Biomedical subjects

S Ono

Publications and source records attributed to S Ono.

At least 325 records · Page 18Linked to original sources

PubMed1996

Proteins of 30 and 36 kilodaltons, membrane constituents of the Staphylococcus aureus L form, induce production of tumor necrosis factor alpha and activate the human immunodeficiency virus type 1 long terminal repeat.

We have previously demonstrated that the membrane of the Staphylococcus aureus L form induced tumor necrosis factor alpha (TNF-alpha) from murine macrophages. In this study, we purified two proteins which induce TNF-alpha production from a human monocytic cell line, THP-1, and murine macrophages. These molecules were purified from delipidated membranes by deoxycholic acid extraction, two-step anion-exchange chromatography, and preparative electrophoresis. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of the purified proteins showed for each a single band with a molecular mass of 30, and 36 kDa. These proteins were heat stable. Polymyxin B did not affect the production of TNF-alpha induced by these proteins. Furthermore, these proteins induced comparable levels of TNF-alpha in both lipopolysaccharide-responsive and -nonresponsive mouse macrophages. Pretreatment of murine macrophages with gamma interferon enhanced 30- and 36-kDa protein-mediated TNF-alpha production. The 30-kDa protein showed lethal toxicity to D-galactosamine-treated mice. The 30- and 36-kDa proteins stimulated the human immunodeficiency virus type 1 long terminal repeat in a monocytic cell line but not a T-cell line. This effect appeared to be mediated through the induction of nuclear factor kappaB. These results indicate that the 30- and 36-kDa proteins, membrane constituents of the S. aureus L form, may play a role in S. aureus infection and/or in human immunodeficiency virus type 1-infected individuals.

Animals↗

PubMed1996

Role of H(+)-K(+)-ATPase in pHi regulation in inner medullary collecting duct cells in culture.

Studies in inner medullary collecting duct (IMCD) cells in primary culture have proposed two mechanisms for Na(+)-independent hydrogen ion transport: an H(+)-adenosinetriphosphatase (H(+)-ATPase) and an H(+)-K(+)-ATPase. In the present study, we have employed two sources of IMCD cells, cells in primary culture derived from the terminal papilla of the Munich-Wistar rat (IMCDp) and an established murine cell line (mIMCD-3), to define the predominant mechanism(s) of Na(+)-independent intracellular pH (pHi) recovery in the IMCD. In confluent monolayers of IMCDp and mIMCD-3 cells, pHi was measured using the pH-sensitive dye 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein (BCECF) following addition and withdrawal of NH4Cl. Removal of K+ completely abolished Na(+)-independent pHi recovery in both IMCDp (delta pHi/min = 0.039 +/- 0.006 to 0.005 +/- 0.003; P < 0.001) and in mIMCD-3 (delta pHi/min = 0.055 +/- 0.009 to -0.003 +/- 0.002; P < 0.001) cells, respectively. In mIMCD-3 cells, K(+)-dependent pHi recovery was abolished by either of two specific inhibitors of the H(+)-K(+)-ATPase, Sch-28080 (5 or 10 microM) or A-80915A (10 microM). In contrast, bafilomycin A1 (2.5 and 10 nM), an inhibitor of the H(+)-ATPase, failed to attenuate K(+)-dependent pHi recovery. Moreover, sequence verified mouse gastric and colonic alpha-H(+)-K(+)-ATPase probes hybridized to total RNA from mIMCD-3 cells. Based on these findings, we conclude that Na(+)-independent pHi recovery from an acid load in both IMCDp and mIMCD-3 cells in critically dependent on extracellular K(+)-That K(+)-dependent pHi recovery was inhibited by both Sch-28080 and A-80915A but not by bafilomycin A1 suggests that the predominant mechanism by which Na(+)-independent pHi recovery is accomplished in IMCD is through the H(+)-K(+)-ATPase. Expression of both gastric and colonic alpha-H(+)-K(+)-ATPase mRNA in mIMCD-3 cells suggests that one or both of these H(+)-K(+)-ATPases may be responsible for proton secretion in the IMCD.

