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  • 1
    Electronic Resource
    Electronic Resource
    Abnormal messenger ribonucleic acid (mRNA) transcribed from a mutant insulin receptor gene in a patient with type A insulin resistance (1992)
    Springer
    Diabetologia 35 (1992), S. 639-644 
    Details
    ISSN: 1432-0428
    Keywords: Insulin receptor ; type A insulin resistance ; deletion ; polymerase chain reaction ; insulin receptor gene ; direct sequence ; mRNA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In a previous report on a 16-year-old Japanese girl with type A insulin resistance, we found that one allele of the insulin receptor gene was inherited from her mother and contained a 1.2 kilobase pair deletion which removed the 14th exon in the β subunit. We extended investigation of the proband and found the deletion between two Alu sequences. To determine the effect of the deletion on the level of transcription and the splicing pattern of messenger ribonucleic acid (mRNA), we synthesized the complimentary DNA and used the polymerase chain reaction to amplify the region which included the deleted area. The deletion shifted the reading frame, resulting in a termination codon after amino acid 867 (Glu), thereby producing a truncated insulin receptor without a transmembrane region and cytoplasmic domain. We also sequenced each of 22 exons of the insulin receptor gene but found no mutation in exons of the insulin receptor gene, except for deletion of exon 14 of the maternal allele. Thus, the proband is a heterozygote for a single mutant allele. Abnormal mRNA transcribed from the mutant allele resulted in a decrease in insulin binding.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400255
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  • 2
    Electronic Resource
    Electronic Resource
    Defects in insulin binding and receptor kinase in cells from a woman with type A insulin resistance and from her family (1991)
    Springer
    Diabetologia 34 (1991), S. 86-92 
    Details
    ISSN: 1432-0428
    Keywords: Insulin receptor ; type A syndrome of insulin resistance ; insulin binding ; autophosphorylation ; kinase activity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Defects in insulin receptor function lead to impairment of the insulin response. We treated a patient with the typical phenotype of type A syndrome of insulin resistance whose insulin receptor seemed to lack the transmembrane region and cytoplasmic domain. Hyperinsulinaemia and resistance to exogenous insulin were evident, and insulin binding to cells and uptake of 2-deoxyglucose into fibroblasts were greatly decreased. Molecular weight of the α-subunit of the insulin receptor was normal, but autophosphorylation and kinase activity were impaired. In the pedigree analysis, defects in insulin binding were also observed in the mother, maternal grandfather and two maternal aunts, corresponding with the abnormality of the insulin receptor gene and mild insulin resistance. In the mother, much the same kinase defects as were seen in the patient became evident. However, no relatives had clinical symptoms similar to those seen in the patient. In the father there was a mild insulin resistance in the glucose clamp study and a borderline impaired glucose tolerance. Although insulin binding to cells was normal in the father, both autophosphorylation and kinase activity were reduced. Our findings suggest that insulin resistance in the patient may be caused by the defects in insulin receptor kinase activity as well as by a reduction in insulin binding activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00500378
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  • 3
    Electronic Resource
    Electronic Resource
    Type 2 (non-insulin-dependent) diabetes mellitus associated with a mutation of the glucokinase gene in a Japanese family (1993)
    Springer
    Diabetologia 36 (1993), S. 433-437 
    Details
    ISSN: 1432-0428
    Keywords: Glucokinase gene ; mutation ; Type 2 (non-insulin-dependent) diabetes mellitus ; polymerase chain reaction ; single stranded conformation polymorphism ; insulin secretion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Mutations were screened for in the glucokinase gene of 25 Japanese patients with Type 2 (non-insulin-dependent) diabetes mellitus. Each exon was scanned by electrophoresis of enzymatically amplified DNA segments under non-denaturing conditions and variants were sequenced. A variant pattern was detected in exon 5 of one patient. Direct sequencing of this exon revealed a single nucleotide substitution in codon 188 (GCT→ACT) of one of two alleles resulting in the mutation of Ala188→Thr, an invariant residue in the sequence of all mammalian glucokinases and hexokinases. This mutation was not found in 40 normal control subjects. The proband had been diagnosed with Type 2 diabetes at the age of 62 years. Four other members of her family have the same mutation and all have Type 2 diabetes or impaired glucose tolerance. The youngest age at diagnosis of Type 2 diabetes in these other members was 13 years, suggesting that her pedigree was maturity-onset diabetes of the young (MODY). All subjects with the Thr188 mutation show a decreased insulin secretory response during oral glucose tolerance testing. Mutations in the glucokinase gene associated with Type 2 diabetes have been previously identified in Caucasian (French and British) subjects. This study indicates that mutations in this gene are also implicated in the development of Type 2 diabetes in Asians. Further studies are required to determine the frequency of mutations in glucokinase among Japanese patients with Type 2 diabetes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00402280
