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Biomedical subjects

T Suga

Publications and source records attributed to T Suga.

At least 91 records · Page 5Linked to original sources

Convulsions in hemodialysis (HD) patients with elevated polymorphonuclear leukocyte elastase (PMNE) levels.

Eight hemodialysis (HD) patients with convulsions of unknown cause were monitored for serum levels of uremic toxins such as methylguanidine(MG), and polymorphonuclear leukocyte elastase (PMNE). Twenty HD patients without convulsions served as controls. In the convulsion group, MG and PMNE were high. In 2 patients, convulsions subsided after daily hemodiafiltration (HDF). Although PMNE was thought to be a mediator of injury in the present series, no significant correlation was found between PMNE and either neutrophil numbers or endotoxin levels. PMNE may indicate the over production of cytokines not associated with serious infection or septicemia. In patients with renal failure and complications of unknown cause, intensified dialysis therapy such as frequent HDF may be useful when combined with treatment of the underlying disease producing the toxins. PMNE measurement is useful in assessing the uremia caused by high cytokine levels and, together with methylguanidin (MG) serum levels, can indicate the severity of the convulsion.

Aged↗

[Preliminary screening for antiviral AIDS drugs. VIII. Report for fiscal year 1995].

Preliminary screening of antiviral AIDS drugs has been carried out using three different in vitro assay systems. Among 96 samples of different origin tested, two were shown to inhibit the growth of HIV in vitro. One of the positive samples (plant origin) has hopeful signs, as the ranges of effective doses are wider than those of most of positive samples which had been found by us.

Acquired Immunodeficiency Syndrome↗

Long-chain acyl-CoA hydrolase from rat brain cytosol: purification, characterization, and immunohistochemical localization.

Long-chain acyl-CoA hydrolase (EC 3.1.2.2), which is found primarily in the brain in rats, catalyzes the hydrolysis of fatty acyl-CoA thioesters. We purified this enzyme, referred to as ACH, from the rat brain cytosol. The molecular masses of the native enzyme and the subunit were estimated to be 104 and 36 kDa, respectively. The enzyme showed high activity with long-chain acyl-CoAs, e.g., with maximal velocity of 262 mumol/min/mg and Km of 5.7 microM for palmitoyl-CoA, but acyl-CoAs with carbon chain lengths of C8-18 were also good substrates. The enzyme was refractory to the inhibitory effect of diisopropyl fluorophosphate and phenylmethylsulfonyl fluoride, but sensitive to p-chloromercuribenzoate. In the rat brain cytosol, about 90% of palmitoyl-CoA hydrolase activity was titrated by anti-ACH antibody, which accounted for over 70% of the enzyme activity found in the brain tissue. Immunoblots of the cytosol prepared from rat brain regional blocks indicated the broad distribution of ACH over the brain, with a relatively high level in the pons and medulla. Immunohistochemically, ACH was localized to neurons. In addition to various nuclei, some neuronal cells, such as mitral cells in the olfactory bulb, pyramidal cells in the cerebral cortex, and Purkinje cells in the cerebellum, were also immunostained with anti-ACH antibody. Brain cytosols prepared from ten mammalian species including human contained a single polypeptide reactive to anti-ACH antibody with molecular masses of 34-36 kDa, together with high activities of palmitoyl-CoA hydrolase. These findings suggest the physiological significance of ACH in the brain, although its precise role remains to be determined.

Animals↗

In vitro and in vivo analysis of human leukocyte binding by the antitumor polysaccharide, lentinan.

