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Biomedical subjects

G Huber

Publications and source records attributed to G Huber.

At least 19 recordsLinked to original sources
PubMed1992

Beta-amyloid precursor protein isoforms in various rat brain regions and during brain development.

To address the question of the possible functions of different Alzheimer's disease beta-amyloid precursor protein (beta-APP) isoforms in the brain, we studied their expression at different times during postnatal rat brain development and in various regions of the adult rat brain. Polyclonal antibodies directed to two peptide antigens were used. The majority of all beta-APP forms was found to be soluble as revealed by western blot analysis. The highest level of most beta-APP forms was reached in the second postnatal week, which is the time of brain maturation and completion of synaptic connections. Strikingly high concentrations of the Kunitz protease inhibitor-containing beta-APP were present in the adult olfactory bulb, where continuous synaptogenesis occurs in the adult animal. These findings support the idea of an involvement of beta-APPs in the processes of cell differentiation and, probably, in the establishment of synaptic contacts.

Amyloid beta-Protein Precursor↗
PubMed1991

Characterization of a new 120 kDa microtubule-associated protein (MAP) of rat brain.

A novel protein was identified in rat brain microtubules using a monoclonal antibody. The immunoreactive protein is a microtubule-associated protein (MAP) by the criteria of co-purification with tubulin through repeated cycles of microtubule polymerisation in vitro. It belongs to the class of thermostable MAPs and runs as a closely spaced polypeptide doublet of 120 kDa on SDS-PAGE gels. MAP-120 kDa is brain- and neuron-specific and is localized predominantly in Purkinje cell bodies and dendrites in the cerebellum and in dendritic compartments of pyramidal and granule neurons in the hippocampus and dentate gyrus. During postnatal brain development, MAP-120 kD levels increase about 3 to 4-fold.

Animals↗
PubMed1991

Long-term prognosis of schizophrenia.

The question of determining prognostically relevant features for schizophrenia was approached with multivariate statistical methods applied to the data from the Bonn longitudinal study of 502 schizophrenic patients. In this study, personal interviews according to a clinical classification scheme allowed every patient to be ranked within each of three different outcome classes: psychopathological remission, occupational remission, and course type. Our multivariate analysis encompassed a total of 50 items pertinent to the time up to and including the first 6 months after the first psychotic manifestation. Despite the introduction of mathematical methods considerably more sophisticated than those employed in earlier studies, no satisfactory solution could be found to the problem of predicting end states of schizophrenia. Reliable predictions could be made only for 'extreme' end states (i.e. full remission versus (1) characteristic residues in the narrower sense; (2) total unemployment, or (3) surging or simple courses to mixed residues or to typical schizophrenic defect psychoses). Accordingly, sufficiently reliable assertions applied only to a minority of about 1/3 of patients, whereas for the majority of 2/3, no generalizable prognostication was possible (67-71% true-positive predictions on 36-63% of total population in extreme states). By contrast, our analyses have clearly uncovered a fundamental problem of investigations into the long-term prognosis of schizophrenia: the extreme dependence of results on the clinical definition of end states. The further the phenomenon 'end state' is qualitatively subdivided, the poorer and less reproducible is the mutual discrimination between intermediate states and the less reliable are allocations of patients to these intermediate states by means of multivariate classifiers. Furthermore, our analyses have also demonstrated the usefulness of multivariate, adaptive procedures for investigations into the structural properties of long-term courses, so that predictions might be considerably improved if more reliable definitions of schizophrenic end states are available.

Activities of Daily Living↗
PubMed1991

[Venous anomalies of the brain. The clinical significance of the so-called venous angioma].

In contrast to angiography, MRI not only allows the diagnosis of DVA (developmental venous anomaly, so-called venous angioma), but also shows up cavernomas and other angiographically occult vascular malformations. It also differentiates between DVAs and occult true malformations. This has completely changed the pathological assessment of DVAs. In a retrospective study on 31 patients with angiographically proven DVAs neighbouring cavernoma was a frequent finding (15 patients, 48% group I). Symptoms caused by cavernoma were present in 6 (40%) of these 15 patients. The following associations were also found: cerebral arterial aneurysm (2), spinal arterio-venous dural fistula (1), dermal haemangioma (1), Klippel-Trénauny syndrome (1). Only 16 (52%) of the 31 cases with DVA were free of associated cavernoma (group II). Only 3 (19%) of these patients with a solitary DVA were symptomatic. In our series we have seen no case of bleeding from a DVA. A DVA is a vascular anomaly characterized, like other anomalies, by reduced resistance and limited capacity for regulation and adaptation. In rare cases this can result in haemodynamic disturbances, thrombosis and ischaemia. Wall rupture with bleeding does not occur in DVA. It must be assumed that bleeding reported in patients with DVAs before the availability of MRI resulted from an associated true vascular malformation in most cases.

