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K Kamakura

Publications and source records attributed to K Kamakura.

At least 73 records · Page 4Linked to original sources
PubMed1994

[A case of vertical gaze palsy associated with a unilateral infarct in the thalamo-mesencephalic junction on MR imaging].

We report a case of a 54-year-old man with sudden-onset double-vision. On admission, neurological examination showed upward and downward gaze palsy on voluntary and smooth pursuit movements, and vertical oculocephalic maneuver elicited a full upward and downward response. Bell's phenomenon, horizontal eye movements and convergence were not impaired. Based on these findings, supranuclear dissociated vertical gaze palsy was diagnosed. T1-weighted MR images revealed low intensity on the medial side of the right thalamo-mesencephalic junction, which impaired the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF). T2-weighted MR images revealed a high-intensity area. The posterior commissure was spared. The clinical signs gradually improved, and the vertical gaze palsy almost disappeared one month after onset. Based on these findings, unilateral infarct in the thalamo-mesencephalic junction in the distribution of the right paramedian thalamic artery was diagnosed. Only two cases of upward and downward gaze palsy in association with unilateral upper midbrain lesion without posterior commissure have been previously reported. Since we did not perform a pathological examination, we cannot deny that there may have been some denervation of fibers at the posterior commissure. Cases of upward and downward gaze palsy in association with unilateral upper midbrain lesion without posterior commissure are rare, and it is very interesting that the lesion in our patients, like that seen in the two pathological reports, was right-sided.

Cerebral Infarction↗
PubMed1993

Immunoblot analysis of dystrophin-related protein (DRP).

Polyclonal antibodies against the carboxy-terminal portion of dystrophin-related protein (DRP), the putative autosomal gene product which shares sequence homology with dystrophin, show the clear expression of DRP in mouse fetal muscle and in cultured human muscle cells, but not in mature mouse or human muscle. DRP has the same molecular mass as X-linked dystrophin and is recovered from the membrane fraction, but is associated with membranes more loosely than dystrophin.

Amino Acid Sequence↗
PubMed1993

MR imaging findings of tremors associated with lesions in cerebellar outflow tracts: report of two cases.

Two cases with severe tremors were studied by means of electromyograms using surface electrodes and also by magnetic resonance (MR) imaging. The first case was associated with multiple sclerosis and demonstrated a severe postural cerebellar tremor and an alternate activation of antagonist muscles in the right arm. The second case, with hemorrhage in the brainstem, demonstrated a severe tremor at rest and mixed synchronous and alternating activation of antagonist muscles in the left forearm. MR imaging studies localized lesions possibly responsible for these tremors. In the first case a lesion was located in the superior cerebellar peduncle just under the decussation, and in the second case a lesion was found between the red nucleus and the thalamus, with possible involvement of both the cerebellothalamic and nigrostriatal pathways. The first case accords with the theory that a lesion located in the dentate nucleus and its projection can cause severe postural cerebellar tremor. The lesion demonstrated in the second case may be responsible for "cerebellar tremor at rest" or "static (resting) cerebellar tremor."

Adult↗
PubMed1993

[Studies on the identification of sulfadimidine in pork by high performance liquid chromatography with photodiode array detector and gas chromatograph-mass spectrometry].

Sulfadimidine (SDD) was detected in pork imported from Mexico by HPLC with gradient elution system. UV spectrum of the peak was measured and confirmed by photodiode array detector, moreover identified by GC/MS after methylation with diazomethane. Content of SDD in the sample was 0.1 ppm and detection limit of SDD by the proposed method was 0.02 ppm. Application of this method to CLP, SMR, SMM, SDM and SQX was studied, and satisfactory results were obtained.

Animals↗
PubMed1993

[Cranial MRI in hepatic disease--relationship between MR imaging and clinical symptoms and laboratory analysis of liver function].

Magnetic resonance imaging studies on 12 cases with hepatic disease were performed. In 11 adult patients with chronic hepatic failure, T1-weighted images demonstrated increased signal in the globus pallidus in 7 patients (63.6%) and in some parts of the cerebral peduncles in 6 patients (54.5%), in the substantia innominata in 4 patients (36.3%). There might be some correlation between the abnormality of MR imaging and clinical symptoms of hepatic encephalopathy. There was a significant correlation between the intensity of the signal and Fischer's ratio of amino acid analysis. In one patient with Wilson's disease, who developed symptoms of central nervous system, T1-weighted images demonstrated increased signal in the globus pallidus. After treatment of D-penicillamine, the signal of the globus pallidus decreased.

