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Biomedical subjects

T Koide

Publications and source records attributed to T Koide.

At least 325 records · Page 18Linked to original sources
PubMed1985

Alterations of the eicosanoid synthetic capacity of rat brain microvessels following ischemia: relevance to ischemic brain edema.

To know the mechanism underlying ischemic brain edema, a time-course analysis of the eicosanoid synthetic capacity of brain microvessels was carried out using unilateral, middle cerebral artery (MCA)-occluded rats. Concomitant with the development of brain edema the synthetic capacity of all products, including cyclooxygenase and lipoxygenase products, increased significantly. Next the effects of 15-hydroperoxyarachidonic acid (15-HPAA) on the synthetic capacity of microvessels were examined. The drug caused a generalized increase of each product, the profile of which was similar to that obtained with ischemic hemispheres, although the ratios of each product differed somewhat among them. The enhanced synthesis of eicosanoids by 15-HPAA was markedly suppressed by radical scavengers such as alpha-tocopherol, hydroquinone, and 1,2-bis(nicotineamide)-propane. Furthermore, the evolution of brain edema was virtually suppressed by the systemic administration of 1,2-bis(nicotineamide)-propane. The above result suggests that the enzyme activity of the arachidonic acid (AA) cascade of microvessels is stimulated by its own products. Such a mechanism will form a vicious cycle that accelerates the accumulation of free radicals within microvessels and thus may play a role in the progressing disruption of the blood-brain barrier (BBB) following ischemia.

Animals↗
PubMed1985

Xanthine calculi in the patient with the Lesch-Nyhan syndrome associated with urinary tract infection.

A Japanese boy with Lesch-Nyhan syndrome who passed xanthine calculi is reported. After pyelolithotomy for a left renal stone, made up of ammonium urate, associated with urinary tract infection, a high dose of allopurinol was given because of the persistence of pyuria. In the present case, the administration of a high dose of allopurinol, given for the prevention of ammonium urate stone formation in infected urine, induced xanthine calculi formation and we had difficulty in the management of this patient with Lesch-Nyhan syndrome associated with urinary tract infection. However, we believe it a basic necessity to cure our patient of his urinary tract infection and prevent recurrent ammonium urate stone formation because of the risk of renal deterioration.

Allopurinol↗
PubMed1985

Necropsy finding in a patient with apical hypertrophic cardiomyopathy.

Whether apical hypertrophic cardiomyopathy is a variant of classic hypertrophic cardiomyopathy or a separate entity is controversial. This is a case report of an apical hypertrophic cardiomyopathy. The patient was a 67-year-old man associated with giant negative T waves in electrocardiogram and asymmetric apical hypertrophy on echocardiogram. He died of liver cirrhosis and liver cell carcinoma. At necropsy the heart showed apical hypertrophy grossly and extensive disarray of myocardial fibers near the apex of the left ventricle histologically. The necropsy findings were indistinguishable from those of classic hypertrophic cardiomyopathy. This suggests that apical hypertrophic cardiomyopathy is a variant of hypertrophic cardiomyopathy.

Aged↗
PubMed1985

Large cell carcinoma of the lung--ultrastructural and immunohistochemical studies.

Twenty-seven cases of surgically resected large cell carcinoma of the lung including nine cases of giant cell carcinoma were examined ultrastructurally and immunohistochemically. Ultrastructurally, of 18 large cell carcinomas other than giant cell carcinoma eight showed characteristic differentiation toward adenocarcinoma, four toward adenosquamous carcinoma, and one each toward squamous cell carcinoma and neuroendocrine cell carcinoma, but the remaining four were undifferentiated. Six of the nine giant cell carcinomas also showed features of adenocarcinoma, two showed features of squamous cell carcinoma, and one was undifferentiated carcinoma. Immunohistochemically, secretory component (SC) was observed in seven of 14 cases with features of adenocarcinoma and two of four cases with features of adenosquamous carcinoma. Carcinomas with only squamous cell differentiation did not stain for SC. Keratin staining was positive in five of the 14 with features of adenocarcinoma, three of the four cases with features of adenosquamous carcinoma and two of the three cases with features of squamous cell carcinoma. The numbers of tumor cells positive for keratin and/or SC were small. One carcinoma with neurosecretory type granules was stained positively for calcitonin. These findings indicate that many large cell carcinomas showed differentiation toward glandular cells and/or squamous cells, and some did not show any differentiation ultrastructurally or immunohistochemically, indicating that the majority of large cell carcinomas are poorly differentiated form of either adenocarcinomas or squamous cell carcinomas.

