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Biomedical subjects

Y Shiga

Publications and source records attributed to Y Shiga.

At least 19 recordsLinked to original sources
PubMed2003

CSF hypovolemia vs intracranial hypotension in "spontaneous intracranial hypotension syndrome".

OBJECTIVES: To investigate the role of CSF hypovolemia in spontaneous intracranial hypotension (SIH) syndrome because so-called SIH syndrome sometimes lacks intracranial hypotension. METHODS: Ten women (aged from 28 to 49 years) with characteristic orthostatic headache without a previous history of dural tear were investigated. In addition to gadolinium (Gd)-enhanced brain MRI, spinal MRI with and without Gd enhancement was performed. RESULTS: Gd-enhanced brain MRI demonstrated diffuse pachymeningeal enhancement in all patients. Sagittal T2-weighted spinal MRI revealed a variable amount of CSF in the extradural space in all patients. Sagittal T2-weighted MRI or axial Gd-enhanced T1-weighted MRI showed dilated epidural veins located in the high cervical portion in each patient. The intensity of dilatation of the epidural veins correlated significantly with the amount of CSF in the epidural space. This suggested that the Monro-Kellie doctrine was applicable in this circumstance. CONCLUSIONS: Since some patients with SIH syndrome have normal CSF pressure and since a downward displacement of the brain due to a reduction of the buoyant action of CSF may induce symptoms, CSF hypovolemia, not intracranial hypotension, may be the cause. Based on the Monro-Kellie doctrine, detecting leaked CSF and venous engorgement (epidural vein dilatation and pachymeningeal enhancement) is an important clue to diagnose so-called SIH syndrome. Dilatation of epidural veins suggests CSF hypovolemia in appropriate conditions.

Adult↗
PubMed2002

Mutation in the caveolin-3 gene causes a peculiar form of distal myopathy.

The authors describe a patient with sporadic distal myopathy associated with reduced caveolin-3 in muscle fibers in which the muscle atrophy was restricted to the small muscles of the hands and feet. Gene analysis disclosed a heterozygous 80 G-->A substitution in the caveolin-3 gene that was identical to that of reported cases of elevated serum creatine kinase. This patient further demonstrated possible clinical heterogeneity of myopathies with mutations in the caveolin-3 gene.

Adolescent↗
PubMed2001

Clinical and physiological significance of abnormally prolonged central motor conduction time in HAM/TSP.

We measured the central motor conduction time (CMCT), central sensory conduction time (CSCT), F wave and mean F wave/M wave amplitude ratio in patients with HTLV-I associated myelopathy/tropical spastic paraparesis (HAM/TSP) and controls. CMCTs in upper (U) and lower (L) limbs were significantly prolonged in HAM/TSP. L-CSCT was significantly prolonged in HAM/TSP, but U-CSCT in HAM/TSP and controls were not significantly different. CMCT and CSCT were significantly correlated in HAM/TSP. U-CMCT, but not L-CMCT, correlated with the clinical severity of HAM/TSP. Although F wave conduction velocity and its occurrence were normal in HAM/TSP, U- and L-mean F wave/M wave amplitude ratio tended to be higher in HAM/TSP, and the L-mean F wave/M wave amplitude ratio was significantly correlated with the L- and thoracic CMCT. These findings demonstrate that the prolongation of CMCT sensitively reflects the extension of the lesions and the disinhibition to the anterior horn cells in HAM/TSP.

Aged↗
PubMed2001

Effect of digoxin noncompliance on hospitalization and mortality in patients with heart failure in long-term therapy: a prospective cohort study.