Animals↗

PubMed1996

Improvement of atherosclerosis and stiffness of the thoracic descending aorta with cholesterol-lowering therapies in familial hypercholesterolemia.

The thoracic aorta is frequently involved in atherosclerotic lesions associated with familial hypercholesterolemia (FH). Transesophageal echocardiography (TEE) allows quantitative evaluation of the wall properties of the thoracic aorta. Using TEE, we tested whether atherosclerosis of the thoracic aorta in FH could be improved by cholesterol-lowering therapies. The subjects investigated were 22 FH patients and 22 age-matched normal subjects. The descending aorta (DA) was divided into four longitudinal portions of equal length. Atheromatous lesions of each portion of the DA were scored by character and extension of lesions by biplane two-dimensional TEE. The scores of atheromatous lesions from all four portions of the DA were added together to give the total atheromatous score (TAS). We also measured instantaneous dimensional changes of the DA in a cardiac cycle by M-mode TEE and blood pressure by a cuff method and calculated the stiffness parameter beta (In[SBP/DBP]/[Dmax-Dmin]/Dmin), where SBP is the systolic arterial blood pressure, DBP is the diastolic arterial blood pressure, Dmax is the maximum aortic dimension during the ejection period, and Dmin is the minimum aortic dimension during the preejection period. TAS was higher in FH (3.70 +/- 1.32) than normal (0.62 +/- 0.54, P < .0001) subjects. Beta in FH (10.35 +/- 4.87) was greater than in normal (5.10 +/- 1.25, P < .0001) subjects, but there were no significant differences of DA dimensions between the groups. In both normal subjects and FH patients, beta correlated with age (r = .52, P < .02 and r = .59, P < .005, respectively). In FH patients, beta and TAS correlated well with pretreatment total cholesterol levels (r = .43, P < .05 and r = .60, P < .005, respectively). In 12 of 22 FH patients, strict cholesterol-lowering therapies with diet and cholesterol-lowering drugs (pravastatin and probucol) were undertaken for 13 months. Cholesterol levels were significantly decreased from 333 +/- 45 to 219 +/- 39 mg/dL (P < .0001); this was associated with significant decreases in beta and TAS (from 9.88 +/- 5.03 to 7.88 +/- 3.92, P < .005, and from 3.61 +/- 1.50 to 2.94 +/- 1.22, P < .0005, respectively). In FH patients, the incidence and severity of morphological and physiological atherosclerosis of the DA were significantly higher than in age-matched normal subjects. A significant regression of atherosclerosis was achieved by strict cholesterol-lowering therapies in relatively young FH patients.

Adult↗

PubMed1996

Role of extracellular matrix in experimental vasospasm. Inhibitory effect of antisense oligonucleotide on collagen induction.

BACKGROUND AND PURPOSE: Although it has been suggested that collagen plays a role in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage, there has been no constructive research to prove it directly. In this study we stopped the transcription of the procollagen type I gene by introducing antisense oligonucleotides for its mRNA in a rat femoral artery model of vasospasm induced by blood and assayed the changes in the vasoconstrictive activity of the vessel and expression of the procollagen mRNA. METHODS: We applied antisense, sense, or missense oligonucleotides, located at the carboxyl propeptide region for alpha 1(I) procollagen mRNA, onto the femoral artery in a rat femoral artery model of vasospasm. The diameter of the artery was measured by angiography. The transcription level of the procollagen gene in the arterial tissue was assayed by use of reverse transcription-polymerase chain reaction. Morphological change in the artery was observed with aldehyde-fuchsin-Masson-Goldner staining. RESULTS: In the model, when the artery was exposed to antisense oligonucleotides in pluronic gel for 5 days to prevent arterial contraction, the contraction was inhibited at a significant level (76.0% +/- 5.6) when compared with that in control experiments using sense oligonucleotides (64.0% +/- 2.4), missense oligonucleotides (63.5% +/- 3.5), or gel alone (62.1% +/- 5.8). The application of antisense oligonucleotide resulted in a marked decrease in alpha 1(I) procollagen mRNA expression as determined by polymerase chain reaction, indicating that the collagen reduction by antisense oligonucleotides occurred at the transcription level. Histological staining suggested that collagen accumulation at the site in the artery where antisense oligonucleotide had been administered was indeed less than that in the control artery. CONCLUSIONS: The results indicate that the induction of procollagen type 1 could cause pathogenesis of the arterial contraction induced by blood in a rat femoral vasospasm model.

