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Biomedical subjects

S Katayama

Publications and source records attributed to S Katayama.

At least 127 records · Page 7Linked to original sources

[A case of Churg-Strauss syndrome presented as right thalamic hemorrhage].

Intracerebral hemorrhage is an uncommon sequel of Churg-Strauss syndrome (CSS). We report the first case of CSS accompanied by right thalamic hemorrhage. The patient was 59-year-old male who experienced a sudden onset of left hemiplegia. Magnetic resonance imaging of the brain revealed right thalamic hemorrhage. Although several reports had pointed out a close relationship between hypertension and cerebral hemorrhage in patients with CSS, this patient had no apparent prior history of hypertension. The cause of thalamic hemorrhage in this patient might be probably due to cerebral vasculitis and an effect of abnormal coagulation and fibrinolytic agents.

Cerebral Hemorrhage↗

[Hepatic arterial infusion of low-dose cisplatin, 5-fluorouracil for hepatocellular carcinoma with tumor thrombi in the portal vein].

Hepatic arterial infusion of low-dose CDDP (10 mg/day), 5-FU (250 mg/day) was performed in 5 unresectable hepatocellular carcinoma (HCC) patients with tumor thrombi in the trunk and/or the first branch of the portal vein. Infusion chemotherapy was continued for five days, then discontinued for the subsequent two days. This procedure was performed repeatedly for at least three weeks. Decrease in the serum levels of the alpha-fetoprotein after the treatment was found in 3 of 4 patients. In one patient, the size of the primary tumor decreased 92%. In two of five patients, the tumor thrombi in the portal vein disappeared, or decreased in size. Side effects of the chemotherapy included liver functional disorder (Grade 3; 1 case), thrombocytopenia (Grade 3; 1 case, Grade 2; 1 case), and leukopenia (Grade 2; 1 case). The present protocol proved to be effective and applicable for patients with advanced HCC associated with severe cirrhosis.

Aged↗

[Percutaneous microwave coagulation therapy for hepatocellular carcinoma].

We performed percutaneous microwave coagulation therapy (PMCT) for 34 hepatocellular carcinoma (HCC) patients, including 18 primary and 16 recurrent HCC ones. Cumulative 1, 2-, 3- and 4-year survival rates of primary HCC patients were 94, 78, 78% and 62%, respectively, while those of recurrent HCC patients were 100, 79, 62% and 41%, respectively. There were no differences between groups. In both groups, local recurrence was found in about 50% of patients. The mean tumor size (diameter 2.6 +/- 0.6 cm) of patients with local recurrence was relatively larger than that (2.2 +/- 0.6 cm) of patients without local recurrence (p = 0.081). Seventeen of 27 patients with moderately or poorly differentiated HCC had local recurrence, while none of patients with well-differentiated HCC did (p = 0.005). Subsequently, local control failure led some patients to have progressive diseases such as multiple intrahepatic metastasis, tumor thrombi in the portal vein, and distant metastasis. From these findings, PMCT should be performed only for well-differentiated HCC less than 2 cm in diameter. If the patients with moderately or poorly differentiated HCC larger than 2 cm in diameter cannot tolerate hepatic resection because of their poor hepatic functional reserve, PMCT should be performed in combination with other non-surgical treatment modalities.

Aged↗

[A case report of valproate encephalopathy].

A 24-years-old woman with epilepsy treated with valproic acid developed disorientation, acalculia, perseveration, slow responsiveness and loss of memory. The drug withdrawal induced a quick improvement of mental function. In this case, hyperammonemia, hypocarnitinemia, increased protein in cerebrospinal fluid were found. When the drug was discontinued, she had a dramatic improvement. Valproic acid caused encephalopathy because of metabolic abnormality in mitochondria in this case. In the cases of encephalopathy caused by valproic acid, the drug administration should be withdrawn, and appropriate measures had to be taken. In addition, elevation of ammonia in the blood, lactic acid and pyruic acid in the serum and cerebrospinal fluid, and decreased carnitine level in the serum will be useful to make a diagnosis of valproate-induced encephalopathy.