Lentinan (LNT), a (1-->3)-beta-D-glucan with (1--6)-beta-D-glucopyranoside branches, has marked antitumor effects in syngeneic and autochtonous hosts. Clinically, LNT has proved effective with chemotherapeutic agents in patients with recurrent gastric and colorectal cancer. However, the mechanism that triggers subsequent immunologic reactions remains obscure. We hypothesized that LNT must first bind to the host cells. Accordingly, we analyzed LNT binding to host cells in healthy volunteers after incubating their cells under a variety of conditions as well as intravenously injecting LNT then subjecting them to flow cytometry and immunofluorescent staining using monoclonal antibody (anti-LNT mAb). LNT bound to monocytes and neutrophils, but not to lymphocytes in vitro. The most avid LNT binding was to monocytes. The percentage of LNT-bound monocytes after 60 min incubation at 4 degrees C was greater than that at 37 degrees C. The binding of LNT to monocytes was inhibited slightly by anti-iC3b receptor (anti-CR3) mAb, strongly by anti-C3b receptor (anti-CR1) mAb, and completely by anti-CR1 and anti-CR3 mAb together. The percentages of LNT-binding monocytes in the peripheral blood increased significantly 3 and 4 after 2 mg LNT-injection and returned to low levels 5 h later. However, no increase in LNT-binding neutrophils and lymphocytes was observed. We concluded that binding of LNT to human monocytes may initiate the influence of this compound on the immune system and differ between individuals. Its binding site may be similar to the C3b receptor.

Adult↗

Transcriptional induction of Acyl-CoA oxidase by dehydroepiandrosterone sulfate in cultured rat hepatocytes.

To elucidate the molecular basis of the induction of peroxisomal enzymes, transcriptional regulation of the acyl-CoA oxidase (AOX) gene by dehydroepiandrosterone sulfate (DHEAS) was examined using primary cultures of rat hepatocytes. Incubation of the hepatocytes with 0.1 mM DHEAS resulted in a progressive increase in the cellular AOX mRNA level, which after 24 h reached a 5.6-fold higher level than that in the control cells treated with vehicle alone. However, this mRNA induction was completely inhibited by alpha-amanitin, an RNA polymerase II inhibitor. When examined by the nuclear run-on transcription assay, the rate of de novo synthesis of AOX mRNA was 3- to 4-fold higher in the hepatocytes exposed to DHEAS than in the control cells, even after 3h. These results indicate that DHEAS acts directly on hepatocytes to activate the transcription of the AOX gene, which leads to the marked induction of AOX in the cell.

Acyl-CoA Oxidase↗

Effect of nicardipine, a calcium antagonist, on induction of peroxisomal enzymes by dehydroepiandrosterone sulfate in cultured rat hepatocytes.

We examined the effect of nicardipine, a calcium antagonist, on the induction of peroxisomal enzymes, such as acyl-CoA oxidase and carnitine acetyltransferase, by dehydroepiandrosterone sulfate (DHEAS) and clofibric acid (CPIB), in primary cultured rat hepatocytes. Peroxisomal beta-oxidation and carnitine acetyltransferase activities were increased 11- and 20-fold, respectively, after 5 days of treatment with DHEAS (40 microM). However, 60 microM nicardipine significantly suppressed the induction of both of these activities by DHEAS to about 2-fold that of the control. This suppression was found to be both dose- and time-dependent. Immunoblot and Northern blot analyses of acyl-CoA oxidase revealed that suppression by nicardipine of the induction of peroxisomal beta-oxidation activity would be responsible for an increase in the amount of mRNA. In addition, the manner in which nicardipine suppressed the induction of peroxisomal beta-oxidation and carnitine acetyltransferase activity, was similar to that of clofibric acid. These findings suggest that in the calcium-dependent pathway, the mechanism for the induction of peroxisomal enzymes by DHEAS is basically the same as that by clofibric acid, a typical peroxisome proliferator. The present results also support our previous hypothesis that calcium may play an important role in the induction of these enzymes by peroxisome proliferators.

Animals↗

[A case of thoracic meningioma presenting paraplegia at 4.5 years after removal of a falx meningioma].

