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J Schepers

Publications and source records attributed to J Schepers.

11 recordsLinked to original sources
PubMed2005

Magnetic resonance imaging in experimental subarachnoid haemorrhage.

BACKGROUND: We developed an MRI protocol to measure cerebrovascular diameter and blood flow velocity, and if we could detect cerebrovascular alterations after SAH and their impact on cerebral ischaemia. METHOD: SAH was induced in 15 Wistar rats by means of the endovascular filament method; 6 other rats served as control. MRI measurements were performed on a 4.7T NMR spectrometer 1 and 48 hours after SAH and 9 days thereafter. Diffusion-weighted and T2-weighted images were acquired to detect cerebral ischaemia. The arterial spin labelling method was used to measure CBF. MR angiography was used to measure vessel diameter and blood flow velocity, from which the arterial blood flow was calculated. FINDINGS: The ischemic lesion volume increased between 1 and 48 hours after SAH from 0.039 to 0.26 ml (P = 0.003). CBF decreased from 53.6 to 39.1 ml/100 g/min. The vessel diameter had narrowed, the blood flow velocity diminished as did the arterial blood flow in most vessels, but only the vasoconstriction in the right proximal ICA reached significance (0.49 mm to 0.43 mm, P = 0.016). Baseline values were restored at day 9. CONCLUSIONS: We showed that it is feasible to detect alterations of in-vivo vessel diameter and blood flow velocities and their consequences for brain damage after experimental SAH in the rat. The growth of the infarct volume between day 0 and 2 after SAH and the parallel vasoconstriction suggest that delayed cerebral ischaemia after SAH occurs in rats and that this may be caused by vasoconstriction.

Animals↗
PubMed2005

Comparison of perfusion MRI by flow-sensitive alternating inversion recovery and dynamic susceptibility contrast in rats with permanent middle cerebral artery occlusion.

We compared cerebral blood flow (CBF) parameters obtained by dynamic susceptibility contrast magnetic resonance imaging (DSC-MRI) with those obtained by flow-sensitive alternating inversion recovery (FAIR) in brain regions with different perfusion levels in rats with permanent middle cerebral artery (MCA) occlusion. MCA occlusion was performed in 19 rats. T2-weighted MRI, FAIR and DSC-MRI were performed within 48 h after occlusion. CBF parameters were analyzed in regions of interest with either prolonged or less prolonged mean transit time (MTT). Ratios of ipsi- vs contralateral CBF values were calculated and tested for correlation and differences between FAIR and DSC-MRI. FAIR-aCBF ratios correlated significantly with DSC-rCBF ratios. The mean FAIR-aCBF ratio was significantly lower than mean DSC-rCBF ratio in the area with prolonged MTT. In the area with less prolonged MTT, the mean FAIR-aCBF ratio and mean DSC-rCBF values did not differ significantly. We conclude that FAIR correlates with DSC-MRI if perfusion is preserved. FAIR provides lower CBF values than DSC-MRI if perfusion is reduced and MTT is prolonged. This probable underestimation of perfusion may be caused by transit delays. Care should be taken when quantifying CBF with FAIR and when comparing the results of FAIR- and DSC-MRI in areas with hypoperfusion.

Animals↗
PubMed2004

The time course of ischemic damage and cerebral perfusion in a rat model of space-occupying cerebral infarction.

We aimed to establish a rat model of space-occupying hemispheric infarction to evaluate potential treatment strategies. For adequate timing of therapy in future experiments, we studied the development of tissue damage, edema formation, and perfusion over time with different MRI techniques. Permanent middle cerebral artery (MCA) occlusion was performed in 32 Fisher-344 rats. Forty-six MRI experiments including diffusion weighted (DW), T2-weighted (T2W), flow-sensitive alternating inversion recovery (FAIR) perfusion-weighted, and T1-weighted (T1W) imaging before and after gadolinium were performed at 1, 3, 8, 16, 24, and 48 h of ischemia. MCA occlusion consistently led to infarction of the complete MCA territory. Mortality was 75%. Lesion volumes as derived from apparent diffusion coefficient (ADC) and T2 maps increased to maximum values of 400+/-48 mm3 at 24 h and 420+/-54 mm3 at 48 h of ischemia, respectively. Midline shift peaked at 24 h. The area with diffusion-perfusion deficit decreased to a minimum at 24 h after onset of ischemia and perfusion of the contralateral hemisphere dropped at the same time point. Leakage of gadolinium through the blood-brain barrier in the entire infarct occurred within 3 h of ischemia. Permanent intraluminal MCA occlusion in Fisher-344 rats is an adequate model for space-occupying cerebral infarction. Rats may benefit from intervention aimed at reducing tissue shift and intracranial pressure (ICP), and at improving cerebral blood flow, if initiated before 24 h after MCA occlusion. The value of treatment modalities depending on an intact blood-brain barrier should be questioned.

