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Biomedical subjects

M Koch

Publications and source records attributed to M Koch.

At least 181 records · Page 10Linked to original sources

Stabilization of human immunodeficiency virus type 1 envelope glycoprotein trimers by disulfide bonds introduced into the gp41 glycoprotein ectodomain.

Biochemical and structural studies of fragments of the ectodomain of the human immunodeficiency virus type 1 (HIV-1) gp41 transmembrane envelope glycoprotein have demonstrated that the molecular contacts between alpha helices allow the formation of a trimeric coiled coil. By introducing cysteine residues into specific locations along these alpha helices, the normally labile HIV-1 gp160 envelope glycoprotein was converted into a stable disulfide-linked oligomer. Although proteolytic cleavage into gp120 and gp41 glycoproteins was largely blocked, the disulfide-linked oligomer was efficiently transported to the cell surface and was recognized by a series of conformationally dependent antibodies. The pattern of hetero-oligomer formation between this construct and an analogous construct lacking portions of the gp120 variable loops and of the gp41 cytoplasmic tail demonstrates that these oligomers are trimers. These results support the relevance of the proposed gp41 structure and intersubunit contacts to the native, complete HIV-1 envelope glycoprotein. Disulfide-mediated stabilization of the labile HIV-1 envelope glycoprotein oligomer, which has been suggested to possess advantages as an immunogen, may assist attempts to develop vaccines.

Amino Acid Sequence↗

Expression of glutamine:fructose-6-phosphate amidotransferase in human tissues: evidence for high variability and distinct regulation in diabetes.

Recent in vitro and in vivo studies suggested that the increased flux of glucose through the hexosamine biosynthetic pathway may contribute to glucose-induced insulin resistance and to the induction of the synthesis of growth factors. Because glutamine:fructose-6-phosphate amidotransferase (GFAT) catalyzes the first and rate-limiting step in the formation of hexosamine products, this enzyme is the key regulator in this pathway and is therefore possibly also involved in the alterations occurring in preclinical or manifest diabetic patients. To study the expression of GFAT in human tissues, we produced and characterized a peptic antiserum specifically recognizing GFAT protein and a riboprobe for the detection of GFAT mRNA. Immunohistochemical and nonradioactive in situ hybridization analysis revealed high levels of expression of GFAT protein and mRNA in adipocytes and skeletal muscle. Furthermore, a marked GFAT expression was found in vascular smooth muscle cells with unexpectedly high variability and lower levels in other cells, e.g., peripheral nerve sheath cells or endocrine-active cells, including the pancreatic islet cell. GFAT protein expression was below detection level in endothelium, osteocytes, lymphocytes, granulocytes, and in most quiescent fibroblasts. In renal tissue, GFAT was expressed in tubular epithelial cells, while glomerular cells remained essentially unstained. Renal sections obtained from patients with diabetic nephropathy showed significant GFAT expression in some glomerular epithelial and mesangial cells, indicating that GFAT expression may be induced by manifest diabetes. Our data indicate that GFAT is expressed in most tissues involved in the development of diabetic late complications. Furthermore, the results suggest that GFAT gene expression is highly regulated.

Adipocytes↗

Latent inhibition of fear potentiated startle in rats.

Non-reinforced pre-exposure to a prospective conditioned stimulus impairs subsequent conditioning. This phenomenon is termed latent inhibition. In this report, we demonstrate latent inhibition in a classical conditioning procedure, the fear-potentiated startle reflex. Normally, the startle response is enhanced in the presence of a conditioned stimulus that has previously been paired with an aversive stimulus. We show that fear-potentiation of the startle response is significantly less pronounced in rats that have been repeatedly pre-exposed to a conditioned light stimulus. Similar to other procedures reported in the literature, the administration of the psychostimulant drug amphetamine (1.0 mg/kg) before pre-exposure and conditioning disrupts latent inhibition. A good deal is known about the neuronal mechanisms underlying the acquisition and expression of fear-potentiated startle, and therefore this new procedure could be a useful tool for investigating the neuronal basis of latent inhibition.

Acoustic Stimulation↗

Doxorubicin prodrugs with reduced cytotoxicity suited for tumour-specific activation.

The three new hydrophilic prodrugs 2, 3 and 4 have been prepared from methyl (4-hydroxymethyl-2-nitrophenyl 2,3,4-tri-O-acetyl-beta-D-glucopyranosid)uronate (5) and doxorubicin. Their low cytotoxicity, efficient release of doxorubicin after hydrolysis by beta-D-glucuronidase, and in the cases of 2 and 3 stability at pH 7.2 fulfil the preliminary requirement for their use in antibody-directed enzyme prodrug therapy or prodrug monotherapy.