Adult↗
PubMed1992

Distribution of calcium-activated neutral protease inhibitor in the central nervous system of the rat.

The ubiquitous existence of calcium-activated neutral protease (CANP, calpain), an enzyme whose activity is regulated by calcium ions and a specific endogenous CANP inhibitor (calpastatin), is well known. Although there has been much investigation concerning the distribution and role of CANP, investigations of the distribution of the CANP inhibitor using immunohistochemical techniques are rare. We made antiserum against a 40K fragment of cDNA corresponding to two C-terminal repeats of rat liver CANP inhibitor expressed in Escherichia coli. Using this antiserum, we examined the distribution of CANP inhibitor in the rat central nervous system by the ABC technique and compared it with the distribution of CANP. Neurons and glias were stained, with the cytosol stained diffusely and the cell membranes stained clearly and strongly. Axons and myelin were stained faintly, but nuclei and vessels were not stained. The distribution of CANP inhibitor was thus found to be similar to that of CANP.

Animals↗
PubMed1992

Somatosensory conduction delay in central and peripheral nervous system of diabetic patients.

Fifty-four diabetic patients with or without clinical evidence of neuropathy and with no clinical evidence of CNS dysfunction were studied by somatosensory-evoked potentials after electrical stimulation of the median nerve at the wrist and recorded from the scalp electrode against a noncephalic reference. Peripheral conduction index, calculated as the distance from the wrist to the C7 spinous process divided by the P9 latency, was significantly decreased (P less than 0.01) in diabetic patients (69.81 +/- 6.47 m/s) compared with 28 age-matched nondiabetic subjects (76.85 +/- 5.65 m/s). The P11-P13 interpeak latency, representative of the transit time from the dorsal column at the level of the sensory input into the cervical cord to the brain stem along the somatosensory pathways (CCT1), and the P13-N19 interpeak latency, representative of the transit time from the brain stem to the somatosensory cortex (CCT2), were significantly increased in diabetic patients (CCT1, 2.51 +/- 0.63 ms; CCT2, 5.76 +/- 0.92 ms) compared with nondiabetic subjects (CCT1, 2.28 +/- 0.36 ms, P less than 0.05; CCT2, 5.18 +/- 0.51 ms, P less than 0.01). We conclude that, in diabetic patients, neurophysiological abnormalities may be present in two distinct parts of the CNS and the peripheral nervous system.

Blood Pressure↗
PubMed1991

Dystrophin-related protein in the fetal and denervated skeletal muscles of normal and mdx mice.

The amino acid sequence of the polyclonal antibodies we developed against the carboxyl terminus of the dystrophin-related protein, the putative gene product of B3 cDNA, had no homologous sequence to the dystrophin molecule except for two amino acids located at its ends for immunization. By immunohistochemical examination in C57B1/10ScSn and C57B1/10ScSn-mdx mice we found that the DRP was expressed on the surface membrane of fetal muscle fibers, was assembled at the neuromuscular junctions of the mature muscle fibers, and reappeared on the surface membrane of muscle fibers after denervation. Its localization was similar to that of the acetylcholine receptor, suggesting that DRP is one of the cytoskeletons which organize and stabilize the cytoplasmic domain of the acetylcholine receptor.

Aging↗
PubMed1991

[A case of whole visual field visuomotor ataxia of bilateral hands associated with bilateral parietooccipital lesions in the white matter].

A 29-year-old male with visuomotor ataxia was reported. Visuomotor ataxia of bilateral upper extremities was noted in whole visual field including central visual field (optische Ataxie). Neither contraction nor depression of visual field was detected by the test using kinetic or static perimeter, respectively. Magnetic resonance imaging and computed tomography of the brain revealed bilateral parietooccipital lesions in the white matter, and pathological examination of brain biopsy specimen demonstrated demyelination. We considered that bilateral parietooccipital lesions in the white matter were responsible for visuomotor ataxia in this case.

Adult↗
PubMed1990

A manifesting carrier of Duchenne muscular dystrophy with severe myocardial symptoms.

A 42-year-old so-called manifesting carrier of Duchenne muscular dystrophy (DMD), whose first complaints were severe myocardial symptoms, is described. Immunohistochemical study using anti-dystrophin anti-serum and analysis of cloned segments of X chromosome DNA were performed. Her two sons and one of her brothers appear to have had the same disease. She was admitted to the hospital complaining of dyspnoea, back pain and palpitations and was first diagnosed as having myocardial infarction. However, this diagnosis was excluded. The echocardiogram showed diffuse abnormalities of myocardial function. Serum enzymes were increased. Minimal weakness and decreased deep tendon reflexes were detected in her left lower extremity. Muscle biopsy revealed a small number of necrotic fibres. Immunohistochemical study using anti-dystrophin antiserum showed a mosaic pattern of the surface membrane. Analysis of cloned segments of X chromosome DNA from the patient and her son showed the XmnI(Asp) alleles of pERT 87-15 and the TaqI alleles of pERT 87-8 in both patients.

