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| Vopr Med Khim, 1978 Jul-Aug, 24(4), 505 - 10 {Effect of the activity of adrenergic processes on tissue catecholamine concentrations}; Chesnokova NP; Demedullation of adrenal glands caused a decrease in excretion of adrenaline and vanilyl mandelic acid with simultaneous increase of adrenaline content in various rat tissues . Predemedullation of adrenal glands prevented distinctly the alterations in catecholamine metabolism, which developed in botulinic and tetanic neurointoxications . The data obtained suggest that activation of adrenergic processes is of importance in genesis of the alterations observed in catecholamine metabolism under conditions of botulinic and tetanic intoxications. Vopr Med Khim, 1978 Jul-Aug, 24(4), 490 - 5 {Interrelationship between the activity of cholinergic processes and catecholamine metabolism in botulin poisoning}; Chesnokova NP; Reversible inhibition of cholinergic processes in cats after pancreatectomy was accompanied by decreased urinary excretion of adrenaline, increased excretion of vanilyl mandelic acid, exhaustion of catecholamine stores in adrenal glands and increased content of noradrenaline in some tissues . Similar alterations occurred in the paralytic step of botulinic intoxication . Metabolism of catecholamines was much more distinctly impaired in previously pancreatectomized animals after development of botulinic and tetanic neurointoxications, which were accompanied by irreversible inhibition of acetylcholine liberation in myoneural synapses . Impairments of catecholamine metabolism were manifested in a decrease in total content of the substances studied in various tissues. Naunyn Schmiedebergs Arch Pharmacol, 1978 Jun 27, 303(2), 133 - 8 Suppression of 3H-acetylcholine release from primary nerve cell cultures by tetanus and botulinum-A toxin; Bigalke H et al.; Primary nerve cell cultures derived from embryonic rat central nervous system form {3H}ACh from exogenous {3H}Ch, and release it upon potassium depolarization . Pretreatment of the cultures with botulinum-A toxin or tetanus toxin diminishes the cellular accumulation of {3H}ACh . Poisoning the cultures during the period of {3H}Ch uptake fails to lower {H}ACh formation . Dependent on dosage, both toxins suppress the release of {3H}ACh upon potassium depolarization . Heat-denaturated toxins as well as tetanus toxin preincubated with tetanus antitoxin were without effect. Parazitologiia, 1978 May-Jun, 12(3), 201 - 5 {Specification of the systematic position of Botulus alepidosauri (Trematoda, Hirudinellidae)}; Aleshkina LD; The detailed description of Botulus alepidosauri Guiart, 1938 from Thunnus obesus, Alepisauris ferox, A . brevirostris in tropical East Atlantic is presented . The described species is compared with literary data . Some changes were introduced into the taxonomic position of the genus Botulus, considered as a representative of the subfamily Botulinae in the family Hirudinellidae. Appl Environ Microbiol, 1978 May, 35(5), 878 - 80 Affinity chromatography purification of type A botulinum neurotoxin from crystalline toxic complex; Moberg LJ et al.; Type A botulinum neurotoxin was purified from toxic crystals by adsorption to p-aminophenyl-beta-D-thiogalactopyranoside coupled to CH-Sepharose 4B . At pH 6.3, the toxic complex was held by the binding between the ligand and the hemagglutinin of the complex; the toxin is eluted selectively by dissociating the complex with buffer-saline of pH 7.9 . The single-step affinity chromatography recovered 50 to 60% of applied toxicity as preparations of greater than 99% purity. C R Acad Sci Hebd Seances Acad Sci D, 1978 Mar 13, 286(10), 793 - 5 {Action of serotonin on neuromuscular transmission in normal guinea pigs and those treated with paralyzing doses of botulinum toxin type A}; Tazieff-Depierre F; Serotonin inhibits the muscular contractions elicited by indirect stimulation; injected before Botulinum toxin it prevents the paralysis induced by this toxin. Vopr Med Khim, 1978 Mar-Apr, 24(2), 224 - 7 {Change in the histamine and serotonin levels in the external respiratory apparatus in botulinic poisoning in cats}; Morrison VV; General botulinic intoxication in cats, accompanied by severe respiratory insufficiency, was characterized by distinct impairments in histamine and serotonin metabolism in external respiratory system . Pronounced increase in content of histamine was observed in impaired muscles and their corresponding regional centers of medulla spinalis, when botulinic intoxication had the local type with unilateral paralysis of diaphragm and intercostal muscles . Content of serotonin was increased in the tissues studied only at the later steps of local botulinic intoxication. C R Acad Sci Hebd Seances Acad Sci D, 1978 Feb 27, 286(8), 655 - 8 {Action of toxin II isolated from the tentacles of sea anemones on the neuromuscular transmission on normal and botulin toxin inhibited frogs}; Tazieff-Depierre F et al.; In our experimental conditions, toxin II from Anemonia sulcata restored Frog neuromuscular transmission blocked by botulinum toxin, type A. J Hyg Epidemiol Microbiol Immunol, 1978, 22(4), 449 - 52 Histochemical investigation of some mitochondrial and microsomal enzymes in the kidneys of rabbits immunized with type B botulinus anatoxin; Gendler IE et al.; Immunization of rabbits with botulinus anatoxin containing a number of proteins of bacterial origin causes a statistically significant increase in the activity of succinate dehydrogenase, NAD diaphorase and NADP diaphorase as early as after 24 hours . After 5-7 days, the activity of all mitochondrial enzymes drops below the control level and returns to normal by the 14th day . The activity of glucose 6-phosphatase decreases significantly already 24 hours after immunization and returns to normal by the end of the 7th day . The mechanism of excretion of foreign protein in the kidneys of immunized animals is discussed. J Physiol, 1977 Dec, 273(2), 443 - 57 Action of brown widow spider venom and botulinum toxin on the frog neuromuscular junction examined with the freeze-fracture technique; Pumplin DW et al.; 1 . Structural changes which normally accompany transmitter release at frog neuromuscular junctions are visualized with the freeze-fracture technique . The effects of brown widow spider venom and botulinum toxin were evaluated in terms of their ability to block or produce these structural changes . Changes produced by these neuropoisons were correlated with their known effects on neurotransmitter release . 3 . Fusion of synaptic vesicles with the presynaptic plasmalemma, normally evoked by electrical stimulation, was abolished at neuromuscular junctions from frogs treated with botulinum toxin . 3 . The concentration of large intramembranous particles in the presynaptic plasmalemma, an indication of the excess of synaptic vesicle fusion over recovery of synaptic vesicle membrane, was increased by treatment with brown widow spider venom, even in the presence of botulinum toxin . 4 . When external calcium was present, sites of vesicle fusion induced by brown widow spider venom, as well as by electrical stimulation, were located mainly in the active zone . In the absence of external calcium, many plasmalemmal deformations, also though to be sites of vesicle fusion, were more evenly dispersed over the presynaptic surface of nerve terminals . 5 . Botulinum toxin decreased the number of vesicle fusion sites in the active zone induced by spider venom in the presence of external calcium but had little effect on the number of fusion sites induced by spider venom in the absence of external calcium . 6 . Nerve terminals soaked in a sodium-free Ringer solution were partially depleted of vesicles . Addition of spider venom to this Ringer did not cause additional depletion of vesicles . 