Antibiotics, Antineoplastic↗

Regulation of sensorimotor gating by interactions of dopamine and adenosine in the rat.

Prepulse inhibition (PPI) of the acoustic startle response is a behavioural tool used to assess sensorimotor gating processes and its disturbances in rats and in humans. PPI in rats is reduced by an overactivity of the dopamine (DA) system. Because there are functional interactions between DA and adenosine receptors, we tested whether PPI can be influenced by the mixed DA receptor agonist apomorphine (APO) and by the unselective adenosine antagonist theophylline (THEO). Combined administration of APO (0.5 mg/kg, i.p.) and THEO (20 mg/kg, i.p.) in doses devoid of significant effects on their own significantly reduced PPI. The PPI-disrupting effect of the combined THEO plus APO treatment was dose-dependently antagonized by co-administration of the selective adenosine A1 agonist CPA (0.15-1.5 mg/kg, i.p.), but not by the A2A agonist CGS21680 (0.1-2 mg/kg, i.p.). These data demonstrate that antagonistic interactions between DA and adenosine, involving adenosine A1 receptors, play an important role in the regulation of PPI. The possible implications of these findings for the use of adenosine agonists in the treatment of schizophrenia are discussed.

Acoustic Stimulation↗

ACEA 1021, a glycine site antagonist with minor psychotomimetic and amnestic effects in rats.

Antagonists of the allosteric glycine site of the NMDA receptor complex have been suggested to be beneficial in the treatment of neurodegenerative disorders. However, unwanted side effects like psychomotor stimulation and amnesia must be expected. ACEA 1021 (5-nitro-6,7-dichloro-1,4-dihydroquioxaline-2,3dione) is one of the first high-selective glycine site antagonists which passes the blood-brain barrier and which has promising anticonvulsive and neuroprotective properties. In the present study the effects of ACEA 1021 (5, 7.5, 8, 10, 15 and 20 mg/kg i.p.) on sniffing stereotypy, locomotor activity, prepulse inhibition of the acoustic startle response, the anti-cataleptic properties and spatial learning were tested. Only 7.5 mg/kg ACEA 1021 induced a sniffing stereotypy which was antagonized by the partial glycine site agonist D-cycloserine (D-4-amino-3-isoxazolidinone). ACEA 1021 had neither an effect on motor behavior measured in the open field nor on the acoustic startle response in the prepulse inhibition paradigm nor on the acquisition of spatial learning in the 8-arm-radial maze. Anti-cataleptic properties of ACEA 1021 in dopamine D2 (haloperidol (4'fluoro-4-(1-(4-hydroxy-4-p-chlorophenyl-piperidino)-butyrophe non)) or D1 (SCH 23390 (7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzaze pin e hydrochloride)) receptor antagonist-pretreated rats were only minor. Thus, ACEA 1021 is a glycine site antagonist with minimal psychotomimetic side effects and with no amnesia properties. However, it has only minor anti-parkinsonian effects.

Amnesia↗

Complete primary structure of two splice variants of collagen XII, and assignment of alpha 1(XII) collagen (COL12A1), alpha 1(IX) collagen (COL9A1), and alpha 1(XIX) collagen (COL19A1) to human chromosome 6q12-q13.

Overlapping cDNA clones that encode the full-length human alpha 1(XII) collagen polypeptides were isolated. The long variant molecule cDNA of 9750 nucleotides (nt) contains a 9189-nt open reading frame encoding 3063 amino acid residues. The short variant molecule cDNA of 6258 nt contains a 5697-nt open reading frame encoding 1899 amino acid residues. At the amino terminus of each variant is a 24-residue signal peptide that is followed by the mature polypeptides of 3039 amino acid residues with a calculated molecular mass of 330,759 Da for the long variant and 1875 amino acid residues with a calculated molecular mass of 203,163 Da for the short variant polypeptide. The human collagen XII chains are predicted to have all the structural domains described for the molecules in chicken and mouse, including, fibronectin type III repeats, von Willebrand factor A domains, and two triple-helical domains similar to those of all the other collagen family members. The amino acid residue sequence of human alpha 1(XII) collagen showed 92% identity to the mouse chain and 78% identity to the chicken chain. The sequence of three peptide fragments of collagen XII isolated from human placenta was identical to the sequence predicted from the deduced cDNA sequence and confirms that the cDNA encodes human alpha 1(XII) collagen. An isolated genomic clone was used to map the locus of the COL12A1 gene to chromosome 6q12-q13, very close to the locus of the FACIT collagen genes COL9A1 and COL19A1. RT-PCR on a variety of cDNAs demonstrates that both variant transcripts appear in human amnion, chorion, skeletal muscle, small intestine, and in cell cultures of human dermal fibroblasts, keratinocytes, and endothelial cells. Only the small variant transcript is apparent in human lung, placenta, kidney, and a squamous cell carcinoma cell line. These results confirm the previous observations showing that collagen XII is found in collagen I-containing tissues.

