Combined abnormalities of semilunar valves: quadricuspid pulmonary and bicuspid aortic valves.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to N Yamada.
Explore the source record for details and available documents.
BACKGROUND: Although the incidence of acute pulmonary thromboembolism (APTE) has been increasing in Japan, patient characteristics, management strategies, and outcome have not yet been assessed in large series. HYPOTHESIS: The present study was designed to investigate the current status of APTE in Japan. METHODS: Of a total of 533 registry patients with pulmonary thromboembolism, 309 with APTE were analyzed with respect to clinical symptoms and signs, predisposing factors, diagnostic procedures, estimation of deep venous thrombosis, treatment, and clinical course. RESULTS: Main risk factors were recent major surgery, cancer, prolonged immobilization, and obesity; only a few patients had coagulopathy and 36% were in cardiogenic shock at presentation. The majority of registry patients underwent lung scans or pulmonary angiography; 30% were diagnosed only by lung scanning. Venous ultrasonography was used in only 34 patients, while 188 patients underwent at least one diagnostic procedure for deep venous thrombosis. Thrombolysis was more frequently performed in patients with cardiogenic shock, and only a few patients received thromboembolectomy. In-hospital mortality rate was 14%. In patients with cardiogenic shock, the mortality rate was reduced by thrombolysis. The predictors of in-hospital mortality were male gender, cardiogenic shock, cancer, and prolonged immobilization. CONCLUSIONS: The patients in this registry had almost the same findings as those in Western patients, except for some points that had the possibility of demonstrating a difference between Westerners and Japanese in the development of APTE. These results can prove especially helpful in planning prospective, randomized trials that will clarify the impact of widely used treatment modalities on the outcome of patients with APTE.
A three-dimensional laser scanner enables the measurement of surface data from objects with no contact, both quickly and in three dimensions. A 40-year-old woman with a right breast cancer had undergone a simple mastectomy. The surface of the chest was then measured with the non-contact three-dimensional laser scanner. Using the mirror image of data obtained by the same system, a mask-like model of the breast was made using laser lithography technology. This model was used for reconstruction of the breast after mastectomy. It was effective in determining the position and form of the breast which was to be repaired.
Voluntary arm movements frequently perturb body equilibrium in an upright posture. The motions of leg joints need to be coordinated according to the properties of voluntary arm movements in order to maintain body equilibrium, and this may cause a change in postural pattern. The purpose of this study was to determine whether the kinematic pattern generation of upright posture is influenced by a change in the swinging frequency of arm movements and whether the pattern generation is correlated with a change in joint torque about the shoulder joint. Four male subjects in an upright posture were instructed to swing their arms at seven different frequencies, determined by the maximum swinging frequency of each subject (35%max, 40-60%max, 65%max). Segment rotations around the shoulder, hip, and ankle joints were analyzed at kinematic and kinetic levels. The results of kinematic analysis indicated that tight coupling between motions of the shoulder and hip joints was generated in lower-frequency trials (under 40-45%max), whereas tight coupling between motions of the shoulder and ankle joints was generated in higher frequency trials (more than 40-45%max). Furthermore, the results of kinetic analysis revealed that changes in the joint torque patterns about the shoulder and hip joints occurred in trials at 40-45%max. The mean value of 40-45%max was close to the eigenfrequency of each subject's arm. We concluded that (1) postural patterns associated with a gradual change in the swinging frequency of the arms can be divided into two coordination modes (a hip-shoulder in-phase mode and an ankle-shoulder in-phase mode), and (2) these two patterns may be divided by the eigenfrequency of the arm.
Sizable glomus tumors with cystic changes in the ankle are extremely uncommon. This paper describes painless glomus tumors with cystic changes arising in the ankle of a 22-year-old woman. At the age of 14, a painless mass was noticed on the lateral side of the left ankle, and at age 21, another mass appeared on the medial side of the same ankle. Magnetic resonance imaging (MRI) and computed tomography (CT) scanning revealed 4.5 x 4.0 cm and 2.0 x 2.0 cm sized masses on the medial side and a 3.0 x 4.0 cm sized cystic mass on the lateral side of the ankle. The tumors were removed en bloc. Microscopically, the tumor consisted of perivascularly arranged cells with punched-out, round, and regular nuclei. Immunohistochemically, the tumor cells expressed SMA and HHF-35, indicating smooth muscle cell characters. The patient had no recurrence at 2 years after surgery.
