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B Schmitz

Publications and source records attributed to B Schmitz.

At least 55 records · Page 3Linked to original sources

Fenfluramine blocks low-Mg2+-induced epileptiform activity in rat entorhinal cortex.

PURPOSE: The entorhinal cortex (EC) represents the main input structure to the hippocampus and seems to be critically involved in temporal lobe epilepsy. Considering that the EC receives a strong serotonergic projection from the raphe nuclei and expresses a high density of serotonin (5-HT) receptors, the effect of the 5-HT-releasing drug fenfluramine (FFA) on epileptiform activity generated in the EC was investigated in an in vitro model of epilepsy. METHODS: The experiments were performed on 43 horizontal slices containing the EC, the subiculum, and the hippocampal formation obtained from 230-250 g adult Wistar rats. Using extracellular recording techniques, we investigated the effect of bath-applied FFA (200 micromol/L to 1 mmol/L) on epileptiform activity induced by omitting MgSO4 from the artificial cerebrospinal fluid. RESULTS: We demonstrate that FFA reversibly blocks epileptiform activity in the EC. Surprisingly, in the presence of the 5-HT uptake blocker paroxetine, the FFA-induced effect was diminished. Coapplication of the 5-HT1A receptor antagonist WAY100635 prevented the FFA-induced anticonvulsive effect, suggesting that (a) the FFA-induced suppression of epileptiform activity is mediated by the release of 5-HT from synaptic terminals within the EC rather than by an unspecific effect of FFA and (b) released 5-HT most likely blocks the activity by activation of 5-HT1A receptors. CONCLUSION: FFA, which is primarily used because of its anorectic activity, might get an additional therapeutic value in the treatment of temporal lobe epilepsy with parahippocampal involvement.

Animals↗

Penumbral tissue alkalosis in focal cerebral ischemia: relationship to energy metabolism, blood flow, and steady potential.

The effect of focal ischemia on tissue pH was studied at various times up to 6 hours after permanent middle cerebral artery occlusion in rats. Tissue pH was imaged by using umbelliferone fluorescence and correlated with cerebral blood flow, ATP content, and recordings of the steady potential. Circumscribed foci of allalosis (pH 7.32+/-0.11) were detected with increasing frequency in penumbral regions having near-to-normal ATP concentrations and cerebral blood flow values between 20% and 40% of control. Both the infarct core, defined by ATP loss and cerebral blood flow values of less than 20% of control, and the inner peri-infarct rim were consistently acidic (pH 6.03+/-0.36 and 6.53+/-0.24, respectively). Treatment with the glutamate antagonist dizocilpine (MK-801) suppressed negative shifts of the steady potential and reduced significantly the occurrence of alkalosis observed in 90% of untreated but only in 44% of treated animals. Penumbral alkalosis appeared to be a time-dependent event occurring 30 to 60 minutes after the passage of peri-infarct depolarizations. The diversity of penumbral pH changes reflects the local disturbance of pH regulation and, possibly, the differential fate of penumbral subareas.

Acidosis↗

Global cerebral ischemia due to cardiocirculatory arrest in mice causes neuronal degeneration and early induction of transcription factor genes in the hippocampus.

To analyze the role of specific genes and proteins in neuronal signaling cascades following global cerebral ischemia, it would be useful to have a reproducible model of global cerebral ischemia in mice that potentially allows the investigation of mice with specific genomic mutations. We first report on the development of a model of reversible cardiocirculatory arrest in mice and the consequences of such an insult to neuronal degeneration and expression of immediate early genes (IEG) in the hippocampus. Cardiocirculatory arrest of 5 min duration was induced via ventricular fibrillation in mechanically ventilated NMRI mice. After successful cardiopulmonary resuscitation (CPR), animals were allowed to reperfuse spontaneously for 3 h (n=7) and 7 days (n=7). TUNEL staining revealed a selective degeneration of a subset of neurons in the hippocampal CA1 sector at 7 days. About 30% of all TUNEL-positive nuclei showed condensed chromatin and apoptotic bodies. Immunohistochemical studies of IEG expression performed at 3 h exhibited a marked induction of c-Fos, c-Jun, and Krox-24 protein in all sectors of the hippocampus, peaking in vulnerable CA1 pyramidal neurons and in dentate gyrus. In contrast, sham-operated animals (n=3) did not reveal neuronal degeneration or increased IEG expression in the hippocampus when compared with untreated control animals (n=3). In conclusion, we present a new model of global cerebral ischemia and reperfusion in mice with the use of complete cardiocirculatory arrest and subsequent CPR. Following 5 min of ischemia, a subset of CA1 pyramidal neurons was TUNEL-positive at 7 days. The expression of IEG was observed in all sectors of the hippocampus, including selectively vulnerable CA1 pyramidal neurons. This appears to be a good model which should be useful in evaluating the role of various genes in transgenic and knockout mice following global ischemia.

