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Biomedical subjects

N Oka

Publications and source records attributed to N Oka.

At least 55 records · Page 3Linked to original sources
PubMed1999

Nephrogenic adenoma of the bladder in a chronic hemodialysis patient.

BACKGROUND: Nephrogenic adenoma is an uncommon, benign metaplastic lesion occurring in the urothelium, usually as a response to chronic irritation or trauma. It is rarely encountered in hemodialysis patients. Endoscopically, these lesions can easily be mistaken for malignant tumors. METHODS/RESULTS: We report on a case of nephrogenic adenoma of the bladder in a chronic hemodialysis patient that was large and mistakenly diagnosed as transitional cell carcinoma in the initial biopsy. Histopathological examination of the total cystectomy specimen demonstrated the correct diagnosis of nephrogenic adenoma. CONCLUSION: Increased awareness by urologists and pathologists of nephrogenic adenoma may lead to its more accurate diagnosis.

Adenoma↗
PubMed1999

[Immunopathology of inflammatory neuropathies].

With the use of immunohistochemical technique, nerve biopsy is more informative for the diagnosis of inflammatory neuropathies. In chronic inflammatory demyelinating neuropathy, an increased number of T cells are frequently present in endoneurium, which is in contrast to hereditary neuropathies. In active demyelinating lesions, macrophages adhering nerve fibers showed stainings with TNF-alpha. NOS and cyclooxygenase-2 (COX-2). These molecules may act in concert to promote nerve damage. The inhibitor of COX-2, nimesulide, was effective on experimental allergic neuritis, even if given after the onset of clinical signs. A COX-2 inhibitor may have potential as an additional therapeutic agent in human inflammatory neuropathies. In vasculitic neuropathies, cell-mediated cytotoxicity may be involved in the pathogenesis of small vessel injury. Axonal injury may be caused by focal ischemia. However, an immune attack might be involved in nerve damage, since T cells and IL-12 positive cells were found in endoneurium of some patients with active vasculitis.

Chronic Disease↗
PubMed1999

[A family of hereditary motor and sensory neuropathy with spastic paraplegia (HMSN type V) presenting with phenotypic uniformity including onset in early childhood].

The proband was a 38 year old mother, who had begun to walk abnormally at one year old. She developed weakness and wasting in the intrinsic hand muscles in the third decades. On neurological examinations, she showed weakness with atrophy in the distal muscles of the upper and lower limbs, mild impairment of deep sensation in the feet, and severe spastic gait with scissoring. Deep tendon reflexes were hypoactive in the arms and at the ankles, and brisk at the knees. Babinski sign was present bilaterally. Nerve conduction studies revealed mild slowing of conduction velocities and reduction of muscle and sensory action potential amplitudes. Sural nerve biopsy showed a prominent decrease in myelinated fiber density, especially in the large fibers. Neither demyelination nor typical onion-bulb was found. Results of gene analysis of PMP-22 was negative. Her two daughters, 14- and 11-year-old, respectively, also presented with gait disturbance from the beginning of walking at one year old and had almost the same clinical manifestations as their mother, indicating autosomal dominant inheritance. This family of the hereditary motor and sensory neuropathy with spastic paraplegia (HMSN type V) was distinctive in having phenotypic uniformity including onset in early childhood.

Adolescent↗
PubMed1999

[A case of anti-GM1 antibody positive HTLV-I associated myelopathy (HAM) with polyneuropathy].

