adrenoceptors. Beta-1 adrenoceptors were significantly reduced only in the left bundle branch whereas there were trends toward a reduction in the right bundle branch, bundle of His and an increase in the atrioventricular node. There was no alteration in beta-1 adrenoceptor density in myocardium. Loss of beta adrenoceptor binding produced by (-)-isoproterenol was mainly confined to beta-2 adrenoceptors.