A case of a thoracic meningioma presenting paraplegia 4.5 years after removal of a falx meningioma is reported. A 73-year-old woman, complaining of diplopia, was admitted to our department. Neurological examination revealed right abducens palsy. CT demonstrated a well-enhanced right frontal mass beneath the falx. The mass was totally removed under right frontal craniotomy. Its histology was transitional meningioma with rich fibroblasts. 4.5 years after craniotomy, she complained of progressing gait disturbance and nocturnal leg pain. Neurological examination revealed paraplegia, complete loss of leg sensation, loss of patellar and ankle reflex, bilateral positive Babinski reflex and urinary disturbance. Rectal function and anal reflex were preserved. Thoracic MRI demonstrated an intradural extramedullary mass which was well enhanced with Gd-DTPA at Th6-7. Under laminectomy, the mass was totally removed. Its histology was transitional meningioma with rich psammoma bodies and whirl formations. 4 months after removal, her palsy and sensory loss were almost completely recovered. We were able to find 15 cases of combined intracranial and spinal meningiomas in the literature. A young woman of neurofibromatosis suffered from tentorial, intraventricular and C1-2 meningiomas. Of 15 cases without neurofibromatosis including our case, 4 cases were of young boys and 11 cases were of women. Their initial symptoms originated from intracranial meningiomas in 8 cases. Multiple intracranial meningiomas were revealed in only 4 cases. In 9 cases, one case presented a combination of one intracranial meningioma and one spinal meningioma. Histology of intracranial meningioma was almost the same that of spinal meningioma in almost half of the 10 cases. These findings suggest the multi sentricity theory of multiple meningiomas originating in other neuroaxial compartments. Severe spinal dysfunction was recovered after removal in our case. Rectal function and anal reflex were preserved. These anorectal findings suggest that spinal dysfunction is either complete or incomplete. Motor evoked potentials are hopeful tools which can select reversible spinal motor dysfunctions.

Aged↗

[A case of pituitary adenoma progressing to pituitary apoplexy on the occasion of cerebral angiography].

A case of pituitary adenoma which had progressed from subclinical pituitary apoplexy to subacute pituitary apoplexy on the occasion of cerebral angiography is reported. A 29-year-old man, complaining of bitemporal hemianopsia, was admitted to our department. Plain skull X-p revealed enlargement and double floor of the sella turcica. No abnormal calcification was revealed. CT demonstrated an isodensity mass with a diameter of 4 x 4 cm, and with ring enhancement in the suprasellar region. The mass extended from the intrasellar region to the suprasellar region and had a signal of high intensity on T1-weighted images. Endocrinological examination revealed hyperprolactinemia with a serum level of 422 ng/ml and normal reaction of anterior pituitary hormones. On 3rd March, digital subtraction angiography with 5F catheter was performed with the patient under sedation. The contrast medium was ioxaglic acid (Hexabrix 320). A volume of 6 ml with a speed of 4 ml per second was injected for the internal carotid angiogram. A total volume of 60 ml was used. Serum saline with 10 unit per ml of heparin sodium was also used for flushing. During angiography, the patient's blood pressure was 125/60-115/60mm Hg. DSA revealed upward displacement of the proximal portion of the anterior cerebral artery, pocket formation, and staining of the tumor capsule. Six hours later, he complained of retroorbital headache. Next morning, he noticed complete lack of left visual acuity. On 7th March, right visual acuity degenerated to blindness. CT revealed that the mass had increased its density. With bifrontal osteoplastic craniotomy, the tumor with marked intratumoral hemorrhage was resected. Its histology was chromophobe adenoma. The patient's right visual acuity improved rapidly. On the occasion of cerebral angiography, we could observe that subclinical pituitary apoplexy deteriorated to subacute pituitary apoplexy. Rosenbaum postulated that injection of contrast media increased intravascular pressure leading to pituitary apoplexy. At present, we cannot postulate increased intravascular pressure with 5F catheter and DSA. We cannot rule out that, with underlying subclinical pituitary apoplexy, hemorrhagic infarction due to contrast media and the anti-coagulate effect of heparin sodium accelerated the intratumoral bleeding. Subclinical pituitary apoplexy is a vulnerable state because of its aggravation to symptomatic apoplexy under mild stress. We emphasize that an operation should be performed as early as possible in the case of subclinical pituitary apoplexy.

Adenoma↗

[Cardiac output in patients in their 90's].

Cardiac output was measured by the thermodilution method in nine patients aged 90 to 97 years. The patients were capable of walking in their daily lives before the injury or admission to the hospital, after which they were scheduled for operations. The causes for operations were localized and did not markedly influence general conditions of the patients. After heart rate, arterial blood pressure and mental condition of the patients had been stabilized, their cardiac outputs were determined before the induction of anesthesia. The results are as follows: Cardiac output: 3.58 +/- 0.90 l.min-1, cardiac index: 2.72 +/- 0.57 l.min-1.m-2. Previously published reports in Japan and the results of this study about the relationship between cardiac index and age suggest that as a whole there is a tendency for the cardiac index to decrease with aging.

