Limitation of implantation of endovascular stent-graft: case report of a patient with thoracoabdominal aneurysm.
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Aged↗
Biomedical subjects
M Kato
Publications and source records attributed to M Kato.
Effects of spironolactone on exercise capacity and neurohormonal factors in patients with heart failure treated with loop diuretics and angiotensin-converting enzyme inhibitor.
1. Treatment with spironolactone is reported to be useful when combined with loop diuretics and an angiotensin-converting enzyme (ACE) inhibitor in severe congestive heart failure (CHF). However, the effects of the addition of spironolactone on exercise capacity and neurohormonal variables have not been demonstrated. This study determined the effects of additive spironolactone on exercise capacity and neurohormonal factors in patients with mild CHF. 2. Oxygen uptake (VO2), plasma norepinephrine (NE), renin activity (PRA), angiotensin II (AII), aldosterone (ALD), and atrial natriuretic peptide (ANP) were measured at rest and after peak exercise in nine patients with CHF (six idiopathic and three ischemic cardiomyopathy; New York Heart Association (NYHA) classes II and III) who were already taking furosemide (mean 29 +/- 5 mg/day) and enalapril (mean 4.7 +/- 0.8 mg/day). Studies were repeated after 16 weeks of treatment with additive single daily dose of 25 mg of spironolactone. In four of nine patients, the exercise test was repeated after a 4-weeks washout of spironolactone. 3. Treatment with spironolactone caused natriuresis, decreased cardiothoracic ratio in chest X-ray (before vs. after treatment: 53.7 +/- 1.2 vs. 50.7 +/- 1.4%, P < 0.01), and improved NYHA functional class. Peak VO2 (17.1 +/- 1.6 vs. 17.5 +/- 2.2 ml/min/kg, NS) and heart rate and blood pressure responses to exercise were not altered. Resting NE (215 +/- 41 vs. 492 +/- 85 pg/ml, P < 0.01) and resting PRA (8.2 +/- 2.3 vs. 16.2 +/- 4.1 ng/ml/hr, P < 0.01) as well as peak NE (1618 +/- 313 vs. 2712 +/- 374 pg/ml, P < 0.01) and peak PRA (12.8 +/- 3.2 vs. 28.1 +/- 11.8 ng/ml/hr, P = 0.17) were augmented after additive spironolactone. ALD and AII were insignificantly increased, and ANP was insignificantly decreased at peak exercise after spironolactone treatment. Spironolactone washout was associated with a trend of the neurohormones to return toward pretreatment values. 4. In conclusion, chronic additive treatment with spironolactone was associated with neurohormonal activation both at rest and during exercise without changing the exercise capacity of patients with mild CHF who were already on loop diuretics and ACE inhibitor therapy.
Adult↗
Adenomatous hyperplasia with unusual imaging findings at combined helical CT hepatic arteriography and CT during arterial portography.
We examined a patient with a hepatocellular carcinoma and multiple adenomatous hyperplasias in the cirrhotic liver. Helical CT hepatic arteriography (CTA) showed the adenomatous hyperplasias as areas of discrete hypoattenuation, and the combined CT during arterial portography (CTAP) showed corresponding areas of subtle hyperattenuation. Such imaging findings at combined CTA and CTAP were seen in only one patient in a series of more than 80 patients in whom we performed angiographically-assisted CT. We demonstrate these unusual imaging findings of adenomatous hyperplasia in the report.
Adenoma↗
Loss of neurofibromin in the leptomeningeal astroglial heterotopia of NF-1.
Neurofibromin, the protein product of the neurofibromatosis type 1 (NF-1) gene, has important roles in tumor suppression or normal embryogenesis. Cerebellar leptomeningeal astroglial heterotopia (LAH) is a proliferation of heterotopic astroglial cells and fibers in the cerebellar leptomeninges, which is characteristically demonstrated in the NF-1 patients. In this study, neurofibromin expression was investigated in NF-1 and non-NF-1 human tissues, especially in the cerebellum of NF-1 patients. Neurofibromin was found by immunoblotting in the CNS but not in the heart, liver, and kidney. Immunohistochemistry in the normal areas of the brains with NF-1 demonstrated neurofibromin immunoreactivity as did the brains of unaffected controls. Cerebellar LAH showed no neurofibromin immunoreactivity. The results of this study suggest that neurofibromin expression remains unchanged in the nonproliferated region of the CNS of the NF-1 patient but changes occur in the abnormally proliferated region, resulting in cerebellar LAH. Loss of neurofibromin may result in the excessive migration and growth of astrocytes in the early fetal period.
