Secondary electrons induced by fast ions under channeling conditions. II. Screening of fast heavy ions in solids.
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Biomedical subjects
Publications and source records attributed to K Shima.
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We have carried out a long-term study of lesions found in a man who had a demyelinating disease of both central and peripheral nervous systems. During the 10 years of his clinical course, he suffered from optic neuritis, multifocal myelitis, and chronic multifocal demyelinating neuropathy, with persistent conduction block. Our study revealed that both central and peripheral nervous system demyelination occurred repeatedly and simultaneously.
The supplementary motor area (SMA) of primates has been implicated in the initiation and execution of limb movements. However, when a motor task was extensively overlearned, few SMA neurons, if any, were active before the movement onset. Subsequent lesions of the primary motor cortex gave rise to the appearance of premovement activity changes, indicating usedependent reorganization of the neuronal activity in SMA.
Inflammatory pseudotumor of the spleen in a 50-year-old man was encountered in our surgical clinic. This splenic tumor is very rare and in the ninth of the cases in the literature. The removed spleen, weighting 255g, revealed the presence of a firm, circumscribed mass, measuring 4.5 x 4.0 x 4.5 cm, and histologically presenting marked lamination of collagen fibers around the small vessels associated with granulomatous lesions. The implications of its pathogenesis was analyzed with a review of the literature.
Chronological changes in plasma or serum concentrations of various fibrinolytic parameters, such as tissue-type plasminogen activator, plasminogen activator inhibitor, fibrinopeptide B beta 15-42 and FDP, were examined in 31 healthy volunteers before and after venous occlusion to determine a suitable time of venous stasis and a good parameter for use in a simplified venous occlusion test. After venous stasis for 5 min, a significant increase in the serum concentration of FDP (from 38.3 +/- 21.1 to 100.9 +/- 87.2 ng/ml (n = 24)) was observed, and the increase was parallel with changes in the plasma concentrations of other fibrinolytic parameters. The serum FDP level after 10 min VO was not significantly higher than that after 5 min VO. A significant decrease in ADP-induced platelet aggregation was observed after venous occlusion when measured by the impedance method, but not by the turbidimetric method. Therefore, as a simplified test, the change in the serum concentration of FDP after VO for 5 min was measured. The clinical significance of this simplified test was evaluated in fourteen patients with stenosis of cerebral artery. The mean percentage change in serum FDP concentration after venous stasis in the patients, 34.5 +/- 54.8%, was significantly less than that in normal subjects, 156.5 +/- 90.9%. Similar results were obtained on changes in plasma responses of other fibrinolytic parameters. Measurement of increase in serum FDP concentration after venous occlusion for 5 min should be useful as a screening tests for the hypofibrinolytic or thrombotic state due to vascular dysfunction.
In order to investigate whether urinary C-peptide (UCP) excretion can be a useful index of insulin-dependent diabetes mellitus (IDDM) with unstable glycemic control, UCP was measured in nine IDDM patients with unstable glycemic control, nine IDDM patients with stable glycemic control, and 12 non-insulin-dependent diabetic (NIDDM) patients treated with insulin. The UCPs in overnight urine (U1) and fasting single void urine (U2) in IDDM patients with unstable glycemic control were significantly lower than those in IDDM patients with stable glycemic control (U1: 0.03 +/- 0.03 vs 0.24 +/- 0.20 nmol/mmol-Creatinine, U2: 0.02 +/- 0.01 vs 0.20 +/- 0.20 nmol/mmol-Cr, mean +/- SD, both P less than 0.01). The UCPs in U1 and U2 in both groups of IDDM were significantly lower than those in NIDDM (U1: 0.97 +/- 0.52, U2: 0.73 +/- 0.41 nmol/mmol-Cr, both P less than 0.01). The UCPs in U1 and U2 significantly correlated with incremental C-peptide response to intravenous glucagon injection and with glycemic stability assessed by the standard deviation of 10 previous fasting plasma glucose levels. These results suggest that UCP reflects their residual insulin secretory capacity and that UCP can be a useful index which distinguishes patients with unstable IDDM from those with stable diabetes mellitus.
