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R Veltkamp

Publications and source records attributed to R Veltkamp.

18 recordsLinked to original sources
PubMed2005

Regulatory CD4+CD25+ cells reverse imbalances in the T cell pool of bone marrow transplanted TGepsilon26 mice leading to the prevention of colitis.

BACKGROUND AND AIMS: Erroneous thymic selection of developing T lymphocytes may be responsible for the expansion of self reactive T cells or may contribute to the absence of regulatory T cells important in controlling peripheral inflammatory processes. Colitis in bone marrow (BM) transplanted Tgepsilon26 mice is induced by abnormally activated T cells developing in an aberrant thymic microenvironment. We investigated the protective role of regulatory CD4+CD25+ T cells in this model. METHODS: BM from (C57BL/6 x CBA/J) F1 mice was transplanted into specific pathogen free Tgepsilon26 mice (BM-->Tgepsilon26). Transplanted mice received no cells (control), sorted CD4+CD25+, or CD4+CD25- cells from mesenteric lymph nodes (MLN) of normal mice. MLN cell subsets were analysed using membrane markers. Cytokine secretion of MLN cells was measured using intracellular cytokine staining and cytokine secretion in anti-CD3 stimulated cell cultures. Colitis was measured by histological scores. RESULTS: CD4+CD25+ cells were reduced in the MLNs of BM-->Tgepsilon26 mice. Transfer of regulatory CD4CD4+CD25+ but not of CD4+CD25- cells reduced the number of MLN CD4+ T cells in BM-->Tgepsilon26 recipients and increased the number of MLN CD8+ cells, thereby normalising the CD4+/CD8+ ratio. CD4+CD25+ but not CD4+CD25- cell transfer into BM-->Tgepsilon26 mice reduced the number of tumour necrosis factor alpha+ CD4+ cells and increased the secretion of transforming growth factor beta by MLN cells. Transfer of 3 x 10(5) CD4+CD25+ cells after BM transplantation into Tgepsilon26 mice prevented colitis whereas CD4+CD25- cells had no protective effect. CONCLUSIONS: These results suggest that defective selection or induction of regulatory T cells in the abnormal thymus is responsible for the development of colitis in BM-->Tgepsilon26 mice. Transfer of CD4+CD25+ cells can control intestinal inflammation in BM-->Tgepsilon26 mice by normalising the number and function of the MLN T cell pool.

Animals↗
PubMed2004

[Symptomatic dissection of the internal carotid artery. A rare manifestation of autosome dominant polycystic kidney disease?].

Autosomal dominant polycystic kidney disease (ADPKD) is a frequent, genetically heterogenous disease with renal and extrarenal manifestations. Intracranial aneurysms are found in about 10% of cases. Other vascular manifestations of ADPKD have been described only in small case series. We report a 44-year-old ADPKD patient who developed acute large middle cerebral artery infarction secondary to subpetrous dissection of the internal carotid artery. Six months after the stroke, pseudoaneurysm was demonstrated on magnetic resonance angiography at the site of a previous dissection. Based on this case report, we review the spectrum of neurovascular manifestations and stroke associated with ADPKD and summarize current concepts of the pathogenesis of this disease. Finally, special aspects of the diagnostic evaluation and therapeutic management in patients with ADPKD and cervicocephalic dissection are discussed.

Aneurysm, False↗
PubMed2003

Progressive arm weakness and tonic hand spasm from multifocal motor neuropathy in the brachial plexus.

A 50-year-old waitress presented with a 10-year history of progressive weakness in her right arm without atrophy and with tonic hand spasms suggesting a central motor disorder. Electromyography, however, disclosed chronic neurogenic changes including fasciculations and atypical cramps. Isolated motor conduction block in the right brachial plexus suggested a variant of multifocal motor neuropathy. Strength recovered and cramps disappeared after intravenous immunoglobulins. Motor neuropathies may thus manifest with features of central motor disorders.

Action Potentials↗
PubMed2001

Influence of positive end-expiratory pressure on intracranial pressure and cerebral perfusion pressure in patients with acute stroke.