Adolescent↗
PubMed1991

[Sturge-Weber syndrome. Diagnostic imaging relative to neuropathology].

Clinical presentation of a child with port-wine stain and seizures leads to the suspicion of Sturge-Weber disease (SWD). This diagnosis can be confirmed by the detection of a meningeal angiomatosis. In rare cases, early detection of meningeal pathology by ultrasound has been reported. Key findings are brain atrophy, gyriform cortical calcifications demonstrated by skull radiographs after the first year of life or earlier by cranial CT, and dys- or aplasia of the deep cerebral veins on angiography. Radionuclide imaging shows focal or diffuse tracer accumulation over the affected brain regions. MR demonstrates an abnormal appearance of the affected meninges, especially thickening and pathologically increased signal intensity after Gd-DTPA application. This, in association with the demonstration of abnormal enhancement in deep medullary veins, is the most characteristic finding. Contrast-enhanced MR allows early and non-invasive diagnosis of SWD, mainly by revealing leptomeningeal angiomatosis and abnormal venous vessels.

Adolescent↗
PubMed1991

[Radionuclide cisternography: SPECT- and 3D-technique].

Radionuclide cisternography is indicated in the clinical work-up for hydrocephalus, when searching for CSF leaks, and when testing whether or not intracranial cystic lesions are communicating with the adjacent subarachnoid space. This paper demonstrates the feasibility and diagnostic value of SPECT and subsequent 3D surface rendering in addition to conventional rectilinear CSF imaging in eight patients. Planar images allowed the evaluation of CSF circulation and the detection of CSF fistula. They were advantageous in examinations 48 h after application of 111In-DTPA. SPECT scans, generated 4-24 h after tracer application, were superior in the delineation of basal cisterns, especially in early scans; this was helpful in patients with pooling due to CSF fistula and in cystic lesions near the skull base. A major drawback was the limited image quality of delayed scans, when the SPECT data were degraded by a low count rate. 3D surface rendering was easily feasible from SPECT data and yielded high quality images. The presentation of the spatial distribution of nuclide-contaminated CSF proved especially helpful in the area of the basal cisterns.

Adult↗
PubMed1991

Diagnostic aspects of depression.

In this review the traditional concepts of endogenous depression and modern trials of classification in operationalized diagnostic systems, especially in DSM and ICD, are critically discussed. The psychopathological and other phenomenological symptomatologies of endogenous (cyclothymic) depression within monopolar and bipolar affective psychoses and the diagnosis and differential diagnosis above all against schizophrenia, organic brain diseases and psychoreactive disorders, are described. The possibilities and limitations of operationalized classifications with regard to diagnostic reliability and validity are presented. At present state of research homogeneous groups of patients with regard to affective and other idiopathic psychoses and here depressive syndromes and episodes cannot be defined, neither with the traditional concepts nor with the up to now available operationalized diagnostic classifications. In contemporary operationalized diagnostic systems among others the psychopathological and other phenomenological criteria are not sufficiently or too vaguely defined, the different significance of the requested inclusion-criteria and the intraindividual variability with regard to single episodes and subsequent phases of the depression are too little considered. Up to now all trials failed to validate different diagnostic concepts of depression by biological markers. Clinical psychopathological diagnosis of endogenous depression according to the traditional psychiatry criteria may reach a better validity under certain conditions than diagnoses according to DSM-III-R or ICD 10. To use exclusively operationalized diagnostic systems instead of clinical diagnosis in the diagnostic practice but also in research would be too early at present. Modern diagnostic systems can complete the clinical diagnosis but not replace it.

Affective Disorders, Psychotic↗
PubMed1990

[Clinical efficacy and nephrotoxicity of gentamicin in single-dose parenteral administration of total individually adapted daily dosage].

The efficacy of gentamicin given intravenously once daily in a single, individually-adapted dose in form of a short infusion was confirmed in 30 patients with febrile urogenitary infections, taking nephrotoxicity into consideration. Antibiotic therapy was given for 7 days in each case, the individual dose of gentamicin being chosen from the dosage schedule according to Mawer. Depending on weight, age and renal function we used daily doses ranging from 160 to 480 mg (i.e. 2 to 5 mg/kg) of gentamicin. All patients were cured and all gram-negative bacteria were eliminated; no nephrotoxicity was recorded, as verified by constantly low serum levels of gentamicin (below the recommended peak level of 2 micrograms/ml) and non-significant changes in serum creatinine level. According to our results and to the findings of other investigations cited in the literature we conclude that in gentamicin therapy the once-daily individually--adapted intravenous dosage regimen is superior to to continuous administration by means of repeated daily doses with regard to efficacy and absence of nephrotoxicity.

