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Biomedical subjects

E Bock

Publications and source records attributed to E Bock.

At least 91 records · Page 5Linked to original sources
PubMed1994

Transfection of glioma cells with the neural-cell adhesion molecule NCAM: effect on glioma-cell invasion and growth in vivo.

The tumor growth and the invasive capacity of a rat glioma cell line (BT4Cn) were studied after transfection with the human transmembrane 140-kDa isoform of the neural-cell adhesion molecule, NCAM. After s.c. injection, the NCAM-transfected cells showed a slower growth rate than the parent cell line (BT4Cn). Upon intracerebral implantation with BT4Cn cells and different clones of NCAM-transfected cells, all animals developed neurological symptoms within 13-16 days. However, the tumors showed different growth characteristics. The NCAM-transfected BT4Cn cells were localized in the region of the injection site, with a sharply demarcated border between the tumor and brain tissue. In contrast, the parental cell line showed single-cell infiltration and more pronounced destruction of normal brain tissue. Using a 51Cr-release assay, spleen cells from rats transplanted with BT4Cn tumor cells generally showed a lower cytotoxic response than the spleen cells from rats transplanted with the transfected variants of BT4Cn cells, indicating that the transfection procedure in itself mediated an activation of the immune system. The present data suggest that NCAM may influence the malignant behavior of rat glioma cells in vivo.

Animals↗
PubMed1994

Characterization of N-cadherin messenger RNA and polypeptide expression in rat.

The cell adhesion molecule N-cadherin is a member of the cadherin gene superfamily. The protein is involved in morphogenetic processes, including neurite extension. In this study, N-cadherin mRNA and polypeptide expression were investigated in rat brain, liver, muscle, heart, kidney and lung during postnatal development and aging. Six synthetic oligonucleotide probes covering different parts of mouse N-cadherin cDNA all hybridized to 5.2, 4.3-4.4 and 3.5 kb mRNAs in rat tissues. The mRNA pattern differed between tissues and, furthermore, the amount of N-cadherin mRNA and polypeptides in brain, liver and heart was higher than in muscle, kidney and lung. N-cadherin expression decreased slightly during early postnatal development in all tissues, whereas no changes in N-cadherin expression were observed during aging. Antibodies against a fusion protein containing the transmembrane and cytoplasmic sequence of chick N-cadherin were produced. These antibodies, termed anti-N-cad-cyt, were compared to the R-156 antibodies which recognize the 24 C-terminal amino acids of N-cadherin and which have been shown to react with a broad spectrum of cadherins. Using these two antibodies, it was shown that the 130 kDa N-cadherin polypeptide was subject to calcium-dependent cleavage of the cytoplasmic domain. Conversely, in the absence of calcium the polypeptide was cleaved extracellularly, producing two C-terminal fragments of 85 and 95 kDa. A 122 kDa polypeptide was recognized by both antibodies and may be either an alternatively spliced form of N-cadherin or a closely related cadherin.

Aging↗
PubMed1994

Anticardiolipin antibodies in HIV infection: association with cerebral perfusion defects as detected by 99mTc-HMPAO SPECT.

Anticardiolipin antibodies (ACA) belong to a heterogeneous group of antibodies directed against negatively charged phospholipids. In patients with rheumatic disorders, their presence has been correlated to the occurrence of thromboembolic complications, thrombocytopenia, abortions and other disease manifestations. Several studies have revealed the detection of mostly high-titre ACA in a significant proportion of HIV-infected patients without any known clinical relationship. In our study, ACA were detected in 17/34 HIV-infected patients, and their presence was significantly associated with the detection of cerebral perfusion abnormalities by 99mTc-HMPAO SPECT. SPECT scans were classified as normal or as focal or diffuse defects in uptake. Most patients (13/16) with cerebral perfusion defects had elevated ACA titres in contrast to 4/18 patients with normal SPECT findings (P = 0.002). Focal uptake defects were always associated with the presence of ACA. No correlation to clinical features or other laboratory parameters was evident. Our results suggest a possible implication of autoimmune mechanisms in the pathogenesis of cerebral perfusion abnormalities detected by SPECT scanning in HIV-infected patients. However, further studies are needed to evaluate the clinical significance and to develop possible therapeutic consequences.

AIDS-Related Opportunistic Infections↗
PubMed1994

New serum markers for small-cell lung cancer. II. The neural cell adhesion molecule, NCAM.