We report a case of HTLV-I associated myelopathy (HAM) with polyneuropathy. A 59-year old man suffering from progressive paraparesis associated with subclinical polyneuropathy was admitted to our hospital. HTLV-I antibodies in the serum and CSF were positive, and a diagnosis of HAM was made. His laboratory investigation revealed elevated serum IgG and IgM anti GM-1 antibodies. The nerve conduction study showed a mild reduction in motor and sensory conduction velocity in all extremities. A sural nerve biopsy revealed active demyelination and globule-like changes, which are specific for HAM neuropathy. Anti-GM1 antibodies are frequently present in autoimmune motor neuropathy. They are thought to inflict a damage on both the myelin and axons of the peripheral nerves. Ours is believed to be the first case of HAM associated with anti-GM1 antibodies, although polyneuropathy is often associated with HAM. While it is not clear whether the lesion observed in HAM neuropathy results from the direct cytopathic effect of the virus or from the immune response, some immune-mediated reactions are thought to play an important role. This case suggests that a case of HAM with polyneuropathy should be examined for the presence of the anti-ganglioside antibodies. More investigations are needed to fully understand the mechanism of the HAM neuropathy.

Autoantibodies↗
PubMed1999

[A juvenile case of chronic inflammatory demyelinating polyradiculoneuropathy with severe onion bulb-like change mimicking hereditary neuropathy].

A 15-year-old male developed symmetrical weakness of the limb muscles. He had not had any previous developmental disorders except delayed initiation of walking. Flexion contraction of ankle joint and pes cavus deformity were seen. The cerebrospinal fluid protein concentration was elevated. Nerve conduction study showed severe conduction block and temporal dispersion. A sural nerve biopsy revealed remarkable onion bulb-like changes and perivascular infiltration of inflammatory cells. After high-dose corticosteroid treatment, he showed improvement in muscle strength. Although there were no abnormalities of genes related to hereditary neuropathy, the atypical findings of severe demyelinating changes of peripheral nerves mimicked hereditary neuropathy.

Adolescent↗
PubMed1998

The effect of cyclooxygenase-2 inhibitor on experimental allergic neuritis.

We studied the effect of the cyclooxygenase (COX)-2 inhibitor nimesulide on experimental allergic neuritis (EAN). In rats fed with nimesulide starting on day 1 post inoculation, the clinical EAN score was significantly lower and the maximal clinical score was reduced compared with the control group. Even if given after the onset of clinical signs, the clinical score was reduced and improvement was faster than the control group. Nimesulide inhibited decreases in weight in the experimental group. The histopathological observations of the sciatic nerve showed a decreased incidence of degenerated nerve fibers in the experimental group. Although the exact mechanism of its efficacy is not clear, a COX-2 inhibitor may have potential as an additional therapeutic agent in human inflammatory neuropathies.

Amino Acid Sequence↗
PubMed1998

Tumor necrosis factor-alpha in peripheral nerve lesions.

Immunocytochemical expression of tumor necrosis factor-alpha (TNF-alpha) was examined in nerve biopsy samples of patients with various disorders, focusing on nerve injury. TNF-alpha was mainly associated with phagocytosing macrophages in acute axonal injury, but the staining was more frequently seen in sections from patients with vasculitis than with metabolic neuropathy. Ramifield macrophages outside nerve fibers were also positive for TNF-alpha in the acute stage of vasculitis. In active demyelinating lesions from patients with chronic inflammatory demyelinating neuropathy (CIDP), macrophages outside nerve fibers showed weak staining with TNF-alpha, but the cells adhering to myelinated nerve fibers showed definite staining. This may be due, in part, to the smouldering course of CIDP, and expression may be up-regulated transiently during the demyelinating process. These results indicate that macrophages, as the effector cells for both axonal injury and active demyelination, express TNF-alpha, buth their activation mechanisms may vary among vasculitis, metabolic axonopathy and inflammatory demyelination.

Adult↗
PubMed1998

Presurgical functional localization of primary somatosensory cortex by dipole tracing method of scalp-skull-brain head model applied to somatosensory evoked potential.

