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Biomedical subjects

T Sander

Publications and source records attributed to T Sander.

82 records · Page 5Linked to original sources
PubMed1991

Localization of idiopathic generalized epilepsy on chromosome 6p in families of juvenile myoclonic epilepsy patients.

Juvenile myoclonic epilepsy (JME) is a distinct subform of idiopathic generalized epilepsy of adolescence. Linkage studies with Bf and serologic HLA markers in families of JME patients have shown a tight linkage on chromosome 6. We present a linkage analysis with HLA-DQ restriction fragment length polymorphisms on more extended families, paying particular attention to the epilepsy type of the affected family members. We studied 21 families of JME patients with a total of 143 family members and obtained a highest logarithm of the odds (lod) score of 3.9 (theta m = 0.01, theta f = 0.01) assuming a dominant mode of inheritance and 70% penetrance when family members with JME, absence epilepsy, or epilepsy with generalized tonic-clonic seizures (GTCS) were considered as affected. When we also classified clinically normal family members with generalized spike-wave discharges in the EEG as "affected," the maximum lod score was 4.1 (theta m = 0.01, theta f = 0.3) under a dominant mode of inheritance and 90% penetrance. These findings support the conclusion that a gene locus for a group of idiopathic generalized epilepsies (JME, epilepsy with absences, and epilepsy with GTCS) maps to chromosome 6p.

Chromosomes, Human, Pair 6↗
PubMed1988

Oligoclonal bands in serum and cerebrospinal fluid of patients with HIV infection.

Matched samples of serum and cerebrospinal fluid (CSF) from 15 human immunodeficiency virus (HIV)-infected patients were examined after isoelectric focusing. The appearance of oligoclonal bands only in the CSF could indicate the primary HIV infection of CNS in early stages of the disease. Later, the increasing number of autochthonous oligoclonal bands in the CSF suggested locally synthesized IgG against opportunistic infections. Because of the immunodeficiency, T cell independent polyclonal B cell stimulation might mask the oligoclonal pattern.

Acquired Immunodeficiency Syndrome↗
PubMed1986

Laser-induced alteration of collagen substructure allows microsurgical tissue welding.

Tissue welding is a potentially important biomedical application of laser technology. The structural alterations basic to this phenomenon were studied in experimental repair of lesions of the rat carotid artery and sciatic nerve. A modified neodymiumdoped yttrium-aluminum-garnet laser operating at a wavelength of 1.319 micrometers was used in conjunction with conventional suture techniques. Histological and fine-structural analysis revealed a homogenizing change in collagen with interdigitation of altered individual fibrils that appeared to be the structural basis of the welding effect.

Animals↗
PubMed1986

Fracture analysis of retrieved orthopedic wires.

Ten retrieved samples of 316L stainless steel wires, implanted for times from 11 months to 11 years, were examined fractographically and metallurgically to evaluate the effects of a physiological environment on their fracture. Seven samples were from L-rod instrumentation, and three samples were from trochanter reattachment. Of 16 breaks in the 10 samples, 94% were caused primarily by cyclic loading (fatigue), and 6% were caused by tensile forces. Two factors were found to influence the effective life of an implanted wire. First, the surface condition (deformation) appeared to be most important, and second, corrosion pits present on most wire surfaces could possibly be an influence in initiating a crack. Biomechanical forces on wires enveloping L-rods tended to promote metal deformation and faceting, which decreased time to fracture. This decrease in wire life was evident from a substantial hardness increase in faceted areas.

Bone Wires↗
PubMed1986

Interaction of the oncogene protein myc with specific DNA fragments.