The neural cell adhesion molecule (NCAM) was recently suggested as a marker for small-cell lung cancer (SCLC). Immunohistochemical analysis demonstrated the presence of the NCAM in 78% of SCLC patients and in 25% of patients with other cancer forms. NCAM was proposed to be the most sensitive marker for SCLC, and it may also be an important prognostic marker for SCLC. We used a competitive ELISA to analyze the concentrations of NCAM in sera from 96 SCLC patients, 16 patients with non-SCLC, 4 patients with other cancer forms, and 16 healthy controls. All sera were collected at the time of diagnosis, before the patients received chemotherapy. The polyclonal antibody used in the assay recognized all three isoforms of NCAM. The concentration of NCAM was related to clinical parameters of the patients such as age, sex, blood group status, stage of disease, organ site involvement of metastases, survival, and expression of the ganglioside fucosyl-GM1 (FucGM1). Sera were considered positive if NCAM concentrations were higher than the mean concentration of healthy controls plus two standard deviations. Twenty-two percent of the sera from SCLC patients were positive for NCAM. No difference in concentration was found between SCLC patients with localized and extensive disease. Serum from one patient with cancer of the thyroid, but no sera from non-SCLC patients or normal healthy controls, was positive. The expression of NCAM did not correlate to any of the clinical parameters, and no correlation was found to the other serum marker, FucGM1.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Expression of N-CAM in fertilized pre- and periimplantation and parthenogenetically activated mouse embryos.

The expression of the cell adhesion molecule of the immunoglobulin family, neural cell adhesion molecule (N-CAM), in the pre- and periimplantation embryo was examined by immunocytochemistry. N-CAM is expressed on unfertilized ovulated oocytes, fertilized preimplantation embryos at all stages of development and parthenogenetically activated eggs and embryos. In fertilized embryos, expression from the 4-cell stage can be partially inhibited by blocking embryonic transcription before 38 h post human chorionic gonadotropin (hCG). Expression of N-CAM was reduced on the trophoblast of day 6 blastocysts in culture, weak on the trophoblast of embryonic outgrowths and disappears from invading trophoblast in utero. An antibody against alpha(2-8) linked polysialic acid, mAb2-2B, reacted with embryos from the 8-cell stage, and staining was similarly reduced on the trophoblast of blastocysts at the time of implantation. These results suggest a role for N-CAM in the interactions of cells of the preimplantation mammalian embryo which requires further investigation.

Amanitins↗
PubMed1994

[Doppler ultrasonography assessment of the inferior mesenteric artery. Feasibility study and definition of morphologic and flowmetric characteristics].

The conventional and Doppler US assessment of the inferior mesenteric artery has not been reported in the literature to date. In the present study, the feasibility of Doppler US of the inferior mesenteric artery was prospectively investigated in 112 consecutive nonselected patients; the corresponding morphological features (size and vessel course) and Doppler flowmetry (peak systolic, peak diastolic and mean velocities; pulsatility index) were defined. In 32 patients (29%) neither conventional nor color-Doppler nor duplex imaging was possible. Of the extant 80 patients, in 65 (81%) all the three methods allowed the correct assessment of the inferior mesenteric artery; in 15 patients (19%) the results were suboptimal (poor US visualization, or inadequate Doppler flowmetry). In 33/80 patients, arterial blood flow was quantitatively assessed in 1/min. As for the patients who underwent further diagnostic procedures--e.g., CT and angiography--a close correlation was demonstrated between the morphological and functional data obtained by Doppler US and the corresponding CT and angiographic features. The possibility of analyzing the inferior mesenteric artery with conventional and Doppler US, besides the celiac trunk and the superior mesenteric artery, should allow splanchnic circulation to be more completely assessed, thanks to information about normal hemodynamics (after a meal or in response to pharmacological treatments) as well as about the diseases known to affect intestinal perfusion--e.g., mesenteric ischemia.

Adult↗
PubMed1993

Demonstration of (Ca(2+)-Mg2+)-ATPase activity of the neural cell adhesion molecule.

