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Biomedical subjects

G Lubec

Publications and source records attributed to G Lubec.

318 records · Page 18Linked to original sources
PubMed1976

[Antibodies against the Epstein-Barr Virus nuclear-antigen in children with malignant disease (author's transl)].

Sera of 25 patients and 50 health children were tested for the presence of antibodies against the Epstein-Barr Virus Nuclear-Antigen (EBNA). We examined 15 children with acute lymphocytic leukemia, who showed a mean arithmatic titer of 1 : 5.33, 1 child with acute myeloblastic leukemia and 1 child with the chronic myeloblastic form showing no reactivity. Two children with lymphogranuloma had titers 1 : 16 and 1 : 32, respectively. 1 patient with lymphoepithelial carcinoma and 5 with lymphosarcoma showed a mean arithmetic titer of 1 : 170.66. Control persons had antibodies against EBNA in the amount of 1 : 2.56. We think that the humoral reactivity against this regularly viral-genome-associated antigen is an additional indicator for the causative role of the Epstein-Barr Virus.

Antibodies, Viral↗
PubMed1976

[Alport's-syndrome: diagnosis, light- and electronmicroscopic findings (author's transl)].

Alport's syndrome is a hereditary nephropathy with grave prognostic consequences. The occurrence of this disease is probably more frequent than was assumed until now - many cases are not immediately recognized as such. It is possible to make a clinical diagnosis from detailed family histories and through careful examinations of family members including audiometric tests. In the early stages of the disease children merely have recurrent macro- or microhematuria. Renal functional tests are normal and there is general well-being of the patient. Whereas the biopsy specimens examined by light microscopy show non-specific alterations, those examined under the electronmicroscope already show specific defects of the basement membrane. Our studies lead us to believe that these morphologic findings correspond with changes of the basement membrane, detectable by immunochemical investigations. 6 of 12 patients have been biopsied in recent time and the above cited typical changes of the basement membrane could be demonstrated. Therefore these investigations are recommended in Alport's syndrome.

Adolescent↗
PubMedDate not supplied

Two-dimensional map of human brain proteins.

Samples of human brain from the parietal cortex lobe were analyzed by two-dimensional gel electrophoresis, using immobilized pH gradient strips covering the various pH regions. The protein spots were visualized with colloidal Coomassie blue stain and identified by matrix-assisted laser desorption/ionization mass spectrometry. Approximately 400 spots were identified, corresponding to 180 different brain proteins. The list of identified proteins includes a large number of structural proteins and of enzymes or enzyme subunits with various catalytic activities. The majority of proteins are localized in the cytoplasma and in mitochondria. The two-dimensional map may be useful as a reference database to study changes in the protein level caused by various disorders, such as Alzheimer's disease, major depression and schizophrenia.

Animals↗
PubMedDate not supplied

Decreased levels of synaptosomal associated protein 25 in the brain of patients with Down syndrome and Alzheimer's disease.

Synaptosomal associated protein 25 kDa (snap-25) is a widely distributed membrane-associated protein in the brain, mainly localized in nerve terminals. In nerve terminals, snap-25 participates in docking and/or fusion of synaptic vesicles with the plasmalemma, a process essential for synaptic vesicle exocytosis. Recent work suggests a role in brain development, forming presynaptic sites by regulating axonal outgrowth and nerve growth-induced neurite elongation. In Down syndrome (DS) brain, it is abnormally developed from early life, and brain pathology becomes even more pronounced when Alzheimer's disease (AD) develops in the fourth decade. This information led us to examine snap-25 in the brain of patients with DS and AD. We studied snap-25 and glial fibrillary acidic protein (GFAP) brain levels in five individual brain areas of 9 aged patients with DS, 9 patients with AD and 9 controls, applying two-dimensional gel electrophoresis. Decreased snap-25 levels were found in the five brain regions of the patients with DS and AD. Increased expression levels of GFAP were found in the frontal, parietal, temporal and occipital cortex regions of the DS and AD patients. Decreased snap-25 protein levels in the brain of DS and AD may reflect impaired synaptogenesis or represent neuronal loss. Findings of increased GFAP, a marker for neuronal loss, along with data from literature would support the notion of decreased snap-25 secondary to neuronal decay in both neurodegenerative disorders.