Adenocarcinoma↗
PubMed1985

[Combination chemotherapy with cis-diamminedichloroplatinum, vinblastine and bleomycin for a rhabdomyosarcoma of the prostate in a child: report of a case].

A case of prostatic rhabdomyosarcoma in a 5-year-old boy is reported. He was brought to our clinic on Apr. 1, 1982 with complaints of pollakisuria and urethral pain. X-ray examinations revealed a huge intrapelvic tumor, and it was histopathologically diagnosed as embryonal rhabdomyosarcoma with a specimen of transrectal needle biopsy. Since the tumor was too huge to resect completely, he was initially treated with combination chemotherapy regimen of vincristine, actinomycin D and cyclophosphamide (VAC therapy), and resulted in failure. Then another combination chemotherapy consisting of cis-diamminedichloroplatinum, vinblastine and bleomycin (PVB therapy) was tried, and the tumor showed reduction in size. On Oct. 15, 1982, total cystectomy with ileal conduit urinary diversion was performed. Histopathologically, degenerative change and partial necrosis of the tumor cell were recognized. After the operation, he was treated with radiation therapy and prophylactic VAC therapy. But six months later, multiple pulmonary metastases occurred and gradually increased in size and number. They did not respond to any other chemotherapy. He died on July 13, 1983. We discussed the chemotherapy for rhabdomyosarcoma, and emphasized that the PVB therapy should be tried on rhabdomyosarcoma as an initial chemotherapy.

Age Factors↗
PubMed1985

[The pathomechanism underlying ischemic brain edema: the role of Na+, K+-ATPase of the brain microvessels].

In the present study, the anti-edema effect of AVS [1,2-bis (nicotineamide)-propane] was evaluated using the cat MCA occlusion model with or without recirculation. In the prolonged ischemia (PI) group, cortical edema as assessed by the changes in specific gravity, developed in those cortical areas where the mean 1-CBF was less than 25-30 ml/100 g/min during MCA occlusion (4 hours). In the recirculation group (2 hours' ischemia followed by 2 hours' recirculation: RC group), the ischemic threshold for edema development was almost the same as in the PI group. In both groups, the drop in cortical specific gravity was significantly suppressed by AVS. Regarding the time-course of 1-CBF, there was no difference between the PI-AVS-treated and PI-saline-treated groups. In the RC group, however, the postischemic hypoperfusion was significantly ameliorated by AVS. Based on the present and previous data showing the antiedema effect of AVS, the mechanism of action of AVS was discussed in relation to the pathomechanism underlying ischemic brain edema. Our new concept of ischemic brain edema is briefly stated below. Related in vitro studies have shown the followings: (i) the influx of sodium not of proteins is the principal cause of ischemic brain edema: (ii) the eicosanoid synthetic capacity of the brain microvessel (MV) is increased simultaneous to edema development (iii) an elevation in the level of hydroperoxides enhances the activities of Na+, K+-ATPase as well as the arachidonate cascade of MV. These data suggest that free fatty acids and free radicals liberated following cerebral ischemia stimulate the activity of the MV-Na+, K+-ATPase, which results in increased sodium influx across the BBB. AVS was shown to scavenge hydroxyl radicals and to inhibit the stimulatory effects of a lipid hydroperoxide (15-HPAA) on the activities of Na+, K+-ATPase and the arachidonate cascade of the MV. These actions of AVS may be linked to its antiedema effect.

Animals↗
PubMed1985

[Two-dimensional echocardiography in ventricular septal rupture after acute myocardial infarction].

