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S Ritter

Publications and source records attributed to S Ritter.

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

Hemolysis and autoantibodies to triosephosphate isomerase in a patient with acute hepatitis A virus infection.

Having returned from a holiday in Southeast Europe, a 30-year-old German woman developed acute hepatitis. Hepatitis A virus (HAV) infection was diagnosed serologically. During the course of the infection, hemolysis was found. IgM antibodies against triosephosphate isomerase (IgM anti-TPI) were detected in the patient's serum from the acute phase of the HAV infection. Affinity purified IgM anti-TPI from the serum reduced the enzyme activity in vitro and caused an increased 51Cr release from erythrocytes. IgM anti-TPI is assumed to be one of the causative agents of hemolysis in HAV infection.

Acute Disease↗
PubMed1993

Z-DNA binding and inhibition by GTP of Drosophila topoisomerase II.

A Z-DNA binding protein has been isolated and characterized by biochemical means from Drosophila melanogaster tissue culture cells and embryos. This protein shares the following properties with the known, cloned Drosophila topoisomerase II: (1) expression of an ATP-dependent relaxation activity on supercoiled DNA; (2) a monomer mass of 165 kDa in SDS denaturing gels; (3) a sedimentation coefficient, S20,w, of approximately 10 S for the active enzyme; (4) cross-reactivity for the respective monoclonal and polyclonal antibodies; (5) generation of covalent enzyme-DNA intermediates at preferred cutting sites in the Drosophila HSP70 intergenic spacer region; (6) inhibition of DNA relaxation activity by antitumor drugs, e.g., the etoposide VM26, and by monospecific antibodies raised against the protein; and (7) in vitro phosphorylation by a casein kinase activity. However, we have identified new properties for our topoisomerase II preparation not previously reported for the conventionally isolated enzyme: (1) The enzyme binds to Z-DNA with an affinity 2 orders of magnitude greater than that for B-DNA. (2) The binding to Z-DNA is increased 5-10-fold by GTP or GTP-gamma-S. (3) GTP and GTP-gamma-S inhibit the catalytic activity of topoisomerase II through a proposed allosteric mechanism. (4) Z-DNA inhibits the relaxation of closed circular supercoiled DNA. (5) The preparation consists of a single polypeptide chain of 165 kDa on denaturing SDS gels with no evidence of proteolytic degradation. We postulate that the Z-DNA binding activity of undegraded topoisomerase II may be important in targeting the enzyme both to structural motifs required for chromatin organization and to sites of local supercoiling. Some of these features arise during processes such as replication and gene expression and may be more frequent during embryogenesis and early development.

Animals↗
PubMed1993

Sympathoadrenal responses to glucoprivation and lipoprivation in rats.

The effects of glucoprivation and lipoprivation on sympathoadrenal outflow were investigated in rats with permanent intra-atrial catheters. Glucoprivation was induced by infusion of a hypoglycemic dose of insulin (3 U/kg) or by infusion of the glucose antimetabolite, 2-deoxy-D-glucose (2-DG, 200 mg/kg). Lipoprivation was induced by infusion of sodium mercaptoacetate (MA, 600 mumol/kg), which blocks beta oxidation of fatty acids. Stress-free blood samples for measurement of blood glucose, plasma nonesterified fatty acids (NEFA), and epinephrine (E) and norepinephrine (NE) concentrations were collected remotely before and after drug injection. Glucoprivation and lipoprivation differed significantly in their effects on the sympathoadrenal system. Both 2-DG- and insulin-induced glucoprivation appeared to increase adrenomedullary secretion selectively, leading to dramatically increased plasma E levels. Although plasma NE levels also rose during glucoprivation, other evidence suggests that this effect may be secondary to the rise in E. In contrast, MA-induced lipoprivation increased the outflow of NE from the sympathetic nerve endings without a significant effect on plasma E concentrations. Plasma E levels rose only late in the test, as blood glucose levels began to fall. Results indicate that glucoprivation and lipoprivation are distinct metabolic signals, each capable of selectively activating one branch of the sympathoadrenomedullary system and thereby facilitating the mobilization of metabolic fuels appropriate for the specific metabolic challenge.