Adult↗

Slowly progressive L-DOPA nonresponsive pure akinesia due to nigropallidal degeneration: a clinicopathological case study.

We report an autopsy case of a 51-year old man who showed slowly progressive pure akinesia: freezing phenomenon and festination during 21 years of illness without tremor, rigidity, upward gaze palsy, bradykinesia and dementia, which were not responded to L-DOPA clinically. Neuropathological findings revealed the circumscribed regions in the substantia nigra and middle portion of the internal globus pallidus (GPi), without neurofibrillary tangles, neuropil threads, and glial fibrillary tangles. So this case was clearly distinguished with progressive nuclear palsy and pallidonigroluisian atrophy. It was first reported to describe that L-DOPA nonresponsive pure akinesia can arise from nigopallidal atrophy.

Disease Progression↗

Expression of peroxisome proliferator-activated receptor alpha (PPAR alpha) in primary cultures of human vascular endothelial cells.

The peroxisome proliferator-activated receptor (PPAR) is a member of the steroid nuclear receptor superfamily. Three types of PPARs have been described in humans: PPAR alpha, PPAR beta, and PPAR gamma. Here we investigated the levels of PPAR alpha mRNA in primary cultures of human umbilical venous endothelial cells (HUVEC), human umbilical arterial endothelial cells (HUAEC), human coronary arterial endothelial cells (HCAEC), and human aortic endothelial cells (HAEC), using the reverse transcriptase-polymerase chain reaction (RT-PCR). The HUVEC, HAEC, and HCAEC, but not the HUAEC, showed relatively low expression of PPAR alpha in comparison with liver, which was used as a positive control. Moreover, the partial sequences of the PCR-amplified products from HUVEC, HAEC, and HCAEC were similar to that of the PPAR alpha from human liver. The expression of PPAR alpha in cultured HAEC, which were induced by dexamethasone, was inhibited by insulin. In addition, PPAR alpha expression was also increased by benzafibrate or eicosapentaenoic acid with the physiological concentration. These results suggest that the PPAR alpha in endothelial cells may have the same physiological role as the expression of PPAR alpha in the liver.

Aorta↗

A study of the collagen-binding domain of a 116-kDa Clostridium histolyticum collagenase.

The Clostridium histolyticum 116-kDa collagenase consists of four segments, S1, S2a, S2b, and S3. A 98-kDa gelatinase, which can degrade denatured but not native collagen, lacks the C-terminal fragment containing a part of S2b and S3. In this paper we have investigated the function of the C-terminal segments using recombinant proteins. Full-length collagenase degraded both native type I collagen and a synthetic substrate, Pz-peptide, while an 88-kDa protein containing only S1 and S2a (S1S2a) degraded only Pz-peptide. Unlike the full-length enzyme, S1S2a did not bind to insoluble type I collagen. To determine the molecular determinant of collagen binding activity, various C-terminal regions were fused to the C terminus of glutathione S-transferase. S3 as well as S2bS3 conferred collagen binding. However, a glutathione S-transferase fusion protein with a region shorter than S3 exhibited reduced collagen binding activity. S3 liberated from the fusion protein also showed collagen binding activity, but not S2aS2b or S2b. S1 had 100% of the Pz-peptidase activity but only 5% of the collagenolytic activity of the full-length collagenase. These results indicate that S1 and S3 are the catalytic and binding domains, respectively, and that S2a and S2b form an interdomain structure.

Catalysis↗

A decrease in cerebral cortex intensity on T2-weighted with ageing images of normal subjects.

To determine the change in intensity in the cerebral cortex on T2-weighted MRI with ageing, we reviewed the T2-weighted images of 83 normal subjects and measured the signal intensity in the cerebral cortex in 30 subjects randomly selected from them. Low-intensity areas were more common in the cerebral cortex of the aged. The intensity of different cortical regions varied, and the intensity in the temporal and parietal to be decreased with ageing. Presumably, this change of the intensity reflects senile changes, although low intensity is not evident in the temporal cortex because of its high basal intensity level.