Aged↗

[A case of acromegaly associated with variegated spinal disorders].

A case of acromegaly associated with variegated spinal disorders was reported. The spinal disorders were multiple cervical disc herniations, spinal epidural cavernous angioma, multiple ossification of the spinal ligament and lumbar canal stenosis. A 51-year-old woman with acromegaly, complaining of disturbances of delicate hand movement and gate, consulted our department. Her past history included diabetes mellitus, hypertension and progressing enlargement of her extremities. Serum growth hormone level was 65.7 ng/ml and somatomedin-c level was 746 ng/ml. Brain MRI showed a pituitary tumor extending to the right cavernous sinus. Cervical MRI revealed disc herniations at C5/6 and C6/7. Thoracic MRI revealed osteoporosis, ossification of the posterior longitudinal ligament and multiple ossification of yellow ligament. Lumbar MRI disclosed ossification of yellow ligament and canal stenosis. Anterior fusion of C5-C7 and an intracapsular removal of the pituitary tumor were performed. Its pathology was that of eosinophilic adenoma. After 3 months, she suffered from paraparesis. On repeating MRI examination with Gd-DTPA, a spinal epidural mass was found at T4. Under laminectomy of Th3-5 and Th8-11, the epidural mass and ossified yellow ligament were removed. The epidural mass was cavernous angioma. She was able to walk without any assistance. An association of spinal canal stenosis with acromegaly is well known. But the association of disc herniation and with the ossification of spinal ligaments is rather rare in the literature. Spinal epidural cavernous angioma is very rare. We discussed the etiological aspects and the management of spinal disorders with acromegaly.

Acromegaly↗

[A case of acute occlusion of left middle cerebral artery due to an embolus treated successfully with percutaneous transluminal angioplasty].

The acute occlusion of cerebral artery by embolism causes severe cerebral infarction. In cases with poor colateral circulation, cerebral infarction develops more severely. In these cases, quick recanalization of the occluded cerebral artery is necessary to prevent severe hemorrhagic infarction and brain edema. We report a case where interventional techniques were used to bring about quick recanalization of occluded cerebral artery. We encountered a case of a sixty-year-old male who experienced complete occlusion of the left middle cerebral artery due to an embolus. It was very hard to pass a guide wire through the embolic lesion. At first, we tried mild local fibrinolysis therapy using tissue plasminogen activator, but we could not get any recanalization. However, after mild local fibrinolysis therapy, the guide wire could be passed through the occlusion point. Secondly, we tried percutaneous transluminal angioplasty (PTA) with 2.0mm diameter angioplastic balloon using up to five atomic pressures, after which we obtained partial recanalization. Finally we achieved total recanalization of the middle cerebral artery by PTA with a 2.5mm diameter angioplastic balloon. We crushed this embolus using the angioplastic balloon with up to six atomic pressures. The point of the techniques is to press the embolus against the arterial wall. After this angioplasty, there was an occlusion of the common trunk of the posterior parietal artery and the angular artery. However there was neither massive hemorrhagic infarction nor massive brain edema on follow up CT. In the treatment of acute occlusion of the cerebral artery due to embolism, we found PTA is very effective against the embolus. In the future, we need to develop a retrieving device and a balloon that will prevent the production of small emboli during the crush process involved when bringing about recanalization using PTA.

Acute Disease↗

[A case of Iotrolan encephalopathy].