The p110gag-myc protein coded for by the retrovirus MC29 was purified 3,000-fold from MC29-Q8 transformed cells by immuno-affinity chromatography using IgG specific for the N-terminal region of the gag protein. Interaction of the protein with DNA fragments was studied by filter binding assay. DNA fragments were obtained from a MC29 DNA clone by restriction endonuclease treatment. Besides the complete DNA provirus the clone contained flanking cellular sequences into which the provirus had integrated. The DNA fragments which were retained by the p110gag-myc protein were eluted from the filter and analyzed by agarose gel electrophoresis. Preferential binding of a DNA fragment originating from the flanking cellular sequences was detected. The protein did not preferentially bind to the viral LTR promoter/enhancer region as suggested by an autoregulatory model, which can therefore no longer be substantiated.

DNA↗
PubMed1985

Isolation and characterization of the human cellular myc gene product.

Antibodies against the product of the human cellular myc gene (c-myc) were prepared against a bacterially expressed human c-myc protein by inserting the ClaI/BclI fragment of the human c-myc DNA clone in an expression vector derived from pPLc24. These antibodies cross-react with viral-coded myc (v-myc) proteins from MC29 and OK10 viruses. Furthermore, IgGs specific for synthetic peptides, corresponding to the 12 carboxy-terminal amino acids of the human c-myc gene and 16 internal amino acids, were isolated. By use of the various myc-specific antisera or IgGs, a protein of Mr 64 000 was detected in several human tumor cell lines including Colo320, small cell cancer of the lung (417d), HL60, Raji, and HeLa. This protein is larger than the corresponding v-myc or chicken c-myc proteins from avian virus transformed cells or avian bursa lymphoma cells (RP9), both of which are proteins of Mr 55 000. The human c-myc protein is located in the nucleus of Colo320 cells, exhibits a half-life of about 15 min, and is expressed at significantly lower levels than the viral protein. The human c-myc protein was enriched about 3000-fold from Colo320 cells using c-myc-specific IgG coupled to Sepharose beads. The protein binds to double-stranded DNA in vitro, a reaction that can be inhibited to more than 90% by c-myc specific IgG.

Antibodies↗
PubMedDate not supplied

Serine- and threonine-specific protein kinase activities of purified gag-mil and gag-raf proteins.

Retroviruses carry cell-derived oncogenes (v-onc) that have the potential to transform cells in culture and induce tumours in vivo. One of the few carcinoma-inducing viruses is the acutely transforming retrovirus MH2, which carries the putative oncogene v-mil and the known oncogene v-myc. Recently, a high degree of homology was discovered between v-mil and v-raf, the transforming gene of the murine retrovirus 3611 murine sarcoma virus (MSV), whereas homology to v-src is low. Both viruses express their oncogenes as the gag-fusion polyproteins p100gag-mil and p75gag-raf (of respective relative molecular mass (Mr) 100,000 and 75,000), while the myc oncogene of MH2 is expressed by means of a subgenomic messenger RNA. We have recently demonstrated that p100gag-mil is not a nuclear protein. Here we report that purified p100gag-mil and p75gag-raf exhibit protein kinase activities in vitro which, in contrast to the src-related p130gag-fps of Fujinami sarcoma virus (FSV) and all other characterized oncogene-encoded protein kinases, phosphorylate serine and threonine but not tyrosine. Both types of protein kinases phosphorylate lipids in vitro.

Animals↗
PubMedDate not supplied

Five exon 1 variants of mu opioid receptor and vulnerability to alcohol dependence.

The human mu opioid receptor (hMOR) gene is a prime candidate gene responsible for addictive disorders. The present association study tested the hypothesis that hMOR exon 1 variants elicit susceptibility to alcohol dependence. We have analyzed five nucleotide changes in exon 1 of the hMOR gene. Three of them are in the 5'untranslated region of exon 1 at positions -172G/T,-111C/T and -3 8C/A, the remaining two variants cause amino acid substitutions: +17C/T (Ala6Val) and +118A/G (Asn40Asp). Our population-based association study included 327 German alcohol-dependent subjects and 340 ethnically matched controls. The lack of an allelic association suggests that the analyzed hMOR exon 1 variants do not contribute a common and substantial effect to the genetically determined vulnerability of alcohol dependence.

5' Untranslated Regions↗