7 . Formation of cation-permeable channels in the presynaptic membrane could account for these effects of spider venom on the frog neuromuscular junction . Botulinum toxin blocks vesicle fusion by some means which is not yet understood. C R Acad Sci Hebd Seances Acad Sci D, 1977 Nov 28, 285(15), 1335 - 8 {Effect of scorpion venom (Androctonus australis) on neuromuscular transmission inhibited by botulinum toxin in the frog}; Tazieff-Depierre F et al.; We have shown that Scorpion venom restores the neuro-muscular transmission inhibited by Botulinum toxin in the Frog . The effectiveness of Scorpion venom was antagonized by excess magnesium. Exp Brain Res, 1977 Nov 24, 30(2-3), 313 - 21 Ultrastructural responses of the hypoglossal nucleus to the presence in the tongue of botulinum toxin, a quantitative study; Sumner BE; The ultrastructural effects of local injection of botulinum toxin into the left half of the tongue of the rat, were studied quantitatively 35 days postoperatively in the left hypoglossal nucleus . The results showed (1) a decrease in somatic and neuropil bouton numbers because of loss of boutons with symmetrical synapses and clear spherical synaptic vesicles, (2) a decrease in the numbers of dendrite profiles in the neuropil, (3) an increase in the proportion of dendrites and boutons with unusual inclusions, suggestive of profile retraction, (4) an increase in the proportion of profiles which were unusually electron-dense, (5) an increase in the amount of astrocyte, and a growth of astrocyte sheaths around bouton-free neurone surfaces, (6) the presence of occasional microglia, and (7) subastrocytic subsurface cisterns . Control rats injected with boiled toxin had no responses except (3) and (4) above, and then only to a modest extent, possibly due to mechanical damage of a few axons or terminals at the time of injection, or to insufficient inactivation of the toxin by boiling . The results were compared with those at 35 days after axotomy, and it was concluded that botulinum toxin, which interrupts neuromuscular transmission, elicits the same responses in the hypoglossal neurones, as does transection of the hypoglossal nerve, even though earlier studies had discovered no glial replication after botulinum toxin, in contrast to axotomy. Experientia, 1977 Nov 15, 33(11), 1458 - 60 Effect of botulinum toxin on the choline acetyltransferase activity in salivary glands of cats; Ekstrom J et al.; The choline acetyltransferase activity of submandibular glands that had previously received a retrograde injection of botulinum toxin via their ducts was found to be markedly lower than in the untreated contralateral glands . In the parotid glands exposed to the same treatment the activity of this enzyme was less affected. Zh Mikrobiol Epidemiol Immunobiol, 1977 Nov, (11), 120 - 5 {Morphologic and histochemical responses of the body to introduction of C1 . botulinum toxin . V . Response of locus coeruleus cells of the brain to introduction of the toxin of C1 . botulinum type B}; Anosov IIa; After the per os administration of 1Dlm/ml of botulin, type B . there were observed at the period of development of the limb paralysis and myasthenia morphological changes in the locus coeruleus cells expressed in the development of a more pronounced than normal perinuclear clarification and some nuclear basophilia . Histochemical study of succinic dehydrogenase, acid phosphatase, cholinesterase, and catecholamines pointed to the intensified neuron metabolism of the locus coeruleus; this could serve as an indication of enhanced energopacemaker function of this nucleus in hypoxia which occurred. Zh Mikrobiol Epidemiol Immunobiol, 1977 Nov, (11), 97 - 106 {The species C . diphtheriae}; Krylova MD; Corynebacteria (C . diphtheriae var . gravis, mitis, minimus, intermedius, C . belfanti, C . ovis, C . ulceraus) producing diphtheria toxin are found as variants sharply differing from one another morphologically (from long branching rods to coccobacilli), culturally, biochemically and by other signs . The toxin synthesis in them was determined by genetically heterogeneous prophages tox+; tox+ virus exchange is possible between the corynebacteria . Since production of specific toxin, the cardinal sign of C . diphtheriae species, is connected with the genoms of genetically heterogeneous viruses tox+, the circle of whose hosts is very wide, it can be supposed that there is no genetically homogeneous taxonomic category "diphtheriae species" . Several species of corynebacteria--lysogenized (toxigenic) or capable of being lysogenized (nontoxigenic) with tox+ viruses are included into the composition of the corynebacteria groups which medicine considers as "species" for over 80 years . A possiblity of becoming a diphtheria causative agent is determined by the capacity of corynebacteria to become infected with the circle of viruses tox+ the DNA of which can become stably integrated with the gene of this bacterium . The mentioned approach to taxonomy is possibly applicable to microorganisms in which the pathogenicity signs (the toxin) were determined, as in C . diphtheriae, in the virus genoms (Bac . botulinus). Naunyn Schmiedebergs Arch Pharmacol, 1977 Oct 6, 299(3), 267 - 72 Effects of type A botulinum toxin on the cholinergic transmission at spinal Renshaw cells and on the inhibitory action at Ia inhibitory interneurones; Hagenah R et al.; 1 . The central action of botulinum toxin A (BTA) on the cholinergic transmission at Renshaw cells (RCs) and on the RC-induced inhibition of Ia inhibitory interneurones (IaINs) was studied in anaesthetized cats . BTA was administered by application directly into the spinal cord, injection into a ventral root (L7) and/or injection into the triceps surae (GS) muscle . 2 . A direct application of BTA into the spinal cord led to a decrease of the early and the late response of RCs . 3 . When the neurotoxin was injected into the GS muscle, the RC activity remained unaffected during the test period (33-46 h after application) . 4 . No effect appeared up to 10 h after an injection into the ventral root L7 . 5 . The RC-induced inhibition on IaINs, when tested in animals with local botulismus, remained intact during the test period . 6 . From the present results it is suggested that on the spinal level the central action of botulinum toxin predominantly passes on the motoneurones. J Neurol Sci, 1977 Oct, 34(1), 37 - 42 Neuromuscular paralysis caused by tick envenomation; Pearn J; The Australian scrub-tick Ixodes holocyclus causes a series of significant toxic effects in its victims . The most important feature of tick envenomation is neuromuscular paralysis . Children poisoned by ticks may manifest only local motoneural effects, usually facial paralysis . Progressive ascending flaccid paralysis occurs if the removal of an embedded tick is delayed . The specific neurological features of tick-bite are discussed in the light of a series of 6 children who all showed signs of tick paralysis . Tick venom is known to slow nerve conduction, and may have a botulinum-like effect at the neuromuscular junction . The literature on the neurological effects of tick-envenomation is reviewed. Acta Neurol Scand, 1977 Aug, 56(2), 141 - 52 Correlation between single fibre EMG jitter and endplate potentials studied in mild experimental botulinum poisoning; Lundh H et al.; To study the correlation between single fibre EMG jitter and endplate potential amplitude we examined neuromuscular transmission in rats paralysed with botulinum toxin type A with single fibre EMG (SFEMG) in vivo and with intracellular microelectrode techniques in vitro . In muscles that were not completely paralysed SFEMG showed an increased neuromuscular jitter on nerve stimulation and in these muscles endplate potentials were of reduced amplitude . When the nerve stimulation