Adrenal Medulla↗
PubMed1993

Lateral parabrachial subnucleus lesions abolish feeding induced by mercaptoacetate but not by 2-deoxy-D-glucose.

Lesions of the area postrema/nucleus of the solitary tract (AP/NTS) region abolish feeding induced by mercaptoacetate (MA) and 2-deoxy-D-glucose (2DG), metabolic inhibitors that selectively impair fatty acid and glucose utilization, respectively. Because the AP/NTS region is important for both MA- and 2DG-induced feeding, the present experiment investigated the involvement of the lateral parabrachial nucleus (1PBN), which is innervated by AP/NTS neurons, in these feeding responses. Electrolytic and ibotenic acid lesions were directed at the entire parabrachial nucleus or at specific lateral parabrachial subnuclei. Rats with electrolytic lesions were tested for feeding in response to 0.9% NaCl (subcutaneous or intraperitoneal), MA (400, 600, and 800 mumol/kg ip), and 2DG (100 and 200 mg/kg sc). Ibotenate-lesioned rats were tested with NaCl and MA only. Lesions were verified either by cresyl violet staining or by glial fibrillary acidic protein immunohistochemistry. Bilateral destruction of the 1PBN severely impaired or abolished MA-induced feeding. Cell bodies important for MA-induced feeding appear to be localized in the dorsal-central 1PBN subnuclear area, because both electrolytic and cytotoxin microlesions centered in this area abolished feeding in response to MA. Fibers of passage important for MA-induced feeding appear to pass through the external and superior 1PBN because electrolytic but not cytotoxin lesions of these subnuclei disrupted the feeding response. In contrast, 2DG-induced feeding did not differ significantly from sham-lesioned controls in any of the 1PBN lesion groups. These results indicate that 2DG and MA stimulate feeding by activating separate central neural pathways and, perhaps, distinct metabolic controls of food intake.

Animals↗
PubMed1992

Immobilized metal affinity chromatography for the separation of photosystems I and II from the thermophilic cyanobacterium Synechococcus elongatus.

Immobilized metal affinity chromatography (IMAC) of solubilized, photosystem II (PS II) enriched particles from the thermophilic cyanobacterium Synechococcus elongatus was studied. A chelating Sepharose Fast Flow column was charged with various metal ions (Mn2+, Fe2+, Fe3+, Ni2+, Co2+, Ca2+, Sr2+, Zn2+ and Cu2+) and their affinity to photosystem I (PS I) and PS II was examined. Among all the metal ions tested, only copper was able to bind the two protein complexes. For elution of the column, a pH gradient, a pH step gradient and gradients of imidazole, amino acids, organic acids and various other eluents were tested; only the pH step gradient, which selectively eluted PS II at a pH between 6 and 5, was useful for the separation of PS I and PS II. All other gradients proved to be inappropriate for the separation of these two photosystems. Mechanisms of protein elution by these compounds are discussed. Alternatively, a separation of PS I and PS II at pH 7.5 could be achieved when an IMAC column was used on which the free coordination positions of the bound copper ions were occupied by imidazole. When solubilized photosystems were loaded on to this column, PS I replaced imidazole and remained bound on the column, whereas PS II was highly enriched in the effluent.

Centrifugation↗
PubMed1992

Hypothalamic paraventricular nucleus lesions do not abolish glucoprivic or lipoprivic feeding.