Animals↗

Regional and directional anisotropy of apparent diffusion coefficient in rat brain.

Quantitative diffusion maps were recorded in normal rat brain. In multi-slice sections covering the whole brain, strong variation of the apparent diffusion coefficient (ADC) was observed depending on slice position at constant gradient direction. Furthermore, a varying difference between apparent diffusion coefficients depending on gradient direction was found, reaching 32% in the cortex of the ventral-most horizontal sections while showing equal ADC on the dorsal cortex side. The regional variation and directional anisotropy of the ADC was not restricted to white matter but was described for both cortical and subcortical brain tissue. From diffusion coefficients along the three major field gradient directions (ADCx, ADCy, ADCz), the average ADC (ADCaverage) was determined from the trace of the diffusion tensor (D) as 653+/-28 microm2/s for parietal cortex and 671+/-32 microm2/s for lateral cortex, independent of position along the sagittal direction. From these observations about the regional diffusion anisotropy, a more stringent protocol for the description of ischemic ADC changes is proposed.

Animals↗

Polycythemia vera megakaryocytes store and release lysozyme to a higher extent than megakaryocytes in secondary polycythemia (polyglobuly).

Lysozyme, a myelomonocytic marker not only exerts bacteriolytic, but also immunomodulatoric properties and was found to bind to the glycosaminoglycan serglycin, an important constituent of the extracellular matrix (ECM). Pathological serum lysozyme levels were described in chronic myeloproliferative disorders (CMPDs) and other hematological conditions. In this context it is remarkable that in polycythemia rubra vera (PV), characterized by a proliferation particularly of the megakaryo- and erythropoiesis, serum lysozyme levels behave independently of the numbers of myelomonocytic cells in peripheral blood. To elucidate whether megakaryopoiesis might be the source of the increased serum lysozyme, we performed an experimental study on isolated and enriched megakaryocytes derived from bone marrow of patients with PV. Findings were compared to a group of patients with reactive (smoker's) polyglobuly (PG). In confirmation of previous results, quantification of serum lysozyme levels showed a slight elevation in the cohort of PV patients which was not correlated with the leukocyte count. Applying an immunohistochemical assay we were able to demonstrate intracytoplasmic lysozyme storage in megakaryocytes. Moreover, performing the reverse hemolytic plaque assay (RHPA), a technique which enables detection of secreted proteins at the single cell level, we found that 54% of the PV, but only 3% of the PG megakaryocytes spontaneously secreted lysozyme. After rhIL-3 treatment the secretion of lysozyme remained unchanged in PV but increased to 14% in PG. These findings suggest that the extent of megakaryocytic lysozyme secretion might discriminate PV from reactive conditions. Although a direct involvement of lysozyme in the regulation of aberrant megakaryopoiesis in PV is not likely, the results of the present study point to the possibility that lysozyme could be involved in the interactions of PV megakaryocytes with ECM. Moreover, the response to rhIL-3 significantly discriminates PV megakaryocytes from megakaryocytes of the PG group.

Female↗

Megakaryocyte induced fibroblast proliferation is enhanced by costimulation with IL-6/IL-3 and dependent on secretory and adhesion events.