Adolescent↗
Brainstem lesion in Aicardi-Goutières syndrome.
Aicardi-Goutières syndrome is characterized by the calcification of basal ganglia, leukodystrophy, and lymphocytosis in cerebrospinal fluid. No brainstem lesion has been described. We report a Japanese girl who presented with delayed development and microcephalus at early infancy. Magnetic resonance imaging revealed T2-weighted high intensity in the cerebral white matter and brainstem, and nerve conduction velocity was delayed in the central nervous system, indicating that she manifested dysmyelination in the brainstem white matter similar to that in the cerebral white matter.
Basal Ganglia Diseases↗
Increased numbers of CD68 antigen positive dendritic epidermal cells and upregulation of CLA (cutaneous lymphocyte-associated antigen) expression on these cells in various skin diseases.
CD68 is a myelomonocytic marker identified in human dermal macrophages. Although the existence of CD68 + dendritic epidermal cells has been reported, their characteristics have not been well elucidated. Cutaneous lymphocyte-associated antigen (CLA) is a homing receptor of cutaneous inflammatory T cells. Our recent report suggested that CLA was a homing molecule of CD1a+ Langerhans cells (LC) in the skin. In the present study we tested whether CD68 and CLA+ dendritic epidermal cells were present in skin specimens of normal skin and diseased skin such as lichen planus (LP), psoriasis vulgaris (PS), discoid lupus erythematosus (DLE), basal cell epithelioma (BCE), squamous cell carcinoma (SCC), irritated seborrheic keratosis (iSK), and Bowen's disease (BD). CD68+ dendritic epidermal cells were identified in normal skin and consisted of half the population of CD1a+ LC. These data indicate that CD68+ dendritic epidermal cells constitute a subpopulation of CD1a+ LC. CLA was expressed on a small percentage of CD68+ dendritic epidermal cells in normal skin. A remarkably increased number of CD68+ dendritic epidermal cells and upregulation of CLA on CD68+ dendritic epidermal cells were observed in diseased skin. The percentage of CLA+ cells among all CD68+ dendritic epidermal cells was less than that of CLA+ cells among all CD1a+ LC in diseased skin. The percentage of CLA+ cells among all CD68+ dendritic dermal cells was much less than that of CLA+ cells among all CD1a+ dendritic dermal cells. In normal skin, the epidermis showed minimal expression of monocyte chemoattractant protein (MCP)-1 and TGF-beta2, and no expression of TGF-beta1. In diseased skin, the epidermis showed elevated, but still moderate immunoreactivity for MCP-1. Slightly enhanced immunoreactivity for TGF-beta2, but not for TGF-beta1, was observed in the epidermis of diseased skin. Increased epidermal MCP-1 immunohistochemical staining was associated with the increased number of CD68 dendritic epidermal cells. These data suggest the possibility that MCP-1 secretion from the epidermis can affect the migration of CD68; Cutaneous lymphocyte-associated antigen; Monocyte chemoattractant protein-1; TAF-beta.
Antigens, CD↗
Interleukin-10 production during and after upper abdominal surgery.
STUDY OBJECTIVE: To evaluate the influence of major abdominal surgery on the plasma levels of interleukin-10 (IL-10). DESIGN: Prospective study. SETTING: University hospital. PATIENTS: 10 ASA physical status I and II patients undergoing upper abdominal surgery. INTERVENTIONS: All patients received combined general-epidural anesthesia with isoflurane and nitrous oxide, after insertion of an epidural catheter at T8-T9 dosed with 1.5% lidocaine. MEASUREMENTS AND MAIN RESULTS: Plasma interleukin-6 (IL-6), interleukin-8 (IL-8), and IL-10 levels were determined with an enzyme-linked immunosorbent assay at preanesthesia, 0, 2, and 4 hours during surgery, and at the end of surgery, followed by sampling on the morning of postoperative days 1 (POD1) and 3 (POD3). Before anesthesia and at 0 hours of surgery, IL-10 was not detected. In all ten patients, the plasma levels of IL-10 showed significant elevations and achieved their maximal value 4 hours after the skin incision (p < 0.05 vs. baseline). The plasma IL-10 levels returned to preanesthesia levels on POD3. The plasma levels of IL-6 and IL-8 also increased in the perioperative period. The peak cytokine levels correlated (r = 0. 915, p = 0.0001 for IL-6 vs. IL-8; r = 0.82, p = 0.025 for IL-6 vs. IL-10; and r = 0.641, p = 0.06 for IL-8 vs. IL-10). The peak plasma IL-10 levels significantly correlated with the amount of intraoperative blood loss (r = 0.69, p < 0.05). CONCLUSIONS: In patients undergoing major abdominal surgery, plasma IL-10 levels were elevated during and after operation. IL-10 may modulate the inflammatory responses in the perioperative period.