Adult↗
PubMed1990

Serum amino acids, central monoamines, and hormones in drug-naive, drug-free, and neuroleptic-treated schizophrenic patients and healthy subjects.

Basal serum amino acids (including central monoamine precursors), central monoamines, and hormones were studied in schizophrenic patients (drug-naive; n = 20; drug-withdrawn for 3 or more days, n = 67; neuroleptic-treated, n = 23) and healthy subjects (n = 90) to answer the following questions: (1) Do neuroleptic-withdrawn and neuroleptic-naive patients differ on these serum measures? (2) What are the effects of neuroleptic treatment on these measures? (3) On which variables do drug-free and neuroleptic-treated patients differ? Because serum amino acid, central monoamine, and hormone levels were similar in drug-naive and drug-withdrawn patients, data from these groups ("drug-free") were combined and compared to those of healthy subjects and neuroleptic-treated patients. Asparagine, citrulline, phenylalanine, and cysteine were higher, while tyrosine, tryptophan, and the ratio of tryptophan to competing amino acids were significantly lower in drug-free schizophrenic patients than in healthy subjects. Dopamine was increased, and melatonin and thyroid hormones were decreased in drug-free schizophrenic patients compared to healthy subjects. Norepinephrine, epinephrine, and prolactin were higher in neuroleptic-treated men compared to drug-free male patients or healthy men. These results are consistent with the hypothesis of dopaminergic overactivity in schizophrenia, which might be caused by altered amino acid precursor availability and could be related to the decrease in melatonin and reduction in thyroid hormone levels.

Adult↗
PubMed1990

[Status-dependent neurochemical parameters in schizophrenic and affective diseases].

The dynamics of course, i.e., the marked psychopathological fluctuation in acute phases of schizophrenic and other idiopathic psychoses was little considered up to now in investigations referred to correlating clinical and neurochemical findings. Therefore, we selected subgroups of patients, classified as inactive or slight, moderate or severe process-active according to the operational defined actual psychopathological syndrome (Gross et al. 1988, Klosterkötter et al. 1989) at the time of taking of blood samples. We demonstrated in previous studies that the fluctuation and/or sudden development (minutes, hours, up to six days at the latest) of schizophrenic first rank symptoms and certain basic symptoms may reflect also an instability and process-activity of underlying neurochemical changes. In this study we have measured the concentrations of dopamine, noradrenaline, adrenaline, 5-HT, TSH, prolactin, HGH, melatonin, cortisol, T 3, T 4 and 28 amino acids in blood samples (examined 8 times within 24 hours) from 48 schizophrenic patients, divided in 4 subgroups (each 12 cases) with severe, moderate, slight or lacking process-activity, from 20 patients with (inactive or only slight active) depressive phases of affective psychoses and from normal controls. Marked process-active schizophrenics showed significantly higher levels of dopamine, noradrenaline and 5-HT, and significantly lower levels of TSH, compared to healthy controls and process-inactive schizophrenics with pure deficiency syndromes, that reveal a relative hypo-activity of catecholaminergic and presumably also of serotoninergic systems. In the subgroup of depressions were found decreased concentrations of noradrenaline, 5-HT, adrenaline and melatonin when compared to marked process-active schizophrenics.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Antibiotic prophylaxis of infectious complications with endoscopic retrograde cholangiopancreatography. A randomized controlled study.

Biliary sepsis represents a major percentage of fatal complications after endoscopic retrograde cholangiopancreatography. We performed a randomized controlled study to investigate the value of antibiotic prophylaxis, and to assess the frequency and source of infectious complications associated with ERCP. Ninety-six patients who underwent 100 endoscopic retrograde cholangiopancreatographies were included in the study. Half of the patients received antibiotic prophylaxis (Cefotaxime 2 g i.v. 15 min before the procedure). Bacteremia was detected in 2% of the patients receiving antibiotic prophylaxis, as compared with 16% (p less than 0.02) in the control group. In order to determine the source of bacteremia, bile samples and irrigation fluid from the suction channel of the endo-scope were obtained for bacteriological evaluation. Several lines of evidence suggested that bacteremia associated with ERCP was essentially caused by mucosal lesions of the oropharynx. Bacteremia was asymptomatic, with the exception of two patients who subsequently developed fever, but recovered rapidly under antibiotic therapy. The frequency of cholangitis following ERCP was not significantly reduced by antibiotic prophylaxis (4% vs. 2%). Recommendations for antibiotic prophylaxis are discussed.