Animals↗
PubMed2004

Delayed decompressive surgery increases apparent diffusion coefficient and improves peri-infarct perfusion in rats with space-occupying cerebral infarction.

BACKGROUND AND PURPOSE: There is no conclusive experimental support that decompressive surgery in late stages of space-occupying cerebral infarction will improve outcome. We studied the effects of delayed decompressive surgery on the development of tissue damage, edema formation, and cerebral perfusion with different MRI techniques in a rat model of space-occupying cerebral infarction. METHODS: Permanent middle cerebral artery (MCA) occlusion was performed in 6 Fisher 344 rats. Decompressive surgery was performed 17 hours after the occlusion. Each animal was assessed before surgery and 2 and 4 hours after surgery by means, of diffusion-weighted T2-weighted, and flow-sensitive alternating inversion recovery perfusion-weighted MRI. Ischemic damage was also evaluated in hematoxylin-eosin-stained brain sections. RESULTS: Lesion volume as derived from apparent diffusion coefficient (ADC) maps decreased from 522+/-98 mm3 before to 405+/-100 mm3 (P=0.016) 4 hours after decompressive surgery, whereas lesion volume from T2 maps increased from 420+/-66 mm3 before to 510+/-92 mm3 (P=0.048) 4 hours after decompressive surgery. Midline shift decreased from 1.4+/-0.1 mm to 0.5+/-0.2 mm (P=0.001). Blood flow in the noninfarcted area of the ipsilateral hemisphere improved from 25+/-9 mL/min/100 g of tissue to 38+/-9 mL/min/100 g of tissue (P=0.035). Despite the pseudonormalization of ADC, irreversible damage was found in the entire MCA territory on histological evaluation. CONCLUSIONS: In rats with space-occupying cerebral infarction, delayed decompressive surgery leads to a decrease in lesion volume derived from ADC maps, which is probably because of an increase of extracellular water formation. There are no signs that this reflects rescue of ischemic tissue.

Animals↗
PubMed2000

Analysis of three Ptx2 splice variants on transcriptional activity and differential expression pattern in the brain.

Three different transcripts of the homeodomain gene termed pituitary homeobox (Ptx) 2 (Pitx2/Brx/Rieg/Solurshin/Arp) were cloned from different species encoding proteins belonging to the paired-like family of homeodomain proteins. Ptx2a (324 amino acids), Ptx2b (271 amino acids), and Ptx2c (318 amino acids) share the C terminus, including the homeodomain, and have different N termini. Here we report the comparative analysis of all three different Ptx2 splice variants for their transcriptional activity and their expression pattern in the adult rat brain. Ptx2 is able to trans-activate via different model promoters in different cell lines. A mild difference in trans-activating potential is observed among the splice variants, but the underlying mechanism is at present unknown. It is surprising that all Ptx2 transcripts displayed an identical expression pattern in the brain. This markedly restricted pattern is limited to the following brain areas: the anterior and intermediate lobes of the pituitary gland, the subthalamic nucleus, the posterior hypothalamic nucleus, the mammillary bodies, the red nucleus, and the deep gray layer of the superior colliculus. The data presented suggest that all variants of Ptx2 are involved in the development and regulation of distinct neuronal cell groups and the pituitary gland.

Alternative Splicing↗
PubMed1999

Cyclophosphamide, epirubicin and cisplatin (CEP) versus epirubicin plus cisplatin (EP) in stage Ic-IV ovarian cancer: a randomized phase III trial of the Gynecologic Oncology Group of the Comprehensive Cancer Center Limburg.