BACKGROUND: This study was designed to compare genetic differences in single-nucleotide polymorphisms of the S-mephenytoin 4'-hydroxylation (CYP2C19) gene among four Asian populations. METHODS: Polymerase chain reaction with restriction fragment length polymorphism (PCR-RFLP) analysis of CYP2C19 was conducted in Japanese, Chinese, Thai, and Vietnamese populations. All genotype frequencies were analyzed. Wild-type homozygote and wild-type heterozygote genotypes were extensive proton pump inhibitor (PPI) metabolizers. Mutant-type heterozygote and mutant-type homozygote genotypes were poor PPI metabolizers. RESULTS: No significant differences in CYP2C19 phenotype, calculated based on genotype frequencies, (P > 0.05) were found among the four populations. CONCLUSIONS: Many factors, including CYP2C19 polymorphisms, affect the success rate of Helicobacterpylori eradication with PPI-based therapy. We suspect that CYP2C19 polymorphisms may not be the main factor associated with differences among these four Asian populations in the success rates of H. pylori eradication with PPI-based therapy.
It has recently been proposed that gastrointestinal stromal tumors (GISTs) originate from stem cells that differentiate toward a phenotype of interstitial cells of Cajal (ICCs). Nestin is a newly identified intermediate filament protein, and is predominantly expressed in immature cells, such as neuroectodermal stem cells and skeletal muscle progenitor cells, and tumors originating from these cells. In this study, we examined, using immunohistochemistry, the nestin expression in GISTs and ICCs to clarify the origin of GISTs. Strong immunoreactivity for nestin was observed in all 18 GISTs, and its expression was confirmed by Western blot and Northern blot analyses. In contrast, three leiomyomas and a schwannoma that developed in the gastrointestinal tract showed no apparent immunoreactivity for nestin. Among 17 mesenchymal tumors (seven leiomyosarcomas, five malignant peripheral nerve sheath tumors, and five fibrosarcomas) that occurred in sites other than the gastrointestinal tract, only two malignant peripheral nerve sheath tumors were moderately immunoreactive for nestin. Furthermore, with fluorescence double immunostaining of the normal small intestine, nestin expression was demonstrated in ICCs. These results show that nestin may be a useful marker for diagnosis of GISTs, and support the current hypothesis that GISTs are tumors of stem cells that differentiate toward an ICC phenotype.
Resection of a saccular aneurysm that developed in a remnant of aorta in a patient with Marfan's syndrome, who previously underwent aortic aneurysmectomy, is described. The intercostal arteries were reconstructed end-to-end using small-caliber interposition grafts to the aortic prosthesis. Preoperative magnetic resonance angiography identified the artery of Adamkiewicz and facilitated its preservation.
A double-blind, placebo-controlled, parallel-group study was performed to determine whether atorvastatin, a new HMG-CoA reductase inhibitor, could effectively and safely reduce plasma LDL-cholesterol concentrations in Japanese patients with type-2 diabetes without influencing glycemic control. The subjects were patients with hypercholesterolemia (serum cholesterol concentration > or =5.7 mmol/l (220 mg/dl)) and stable glycemic control. The fasting concentrations of hemoglobin A(1C) (HbA(1C)), fructosamine, and 1,5-anhydroglucitol (1,5-AG) were measured as indices of glycemic control. Plasma lipid concentrations and the safety of the drug were also examined. Forty eligible patients in two groups of 20 each were administered atorvastatin (10 mg/day) or placebo. Neither atorvastatin nor placebo caused a significant change in HbA(1C), fructosamine, or 1,5-AG concentrations. Atorvastatin significantly reduced total cholesterol and LDL-cholesterol concentrations from baseline by 29.7% (p<0.0001) and 41.6% (p<0.0001), respectively. The incidence of clinical adverse events and that of abnormal changes in laboratory test values did not differ between the two groups. In this trial, atorvastatin effectively and safely reduced LDL-cholesterol concentrations in diabetic patients with hypercholesterolemia without influencing glycemic control. These findings are clinically important because there are many diabetic patients with hypercholesterolemia and such patients have a high risk of developing arteriosclerotic disease.
