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Biomedical subjects

E Koenig

Publications and source records attributed to E Koenig.

At least 37 records · Page 2Linked to original sources
PubMed1991

Transmembrane cytoskeletal modulation in preterminal growing axons. II. Limax flavus agglutinin-induced receptor redistribution, capping and internalization in varicosities of growing axons.

Growing retinal ganglion cell axons of the goldfish exhibit varicosities of varying sizes and smaller non-protruding phase-dense inclusions that are mobile and mediate rapid bulk redistribution of axoplasm. In fixed axons, Limax flavus agglutinin, a lectin specific for sialic acid which has been shown to inhibit organelle transport in these axons, preferentially labels surface membrane associated with varicosities and inclusions in preterminal axons. In viable axons, Limax flavus agglutinin causes: (1) agglutination of closely apposed axons, (2) redistribution of lectin-binding sites on varicosities to surfaces of interaxonal contact with other varicosities, forming 'fused' multivaricosity complexes, and (3) formation of vacuoles in many single varicosities and some multivaricosity complexes. Vacuoles contain Limax flavus agglutinin binding sites distributed circumferentially. On the basis of immunocytochemistry, actin, myosin, calmodulin and alpha-spectrin are co-localized with redistributed Limax flavus agglutinin binding sites. The agglutination, redistribution of lectin binding sites and changes in the cytoskeleton can be reversed by treatment with sialic acid. The lectin-induced vacuole formation and internalization of Limax flavus agglutinin receptors can also be blocked either by sodium azide in a glucose-free medium, or by pretreatment with cytochalasin D and indicate an energy and a cytoskeletal dependence. The Limax flavus agglutinin-induced structural rearrangements are not altered after limited digestion with pronase. Western blots after ultramicroelectrophoresis of retinal ganglion cell axons subjected to limited digestion reveal Limax flavus agglutinin labelling of bands with apparent Mr of 64 and 70 KDa. In undigested axons, some 70 KDa protein remains unextracted with Triton X-100 lysis of axonal fields, and more remains unextracted when axonal fields are pretreated with Limax flavus agglutinin before Triton lysis, suggesting increased association with the cytoskeleton in response to lectin binding. The results indicate that cross-linking of one or more sialoglycoconjugates on the surface of varicosities of preterminal growing retinal ganglion cell axons causes a constellation of transmembrane-mediated cytoskeletal and membrane changes that are akin to those described for capping in motile cells.

Actins↗
PubMed1991

T-wave response in cervical root lesions.

T-wave responses of biceps and triceps brachii muscles were recorded electrophysiologically from 31 normal subjects and 15 patients with unilateral lesions of the cervical C6 or C7 roots. Pathological T-wave responses were found in 11 (73%) patients. Patients with radiological correlate showed electromyographic (EMG) pathology in 60% but a pathological T-wave response in 90%. All patients with radiological correlate also showed pathological electrophysiological tests (EMG or T-wave responses). Electrophysiological measurement of the T-wave response appears to be a potentially useful tool in the diagnosis of cervical radiculopathies.

Adult↗
PubMed1990

Volume regulation in response to hypo-osmotic stress in goldfish retinal ganglion cell axons regenerating in vitro.

Goldfish retinal ganglion cell (RGC) axons regenerating in vitro were used to investigate the volume regulatory response to hypo-osmotic stress. Reducing the tonicity of the bathing medium to half strength caused an immediate swelling of axons; however, within 1 min a progressive volume reduction ensued which stabilized at near control volume over a period of 10 min. This regulatory volume decrease (RVD) was attenuated by elevated [K+]o, Ca2(+)-activated K+ channel antagonists, and calmidazolium, a potent calmodulin inhibitor. Inclusion of ATP-gamma S in the hypotonic bathing medium led to a loading of stressed axons which resulted in an excessive volume reduction that reflected an overshooting of the RVD response. The latter suggested the importance of phosphorylation/dephosphorylation reactions in the RVD response pathway. Cytochalasin D and colchicine had no effect on the development of the typical RVD response, providing no evidence of involvement of actin or microtubule cytoskeletons in the volume reduction mechanism of the immature axons. The results are consistent with the hypothesis that hypo-osmotic stress activates a calcium/calmodulin dependent membrane pathway, which probably involves transient phosphorylation, leading to a loss of cellular K+ and osmotically obligated water which restorates normal axonal volume.