Cefotaxime↗
PubMed1990

Heart rates, cardiac arrhythmia, lactate levels and catecholamine excretions in CHD patients during cross-country skiing.

We examined cross-country skiing-related strain in 10 less experienced postinfarction patients, performing a skiing test, covering a distance of approximately 7 km in 90 min. Heart rates, cardiac arrhythmia, lactic acid levels and catecholamine excretions were determined as strain indicators. The patients' exercise capacity, estimated during graded ergometric cycling, was 2.1 +/- 0.4 watts.kg-1, indicating a nearly age-appropriate submaximum performance ability. They had suffered myocardial infarction 2.8 +/- 0.7 years previously, participated regularly in a rehabilitation program for at least one year, and they did not show coronary insufficiency or significant cardiac dysrhythmias during laboratory testing under their usual medications. They went cross-country skiing during a 4-day instruction period and subsequently performed a cross-country skiing test on the 5th day. Mean skiing-related heart rates (124 +/- 9 bpm) and adrenaline excretions (124 +/- 88 pmol.min-1) corresponded on average to an exercise level of 1.85-2.0 watts.kg-1 during laboratory testing, and mean noradrenaline excretions (586-343 pmol.kg-1) and lactate concentrations (3.83 +/- 2.18 mmol.l-1) to a level of 1.48-1.73 watts.kg-1. Cardiac dysrhythmias were observed in a moderate number of 6-8 SVES, 9 to 12 VES and 4 to 7 couplets of VES per 1000 beats during cross-country skiing. The present results point to a comparatively high cardiovascular strain in less experienced postinfarction patients during a cross-country skiing test at an intensity level thought to be moderate.

Adult↗
PubMed1990

Molecular cloning of microtubule-associated protein 1 (MAP1A) and microtubule-associated protein 5 (MAP1B): identification of distinct genes and their differential expression in developing brain.

cDNA clones encoding microtubule-associated proteins 1 (MAP1/MAP1A) and 5 (MAP5/MAP1B) were isolated and have been used to study their structural relationship as well as their regulated expression in developing rat brain. cDNA clones specific for MAP1 hybridized to a single 10-kb rat brain mRNA, and analysis of genomic DNA by Southern blotting indicated the existence of a single MAP1 gene. A second set of cDNAs specific for MAP5 hybridized to a single 11-kb mRNA in rat brain and also detected a single gene. By analysis of hybrid mouse-hamster cell lines, the MAP1 gene was located to mouse chromosome 2, designated Mtap-1, and the MAP5 gene to chromosome 13, designated Mtap-5. MAP1 and MAP5 mRNAs were expressed with different temporal patterns during rat brain development that mirrored the appearance of their protein products, suggesting that expression of these proteins is under transcriptional control. These results taken together demonstrate that although MAP1 and MAP5 have some properties that are similar, they are structurally distinct proteins whose transcription is differently regulated from separate genes.

Animals↗
PubMed1990

Generation of intercellular heterogeneity of growth and function in cloned rat thyroid cells (FRTL-5).

The most characteristic hallmarks of human nodular goiters are nodular growth and heterogeneity of structure and function between different areas of the same goiter. In search of the earliest detectable stage of thyroid heterogeneity we have observed doubling times, TSH dependency, and thyroglobulin production in colonies formed from individual FRTL-5 cells growing as monolayers in slide flasks. Single cells and the colonies derived thereof were followed on photographs taken daily until confluence. We observed that each cell had its individual stable multiplication rate throughout the observation period. This was true for all TSH doses tested (0.625-10 mU/ml). A wide range of doubling times (20 h to almost infinite) in the individual cells was observed. The mean growth velocity of subcloned cell lines was highly reproducible in consecutive passages, although a minority of cells escaped this rule. Cells with either high or low thyroglobulin content occurred in clusters, indicating again that specific traits tend to remain stable in the offspring. We conclude that a highly individual growth program, unrelated to mutation, appears to be switched on at the very moment a cell is generated and that this program is passed on to the majority of the offspring, with a minority of cells acquiring qualities differing from those of their sister cell. Therefore, goiter heterogeneity may be the in vivo amplification of a natural phenomenon occurring in all growing cells. Monoclonal adenomas in vivo and nontransformed immortal cell lines in vitro may represent the far end of the large spectrum of individual growth potency among normal thyrocytes.