This experiment assessed the importance of the hypothalamic paraventricular nucleus (PVN) for feeding stimulated by blockade of glucose utilization (glucoprivic feeding) and fatty acid oxidation (lipoprivic feeding). The PVN was investigated because it is innervated by neurons residing in the area postrema and nucleus of the solitary tract (AP/NTS) region where lesions have been shown to abolish both glucoprivic and lipoprivic feeding, and because the PVN appears to be a site of action for certain feeding-stimulatory peptides and amines. Bilateral electrolytic lesions were placed in the PVN and adjacent areas. Lesioned rats were subsequently tested for feeding in response to 2-deoxy-D-glucose (2DG)-and mercaptoacetate (MA)-induced blockade of glucose and fatty acid oxidation, respectively. Results revealed that total destruction of the PVN does not impair either 2DG- or MA-induced food intake and suggest that this structure is not essential for these particular controls of feeding.

Animals↗
PubMed1992

Age-related changes in capsaicin-induced degeneration in rat brain.

Previous results indicate that the pattern of capsaicin-induced degeneration in the rat central nervous system is age-related. Experiments utilizing capsaicin's selective neurodegenerative effects to study the function of central neural circuits will therefore require a detailed understanding of capsaicin's central neurotoxicity in rats of different ages. The goal of this experiment was to characterize the degeneration induced in the rat brain by systemic treatment with capsaicin at different ages (10, 15, 20, 25, 30 or 75 days, or 11 months), using a cupric silver stain to label degenerating neurons. Results revealed degenerating cell bodies in the ventromedial brainstem in capsaicin-treated rats of all age groups, though they were more numerous in adult rats than in pups. In addition, many areas contained capsaicin-induced nerve terminal degeneration both in rat pups and in adult rats. These areas were the substantia gelatinosa of the spinal cord dorsal horn; the solitary tract; the nucleus of the solitary tract, visceral portion; the area postrema; the trigeminal nerve and spinal trigeminal nucleus; the medial nucleus of the inferior olive; the rostral, dorsomedial and dorsolateral interpeduncular subnuclei and overlying interfascicular nucleus; the supramammillary area; the lateral septal nucleus; the bed nucleus of the stria terminalis, anterior medial portion; the optic nerve and tract; the suprachiasmatic nucleus, ventroposterolateral portion; the magnocellular subnucleus of the ventrolateral geniculate nucleus; the intergeniculate leaf; the medial pretectal nucleus and the olivary pretectal nucleus. In several, but not all of these areas, the apparent density of degenerating terminals was significantly less in adult rats than in pups. In other brain sites, capsaicin-induced degeneration was observed only in rats younger than 30 days of age. These areas were the lateral habenula, medial part; the sphenoid nucleus; and the stria medullaris. Still other brain sites lost their sensitivity to capsaicin sometime between 30 and 75 days of age. These areas were the bed nucleus of the stria terminalis, medial posteromedial part; the medial preoptic nucleus, central part; the septohypothalamic nucleus; the ventral reuniens area; and the ventromedial hypothalamic nucleus. Adult rats 75 days and 11 months of age did not differ detectably in their response to capsaicin. Thus, loss or attenuation of capsaicin sensitivity is not progressive throughout life. It does not occur in all capsaicin-sensitive sites. Where it does occur, loss of sensitivity occurs prior to adulthood and follows a distinct and reproducible time course that may differ for different sites.

Aging↗
PubMed1992

Presence of galanin in rat vagal sensory neurons: evidence from immunohistochemistry and in situ hybridization.

Galanin (GAL), a 29 amino acid peptide originally isolated from the porcine upper small intestine, is widely distributed in the rat central nervous system, including the area postrema (AP) and nucleus of the solitary tract (NTS). Although vagal sensory neurons terminate in the AP/NTS, it is not known whether these neurons contain GAL in the rat. Therefore, we examined the presence and distribution of GAL in the rat nodose ganglia which contain the cell bodies of vagal sensory neurons. We used avidin-biotin-peroxidase immunohistochemistry and in situ hybridization histochemistry with a 35S-labeled oligonucleotide probe. Results with both techniques revealed the presence of GAL-containing cell bodies and fibers in the nodose ganglion. GAL-like immunoreactive cell bodies, mostly between 25 and 40 microns in diameter, were unevenly scattered throughout the nodose ganglia. The distribution and cell diameter range of GAL mRNA-labeled neurons appeared similar to those of GAL-like immunoreactive cells. These findings suggest a role for GAL in the transmission of visceral sensory information by the vagus nerve in rats.