Cisplatin is the most important drug in the treatment of advanced ovarian cancer. The role of anthracyclines is controversial. We compared a combination of epirubicin plus cisplatin (EP) with a regimen of cyclophosphamide, epirubicin and cisplatin (CEP). Patients with stage Ic-IV ovarian cancer were randomized to receive either epirubicin 100 mg/m2 plus cisplatin 75 mg/m2 q 4 weeks or cyclophosphamide 500 mg/m2 plus epirubicin 75 mg/m2 plus cisplatin 50 mg/m2 q 4 weeks, which we considered the reference treatment based on our previous experience. Patients were initially debulked, followed by six cycles of chemotherapy, or in case primary debulking was insufficient or considered inappropriate, secondary debulking was attempted in selected cases after sufficient chemotherapy-induced regression. Optimal debulking was defined as residual lesions < or = 2 cm. A total of 210 patients (191 eligible) were randomized. Results did not show significant differences in all major endpoints (pathologically documented complete response and survival). The median survival for all patients was 34 months, for patients with stage III 26 months, for patients with stage IV 20 months and it has not been reached for patients with stage Ic-II. As no significant differences between an equitoxic regimen of EP and CEP were detected, it might be more useful to look again at the anthracyclines as part of combination chemotherapy instead of the alkylating agents.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1991

Correlation of bovine viral diarrhoea virus induced cytopathic effects with expression of a biotype-specific marker.

The purpose of this study was the identification antigenic differences between cytopathic (cp) and noncytopathic (ncp) bovine viral diarrhoea viruses (BVDV). Cells infected with 19 strains of each viral biotype were analyzed for reactivity with the monoclonal antibody (mab) BVD/C38. Reactivity was examined using an enzyme immunoassay on fixed infected monolayers of fetal calf kidney cells. In the majority of cases, the mab discriminated between cells infected with each of the two viral biotypes. Three reactivity patterns could be distinguished. Most cpBVDV strains yielded monolayers where 80-100% of infected cells reacted with the mab. Most of the ncpBVDV infected cells showed either no reaction, or only single cells of foci were stained. However, about one third of either cp- or ncpBVDV strains tested yielded infected monolayers where 30-50% of the cells reacted with the antibody. Cell damage other than the typical cytopathic effect might be responsible for the BVD/C38 reactivity of cells infected with BVDV. In addition, it was analyzed whether the antigenic marker associated with cpBVDV was expressed in cells infected with viral isolates from 21 animals with clinical mucosal disease. In 14 cases cpBVDV was isolated and the antigenic marker was found throughout. In seven cases ncpBVDV was cultivated and the antigenic marker was detected in four isolates.

Animals↗
PubMed1984

[Incidence and prognostic significance of inducible ventricular arrhythmias in the early post-infarction phase].

To identify patients at risk of sudden cardiac death or sustained ventricular tachycardia (VT) after recent acute myocardial infarction, 100 patients younger than 70 years (80 male, 20 female; 47 anterior wall infarction, 53 inferior wall infarction) were studied prospectively. 25 days (mean) after onset of myocardial infarction, programmed ventricular stimulation was performed, including the introduction of single (S2) and double (S2-S3) ventricular extrastimuli both during sinus rhythm and at paced ventricular cycle lengths (S1-S1) of 500, 430, 370, and 330 ms. The end of the protocol was reached as soon as 4 or more consecutive ventricular echo beats (VE) were initiated. Four or more VE were initiated in 46% of patients, 4 to 9 VE in 21%, greater than or equal to 10 VE or sustained VT in 25%. During follow-up (15 +/- 8 months), 5 patients died suddenly (less than or equal to 1 h), and 5 further patients developed spontaneous sustained ventricular tachycardia. In 3 patients who died suddenly and 4 with spontaneous sustained VT, greater than or equal to 4 VE had been induced by programmed ventricular stimulation (sensitivity 60% and 80% respectively). With regard to sudden cardiac death and spontaneous ventricular tachycardia, the predictive value of a positive test was 15%, that of a negative (normal) test 94%. False negative results occurred in 6%, whereas 85% of all abnormal results had to be regarded as false positive, as these patients did not develop an arrhythmic event during follow-up. Thus patients after recent myocardial infarction frequently have signs of increased ventricular vulnerability during programmed ventricular stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