Animals↗

PubMed1996

Maturation of rat renal tubular response to alpha-adrenergic agonists and neuropeptide Y: a study on the regulation of Na+,K+-ATPase.

Na+,K+-ATPase in tubular cells plays a pivotal role for the regulation of renal sodium excretion. In adult rats the activity of this enzyme is inhibited by natriuretic hormones and stimulated by antinatriuretic hormones. Here we have examined the tubular response to alpha-adrenergic agonists and neuropeptide Y (NPY) in both infant and adult rats. In the adult kidney, alpha-adrenergic agonists and NPY stimulate Na+,K+-ATPase activity via Ca2+-dependent pathways. Oxymetazoline, a selective alpha-adrenergic agonist, and NPY failed to stimulate proximal tubular (PT) Na+,K+-ATPase activity in 10-d-old rats in doses of 10(-8) to 10(-5) M and 10(-8) to 10(-6) M, respectively, but when tubules were incubated simultaneously with both oxymetazoline 10(-8) M and NPY 5 x 10(-9) M, stimulation was observed in both 10- and 40-d-old rat PT. This effect was abolished by FK 506, an inhibitor of Ca2+ and calmodulin-dependent protein phosphatase 2B in both age groups. A23187, a calcium ionophore, stimulated Na+,K+-ATPase in both infant and adult PT, but 10-fold higher doses were required for the infant tubules. The effect of alpha-adrenergic agonists and NPY on free intracellular Ca2+ was studied in PT cells in primary culture. The Ca2+ response to each agent was less pronounced in infant than in adult cells. Preincubation with NPY, which increases Ca2+ influx into the cells, enhanced the response to the alpha-adrenergic agonist in both infant and adult cells. The results support the concept that the systems regulating renal tubular Na+, K+-ATPase and sodium metabolism undergo postnatal maturation.

Adrenergic alpha-Agonists↗

PubMed1996

Neuronal loss in the medullary reticular formation in myotonic dystrophy: a clinicopathological study.

Respiratory insufficiency occurs frequently in patients with myotonic dystrophy (MyD). We have performed a quantitative study of neurons linked to respiratory function in the dorsal central medullary nucleus (DCMN), the ventral central medullary nucleus (VCMN), and the subtrigeminal medullary nucleus (SMN) in seven patients with MyD and eight age-matched controls. Alveolar hypoventilation of the central type occurred in three of the MyD patients but not in the remaining MyD patients or controls. The densities of neurons of the DCMN, the VCMN, and the SMN in MyD patients with hypoventilation were significantly lower than in MyD without hypoventilation and controls. These data suggest the neuronal loss of the DCMN, VCMN, and SMN is associated with the presence of hypoventilation in MyD and may be an important feature of MyD.

Aged↗

PubMed1996

Stimulus-dependent disorganization of actin filaments induced by overexpression of cofilin in C2 myoblasts.