frequency increased the jitter decreased . Intravenous injection of drugs that increase the acetylcholine release and endplate potential amplitude markedly reduced the jitter and the frequency dependence disappeared. Experientia, 1977 Jun 15, 33(6), 750 - 1 Modification of the action of pentagastrin on acid secretion by botulinum toxin; Kondo T et al.; I.v botulinum toxin after 60-90 min abolished the dose-response relationship between pentagastrin and gastric acid secretion in anesthetized rats and guinea-pigs . The toxin reduced but did not abolish the acid stimulatory effect of histamine . As expected, the acid response to vagal stimulation was abolished and that to methacholine in rats was unaltered by the toxin. Biull Eksp Biol Med, 1977 Jun, 83(6), 651 - 4 {Mechanism of disorders of inhibition of electrogenesis in spinal alpha-motor neurons in experimental local botulin poisoning}; Mikhailov VV et al.; Disorders of postsynaptic inhibition and of the spinal cord alpha-motoneurons were studied in cats with experimental local botulinum intoxication . A significant decrease of the reciprocal, and, to a lesser extent, of polysynaptic inhibitory postsynaptic potential (IPSP) was noted . With the appearance of total paralysis of the muscles in the poisoned extremity there proved to be an even greater depression of the reciprocal and polysynaptic IPSP; however, they never disappeared or turned into depolarization potentials . Synaptic permeability of motor neurons as a rule decreased during the IPSP development, this indirectly indicating a reduction of ion transport. J Pharmacol Exp Ther, 1977 May, 201(2), 312 - 9 The release of acetylcholine elicited by extracts of black widow spider glands: studies using rat superior cervical ganglia and inhibitors of electrically stimulated release; Pumplin DW et al.; An extract of the venom glands of black widow spiders (BWGE) induces the release of acetylcholine (ACh) from the superior cervical ganglia of rats . The release of ACh follows first-order kinetics, which suggests that the venom either lowers the ganglionic store of ACh, or continually reduces the rate of release . Since ganglionic ACh did not decrease in the presence of BWGE, it is likely that the venom continually reduces the rate of release . The rate constant for BWGE-induced release of ACh is depressed about 45% by treatment of the ganglion with either botulinum toxin or a low Ca++/high Mg++Ringer's solution . The rate constant is depressed about 30% by treatment of the ganglion with 8.3 microng/ml of cytochalasin-B . Since these agents inhibit the release of ACh which is elicited by electrical stimulation of the ganglion, it is suggested that one action of BWGE is the stimulation of some step in the physiological mechanism involved in the release of neurotransmitters . Treatment of the ganglion with tetrodotoxin had no effect on the rate constant for release induced by BWGE . The action of BWGE on the ganglion was not reversible after 10 minutes . When treated with BWGE, ganglia whose stores of transmitter had been labeled by electrical stimulation in the presence of {3H}choline released ACh having uniform specific activity . The data suggest the presence of more than one activity in the extracts. Zh Mikrobiol Epidemiol Immunobiol, 1977 May, (5), 81 - 6 {Evaluation of the quality of dry anatoxins in the process of their production}; Vorontsov IV et al.; On the example of production of botulin toxoids of A, B and E types the authors demon strated the expediency of using the agar gel diffuse precipitation test for preliminary assessment of the toxoid activity, instead of a more expensive and complicated antitoxin-binding test. J Neurol Sci, 1977 May, 32(1), 29 - 43 Antagonism of the paralysis produced by botulinum toxin in the rat . The effects of tetraethylammonium, guanidine and 4-aminopyridine; Lundh H et al.; The injection of botulinum toxin type A into the hind-leg of adult rats causes complete paralysis of the leg lasting for several weeks . In the extensor digitorum longus (EDL) muscle transmitter release is reduced to a level of less than 1% of normal . Tetraethylammonium (TEA) and guanidine in concentrations of about 3 mM restore, in EDL muslces in vitro, neuromuscular transmission to about the normal level, provided that the external calcium concentration is 4 mM or higher . 4-Aminopyridine (4-AP) has similar restorative effect but is about 20-30 times more potent . Unlike TEA and guanidine, 4-AP is effective when the ambient calcium concentration is 2 mM; this drug is therefore also active in vivo . The intravenous injection of 4-AP (5 mg/kg body weight) restores neuromuscular transmission from complete paralysis by botulinum toxin to a normal level as shown by the recording of almost normal twitch and tetanic tensions in the EDL muscle . In rats paralysed by a lethal dose of botulinum toxin, the intraperitoneal administration of 4-AP restores general motor activity, the effect lasting 1-2 hours . A study of the effects of these drugs on spontaneous and evoked transmitter release suggests that all three compounds increase the level of free calcium inside the nerve terminals . In botulinum poisoning the transmitter release mechanism appears to be intact, but a reduced sensitivity to calcium has been shown (Cull-Candy et al . 1976), and this could explain why the drugs restore evoked transmitter release in botulinum poisoning. Zh Mikrobiol Epidemiol Immunobiol, 1977 Apr, (4), 91 - 4 {Detection of the localization of C1 . botulinum antigens in regional lymph node cells by the immunofluorescence technic}; Vasil'eva TA et al.; As a result of the study of lacalization of the C1 . botulinum toxoids of the A, B, and E types in cells of the regional lymph nodes of rabbits by the indirect Coons' method and by the smear-print method it was revealed that different types of lymphoid tissue cells took part in the ingestion and digestion of these antigens; the antigens of the A and B types were at first revealed in the cytoplasm of pseudoeosinophils, and then in the macrophages . The antigen of the E type was revealed in the course of the whole experiment in the macro phages of the regional lymph node, although the number of pseudoeosinophils also increased . Apparently there was a different activity of pseudoeosinophils against the C1 . botulinum toxoids, the types A, B and E. Zh Mikrobiol Epidemiol Immunobiol, 1977 Apr, (4), 125 - 9 {Patterns in the formation of proteolytic enzymes by different strains of C1 . botulinum type F}; Egorova EN et al.; The authors studied regularities attending the accumulation of proteolytic enzyme and toxin by C1 . botulinum, type F, strains in the medium . Strains No . 470, 200, 76, 55 proved to possess caseinolytic capacity, whereas strains Eklund and Craig were "nonproteolytic" . C1 . botulinum strain, type F, medium and growing conditions providing a high yield of proteolytic enzymes were selected . Some properties of proteolytic enzyme of strain No . 470 were studied. Vopr Med Khim, 1977 Mar-Apr, 23(2), 261 - 6 {Role of disorders in biogenic amine metabolism in the pathogenesis of botulin poisoning}; Chesnokova NP; A depotentiating effect of prednisolone, benactyzine, reserpine, propranolole and large doses of serotonin on the development of the intoxication was shown to occur in combination with inhibition of the biogenic amines accumulation in various tissues of cats with botulinic paresis . The same phenomenon was observed in intoxicated animals maintained without pharmacological treatment. J Physiol, 1977 Mar, 265(3), 809 - 20 Effect of implantation of an extra nerve on the recovery of neuromuscular transmission from botulinum toxin; Tonge DA; 1 . The common peroneal nerve was implanted into soleus in the mouse and 2 weeks later a sublethal dose of botulinum toxin injected causing a block of neuromuscular transmission at the terminals of the soleus nerve . Most muscle fibres became innervated by the common peroneal nerve . 