Adenosine Triphosphate↗
PubMed1990

Transmembrane cytoskeletal modulation in preterminal growing axons: I. Arrest of bulk and organelle transport in goldfish retinal ganglion cell axons regenerating in vitro by lectins binding to sialoglycoconjugates.

Goldfish retinal ganglion cell (RGC) axons regenerating in vitro exhibit a novel mode of axoplasmic transport that entails a rapid bidirectional bulk redistribution of axoplasm, "packaged" as protruding varicosities and non-protruding phase-dense inclusions (Koenig et al.: J. Neurosci. 5:715-729, 1985; Edmonds and Koenig Brain Res. 406:288-293, 1987). We have used phase-contrast video microscopy to study transmembrane effects of surface-binding lectins on bulk transport and transport of single visible organelles in RGC axons. Our findings show that certain lectins which crosslink sialoglycoconjugates, such as wheat germ agglutinin (WGA) and the more specific sialic acid-binding lectin Limax flavus agglutinin (LFA), induce a rapid inhibition of transport activity. The LFA-induced inhibition of transport can be reversed by appropriate simple sugar haptens, and can also be antagonized by pretreatment with cytochalasin D. One of the consequences of LFA binding is an increase in RITC-conjugated phalloidin fluorescence staining of preterminal axons. The latter observation in conjunction with the antagonistic action of cytochalasin D suggests that one possible explanation for the transmembrane arrest of transport induced by crosslinking of surface sialoglycoconjugates may involve a polymerization and/or reorganization of the actin filament network which hinders translocation of mobile axoplasmic components.

Animals↗
PubMed1990

Trypanosoma brucei: constitutive activity of the VSG and procyclin gene promoters.

The variant surface glycoprotein (VSG) and procyclin are the major surface proteins of the bloodstream and procyclic stages, respectively, of Trypanosoma brucei. The promoter regions of the VSG and procyclin gene transcription units could be mapped thanks to the specific enrichment of initial transcripts that occurs following UV irradiation. Whereas the VSG gene is 45 kb distant from its promoter, procyclin genes are located immediately downstream. We show, by run-on assays on isolated nuclei and by cDNA analysis, that transcription occurs from both promoters in bloodstream as well as in procyclic forms. It is inferred that the control of the stage-specific expression of VSG and procyclin genes is not effected at the level of transcription initiation, but most probably by interfering with the elongation and stability of the specific transcripts.

Animals↗
PubMed1990

Calcium-dependent volume reduction in regenerating ganglion cell axons in vitro.

The effects of increasing [Ca2+]i on volume regulatory behavior was investigated by phase-contrast videomicroscopy in immature axons regenerating from goldfish retinal explants in vitro. Elevating [Ca2+]i by using EGTA-buffered, ionomycin-containing bathing media with either greater than or equal to 100 microM [Ca2+]o or 1 microM [Ca2+]o with N-methylglucamine substituted for Na+ caused axons to undergo a "syneresis." The syneresis was characterized by a marked loss in volume and condensation of axoplasm, accompanied by a proliferation of lateral processes, which resulted ultimately in an arrest of visible particle transport. The random appearance of dynamic phase-lucent axial protrusions in the distal axon, apparently caused by microtubules, was a frequent early manifestation. Syneresis was also produced by increasing the tonicity of the Cortland saline with sorbitol or treating axons with either valinomycin or with permeant cyclic AMP analogs in normal Cortland saline. In the latter case, extracellular Ca2+ was required. Preterminal axons showed an increase in phalloidin fluorescence after syneresis, suggesting polymerization and/or rearrangement of the actin cytoskeleton. Digitonin-permeabilized axonal field models, which maintained good morphology and particle transport, failed to develop a syneresis even when [Ca2+]o was increased to 250 microM. Cytochalasin D did not interfere with the development of a syneresis, but did suppress the proliferation of lateral processes. Syneresis could be blocked by high [K+]o, putative antagonists of Ca2(+)-activated K+ channels, or by calmidazolium, a calmodulin antagonist. The experimental findings suggest that cytoskeletal changes associated with volume reduction in growing retinal ganglion cell axons are secondary to a loss of cell water and that calcium/calmodulin-activated K+ channels very likely play a primary role in dehydration through the loss of K+ and osmotically obligated water.