Abdomen↗
Syntheses and preventive effects of analogues related to 1alpha,25-dihydroxy-2beta-(3-hydroxypropoxy)vitamin D3 (ED-71) on bone mineral loss in ovariectomized rats.
Analogues related to 1alpha,25-dihydroxy-2beta-(3-hydroxypropoxy)vitamin D3 (ED-71) (2), 26,27-dimethyl ED-71 (3) and 26,27-diethyl ED-71 (4), were synthesized from lithocholic acid (5). In the study of the preventive effects of these analogues and ED-71 (2) on bone mineral loss in ovariectomized rats, 26,27-dimethyl ED-71 (3) showed the most potent activity.
Animals↗
Antiangiogenic agent (TNP-470) inhibition of ectopic bone formation induced by bone morphogenetic protein-2.
Bone morphogenetic protein (BMP) is a potent inducer of ectopic bone formation, and TNP-470, a synthetic analog of fumagillin, is an antiangiogenic agent that strongly inhibits neovascular formation in vivo. We investigated the effects of TNP-470 on BMP-induced ectopic bone formation to clarify the role of angiogenesis in bone formation. Collagen pellets containing recombinant human BMP-2 (rhBMP-2) were implanted beneath the fasciae of dorsal muscles in mice. By daily subcutaneous administration of TNP-470, ectopic new bone formation was inhibited in a dose-dependent manner. Histological examination revealed that TNP-470 prevented proliferation of mesenchymal cells and chondrogenesis at the initial step of endochondral bone formation. Immunohistochemical staining with a specific antibody against bone morphogenetic protein type IA receptor showed that TNP-470 reduced the number of receptor-positive cells surrounding the BMP pellets. The inhibitory effect of TNP-470 on bone formation continued during the period of its administration, and discontinuation of treatment was followed by the resumption of the whole process of endochondral bone formation. This study showed that TNP-470 reversibly inhibits the biological activity of rhBMP-2 in the early stage of bone induction, suggesting that angiogenesis may play an essential role in the recruitment of BMP-receptor-positive cells that can respond to rhBMP-2 and differentiate into chondrocytes and/or osteoblasts.
Animals↗
Distinct and overlapping patterns of localization of bone morphogenetic protein (BMP) family members and a BMP type II receptor during fracture healing in rats.
Bone morphogenetic proteins (BMPs) and their receptors (BMPRs) are thought to play an important role in bone morphogenesis. The purpose of this study was to determine the locations of BMP-2/-4, osteogenic protein-1 (OP-1, also termed BMP-7), and BMP type II receptor (BMPR-II) during rat fracture healing by immunostaining, and thereby elucidate the possible roles of the BMPs and BMPR-II in intramembranous ossification and endochondral ossification. In the early stage of fracture repair, the expression of BMP-2/-4 and OP-1 was strongly induced in the thickened periosteum near the fracture ends, and coincided with an enhanced expression of BMPR-II. On day 7 after fracture, staining for BMP-2/-4 and OP-1 immunostaining was increased in various types of chondrocytes, and was strong in fibroblast-like spindle cells and proliferating chondrocytes in endochondral bone. On day 14 after fracture, staining with OP-1 antibody disappeared in proliferating and mature chondrocytes, while BMP-2/-4 staining continued in various types of chondrocytes until the late stage. In the newly formed trabecular bone, BMP-2/-4 and OP-1 were present at various levels. BMPR-II was actively expressed in both intramembranous ossification and endochondral ossification. Additionally, immunostaining for BMP-2/-4 and OP-1 was observed in multinucleated osteoclast-like cells on the newly formed trabecular bone, along with BMPR-II. In reference to our previous study of BMP type I receptors (BMPR-IA and BMPR-IB), BMPR-II was found to be co-localized with BMPR-IA and BMPR-IB. BMP-2/-4 and OP-1 antibodies exhibited distinct and overlapping immunostaining patterns during fracture repair. OP-1 may act predominantly in the initial phase of endochondral ossification, while BMP-2/-4 acts throughout this process. Thus, these findings suggested that BMPs acting through their BMP receptors may play major roles in modulating the sequential events leading to bone formation.