BACKGROUND AND PURPOSE: We undertook this study to evaluate the influence of positive end-expiratory pressure (PEEP) on intracranial pressure (ICP) and cerebral perfusion pressure (CPP) in patients with acute stroke. METHODS: A total of 20 ventilated patients of a neurological intensive care unit were examined under a protocol entailing variation of PEEP to 4, 8, 12, and 4 mm Hg; mean arterial blood pressure (MAP), ICP, heart rate, and mean velocity of the middle cerebral arteries (V(m) MCA) were recorded. RESULTS: CPP significantly changed depending on the various PEEP levels. No significant differences in remaining parameters were evident. Three distinct reaction patterns of the parameters monitored were observed: (1) All parameters remained stable through the various PEEP levels (15 patients, 40 examinations). (2) Increase in PEEP resulted in a significant decrease of MAP, while V(m) MCA remained unchanged, indicating an intact cerebral autoregulation. A slight (statistically insignificant) increase in ICP, which was significantly related to the MAP changes, was evident (7 patients, 16 examinations). (3) Increase in PEEP resulted in a decrease of MAP and V(m) MCA; ICP remained unchanged or demonstrated a slight decline (3 patients, 6 examinations). CONCLUSIONS: PEEP increase up to 12 mm Hg does not significantly influence ICP. The observed marked changes in CPP are mediated through the MAP. Thus, PEEP application should be safe, provided that MAP is maintained.

Adult↗
PubMed2000

Low mini-mental status predicts mortality in asymptomatic carotid arterial stenosis. Asymptomatic Carotid Atherosclerosis Study investigators.

OBJECTIVE: To determine whether carotid endarterectomy is superior to best medical therapy in preserving cognition, and whether low Mini-Mental State Examination (MMSE) scores predict TIA, stroke, myocardial infarction, or death. METHODS: Subjects participating in the Asymptomatic Carotid Atherosclerosis Study were administered the MMSE at periodic intervals. Group means were calculated at randomization, 1 and 3 months later, and every 6 months thereafter. The group means were compared by treatment and over time. A proportional hazard regression model incorporating postrandomization MMSE score as a predictor variable was used to estimate risk of death, stroke, or other outcome events. RESULTS: There was no intergroup difference in mean MMSE score during 5 years of observation. For individual patients, the relationship between a low postrandomization score on the MMSE and increased risk of death was significant (p </= 0.0001). Patients who experienced stroke after randomization also had a significant and persistent reduction in MMSE score (p </= 0.0001). CONCLUSIONS: Carotid endarterectomy had no impact on MMSE score in this study. Patients with low postrandomization MMSE scores had a greater likelihood of death. Stroke reduced MMSE scores and may portend cognitive impairment. The authors recommend the routine inclusion of cognitive testing in future clinical trials designed to evaluate prophylaxis or acute therapy of stroke.

Carotid Stenosis↗
PubMed2000

Characteristics of induced spreading depression after transient focal ischemia in the rat.

We examined characteristics of spreading depression (SD) induced on the rat cortex 1 day after transient focal ischemia. Male Wistar rats (n=21) were subjected to transient intraluminal thread occlusion of the right middle cerebral artery for 75 min. Twenty-four hours after the reperfusion, cerebral blood flow (CBF) was determined using laser Doppler flowmeter during multiple SDs elicited on both non-stroke (left) and stroke (right) cortex by the topical application of 2 M KCl. We also examined CBF responses before and after the intravenous administration of the nonspecific NOS inhibitor Nomega-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg) in normal and stroke cortex. Animals were divided into two groups; Group 1 (n=12), animals with subcortical infarction and Group 2 (n=9), animals with subcortical plus cortical infarction. There were no differences between non-stroke and stroke sides in the duration or amplitude of the DC potential shifts in either group. The transient CBF hyperemia during SD was not different between non-stroke (372+/-23% of baseline, mean+/-S.E.) and stroke sides (383+/-30%) in Group 1. However, in Group 2, CBF was significantly restricted on the stroke side (192+/-15% vs. non-stroke side, 374+/-33%). In four normal animals without ischemia, there were no differences in CBF response between both sides. L-NAME had no effect on the transient CBF hyperemia during SD in any of the groups. These data suggest that the CBF responses during SD in the peri-infarction area is restricted 1 day after the transient focal ischemia, while CBF responses are intact in normal cortex overlapping a subcortical infarct. Further, our results indicate that nitric oxide does not promote CBF responses during SD in normal cortex or in tissue surrounding infarction.