Renal handling of glycated albumin in diabetic nephropathy was examined by studies on renal selectivity for glycated albumin in 23 normal controls and 52 patients with non-insulin-dependent diabetes mellitus (NIDDM) with various degrees of nephropathy. The serum and urinary levels of glycated albumin were measured by enzyme-immunoassay with monoclonal antibody to glucitol-lysine residues in human glycated albumin. The diabetic patients were divided into 3 groups according to the albumin index (AI): patients with normoalbuminuria [AI less than or equal to 30 mg/g creatinine(Cr)], with microalbuminuria (30 less than AI less than or equal to 270 mg/g Cr), and with macroalbuminuria (AI greater than 270 mg/g Cr). The renal selectivity for glycated albumin was calculated from the ratio of the urinary to serum level of glycated albumin. In the controls, the renal selectivity was as high as 4.40 +/- 0.48, and significantly higher than those in patients with normo- (2.87 +/- 0.29), micro- (1.72 +/- 0.20) and macroalbuminuria (1.26 +/- 0.23). The renal selectivity was inversely correlated with the AI in diabetic patients (r = -0.58, P less than 0.01). These data indicate that glycated albumin was selectively excreted in the urine and that the renal selectivity in diabetic patients gradually decreased to a value of 1 with increase in albuminuria. When the patients with normoalbuminuria were divided into two subgroups with high and low albumin excretion, the renal selectivities for glycated albumin in both subgroups were still significantly lower than that in controls. These results suggested that early diabetic nephropathy which cannot be detected clinically by albuminuria can be diagnosed by measurement of renal selectivity for glycated albumin.
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1. Single-unit activity in the cingulate cortex of the monkey was recorded during the performance of sensorially (visual, auditory, or tactile) triggered or self-paced forelimb key press movements. 2. Microelectrodes were inserted into the broad rostrocaudal expanse of the cingulate cortex, including the upper and lower banks of the cingulate sulcus and the hemispheric medial wall of the cingulate gyrus. 3. A total of 1,042 task-related neurons were examined, the majority of which were related to the execution of the key press movements. In greater than 60% of them, the movement-related activity preceded the activity in the distal flexor muscles. 4. The movement-related neurons were distributed, in two foci, in the posterior and anterior parts of the cingulate cortex, both including the upper and lower banks of the cingulate sulcus. The posterior focus was found to largely overlap the area projecting to the forelimb area of the primary motor cortex by the use of the horseradish peroxidase (HRP) method. 5. About 40% of the cingulate cortical neurons showed equimagnitude responses during the signal-triggered and self-paced movements. The neurons exhibiting a selective or differential response to the self-paced motor task were more frequently observed in the anterior than in the posterior cingulate cortex. 6. The long-lead type of changes in activity, ranging from 500 ms to 2 s, were observed mainly before the self-paced and, much less frequently, before the triggered movements. They were particularly abundant in the anterior cingulate cortex. 7. Only a few of the neurons showed activity time-locked to the onset of the sensory signals. 8. These observations indicate that the anterior and posterior parts of the cingulate cortex are distinct entities participating in the performance of limb movements, even if the movements are simple, such as those in this study.
We describe two patients with autopsy-proven neoplastic angioendotheliomatosis (NAE) presenting only as a transverse myelopathy for 10 to 12 months, followed by disseminated intracranial manifestations. Postmortem examination disclosed a vasculocentric distribution of neoplastic cells in various organs that stained positively with B-lymphocyte-specific monoclonal antibody. These cases were unusual because they manifested as an isolated myelopathy for many months.
The degree of brain-stem dysfunction associated with high-level fluid-percussion injury (3.0 to 3.8 atm) was investigated in anesthetized cats. Measurements were made of the animals' intracranial pressure (ICP) pressure-volume index (PVI), far-field brain-stem auditory evoked responses (BAER's), and cerebral blood flow (CBF). The animals were classified into two groups based on the severity of neuropathological damage to the brain stem after trauma: Group 1 had mild intraparenchymal and subarachnoid hemorrhages and Group 2 had severe intraparenchymal and subarachnoid hemorrhages. The ICP values in Group 1 were insignificantly lower than those in Group 2, while the PVI values in Group 2 were clearly lower (p less than 0.05). Immediately after the injury, peaks II, III, and IV of the BAER's demonstrated a transitory and marked suppression. One Group 1 and two Group 2 animals showed the disappearance of peak V. In Group 1, the latencies of peak II, III, and IV gradually increased until 60 to 150 minutes postinjury, then returned to 95% of baseline value at 8 hours; however, the animals in Group 2 showed poor recovery of latencies. Two hours after brain injury, the CBF decreased to 40% of the preinjury measurement in both groups (p less than 0.001). In contrast to Group 2, the CBF in Group 1 returned to 86.8% of the preinjury measurement by 8 hours following the injury. Changes in PVI, BAER, and CBF correlated well with the degree of brain-stem injury following severe head injury. These data indicate that high-level fluid-percussion injury (greater than 3.0 atm) is predominantly a model of brain-stem injury.