Aging↗

Bezafibrate has an antioxidant effect: peroxisome proliferator-activated receptor alpha is associated with Cu2+, Zn2+-superoxide dismutase in the liver.

Administration of bezafibrate in rats significantly reduced the levels of plasma thiobarbituric acid-reactive substances (TBARS) in comparison with those obtained in rats fed a soy or lard chow. Moreover, an elevation of in vitro conjugated diene production and linoleic acid levels in the high-density lipoproteins and low-density lipoproteins induced by a soy or lard chow, was reduced by bezafibrate administration. In addition, the liver Cu2+, Zn2+-superoxide dismutase (SOD) gene expression showed a significant positive correlation with the liver peroxisome proliferator-activated receptor alpha (PPARalpha) mRNA level (R=0.769, p<0.0001). This unique characteristic of bezafibrate, which possesses both a hypolipidemic effect and antioxidant activity, may be beneficial in preventing vascular complications in hyperlipidemia.

Acyl-CoA Oxidase↗

Increased night:day blood pressure ratio in microalbuminuric normotensive NIDDM subjects.

OBJECTIVE: To determine the relationship of day- and night-time blood pressure (BP) with the degree of albuminuria in subjects with non-insulin-dependent diabetes (NIDDM). RESEARCH DESIGN AND METHODS: BP was determined hourly for 24 h in 27 NIDDM normotensive patients, and 10 age- and BMI-matched controls. Diabetic subjects were separated into normo- and microalbuminuric groups according to the urinary albumin excretion rate (AER < 15 and > or = 15 micrograms/min), respectively. RESULTS: Non-dippers defined by a nocturnal fall in BP of less then 10/5 mmHg represented 68.8% of the normo- and 81.8% of the microalbuminuric patients. Microalbuminuric diabetics demonstrated a significantly higher ratio of night:day BP in comparison to controls, but not to normoalbuminuric diabetics. AER was significantly correlated with BP ratio in the normoalbuminuric, but not in microalbuminuric group. CONCLUSIONS: Ambulatory 24-h BP monitoring is useful to find blunted nocturnal fall in BP even in normotensive NIDDM subjects with or without microalbuminuria. However, whether or not an increase in the night-time BP and/or the night:day ratio in NIDDM patients plays a pathogenetic role in the progression of diabetic nephropathy remains to be clarified.

Albuminuria↗

Reduced alkaline phosphatase activity in diabetic rat bone: a re-evaluation.

We found previously that human bone alkaline phosphatase (AP) was glycated by aseptic incubation with glucose, and partially broken down by reactive oxygen species. In this study, we examined whether selective in vivo glycation of AP molecules occurred in bone tissue, using experimental diabetic rats induced by streptozotocin and spontaneously diabetic rats. Additionally, the effects of hyperlipidemia on bone AP activity were examined. Serum AP activity was significantly elevated after incipient onset of diabetes, and the increased activity originated from the intestinal isozyme. High levels of intestinal AP activity were also observed in rats with hyperlipidemia induced by feeding high-fat or high-fructose chow, but the AP activity in bone tissues was maintained at a constant level. AP activity in bone was reduced after the onset of diabetes. The resulting bone AP molecule bound to an aminophenylboronic acid column, which had affinity for glycated proteins, and contained smaller molecular sizes than the native bone AP. These results suggest that elevated levels of serum AP activity originated from the intestinal isozyme accompanied with hyperlipidemia induced by diabetes. In contrast, the reduced serum levels of AP activity in diabetic rats might be dependent on inactivation of bone AP, which was glycated, followed by partial breakdown of bone AP molecules, possibly due to reactive oxygen species.