Animals↗
PubMed2000

Hyperbaric oxygen decreases infarct size and behavioral deficit after transient focal cerebral ischemia in rats.

Cerebral hypoxia is a major component of immediate and secondary cell damage caused by ischemia. Hyperbaric oxygen (HBO) is a potent means to increase the amount of oxygen dissolved in blood plasma. The effectiveness of HBO in clinical and experimental cerebral ischemia, however, is controversial. We sought to determine whether treatment with HBO initiated early after focal cerebral ischemia-onset protects the brain when experimental conditions such as brain temperature are controlled. Male Wistar rats (n=57) underwent reversible filament occlusion of the right middle cerebral artery (MCA) for 75 min. Animals were awakened after filament introduction and assessed for presence of forelimb paresis. Rats then underwent a 60-min course of either 100% O(2) at 1.0 atmosphere absolute (ata; control group), HBO 1.5 ata, or HBO 2.5 ata in a customized HBO chamber allowing physiological monitoring and pericranial temperature control. The filament was then removed. Seven days after ischemia, rat behavior was scored from 3-18 (18=normal) and brains were removed for histological analysis of infarct volume. Rats treated with HBO 2.5 ata had better mean+/-standard deviation (S.D.) behavioral scores (14+/-2; p<0.05) than control (10+/-3) or HBO 1.5-ata-treated animals (11+/-3). Similarly, total infarct volumes (mean+/-S.D.) were smaller in animals receiving HBO at 2.5 ata (76+/-65 mm(3); p<0.05) compared to control (129+/-83 mm(3)) and HBO 1.5-ata (119+/-68 mm(3))-treated groups. Cortical infarction occurred less frequently in HBO 2. 5-ata-treated than in control animals (44% vs. 71%; p<0.05). We conclude that HBO can improve outcome after temporary focal ischemia when treatment is started early after ischemia-onset but HBO dose appears important. Potential mechanisms include enhanced oxygen supply to marginally perfused cells.

Animals↗
PubMed2000

Late onset postpartum eclampsia without pre-eclamptic prodromi: clinical and neuroradiological presentation in two patients.

In two patients eclampsia started 9 days postpartum. Headache and visual disturbances preceded seizures but none of the classic pre-eclamptic signs oedema, proteinuria, and hypertension were present until shortly before seizure onset. Brain herniation (patient 1) and status epilepticus (patient 2) necessitated neurointensive care management. Brain MRI initially showed only frontal sulcal effacement in one patient but later showed white matter hyperintensities on T2 weighted images and a previously undescribed pattern of cortical-subcortical postgadolinium enhancement on T1 weighted images in both. Neurological deficits and MRI findings were reversed with therapy in both patients. It is concluded that late postpartum eclampsia can manifest without classic prodromi and that characteristic MRI findings may lag behind clinical manifestation.

Adult↗
PubMed1999

Cycloheximide rapidly inhibits cortical COX activity and COX-dependent pial arteriolar dilation in piglets.