Animals↗
PubMed1992

Induction of chromosome aberrations in mammalian cells after heavy ion exposure.

The induction of chromosome aberrations by heavy charged particles was studied in V79 Chinese hamster cells over a wide range of energies (3-100 MeV/u) and LET (20-16000 keV/micrometer). For comparison, X-ray experiments were performed. Our data indicate quantitative and qualitative differences in the response of cells to particle and x-ray irradiation. For the same level of cell survival the amount of damaged cells which can be observed is smaller in heavy ion (11.4 MeV/u Ar) irradiated samples. The highest yield of damaged cells is found 8 to 12 hours after particle irradiation and 4 hours after x-irradiation. Differences in the amount of damaged cells are attributed to cell cycle perturbations which interfere with the expression of damage. After heavy ion exposure the amount of cells reaching mitosis (mitotic index) decreases drastically and not all damaged cells reach mitosis within 48 hours after exposure. A portion of cells die in interphase. Cell cycle delays induced by x-ray irradiation are less pronounced and all cells reach the first post-irradiation mitosis within 24 hours after irradiation. Additionally, the damage produced by charged particles seems to be more severe. The disintegration of chromosomes was only observed after high LET radiation: an indication of the high and local energy deposition in the particle track. Only cross sections for the induction of chromosome aberrations in mitotic cells were reported in this paper because of the problems arising from the drastic cell cycle perturbations. In this case, cells were irradiated in mitosis and assayed immediately.

Animals↗
PubMed1992

Low-dose near-celiac arterial cholecystokinin suppresses food intake in rats.

Exogenous cholecystokinin (CCK) suppresses food intake by acting on vagal sensory neurons. However, CCK doses used in behavioral experiments are generally much larger than those necessary to produce electrophysiological changes in vagal afferents. We made automated measurements of liquid food intake before, during, and after infusion of low doses of CCK octapeptide (CCK-8) through a chronic aortic catheter with its tip seated just above the celiac juncture. In parallel experiments, we made similar infusions while collecting blood from the hepatic portal and jugular veins for CCK assay. Injection of 10, 30, 50, and 70 pmol of CCK-8 suppressed feeding in a dose-dependent manner beginning 1 min postinfusion. The lowest dose to produce statistically significant suppression of preinfusion intake was 30 pmol. Infusion of the same CCK-8 doses into the jugular vein did not suppress feeding. Near-celiac injection of 30 pmol of CCK-8 produced systemic plasma CCK concentrations averaging 6.5 +/- 1 pM compared with less than 1 pM after saline injection. These findings show that exogenous CCK, by acting on tissues perfused by the celiac artery, can suppress feeding at doses that 1) are similar to those producing effects on the firing of vagal neurons and 2) do not increase plasma CCK concentrations above postprandial levels.

Animals↗
PubMed1991

Prior optic nerve transection reduces capsaicin-induced degeneration in rat subcortical visual structures.