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  • 4
    Electronic Resource
    Electronic Resource
    Effect of nicardipine on haemodynamic response to stress in hypertension (1992)
    Springer
    European journal of clinical pharmacology 42 (1992), S. 265-269 
    Details
    ISSN: 1432-1041
    Keywords: Nicardipine ; Hypertension ; calcium antagonist ; mental arithmetic ; cold pressor test ; exercise test ; haemodynamics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The effects of the calcium antagonist nicardipine on the pressor response to mental arithmetic, cold pressor and exercise tests have been studied in fifteen patients with established mild to moderate essential hypertension. Nicardipine 20 mg p.o. showed a hypotensive effect within 60 min, associated with a fall in total peripheral resistance and an increase in heart rate. As the pressor response to each stress was not affected by nicardipine, the peak blood pressure reached during each stress was lower. Nicardipine lowers blood pressure at rest as a result of arteriolar dilatation, associated with reflex tachycardia. The pressor responsiveness to various stresses was not affected by nicardipine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00266346
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  • 5
    Electronic Resource
    Electronic Resource
    Pharmacokinetics of SUN 1165, a new antiarrhythmic agent, in renal dysfunction (1991)
    Springer
    European journal of clinical pharmacology 40 (1991), S. 411-414 
    Details
    ISSN: 1432-1041
    Keywords: SUN 1165 ; renal failure ; antiarrhythmic agent ; pharmacokinetics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The pharmacokinetics of a new Class I antiarrhythmic agent, SUN 1165, has been studied in 32 patients with varying degrees of renal impairment following a single oral dose of 50 mg. The apparent volume of distribution at steady state was 1.48 1 · kg−1, the absorption rate constant was 2.2 h−1, and plasma protein binding was 26.8% in subjects with normal renal function. These variables were not altered with renal impairment. More than 60% of SUN 1165 given orally was excreted unchanged via the kidney, both by tubular secretion and glomerular filtration. The elimination rate constant, the apparent total body clearance and the apparent renal clearance were linearly correlated with the endogenous creatinine clearance. The half-time of elimination was 3.4 h in normal subjects and it was prolonged to 23.7 h in severe renal failure (creatinine clearance below 20 ml · min−1 · 1.48 m−2). Dosage adjustment of SUN 1165 is necessary in renal failure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00265853
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  • 6
    Electronic Resource
    Electronic Resource
    Degenerative changes in the internal elastic lamina relating to the development of saccular cerebral aneurysms in rats (1993)
    Springer
    Acta neurochirurgica 121 (1993), S. 76-81 
    Details
    ISSN: 0942-0940
    Keywords: Cerebral aneurysm ; internal elastic lamina ; degenerative changes ; catabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In order to investigate the developmental mechanism of saccular cerebral aneurysms, changes in the internal elastic lamina at the junction of the anterior cerebral artery and the olfactory artery were electronmicroscopically studied in 6 control and 6 experimental rats undergoing ligation of the left carotid artery and branches of both renal arteries. In the control group, spontaneous destructive changes occurred on the luminal side of the internal elastic lamina and progressed from the luminal towards the abluminal side as the elastic lamina advanced to the apex. Close to the apex, these changes invaded and disrupted the whole elastic lamina. The elastic lamina was replaced by sparsely lined up lumps of elastic tissue in the walls of early aneurysmal alterations, and was atrophied and disappeared totally in the walls of aneurysmal alterations that had reached an advanced stage. These spontaneous changes were in agreement with reports in the literature and our own previous investigations. From the findings in the experimental rats it becomes likely that the aneurysmal changes in the elastic lamina are exaggerated forms of the normal catabolic metabolism. Therefore its synthesis on the abluminal side no longer balances with the catabolism on the luminal side. It is strongly suggested that aneurysmal alterations progress from the luminal towards the abluminal side of arterial walls and that the lytic process of elastase might play a role in the degenerative changes in aneurysmal development.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01405187
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  • 7
    Electronic Resource
    Electronic Resource
    In vivo flow visualization of induced saccular cerebral aneurysms in rats (1993)
    Springer
    Acta neurochirurgica 122 (1993), S. 244-249 
    Details
    ISSN: 0942-0940