2 . Recovery of neuromuscular transmission at the soleus nerve terminals was delayed in the common peroneal nerve implanted muscles . 3 . Stimulation of the soleus nerve after botulinum-evoked subthreshold end-plate potentials (e.p.p.s) in virtually every fibre tested in unoperated muscles . In common peroneal nerve-implanted muscles stimulation of the soleus nerve failed to evoke e.p.p.s in about 40% of fibres tested and where e.p.p.s were recorded their amplitudes were generally smaller . 4 . When the common peroneal nerve was cut 2 months after botulinum, neuromuscular transmission at soleus nerve terminals occurred after 4 weeks . When the common peroneal nerve was cut 6 months after botulinum, transmission was found at soleus nerve terminals within 1 week . 5 . Recovery of transmission at soleus nerve terminals from the effects of botulinum toxin is delayed if the muscle fibres become innervated by the common peroneal nerve and a proportion of soleus nerve terminals cease to release acetylcholine (ACh) until after the peroneal nerve has been cut. J Pharmacol Exp Ther, 1977 Feb, 200(2), 343 - 51 The effects of acute and chronic botulinum toxin treatment on receptor number, receptor distribution and tissue sensitivity in rat diaphragm; Simpson LL; Tritiated alpha-bungarotoxin was used to determine the number and distribution of acetylcholine receptors in innervated, denervated and botulinum toxin-treated muscles . Innervated hemidiaphragms bound approximately 2.3 x 10(11) molecules of alpha-bungarotoxin; binding sites were restricted to the end-plate region . Neither acute denervation nor acute poisoning with botulinum toxin altered the number or distribution of alpha-bungarotoxin binding sites . In chronically denervated hemidiaphragms, there was an increase in alpha-bungarotoxin binding sites (maximum about 5.7 x 10(12); these sites were distributed across the muscle surface . In chronically poisoned hemidiaphragms, there was also an increase in the number (maximum about 4.7 x 10(12)) and distribution of binding sites . Chronic denervation and chronic botulinum toxin treatment both produced supersensitivity to acetylcholine . At maximal sensitivity, the respective ED50 values were: denervated muscle, 1.1 x 10(-6) M; botulinum toxin-treated muscle, 5.0 x 10(-6) M . The combination of denervation plus botulinum toxin treatment did not have additive or synergistic effects on alpha-bungarotoxin binding (4.9 x 10(12) molecules/hemidiaphragm) or on tissue sensitivity to acetylcholine (ED50 = 2.1 x 10(-6) M) . It is concluded that denervation and botulinum toxin have rather similar effects on the number and distribution of acetylcholine receptors in rat hemidiaphragm. Zh Mikrobiol Epidemiol Immunobiol, 1977 Feb, (2), 48 - 53 {Comparative immunochemical study of the hemagglutinins of Cl . botulinum A and B}; Ivanova LG et al.; The authors demonstrated an incomplete indentity of Cl . botulinum hemagglutinins of types A and B in the double diffusion reaction in agar gel, and their difference by electrophoretic mobility . Some differences in the interaction of hemagglutinins A and B with human erythrocytes were found by the hemagglutination inhibition method; apparently, of the principal significance in the relization of the reaction of human erythrocyte hemagglutination with hemagglutinins of Cl . botulinum, types A and B, was the OH-group position in the C4 galactose of the mucopolysaccharides of the erythrocyte cell wall . Apart from C4, apparently, for hemagglutinin of types A of significance was the reactive capacity of C1 and C2 galactose atoms, whereas for hemagglutinin of type B--free OH-group in C2 galactose atom. Acta Histochem, 1977, 60(2), 169 - 72 {Histochemical studies of the dynamic of activity of some mitochondrial enzymes in the rabbit liver during the process of the primary immune answer (author's transl)}; Gendler IE; With the histochemical methods were investigated the dynamic of activity of the succino-dehydrogenase, the NAD- und NADP-depended diaphorase in the rabbit liver after a one time immunisation with botulinus anatoxin typ B . The animals were killed in different steps after the immunity . Their was observed significant variety of the activity of investigated enzymes . This was discussed in connexion with the catabolic processes of the antigen and the stimulation of the synthesis unspecific proteins in the parenchymatous cells. J Physiol, 1976 Nov, 262(3), 553 - 81 Spontaneous subminature end-plate potentials in mouse diaphragm muscle: evidence for synchronous release; Kriebel ME et al.; 1 . Miniature end-plate potentials (min.e.p.p.s) were recorded from small muscle cells of mouse diaphragms . Min.e.p.p . amplitude histograms showed successive peaks which were integral multiples of the smallest peak . The smallest potentials (submin.e.p.p.s) averaged 0-3-0-6mV and the mean of the larger min.e.p.p.s averaged 3-7 mV, depending on the muscle cell diameter . There was a positive correlation between time-to-peak and min.e.p.p . amplitude . Time-to-peak of the submin.e.p.p.s fell slightly below the regression line through the larger min.e.p.p.s . 2 . Sometimes min.e.p.p . amplitude distributions changed spontaneously such that the mean of the major mode min.e.p.p.s decreased twofold during which time the mean of the submin.e.p.p.s did not change . Spontaneous decreases were most pronounced during low frequencies of release (10/min) achieved at 32 degrees C . 3 . Small changes in temperature (2 degrees C steps in the range 32-40 degrees C) greatly altered the number of peaks of min.e.p.p . amplitude histograms without noticeably changing the position of the submin.e.p.p . peak . At 32 degrees C submin.e.p.p.s composed 5-20% of the histograms and the amplitude of the major mode peak was twelve to fifteen-times that of the submin.e.p.p.s . Over-all bell-shaped distributions were obtained at 37 degrees C which showed up to eight peaks with the major peak at the fourth to sixth peak . Temperatures slightly above 37 degrees C gave a flat distribution with the mean amplitude at the third peak . Min.e.p.p . amplitude histograms were initially skewed (mostly small min.e.p.p.s) after a 40 degrees C heat challenge . 4 . Two to eight-times the normal concentration of Ca2+ in the saline reversibly increased the min.e.p.p . frequency and also decreased the mean of the major mode min.e.p.p.s (two to nine-times) without noticeably changing the mean of the submin.e.p.p.s . 5 . Botulinum toxin A, 10(5) X intraperitoneal median lethal dose (10(5)I.P.LD50)/ml., almost abolished min.e.p.p.s in 30-90 min . The relative proportion of submin.e.p.p.s increased and the mean of the major mode min.e.p.p.s usually did not change during the initial decrease in frequency . Major mode min.e.p.p.s essentially ceased after 200-1000 were generated and remaining min.e.p.p.s of some cells showed skewed distributions with three small peaks that were integral multiples of the submin.e.p.p . peak . Smaller min.e.p.p.s were more resistant to block than the larger min.e.p.p.s and, although frequencies were low, small min.e.p.p.s were recorded after 4 hr of botulinum toxin incubation . 6 . Colchicine (5 X 10(-4)M) within minutes reduced the major mode min.e.p.p.s by half (mean of major peak reduced to sixth or seventh peak) . Additional colchicine (10(-3)M reduced the major mode min.e.p.p . amplitude to a fifth of that of control (mean of major mode min.e.p.p.s at the third peak) with no change in position of the submin.e.p.p . peak . Min.e.p.p . amplitudes slowly recovered to half control values after washing . 