The aim of the present study was to explore the utility of dipole tracing (DT) of a scalp-skull-brain (SSB) head model in preoperative functional localization of the human brain. Nine patients who underwent surgery of mass lesions around the central sulcus (CS) were employed. By using SSB/DT, dipole source location of early cortical components of the somatosensory evoked potential (SEP) was estimated before surgery. Motor cortex, CS and primary somatosensory cortex were determined by cortical SEP during surgery. After surgery precise functional mapping was reproduced in MRI, and the accuracy of DT was evaluated by measuring the distance between estimated dipole source and the posterior bank of the CS. We defined this distance as localization error of DT. In 4 cases without structural change around the sensorimotor cortex, localization error ranged from 1 to 4 mm with an average of 2 mm. In 5 cases with structural alteration of sensorimotor cortex, localization error ranged from 6 to 10 mm with an average of 8 mm. The difference in localization error between the two groups was statistically significant, and may have been caused by changes of conductance near sensorimotor cortex in the latter group. Functional localization by DT was accurate and useful. But localization error could not be ignored in cases with structural alteration in the sensorimotor cortex.

Aged↗
PubMed1998

Mechanisms of tissue injury in vasculitic neuropathies.

We studied the expression of candidate molecules for tissue injury in vasculitic neuropathies immunohistochemically, using samples obtained by nerve biopsy from seven patients with necrotizing angitis. In the involved vessels of all samples, numerous infiltrating cells were positive for perforin, nitric oxide synthase (m-NOS), cyclooxygenase-2 (COX-2), or matrix metalloproteinase-1 (MMP-1). Cell-mediated cytotoxicity may be involved in the pathogenesis of small vessel injury in vasculitic neuropathies. In the endoneurium following axonal degeneration, scattered and phagocytosing macrophages showed immunostaining for m-NOS and MMP-1, but COX-2 was all but restricted to phagocytosing macrophages. This suggests a role for prostaglandins in nerve damage.

Adolescent↗
PubMed1998

[Spontaneous rupture of malignant fibrous histiocytoma arising from the renal capsule: a case report].

We report a case of spontaneous rupture of malignant fibrous histiocytoma. A 50-year-old male with right flank pain was referred to our hospital. Computed tomography (CT) showed a heterogeneous space-occupying lesion on the upper pole of the right kidney. Selective right renal arteriography revealed a hypovascular mass. Preoperative clinical diagnosis was spontaneous rupture of renal cell carcinoma. Radical nephrectomy was performed. Histopathological diagnosis was malignant fibrous histiocytoma arising from the renal capsule.

Histiocytoma, Benign Fibrous↗
PubMed1998

[Dissecting aneurysm of the extracranial vertebral artery causing TIA: a case report].

Spontaneous dissecting aneurysm of the extracranial vertebral artery is not frequent. We report a case of dissecting aneurysm of the left extracranial vertebral artery causing TIA. A 44-year-old man was admitted to our hospital with severe occipitalgia of sudden onset on Dec. 21, 1995. On admission, he presented with left hemiparesis and left hemidysesthesia. CT scan and SPECT showed no abnormal findings. His neurological deficits completely improved on the following day. Initial cerebral angiography performed on Dec. 27, 1995 showed pearl and string sign at V3 segment and irregular stenosis at V2 segment suggesting a dissecting aneurysm. We treated conservatively. Repeated angiography performed four weeks after the onset showed resolution of the stenosic lesion and disappearance of the aneurysm. We discussed diagnosis and etiology and treatment of dissecting aneurysm of the extracranial vertebral artery.

Adult↗
PubMed1998

[Long-term clinical outcome of extracorporeal shock wave lithotripsy monotherapy for staghorn calculi].