    Keywords: Cerebral aneurysm ; experimental aneurysm ; rheology ; haemodynamics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A surgical procedure to expose the arterial bifurcation at the base of the rat brain was developed without sacrificing the animal. Using this technique, visualization of flow in and around the induced cerebral aneurysm was achieved by detecting and following fluorescent particles in the blood stream. Cerebral aneurysms were produced by ligating one common carotid artery, inducing experimental hypertension and feeding them with beta-aminopropionitrile. Flow studies of the arterial bifurcation with an early aneurysmal formation showed that there were spiral flows proximal and distal to the bifurcation. This was the first direct visualization of the actual flow in and around cerebral aneurysms in a vital state. This technology can add further information on the development, growth and rupture of cerebral aneurysms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01405537
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  • 8
    Electronic Resource
    Electronic Resource
    Effect of nerve growth factor on delayed neuronal death after cerebral ischaemia (1994)
    Springer
    Acta neurochirurgica 129 (1994), S. 64-71 
    Details
    ISSN: 0942-0940
    Keywords: Cytoskeleton ; delayed neuronal death ; nerve growth factor (NGF) ; neurofilament (NF)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We investigated the protective action of nerve growth factor (NGF) on delayed neuronal death, and we also studied the involvement of the 200 kDa neurofilament (NF 200) cytoskeletal proteins. Wistar rats were divided into three groups: Group I, in which transient forebrain ischaemia was produced; Group II, ischaemic group which received intraventricular administration of artificial cerebrospinal fluid (CSF); and Group III, ischaemic group which received intraventricular administration of 2 Μg of 2.5 S NGF. Forebrain ischaemia in these rats was produced by causing transient bilateral occlusion of the common carotid arteries and lowering the mean blood pressure to 50 mmHg for 8 minutes. On the 1st and 7th day after ischaemia we histologically examined neuronal death in the hippocampal CA1 sector. On the 7th day after ischaemia, mean cell death (degenerative cell number/total cell number) was 87±9% in group I (n=7), 51±36% in group II (n=7), and 14±16% in group III (n=8) (p〈0.05 vs. group II). The concentration of NF 200 in the hippocampal homogenate was measured by the Western blotting method on the 1st and 7th day after ischaemia. On the 1st day it was found to be 67±11% of that in the control group in group I (n=6), 73±21% in group II (n=6), and 84±7% in group III (n=6) (p〈0.05 vs. group II). The concentration of NF 200 in all groups remained at the same level until the 7th day after ischaemia (each group, n=6). These results suggest that 1) intraventricular NGF has a protective effect on delayed neuronal death, 2) these protective actions occur within one day after ischaemia, and 3) these effects may be mediated by the suppressed degradation and/or promoted restoration of neuronal cytoskeletal proteins.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01400875
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  • 9
    Electronic Resource
    Electronic Resource
    Protective role of antigenic sites on the envelope protein of Hantaan virus defined by monoclonal antibodies (1992)
    Springer
    Archives of virology 126 (1992), S. 271-281 
    Details
    ISSN: 1432-8798
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To investigate the role of Hantaan virus envelope glycoprotein in infection, a panel of monoclonal antibodies (MAbs) was examined in vitro with several serological tests and in vivo by passive transfer experiments in mice. An antigenic site, specific for the inhibition of infected cell focus was detected with the focus inhibition neutralization test (FINT), in addition to the neutralization related antigenic sites, which were revealed by the ordinary focus reduction neutralization test (FRNT). Suckling mice were given the MAbs by passive transfer followed by lethal Hantaan virus challenge. All neutralizing MAbs detected by either FRNT or FINT protected all mice from lethal infection, confirming the importance of the antigenic sites as a protective antigen. Mice given non-neutralizing MAbs by passive transfer, however, began to die earlier than the control group; mean time to death (18.2±2.1 to 21.5±2.8 days) being significantly shorter than that of the control group (25.8±1.8, p〈0.01, Mann-Whitney,U probability test). Virus titers in brains of mice which died early, were about 10 times higher than those of control mice. These results indicated the early death phenomenon of mice which was mediated by the antivirus antibody.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01309700
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  • 10
    Electronic Resource
    Electronic Resource
    Antibody-dependent enhancement of hantavirus infection in macrophage cell lines (1992)
    Springer
    Archives of virology 122 (1992), S. 107-118 
    Details
    ISSN: 1432-8798
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Antibody-dependent enhancement (ADE) of hantavirus infections (strains Hantaan 76–118 and SR-11) was studied using macrophage-like cell lines (J774.1, P388D1, and U937). Significantly higher virus titers (1,000 to 4,000 FFU/ml) were obtained by pretreatment of the virus with immune serum as compared to normal serum (〈20 FFU/ml). Monoclonal antibodies (MAbs) to strain Hantaan 76–118 were employed to determine the antigenic determinants responsible for the ADE activity. ADE of the infection occurred with MAbs to both G1 and G2 envelope glycoproteins, but not with MAbs to nucleocapsid protein. Antigenic determinants related to haemagglutination or virus neutralization were found to cause ADE of the infection.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01321121
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