Animals↗
PubMed1990

ATP and calmodulin dependent actomyosin aggregates induced by cytochalasin D in goldfish retinal ganglion cell axons in vitro.

Growing retinal ganglion cell (RGC) axons of the goldfish have mobile varicosities, which play a role in rapid bulk redistribution of axoplasm (Koenig, Kinsman, Repasky, and Sultz, 1985; Edmonds and Koenig, 1987). Varicosities contain a tubulo-vesicular SER embedded in an actin-containing cytomatrix (Koenig et al., 1985). Cytochalasin D (CD) induces the formation of focal cytoskeletal aggregates throughout preterminal axons and especially in varicosities. The aggregates are visible when labelled with fluoroscein isothiocyanate (FITC)-conjugated phalloidin. Double-labelling experiments show that Texas red-myosin or rhodamine isothiocyanate (RITC)-calmodulin immunofluorescence co-localizes with FITC-phalloidin-labelled aggregates. Formation of aggregates is blocked by calmidazolium, a calmodulin antagonist. Axon models permeabilized with digitonin retain the capacity to form focal aggregates in response to CD, when ATP or adenosine-5'-O(3-thiotriphosphate) (ATP-gamma S) is present in the permeabilization buffer, but not when 5'-adenylylimidodiphosphate (AMP-PNP) is present. The latter result indicates that formation of focal aggregates depends on ATP. The findings suggest that the formation of focal aggregates in immature axons is a manifestation of actomyosin interactions after free actin-filament ends are generated by CD treatment.

Actomyosin↗
PubMed1990

Impairment of vertical motion detection and downgaze palsy due to rostral midbrain infarction.

We present two cases with acute onset of vertical gaze palsy, mainly consisting of impaired downgaze and apraxia of downward head movements, together with neuropsychological deficits (hypersomnia, impaired attention and disorders of memory and affective control). CT and MRI revealed bilateral post-ischaemic lesions in the dorsomedial thalamus and the mesodiencephalic junction, dorsomedial to the red nucleus, thus being restricted to the territory of the posterior thalamosubthalamic paramedian artery, which includes the region of the rostral interstitial nucleus of the medial longitudinal fascicle as the main premotor nucleus for the generation of vertical saccades. In our patients, oculographic examination with electro-oculography and magnetic search coil recording showed severe impairment of downward more than upward saccades and only minor deficits of vertical pursuit and the vestibulo-ocular reflex. Visual functions were normal, with one exception: a psychophysical test of motion perception revealed a significant deficit in the detection of vertical movements. This could be due to a central adaptive mechanism which, in order to minimize oscillopsia, might elevate thresholds for vertical motion perception in cases of vertical gaze palsy. As an alternative explanation, lesions within the midbrain tegmentum could have damaged subcortical visual pathways involved in motion perception.

Cerebral Infarction↗
PubMed1990

Central spinal cord lesions in stenosis of the cervical canal.

34 patients suffering from cervical spondylotic myelopathy confirmed by myelography were examined by delayed CT 6-10 h after myelography. Twelve patients showed bilateral intramedullary collections of contrast medium, predominantly cranial to the stenosis. In these patients males predominated, the duration of clinical symptoms lasted longer although their age was lower. There was no correlation to the degree and the extension of the narrowing of the cervical spinal canal. Half of 20 patients undergoing consecutive decompressive surgery showed intramedullary contrast enhancement, and this was shown again by postoperative MRI in eight. The postoperative clinical and neurophysiological results revealed no change in the majority of patients, but three patients showing intramedullary contrast medium deteriorated in neurophysiological outcome, while only one of the patients in whom intramedullary contrast medium was not noticed got worse.