A case of Iotrolan encephalopathy is reported. A 66-year-old woman, suffering from subarachnoid hemorrhage, was admitted to our department on January 17th, 1995. After an operation for aneurysmal clipping and ventriculo-peritoneal shunt, she was discharged with no neurological deficiency. CT scan revealed ventricular enlargement and slight periventricular lucency. She was re-admitted on January 4th, 1996. She was suffering from nausea, vomiting, right hemiparesis, right hemi-hypesthesia and disturbance of consciousness. CT scan demonstrated right thalamic bleeding and bilateral ventricular hemorrhage. Further ventricular enlargement was also revealed. With medical treatment, her symptoms were relieved gradually. But disorientation and memory disturbance continued. Shuntography with Iotrolan was performed on February 2nd, 1996. The ventriculo-peritoneal shunt was demonstrated to be occluded on the abdominal side. The volume of Iotrolan used was about 8cc. She became very restless on the night of the examination. Her temperature was up to 38. CT on February 4th demonstrated brain penetration of the Iotrolan. Revision of ventriculo-peritoneal shunt, administration of steroids and hydration was performed. CSF findings demonstrated no abnormalities. Her symptoms were relieved gradually. Iotrolan is a non-ionic contrast media of dimer type, composed of C37 H48 I6 N6 O18. Its distinctive features are low distributing coefficient and high affinity with water. Contrasting several reports of Metrizamide encephalopathy, only 2 cases of Iotrolan encephalopathy were reported. Iotrolan is reported to be much safer than Metrizamide. We were able to find brain penetration by Iotrolan. It is expected to be a characteristic radiological finding of encephalopathy induced by contrast media. The mechanism of Iotrolan encephalopathy is obscure. Several theories concerning Metrizamide encephalopathy are proposed. These are (1) inhibition of hexokinase, (2) inhibition of acethylcholinesterase, (3) immunological mechanism and (4) vascular disturbance. Iotrolan has no 2-deoxy-glucose structure. The inhibition theory of hexokinase is least expected. Related matters are circulatory disturbance of liquor, dehydration, excessive contrast media, advanced age, diabetes mellitus, hypertension, epileptic patients and patients taking phenothiazines. Prompt therapy is important. Removal of contrast media, hydration and administration of steroids should be performed as early as possible.

Aged↗

[A case of acute occlusion of the cervical portion of the right internal carotid artery with successful stepwise vascular dilatation by rescue PTA and deferred PTA].

A case is reported of acute occlusion of the cervical portion of the internal carotid artery, which was recanalized and dilated by steps through rescue percutaneous transluminal angioplasty (PTA) and deferred PTA. A 53-year-old man, complaining of progressive disturbance of consciousness and hemiplegia, was admitted to our department at about 7 hours after onset. CT demonstrated no abnormality. Digital subtraction angiography revealed an occlusion of the right cervical internal carotid artery. After intra-arterial injection of t-PA, a guide wire was able to be passed through the artery. Recanalization of internal carotid artery was performed by rescue PTA with Stealth FS angioplastic balloons of small diameter. Residual stenosis ratio was about 80%. After rescue PTA, his symptoms improved. On the following day, deferred PTA with Stealth FS angioplastic balloons of larger diameter was performed. Stenosis ratio was 30%. After the procedure, his palsy was relieved. DSA in the 3rd week after the PTA revealed that the stenosis ratio had changed from 30% to 13%. Rescue PTA is very effective for prompt recanalization. Stepwise vascular dilatation by rescue PTA with small balloons followed by deferred PTA can improve symptoms and prevent fatal hemorrhagic infarction. This method is especially useful for high risk patients of cervical internal carotid artery occlusion.

Acute Disease↗

Enhancement by peroxisome proliferators of the susceptibility to DNA damage in the liver of male F344 rats.

Effects of [4-chloro-6-(2,3-xylidino)-2-pyrimidinylthio] acetic acid (Wy-14643) or di(2-ethylhexyl) phthalate (DEHP) as peroxisome proliferators on the susceptibility of liver DNA to damage by N-nitrosodimethylamine (DMN) or methyl methane sulfonate (MMS) were investigated. Male F344 rats were administered Wy-14643 or DEHP, orally, for 1 or 10 weeks. At 1 week, the susceptibility to hepatic DNA damage by DMN or MMS was significantly increased in the Wy-14643- or DEHP-treated rats. The enhancement of the susceptibility persisted for up to 10 weeks in both peroxisome proliferator-treated groups. These findings suggest that the high susceptibility to DNA damage caused by peroxisome proliferators would amplify the DNA damage action such as spontaneous damage, leading to an increase in the risk of initiation in the hepatocarcinogenesis.

Animals↗