Experimental data are in keeping with the finding that megakaryocytes isolated from normal human bone marrow may promote fibroblast growth. This effect can be significantly enhanced by interleukin (IL)-3. In this context it has been demonstrated that IL-3 induces the release of platelet-derived growth factor (PDGF) and transforming growth factor beta1 (TGFbeta1) from megakaryocytes, factors known to enhance fibroblast proliferation. The present in vitro study was performed to elucidate the action of several other cytokines which are able to influence the different steps of megakaryocyte maturation and function like stem cell factor (SCF), IL-6, and leukemia inhibitory factor (LIF) as well. Following an appropriate experimental design we were able to show that none of the mentioned cytokines enhanced megakaryocyte dependent fibroblast proliferation in the coculture assays. On the other hand, IL-6 in combination with IL-3 surpassed the IL-3 dependent action significantly. However, the combined IL-3/IL-6 effect was not explainable by an increased PDGF/TGF-beta secretion of the megakaryocytes. In transwell experiments the inhibition of cell-to-cell contact via tissue culture inserts generated a conspicuous impairment of fibroblast growth in the IL-3/IL-6 treated cocultures. This reversal surpassed even the effect on the untreated and IL-3 stimulated cocultures. Hence, a direct contact of both cell types probably inducing adhesion phenomenons and warranting a certain threshold of local PDGF/TGF-beta concentration is a prerequisite for the proliferative effect on fibroblasts in the costimulation experiments. These results are of special interest regarding the evolution of myelofibrosis in chronic myeloproliferative disorders (CMPDs) because (1) various progenitor cells including the megakaryocytic lineage are hypersensitive towards IL-3 and (2) an abnormal secretion of IL-6 is described for megakaryocytes in these disorders.

Cell Adhesion↗

Polycythemia vera megakaryocytes but not megakaryocytes from normal controls and patients with smokers polyglobuly spontaneously express IL-6 and IL-6R and secrete IL-6.

Polycythemia rubra vera (PV) represents a clonal hematological disorder defined by an abnormal expansion of erythroid precursors and megakaryopoiesis, in particular. Ample evidence has been provided that the IL-6/1L-6R complex may be responsible for the proliferation of normal and neoplastic megakaryocytes in vitro and this fact lead us to the hypothesis, that defects in the regulation of IL-6 synthesis take part in the pathogenesis of PV. The study was carried out to determine the IL-6 serum levels and the megakaryocytic IL-6 production in patients with PV and to compare these data with the situation in hematologically healthy donors as well as in patients suffering from spurious polycythemia--smokers polyglobuly (PG). For this purpose, IL-6 serum levels were measured by ELISA and the megakaryocytic production studied by immunohistochemistry, reverse hemolytic plaque assay (RHPA) together with reverse transcription/polymerase chain reaction (RT-PCR) in highly enriched megakaryocyte preparations. In additional experiments, the influence of IL-3 stimulation and the expression of IL-6R were tested. Serum levels of IL-6 did not differ between the three groups under study. In contrast, immunohistochemistry revealed a raised proportion of megakaryocytes expressing IL-6 in PV as compared to normal donors and patients suffering from PG. The percentage of megakaryocytes actively secreting this cytokine as detected by the RHPA was 20 times greater than in both the other groups. This phenomenon was further substantiated by the fact that IL-6 mRNA could only be shown in PV megakaryocyte preparations. The regulation of IL-6 secretion appears to be abnormal in PV. Whereas in the normal and in the PG group IL-3 stimulation exerts a marked increase in megakaryocytic IL-6 secretion, PV megakaryocytes responded with a paradoxical down-regulation of IL-6 synthesis combined with the loss of IL-6R. Our data describe for the first time an abnormally raised IL-6 production by PV megakaryocytes and point towards fundamental regulatory alterations of the IL-6 synthesis in this disease.

Bone Marrow↗

O-linked N-acetylglucosamine levels in cerebellar neurons respond reciprocally to pertubations of phosphorylation.