We treated 97 patients with staghorn calculi by ESWL monotherapy using a Lithostar Lithotriptor (Siemens) between January 1989 and December 1996. Seventeen patients (18 renal units) out of 45 patients (47 renal units) who could be followed up for more than 12 months after ESWL had no stones on radiographs at 3 months after the treatment. The actuarial non-recurrence (or stone-free) rate was 88.9% at 1 year, 79.0% at 3 years, and 63.2% at 5 years after ESWL (Kaplan-Meier method). The actuarial non-regrowth rate (regrowth < 1 mm) was 96.6% at 1 year, 72.8% at 3 years, and 63.7% at 5 years (Kaplan-Meier method). History of urinary stones was a significant risk factor for stone recurrence, while patient sex, affected side, stone number, pyuria (> or = 10/HPF), hydronephrosis on DIP, and staghorn type were not significantly associated with stone recurrence or regrowth (Cox proportional hazard model). Late complications associated with ESWL included renal dysfunction (serum Cr > or = 1.1 mg/dl) in 2 patients, hypertension (> or = 160 mmHg) in 3, and renal atrophy (two-dimensional size < or = 80%) in 5. ESWL exerted adverse effects in a session-dependent manner on the kidney resulting in renal atrophy. Therefore, we highly recommend that ESWL should be limited to less than 10 sessions.

Adult↗
PubMed1997

Caveolin interaction with protein kinase C. Isoenzyme-dependent regulation of kinase activity by the caveolin scaffolding domain peptide.

Caveolar localization of protein kinase C and the regulation of caveolar function by protein kinase C are well known. This study was undertaken to examine whether caveolin subtypes interact with various protein kinase C isoenzymes using the caveolin scaffolding domain peptide. When protein kinase C-alpha, -epsilon, and -zeta were overexpressed in COS cells followed by subcellular fractionation using the sucrose gradient method, all the isoenzymes (alpha, epsilon, and zeta) were detected in the same fraction as caveolin. The scaffolding domain peptide of caveolin-1 and -3, but not -2, inhibited the kinase activity and autophosphorylation of protein kinase C-alpha and -zeta, but not of protein kinase C-epsilon, overexpressed in insect cells. Truncation mutation studies of the caveolin-1 and -3 peptides demonstrated that a minimum of 16 or 14 amino acid residues of the peptide were required for the inhibition or direct binding of protein kinase C. Thus, the caveolin peptide physically interacted with protein kinase C and regulated its function. Further, this regulation occurred in a protein kinase C isoenzyme-dependent manner. Our results may provide a new mechanism regarding the regulation of protein kinase C isoenzyme activity and the molecular interaction of protein kinase C with its putative binding proteins.

Amino Acid Sequence↗
PubMed1997

Isoform-dependent activation of adenylyl cyclase by proteolysis.

Recent findings have suggested that the cellular proteolytic system plays a major role in the regulation of various intra- and extra-cellular signaling. It was previously shown that proteolytic treatment of adenylyl cyclase leads to the activation of this enzyme. We demonstrate that this activation occurs in an adenylyl cyclase isoform-dependent manner. The type II isoform was strongly activated (approximately 500%), the type III isoform was modestly activated (approximately 30%),and the type V isoform was inhibited by trypsin. Activation of type II adenylyl cyclase occurred in trypsin dose- and time-dependent manners and was blocked by a trypsin inhibitor in a dose-dependent manner. Other proteases, such as thrombin and plasminogen, similarly activated the type II isoform, but not the others. Our data suggest that proteolytic activation is an isoform- and thus cell type-dependent mechanism of altering adenylyl cyclase catalytic activity.

Adenylyl Cyclases↗
PubMed1997

Isoform-specific regulation of adenylyl cyclase by oxidized catecholamines.

Both epinephrine and manganese are known to stimulate cAMP production in cardiac homogenates. When added together, however, they inhibited adenylyl cyclase catalytic activity. Type V adenylyl cyclase, the major isoform in the heart, was also inhibited when an increasing concentration of epinephrine was added in the presence of manganese. Inhibition was not dependent on the condition of stimulation or preparation of the enzyme. However, this inhibition was abolished in the presence of anti-oxidant. Other catecholamines, including dopamine and isoproterenol, as well as adrenochrome, an oxidized product of epinephrine, similarly inhibited the activity of this enzyme. Kinetic analyses revealed that the K(m) for the substrate ATP was unchanged, but the V(max) was significantly decreased. In contrast, type II adenylyl cyclase, a non-cardiac isoform, was resistant to such inhibition by adrenochrome and was somewhat stimulated by it. Thus, catecholamines, when oxidized, directly interacted with adenylyl cyclase in an isoform-specific manner in the absence of G proteins. Our findings suggest that adenylyl cyclase isoforms have different sensitivity to various stresses, including oxidative stress.