Alkaline Phosphatase↗

TSH receptor antibody-associated thyroid dysfunction following subacute thyroiditis.

OBJECTIVE: Autoimmunity plays an important role in the development of thyrotrophin (TSH) receptor antibodies and the pathogenesis of Graves' disease and Hashimoto's thyroiditis. On the other hand, subacute thyroiditis is a self-limited inflammatory disease of presumed viral aetiology. The aim of this study was to examine whether subacute thyroiditis triggers TSH receptor antibody-associated thyroid disorders. PATIENTS: We reviewed 1,697 patients with subacute thyroiditis seen between 1985 and 1995. DESIGN AND MEASUREMENTS: We measured antibodies which inhibit the TSH binding to the TSH receptor (TBIAb), thyroid stimulating antibodies (TSAb) and antibodies that block TSH action (TBAb). Other thyroid autoantibodies were also determined. RESULTS: TBIAb became positive in 38 patients following subacute thyroiditis. Thyroid function after the development of TBIAb appeared to be influenced by the bioactivity of the antibody. Hyperthyroidism developed in the presence of TSAb, and so did hypothyroidism in the presence of TBAb, although 21 patients did not have thyroid dysfunction despite high titres of TBIAb. Fifteen out of 17 patients recovered from hyperthyroidism or hypothyroidism after the disappearance of TBIAb sometimes even without medication. TBIAb-positive patients had a high incidence of a family history of thyroid disease and positive anti-thyroid microsomal antibodies. An ophthalmopathy similar to Graves' disease was also observed in 3 patients. CONCLUSIONS: Subacute thyroiditis may trigger autoreactive B cells to produce TSH receptor antibodies, resulting in TSH receptor antibody-associated thyroid dysfunction in some patients.

Adult↗

Serum substances that interfere with thyroid hormone assays in patients with chronic renal failure.

OBJECTIVE: Serum thyroid hormone concentrations in patients with chronic renal failure are usually low, despite normal serum TSH levels. We investigated the effect on thyroid hormone assays of serum dialysable organic acids that are elevated in uraemic patients. PATIENTS: Serum samples from 42 patients with chronic renal failure who were receiving haemodialysis and 37 sex- and age-matched healthy subjects were examined. DESIGN AND MEASUREMENTS: Serum thyroid hormone concentrations were measured with an analogue radioimmunoassay (RIA), a labelled antibody assay, and an equilibrium dialysis/RIA method. Serum concentrations of organic acids were determined with high performance liquid chromatography. RESULTS: Serum thyroid hormone levels determined by an analogue RIA and a labelled antibody assay in uraemic patients increased, and serum concentrations of organic acids decreased following haemodialysis. A significant association existed between serum free T3 (FT3) levels determined by an analogue RIA and serum concentrations of indoxyl sulphate (IS) prior to dialysis. There was also a significant association between serum free T4 (FT4) levels determined by an analogue RIA and serum concentration of IS and hippuric acid (HA) prior to dialysis. There was a significant association between the changes of serum concentrations of indole acetic acid (IAA) and FT4 concentrations prior to and following haemodialysis when determined by an analogue RIA. Serum FT3 and FT4 levels significantly decreased after the addition of IS to serum from healthy subjects when determined by an analogue RIA but not by a labelled antibody assay. Serum FT4 levels, but not FT3 levels, decreased after addition of IAA when determined by an analogue RIA. Serum FT4 concentrations determined by an equilibrium dialysis/RIA were significantly higher than those determined by the other two methods. The addition of IS, IAA, and HA to serum samples from healthy subjects significantly increased FT4 concentrations when determined by an equilibrium dialysis/RIA method. CONCLUSIONS: Increased serum levels of indoxyl sulphate, indole acetic acid and hippuric acid in sera of uraemic patients may interfere with thyroid hormone measurements when an analogue radioimmunoassay is used. In contrast, there was little Interference with a labelled antibody assay. Dialysable organic acids may also interfere with thyroid hormone assays determined by an equilibrium dialysis/radioimmunoassay method.