The novel intracellular carbohydrate O-linked N-acetylglucosamine (O-GlcNAc) is present on proteins ranging from those of viruses to those of humans and include cytosolic, nuclear and plasma-membrane proteins. In this report we have examined the effect of manipulation of phosphorylation on the levels of O-GlcNAc in cerebellar neurons from early postnatal mice. Our results indicate a reciprocal response of O-GlcNAc levels to phosphorylation. Activation of protein kinase A or C, for example, results in reduced levels of O-GlcNAc specifically in the fraction of cytoskeletal and cytoskeleton-associated proteins, while inhibition of the same kinases results in increased levels of O-GlcNAc. These data are in keeping with a reciprocal action of O-GlcNAc with respect to phosphorylation and suggest that this modification may have a role in signal transduction.

Acetylglucosamine↗

Psychiatric syndromes related to antiepileptic drugs.

All antiepileptic drugs may provoke positive or negative psychiatric reactions in individual patients. These psychotropic effects are not simply idiosyncratic but depend on the drug's anticonvulsive strength and the person's genetic and biographic psychiatric predisposition. Mechanisms related to psychiatric adverse events are polytherapy and folate deficiency, forced normalization, drug toxicity, and withdrawal. Our knowledge on dose independent, idiosyncratic psychotropic side effects is still limited. With respect to the older antiepileptic drugs there are almost no systematic data, and knowledge is largely empirical and based on anecdotal reports. With respect to the new generation of anticonvulsants there are data on psychiatric side effects from drug trials. However, these data are not always entirely transparent to the interested epileptologist. Moreover, drug trials are designed to test anticonvulsive efficacy and psychiatric adverse events are not systematically reported, thus severity psychopathologic nature of behavioral problems remain obscure. Differences in patients included in trials do not allow comparisons of psychiatric risks of specific drugs, particularly since following the vigabatrin experience, patients with a psychiatric history were often excluded from trials. In this chapter, methodological issues related to data on psychiatric adverse events of AED are discussed followed by an overview on the current knowledge on psychiatric side effect profiles of old and new antiepileptic drugs.

Anticonvulsants↗

Insertion of foreign DNA into an established mammalian genome can alter the methylation of cellular DNA sequences.

The insertion of adenovirus type 12 (Ad12) DNA into the hamster genome and the transformation of these cells by Ad12 can lead to marked alterations in the levels of DNA methylation in several cellular genes and DNA segments. Since such alterations in DNA methylation patterns are likely to affect the transcription patterns of cellular genes, it is conceivable that these changes have played a role in the generation or the maintenance of the Ad12-transformed phenotype. We have now isolated clonal BHK21 hamster cell lines that carry in their genomes bacteriophage lambda and plasmid pSV2neo DNAs in an integrated state. Most of these cell lines contain one or multiple copies of integrated lambda DNA, which often colocalize with the pSV2neo DNA, usually in a single chromosomal site as determined by the fluorescent in situ hybridization technique. In different cell lines, the loci of foreign DNA insertion are different. The inserted bacteriophage lambda DNA frequently becomes de novo methylated. In some of the thus-generated hamster cell lines, the levels of DNA methylation in the retrotransposon genomes of the endogenous intracisternal A particles (IAP) are increased in comparison to those in the non-lambda-DNA-transgenic BHK21 cell lines. These changes in the methylation patterns of the IAP subclone I (IAPI) segment have been documented by restriction analyses with methylation-sensitive restriction endonucleases followed by Southern transfer hybridization and phosphorimager quantitation. The results of genomic sequencing experiments using the bisulfite protocol yielded additional evidence for alterations in the patterns of DNA methylation in selected segments of the IAPI sequences. In these experiments, the nucleotide sequences in >330 PCR-generated cloned DNA molecules were determined. Upon prolonged cultivation of cell lines with altered cellular methylation patterns, these differences became less apparent, perhaps due to counterselection of the transgenic cells. The possibility existed that the hamster BHK21 cell genomes represent mosaics with respect to DNA methylation in the IAPI segment. Hence, some of the cells with the patterns observed after lambda DNA integration might have existed prior to lambda DNA integration and been selected by chance. A total of 66 individual BHK21 cell clones from the BHK21 cell stock have been recloned up to three times, and the DNAs of these cell populations have been analyzed for differences in IAPI methylation patterns. None have been found. These patterns are identical among the individual BHK21 cell clones and identical to the patterns of the originally used BHK21 cell line. Similar results have been obtained with nine clones isolated from BHK21 cells mock transfected by the Ca2+-phosphate precipitation procedure with DNA omitted from the transfection mixture. In four clonal sublines of nontransgenic control BHK21 cells, genomic sequencing of 335 PCR-generated clones by the bisulfite protocol revealed 5'-CG-3' methylation levels in the IAPI segment that were comparable to those in the uncloned BHK21 cell line. We conclude that the observed changes in the DNA methylation patterns in BHK21 cells with integrated lambda DNA are unlikely to preexist or to be caused by the transfection procedure. Our data support the interpretation that the insertion of foreign DNA into a preexisting mammalian genome can alter the cellular patterns of DNA methylation, perhaps via changes in chromatin structure. The cellular sites affected by and the extent of these changes could depend on the site and size of foreign DNA insertion.