Adult↗
PubMed1990

[MRI findings in a patient with multiple sclerosis and "hyperkinésies voltionnelles" as a main symptom].

A 23-year-old female was admitted to our hospital complaining of tremor in the upper extremities and gait disturbance. Beginning at age 18, this patient experienced tingling of the right fingers, gait disturbance, dysesthesia of both hands, and tremor in the upper extremities. These symptoms disappeared several weeks after each onset. At age 21, gait disturbance and coarse tremor in the upper extremities developed. They were exaggerated and occurred repeatedly. On neurological examination, the right optic disc was slightly pale. She had nystagmus in all directions with ocular movements. Deep tendon reflexes were hypoactive throughout. There was no tremor in the upper extremities at rest, but during the voluntary movements especially in maintaining certain posture coarse tremor developed. When performing goal-directed motion, such as finger-nose test, the tremor became worse near the terminal position. The patient's gait was broad-based, with the trunk trembling. There were no sensory disturbances, dysarthria, or bowel or bladder dysfunction. Laboratory studies were normal except for high IgG% in the cerebrospinal fluid. An electromyogram using surface electrodes recorded rhythmic bursts of about 4c/s, alternating between the extensor and the flexor muscles of the right arm. MRI of T2-weighted images showed many high-intensity areas located around the bilateral ventricles and near the area of the decussation of superior cerebellar peduncle. A diagnosis of multiple sclerosis was made in this case based on the patient's history of illness and MRI findings. The tremor in her right upper extremity was too intense and coarse to be described as tremor, and should better be called "hyperkinésies volitionnelles (HV)".(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Mosaic expression of dystrophin in symptomatic carriers of Duchenne's muscular dystrophy.

A deficiency of the protein dystrophin is known to be the cause of Duchenne's muscular dystrophy. To examine the expression of dystrophin in symptomatic female carriers of this X-linked recessive disorder, we performed immunohistochemical studies on muscle-biopsy specimens from three such carriers, using an antiserum raised against a synthetic peptide fragment of dystrophin. In all three carriers, most individual muscle fibers reacted either strongly or not at all to the antiserum for dystrophin; only 2 to 8 percent of fibers showed partial immunostaining. This mosaic staining pattern was present on both cross-sectional and longitudinal muscle specimens. Although the mosaic pattern was seen in all fiber types, more than 80 percent of type 2B and 2C fibers from two of the carriers did not react with the antiserum. Similar studies in nine normal subjects showed consistently strong staining of all muscle fibers. No muscle fibers from 31 patients with Duchenne's muscular dystrophy reacted with the antiserum. We conclude that symptomatic carriers of Duchenne's muscular dystrophy can be identified by a distinct mosaic pattern in the immunohistochemical staining of the surface membrane of skeletal-muscle specimens. This finding may have practical implications for genetic counseling, although it remains to be shown whether the same staining pattern will be found in muscle specimens from asymptomatic carriers of Duchenne's muscular dystrophy.

Adolescent↗
PubMed1989

[31P-NMR spectroscopy of mitochondrial myopathies: the relation between abnormal energy metabolism and muscle biopsy findings].

31P-NMR spectra were obtained from the quadriceps femoris muscle (at rest and after aerobic exercise) of the 7 cases of mitochondrial myopathies (2 cases of mitochondrial encephalomyopathy and lactic acidosis(MELA), 1 case of myoclonus epilepsy with regged red fiber, 1 case of Kearns-Sayre syndrome, 3 cases of progressive external ophthalmoplegia), using superconducting whole body MR (Magnetom, Siemens). One case showed abnormally low Pcr/Pi ratio in the resting state. An aerobic exercise using ergometer was performed on the other 6 patients. Three of them demonstrated significant reduction and delayed recovery of the Pcr/Pi ratio after exercise. This reduction was not detected in the control subjects. Histological studies of biopsied muscles revealed ragged red fibers in all the cases, the number varies, however, from 0.5 to 15.3 per cent of the total fibers. Abnormalities in the Pcr/Pi ratio of phosphorus spectra, in resting state or after exercise, tend to be observed in patients showing abundant ragged red fibers. Focal cytochrome c oxidase deficiency with relatively small amount of ragged red fibers (less than 10 per cent of the total fibers) was histologically noted in five of our patients, excluding 2 MELA patients. Biochemical assay of mitochondria enzyme was normal. It has been assumed that these patients have no primary defect in energy metabolism and the occasionally observed cytochrome c oxidase deficient fibers are non-specific findings probably caused by some devastating process occurring in these fibers. However, our present studies revealed abnormal reduction and delayed restoration of the Pcr/Pi ratio in 2 out of 5 focal cytochrome c oxidase deficiency cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Lactic↗
PubMed1989

[A case of progressive myopathy with tubular aggregates].