BACKGROUND: As outpatients with long-term chronic illness often show a high incidence of medication noncompliance, we investigated the influence of digoxin noncompliance on hospitalization, left ventricular ejection fraction, and mortality in outpatients in long-term therapy having congestive heart failure with tachycardia at a rate over 100 beats/min before starting digoxin therapy, but abnormal sinus rhythm. METHODS: Before starting this study, the digoxin compliance/noncompliance of patients was determined by measuring the serum digoxin concentration (SDC). SDC was determined once a month, followed for six consecutive months, and patients were defined as noncompliant if their SDC was zero (0.0 ng/ml) on at least three consecutive occasions. According to SDC data, 218 patients were assigned to the compliant group and 213 patients were assigned to the noncompliant group. All 431 patients received diuretics, angiotensin converting-enzyme inhibitors, or nitrates as well as conventional therapy with digoxin throughout the trial. The duration of follow-up was 72 months. FINDINGS: After 72 months of follow-up, the digoxin noncompliant patients showed significant increases in the number and duration of hospitalizations compared with the compliant patients. The digoxin noncompliant patients had a marked decrease in the left ventricular ejection fraction from 49.1% to 41.8%. The cumulative rate of mortality from any cause in noncompliant patients was twofold higher (15.0%) than in compliant patients (7.8%; risk ratio when noncompliant was compared with compliant: 1.95; 95% confidence interval 1.11, 3.45; P = 0.029) at the 72-month follow-up. The higher mortality in digoxin noncompliant patients was exclusively attributed to worsening heart failure rather than other cardiac and noncardiac causes (risk ratio 2.13; 95% confidence interval 1.12, 4.07; P = 0.033). In addition, multiple regression analyses demonstrated that patient noncompliance as well as lower left ventricular ejection fraction at baseline were significantly involved in increased mortality. CONCLUSION: These results indicate that digoxin noncompliance, at least in part, increases the rate of both hospitalization and mortality due to worsening heart failure in outpatients who have congestive heart failure with tachycardia in long-term therapy.

Aged↗
PubMed2001

Diabetogenic activity of 20 kDa human growth hormone (20K-hGH) and 22K-hGH in rats.

To compare the diabetogenic activity of 20 kDa human growth hormone (20K-hGH) with that of 22K-hGH, we evaluated insulin sensitivity with a euglycaemic clamp in rats. The glucose infusion rate (GIR) in euglycaemic clamp studies was measured as an indicator of insulin sensitivity. [(14)C]glucose and 2-[(3)H] deoxy- D -glucose injection were used to calculate the rate of glucose utilization (R(d)), the hepatic glucose output (HGO), and the glucose metabolic index (R(g)'). Both 20K- and 22K-hGH were infused at equivalent rates (1.0 (mg/kg)/day). A 24 h infusion of 20K-hGH had no significant effects on the GIR, R(d), HGO and R(g)(')except for in gastrocnemius muscle. In contrast, 22K-hGH significantly lowered the GIR compared with the control (P< 0.001) and 20K-hGH groups (P< 0.01). The infusion of 22K-hGH also reduced R(d)compared with the controls and the 20K-hGH rats by 46.6% (P< 0.001) and 39.6% (P< 0.05) respectively, while no differences were observed in the HGO. Moreover, 22K-hGH inhibited glucose uptake, which was estimated from the insulin-stimulated R(g)' in some tissues. These results suggest that 22K-hGH inhibits the uptake and use of glucose in various tissues, which then leads to insulin resistance. In conclusion, the diabetogenicity of 20K-hGH is much weaker than that of 22K-hGH, and the reduced insulin-antagonizing action of 20K-hGH could have important clinical benefits.

Adipose Tissue↗
PubMed2001

Decrement of N20 amplitude of the median nerve somatosensory evoked potential in Creutzfeldt-Jakob disease patients.

We studied somatosensory evoked potentials (SSEPs) in eight Creutzfeldt-Jakob disease (CJD) patients presenting with subacute progressive dementia, generalized myoclonus, and characteristic periodic sharp wave complexes in EEG. Somatosensory evoked potentials were elicited by median nerve stimulation at the wrist. We compared SSEP findings with EEG and the clinical stage proposed by the Japanese Slow Virus Infection Research Committee (stage 1: early stage to stage 5: terminal stage). Until clinical stage 3, short-latency SSEPs showed normal findings despite the severely abnormal EEG. With the progression to clinical stages 4 and 5, however, the amplitude of N20 began to decrease and finally disappeared without prolongation of the latency of N20, whereas other short-latency components were preserved. We recorded giant SSEPs in two of three patients in stage 4, when the periodic sharp wave complex in EEG began to decrease in amplitude. The giant SSEPs decreased in amplitude with the progression of the illness. These findings suggest that the short-latency SSEP is relatively preserved until the middle phase of the disease but that it is eventually affected in the terminal phase. We conclude that our results are compatible with the CJD pathologic findings and that the amplitude of N20 reflects the extent of cortical damage in CJD patients.