Adenylyl Cyclases↗
PubMed1997

Effects of chronic beta-adrenergic receptor stimulation in mice.

The goal of the present study was to determine the effects of chronic beta-adrenergic receptor stimulation with isoproterenol (ISO) on cardiac tissue, systemic trophic changes and on beta-adrenergic receptor desensitization in mice. Mice (n=36) received continuous ISO (30 microg/g/day) via osmotic minipump for 13 days. Left ventricle (LV)/body weight (BW) ratio was increased by 27% in ISO v control (CON) mice. The extent of cardiac hypertrophy induced by chronic ISO was offset in part by concomitant increases in body weight, which were greater in ISO than CON mice (22 v 8%), and occurred with increases in both muscle mass and brown fat to BW ratios. Histological analysis of mice revealed a three-fold increase in subendocardial interstitial connective tissue with no evidence of acute cellular necrosis or chronic inflammation. Acute i.v. ISO challenges induced dose-dependent increases in LV fractional shortening (FS) and ejection fraction (EF) using echocardiography (9 MHz), which were attenuated after chronic ISO, i.e. physiological desensitization was observed. Cellular mechanisms of beta-adrenergic receptor desensitization included decreases in beta-adrenergic receptor density (-49%) and decreased basal (-45%) and ISO-stimulated (-61%) adenylyl cyclase activities. Lesser decreases in forskolin-stimulated adenylyl cyclase activity (-16%) and adenylyl cyclase mRNA levels for both type V (-17%) and type VI (-23%) isoforms were observed following chronic ISO. Thus, chronic ISO (30 microg/g/day) induced cardiac hypertrophy without cellular necrosis, increased weight gain and clear physiological desensitization in mice, with more extensive biochemical mechanisms than expected from simple catecholamine-specific (homologous) desensitization.

Adenylyl Cyclases↗
PubMed1997

The physiological effect of anti-GM1 antibodies on saltatory conduction and transmembrane currents in single motor axons.

Anti-ganglioside (anti-GM1) antibodies have been implicated in the pathogenesis of Guillain-Barré syndrome, multifocal motor neuropathy and motor neuron diseases. It has been held that they may interfere with saltatory conduction by blocking sodium channels. We tested this hypothesis by analysing action potentials from 140 single nerve fibres in 22 rat ventral roots using external longitudinal current measurement. High-titre anti-GM1 sera from Guillain-Barré syndrome or multifocal motor neuropathy patients, or anti-GM1 rabbit sera were applied to the rat ventral root, where saltatory conduction in single motor fibres was serially observed for 4-12 h (mean 8.2 h). For control experiments, we also tested anti-galactocerebroside (anti-GalC) sera, which causes acute demyelinative conduction block, and tetrodotoxin (TTX), a sodium channel blocker. Conduction block was found in 82% of the fibres treated with anti-GalC sera and 100% treated with TTX, but only in 2% (one out of 44) treated with the patients' sera and 5% (two out of 38) treated with rabbit anti-GM1 sera. All the nodes blocked by anti-GM1 sera revealed intense passive outward membrane current, in the internode just beyond the last active node. This pattern of current flow was similar to that in fibres blocked by demyelination with anti-GalC sera, and quite different from that seen in fibres blocked by reducing sodium currents with TTX. Our findings suggest that anti-GM1 sera neither mediate conduction block nor block sodium channels on their own. We conclude that physiological action of the antibody alone is insufficient to explain clinically observed conduction block in human diseases.

Action Potentials↗