In this study a possible association between (Ca(2+)-Mg2+)-ATPase activity and the neural cell adhesion molecule, NCAM, was investigated. The effects of various detergents on ATPase activity were evaluated, and it was found that solubilization of rat brain microsomes with 3-[(3-cholamidopropyl)dimethylammonio]-1-propanesulfonate, CHAPS, released a major fraction of the (Ca(2+)-Mg2+)-ATPase activity together with NCAM. Using different types of solid phase immunoadsorption it was shown that NCAM antibodies selectively isolated ATPase activity. Furthermore, agarose gel immunoelectrophoresis of solubilized brain microsomes followed by ATPase assay directly in the gel revealed ATPase activity associated with the NCAM immunoprecipitate. The NCAM-associated enzyme activity had a broad nucleoside triphosphate specificity and no strict selectivity for divalent cations, indicating that the enzyme probably is an ecto-ATPase. This raises a series of intriguing questions in relation to NCAM adhesive functions.

Adenosine Triphosphate↗
PubMed1993

Electrocardiographic characteristics indicating a risk of irreversibly impaired myocardial function in chronic aortic regurgitation.

In order to define which of selected ECG variables could indicate irreversibly impaired myocardial function in chronic aortic regurgitation 54 patients were stratified according to normal (> or = 50%; Group A, n = 41) or subnormal radionuclide left ventricular ejection fraction (LVEF < 50%; Group B, n = 13) late after aortic valve replacement. Preoperatively, Group B patients had a significantly greater QRS duration, greater R-peak time (RPT) prolongation in I, V5 or V6, greater RPT relative to the S-peak time of the maximum S in V1, V2 or V3 (R-peak delay) and a greater negative T-wave in I or V6, as compared with Group A. These ECG variables together with preoperative angiocardiographic LVEF and end-systolic volume index were subjected to stepwise linear discriminant analysis. The maximum RPT, angio-LVEF and the maximum RPT relative to the S-peak time of the maximum S in V1, V2 or V3 emerged as the most promising variables. Of of Group A patients 82.9% and 84.6% of Group B patients were correctly classified by the three variables. If applied separately, APT prolongation or the presence of the R-peak delay in the left-sided leads, although less sensitive, have reasonably high specificity as risk indicators of irreversibly impaired chamber function, their positive predictive value being 60 and 62.5%, respectively. In conjunction with preoperative LVEF the diagnostic contribution of the two ECG variables amounts to the greatest overall separation of postoperatively preserved from irreversibly impaired systolic function.

Aortic Valve Insufficiency↗
PubMed1993

Transmembrane neural cell-adhesion molecule (NCAM), but not glycosyl-phosphatidylinositol-anchored NCAM, down-regulates secretion of matrix metalloproteinases.

During embryogenesis interactions between cells and extracellular matrix play a central role in the modulation of cell motility, growth, and differentiation. Modulation of matrix structure is therefore crucial during development; extracellular matrix ligands, their receptors, extracellular proteinases, and proteinase inhibitors all participate in the construction, maintenance, and remodeling of extracellular matrix by cells. The neural cell-adhesion molecule (NCAM)-negative rat glioma cell line BT4Cn secretes substantial amounts of metalloproteinases, as compared with its NCAM-positive mother cell line BT4C. We have transfected the BT4Cn cell line with cDNAs encoding the human NCAM-B and -C isoforms. We report here that the expression of transmembrane NCAM-B, but not of glycosyl-phosphatidylinositol-linked NCAM-C, induces a down-regulation of 92-kDa gelatinase (matrix metalloproteinase 9) and interstitial collagenase (matrix metalloproteinase 1), indicating that cellular expression of the recognition molecule NCAM regulates the metabolism of the surrounding matrix.

Animals↗
PubMed1993

Intact transmembrane isoforms of the neural cell adhesion molecule are released from the plasma membrane.