Aged↗

Elevated serum granulocyte colony-stimulating factor levels in patients with Graves' disease.

OBJECTIVE: Agranulocytosis is a serious side effect of anti-thyroid drugs (ATD). Granulocyte colony-stimulating factor (G-CSF) is one of the cytokines that increase granulocyte number. The aim of this study was to examine the sequential variation of serum G-CSF levels in patients with Graves' disease before and after ATD therapy. PATIENTS: Sixty-three patients with Graves' disease were studied before, during and after treatment with methimazole (MMI). Serum samples from 71 healthy subjects were used as controls. DESIGN AND MEASUREMENTS: Serum levels of G-CSF were measured by a novel chemiluminescent enzyme immunoassay, which was sensitive enough to determine G-CSF levels in healthy subjects. Blood granulocyte counts, serum, thyroid hormone and TSH levels, and titres of thyroid autoantibodies were also measured. RESULTS: Serum G-CSF levels in Graves' patients before and 2 weeks after MMI were significantly higher than in healthy subjects. There was a significant correlation between serum G-CSF levels and granulocyte counts in untreated patients with Graves' disease. Untreated patients with granulocyte counts less than 2 x 10(9)/I had significantly lower serum G-CSF levels as compared with other untreated patients. Serum G-CSF levels gradually decreased thereafter. No correlation was observed between serum G-CSF levels and serum thyroid hormone levels or titres of thyroid autoantibodies. After ATD treatment, no correlation was found between serum G-CSF levels and granulocytes counts. There was no significant correlation between the change of serum G-CSF levels and that of granulocyte counts before and after MMI treatment. Graves' patients with mild agranulocytosis had normal or elevated serum G-CSF levels. CONCLUSIONS: Significantly elevated serum G-CSF levels were observed in patients with Graves' hyperthyroidism. During ATD therapy, deficiency of G-CSF was not identified as a cause of agranulocytosis in this study.

Adult↗

Argyrophilic structures stimulate glial reactions in neurofibrillary tangles and senile plaques.

Neurofibrillary tangles (NFT) and senile plaques (SP) contain various pathological structures, and the majority of these pathological structures are argyrophilic. To investigate the glial reactions of the argyrophilic substance, we performed immunohistochemistry for microglia or for astroglia after Gallyas-Braak staining, which is one of the most sensitive silver impregnation techniques detecting argyrophilic structures in NFT and SP. We found that extracellular argyrophilic structures in NFT and SP showed glial reactions, and we observed reactive microglia in the center of NFT and SP in contrast to astroglia, which were situated in the periphery. These findings suggest that the exposed argyrophilic components in the extracellular space stimulate both glial reactions, but that there is a striking difference in localization between microglia and astroglia.

Alzheimer Disease↗

A case of Arnold-Chiari Type I malformation presenting with dysrhythmic breathing during sleep.

A 43-year-old woman presented with dull headache, left tinnitus and dizziness. Neurological examination revealed down-beat gaze nystagmus, left tinnitus, positive Romberg sign, poor standing on the left foot, poor tandem gait, left spastic gait and positive pathological reflexes in the bilateral upper and lower extremities. Plain X-ray of the skull and cervical vertebrae demonstrated basilar impression and atlantoaxial fusion. Magnetic resonance imaging of the brain and cervical spine showed cerebellar tonsil descent and syringomyelia located in the left side of the spine at the II-III vertebral level which communicated with the fourth ventricle. The patient was diagnosed as having cervical syringomyelia. Arnold-Chiari type I malformation and basilar impression. Preoperative polysomnography showed dysrhythmic breathing and bradypnea during sleep. Abnormal breathing improved after suboccipital decompression craniotomy and upper cervical laminectomy. It was suggested that dysrhythmic breathing was caused by a disorder of the medullary respiratory center. Herniation of the cerebellar tonsil and syringomyelia might have compressed the medulla.

Adult↗