The present study was undertaken to examine the genetic relationships among the closely related species, Clostridium novyi types A and B, C. haemolyticum and C. botulinum type C. These species were tested for DNA-DNA homology and thermostability of DNA duplexes and sorted into three genetically related groups: I, C. novyi type A; II, C. novyi type B, C. haemolyticum and one C. botulinum type C strain (Stockholm); III, the remaining C. botulinum type C strains. A few biochemical criteria corresponding to the genetic differences were recommended to differentiate each group. These studies imply that C. haemolyticum might be considered as C. novyi type D and that there are two genetically different groups in C. botulinum type C.
The precise mechanism involved in the restoration by glucose of action potentials and membrane currents has not been established, so we studied it in single guinea pig ventricular cells under conditions of metabolic inhibition by 2,4-dinitrophenol (DNP). Application of DNP (50 μmol·litre−1) significantly shortened the action potential duration (APD) from 276.3(SD 47.5) to 43.0(3.9) ms (n=10). The increase in glucose concentration from 5.5 (control) to 22 mmol·litre−1significantly restored the APD within 10 min, to 233.2(51.2) ms. In tight seal whole cell clamp studies, we found that DNP increased the steady state outward currents at potentials positive to −60 mV, and that this current was all but suppressed by 22 mmol·litre−1 glucose. The glucose induced recovery in the APD and membrane current was not seen in the presence of 2-deoxyglucose (2 mmol·litre−1), an inhibitor of glycolysis. Insulin (40 mIU·ml−1) reversed the DNP induced shortening of APD and abolished the increase in the outward current in the presence of 11 mmol·litre−1 glucose, though the application of glucose alone at this concentration failed to reverse these changes. Glucose (5.5 to 44 mmol·litre−1) did not directly affect single channel currents of ATP regulated K channels of the excised patch membrane in an outside out mode. These results suggest that the antagonising effects of glucose on the DNP induced alterations in APD and membrane currents are mediated by an increase in intracellular ATP concentration via enhanced glycolysis. Insulin might enhance this effect by facilitating the transport of glucose across the cell membrane.
Since Young et al 1described a patient with acute loss of sympathetic and parasympathetic functions in 1969, many similar cases have been reported as being acute idiopathic autonomic neuropathy.2 Apart from acute cholinergic neuropathy, there are four types of acute idiopathic autonomic neuropathy, classified according to somatic nerve involvement: acute pandysautonomia, which has minimal or no motor or sensory dysfunctions3;acute autonomic and sensory neuropathy in which sensation is seriously involved4-6; Guillain-Barre syndrome with prominent dysautonomia, manifesting autonomic and somatic motor dysfunctions; and acute autonomic sensory and motor neuropathy, characterised by prominent dysautonomia and severe motor and sensory impairment. Despite minimal or no sensory disturbance, reduction of myelinated fibres in biopsied sural nerve has been found in several cases with acute pandysautonomia.3However, the exact site of pathological involvement in the sensory system remains unknown, because postmortem examinations have seldom been performed. We report a case of acute pandysautonomia with no evidence of significant somatic nerve involvement, accompanied by dorsal root ganglionopathy shown by postmortem examinations.
An 18 year old male student experienced low grade fever, vomiting, and tingling pain in the limbs on 26 February 1987. Orthostatic syncopy occurred three times on the next day. Difficulty in emptying the bladder, alternate diarrhoea and constipation, and lack of sweating over the whole body developed rapidly. He was admitted to the Third Department of Internal Medicine, Medical College of Oita on 24 April 1987. On physical examination, he weighed 46 kg, with a recent weight loss of 14 kg. Blood pressure was 108/78 mm Hg in the supine position and heart rate was 88/min. When changing from the supine to theupright position, he …
Colicin E5 cleaves tRNAs for Tyr, His, Asn and Asp in their anticodons to abolish protein synthesis in Escherichia coli. We previously showed how its C-terminal RNase domain, E5-CRD, recognizes the anticodon bases but the catalytic mechanism remained to be elucidated. Although the reaction products with 5′-OH and 2′,3′-cyclic phosphate ends suggested a similar mechanism to those of RNases A and T1, E5-CRD does not have the His residues necessary as a catalyst in usual RNases. To identify residues important for the catalytic reaction, mutants as to all residues within 5 Å from the central phosphorus of the scissile phosphodiester bond were prepared. Evaluation of the killing activities of the mutant colicins and the RNase activities of the mutant E5-CRDs suggested direct involvement of Arg33, Lys25, Gln29 and Lys60 in the reaction. Particularly, Arg33 plays a critical role and Ile94 provides a structural support of Arg33. Crystal structure of the complex of E5-CRD(R33Q)/dGpdUp showed structural and binding functional integrity of this mutant protein, suggesting involvement of Arg33 in the catalytic reaction. The structure of the free E5–CRD, we also determined, showed great flexibility of a flap region, which facilitates the access of Lys60 to the substrate in an induced-fit manner.
Resistance patterns against 23 antimicrobial agents were examined for 42 strains of methicillin-resistant Staphylococcus aureus (MRSA). Thirty-four strains were isolated at Hiroshima University Hospital during 1984-1990 and 8 strains were collected in Tokushima city in 1986. Overall resistance to the antimicrobial agents in clinical use is summarized as follows: methicillin 100%, flomoxef 93% (beta-lactams); kanamycin 98%, tobramycin 88%, amikacin 83%, isepamicin 81%, gentamicin 60%, dibekacin 64%, arbekacin 0% (aminocyclitol aminoglycosides); ofloxacin 31%, TA-167 33% (fluoroquinolones); erythromycin 100%, clarithromycin 100%, josamycin 71% (macrolides); vancomycin 0% (glycopeptide); tetracycline 43%, minocycline 31% (tetracyclines); fosfomycin 93%. The MRSA strains remained susceptible to the non-clinical peptide group of antibiotics except for mikamycin B: mikamycin A 2%, mikamycin B 69%, nosiheptide 0%, bottromycin A2 0%, bottromycin D-1 0%, bottromycin D-2 0%. Since April 1990, the MRSA strains isolated at Hiroshima University Hospital showed a tendency to acquire resistance to tetracyclines and fluoroquinolones and to lose mikamycin B-resistance. As of August 1990, none of the MRSA strains isolated at Hiroshima University Hospital was resistant to vancomycin and arbekacin.
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