7... Naunyn Schmiedebergs Arch Pharmacol, 1976 Nov, 295(2), 171 - 5 Binding of botulinum neurotoxin to the synaptosome fraction of rat brain; Kitamura M; The radioactive 125I-labelled neurotoxin of C . botulinum type A, when incubated with rat brain homogenate, is bound selectively to the synaptosome fraction . Intact toxin was liberated from the synaptosome fraction by treatment with Triton X-100, SDS, trypsin or neuraminidase. Science, 1976 Sep 24, 193(4259), 1256 - 8 Botulinum toxin: mechanism of presynaptic blockade; Kao I et al.; The mechanism of action of botulinum toxin was analyzed by the use of calcium ionophores and black widow spider venom . Addition of calcium ionophores to nerve-muscle preparations blocked by botulinum toxin did not increase the frequency of miniature end plate potentials . However, the spider venom elicited a barrage of miniature end plate potentials after blockade by botulinum . Electron micrographs of preparations treated with botulinum toxin and then the spider venom revealed clumping of synaptic vesicles at release sites in the otherwise depleted nerve terminals . These findings indicate that the action of botulinum toxin is not due to deficient storage of acetylcholine in vesicles or blockade of calcium entry into nerve terminals . They suggest that the toxin interferes with the acetylcholine release process itself, possibly by blocking exocytosis at the release sites. J Physiol, 1976 Aug, 260(1), 177 - 203 Effects of botulinum toxin on neuromuscular transmission in the rat; Cull-Candy SG et al.; 1 . Botulinum toxin (BoTx) type A partially blocks spontaneous transmitter release from nerve terminals in the rat . Minature end-plate potentials (m.e.p.p.s) are present at all end-plates, initially with a low frequency but increasing with time after posoning . Their amplitude distribution is at first skew with a predominace of very small m.e.p.p.s but, after a few days, larger than normal m.e.p.p.s appear . 2 . Tetanic nerve stimulation, Black Widow Spider Venom, the Caionophore A 23187 or mechanical damage to nerve terminals increases the frequency of m.e.p.p.s and alters the amplitude distribution of m.e.p.p.s towards a normal Gaussian one; the m.e.p.p . size approaches that seen at normal end-plates . This was seen at any time after poisoning . 3 . Nerve stimulation gives rise to end-plate potentials (e.p.p.s) of low amplitude and high failure rate . Statistical analysis indicates that evoked release is quantal in nature and follows Poisson statistics, quantum size being initially very small, but after a few days approaching normal size . Short-term tetanic nerve stimulation reversibly increases the quantum content of e.p.p.s and during early stages of paralysis long-term (2 hr) stimulation causes an apparently permanent increase in quantum size . 4 . Raising the extracellular Ca concentration from 2 to 16 mM increases the frequency of m.e.p.p.s in normal muscle but not in BoTx poisoned ones . K-free medium or ouabain, which are believed to raise the intracellular Ca concentration in nerve terminals, similarly increases m.e.p.p . frequency in normal but not in poisoned muscles . When the Ca-ionophore A 23187 is used together with high extracellular Ca (greater than 4 mM) massive release of transmitter occurs from poisoned terminals . 5 . The extracellular Ca concentration which causes a certain level of transmitter release in reponse to nerve impulses is considerably higher at BoTx poisoned end-plates than at normal ones . The slope value for Ca dependence of transmitter release is about 1-5 compared with about 3 at normal end-plates . 6 . Tetraethylammonium (TEA) greatly increases the amount of transmitter released by nerve impulses and restores neuromuscular transmission during all stages of poisoning, although it has not effect on spontaneous transmitter release . In the presence of TEA the power relation between Ca concentration and quantum content at the BoTx poisoned end-plate is similar to that seen at normal end-plates . 7 . It is suggested that in BoTx poisoning the mechanism for transmitter release has a reduced sensitivity to Ca, and the level for activation by intracellular Ca is elevated . Once the intracellular concentration of Ca is raised to this level, by tetanic nerve stimulation, mechanical injury to nerve terminals, the Ca-ionophore or the prolongation of the nerve action potential with TEA, augmented transmitter release occurs, similar to that which occurs in normal nerve terminals at a lower level of Ca. C R Acad Sci Hebd Seances Acad Sci D, 1976 Jul 19, 283(3), 271 - 4 {Comparative action of chronic injection of alpha toxin from Naja nigricolis and of botulinum toxin A on the development of chick embryo dorsal and ventral spinal roots}; Giacobini-Robecchi MG et al.; The chronic injection of high doses of alpha toxin from Naja nigricollis or botulinum toxin type A in the yolk sack of developing Chick embryos causes a selective decrease of the number of fibers in the ventral roots of the spinal nerves; at the concentrations needed this reduction is more important with the alpha toxin than with the botulinum toxin. Zh Mikrobiol Epidemiol Immunobiol, 1976 Jul, (7), 38 - 41 {Histological and histochemical changes in the kidneys of rabbits immunized with Cl . botulinum toxoid type B in combination with blood loss}; Gendler IE et al.; Immunization of rabbits with increasing doses of Cl . botulinum toxoid, type B, led to the development in the kidneys of a focal intracapillary productive glomerulonephritis, and also of productive endo- and perivasculites . Blood letting (in the amount of 1% of body weight) aggravated the morphological picture of the affection on account of supervention of the alternative and exudative components . At the same time blood letting led to reduction of the NAD-diaphorase, succinic dehydrogenase and glucose-6-phosphatase activity in the epithelium of the proximal portions of the nephrons. Zh Mikrobiol Epidemiol Immunobiol, 1976 Jul, (7), 33 - 7 {Morphological and histochemical characteristics of the organism's reaction to administration of Cl botulinum toxin . IV . Cytochemical changes in the cells of the mesencephalic nucleus of trigeminal nerve following administration of Cl . botulinum type B toxin}; Anosov IIa et al.; After the administration to guinea pigs per os of 1 Dlm of botulin toxin, type B, a change of the RNA synthesis in the nucleoli and DNA depolymerization in the nuclei was observed in some of the cells of the mesencephalic nucleus of the trigeminal nerve . An increase in the activity of succinic dehydrogenase and of acid phosphatase coursed without any necrotic processes in the cells . Basing upon the changes in the activity of succinic dehydrogenase in the neurons of the mesencephalic nucleus a conclusion was drawn that hypoxia began to develop at the period of appearance of paralyses of the limbs and reached its maximum in myasthenia. Biochem J, 1976 Jun 15, 156(3), 701 - 12 Inhibition by botulinum toxin of depolarization-evoked release of (14C)acetylcholine from synaptosomes in vitro; Wonnacott S et al.; 1 . Cerebral-cortex synaptosomes were shown to synthesize (14C)acetylcholine after incubation with (14C)choline, and 25mM-KCl released (14C)acetylcholine (but not (14C)choline) into the medium by a Ca2+-dependent and Mg2+-sensitive process . 2 . The K+-stimulated release of (14C)acetylcholine was inhibited by more than 80% after preincubation of the synaptosomes with 10(5) mouse lethal doses of botulinum toxin/ml . (14C)choline uptake, (14C)acetylcholine synthesis, intrasynaptosomal K+ and occluded lactate dehydrogenase were unaffected by the toxin . It also failed to prevent the K+-stimulated release of (3H)noradrenaline and (14C)glycine from synaptosomes . 