Tubular aggregates (TA) are unusual intramuscular structures stained basophilic on hematoxilin and eosin (HE) staining and red on modified Gomori trichrome (GT) staining. The structures are said to be originated from sarcoplasmic reticulum and are collections of tubules with double membranes on electron microscopic studies. The TA are usually seen in biopsy muscles from patients with muscle pain and cramps but without muscle weakness, periodic paralysis or alcoholic myopathy. In addition, there are five reports on families with progressive myopathy and tubular aggregates in the literature. We presented here a 48-year-old postman without any family history, who had had progressive muscle weakness for 17 years. He had never noticed pain or cramps in his muscles, not taken any particular medicine, and not had regular alcoholic beverages. There was no ptosis, facial weakness, masticatory muscle weakness or dysphagia. Muscle wasting, started from the proximal part of four extremities had progressed to the distal part of them. He could not walk on heels or toes and walked with waddling gait. He stood up with Gowers' maneuver. Serum GOT, GPT and CK were elevated. EMG showed myogenic pattern and MCV was normal. The muscle biopsies were performed; the first one taken from quadriceps femoris muscle at 42 years old showed myopathic changes including marked variation in fiber sizes, with scattered necrotic fiber splitting and TA in type 2B fibers. The second biopsy from biceps brachii muscle at the age of 48 years, showed densely proliferated fibrous tissues, marked variation fiber sizes and scattered split fibers. The TA were rarely seen and type 2B fibers were decreased in number.(ABSTRACT TRUNCATED AT 250 WORDS)

Biopsy↗
PubMed1989

[Asymmetrical patchy muscle involvement in manifesting carriers of Duchenne muscular dystrophy--computed tomographical and histological study].

Two cases of manifesting carriers of Duchenne muscular dystrophy (DMD) were described. Case 1. The 41 year-old woman presented gait disturbance at the age of 40. She had two sons. The first son died of pneumonia soon after birth. The second son developed DMD and died of heart failure when he was 17 years old. Neurological examination revealed mild muscle weakness in neck flexors, gluteus maximus (left side dominance) and hamstrings (right side dominance) as well as bilateral calf pseudohypertrophy. Electromyography showed myopathic changes and serum creatine kinase (CK) was elevated (1941IU/l). The karyotype was 46XX. Computed tomography (CT) of skeletal muscles showed that the following muscles were partly replaced by fatty tissue: bilateral paravertebral muscles, left gluteus maximus, left quadriceps femoris, right adductor magnus, long head of right biceps femoris, bilateral peroneus longus and medial head of left gastrocnemius. Histological examination of left quadriceps femoris revealed only minimal change of focal endomysial proliferation and fiber size variation, demonstrating no necrotic fiber or no abnormalities in fiber type. Case 2. The 42 year-old woman was admitted to the hospital complaining of dyspnea and palpitation. The disease was initially diagnosed as myocardial infarction based on cardiomegaly, ECG abnormality (Q in aVL, V5,6., ST depression and negative T in V5,6, ST elevation in I, aVL) and elevated serum CK. However, the diagnosis was rejected due to the lack of subsequent changes in ECG and the continued elevation of serum CK even after her complaints had disappeared.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Localization of ingensin in rat central nervous system and skeletal muscle.

A high molecular weight, fatty acid- and SDS-sensitive protease named ingensin was purified from rat brain in this study. The enzyme purified from rat brain has the same biochemical properties as those purified from other tissues, e.g., porcine skeletal muscle, human placenta, and rat liver in our laboratory, and rat skeletal muscle and bovine pituitary gland in other laboratories, independently. Immunoblot bands were detected in the same positions as those in the case of ingensin from rat liver. In addition, its topographical distribution was studied in rat brain and muscle by means of the immunohistochemical method. The cytoplasm of motor neurons of the spinal cord, pyramidal cells, and granular cells of the hippocampus, Purkinje cells, and glial cells were stained. Axons were stained. The cytoplasm of muscle was also stained, especially that of type 2 fibers.

Animals↗