Adult↗
PubMed1989

Cycloheximide-sensitive [35S]methionine labeling of proteins in goldfish retinal ganglion cell axons in vitro.

Polypeptides of retinal ganglion cell axons of the goldfish, regenerating in culture, were labeled by [35S]methionine after decentralization from the explant. Microscopic samples, composed of isolated axonal fields, were analyzed by SDS ultramicroelectrophoresis and autoradiography. Of the several proteins exhibiting cycloheximide-sensitive labeling, beta-tubulin and actin were consistently and prominently labeled, although the possibility of a labeled alpha-isoform with a lower mol. wt. could not be ruled out.

Actins↗
PubMed1989

Spinal arteriovenous malformations and fistulae: clinical, neuroradiological and neurophysiological findings.

Twenty-six patients with myelographic signs suggestive of a spinal arteriovenous malformation (AVM) were examined neurologically and neurophysiologically. By selective spinal angiography it was possible to differentiate between dural arteriovenous fistulae (dAVF 20 patients) and intradural AVMs (iAVM, 6 patients). Initial complaints were nonspecific and variable, mainly consisting of sensory disorders and muscle weakness. Later, patients suffered involvement of both the upper and lower motor neurons. There was a high percentage of lower motor neuron lesions (95%), especially in dAVF patients, which were mostly of widespread distribution and included several myotomes. Electrophysiological examination regularly revealed lower neuron involvement, frequently with pathological spontaneous activity in several myotomes, pathological sensory-evoked potentials after tibial nerve stimulation, but normal sensory conduction velocities of the sural nerve, indicating sparing of the sensory ganglion. Frequently there was a discrepancy between the localization of the dural fistula or angioma and the spinal level responsible for clinical symptoms. This suggests that it may be the inadequacy of the venous drainage system to cope with the blood volume rather than the AV-shunt that is responsible for the symptoms. An early diagnosis is essential, as removal of the shunt before there has been progression to severe neurological deficits (paraplegia) is the only way to ensure a satisfactory outcome.

Adult↗
PubMed1989

Different affinities of alpha 2-agonists for imidazoline and alpha 2-adrenergic receptors.

It has recently been shown that imidazoline alpha 2-adrenergic agonists, such as clonidine and UK 14,304, selectively bind to both alpha 2- and imidazoline receptors in basolateral membranes from rabbit renal proximal tubule. In order to define the relative affinity of three antihypertensive alpha 2-agonists for the two classes of receptors, we performed competition studies of imidazoline alpha 2-antagonist 3H-RX 781094 and nonimidazoline antagonist 3H-rauwolscine binding to basolateral membranes from rabbit proximal tubule. The order of potency for inhibition of radioligand binding to basolateral membranes was rilmenidine greater than clonidine greater than guanfacine and clonidine greater than guanfacine greater than rilmenidine for 3H-RX 781094 and 3H-rauwolscine binding, respectively. These data show that not only clonidine, but also rilmenidine and guanfacine, drugs usually used as specific alpha 2-agonists, bind to both alpha 2- and imidazoline receptors. The higher affinity of these molecules for one or the other class of receptors could explain their different capacity to induce hypotension and side effects.

Adrenergic alpha-Agonists↗
PubMed1989

[Selectivity of alpha 2-adrenergic agonists for the imidazoline-guanidine and alpha 2-adrenergic receptors].