We studied the echocardiographic findings of 11 patients with proven ventricular septal defect following acute myocardial infarction. There were seven men and four women whose ages ranged from 48 to 77 years, with an average of 66 years. Nine patients had acute anterior and two acute inferior myocardial infarctions. Two-dimensional echocardiography (2DE) was performed for eight patients and M-mode echocardiography for all 11 patients. In all eight patients with apical four-chamber view, in whom four had additional apical short-axis view, the septal defect was directly visualized, but it was not detected by M-mode echocardiography. The defect was visualized in the apical region of the septum in all eight patients by the apical four-chamber view. The anteroapical region of the septum was the site in three with anterior infarction and the inferoapical region in one with inferior infarction by the apical short-axis view. In five of the eight patients who underwent 2DE, surgical or autopsy confirmation of the defects was obtained, with a complete agreement with the echocardiographic findings. In two patients with echocardiographic findings of septal defects, the perforations were confirmed at surgery. Two cases with aneurysmal bulges of thin septum into the right ventricle had the thin necrotic muscle in the anteroapical regions. One patient with a cystic bulge into the septum showed an irregular tear in the inferoapical region of the septum at surgery. In eight patients, the left ventricular wall motion was assessed by 2DE. Six patients revealed hyperkinetic motion in the non-infarcted areas of the basal septum or posterior wall, and these cases had good prognosis. We concluded that 2DE is a sensitive, prompt and safe technique for diagnosing and observing the risk of complicating septal defects in acute myocardial infarction. In this respect, both the apical four-chamber and short-axis views should be utilized for the topographic diagnosis of the defect.

Aged↗
PubMed1985

Pharmacokinetics of the new antihypertensive agent nipradilol in rats. 1st communication: Metabolism and disposition after single oral administration of [14C]nipradilol.

The metabolism and disposition of a new antihypertensive and antianginal agent, 3,4-dihydro-8-(2-hydroxy-3-isopropylamino)propoxy- 3-nitroxy-2H-1-benzopyran (nipradilol, K-351) were studied using its [14C]-labelled compound in rats. The plasma level of radioactivity reached the maximum 1 h after oral administration, and the majority of radioactivities administered were recovered in urine and via the bile in feces within 48 h. From the foregoing it is obvious that the drug was absorbed from the gastrointestinal tract rapidly and well, and was eliminated from the body completely. The unchanged drug detected in the plasma and urine after oral administration of 30 mg/kg was more than 10 times as much as that after 3 mg/kg. This fact indicates that the first-pass metabolism of the drug has been saturated. Denitronipradilol, 4- and 5-hydroxynipradilol, and 4- and 5-hydroxydenitronipradilol were identified as major metabolites in the plasma and excreta, and the degradation compounds of the aminohydroxypropoxy side chain were also found as minor metabolites. Among these metabolites, 4-hydroxy metabolites were found mainly as unconjugates and 5-hydroxy metabolites as glucuronides, respectively. These findings suggest that the possible metabolic pathways of nipradilol in rats involve reductive denitration of the nitroxy group, hydroxylation at the benzopyran skeleton, oxidative degradation of the beta-blocking side chain and their glucuronidation.

Administration, Oral↗
PubMed1985

Situs ambiguous with polysplenia complicated by renal adenocarcinoma.

Two men developed renal adenocarcinoma in association with situs ambiguous off with polysplenia (SAP) (also known as the polysplenia syndrome). Features of their diseases included (1) no normal spleen--just splenuli, (2) interruption of the inferior vena cava with azygos or hemiazygos continuation, (3) bilateral hyparterial bronchi, (4) cardiac malformations, (5) renal adenocarcinomas originating from the kidneys, ipsilateral to the anomalous spleens. The association of renal adenocarcinomas and SAP has not been previously reported, to our knowledge. We suggest that renal adenocarcinoma and SAP may share a common pathogenetic link.

Abnormalities, Multiple↗
PubMed1985

[A study of allopurinol in the prevention of recurrent calcium oxalate stones].

We studied the effect of allopurinol on the prevention of stone recurrence in 134 patients with recurrent, idiopathic calcium nephrolithiasis. They consisted of 113 male patients and 21 female, between 16 and 72 years with an average age of 42.7. The patients were divided into two groups according to the type of stone occurrence; those with multiple stones without previous stone episodes (multiple stone group), and the those with recurrent stones (stone episode group). Twenty three patients belonged to the multiple stone group and 111 patients belonged to the stone episode group. The stones in 19 of the 23 patients in the multiple stone group remained stable throughout the study, while stones in 4 grew. Fifty-nine of the 111 patients in the stone episode group were free from recurrence, but the others showed recurrence. Statistical analyses was done on the stone episode group. The stone recurrence rate of all of the 111 cases showed significant decrease during prophylactic treatment with allopurinol (p less than 0.01), although the observation period before treatment was 73.0 +/- 65.8 months and that during and after treatment was 28.2 +/- 12.1 months. During the two years before and after prophylaxis 79 patients also showed a significantly decreased recurrence rate. Moreover, regarding 37 cases without any stones at the start of treatment, stone recurrence rate decreased significantly after the administration of allopurinol. Throughout this study, we used a new method for evaluating reasonable stone recurrence. It did not calculate the number of stones recurred, but the stone-forming circumstance in each kidney.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1985

Pharmacokinetics of the new antihypertensive agent nipradilol in rats. 2nd communication: A single oral administration of [14C]nipradilol to spontaneously hypertensive rats.