We have previously shown that cycloheximide (CHX) preserved neuronal function after global cerebral ischemia in piglets, in a manner similar to indomethacin. To elucidate the mechanism of this protection, we tested the hypothesis that CHX would inhibit cyclooxygenase (COX) activity in the piglet cerebral cortex and vasculature. Pial arteriolar responses to hypercapnia, arterial hypotension, and sodium nitroprusside (SNP) were determined before and 20 min after treatment with CHX (0.3-1 mg/kg iv) using a closed cranial window and intravital microscopy. We also determined baseline and arachidonic acid (AA)-stimulated cortical PGF(2alpha) and 6-keto-PGF(1alpha) production before and 20-60 min after CHX (1 mg/kg iv) treatment, using ELISA kits. CHX did not affect baseline diameters (approximately 100 microm) but significantly decreased arteriolar dilation to COX-dependent stimuli, such as hypercapnia and hypotension, but not to COX-independent SNP. In the 1 mg/kg CHX-treated group, increases in vascular diameters were reduced from 22 +/- 2 to 10 +/- 2%, from 49 +/- 5 to 31 +/- 3% (means +/- SE, 5 and 10% CO2, respectively, n = 8), from 12 +/- 3 to 3 +/- 1%, and from 26 +/- 5 to 6 +/- 2% ( approximately 25 and 40% decreases in blood pressure, respectively, n = 6). CHX also inhibited conversion of exogenous AA to both PGF(2alpha) and 6-keto-PGF(1alpha); for example, 20 min after CHX treatment 10 microg/ml AA-stimulated PGF(2alpha) concentrations in the artificial cerebrospinal fluid decreased from 14.28 +/- 3.04 to 5.90 +/- 1.26 ng/ml (n = 9). Thus CHX rapidly decreases COX activity in the piglet cerebral cortex. This result may explain in part the preservation of neuronal function of CHX in cerebral ischemia.

Animals↗
PubMed1999

Ischemia-reperfusion rapidly increases COX-2 expression in piglet cerebral arteries.

In the newborn, cyclooxygenase (COX)-derived products play an important role in the cerebrovascular dysfunction after ischemia-reperfusion (I/R). We examined effects of I/R on expression of COX-1 and COX-2 isoforms in large cerebral arteries of anesthetized piglets. The circle of Willis, the basilar, and the middle cerebral arteries were collected from piglets at 0.5-12 h after global ischemia (2.5-10 min, n = 50), hypoxia (n = 3), or hypercapnia (n = 2) and from time-control (n = 19) or untreated animals (n = 7). Tissues were analyzed for COX-1 and COX-2 mRNA and protein using RNase protection assay and immunoblot analysis, respectively. Ischemia increased COX-2 mRNA by 30 min, and maximal levels were reached at 2 h. Hypoxia or hypercapnia had minimal effects on COX-2 mRNA. COX-2 protein levels were also consistently elevated by 8 h after I/R. Increases in COX-2 mRNA or protein were not influenced by pretreatment with either indomethacin (5 mg/kg iv, n = 5) or nitro-L-arginine methyl ester (15 mg/kg iv, n = 7). COX-1 mRNA levels were low in time controls, and ischemic stress had no significant effect on COX-1 expression. Thus ischemic stress leads to relatively rapid, selective induction of COX-2 in cerebral arteries.

Animals↗
PubMed1999

Inhibitors of protein synthesis preserve the N-methyl-D-aspartate-induced cerebral arteriolar dilation after ischemia in piglets.