Three soluble neural cell adhesion molecule (NCAM) polypeptide classes of M(r) values 190,000 (NCAM-s1), 135,000 (NCAM-s2) and 115,000-110,000 (NCAM-s3) have been demonstrated in rat brain and cerebrospinal fluid [Krog, Olsen, Dalseg, Roth and Bock (1992) J. Neurochem. 59, 838-847]. NCAM-s3 is known to arise from released glycosylphosphatidylinositol (GPI)-linked NCAM [He, Finne and Goridis (1987) J. Cell. Biol. 105, 2489-2500] as well as from extracellularly cleaved transmembrane NCAM isoforms [Nybroe, Linnemann and Bock (1989) J. Neurochem. 53, 1372-1378]. In this study the origin of NCAM-s1 and NCAM-s2 and the function of soluble NCAM forms were investigated. It was shown that all three soluble forms could be released from brain membranes with M(r) values identical to the three major membrane-associated forms: the large transmembrane 190,000-M(r) form (NCAM-A), the smaller transmembrane 135,000-M(r) form (NCAM-B) and the GPI-anchored 115,000-110,000-M(r) form (NCAM-C). A polyclonal antibody, directed against transmembrane and cytoplasmic epitopes common to NCAM-A and NCAM-B, was shown to react with NCAM-s1 and NCAM-s2. Furthermore, NCAM-B was shown to be shed in a presumably intact soluble form from membranes of cells transfected with this isoform. Thus, NCAM-s1 and NCAM-s2 probably represent intact released transmembrane NCAM-A and NCAM-B. The soluble transmembrane forms are likely to exist in vivo, as NCAM-s1 and NCAM-s2 were readily demonstrated in cerebrospinal fluid. By density-gradient centrifugation it was shown that shed transmembrane NCAM-B was present in fractions of high, as well as low, density, indicating that a fraction of the shed NCAM is associated with minor plasma membrane fragments. Finally, it was shown that isolated soluble NCAM inhibited cell binding to an immobilized NCAM substratum, attributing a pivotal role to soluble NCAM in vivo as a modulator of NCAM-mediated cell behaviour.

Animals↗
PubMed1993

Characterization of NCAM diversity in cultured neurons.

A single transcript of the NCAM gene undergoes differential processing resulting in a multiplicity of mRNAs and their translation products. In this study, the diversity of NCAM in rat primary neuronal cultures was investigated utilizing immuno- and Northern blot analyses. NCAM polypeptides of 190 kDa (NCAM-A) and 135 kDa (NCAM-B) were shown to be associated with the neuronal phenotype. These data were confirmed by Northern blotting, which in both neocortical neurons and cerebellar granule neurons revealed mRNA classes of 7.4 kb and 6.7 kb encoding for NCAM-A and -B, respectively. However, oligonucleotide probes, specific for selected exons or exon combinations, revealed special features of cerebellar granule neurons as compared to neocortical neurons: expression of 4.3 kb NCAM mRNA, a relatively low amount of VASE-containing variants, and an apparent lack of mRNA species containing exons alpha and an AAG insert between exons 12 and 13. Distinct patterns of NCAM mRNA may putatively be related to the regional origin and functional specificity of the investigated neurons.

Alternative Splicing↗
PubMed1993

Different isoforms and stock-specific variants of the cell adhesion molecule C-CAM (cell-CAM 105) in rat liver.

C-CAM is a cell adhesion molecule of the immunoglobulin superfamily with homophilic binding properties. Here we used the polymerase chain reaction to isolate clones of C-CAM from a rat liver cDNA library. Sequence analyses identified two major isoforms, C-CAM1 and C-CAM2, which differed in their 3' ends. C-CAM2 lacked a sequence of 53 nucleotides that was present in C-CAM1. This causes a frame shift and new stop codons, which gives rise to cytoplasmic domains of different sizes in the two isoforms (10 versus 71 amino-acid residues). In addition, all the clones had a different nucleotide and deduced amino-acid sequence (variant b) in the most N-terminal of the four immunoglobulin-like domains, compared to a previously published C-CAM sequence (variant a). Northern-blot analyses with specific oligonucleotide probes demonstrated that two different rat stocks expressed either variant a or variant b. Northern-blot analyses of rat liver and lung also showed that at least five different C-CAM transcripts are produced. Two major mRNA size classes of 4.0 kb and 6.0 kb, and one minor class of 3.0 kb were found. Both the 4.0-kb and 3.0-kb messenger classes reacted with two different probes that could distinguish between C-CAM1 and C-CAM2, while the 6.0-kb population only reacted with the probe selective for C-CAM1. Taken together these data demonstrate the existence of four different protein-coding sequences of rat liver C-CAM (C-CAM1 a and b, and C-CAM2 a and b). We suggest that both allelic variation and alternative splicing may contribute to the isoform-expression pattern of C-CAM in rats.

Amino Acid Sequence↗
PubMed1993

Age-related changes in expression of the neural cell adhesion molecule in skeletal muscle: a comparative study of newborn, adult and aged rats.