Alternative Splicing↗

Adenosine A2a receptors in the nucleus accumbens modulate prepulse inhibition of the startle response.

Prepulse inhibition (PPI) of the acoustic startle response (ASR) was disrupted by systemic administration of apomorphine (APO) (2 mg/kg, i.p.). Microinfusion of the selective adenosine A2a-recceptor agonist CGS21680 (0.05 microgram in 1.0 microliter per side) into the nucleus accumbens (NAc), had no significant effect in animals with systemic vehicle pretreatment, but significantly reversed the disruption of PPI in rats pretreated with APO. Adenosine is, therefore, involved in the control of PPI through its actions on A2a receptors in the NAc. APO-induced disruption of PPI is considered to represent an animal model useful for screening both typical and atypical antipsychotic agents. The present results add further support to the view that A2a-receptor agonists may be potentially useful antipsychotic agents.

Adenosine↗

Variability in the measurement of intracoronary ultrasound images: implications for the identification of atherosclerotic plaque regression.

BACKGROUND AND HYPOTHESIS: Serial coronary angiography cannot reliably detect the small changes in arterial dimensions. Measurement of arterial dimensions by intracoronary ultrasound (ICUS) may be a superior method to determine the extent of atherosclerotic burden since it directly images the diseased portion of the vessel. METHODS: To quantify inter- and intraobserver variability of ICUS measurements, 27 images of atherosclerotic coronary lesions were measured by two study physicians and repeated 14 days later. RESULTS: Interobserver correlation coefficients for external elastic lamina, lumen, and effective plaque area were 0.96, 0.99, and 0.91, respectively. Intraobserver correlation coefficients for external elastic lamina, lumen, and effective plaque area were 0.99, 0.99, and 0.97, respectively. To determine progression or regression in effective plaque area, a minimal difference of 2.77 mm2 (which represents a 23% change in plaque area) is needed. CONCLUSIONS: Direct visualization of the extent of atherosclerosis by ICUS can be accomplished with a low degree of inter- and intraobserver variability. ICUS may be a preferable alternative to angiography in atherosclerosis regression trials.

Coronary Artery Disease↗

[Effects of leukocyte depletion on the storage quality of whole blood].

BACKGROUND: According to the German Guidelines for Hemotherapy, preoperative autologous blood donations can be stored and transfused as whole blood. In contrast to the storage of blood components, however, storage of whole blood results in deterioration of the biological quality due to contamination with leukocytes and platelets. In this study we examined the influence of prestorage leukocyte depletion on the quality of filtered whole blood donations during storage. MATERIAL AND METHODS: Whole blood was donated by healthy volunteers (n = 14,500 ml, 70 ml CPDA-1) and was filtered using an integrated whole blood filter system (Leukotrap A1, Fa.Pall, Dreieich, Germany). The leukocyte-depleted whole blood units were then stored for up to 49 days. Several hematological and biochemical parameters indicative of the quality of blood donations were determined during storage. RESULTS: Our data indicate a quality of leukocyte-depleted whole blood donations comparable to buffy-coat-free red blood cell units. CONCLUSIONS: The Leukotrap A1 whole blood filter system is an interesting option for hospitals lacking the technical capacity to separate whole blood into components. The clinical suitability remains to be investigated by means of clinical studies.

Adult↗

Leptin activates PI-3 kinase in C2C12 myotubes via janus kinase-2 (JAK-2) and insulin receptor substrate-2 (IRS-2) dependent pathways.