Aged↗
PubMed2001

Structural and functional characterization of IS679 and IS66-family elements.

A new insertion sequence (IS) element, IS679 (2,704 bp in length), has been identified in plasmid pB171 of enteropathogenic Escherichia coli B171. IS679 has imperfect 25-bp terminal inverted repeats (IRs) and three open reading frames (ORFs) (here called tnpA, tnpB, and tnpC). A plasmid carrying a composite transposon (Tn679) with the kanamycin resistance gene flanked by an intact IS679 sequence and an IS679 fragment with only IRR (IR on the right) was constructed to clarify the transposition activity of IS679. A transposition assay done with a mating system showed that Tn679 could transpose at a high frequency to the F plasmid derivative used as the target. On transposition, Tn679 duplicated an 8-bp sequence at the target site. Tn679 derivatives with a deletion in each ORF of IS679 did not transpose, finding indicative that all three IS679 ORFs are essential for transposition. The tnpA and tnpC products appear to have the amino acid sequence motif characteristic of most transposases. A homology search of the databases found that a total of 25 elements homologous to IS679 are present in Agrobacterium, Escherichia, Rhizobium, Pseudomonas, and Vibrio spp., providing evidence that the elements are widespread in gram-negative bacteria. We found that these elements belong to the IS66 family, as do other elements, including nine not previously reported. Almost all of the elements have IRs similar to those in IS679 and, like IS679, most appear to have duplicated an 8-bp sequence at the target site on transposition. These elements have three ORFs corresponding to those in IS679, but many have a mutation(s) in an ORF(s). In almost all of the elements, tnpB is located in the -1 frame relative to tnpA, such that the initiation codon of tnpB overlaps the TGA termination codon of tnpA. In contrast, tnpC, separated from tnpB by a space of ca. 20 bp, is located in any one of three frames relative to tnpB. No common structural features were found around the intergenic regions, indicating that the three ORFs are expressed by translational coupling but not by translational frameshifting.

Amino Acid Sequence↗
PubMed2001

Involvement of H-NS in transpositional recombination mediated by IS1.

IS1, the smallest active transposable element in bacteria, encodes a transposase that promotes inter- and intramolecular transposition. Host-encoded factors, e.g., histone-like proteins HU and integration host factor (IHF), are involved in the transposition reactions of some bacterial transposable elements. Host factors involved in the IS1 transposition reaction, however, are not known. We show that a plasmid with an IS1 derivative that efficiently produces transposase did not generate miniplasmids, the products of intramolecular transposition, in mutants deficient in a nucleoid-associated DNA-binding protein, H-NS, but did generate them in mutants deficient in histone-like proteins HU, IHF, Fis, and StpA. Nor did IS1 transpose intermolecularly to the target plasmid in the H-NS-deficient mutant. The hns mutation did not affect transcription from the indigenous promoter of IS1 for the expression of the transposase gene. These findings show that transpositional recombination mediated by IS1 requires H-NS but does not require the HU, IHF, Fis, or StpA protein in vivo. Gel retardation assays of restriction fragments of IS1-carrying plasmid DNA showed that no sites were bound preferentially by H-NS within the IS1 sequence. The central domain of H-NS, which is involved in dimerization and/or oligomerization of the H-NS protein, was important for the intramolecular transposition of IS1, but the N- and C-terminal domains, which are involved in the repression of certain genes and DNA binding, respectively, were not. The SOS response induced by the IS1 transposase was absent in the H-NS-deficient mutant strain but was present in the wild-type strain. We discuss the possibility that H-NS promotes the formation of an active IS1 DNA-transposase complex in which the IS1 ends are cleaved to initiate transpositional recombination through interaction with IS1 transposase.