Aged↗
PubMedDate not supplied

Fluorescence angiography of the paramacular retinal vessels and altered glomerular basement membrane in children with juvenile onset diabetes mellitus.

Eighteen diabetic children aged between 8.5 and 16.5 years (mean 12.5 years) who had been diabetic for 1 to 10 years (mean 4.1 years) were examined for their urinary glomerular basement membrane (GBM) antigen excretion by means of immunoelectrophoresis and for alterations of the retinal vessels by fluorescence angiography. None of these patients showed albuminuria or hypertension. As compared to 40 healthy controls aged between 5 and 17 years, altered GBM antigen mobility (alpha-1) was found in 9 out of these 18 diabetics, whereas the remaining 9 children had normal GBM antigen mobility (alpha-2). Pathological fluorescence angiography findings on the other hand were evident in 7 children with altered GBM mobility, but only in 4 diabetics with normal GBM antigen mobility. This trend reflects the similarity of biochemical and functional characteristics of basement membranes in the retinal and kidney vessels supporting the well established association of vascular changes in both organs in patients with diabetes mellitus. GBM antigen excretion into urine could be useful for detecting early microvascular alterations in the kidneys in juvenile diabetics where diagnosis of early glomerulosclerosis is important.

Adolescent↗
PubMedDate not supplied

Influence of glucose fluctuations on alkaline phosphatase activity.

It has been suggested previously that non-enzymatic glycosylation of certain enzymes results in decreased enzymatic activity. In order to examine the role of high blood glucose concentrations (BG) on serum alkaline phosphatase (AP) activity, we determined BG and serum AP in 32 healthy children during an oral glucose tolerance test (OGTT) and in 10 type I diabetic children at 30-min intervals for at least 150 min. A significant negative correlation was noted for BG and AP during the oral glucose load (r = -0.57, p less than 0.01). In diabetics, however, only children with marked BG fluctuations showed this inverse relationship between BG and AP. These observations could be explained by the formation of a Schiff base as the initial step of non-enzymatic glycosylation of AP. This assumption was further confirmed by in vitro experiments, in which AP was incubated with glucose resulting in decreased enzymatic activity. The dialyzable aldimine formed initially is subsequently stabilized as ketoamine after long-term incubation.

Adolescent↗
PubMedDate not supplied

Decreased brain levels of 2',3'-cyclic nucleotide-3'-phosphodiesterase in Down syndrome and Alzheimer's disease.

In Down syndrome (DS) as well as in Alzheimer's disease (AD) oligodendroglial and myelin alterations have been reported. 2',3'-cyclic nucleotide-3'-phosphodiesterase (CNPase) and carbonic anhydrase II (CA II) are widely accepted as markers for oligodendroglia and myelin. However, only data on CNPase activity have been available in AD and DS brains so far. In our study we determined the protein levels of CNPase and CA II in DS, AD and in control post mortem brain samples in order to assess oligodendroglia and myelin alterations in both diseases. We used two dimensional electrophoresis to separate brain proteins that were subsequently identified by matrix assisted laser desorption and ionization mass-spectroscopy (MALDI-MS). Seven brain areas were investigated (frontal, temporal, occipital and parietal cortex, cerebellum, thalamus and caudate nucleus). In comparison to control brains we detected significantly decreased CNPase protein levels in frontal and temporal cortex of DS patients. The level of CA II protein in DS was unchanged in comparison to controls. In AD brains levels of CNPase were decreased in frontal cortex only. The level of CA II in all brain areas in AD group was comparable to controls. Changes of CNPase protein levels in DS and AD are in agreement with the previous finding of decreased CNPase activity in DS and AD brain. They probably reflect decreased oligodendroglial density and/or reduced myelination. These can be secondary to disturbances in axon/oligodendroglial communication due to neuronal loss present in both diseases. Alternatively, reduced CNPase levels in DS brains may be caused by impairment of glucose metabolism and/or alterations of thyroid functions.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMedDate not supplied

Synaptosomal proteins, beta-soluble N-ethylmaleimide-sensitive factor attachment protein (beta-SNAP), gamma-SNAP and synaptotagmin I in brain of patients with Down syndrome and Alzheimer's disease.