3 . Fractionation of hypo-osmotically shocked synaptosomes revealed that more than 75% of the radioactive acetylcholine was in the cytoplasmic compartment, although the vesicle pellet contained more total acetylcholine than the cytoplasmic pool . Consequently the specific radioactivity of acetylcholine in the cytoplasmic pool was almost 5 times that of the vesicles . This distribution was unaffected by preincubation with botulinum toxin . It is concluded that the toxin acts directly on the release of acetylcholine, rather than influencing its storage . 4 . After K+-stimulation, toxin-inhibited synaptosomes contained increased amounts of total acetylcholine, which suggests that its rate of synthesis is controlled by depolarization rather than release. Naunyn Schmiedebergs Arch Pharmacol, 1976 Mar 24, 293(1), 1 - 9 Affinity chromatography of tetanus toxin, tetanus toxoid, and botulinum A toxin on synaptosomes, and differentiation of their acceptors; Habermann WE; 125I-labelled tetanus toxin and 125I-labelled botulinum A neurotoxin are known to be specifically bound to brain synapotosomes . In order to discriminate between active toxin and inactive admixtures present in the starting material or arising during iodination, synaptosome columns were prepared using bromacetylcellulose and/or kieselgur (Celite) as carriers . Both types of columns absorb the toxins from low ionic strength medium and release them if the pH and ionic strength are raised . Botulinum toxin was eluted with lower ionic strength than tetanus toxin, and could be freed from nontoxic admixtures . Analysis by affinity chromatography disclosed partially toxoided tetanus toxin in both labelled and unlabelled toxin samples . High concentrations of formaldehyde (0.5%) destroyed both toxicity and affinity to the synaptosomes of tetanus toxin . Low concentrations of formaldehyde (0.05%) yielded a derivative of low toxicity which was still however less firmly, bound to synaptosomes . Tetanus and botulinum toxin differ by their acceptors . Whereas unlabelled botulinum toxin is unable to compete with labelled tetanus toxin, unlabelled tetanus toxin slightly competes with botulinum toxin . Both labelled toxins display anomalous binding behavior in that they cannot be displaced completely even with a large excess of unlabelled toxin. Naunyn Schmiedebergs Arch Pharmacol, 1976 Feb 25, 292(2), 161 - 5 125I-labelled botulinum A neurotoxin: pharmacokinetics in cats after intramuscular injection; Wiegand H et al.; 1 . On unilateral injection of sublethal doses of 125I-botulinum A neurotoxin (BTA) into one gastrocnemius muscle of the cat we found after 48 h: a) A disto-proximal gradient of radioactivity (RA) had developed in the sciatic nerve of the injected side . b) The ventral roots of the spinal cord half segments supplying the injected muscle showed a higher RA than the ventral roots of the contralateral control side . c) The spinal cord half segments innervating the injected muscle had a RA much higher than the corresponding segments of the contralateral side . However, a small rise of RA was also observed in the contralateral half segments . 2 . In histoautoradiographs of the (ligatured) ventral roots the RA was strictly confined to the intraaxonal space of a few nerve fibres . 3 . On injection of equal doses of 125I-BTA into either gastrocnemius muscle we found after 38 h: a) Direct stimulation of only one of the injected muscle caused the RA to reach a higher level in the spinal cord half segments ipsilateral to the stimulated muscle than in the spinal cord half segments of the non-stimulated side . b) Unilateral stimulation of one gastrocnemius nerve under the influence of gallamine or unilateral antidromic stimulation of the dorsal roots L7, S1 failed to cause a difference in RA between stimulated and non-stimulated side. Biull Eksp Biol Med, 1976 Jan, 81(1), 25 - 7 {Changes in the acetylcholine--cholinesterase system in the dynamics of experimental boltulin poisoning}; Khotenko SG et al.; A study was made of the effect of botulin, type B, on the acetylcholine-cholinesterase system . High doses of the toxin increased the level of acetylcholine in the peripheral blood nervous system, as well as in the central nervous system . Injection of DLM of the toxin results in elevation of the acetylcholine level in the peripheral nervous system . Cholinesterase activity was practically unchanged. Ann N Y Acad Sci, 1976, 274, 46 - 59 Experimental acetylcholine blockade of the neuromuscular junction . Effects on end plate and muscle fiber ultrastructure; Freeman SS et al.; To investigate the effect of acetylcholine on the formation and maintenance of the end plate, presynaptic (hemicholinium-3 and botulinum toxin) and postsynaptic (curare and alpha-bungarotoxin) blocking agents were injected into the amniotic sac or chorioallantoic circulation of chick embryos during different stages of their development (days 3 to 11, 3 to 18, and 12 to 18) . Tntercostal or anterior and posterior latissimus dorsi muscles were examined by electron microscopy . Regardless of the duration of treatment, the type of agent, or the type of muscle, nerve ingrowth into muscle and end-plate formation were not arrested and the ultrastructure of nerve terminals and postsynaptic regions was normal . By contrast, muscle fiber ultrastructure was affected by acetylcholine blockade if continued beyond day 11 . By day 11 both treated and control muscles were composed primarily of myotubes . Muscles treated beyond day 11 showed impaired fiber differentiation and persistence of many myotubes . In addition, many fiber regions contained unassembled fine filaments intermingled with other organelles . In hemicholinium-3 treated muscles ther were also mitochondrial abnormalities and an increased number of lipid droplets . The findings suggest that the altered structure of the neuromusclar junction in myasthenia gravis is not due to the lack of a trophic effect of acetylcholine . The impaired fiber maturation in the chick embryos may be related to the lack of acetylcholine mediated fiber activity. Arch Immunol Ther Exp (Warsz), 1976, 24(5), 641 - 54 Botulinum antitoxins and antibacterial IgM and IgG antibodies in sera of persons immunized with botulinum polytoxoid combined with cholera vaccine . II . Response to cholera vaccine; Galazka A et al.; The response of humans to cholera vaccine was very heterogeneous . The proportion of IgG vibriocidal antibodies was high in persons having previous natural or artificial contact with V . cholerae antigens . Predominance of IgM antibody response was seen in persons vaccinated for the first time . This type of response was sometimes evoked by unspecific stimuli such as botulinum polytoxoid without cholera vaccine . Antibodies passively protecting mice were found both in IgM and IgG globulins but the activity of these antibodies was higher in IgG than in IgM globulins. Dev Biol Stand, 1976, 32, 185 - 91 Results of potency tests of a vaccine against Cl . botulinum type C by different methods; Pranter W; The potency of vaccine against Cl . botulinum type C was tested comparatively in mice, guinea pigs and mink, using the test methods employed in the United States, Great Britain and Sweden . Additionally the capacity to withstand challenge to toxin in ferrets was investigated . All species of laboratory animals proved to be protected against high toxin doses . On the other hand the humoral antitoxin titer of the immunized animals was low after one injection . After a second injection or after challenge with toxin the titer increased considerably. J Physiol, 1975 Dec, 253(1), 53 - 77 Dissociation between nerve-muscle transmission and nerve trophic effects on rat diaphragm using type D botulinum toxin; Bray JJ et al.; Small doses of botulinum toxin can produce partial blockage of transmitter release at the nerve--muscle junction . 2 . Subthreshold e.p.p.s, 3--10 days after poisoning, show a distribution of amplitudes that is fitted by Poisson statistics . Successive e.p.p.s . in a short train show a marked facilitation . 