Bacterial Proteins↗
PubMed2001

Inhibitory effects of nicorandil on rat mesangial cell proliferation via the protein kinase G pathway.

We investigated the effects of nicorandil, which is a hybrid between a nitrate and an ATP-sensitive potassium channel (K(ATP)) opener, on cultured rat mesangial cell proliferation. Nicorandil (1 microM to 1 mM inhibited [(3)H]thymidine incorporation into rat mesangial cells in a concentration-dependent manner. Nicorandil (1 microM to 1 mM) also inhibited the number of cells. Nicorandil increased cyclic guanosine 3',5'-cyclic monophosphate accumulation in mesangial cells. A protein kinase G inhibitor, KT5823, partially eliminated the inhibition of mesangial cell proliferation by nicorandil. Methylene blue, a guanylate cyclase inhibitor, blocked the inhibitory effect of nicorandil on mesangial cell proliferation. We also examined the effects of K(ATP) mediators. Cromakalim, a K(ATP) activator, and glibenclamide, a K(ATP) inhibitor, had little effect on the proliferation of mesangial cells. These results suggest that the inhibitory effects of nicorandil on mesangial cell proliferation are mediated via the protein kinase G pathway.

Alkaloids↗
PubMed2001

Effects of stimulus intensity on latency and conduction time of short-latency somatosensory evoked potentials.

We studied the effect of stimulus intensity on latencies of short-latency somatosensory evoked potentials (SSEP) by measuring both onset and peak latencies individually. The latencies of N9, N13, N20 and N9-N13 peripheral conduction time (PCT) of median nerve (MN) SSEP, and N8, N23, P37 and N8-N23 PCT of tibial nerve (TN) and sural nerve (SN) SSEP significantly shortened with increasing stimulus intensity by onset latency measurement. However, those latencies by peak latency measurement were less significantly shortened or had only a trend of latency shortening without statistical significance. In contrast to PCT, N13-N20 central conduction time (CCT) of MN-SSEP and N23-P37 CCT of TN- or SN-SSEP showed no latency changes with the increased stimulus intensity by both onset and peak latencies measurement. As peak latencies had greater interindividual variability than onset latencies shown by larger standard deviation, shortening of onset latencies were more consistent than that of peak latencies. We think shortening of onset latencies indicates the recruitment of faster conduction fiber along with increased stimulus intensity. As the degree of latency shortening was less if stimulus intensity was above 2.5 times sensory threshold, the stimulus intensity greater than 2.5 times the sensory threshold should be used for clinical application.

Adult↗
PubMed2001

Adrenomedullin inhibits the pressor effects and decrease in renal blood flow induced by norepinephrine or angiotensin II in anesthetized rats.

Adrenomedullin (AM), a hypotensive peptide originally isolated from human pheochromocytoma, has been reported to regulate renal functions. In patients with glomerulonephritis, the serum levels of AM are elevated as well as hypertensive agents norepinephrine (NE) and angiotensin II (AII). The effects of AM on the NE- or AII-induced pressor effects and renal blood flow responses, however, are not well clarified. We examined the effects of AM on blood pressure and renal blood flow induced by NE or AII in anesthetized rats. Arterial blood pressure and renal blood flow were measured using a calibrated pressure transducer and a laser Doppler flowmeter, respectively. Drugs were injected into the tail vein with a syringe. Intravenous administration of AM (1-3 nmol/kg) decreased the arterial blood pressure in anesthetized rats in a dose-dependent manner, whereas it did not affect the renal blood flow. NE or AII administration in anesthetized rats caused both increases in blood pressure and decreases in renal blood flow. Simultaneous administration of AM with NE or All prevented the increasing effects of blood pressure and inhibited the decreases in renal blood flow caused by NE or AII. These findings suggest that AM may have a protective role against the pressor effects and decrease in renal blood flow caused by NE or AII.

Adrenomedullin↗
PubMed2001

[A case of potassium-sensitive periodic paralysis with cardiac dysrhythmia controlled with imipramine and acetazolamide].