Actin depolymerizing factor (ADF)/cofilin is a widely distributed family of actin-binding proteins which regulate actin polymerization in a pH-dependent manner. In cultured cells, cofilin, as well as ADF, translocates from the cytoplasm into the nucleus together with actin and forms rod-like structures in response to heat shock or dimethylsulfoxide (DMSO) treatment. In order to study in vivo interaction of cofilin with actin, we examined the effects of cofilin overexpression on actin cytoskeleton in C2 myoblasts. Interestingly, no remarkable effect was observed on phalloidin-stained patterns in cells overexpressing cofilin as compared with normal cells. However, upon treatment with DMSO, cytoplasmic actin filaments were disrupted and intranuclear rod structures containing cofilin and actin were apparently larger and thicker in cells overexpressing cofilin than in normal cells. Heat shock also stimulated disruption of microfilaments and formation of both intranuclear and prominent cytoplasmic cofilin-actin rods in cofilin-transfected cells, suggesting that DMSO-treatment or heat shock triggers cofilin-actin interaction. We further found that a myosin ATPase inhibitor (BDM) induced a reduction in cytoplasmic staining with phalloidin in cofilin-transfected cells. The results suggest that myosin activity might be involved in the regulation of cofilin-actin interactions in vivo.

Actin Cytoskeleton↗

PubMed1996

Comparison of thermal and guanidine hydrochloride denaturation behaviors of glucoamylase from the STA1 gene of Saccharomyces cerevisiae var. diastaticus.

To investigate the relationships between enzyme inactivation and conformational change, the effects of heat and guanidine hydrochloride (GnHC1) on the STA1 gene glucoamylase (STA1GA) of Saccharomyces cerevisiae var. diastaticus were examined by circular dichroism and fluorescence spectroscopies. A conformational change was observed in the thermal denaturation of STA1GA, while extensive enzyme inactivation occurred in GnHC1 denaturation before noticeable conformational change.

Circular Dichroism↗

PubMed1996

PMA and ionomycin differently affect atrial natriuretic peptide stimulated cyclic GMP production in rat mesangial cells.

How 4 beta-phorbol 12-myristate 13-acetate (PMA) and ionomycin (Io), a calcium ionophore, affect on the atrial natriuretic peptide (ANP) stimulated cyclic-3',5'-guanosine monophosphate (cGMP) production in cultured rat mesangial cells was examined. Cultured mesangial cells were prepared by isolated glomeruli from Sprague Dawley rats employing the sieving method and were used between the 3rd and 15th passage for experiments. cGMP and protein contents were measured by radioimmunoassay and Lowry method. Incubations with effectors were carried out either in the presence or absence of 0.5 mM 1-methyl-3-isobutyl-xanthine (MIX). The intracellular concentration of calcium ([Ca2+]i) was determined by using the Fura-2 method. Pretreatment with PMA, an activator of protein kinase C (PKC), attenuated ANP stimulated cGMP production in a time- and dose-dependent fashion, while alpha PDD (an inactive analog of PMA) did not inhibit cGMP production. PMA inhibition was reversed by addition of staurosporine, a protein kinase C inhibitor. Io attenuated ANP stimulated cGMP production in the absence but not in the presence of MIX. These findings suggested that PMA acts on ANP receptor or guanylate cyclase via activation of PKC in rat mesangial cells. Io may inhibit ANP stimulated cGMP production via activation of cyclic nucleotide phosphodiesterase.

1-Methyl-3-isobutylxanthine↗

PubMed1996

Simultaneous estimation of filtration variables in isolated rat lungs in zone 3 conditions.