We have recently shown that leptin mimicks insulin effects on glucose transport and glycogen synthesis through a phosphatidylinositol-3 (PI) kinase dependent pathway in C2C12 myotubes. The aim of the present study was to identify the signalling path from the leptin receptor to the PI-3 kinase. We stimulated C2C12 myotubes with insulin (100 nmol/l, 5 min) or leptin (0.62 nmol/l, 10 min) and determined PI-3 kinase activity in immunoprecipitates with specific non-crossreacting antibodies against insulin-receptor substrate (IRS 1/IRS 2) and against janus kinase (JAK 1 and JAK 2). While insulin-stimulated PI-3 kinase activity is detected in IRS-1 and IRS-2 immunoprecipitates, leptin-stimulated PI-3 kinase activity is found only in IRS-2 immunoprecipitates, suggesting that the leptin signal to PI-3 kinase occurs via IRS-2 and not IRS-1. Leptin-, but not insulin-stimulated PI-3 kinase activity is also detected in immunoprecipitates with antibodies against JAK-2, but not JAK-1. The data suggest that JAK-2 and IRS-2 couple the leptin signalling pathway to the insulin signalling chain. Since we have also detected leptin-stimulated tyrosine phosphorylation of JAK-2 and IRS-2 in C2C12 myotubes it can be assumed that leptin activates JAK-2 which induces tyrosine phosphorylation of IRS-2 leading to activation of PI-3 kinase. As we could not detect the long leptin receptor isoform in C2C12 myotubes we conclude that this signalling pathway is activated by a short leptin receptor isoform.

Animals↗

Role of the strychnine-insensitive glycine binding site in the nucleus accumbens and anterodorsal striatum in sensorimotor gating: a behavioral and microdialysis study.

This study examined the role of the strychnine-insensitive glycine binding site of the NMDA receptor in prepulse inhibition (PPI) of the acoustic startle response (ASR) in rats. PPI is an operational measure of gating processes which normally lead to a diminished ASR when a startling stimulus is preceded by a weak prepulse. PPI is impaired in schizophrenics and, therefore, experimentally induced PPI deficits in rats can be regarded as a model for gating deficits in schizophrenia. Local administration of 7-chlorokynurenate (7-CLKYN), an antagonist of the strychnine-insensitive glycine site of the NMDA receptor, into the nucleus accumbens reduced PPI. This sensorimotor gating deficit was antagonized by systemic pretreatment of the rats with the glycine site agonist D-cycloserine, indicating that the effect of 7-CLKYN was due to a blockade of the NMDA receptor associated glycine binding site. A similar deficit in PPI was observed after intra-accumbal administration of the competitive NMDA receptor antagonist AP-5. PPI was normal after injecting these drugs into the anterodorsal striatum. The hypothesis that the PPI deficit is accompanied by a change in dopamine release was tested by a neurochemical analysis of the effects of local injection of 7-CLKYN. Microdialysis data showed no increase of accumbal and striatal dopamine release after blockade of the glycine site with 7-CLKYN. Our data demonstrate that the glycine/NMDA receptor in the nucleus accumbens plays a important role in sensorimotor information processing that depends not on a hyperactive dopamine system.

Animals↗

Acoustic startle-evoked potentials in the rat amygdala: effect of kindling.

The electroencephalogram (EEG) of the basolateral nucleus of the amygdala (BLA) was recorded during presentation of acoustic stimuli (70-110 dB SPL) in rats. EEG recordings were performed by chronically implanted bipolar electrodes in the BLA. The auditory evoked response consisted of a broad negative wave followed by a slow positive wave. A characteristic pattern of 1 to 3 negative peaks with a latency of about 12 ms and an increased amplitude of the slow positive wave at about 30 ms was observed when an acoustic startle response (ASR) occurred. These findings suggest that the BLA is involved in the processing of adverse auditory stimuli. These ASR-correlated potentials in the BLA were used to characterize changes of the physiological state of the amygdala that occur after chronic epileptogenesis. To achieve this aim, the rats were subsequently partially or fully kindled by daily electrical stimulation via the recording electrode. The negative peak was depressed in the partially kindled rats, but not in fully kindled rats. These changes in the characteristic EEG pattern of the BLA during the ASR indicate alteration of the physiological response of the amygdala after limbic epileptogenesis.

Acoustic Stimulation↗

Pentylenetetrazol kindling changes the ability to induce potentiation phenomena in the hippocampal CA1 region.