Animals↗
Oral supplementation with branched-chain amino acids improves survival rate of rats with carbon tetrachloride-induced liver cirrhosis.
We investigated whether supplementation with branched-chain amino acids (BCAA) improves survival of rats with carbon tetrachloride (CCl4) -induced cirrhosis. Liver cirrhosis was induced in 40 male Sprague-Dawley rats by administering CCl4 for 15 weeks. Twenty rats each were then assigned to the control and BCAA group and fed a casein diet or a BCAA-supplemented casein diet, respectively, for an additional 17 weeks with repeated injections of CCl4. No significant difference occurred in either mean energy or nitrogen intake or in body or liver weight between the two groups. BCAA-supplementation significantly preserved plasma albumin concentrations (P < 0.05) and inhibited significantly the occurrence of ascites and hyperammonemia (P < 0.05). The survival rate was significantly higher in the BCAA group (P=0.03), while no significant difference was found in liver histology between the groups. These results suggest that BCAA improved survival of rats with CCl4-induced cirrhosis by preventing hypoalbuminemia and hyperammonemia without directly reducing hepatic necrosis and fibrosis.
Administration, Oral↗
Response of human insulinoma cells to extracellular calcium is different from normal B cells.
The preoperative determination of the localization of a small insulinoma is sometimes difficult using routine imaging techniques. We have used the selective arterial calcium injection (SACI) test to determine the location of the tumor preoperatively. The pathophysiologic basis of the SACI test is based on the responsiveness of insulinomas to calcium injected into the feeding artery. In this study, we demonstrated the in vitro response of the insulinoma cells to the extracellular calcium challenge by using primary-cultured insulinoma cells. Human insulinoma cells were obtained from three patients. MIN6 cells (normal pancreatic B cells) were used as a control; their insulin response to various stimuli resembles that of normal B cells. The insulin secretory dynamics in response to extracellular calcium were observed using a perfusion system. Second, the change of the concentration of cytosolic free calcium ([Ca2+]i) was monitored by fluorometry using fura-2/AM. When the concentration of extracellular calcium ([Ca2+]o) was changed from 2.54 mM to 10 mM, insulin secretion from the insulinoma cells was markedly increased within 6 min (10- to 18-fold at maximum), and rapidly returned to the basal level; at the same time, [Ca2+]i was immediately elevated and reached a peak within 1 min. In contrast, in the MIN6 cells, the insulin secretion and [Ca2+]i were not significantly changed when [Ca2+]o was switched to 10 mM. The results of these in vitro experiments agreed with the clinical results of the SACI test. The positive response of the insulinoma to the SACI test is probably due to the different response of insulinoma cells to the extracellular calcium challenge compared with normal B cells. The role of [Ca2+]i may be important in the mechanism underlying the SACI test.
Animals↗
Physiological degradation converts the soluble syndecan-1 ectodomain from an inhibitor to a potent activator of FGF-2.
The activity of fibroblast growth factor 2 (FGF-2) is stringently controlled. Inactive in undisturbed tissues, it is activated during injury and is critical for tissue repair. We find that this control can be imposed by the soluble syndecan-1 ectodomain, a heparan sulfate proteoglycan shed from cell surfaces into wound fluids. The ectodomain potently inhibits heparin-mediated FGF-2 mitogenicity because of the poorly sulfated domains in its heparin sulfate chains. Degradation of these regions by platelet heparanase produces heparin-like heparin sulfate fragments that markedly activate FGF-2 mitogenicity and are found in wound fluids. These results establish a novel physiological control for FGF-2 and suggest new ways to modulate FGF activity.
Binding Sites↗
Preparation and evaluation of new Pirkle type chiral stationary phases with long alkyl chains for the separation of amino acid enantiomers derivatized with NBD-F.