Capsaicin is a neurotoxin capable of causing degeneration in specific sites throughout the neuraxis, including the suprachiasmatic nucleus (SCh), the ventrolateral geniculate nucleus (VLG), the intergeniculate leaflet (IGL), and the olivary and medial pretectal nuclei (OPT and MPT). In this experiment, we tested the hypothesis that capsaicin-induced terminal degeneration in the SCh, VLG, IGL, OPT, and MPT results from destruction of retinal ganglion cells and their axonal projections to these sites. In the first experiment, silver stains were used to examine degeneration in the retina induced by systemic capsaicin treatment. Capsaicin caused degeneration of ganglion cells, bipolar cells, and nerve terminals in the retina, which could be observed between 2 and 24 hours after treatment. In the second experiment, 15-day-old rat pups were enucleated unilaterally. Five days or 2, 5, or 10 months later, they were injected systemically with capsaicin and killed 6 hours (pups) or 18 hours (adults) later for analysis with a cupric silver stain. In rats of all ages, prior monocular enucleation reduced or eliminated capsaicin-induced degeneration in the contralateral SCh, VLG, IGL, OPT, and MPT. In the third experiment, rat pups were treated systemically with capsaicin or vehicle solution at 12 days of age and given unilateral intravitreal injections of cholera toxin conjugated to horseradish peroxidase (CT-HRP) 3 days prior to sacrifice at 20 days of age. Transport of CT-HRP to the SCh, VLG, IGL, MPT, and OPT was attenuated but not abolished by capsaicin pretreatment. Results suggest that capsaicin causes degeneration in the SCh, VLG, IGL, MPT, and OPT by selective destruction of a subpopulation of retinal ganglion cells with axonal projections to these sites.

Animals↗
PubMed1991

The mental health component of the general nursing curriculum: a critical review of English National Board guidelines.

The role of the mental health component of general nurse training has been the source of much revision and controversy. Although advocates have proposed a psychiatric experience for general nurses for over thirty years it was only in 1977 following a directive from the General Nursing Council (GNC) that it became a compulsory part of general nurse education. However debate continues; it ranges from whether a specialist psychiatric placement has any academic or clinical merit at all to how issues relating to mental health should be addressed most constructively. After only 11 years the 1977 GNC guidelines changed once again making a distinct psychiatric placement no longer compulsory. This paper critically reviews current guidelines and places the debate once again firmly in the public arena.

Curriculum↗
PubMed1990

Capsaicin-induced neuronal degeneration in the brain and retina of preweanling rats.

Capsaicin is a neurotoxin known for its ability to cause degeneration of small unmyelinated primary sensory neurons in both spinal and cranial nerves. Although lower motor neurons do not degenerate following capsaicin treatment, the extent to which capsaicin may damage neurons in the brain has not been thoroughly evaluated. This study examines the effects of systemic capsaicin (50-150 mg/kg) on the central nervous system of 10-day-old rats. Rat pups were injected with capsaicin or the injection vehicle and sacrificed 6 hours-10 days later. Brains, spinal cords, and retinas were stained with cupric silver to label degenerating neurons. As previously reported for capsaicin-treated rats, degenerating nerve terminals were present in areas receiving primary afferent input: the spinal cord dorsal horn, spinal trigeminal nucleus, nucleus of the solitary tract, and area postrema. However, degenerating terminals were also present in areas not known to receive primary sensory innervation: the inferior olivary nucleus, sphenoid nucleus, medial and olivary pretectal nuclei, interpeduncular nucleus, interfascicular nucleus, caudal linear, dorsal, median, and paramedian raphe nuclei, supramammillary area, lateral habenula, ventrolateral geniculate nucleus, ventral reuniens nucleus, ventromedial hypothalamic nucleus, lateral hypothalamic and preoptic areas, suprachiasmatic nucleus, septohypothalamic nucleus, bed nucleus of the stria terminalis, lateral septal nucleus, accumbens shell, olfactory bulb, and retina. Some areas where capsaicin caused degeneration in rat pups do not appear to be capsaicin-sensitive in adult rats. Results indicate that (1) capsaicin's neurotoxicity is not limited to primary sensory neurons and (2) developmental factors may alter the capsaicin sensitivity of some neuronal projections within the brain.

Animals↗
PubMed1990

Vagal sensory neurons are required for lipoprivic but not glucoprivic feeding in rats.