Animals↗

Galectin-3 promotes neural cell adhesion and neurite growth.

Galectin-3 is a member of the galectin family and belongs to a group of soluble beta-galactoside-binding animal lectins. The molecule is expressed by neural and nonneural cells intra- (cytoplasm and nucleus) as well as extra-cellularly (plasma membrane and extracellular space). By using an in vitro cell-substratum adhesion assay, we have addressed the question whether galectin-3 present in the extracellular milieu may support the adhesion and/or neurite outgrowth of neural cells in a manner analogous to cell adhesion molecules. Galectin-3 was immobilized as a substratum and various cell types, N2A (neuroblastoma), PC12 (pheochromocytoma), and TSC (transformed Schwann cells) cell lines, neural cells from early postnatal mouse cerebellum, and dorsal root ganglion neurons from newborn mice were allowed to adhere to the lectin. Here we show that all cell types studied specifically adhered to galectin-3 by the following criteria: 1) the number of adherent cells was dependent on the galectin-3 concentration used for coating; 2) adhesion of cells to galectin-3, but not to collagen type I or laminin was inhibited by polyclonal antibodies to galectin-3; 3) upon addition of asialofetuin (a polyvalent carrier of terminal beta-galactosides) to the cell suspension prior to the adhesion assay, cell adhesion to galectin-3 was inhibited in a dose-dependent manner; and 4) cell adhesion to galectin-3 was abolished by treatment of cells with endo-beta-galactosidase. In addition, the adhesion of dorsal root ganglion neurons to galectin-3 could be inhibited by lactose. Notably, substratum-bound galectin-3 promoted the outgrowth of neurites from dorsal root ganglia explants and this neurite outgrowth promoting activity could be inhibited by polyclonal antibodies to galectin-3.

Animals↗

A 5'-CG-3'-rich region in the promoter of the transcriptionally frequently silenced RET protooncogene lacks methylated cytidine residues.