We reported a 29-year-old woman who had chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) associated with multifocal nerve hypertrophy. She developed chronic progressive muscular weakness of distal part of her extremities and sensory ataxia of limbs and trunk for five years. Steroid therapy improved most of her signs and symptoms. No recurrence has occurred for the subsequent four years until present time. Magnetic resonance imaging (MRI) revealed multifocal and nodular hypertrophy of her peripheral nerves in the extremities. MRI also detected the hypertrophy of posterior nerve ganglia and extradural nerve roots. Hypertrophic nerve trunk comprised of multifocal and nodular hypertrophy of the nerve fiber fascicles which were detected as abnormal high signal intensity area in MR T2-weighted images. Her sural nerve contained no onion-bulb formations and presented normal low signal in MR T2-weighted images. We concluded that the hypertrophic changes occurred multifocally in and among nerve fascicles predominantly at the proximal part of the nerves of the extremities. MRI is useful method to detect the hypertrophic change of peripheral nerves deep in the trunk and the extremities in CIDP.
An asymptomatic 59-year-old male in whom an abnormal shadow was detected on indirect chest X-ray film, was referred to our hospital for further examination. Further examinations revealed no problem at the previously checked site. However, bronchoscopy revealed a protruding hemispheric lesion on the membranous portion of the trachea 2 cm above the carina. The biopsy specimens revealed that the lesion was leiomyoma of the trachea. Transbronchoscopic biopsy was performed three times and the lesion disappeared. A few small fibrous nodules remained. The incidence of this primary tracheal tumor is rare, and benign lesions are much less common than malignant lesions. Furthermore, leiomyoma of the trachea is extremely rare. Only 20 cases have been reported in Japanese and English literature. The average age of the reported cases, including our case, was 49.3 years old. Among the male patients, most cases were around 50 years old but among female patients, there was no standard age for this disease. Clinical symptoms included coughing, dyspnea, wheezing and bloody sputum. There were several patients with severe dyspnea, two of which died. Ten patients (50%) had been misdiagnosed as having bronchial asthma. If a case is suspected to be bronchial asthma in which and where bronchodilators have little effect, we must always consider the possibility of this type of lesion, and perform further examinations and treatment.
A 63-year-old man developed muscular atrophy and weakness in his four extremities since 1983, and was pointed out to have smoldering ATL by elevated HTLV-1 antibody titers in the serum (x 2,500) and CSF (x 32) in 1985. Neurological examinations revealed proximal muscular weakness and atrophy of four extremities, and mild spasticity of both legs. Deep tendon reflexes were hypoactive in both arms and hyperactive in both lower extremities with ankle clonus and bilateral positive Babinski and Chaddock reflexes. These findings were compatible with HAM. His gait, however, was markedly waddling, requiring support. Muscle biopsy at left biceps muscle revealed inflammatory change with rimmed vacuoles, small group atrophy, and marked type 1 fiber predominance. These findings on muscle biopsy are different from those of previously reported cases with HAM, showing some similarities to inclusion body myositis or distal myopathy with rimmed vacuole.
From the linkage study of D6S89, we previously reported that hereditary OPCA in Japan is genetically heterogenous. Two pedigrees, P2 and P35, reported in this report, were not linked to D6S89. In order to examine possible correlation between OPCA genotypes and disease phenotypes, we studied clinically eight cases in these two pedigrees. One autopsied case in pedigree P2 was proven to have marked neuronal degeneration in the inferior olivary nuclei, pontine nuclei, cerebellar cortex, and substantia nigra. Dentate nucleus and oculomotor nuclei were free from neuronal degeneration. Clinical features of those 8 patients were fairly uniform, characterized by cerebellar ataxia, hypoactive DTR, and slow eye movement. Parkinsonism or choreiform movements were observed in one patient, respectively. Pupillary dilatation, twitching of face and tongue, limb amyotrophy were observed in patients of advanced stages. However, these signs were not dominating nor common throughout clinical course. None of our cases showed hyperactive DTR, limb spasticity, or external ophthalmoparesis. On the other hand, these latter signs were popular in SCA1 so far as reviewing the literature. The present study showed that there was possible correlation between genotypes and phenotypes in hereditary OPCA.
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The cellular mechanism of glucagon gene expression in intact rat islets and their synthesis and release of glucagon were investigated. Arginine significantly increased the amounts of preproglucagon mRNA and glucagon in the islets and glucagon release. H-7, a specific inhibitor of protein kinase C (PKC), significantly inhibited these effects of arginine. However, H-8, a potent inhibitor of cyclic nucleotide-dependent protein kinases, did not affect the arginine-induced biosynthesis of glucagon or glucagon release. These results suggest that the regulation of glucagon gene expression by arginine is mediated by PKC, not by cyclic nucleotide-dependent protein kinases.
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