BACKGROUND AND PURPOSE--Cerebral arteriolar dilation to N-methyl-D-aspartate (NMDA) is a neuronally mediated process that is sensitive to cerebral ischemia. We tested the hypothesis that pretreatment with transcription or translation inhibitors preserves the vascular response to NMDA after global cerebral ischemia. METHODS--Pial arteriolar diameters were measured in anesthetized piglets by use of a closed cranial window and intravital microscopy. Arteriolar responses to NMDA (10(-5) and 10(-4) mol/L) were measured before and 1, 2, and 4 hours after 10 minutes of ischemia. Ischemia was induced by increasing intracranial pressure. Subgroups were pretreated with vehicle, topical actinomycin D (Act-D) 10(-5) or 10(-6) mol/L, or intravenous cycloheximide (CHX) 1.0 or 0.3 mg/kg 15 minutes before ischemia. The effects of Act-D and CHX on vascular responses to NMDA without preceding ischemia were also examined. RESULTS--In the vehicle group, arteriolar responses to NMDA were clearly attenuated 1 hour after ischemia but returned to baseline at 2 to 4 hours. Preischemic compared with 1 hour postischemic arteriolar dilation to NMDA was 10+/-2% versus 1+/-0% at 10(-5) mol/L and 40+/-4% versus 20+/-4% at 10(-4) mol/L NMDA (mean+/-SEM; both P<0.05, n=7). In contrast, pretreatment with Act-D resulted in preservation of the arteriolar responses to NMDA 1 hour after ischemia. For 10(-6) mol/L (n=5) of Act-D, dilations were 6+/-2% versus 6+/-2% at 10(-5) mol/L and 51+/-9% versus 39+/-10% at 10(-4) mol/L of NMDA. For 10(-5) mol/L (n=5) of Act-D, arterioles dilated by 7+/-2% versus 7+/-2% at 10(-5) mol/L and 38+/-4% versus 35+/-4% at 10(-4) mol/L NMDA. Similarly, CHX preserved NMDA-induced vasodilation. For 0.3 mg/kg of CHX (n=5), dilations were 8+/-2% versus 8+/-1% at 10(-5) mol/L and 39+/-4% versus 28+/-6% at 10(-4) mol/L NMDA. For 1.0 mg/kg of CHX (n=5), arterioles dilated by 10+/-2% versus 6+/-2% at 10(-5) mol/L and 37+/-7% versus 35+/-6% at 10(-4) mol/L NMDA. In experiments without ischemia, NMDA-induced vasodilation before and 85 minutes after administration of Act-D or CHX was not significantly different. CONCLUSIONS--Vascular responses of cerebral arterioles to NMDA after ischemia are preserved by pretreatment with either Act-D or CHX. Without preceding ischemia, Act-D and CHX do not potentiate neuronal-vascular responses to NMDA. Our results suggest that continued or augmented protein synthesis is involved in the transient attenuation of NMDA-induced dilation during the early reperfusion phase and that inhibitors of protein synthesis may protect neurons against ischemic stress.

Animals↗
PubMed1999

Mitochondrial potassium channel opener diazoxide preserves neuronal-vascular function after cerebral ischemia in newborn pigs.

BACKGROUND AND PURPOSE: N-Methyl-D-aspartate (NMDA) elicits neuronally mediated cerebral arteriolar vasodilation that is reduced by ischemia/reperfusion (I/R). This sequence has been preserved by pretreatment with the ATP-sensitive potassium (K(ATP)) channel opener aprikalim, although the mechanism was unclear. In the heart, mitochondrial K(ATP) channels (mitoK(ATP)) are involved in the ischemic preconditioning-like effect of K(+) channel openers. We determined whether the selective mitoK(ATP) channel opener diazoxide preserves the vascular dilation to NMDA after I/R. METHODS: Pial arteriolar diameters were determined with the use of closed cranial window/intravital microscopy in anesthetized piglets. Vascular responses to NMDA were assessed before and 1 hour after 10 minutes of global cerebral ischemia induced by raising intracranial pressure. Subgroups received 1 of the following pretreatments before I/R: vehicle; 1 to 10 micromol/L diazoxide; and coapplication of 100 micromol/L 5-hydroxydecanoic acid (5-HD), a K(ATP) antagonist with diazoxide. RESULTS: NMDA-induced dose-dependent pial arteriolar dilation was not affected by diazoxide treatment only but was severely attenuated by I/R. In contrast, diazoxide dose-dependently preserved the NMDA vascular response after I/R; at 10 micromol/L, diazoxide arteriolar responses were unaltered by I/R. The effect of diazoxide was antagonized by coapplication of 5-HD with diazoxide. Percent preservation of 100 micromol/L NMDA-induced vasodilation after I/R was 53+/-19% (mean+/-SEM, n=8) in vehicle-treated controls versus 55+/-10%, 85+/-5%, and 99+/-15% in animals pretreated with 1, 5, and 10 micromol/L diazoxide (n=8, n=8, and n=12, respectively) and 60+/-15% in the group treated with 5-HD+diazoxide (n=5). CONCLUSIONS: The mitoK(ATP) channel opener diazoxide in vivo preserves neuronal function after I/R, shown by pial arteriolar responses to NMDA, in a dose-dependent manner. Thus, activation of mitoK(ATP) channels may play a role in mediating the protective effect of other K(+) channel openers.