Although it is well-known that synaptosomal proteins are deranged in neurodegenerative disorders, no information is available at the protein-chemical level as mainly immunochemical or immunohistochemical data were reported previously. We therefore investigated synaptosomal proteins in brain specimens from patients with Down syndrome (DS) and Alzheimer's disease (AD) to challenge the DS synaptic pathology as well as the relevance of DS to AD in synaptic pathology. For the aim of this study, we employed two-dimensional electrophoresis and matrix-associated laser desorption ionization mass spectroscopy and determined beta-soluble N-ethylmaleimide-sensitive factor attachment protein (beta-SNAP), gamma-SNAP and synaptotagmin I (SYT I) in 7 individual brain regions of controls and patients with DS and AD. In DS brain, beta-SNAP was significantly reduced in temporal cortex (p < 0.01). SYT I (p65) and SYT I (pI 7.0) were significantly reduced in thalamus (p < 0.01 and p < 0.05, respectively). In AD brain, beta-SNAP was significantly decreased in temporal cortex (p < 0.05). SYT I (p65) was significantly reduced in cerebellum (p < 0.05), and temporal (p < 0.001) and parietal cortex (p < 0.01). SYT I (pI 7.0) was significantly reduced in temporal (p < 0.001) and parietal cortex (p < 0.01) and thalamus (p < 0.01). gamma-SNAP did not show any change in both DS and AD. The findings may explain impaired synaptogenesis in DS and AD brain, which is well documented in DS brain already early in life, and/or synaptosomal loss secondary to neuronal loss observed in both neurodegenerative disorders. It may also represent, reflect or account for the impaired neuronal transmission in DS and AD, caused by deterioration of the exocytic machinery. Here, we provide evidence for several deranged synaptosomal proteins in several brain regions at the protein level indicating deficient synaptosomal wiring of the brain in DS and AD.

Adult↗
PubMedDate not supplied

Antigenic changes of the glomerular basement membrane after incorporation of hydroxyproline isomers.

We investigated antigenic changes of murine glomerular basement membrane (GBM) collagen type IV after oral feedings of 3-cis- or 4-cis-hydroxyproline. As shown by thin layer chromatography and gas chromatographic-mass spectrometric studies, 3-cis- and 4-cis-hydroxyproline were incorporated into the GBM collagen instead of the normal trans isomer and led to a considerable reduction of the collagen antibody reactivity on indirect immunofluorescence, passive hemagglutination and radioimmunoassay when compared to GBM collagen of control animals. We speculate that antigen modification due to the incorporation of stereoisomers could serve as a model for basement membrane immunopathology.

Animals↗
PubMedDate not supplied

Neonatal islet cell adenoma: a distinct type of islet cell tumor?

An encapsulated, compact-type islet cell adenoma of the pancreas, found in a newborn infant with hyperinsulinemic hypoglycemia, was investigated by conventional histology and immunofluorescence. Although the histologic structure of the tumor was indistinguishable from that of most islet cell tumors of adults, immunofluorescence revealed that the four islet cell hormones (insulin, glucagon, somatostatin, and pancreatic polypeptide) were all present in the tumor. They were stored in different cells that showed the same spatial distribution usually seen in normal islets. We conclude that neonatal islet cell adenoma can be distinguished from those of adults on the basis of the content and topographic distribution of their constituent endocrine cells.

Adenoma, Islet Cell↗