The present study describes changes of response enhancement of hippocampal field potentials in slices of kindled rats using different methods to induce long-lasting potentiation. Eight-week-old male Wistar rats were subjected to pentylenetetrazol (PTZ) kindling induced by intraperitoneal injection of 45 mg/kg once every 48 h until the occurrence of seizure stages 4-5. Eight to 12 days after the last kindling session, transverse hippocampus slices were prepared and maintained in an artificial medium. Evoked-field potentials were recorded in the CA1 region upon stimulation of the Schaffer collaterals. Potentiation was induced: 1. By moderate tetanic stimulation of the Schaffer collaterals, 2. by changing the perfusion medium to 0-magnesium for 30 min, and 3. by changing the medium to 4 mM Ca2+ for 7 min. In slices from kindled rats, long-term potentiation (LTP) after tetanic stimulation and increase of the evoked potential by 0-magnesium were significantly enhanced in comparison to slices from sham-kindled rats. However, Ca(2+)-induced LTP could not be induced in slices from kindled rats. The results support the assumption that PTZ kindling also induces lasting changes in the responsiveness of hippocampal structures, expressed as an enhanced ability to induce potentiation. An alteration of N-methyl-D-aspartate (NMDA) receptor-coupled processes can be assumed. The inability to induce Ca(2+)-induced LTP points to more complex effects of PTZ, perhaps also on nonNMDA coupled ionic channels.

Animals↗

The acoustic startle response in rats--circuits mediating evocation, inhibition and potentiation.

This review describes the neuronal mechanisms underlying the mediation and modulation of the acoustic startle response (ASR) in rats. The combination of anatomical, physiological and behavioral methods has identified pathways which mediate and modulate the ASR. The ASR is mediated by a relatively simple, oligosynaptic pathway located in the lower brainstem which activates spinal and cranial motor neurons. An important element of the pathway which mediates the ASR is the caudal nucleus of the pontine reticular formation (PnC). Interestingly, this nucleus is also the target of input from various brain nuclei which are involved in the modulation (e.g. fear-potentiation, sensitization, habituation, prepulse inhibition and pleasure-attenuation) of the ASR. Hence, the PnC can be described as a sensorimotor interface, where the transition of sensory input into the motor output can be directly influenced by excitatory or inhibitory afferents. On the basis of these facts we conclude that the ASR may be a valuable model for the study of general principles of sensorimotor-motivational information processing at the behavioral and neurophysiological level in mammals.

Acoustic Stimulation↗

The frameshift mutation oscillator (Glra1(spd-ot)) produces a complete loss of glycine receptor alpha1-polypeptide in mouse central nervous system.

Mice homozygous for the recessive mutation oscillator (Glra1(spd-ot)) suffer from a complex motor disorder leading to death within three weeks after birth. Symptoms of this disorder mimic poisoning by strychnine, the antagonist of the inhibitory glycine receptor. The syndrome has previously been correlated to a 7 base pair microdeletion within the Glra1 gene (chromosome 11) encoding the alpha1-subunit of the adult glycine receptor isoform. As shown by [3H]strychnine binding and western blot analysis employing subunit-specific antibodies, spinal cord of homozygous oscillator mice was totally devoid of alpha1-polypeptide, characterizing the Glra1(spd-ot) gene as a functional null allele of Glra1. Moreover, tissue levels of the postsynaptic anchoring protein gephyrin were drastically reduced in the Glra1(spd-ot)/Glra1(spd-ot) genotype. In contrast, immunoanalysis revealed a persisting low-level expression of non-alpha1 glycine receptor polypeptides. Spinal glycine receptor content was also significantly reduced in the +/Glra1(spd-ot) genotype. This reduction coincided with increased acoustic startle responses in heterozygous animals consistent with haplotype insufficiency of glycine receptor function. Lethality of the murine null allele Glra1(spd-ot) contrasts with the situation in the human, where homozygosity for a GLRA1 null allele produces the phenotype of the non-lethal disorder hyperekplexia (startle disease; stiff baby syndrome). This suggests a disparate regulation of glycine receptor subunit genes and/or diverse compensatory pathways in mice and humans.

Acoustic Stimulation↗

The acoustic startle response in inbred Roman high- and low-avoidance rats.

To investigate the emotional reactions of two rat strains selectively bred for good and poor two-way avoidance acquisition (RHA/Verh and RLA/Verh), male animals of both strains were tested in an acoustic startle response test. They received 40 acoustic stimuli followed by 10 electric foot shocks and another 30 acoustic stimuli. RLA/Verh rats showed a significantly higher startle response compared to RHA/Verh animals, indicating a stronger emotional reaction to acoustic stimuli. In addition, the former showed a stronger response to foot shocks. Combined with earlier findings, we conclude that selection for two-way avoidance learning does not result in cognitive defects in the RLA/Verh strain but, rather, in stronger emotional reactions to fearful stimuli.

Acoustic Stimulation↗