In a large proportion of familial and sporadic cases of Hirschsprung disease (HSCR) mutations in the RET (rearranged during transfection) protooncogene have been described. We have investigated the structure of the RET gene promoter and have analysed a region of approximately 1000 nucleotides in its promoter and 5'-upstream segments for the occurrence of 5-methyldeoxycytidine (5-mC) residues by using the bisulfite protocol of the genomic sequencing method. With an estimated sensitivity of about 93% of this technique, not a single 5-mC residue could be detected in the control region of a gene that seems to be silenced or exhibit low activity in many adult tissues. In these experiments, the DNAs of peripheral white blood cells (PWBC) from four healthy individuals, from seven patients with familial HSCR, as well as DNAs from different human tissues and from a human embryonic kidney (HEK) cell line have been included. In a DNA segment starting 790 nucleotides upstream of the transcriptional start site of the RET gene, a few 5-mC residues have been identified. This region possibly constitutes the transition site from an unmethylated promoter to a more extensively methylated region in the human genome. The data presented are remarkable in that a highly 5'-CG-3'-enriched segment of the human genome with 49 5'-CG-3' dinucleotide pairs in 400 bp within the putative promoter region is completely devoid of 5-mC residues, although this control region is not actively transcribed in most adult human tissues. By hybridization of a PCR-amplified RET protooncogene cDNA probe harboring exons 9-15 to a membrane (Clontech) containing poly-A selected RNAs from 50 different human tissues, weak RET protooncogene expression in many of the neural cell derived tissues has been detected. RNAs extracted from many other human tissues do not share sequence homologies to this 32P-labeled probe. Mechanisms other than DNA methylation obviously play the crucial role in the inactivation of the RET gene promoter in these tissues. We have also demonstrated by the in vitro premethylation of a RET promoter-chloramphenicol acetyltransferase (CAT) gene construct and transient transfection experiments into neuroblastoma cells that the transcriptional activity of the RET promoter is decreased by HpaII (5'-CCGG-3') methylation and abolished by SssI (5'-CG-3') methylation. Hence, the RET promoter region is sensitive to this regulatory signal. However in vivo, DNA methylation of the promoter region seems not to be the predominant regulatory mechanism for the RET protooncogene. Possibly, in adults the RET gene can be occasionally activated.

Adult↗

New 5'-(CGG)n-3' repeats in the human genome.

We identified new, potentially unstable loci in the human genome containing 5'-(CGG)n-3' trinucleotide repeats by screening a human subgenomic library as well as a chromosome 16 library with a 5'-(CGG)17-3' oligodeoxyribonucleotide probe. Five different clones were isolated, two from the chromosome 16 library and three from the subgenomic library. Determinations of the nucleotide sequences have revealed that the E7 clone displayed, in addition to the 5'-(CGG)n-3' trinucleotide repeat, a 5'-(CAG)n-3' and a 5'-(CCT)n-3' trinucleotide repeat. Two clones, CL16-1 and P5-5, had homologies to known genes, the human casein kinase II alpha' subunit (chromosome 16) and the human calcium-activated potassium channel (chromosome 10), respectively. Clones E7 and P4 were assigned to chromosome 6, whereas CL16-8 mapped to chromosome 16. Their potential coding capacities were assessed by RNA transfer (Northern blotting) experiments. Four different transcripts were identified by using the E7 clones as hybridization probes, three of them being brain-specific. The P4 clone was expressed in placenta and skeletal muscle. Minor polymorphisms within the repeats were observed in normal and in fragile X individuals. Lung and colon carcinoma cell lines in which some microsatellites were shown to be unstable were also investigated. Expansions of the 5'-(CGG)n-3' repeats were not found.

Alleles↗

Detection of the bcr/abl gene in bone marrow macrophages in CML and alterations during interferon therapy--a fluorescence in situ hybridization study on trephine biopsies.

A fluorescence in situ hybridization (FISH) study was performed on trephine biopsies of the bone marrow in chronic myelogenous leukaemia (CML) to evaluate the bcr/abl translocation in macrophages before and during interferon (IFN) therapy. Mature macrophages and osteoclasts were identified by the monoclonal antibody PG-M1, which recognizes a fixative-resistant epitope of the CD68 molecule. In contrast to a control group, in 145 of 479 (30 per cent) macrophages of the CML bone marrow, a positive fusion signal was found, together with corresponding translocation sites in the surrounding myeloid cells. In patients following IFN treatment for approximately 12 months and with haematological/cytogenetic remission by clinical standards, this number was reduced to 10 of 136 (9 per cent) macrophages. In addition, the few multinucleated osteoclasts of the untreated CML bone marrow displayed positive translocation spots. This finding supports the hypothesis that stromal macrophages and osteoclasts are of haematogenic stem cell origin. Moreover, clinical remission and reduction of bcr/abl-positive macrophages under IFN therapy lend support to the hypothesis that the presence of malignant stromal macrophages may contribute to the selective expansion of leukaemic precursors and the suppression of normal haematopoiesis in CML.

Antigens, CD↗

Evidence for integrin receptor involvement in megakaryocyte-fibroblast interaction: a possible pathomechanism for the evolution of myelofibrosis.