In order to improve the high-performance liquid chromatographic separation of alpha-amino acids derivatized with the fluorogenic reagent 4-fluoro-7-nitro-2,1,3-benzoxadiazole (NBD-F) on commercially available chiral stationary phases (CSPs) such as SUMICHIRAL OA-2500(S) (CSP 1) and OA-4700 (CSP 3), the preparation of two new CSPs (CSP 2 and CSP 4) having 11-aminoundecanoic acid between the aminopropyl silica gel support and the chiral moiety in CSP 1 and CSP 3 is described. CSP 2 and CSP 4 improved both the mutual and enantiomeric separation of NBD-amino acids compared with CSP 1 and CSP 3. Thus, 17 pairs of NBD-amino acid enantiomers and NBD-glycine were separated on CSP 2 except for six NBD-amino acids (D-Asn, D-Ser, D-Gln, L-Pro, L-Ser and Gly). CSP 2 and CSP 4 also showed better enantiomeric separation of NBD-amino acid esters and amides than CSP 1 and CSP 3. It was considered that the achiral long alkyl chains in the CSPs might form a hydrophobic space which assisted the stereoselective interaction of analytes with the chiral moiety by changing the environment around the chiral moiety. On CSP 1 and CSP 2, NBD-beta-amino acid was also enantiomerically separated.
4-Chloro-7-nitrobenzofurazan↗
Elevated soluble Fas levels in herpes zoster patients.
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Adult↗
Elevated soluble Fas levels in herpes zoster patients.
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Adult↗
Inhaled procaterol inhibits histamine-induced airflow obstruction and microvascular leakage in guinea-pig airways with allergic inflammation.
BACKGROUND: Beta2-adrenoceptor agonists (beta2-agonists) are shown to inhibit airway microvascular leakage in experimental animals. This effect may change in animals with chronic airway inflammation. OBJECTIVE: We examined whether inhaled beta2-agonists inhibit microvascular leakage in guinea-pig airways with chronic allergic inflammation. METHODS: Three weeks after the sensitization with ovalbumin (OA; 6 mg/mL), each guinea pig was challenged with inhaled OA once a day for 1 or 3 weeks. Control animals without sensitization with OA also inhaled vehicle for OA (saline) for 3 weeks. One day after the last challenge, different doses of inhaled procaterol (1, 3 or 10 microg/mL) or vehicle was given to animals for 10 min after an anaesthesia. Fifteen minutes after the end of inhalation, the animals were given i.v. Evans blue dye (EB dye; 20 mg/kg), a marker of microvascular leakage, and then i.v. histamine (3 or 30 microg/kg) or vehicle. Lung resistance, a parameter of airflow obstruction, was measured for 6 min and the lungs were removed to calculate the amount of extravasated EB dye into the airways. RESULTS: A significant increase in eosinophil infiltration into the airways was seen in sensitized and challenged animals compared with control animals without sensitization. Among animals receiving antigenic exposure for either 0 (control), 1 or 3 weeks, 10 microg/mL procaterol significantly inhibited 30 microg/kg histamine-induced increase in EB dye extravasation to a similar degree (ranged from 28.7 to 69.8% inhibition) as well as that in lung resistance (more than 90% inhibition in all groups). The minimal dose of procaterol to inhibit 3 microg/kg histamine-induced microvascular leakage was not different between nonsensitized control animals and those sensitized and challenged for 3 weeks at all airway levels. CONCLUSION: Inhaled beta2-adrenoceptor agonists may be also potent in attenuating microvascular leakage even in the airways with chronic allergic inflammation.
Administration, Inhalation↗
Identification of receptors and Smad proteins involved in activin signalling in a human epidermal keratinocyte cell line.
BACKGROUND: Activin A is a multifunctional protein, which is a member of the transforming growth factor-beta (TGF-beta) superfamily. Smad proteins have recently been shown to transduce signals for the TGF-beta superfamily of proteins, and Smad2 was implicated in activin signalling in Xenopus embryos. RESULTS: We identified the receptors and Smad proteins activated by activin A in a human epidermal keratinocyte cell line, HaCaT. The major activin receptors expressed on HaCaT cells were activin type II receptor (ActR-II) and activin type IB receptor (ActR-IB). We have also shown that in HaCaT cells, activin A induced the phosphorylation of Smad3 and, to a lesser extent, of Smad2. On the other hand, TGF-beta induced an efficient phosphorylation of both Smad2 and Smad3. Activin A preferentially induced the nuclear translocation of Smad3 in HaCaT cells, whereas TGF-beta strongly induced the nuclear translocation of Smad2, as well as other Smads. Moreover, a constitutively active form of ActR-IB efficiently stimulated the formation of a heteromeric complex between Smad3 and Smad4 in COS cells transfected with Smad cDNAs. CONCLUSIONS: These results suggest that activin A binds to a receptor complex of ActR-II and ActR-IB, and preferentially activates Smad3 in HaCaT human keratinocytes.
Activin Receptors↗