We report a patient with potassium-sensitive periodic paralysis with cardiac dysrhythmia. The patient was a 16-year-old man. He presented with asymptomatic ventricular dysrhythmia and periodic paralysis when he was 6 and 12 years old, respectively. Physical examination revealed slight dysmorphic features such as hypoplastic mandible, low-set ears and clinodactyly. Through an exercise test, a potassium tolerance test and a muscle biopsy, his illness was diagnosed as potassium-sensitive periodic paralysis with cardiac dysrhythmia. For the treatment of his episodic paralysis, we started acetazolamide, which improved both the incidence and the severity of paralysis. However, the incidence of cardiac dysrhythmia was increased after the use of acetazolamide. Routine anti-arrhythmic drugs such as lidocaine failed to control his ventricular dysrhythmia. Only imipramine showed its efficacy by improving the degree and the incidence of cardiac dysrhythmia without aggravating periodic paralysis. This syndrome is relatively rare and there have been no standard protocols for the treatment. We propose the combination of acetazolamide and imipramine as the first choice for this clinical entity. We also discussed the efficacy of the exercise test. It enabled us to confirm the diagnosis of periodic paralysis safely and easily by recording the change of compound muscle action potential amplitudes.

Acetazolamide↗
PubMed2001

[Transverse myelopathy with renovascular hypertension caused by fibromuscular dysplasia].

An 18-year-old woman developed subacute transverse myelopathy with renovascular hypertension, hyperlipidemia, and proteinuria. Spinal magnetic resonance imaging(MRI) showed an intra-spinal cord lesion with severe spinal cord swelling at the C 2-Th 2 level. Increased plasma and cerebrospinal fluid interleukin-8(IL-8) levels and the presence of serum antineutrophil cytoplasmic antibody(ANCA) suggested the existence of an ischemic lesion due to vasculitis. Administration of corticosteroids ameliorated the clinical symptoms and MRI findings. Renovascular angiogram revealed the presence of fibromuscular dysplasia(FMD) at the left renal artery but no malformation was found at the cervical arteries. We discussed the possibility of relationships between myelopathy, FMD, IL-8, and ANCA.

Adolescent↗
PubMed2001

[Hand motor cortical area reorganization following cerebral infarction evaluated with functional MRI, near infrared spectroscopic imaging, and transcranial magnetic stimulation].

A 60-year-old, right-handed man suffered from left hemiparesis with upper limb dominance. CT and MRI revealed cerebral infarction of the entire right middle cerebral artery territory. His hemiparesis recovered excellently and residual neurological deficits 6 years later were left hand weakness(grasping power 9 kg vs. 35 kg in the right) and clumsiness. Functional MRI was performed. During right(normal) hand grasping, activation was seen in the left sensorimotor cortex and supplementary motor area. During left(paretic) hand grasping, activation was seen in the left (ipsilateral) sensorimotor cortex, right parietal cortex, and bilateral supplementary motor areas. Near infrared spectroscopic imaging showed similar results. During right hand grasping, left sensorimotor cortex was activated, and during left hand grasping, bilateral sensorimotor cortices were activated with ipsilateral predominance. Transcranial magnetic stimulation of the left motor hand area evoked right hand movement and stimulation of a point near that area evoked ipsilateral left hand muscle movement. Thus, the findings of the three techniques consistently suggest that the recovery of left hemiparesis of this patient was promoted by motor cortical area reorganization including the ipsilateral motor cortex.

Brain↗
PubMed2001

[A case of Tolosa-Hunt syndrome starting from abducens nerve palsy alone].

A 59-year-old man was admitted to our hospital because of right abducens nerve palsy without orbital pain. One month later right orbital pain appeared and two months later the pain changed to an aching severe pain and the right oculomotor, trochlear and trigeminal nerves were also involved. The administration of corticosteroid dramatically reduced these symptoms. The diagnosis was Tolosa-Hunt syndrome (THS) based on these findings. THS starting with abducens nerve palsy alone is rare, representing only 5.1% of 118 patients. In our patient, the newly developed dynamic MRI was able to reveal the right cavernous sinus lesion. The diagnostic usefulness of dynamic MRI for cavernous sinus lesions has been demonstrated for such cases.

Abducens Nerve Diseases↗