Imidazolines have been proposed as highly selective drugs for alpha 2-adrenergic receptors. However, we have recently showed that the imidazoline ligand 3H-RX 781094 (idazoxan) binds to both alpha 2-receptors and imidazoline guanidinium receptive substance (IGRS) in rabbit renal proximal tubule. Binding of 3H-RX 781094 to the purified basolateral membranes (15-fold enriched in Na-KATPase activity) was rapid (t 1/2 = 5 mn.) reversible (t 1/2) = 4 mn.), saturable and of high affinity. Scatchard analysis of equilibrium binding data showed that 3H-RX 781094 labels 566 +/- 118 fmol/mg of proteins of binding sites with an apparent dissociation constant (Kd) of 1.45 +/- 0.14 nM. On the other hand, the non imidazoline ligand 3H-rauwolscine binds only to the alpha 2-adrenergic receptors with a maximal density of 155 +/- 28 fmol/mg of protein and a Kd of 11.5 +/- 1.5 nM. In order to define the relative affinity of the alpha-2-agonists, clonidine, rilmenidine and guanfacine for the two classes of receptors, we performed competition studies of the alpha 2-antagonists 3H-RX 781094 (imidazoline) and 3H-rauwolscine (non imidazoline) binding to basolateral membranes from rabbit proximal tubule. The order of potency for inhibition of the two radioligand binding was rilmenidine greater than clonidine greater than guanfacine for 3H-RX 781094 and clonidine greater than guanfacine greater than rilmenidine for 3H-rauwolscine. Therefore, rilmenidine displayed a higher affinity for IGRS than for alpha 2 adrenergic receptors; on the other hand, clonidine and guanfacine preferentially interact with alpha 2 receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗
PubMed1989

[Hepatic markers (Ac-HVA-IgM and AcHBc-IgM) in cases of infectious hepatitis in Dominican children].

The presence of IgM antibodies for the HVA and HBc antigens in 90 children of 15 or less years with acute hepatitis were investigated, finding that 62% (58) were positive for HVA, 8.9% (8) for HBc and 27.8% (25) did not show antibodies for HVA or HBc (non-A non-B hepatitis); comments are made on some clinical and epidemiological findings such as a higher frequency of blood transfusions in HNANB, more males in HB and HNANB, and more hepatomegaly and liver sensitivity in HNANB.

Adolescent↗
PubMed1989

Neurophysiological characteristics of spinal arteriovenous malformations.

The aim of the study was to identify the clinical and neurophysiological pattern of deficits in spinal arteriovenous malformations (AVM) to allow an early diagnosis which is the prerequisite for effective treatment by early surgery or embolization. Among 26 patients with myelographic signs of a spinal AVM, selective spinal angiography disclosed 20 cases with a dural AV-fistula (dAVF) and 6 patients with an intradural AV-malformation (iAVM). Although the main pathogenetic factor in both disorders may be different, clinical and neurophysiological findings proved to be of limited value in differential diagnosis. Clinical symptoms presented by the patients were a variable combination of lower motor neuron lesion, sphincter disturbance, sensory transverse lesion and partly additional signs of upper motor neuron involvement. Electromyography invariably showed an increased rate of polyphasia and frequently pathological spontaneous activity usually in several myotomes. Normal sensory conduction velocity of the sural nerve contrasted with almost regularly pathological SEP's after tibial nerve stimulation. The distribution if clinical and neurophysiological findings suggests rather widespread lesions of the lower cord and/or cauda equina, frequently at a lower level than the angiographically localized shunt. This suggests a vascular myelopathy on the basis of insufficient venous drainage at least for the frequent dural AV-anomaly.

Adult↗
PubMed1988

Interaction of clonidine and rilmenidine with imidazoline-preferring receptors.

In the present study the imidazoline radioligand 3H-RX 781094 (idazoxan) was used to characterize the alpha 2-adrenergic receptors in basolateral membranes of rabbit proximal tubule. Scatchard analysis of equilibrium binding data showed that 3H-RX 781094 labels 566 +/- 118 fmol/mg protein of binding sites with an apparent dissociation constant (Kd) of 1.45 +/- 0.14 nmol/l. However, in competition studies, only 25% of the 3H-RX 781094 binding was inhibited by catecholamines and alpha 2-adrenergic compounds; the remaining 75% of specific binding was inhibited only by molecules having an imidazoline or oxazoline ring with the following order of potency: cirazoline greater than tolazoline greater than UK 14 304 greater than rilmenidine greater than clonidine. These data suggest that imidazoline compounds bind to both alpha 2-adrenergic receptors and to a 'non-adrenergic site' which might be defined as an imidazoline-preferring receptor. Based on these results, it is possible to hypothesize that imidazoline and oxazoline drugs, such as clonidine and rilmenidine, exert their hypotensive activity partly through the stimulation of imidazoline receptors.

Animals↗