Animals↗
PubMed1999

Cerebrovascular reactivity remains intact after cortical depolarization in newborn piglets.

Cerebrovascular reactivity is severely affected by ischemia, and changes in vascular responses have been reported after cortical spreading depression and head trauma as well. Cortical depolarization (CD) occurs during ischemia, cortical spreading depression, and head trauma, but its effects on cerebrovascular reactivity are unclear. We tested the hypothesis that CD induced by KCl diminishes the vascular responsiveness to various vasodilatory stimuli in piglets. Responses of pial arterioles were determined by changes in vascular diameter by use of a closed cranial window and intravital microscopy. Baseline arteriolar diameters were 105 +/- 3 microm (mean +/- SEM, n = 27). CD was elicited by topical administration of 1 mol/L KCl for 3 min. Vascular responses were measured before and 1 h after CD. KCl elicited CD and constricted arterioles by 54 +/- 4% (n = 27). N-methyl-D-aspartate induced dose-dependent vasodilation that was unaffected by CD; the percent changes were 9 +/- 1 versus 8 +/- 1 (before and after CD) at 10(-5) mol/L, 19 +/- 2 versus 18 +/- 3 at 5 x 10(-5) mol/L, and 29 +/- 2 versus 26 +/- 3 at 10(-4) mol/L (n = 9). Hypercapnic vasodilation was not diminished by CD; the percent changes were 15 +/- 2 versus 16 +/- 4 at 5%, and 27 +/- 5 versus 27 +/- 6 at 10% inspired CO2 (n = 8). Aprikalim and forskolin caused dilation that was also resistant to prior CD; the percent change values were 21 +/- 4 versus 18 +/- 3 and 16 +/- 2 versus 16 +/- 4 at 10(-6) mol/L, 36 +/- 5 versus 34 +/- 5 and 34 +/- 7 versus 37 +/- 7 at 10(-5) mol/L (n = 8), respectively. Finally, calcitonin gene-related peptide-induced vasodilation was unaffected by CD; percent changes were 15 +/- 3 versus 16 +/- 2 at 10(-7) mol/L and 26 +/- 4 versus 22 +/- 3 at 10(-6) mol/L (n = 8). The intact vascular responses after CD suggest that this component is not responsible for decreased cerebrovascular reactivity after ischemia, head trauma, or cortical spreading depression.

Animals↗
PubMed1998

Potassium channel activators protect the N-methyl-D-aspartate-induced cerebral vascular dilation after combined hypoxia and ischemia in piglets.