After oral administration of [14C]-labelled 3,4-dihydro-8-(2-hydroxy-3-isopropylamino)propoxy-3-nitroxy-2H-1-b enzopyran (nipradilol, NP, K-351) to spontaneously hypertensive rats (SHR) at doses of 3 and 30 mg/kg, the blood levels of radioactivity reached a peak at 1 h (197 and 1972 ng eq. NP/ml, respectively), whereas unchanged NP levels showed a peak at 30 min and Cmax values at both doses indicated a great difference (70-fold) in comparison with the dose ratio. Most of the radioactivity was excreted in urine and feces up to 72 h after administration. Large amounts of unchanged NP were distributed in the heart, aorta and vein which were considered to be target organs of NP. The half-lives of NP in those tissues, as well as in the blood, were short. The level of NP in the liver was low in comparison with the blood level. No significantly different levels of NP and its metabolites between SHR and normotensive rats were seen, except that the free type of 5-OH-DN was higher in the liver and urine in SHR.

Administration, Oral↗
PubMed1984

Purification and biological property of heparin cofactor II: activation of heparin cofactor II and antithrombin III by dextran sulfate and various glycosaminoglycans.

Heparin cofactor II (HC II) has been purified from human plasma by a modification of the method described by Tollefsen et al. (J. Biol. Chem., 257, 2162, 1982) and abilities of dextran sulfate and various glycosaminoglycans to activate the antithrombin activities of HC II and antithrombin III (AT III) were studied. By the purification method described here, highly purified HC II with the same specific activity as reported by Tollefsen et al. was obtained with a higher yield and in a shorter purification time. Heparin, dextran sulfate and chondroitin polysulfates 1 and 5 activated both HC II and AT III, while dermatan sulfate activated only HC II. Dextran sulfate was almost as active as heparin in the activation of HC II and AT III, indicating that in the interactions of heparin with HC II and AT III, sulfate groups of heparin are more important than carboxyl groups. When mixed with thrombin in the presence of dermatan sulfate, normal human plasma showed antithrombin activity which was not due to AT III but to HC II only. HC II did not inhibit factor Xa or plasmin in the presence of any glycosaminoglycans or dextran sulfate, suggesting that HC II would be a specific inhibitor of thrombin.

Antithrombin III↗
PubMed1984

Histidine-rich glycoprotein and alpha 2-plasmin inhibitor in inhibition of plasminogen binding to fibrin.

The plasma proteins alpha 2-plasmin inhibitor and histidine-rich glycoprotein were compared directly with respect to their effectiveness in inhibiting the binding of plasminogen to fibrin under the same experimental conditions. At their physiological concentrations, the presence of alpha 2-plasmin inhibitor more markedly decreased the binding of plasminogen to fibrin than histidine-rich glycoprotein. Significance of these findings in inhibition of fibrinolysis is discussed.

Depression, Chemical↗
PubMed1984

Fibrochondrogenesis: radiologic and histologic studies.

Fibrochondrogenesis is a distinct, neonatally lethal, short-limb skeletal dysplasia which was first described in a single patient in 1978. We report the radiographic and morphologic studies of 2 additional unrelated stillborn infants with fibrochondrogenesis. This syndrome has distinct radiographic and chondro-osseous morphologic defects different from those seen in the other known skeletal dysplasias. The long bones are short and dumbbell-shaped with metaphyseal flare. The spine is platyspondylic with superior-inferior clefting defects, and the ribs are short and distally cupped. The growth-plate cartilage is grossly disorganized and has a densely fibrous collagenous matrix when examined by light and electron microscopy. Light, transmission, and scanning electron microscopy shows diaphyseal and metaphyseal trabecular bone to be normal.

Abnormalities, Multiple↗