Neural cell adhesion molecule (NCAM) is expressed by muscle and involved in muscle-neuron and muscle-muscle cell interactions. The expression in muscle is regulated during myogenesis and by the state of innervation. In aged muscle, both neurogenic and myogenic degenerative processes occur. We here report quantitative and qualitative changes in NCAM protein and mRNA forms during aging in normal rat skeletal muscle. Determination of the amount of NCAM by e.l.i.s.a. showed that the level decreased from perinatal to adult age, followed by a considerable increase in 24-month-old rat muscle. Thus NCAM concentration in aged muscle was sixfold higher than in young adult muscle. In contrast with previous reports, NCAM polypeptides of 200, 145, 125 and 120 kDa were observed by immunoblotting throughout postnatal development and aging, the relative proportions of the individual NCAM polypeptides remaining virtually unchanged at all ages examined. However, changes in the extent of sialylation of NCAM were demonstrated. Even though the relative amounts of the various NCAM polypeptides were unchanged during aging, distinct changes in NCAM mRNA classes were observed. Three NCAM mRNA classes of 6.7, 5.2 and 2.9 kb were present in perinatal and young adult skeletal muscle, whereas only the 5.2 and 2.9 kb mRNA classes could be demonstrated in aged muscle. This indicates that metabolism of the various NCAM polypeptides is individually regulated during aging. Alternative splicing of NCAM mRNA in skeletal muscle was studied by Northern blotting using DNA oligonucleotide probes specifically hybridizing to selected exons or exon combinations. Exon VASE, which has previously been shown to be present in both brain and heart NCAM mRNA, was virtually absent from skeletal muscle at all ages studied. In contrast, the majority of NCAM mRNA in postnatal skeletal muscle was shown to contain extra exons inserted between exons 12 and 13. Of the various possible exon combinations at this splice site, the combinations 12-a-AAG-13 and 12-a-b seemed to be prevalent in postnatal skeletal muscle. No significant change in the relative proportion of these two exon combinations occurred during aging. The observed upregulation of NCAM protein in aged muscle supports the assumption that an increasing proportion of muscle fibres are denervated in aged muscle. Selective upregulation of the 5.2 and 2.9 kb mRNA forms have previously been demonstrated in muscle cell lines and in primary cultures of muscle cells during formation of myotubes in vitro, and this switch in NCAM mRNA classes has been suggested to correlate with myogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1993

Regulation of NCAM by growth factors in serum-free myotube cultures.

Regulation of the neural cell adhesion molecule (NCAM) was examined in primary cultures of chick skeletal muscle grown in serum-free defined medium. Relative levels of NCAM (per microgram protein) increased 20-30% in myotubes grown on Matrigel, a reconstituted basement membrane preparation, compared to those grown on collagen; total NCAM levels on Matrigel were increased 40-55% due to the additional increase in total protein. A dose dependent increase in relative NCAM levels in myotubes grown on Matrigel in defined medium was observed with the addition of adsorbed horse serum, while relative NCAM levels in myotubes grown on collagen were unaffected by altering the serum concentration. Thus, extracellular matrix molecules and soluble factors exert trophic effects on myotube NCAM expression. Similar developmental changes in the expression of the different molecular size forms of NCAM occurred in myotubes grown on collagen and Matrigel: levels of 150K and 135K Mr forms decreased during development, while 125K remained prominent in older myotubes. Relative NCAM levels were specifically enhanced 11-26% by several factors: nerve growth factor, thyroxine, insulin-like growth factor II, dibutyryl cyclic AMP, veratridine (a sodium ion channel agonist), and nisoldipine (a calcium ion channel agonist). Total protein and overall myotube development in serum-free cultures were enhanced by fetuin, insulin-like growth factor II, acidic fibroblast growth factor, calcitonin gene-related peptide, dibutyryl cyclic AMP, and veratridine. Thus, changes in extracellular matrix, intracellular calcium, and sodium ions, as well as extracellular trophic factors, such as nerve growth factor, thyroxine, and insulin-like growth factor II, may regulate muscle NCAM expression during embryonic development.

Acetylcholinesterase↗
PubMed1993

Close genetic relationship between Nitrobacter hamburgensis nitrite oxidoreductase and Escherichia coli nitrate reductases.