Megakaryocytes are assumed to be functionally linked with the evolution of myelofibrosis, complicating chronic myeloproliferative disorders. It has already been shown that megakaryocytes will promote fibroblast growth in vitro when in spatial proximity. Here, we demonstrate that the integrin receptors alpha3beta1 and alpha5beta1 are involved in this megakaryocyte-fibroblast interaction. Upon addition of anti-alpha3 and -alpha5 antibodies to megakaryocyte-fibroblast cocultures, fibroblast growth was significantly impaired, and megakaryocyte attachment to the fibroblast feederlayer was significantly reduced. Unilateral blocking of megakaryocytes with anti-alpha3 or -alpha5 antibodies resulted in a suppression of adhesion, probably reflecting the prominent function of fibronectin receptors on the megakaryocyte surface. Moreover, the oligopeptide RGDS (Asp-Gly-Asp-Ser) caused a significant reduction of fibroblast growth as well as megakaryocyte adhesion. This feature reinforces that fibronectin receptors are involved. In addition, fibroblast proliferation was impaired by the application of fibronectin antibodies recognizing the cell-binding domain. However, no effect was observable with respect to megakaryocyte adhesion. In conclusion, our in vitro studies demonstrate the involvement of beta1-integrins, in particular the fibronectin receptor in the megakaryocyte-dependent fibroblast proliferation and therefore suggest a pivotal role of megakaryocytes in the complex pathomechanism causing myelofibrosis.

Adult↗

Functional MRI of somatosensory activation in rat: effect of hypercapnic up-regulation on perfusion- and BOLD-imaging.

Functional activation of somatosensory cortex was studied in alpha-chloralose anesthetized rats by functional magnetic resonance imaging (fMRI), using both perfusion-weighted and T2*-weighted (blood oxygenation level dependent, BOLD) imaging. The sensitivity of functional activation was altered by ventilating animals for 3 minutes with 6% CO2. Before hypercapnic conditioning, electrical stimulation of the left forepaw at a frequency of 3 Hz led to an increase of signal intensity (relative to the unstimulated baseline condition) in the right somatosensory cortex by 6+/-2% (means+/-SD) in T2*-weighted images and by 45%+/-48% in perfusion-weighted images. After hypercapnic conditioning the signal intensity increase in perfusion-weighted images doubled to 91%+/-62% (P=0.034), whereas that of T2*-weighted images only marginally increased to 7+/-4% (not significant). This different behavior in both imaging modalities is interpreted as evidence for an increased flow response in combination with a higher oxygen extraction. Thus, the fMRI data reflect hypercapnia-induced resetting of the functional-metabolic coupling of the tissue during activation.

Animals↗

Recovery of the rodent brain after cardiac arrest: a functional MRI study.

Recovery of the cerebral cortex after 10 min of cardiac arrest was studied in rat using noninvasive MRI techniques. The apparent diffusion coefficient (ADC) of brain water was imaged to document reversal of the metabolic impairment. Perfusion-weighted imaging and blood oxygen level dependent (BOLD) imaging were performed to assess functional recovery. To this purpose, rats were anesthetized with alpha-chloralose, and somatosensory cortex was activated by electrical stimulation of the contralateral forepaw. In sham-operated controls, cortical ADC was 862 +/- 10 microm2/s, and stimulation of forepaw led to a focal increase of signal intensity in somatosensory cortex by 71 +/- 22% in perfusion-weighted images and by 6 +/- 1% in BOLD images. One hour after successful resuscitation following 10 min of cardiac arrest, ADC did not differ from control but functional activation was completely suppressed. After 3 hours of reperfusion, functional activity began to reappear but the recovery of the BOLD signal progressed faster than that of the perfusion-weighted signal. The differences in the recovery of ADC, BOLD, and perfusion imaging are related to differences between metabolic and functional recovery on one hand and between blood flow and oxygen extraction on the other. The combination of these MRI methods thus provides detailed qualitative information about the progression of brain recovery after transient circulatory arrest.

Animals↗