Estimation of filtration variables (filtration coefficient, perimicrovascular pressure, and reflection coefficient) is important for evaluating pulmonary microvascular permeability to fluids, especially when the lungs are inflamed, injured, or being preserved for transplantation. Here we report a new method for estimating filtration variables simultaneously in isolated rat lung lobes in zone 3 conditions (pulmonary arterial pressure > pulmonary venous pressure > alveolar pressure). We used Krebs-Henseleit solution containing 6% bovine serum albumin for the perfusate and maintained perfusion using a constant-pressure circuit system. Pulmonary venous and alveolar pressures were kept at 2.5 and 2.0 cmH2O, respectively, and pulmonary arterial pressure was set so that lung weight did not change. Then we increased both pulmonary arterial and venous pressures by 3 cm H2O simultaneously, and recorded the weight gain. Next, we diluted the perfusate with Krebs-Henseleit solution to about half the original concentration, and recorded the weight gain. Using the Starling equation, the values we obtained for the filtration variables were filtration coefficient, 5.3 mg. min-1.cmH2O-1.g-1; perimicrovascular pressure, 1.1 cmH2O; reflection coefficient, 0.54. These values agree with values from previous reports. Since these 3 filtration variables are interrelated, this method for simultaneous measurement is more accurate than independent measurements are. The advantages of this method are that it does not require direct measurement of interstitial pressure or collection of lymph fluid. What we need to calculate these filtration variables are the initial filtration rates and the albumin osmotic pressures for perfusate.

Animals↗

PubMed1996

Differential assembly of cytoskeletal and sarcomeric actins in developing skeletal muscle cells in vitro.

Monoclonal antibodies (McAb) to actin were prepared to analyze the assembly of actin isoforms in developing muscle cells in vitro. One of the antibodies (SkA-06) was specific for alpha-sarcomeric actin isoforms in skeletal and cardiac muscles, while the others recognized cytoskeletal (beta, gamma) actin isoforms in smooth muscle and non-muscle tissues as well as the sarcomeric (alpha) actins. Using SkA-06 and a polyclonal antibody (PcAb) specific for cytoskeletal actins, the subcellular localization of the actin isoforms was examined by immunocytochemical methods. While in developing young myotubes, cytoskeletal and sarcomeric actins were co-localized in nascent myofibrils or stress-fiber-like structures, sarcomeric actins predominated in striated myofibrils in more developed myotubes. When FITC-labeled cytoskeletal and sarcomeric actins were introduced into young myotubes by a microinjection method, the latter became detectable in striated structures sooner than the former but they were finally incorporated into striated myofibrils. These results suggest that alpha-actin(s) as well as beta- and gamma-actins can be incorporated into myofibrils, but alpha-actin(s) is assembled preferentially into myofibrils in developing muscle cells.

Actins↗

PubMed1996

Specificity of substrate and inhibitor probes for cytochrome P450s: evaluation of in vitro metabolism using cDNA-expressed human P450s and human liver microsomes.

1. We evaluated the specificity of 15 substrates and 14 inhibitors of the cytochrome P450s using nine human P450 forms expressed in HepG2 cells using a recombinant vaccinia virus and also in human liver microsomes. 2. Coumarin, 7-ethoxyresorufin, 7-benzyloxyresorufin, tolbutamide, aniline and diazepam were form-selective substrates towards CYP2A6, the CYP1A subfamily, CYP2B6, the CYP2C subfamily, CYP2E1 and the CYP3A subfamily respectively. However, a selective substrate for CYP2D6 was not found among the chemicals tested. 3. SKF-525A inhibited > 40% of the metabolic activity of all substrates tested, and the inhibitory effects differed among P450 forms. Sulphaphenazole, 7,8-benzoflavone, quinidine and troleandomycin were selective inhibitors of the CYP2C subfamily (except CYP2C19), the CYP1A subfamily, CYP2D6 and the CYP3A subfamily respectively. Methoxsalen (CYP2A6 inhibitor) inhibited the metabolic activity of CYP1A2 as well as that of CYP2A6. Diethyldithiocarbamate (CYP2E1 inhibitor) inhibited the metabolic activities of CYP2A6 and CYP2C19 in addition to that of CYP2E1. 4. Our results indicated that substrates and inhibitors reported as P450 selective probes are not necessarily specific for individual human P450 forms. These results may provide useful information regarding human P450 substrates and inhibitors in vitro using human liver microsomal samples.