This experiment examined the role of subdiaphragmatic vagal sensory neurons in feeding stimulated by pharmacological blockade of fatty-acid oxidation (lipoprivic feeding) and glucose utilization (glucoprivic feeding). Rats prepared by surgical transection of the subdiaphragmatic vagal trunk or aspiration lesion of the vagal sensory terminal fields in the area postrema-nucleus of the solitary tract (AP-NTS) were maintained and tested on a fat-supplemented, high carbohydrate diet. Fatty-acid oxidation was blocked with mercaptoacetate (MA, 400 and 600 mumol/kg ip) and glucose utilization was blocked with 2-deoxy-D-glucose (2-DG, 100 and 200 mg/kg sc). On test days, rats were injected with MA, 2-DG, or saline, and feeding was measured hourly for 6 h beginning immediately after injection. We found that both subdiaphragmatic vagotomy and AP-NTS lesions abolished lipoprivic feeding. In contrast, glucoprivic feeding was abolished by AP-NTS lesions but not by subdiaphragmatic vagotomy. These results indicate that lipoprivic feeding requires intact subdiaphragmatic vagal sensory neurons that terminate in the AP-NTS region. Glucoprivic feeding is not vagally mediated but also requires a neural substate within the AP-NTS region.

Animals↗
PubMed1990

[Is liver biopsy in gallbladder operations still indicated?].

Biopsy of the liver with the Tru-cut needle was done as a routine diagnostic procedure during gallbladder surgery in 166 cases. The data of history, ultrasonography and laboratory were compared with the microscopic liver findings. Preoperatively in 89% of the cases there was an indication for liver biopsy. In 11% of the cases, where there was no indication for preoperative biopsy, we found severe changes in liver histology. Therefore we recommend liver biopsy during gallbladder surgery as a routine procedure.

Adult↗
PubMed1989

Cellular and subcellular effect of heavy ions: a comparison of the induction of strand breaks and chromosomal aberration with the incidence of inactivation and mutation.

Radiobiological effects of heavy charged particles are compared for a large variety of ions from Helium to Uranium and energies between 1 and 1000 MeV/u which correspond to LET values between 10 and 16000 keV/micrometers. The different cross section for the induction of strand breaks and chromosomal aberrations as well as for inactivation and mutation induction exhibit striking similarities when compared as function of the linear energy transfer (LET). At LET values below 100 keV/micrometers all data points of one specific effect form one single curve as a function of LET, independent of the atomic number of the ion. In this LET range, the biological effects are independ from the particle energy or track structure and depend only on the energy transfer. Therefore, LET is a good parameter in this regime. For LET values greater than 100 keV/micrometers, the curves for the different ions separate from the common curve in order of increasing atomic numbers. In this regime LET is no longer a good parameter and the physical parameters of the formation of particle tracks are important. The similarity of the sigma-LET curves for different endpoints indicates that the 'hook-structure' is produced by physical and chemical effects which occur before the biologically relevant lesions are formed. However, from the existing data of biological effects, it can be concluded that the efficiencies for cell killing are always smaller than those extrapolated from X-ray data on the basis of the energy deposition only. Therefore, cells which are directly hit by an HZE particle are not killed and undergo a finite risk of mutation and transformation.

Alpha Particles↗
PubMed1989

Cell cycle delays induced by heavy ion irradiation of synchronous mammalian cells.

Cell cycle effects of very high LET particles on synchronous V79 Chinese Hamster cells have been studied in a track segment experiment by means of flow cytometric methods. Cells were irradiated with 10 MeV/u Pb-ions (LET = 13500 keV/micrometers) at an average fluence of 2 particles per cell nucleus, corresponding to a survival level of about 25%. Instantaneous drastic reductions of cell proliferation in all cycle phases have been observed, which affect the cell cycle for at least 50 hours after exposure to heavy ions. These findings are in clear contrast to the results from low LET radiation experiments, where significant delays can only be observed in S-phase and G2M-phase and for comparatively short time intervals of a few hours. Additionally, high LET radiation gives rise to prolonged DNA synthesis bypassing cell division, which leads to cells with DNA content greater than that of G2M-cells.

Animals↗