BACKGROUND AND PURPOSE: Cerebral arteriolar dilation to N-methyl-D-aspartate (NMDA) is a neuronally mediated multistep process that is sensitive to cerebral hypoxia and ischemia (H/I). We tested the hypothesis that topical pretreatment with the selective potassium channel agonists NS1619 and aprikalim preserves the vascular response to NMDA after consecutive H/I. METHODS: Pial arteriolar diameters were measured in anesthetized piglets with the use of a closed cranial window and intravital microscopy. Arteriolar responses to NMDA (10(-5), 5 x 10(-5), and 10(-4) mol/L) were recorded before and 1 hour after 10 minutes of hypoxia (8.5% O2 in N2) plus 10 minutes of ischemia (H/I). Ischemia was induced by increasing intracranial pressure. Subgroups were topically pretreated with 10(-5) mol/L NS1619, 10(-6) mol/L aprikalim, 10(-6) mol/L calcitonin gene-related peptide (CGRP), or 10(-5) mol/L papaverine. We also examined the effects of H/I on vascular responses to kainate (10(-4) mol/L) to assess specificity of neuronal injury. RESULTS: Arteriolar responses to NMDA were significantly attenuated after H/I. Baseline compared with post-H/I arteriolar diameters were 9+/-4% versus 3+/-2% at 10(-5) mol/L, 22+/-4% versus 4+/-2% at 5 x 10(-5) mol/L, and 33+/-4% versus 7+/-2% at 10(-4) mol/L (mean+/-SE; all P<.05, n=7). Pretreatment with NS1619 and aprikalim preserved the arteriolar responses to NMDA after H/I. For NS1619 (n=6), values were as follows: 9+/-2% versus 6+/-4% at 10(-5) mol/L, 19+/-6% versus 21+/-5% at 5 x 10(-5) mol/L, and 35+/-3% versus 31+/-5% at 10(-4) mol/L. For aprikalim (n=7), values were as follows: 6+/-2% versus 8+/-2% at 10(-5) mol/L, 22+/-6% versus 15+/-3% at 5 x 10(-5) mol/L, and 41+/-5% versus 32+/-6% at 10(-4) mol/L. In contrast, piglets pretreated with CGRP (n=6) or papaverine (n=5) showed no preservation of the vascular response to NMDA after H/I, although these compounds dilated the arterioles to an extent similar to that with NS1619/aprikalim. Kainate-induced arteriolar dilation (n=6) was largely preserved after H/I compared with preischemic responses. CONCLUSIONS: (1) Vascular responses of cerebral arterioles to NMDA after H/I are preserved by pretreatment with NS1619 or aprikalim, indicating a neuroprotective effect. (2) CGRP and papaverine do not preserve the vascular response to NMDA despite causing vasodilation similar to that with NS1619 or aprikalim. This suggests that activation of potassium channels on neurons accounts for the protective effect of potassium channel agonists. (3) Preserved arteriolar dilation to kainate suggests largely intact functioning of neuronal nitric oxide synthase after H/I.

Analysis of Variance↗
PubMed1997

Analysis of dendritic cells at the genetic level.

To increase our understanding of dendritic cell (DC) function we have used two approaches to search at the genetic level for molecules which are specifically expressed by these cells. First, we have performed random sequencing of cDNA libraries prepared from DC. Second, we have employed differential display PCR (DD-PCR). DD-PCR is a powerful technique for the identification at the RNA level of molecules which are expressed in a cell type-specific manner. In our study, we have compared RNA from DC with RNA from a panel of leukocyte cell lines. Here we present a summary of our findings using these two approaches, and show that both methods are complementary and can be used to identify molecules that are specific to DC.

Antigen Presentation↗
PubMed1996

Kinematic analysis of movement imitation in apraxia.

Accuracy of the final position and kinematics of movement were analysed during the imitation of meaningless gestures in patients with unilateral brain lesions who performed with the hand ipsilateral to the lesion and in control subjects. Controls imitated the gestures virtually without spatial errors. The kinematics of their movements was characterized by single-peaked and approximately bell-shaped velocity profiles of the transport phase combined with no or only minor corrective movements in the final phase. Patients with right brain damage (RBD) performed as well as control subjects with respect to both spatial accuracy of final hand-positions and kinematic parameters of the movement trajectories. Patients with left brain damage (LBD) committed spatial parapraxias and had a much higher frequency of kinematic abnormalities. However, there was no correlation between kinematic abnormalities and apraxic errors. There were kinematically abnormal movements which reached a correct final position as well as kinematically normal movements leading to apraxic errors. One possible explanation for the combined occurrence of kinematic abnormalities and parapraxias in LBD patients would be that they are independent sequels of left hemisphere lesions. An alternative account is that the associations and dissociations result from an interaction between one common basic deficit and strategies to cope with this deficit. The basic deficit may concern the mental representation of the target position. The LBD patients may react to the absence of an appropriate representation of the target by one of two alternative strategies; they may switch to a strategy of slowed, on-line controlled movements to find the required final position, or they may move their hand smoothly at normal speed to a roughly specified location without taking note of their deficiency. Depending on whether these strategies are successful or not they would lead to the observed associations and dissociations between kinematic abnormalities and spatial parapraxias.

Adult↗