3 . Two weeks or more after poisoning with a dose of toxin that paralyses the whole muscle, when nerve--muscle transmission is in course of recovery, subthreshold e.p.p.s have an amplitude distribution that is fitted by binomial statistics . This property of transmission is similar to those described in newly formed nerve--muscle junctions, during embryogenesis or regeneration . 4 . Muscle fibres with subthreshold transmission in the 5--10 day group of muscles were all supersensitive to ACh, as were a number of fibres in which nerve stimulation still produced an action potential . 5 . Two weeks or more after poisoning, muscle fibres with subthreshold transmission had lost their extrajunctional ACh-sensitivity, as had many fibres with m.e.p.p.s of roughly normal frequency but no response to nerve stimulation . 6 . In diaphragm muscles poisoned with botulinum toxin between 1 and 4 days previously, the rate of fast axonal transport of radioactively labelled proteins down the phrenic nerve is not greatly affected, but the amount of materials carried is reduced to about one quarter of normal . These labelled proteins accumulate in the intramuscular portion of the phrenic nerve, in or near the nerve terminals, to a much greater extent than in controls, showing that the normal release of some of these materials has been prevented by the toxin . 7 . It is concluded that the blockage of the trophic effects of nerves by botulinum toxin is due to a blockage of release of trophic factors other than ACh . 8 . The muscle nerve cannot maintain a muscle in its normal state simply by activation of contraction, and a regenerating nerve terminal can restore a muscle towards its normal state before it can release enough ACh to produce muscle contraction. Dtsch Med Wochenschr, 1975 Nov 14, 100(46), 2394 - 7 {Mild course of botulinus intoxication (author's transl)}; Richert S et al.; Botulinus poisoning generally ends fatally after an only short course, mild forms being rare . In four members of a family who had eaten deep-frozen grilled sausages symptoms of botulinus poisoning developed, predominantly marked by disturbances of the autonomic nervous system . The course was so mild that hospitalization was not necessary nor was specific antitoxin administration . All clinical symptoms had disappeared after nine weeks . But special clinical and neurophysiological studies (electromyography, pupillography, electroencephalography) demonstrated abnormalities for very much longer . Botulinus poisoning was proven in animal tests and neutralization tests with botulinus antitoxin . The epidemiology, source of infection, and clinical symptoms suggest botulinus type B poisoning. J Physiol, 1975 Nov, 252(3), 657 - 67 Neurotrophic regulation of dynamic properties of skeletal muscle: effects of botulinum toxin and denervation; Drachman DB et al.; In order to determine the role of acetylcholine (ACh) transmission in neurotrophic regulation of dynamic properties of muscle, the effects of botulinum toxin treatment were compared with those of denervation . The extensor digitorum longus (EDL) and soleus muscles of rats were either denervated or injected with botulinum toxin . At times up to 25 days the isometric properties of these muscles were determined . 2 . Both botulinum treatment and denervation produced progressive slowing of the time to peak of the twitch (TPT) and half-relaxation time of the twitch (1/2 RT), which was more pronounced in the EDL than in the soleus . 3 . Both treatments produced slowing of the relaxation curve following tetanic contraction, more marked in the EDL than in the soleus muscle . This indicates a slowing of relaxation, and suggests a prolongation of the active state of the muscle . 4 . The maximum rate of rise of the tetanus did not change significantly in the EDL and soleus muscles after botulinum treatment or denervation . This suggests that there is no major change in the speed of contraction under conditions of botulinum treatment or denervation . 5 . The changes produced by botulinum treatment and denervation were virtually identical in all parameters tested . This is interpreted meaning that cholinergic transmission (including muscle usage), or some other factor closely related to cholinergic transmission, accounts for the motor nerve's trophic influence in maintaining these dynamic properties of skeletal muscles. Nord Vet Med, 1975 Sep, 27(9), 401 - 10 {Intoxication in cattle caused by a batch of sugar beet pulp (author's transl)}; Nielsen K et al.; During the period from Dec . 7th 1972 to Jan . 8th 1973 76 cattle deaths were reported in 20 herds on the island of Moon and the adjacent south-eastern area of Sealand . The disease was characterized by a sudden onset and a rapid and invariably fatal course . Initially, there was a loss of appetite, depression, excessive salivation and incoordination . These symptoms progressed to paralysis and, in some animals, trmor and convulsions . Death usually ensued less than 2 hours after the first observation of symptoms . Losses in the herds varied from 1 to 12 animals . In herds with multiple incidents the majority of deaths occurred in the 24-hour-period following observation of the first case . Pathology: Gross lesions were few and inconclusive . Histology revealed marked dilatation of cerebral and maningeal blood vessels (arterioles, venoles and capillaries), with perivascular edema and haemorrhage . Adjacent neurons and glia cells showed various degrees of degeneration, apparently secondary to the vascular lesion . In all affected herds sugar beet pulp from one particular sugar mill had been used during the period preceding the outbreak . The syndrome was reproduced by feeding sugar beet pulp from this batch to two heifers . The heifers showed symptoms after 19 and 32 days' feeding, resp . and died after a few hours . Clinical and pathological features were identical with those observed in the spontaneous disease . Thus, it was proved that the particular batch of pulp was responsible for the disease . The investigation did not, however, reveal a toxic factor in this batch . Analyses for lead, arsenic, mercury, nitrite, alkyl phosphates, chlorinated insecticides and Cl . botulinum toxin were negative . Batches of the sugar beet pulp showed pronounced microbial deterioration, the flora being dominated by yeasts and filamentous fungi (moulds) . Several species of fungi have been isolated but so fat their possible role in the etiology of the syndrome remains unsettled . The syndrome bears some resemblance to cerebrocortical necrosis (C.C.N.) but differs in several clinical and pathological details . It is tentatively suggested that the beet pulp may have contained one or more toxic substances that interfere with microbial activity in the rumen, resulting in a disturbance of synthesis or absorption of essential metabolites . The clinical, epidemiological and pathological findings are compatible with the hypothesis that the syndrome might be due to fungal toxins . Accordingly, the isolated fungi are now being studied in more detail. Zh Mikrobiol Epidemiol Immunobiol, 1975 Sep, 0(9), 80 - 3 {Deaminase activity of Cl . botulinum type A, B, E and F cultures}; Blagoveshchenskii VA et al.; The authors present the results of a comparative study of desaminase activity in the suspensions of resting cells and in ultrasonic desintegrates of cells of Cl . botulinum types A, B, E and F against a number of amino acids and their amides . It was shown that types A, B, E and F possessed active desamination enzymes; this process, however coursed with a different degree of intensity depending on the substrate . Common for all the 4 types was the presence of desamidase L-asparaginase and L-glutaminase, and also of the desamination enzymes of the aspartic and glutamic acids . Strains of type