Blotting, Western↗

PubMed1996

Human liver microsomal diazepam metabolism using cDNA-expressed cytochrome P450s: role of CYP2B6, 2C19 and the 3A subfamily.

1. We have examined the metabolism of diazepam by ten human cytochrome P450 forms (CYP1A2, 2A6, 2B6, 2C8, 2C9, 2C19, 2D6, 2E1, 3A4 and 3A5) expressed in HepG2 cells using a recombinant vaccinia virus system. 2. Among the P450 forms tested, diazepam was significantly demethylated by CYP2B6, 2C9, 2C19, 3A4 and 3A5, with 2C19 exhibiting the highest rate at concentrations < 0.1 mM, and hydroxylated only by the latter three enzymes, with 3A5 being the most active. The N-demethylation activity of diazepam by 2C19 at a concentration of 20 microM was six times of that by 3A4. However, that by 2C9 was detected at only a trace level. 3. CYP2C19, 3A4 and 3A5 of the ten human P450s catalysed the 3-hydroxylation of nordiazepam, and 2B6, the 2C subfamily and the 3A subfamily catalysed the N-demethylation of temazepam. CYP3A4 exhibited the highest activity of nordiazepam 3-hydroxylation and temazepam N-demethylation. 4. Diazepam N-demethylation by human liver microsomes correlated with diazepam 3-hydroxylation, but not S-mephenytoin 4'-hydroxylation. 5. Our results suggest that in the human liver, the metabolism of diazepam to nordiazepam is mediated by CYP3A4, which has been reported as the most abundant P450 form in human liver as well as 2C19, which has been reported as a polymorphic enzyme.

Anti-Anxiety Agents↗

PubMed1996

Inhibition of vascular contraction by intracisternal administration of preproendothelin-1 mRNA antisense oligoDNA in a rat experimental vasospasm model.

To clarify the role of endothelin-1 (ET-1) in the etiology of hemolysate-induced contraction of vessels, the authors introduced antisense oligoDNA for preproendothelin-1 (ppET-1) messenger RNA in a rat model of vasospasm. Phosphorothioate antisense oligoDNAs for ppET-1 were injected into the cisterna magna. Fluorescein isothiocyanate-labeled phosphorothioate antisense oligoDNAs were proven by fluorescence chasing to be incorporated into the vascular wall. Striking inhibitory effects of experimental vasospasm were observed in the basilar artery (BA) in which the oligoDNAs were injected. The vascular contraction was significantly inhibited by oligoDNAs after 20 minutes of hemolysate exposure, which suggested that ET synthesis started approximately 20 minutes after hemolysate stimulation. Expression of ppET-1 in the BA in which the spasm was inhibited was markedly suppressed at the transcription level. The results indicate that ET-1 may play an important role in hemolysate-induced vasoconstriction in rats. In addition, the antisense approach in the cerebrospinal fluid might be a useful tool for preventing cerebral vasospasm.

Animals↗

PubMed1996

Relaxation of human isolated pulmonary arteries by amrinone.

Amrinone, a selective phosphodiesterase III inhibitor, has been developed as a nonglycoside, noncatecholamine agent with positive inotropic effect. In this study, we examined the effect of amrinone on human pulmonary arterial strips in vitro to understand its action on human pulmonary circulation. Amrinone (10(-5)-10(-3) g/ml) caused dose-dependent relaxation of human pulmonary arterial strips precontracted with 60 mM KCl. Preincubation with either meclofenamate (3.1 microM), a cyclooxygenase inhibitor, or L-N(G)-nitroarginine (100 microM), a competitive inhibitor of EDRF/NO, failed to inhibit amrinone-induced pulmonary vasodilation. The cyclic AMP (cAMP) levels in the supernatant of the lung vessel homogenates increased after incubation with amrinone (10(-3) g/ml). These findings indicate that amrinone causes vasodilation of human pulmonary artery in vitro, and suggest a possible role for cAMP in the mechanisms of amrinone-induced pulmonary vasodilation. Because it is suggested that amrinone has not only positive inotropic effect but also pulmonary vasodilative effect in human in this study, we speculate that amrinone could be an useful agent for the treatment of an increase in right heart afterload and consequent pulmonary hypertension and right heart failure after lung resection in human.