The nitrite oxidoreductase (NOR) from the facultative nitrite-oxidizing bacterium Nitrobacter hamburgensis X14 was investigated genetically. In order to develop a probe for the gene norB, the N-terminal amino acid sequence of the NOR beta-subunit (NorB) was determined. Based on that amino acid sequence, an oligonucleotide was derived that was used for the identification and cloning of gene norB. Sequence analysis of DNA fragments revealed three adjacent open reading frames in the order norA, norX, norB. The DNA sequences of norX and norB represented complete genes while the open reading frame of norA was truncated by the cloning site. The deduced amino acid sequence of protein NorB contained four cysteine clusters with striking homology to those of iron-sulfur centers of bacterial ferredoxins. NorB shares significant sequence similarity to the beta-subunits (NarH, NarY) of the two dissimilatory nitrate reductases (NRA, NRZ) of Escherichia coli. Additionally, the derived amino acid sequence of the truncated open reading frame of norA showed striking resemblance to the alpha-subunits (NarG, NarZ) of the E. coli nitrate reductases.

Amino Acid Sequence↗
PubMed1993

Biochemical correlates to cortical dysplasia, gliosis, and astrocytoma infiltration in human epileptogenic cortex.

The study provides detailed biochemical correlates to the common histopathological diagnoses in epilepsy. A dot immunobinding procedure was used for quantification of NSE, GFA, S-100, NCAM, NF 68 and NF 200. The material consisted of samples from 48 patients either selected for surgical treatment of partial epilepsy or for disorders not related to epilepsy. The histopathological diagnosis of the epileptic cases was: MCD (mild cortical dysplasia, microdysgenesis), gliosis, astrocytoma, ganglioglioma, oligodendroglioma and single cases. The concentration in non-epileptic white matter, in per cent of that in grey matter was: NSE, 85; GFA, 175; S-100, 117; NCAM, 43; NF 68,227 and NF 200, 173. The concentration of NSE as well as of GFA was close to normal in the specimens of the MCD and gliosis groups and of one subgroup of the astrocytomas. There was a striking inverse relationship of the GFA vs the NSE concentrations in the whole material. The concentrations of S-100 showed no such inverse relationship to NSE levels. In all the epileptic groups, total NCAM was lower than 50% of that of the non-epileptic group. The mean NF 68 and NF 200 concentration in the gliosis and astrocytoma groups was 75% of that of the non-epileptic group while the corresponding value for the MCD group was 50%. There was a positive correlation of immunochemically determined GFA and the histopathological gliosis score in the samples of epileptogenic cortex. There was no correlation between the concentration of GFA in the samples and the duration of epilepsy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

CSF and serum brain-specific creatine kinase isoenzyme (CK-BB), neuron-specific enolase (NSE) and neural cell adhesion molecule (NCAM) as prognostic markers for hypoxic brain injury after cardiac arrest in man.

Creatine kinase (CK) and its brain-specific isoenzyme (CK-BB), neuron-specific enolase (NSE), neural cell adhesion molecule (NCAM) and the ions sodium, potassium, chloride and calcium were measured both in CSF and serum and inorganic phosphate in CSF in order to assess their prognostic value in total brain ischemia due to cardiac arrest. The samples were collected at 4, 28 and 76 h after resuscitation. Twenty consecutive patients resuscitated from ventricular fibrillation or asystole were included in the study. Nine of the patients recovered consciousness (recovered) but eleven remained comatose (disabled). The follow-up period was 2 years after which only one patient was still alive. The earliest statistically significant differences between neurologically recovered and disabled patient groups were seen in CSF inorganic phosphate (P = 0.030) already at 4 h and CK-BB (P = 0.046) and NSE (P = 0.020) activity at 28 h. Later, at 76 h after the resuscitation CSF NSE differentiated the groups most clearly (P = 0.014). The values were higher in the disabled patients. A negative correlation between CSF parameters and Glasgow Coma scores was also seen at these timepoints. Statistically significant differences between the groups were seen in both CSF and blood pCO2, pO2, base excess (BE) and actual bicarbonate (HCO3-). CSF or serum NCAM has no prognostic value in anoxic-ischemic coma. The results suggest that in CSF CK-BB and NSE are useful prognostic indicators of hypoxic brain injury when measured 28-76 h after cardiac arrest whereas blood samples have no prognostic value.

Adult↗