B had the greatest set of enzymes, and of type A--the least; bacteria of types E and F occupied an intermediate position . None of the types studied contained tryptophandesaminase . Some of desaminases are bound to subcellular structures. Zh Mikrobiol Epidemiol Immunobiol, 1975 Jul, (7), 47 - 51 {Hemagglutinin specificity of Cl . botulinum types A, B, and F in reaction with erythrocytes of various animals}; Blagoveshchenskii BA et al.; The following differences were revealed in the haemagglutination reaction with the erythrocytes of man, sheep, rabbit, chicks and mice between the haemagglutinins of Cl . botulinum, types A, B and F, having a close affinity with one another: haemagglutinin of type A actively reacted with the erythrocytes of man, sheep, rabbit, rats and chicks; haemagglutinin of type B reacted only with the erythrocytes of man and rabbits; haemagglutinin of type F failed to react with any of the types of the erythrocytes tested; only with the use of erythrocytes treated with neuraminidase was it possible to establish the presence of haemagglutinin fraction in Cl . botulinum, type F . Treatment of human erythrocytes with neuraminidase and proteolytic enzymes caused a marked increase in the sensitivity of the haemagglutination reaction in haemagglutinins of Cl . botulinum, types A, B and F. Zh Mikrobiol Epidemiol Immunobiol, 1975 Jun, (6), 89 - 92 {Detection of atoxigenic variants in Cl . botulinum type A and B cultures exposed to different treatments}; Perova EV et al.; A possibility of detection of atoxigenic clones in the cultures of Cl . botulinum, types A and B, under conditions of treatment with acridine strains, UV-irradiation and heating of spores was studied . Of the 10 strains investigated, atoxigenic variants were obtained only in 3, belonging to type B; the frequency of formation of atoxigenic clones under the effect of ethidium bronide constituted 36--45.7%, and of the UV-irradiation-4.2%; heating of spores proved to be ineffective . A frequent loss of the toxigenicity sign coincided with the view on the elimination of the episomal determinant of the toxin-formation, not with the mutational nature-of this change . An association between the differences in stability of retention of the toxigenicity signs in various strains and types of Cl . botulinum and possible differences of the corresponding genetic determinants of the toxin formation is discussed. Zh Mikrobiol Epidemiol Immunobiol, 1975 May, (5), 111 - 6 {Morphological and histochemical characteristics of the reaction of the body to Cl . botulinum toxin administration . III . The cellular reaction of the diaphragmatic nerve nucleus to the administration of Cl . botulinum type B toxin}; Anosov IIa et al.; On the appearance in the animals (guinea pigs) of paralysis of the limbs and myasthenia after the administration of Cl . botulinum, type B, toxin, there was seen a considerable vascular hyperemia of the spinal cord, and in the neurons of the phrenic nerve nucleus there developed dystrophic-necrotic processes coursing with a marked swelling, hyperchromasia and tigrolysis . As revealed histochemically, at this stage of the botulin intoxication the neurons of the phrenic nerve nucleus displayed metabolic changes expressed in the altered activity of succinic dehydrogenase, acid phosphatase and cholinesterase. Zh Mikrobiol Epidemiol Immunobiol, 1975 Apr, (4), 66 - 70 {Immunochemical study of the toxin of C1 . botulinum type E}; Ispolatovskaia MV et al.; Toxins extracted from the cells and the culture fluid of C1 . butulinum type E had a similar mol wt and antigenic composition . Trypsin activation led to the appearance of an additional antigen . Coefficient of the cell toxin activation was much greater than the coefficient of activation of the toxin contained in the culture fluid. Zh Mikrobiol Epidemiol Immunobiol, 1975 Mar, 0(3), 40 - 3 {Use of a synthetic medium for cultivating pathogenic anaerobes}; Ivanova LG et al.; It was shown that a synthetic medium suggested by the authors earlier was useful for the growth and toxin formation of Cl . tetani, Cl . botulinum and Cl . perfringens, types B and E . A study of the character of growth and toxinogensis, microscopic examination of morphology of culture cells and results of passages showed the suggested synthetic medium to be of value; a possibility of its application for studying the nutrient requirements and the role of individual components of the nutrient media in the process of growth and toxinogenesis was also demonstrated. Zentralbl Bakteriol {Orig A}, 1975 Jan, 230(1), 59 - 66 Sensitivity of eels (Anguilla anguilla) and carp (Cyprinus carpio) to type C and E botulinum toxin; Haagsma J; This study has shown for the first time that fish such as eels (Anguilla anguilla L.) and carp (Cyprinus carpio L.) are sensitive to type E botulinum toxin . With oral administration the MLD for eels was 27.500 mouse LD50 per kg body weight, while for carp it was only 236 mouse LD50 per kg . Carp were also found to be sensitive to a slight degree to type C botulinum toxin, the MLD of the most virulent toxin of this type being 457,000 mouse LD50 per kg with oral administration . Eels, however, showed no sensitivity to type C toxin. Naunyn Schmiedebergs Arch Pharmacol, 1975, 287(1), 97 - 106 Direct evidence for the specific fixation of Cl . botulinum A neurotoxin to brain matter; Habermann E et al.; Rat brain homogenate and synaptosomes from rat brain bind botulinum toxin . The binding is accompanied by partial inactivation . The binding decreases with increasing ionic strength . A considerable fixation of tetanus toxin can still be demonstrated under conditions which prevent the fixation of botulinum toxin . 2 . Only the grey substance, not the white substance from bovine brain is able to bind the toxin . 3 . Upon pretreatment with neuraminidase, synaptosomes lose nearly all of their binding capacity . However, neither gangliosides nor ganglioside-cerebroside mixtures nor brain extracts could replace the synaptosomes . Thus botulinum A toxin closely resembles tetanus toxin in its ability to react with (a) neuraminidase-sensitive site(s) of the grey matter of the CNS . It differs from tetanus toxin by its stronger sensitivity against ionic forces and by its failure to react with certain gangliosides. Brain Res, 1974 Mar 15, 68(1), 157 - 66 The effect of injury on two hydrolases in the hypoglossal nucleus, with quantitative data on N-acetyl-beta-glucosaminidase; Sumner BE; N-acetyl-beta-glucosaminidase and acid phosphatase were studied histochemically in sections of hypoglossal nuclei of normal adult male albino rats, and rats from 1 to 56 days after axotomy of the left hypoglossal nerve, or after injection of botulinum toxin into the left side of the tongue . Both axotomy and botulinum caused a diminution of neurone perikaryal glucosaminidase reaction product on the operated side, but an increase of reaction product elsewhere in the operated nucleus . Whereas the effect of axotomy lasted from 5 to 42 days post-operatively, that of botulinum ceased between 28 and 42 days . Axotomy and botulinum both caused an increase of neuronal acid phosphatase (after a short incubation time) from 2 to 21 days post-operatively in injured nuclei . Glucosaminidase reaction product measured microdensitometrically in isolated cells showed a statistically significant diminution in injured neurones at 18 days after axotomy . There was no change in the amount of reaction product per cell in pericytes, astrocytes, or non-astrocyte glia . Sections scanned quantitatively showed that normal and operated nuclei had a similar amount of reaction product, thus the neuronal diminution must be balanced by the increase elsewhere, either in the elevated numbers of non-astrocyte glia, or in the neuropil.
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