Adult↗

PubMed1996

[Effects of subacute hypoxia on alveolar epithelial ion transport in rats].

To study the effects of subacute hypoxia on alveolar epithelial ion transport, alveolar fluid clearance was measured in isolated fluid-filled rat lungs. After instillation of a solution containing about 5% bovine albumin, an increase in alveolar fluid clearance was measured over 2 hours. Alveolar fluid clearance was lower when rats were kept in hypoxic conditions (FiO2 = 0.1) for 48 hours. Neither 10(-5) M amiloride (a Na(+)-channel blocker) nor 10(-3) M ouabain (an inhibitor of Na(+)-K(+)-ATPase) inhibited fluid clearance in the hypoxia group, but they did in the normoxia group. These results indicate that subacute hypoxia may down-regulate both the Na(+)-channl and Na(+)-K(+)-ATPase, and thus decrease the absorption of excess alveolar fluid.

Animals↗

PubMed1996

[Normal CBF values by the ARG method using IMP SPECT: comparison with a conventional microsphere model method].

N-isopropyl-p[123I]iodoamphetamine (IMP) has been used as a flow tracer for SPECT, and measurement of cerebral blood flow (CBF) using IMP has been performed by conventional microsphere model method (MS method). Recently, the ARG method for measuring CBF by using IMP with one SPECT scan and one point blood sampling has been developed. This method was based on two-compartment model. In the present study, normal CBF values were measured in ten male healthy subjects (mean age +/- S.D.: 29.8 +/- 6.01, age range: 23-41) by the ARG and the MS methods. The mean CBF values (+/- S.D.) for the ARG method in which the Vd value was assumed to be 50 ml/ml were 41.7 +/- 9.4, 31.1 +/- 5.0, 40.7 +/- 9.7, 41.5 +/- 10.0, 38.2 +/- 9.2, 39.0 +/- 9.4, 41.9 +/- 10.6, 38.7 +/- 8.0 and 30.0 +/- 7.7 ml/100 ml/min in the cerebellum, pons, thalamus, basal ganglia, frontal, temporal, parietal, occipital lobe cortex and centrum semiovale, respectively. The mean CBF values for the MS method were 46.8 +/- 8.4, 37.5 +/- 5.6, 45.8 +/- 8.6, 46.5 +/- 8.9, 43.7 +/- 8.3, 44.4 +/- 8.7, 46.8 +/- 9.3, 44.3 +/- 7.3 and 36.3 +/- 8.1 ml/100 ml/min, respectively. The mean CBF values in the cerebral cortex region for the ARG method were lower than those previously reported by PET. This would be caused by low first-pass extraction fraction of IMP compared with oxygen-15 labeled water. The mean CBF values for the MS method were higher than those for the ARG method against previous studies. As reasons for this, errors in estimation of the SPECT brain counts at 8 min in the MS method were considered.

Adult↗

PubMed1996

[Two cases of clear cell tumor of the lung].

We report two cases of benign clear cell tumor of the lung, which were found as well-circumscribed lesions on chest X-ray films without any symptoms, and removed surgically. Light microscopy showed proliferation of clear cells filled with glycogen in both cases. Immunohistochemical examination performed in a case suggested that the tumor cells might be associated to a derivation from neural and/or smooth muscle cells, because of positive staining for NSE and SMA. In another case, the tumor formed a necrotic cavity, which could be detected by the preoperative MRI examination. This report might introduce a note of caution for the pathologic and radiographic diversity of this disease.

Adult↗