Animals↗
PubMed1990

Intercellular propagation of individually programmed growth bursts in FRTL-5 cells. Implications for interpreting growth factor actions.

Five methods are commonly used to quantify FRTL-5 cells' and other thyrocytes' growth in vitro and the impact of growth inhibiting or stimulating maneuvers: Total cell count, mitotic index, DNA measurement, total [3H]thymidine incorporation, and the fraction of [3H]thymidine labeled cells. All of them assess cell growth as though all cells were homogeneous with an identical response to growth factors. We demonstrate here that this assumption is not valid. Rather, some intrinsically growth-prone cells appear to pass a growth signal to neighboring cells so that variably sized colonies of synchronized cells within each cluster growing from monodispersed cells are formed. This is true for FRTL-5 cells growing in vitro in monolayers and in three-dimensional, collagen embedded spheroids. The pattern is the same when cell suspensions or collagen-embedded spheroids are implanted onto nude mice. Patches with alternating high and low growth become particularly prominent in the large tumor-like organoids grown from monodispersed cells in nude mice. The pattern much reminds of similar observations in growing intact thyroids. Since there is no significant correlation between the fraction of [3H]thymidine labeled cells and the size of two- or three-dimensional clusters in any experiment, growth of signal-spreading cells is assumed to occur in leaps and bounds. Growth velocity in each subclone of a cell population depends on the mean interval between bursts of replications and on the number of cells synchronized by cell-to-cell diffusion of the growth signal emanating from one dividing cell. Thus, growth-promoting and growth-inhibiting factors may not only act on the mean interval between successive growth bursts, but they may also change cell-to-cell spreading of growth signals.

Animals↗
PubMed1990

Microtubule-associated protein 3 (MAP3) expression in non-neuronal tissues.

Microtubule-associated protein 3 (MAP3, Mr 180,000), which in previous studies has been shown to be associated with glial processes and neurofilament-rich axons in rat brain, was examined in various non-neuronal rat tissues. Immunoblots of adult rat tissues (brain, liver, heart, spleen, adrenal medulla and kidney) showed that MAP3 is present in all organs tested. In addition we demonstrated that MAP3 is a heat-stable protein. Using immunohistochemistry, we established the localisation of MAP3 in various cell types. MAP3-containing cells appeared to have in common an asymmetric morphology with long processes that need structural support. In kidney MAP3 is limited to epithelial podocytes and in liver to Kupffer cells. In the adrenal gland, the cells of the cortex are devoid of MAP3 compared to the cells of the medulla. High concentrations of MAP3 are also found in cardiac muscle along the Z-disc and in the smooth muscle cells of the digestive tract. In spleen MAP3 is found in cells of the white pulp surrounding central blood vessels. A co-distribution of MAP3 with microtubules and intermediate filaments but not with microfilaments was found in each cell type examined. The widespread distribution pattern of MAP3 together with its molecular size and heat-stability indicate that MAP3 might be a member of the recently postulated family of homologous 200,000 Mr mammalian tissue MAPs. Potential functions for MAP3 in specific cell types are discussed.

Actins↗
PubMed1990

[Does symptomatic schizophrenia exist?].

The question if there are "symptomatic schizophrenias" has been discussed since the 20s. Schizophrenic psychoses caused be definable and well known brain diseases are presented. All schizophrenic symptoms and syndromes, the first rank symptoms (K. Schneider) too, occur in somatically founded psychoses. The group of paroxysmal transition syndromes in the sense of aura prolongata (continua) and the episodic schizophrenic psychoses in psychomotor epilepsy may be a model for the schizophrenia research. Vital threatening, so-called pernicious catatonic schizophrenias are found on the basis of infectious brain diseases, sometimes only diagnosed in autopsy. Beside acute and reversible symptomatic schizophrenic psychoses there are, even if rarely, recurrent and chronic courses of symptomatic schizophrenias. That certain conditions for the developing of symptomatic schizophrenias are rarely realised, could be an explanation for their rarity. Some findings indicate that the limbic system is significant for symptomatic (and idiopathic) schizophrenic psychoses and the pre- and postpsychotic basic stages determined by dynamic and cognitive basic symptoms, which are phenomenologically very similar to aura symptoms released by stereoelectroencephalographic depth recordings (Wieser). The characteristic features of marked fluctuation, discontinuity and insteadiness of the cognitive thought, perception, psychomotor and cenesthetic phenomena do not speak against an organic brain disorder provided that the traditional process hypothesis is abandoned in favor of a neurobiochemic disorder, fluctuating on its part depending on endogenous as well as psychic-reactive factors.

Chronic Disease↗