In order to determine the contribution of the low density lipoprotein receptor (LDL-R) to the removal of apoB-containing native lipoproteins by macrophages, we compared the uptake of beta-VLDL in peritoneal macrophages (MPM) from wild type mice and mice lacking the LDL-R. The d<1.006 g/ml lipoproteins obtained from apoE deficient mice fed a high fat diet were poorly degraded by macrophages and caused only a slight formation of CE in macrophages from both types of mice. On the other hand, d<1.006 g/ml lipoproteins obtained from LDL-R deficient mice fed a high fat diet, beta-VLDL with apoE, were avidly taken up by and markedly stimulated CE formation in wild type macrophages, but not in macrophages lacking the LDL-R. The degradation of 125I-labeled-apoE-containing beta-VLDL by wild type MPM was poorly inhibited by unlabeled human LDL, and beta-VLDL without apoE had no effects. In conclusion, we propose that the in vitro uptake of native apoE-enriched lipoproteins by murine macrophages is primarily mediated by the LDL receptor and not by other apoE-recognizing receptor systems such as: the LDL receptor related protein, the VLDL receptor or the triglyceride-rich lipoprotein receptor.
Explore the source record for details and available documents.
Tympanosclerosis is a condition leading to a calcification process in the middle ear, and often develops after chronic inflammation of the middle ear. Since osteopontin (OPN) has been shown to participate in the pathological calcification, we here investigated whether OPN is involved in the process of calcification in tympanosclerosis. The tympanic membrane and middle ear mucosa, obtained from patients of tympanosclerosis and chronic otitis media, were histologically classified depending on the calcification degree. In hyalinized tissues with macroscopic calcification and fibrous tissues with microscopic calcification, OPN was immunohistochemically found in the calcification sites. In inflammatory tissues with microscopic calcification, OPN was also found in the calcifying foci, and many OPN mRNA-expressing cells, determined by in situ hybridization, located around their foci. Moreover, immunohistochemical double staining of OPN and CD68 showed that the OPN-expressing cells were CD68-positive, indicating these cells were macrophages. In inflammatory tissues without calcification, immunohistochemistry of CD68 and in situ hybridization of OPN mRNA revealed that most OPN mRNA-expressing cells were CD68-positive. The expression of OPN mRNA in inflammatory tissues was also shown by reverse transcriptase polymerase chain reaction. These results suggest that OPN secreted by exudate macrophages might be an important regulator in the calcification of tympanosclerosis.
We have previously reported an important excitatory role of the perirhinal cortex (PRC) in rat kindling development using an immunohistochemistry technique. In this study, we investigated the roles of the PRC and the insular cortex (INS) located rostral to the PRC, in fully-kindled amygdaloid seizures, using a microinjection technique in the rat kindling model of epilepsy. Following the establishment of daily kindling, we investigated the effects of microinjections of procaine hydrochloride, 2-amino-5-phosphonovalerate (APV; an N-methyl-D-aspartate (NMDA) receptor antagonist) and 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(f)-quinoxaline (NBQX; an alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid (AMPA) receptor antagonist). Microinjections of these drugs into the ipsilateral PRC did not suppress kindled seizures. The possibility is that the process of kindling development forms novel seizure-generalization pathways that do not require further activation of the PRC. On the other hand, procaine and APV injected into the ipsilateral INS significantly suppressed kindled seizures. The manner of suppression appeared to be 'all or none'. It is therefore possible that at least the activation of NMDA receptors in the INS is necessary to express generalized kindled amygdaloid seizures.
Insulin resistance and hyperinsulinemia are common pathophysiological features of several metabolic diseases, obesity and diabetes being two notable examples. In this article we review how the use of animal models has increased our understanding of insulin resistance and hyperinsulinemia, with a particular emphasis on the use of mice with targeted disruptions of the insulin signaling pathway.
Deficiency of leptin or its receptor produces hyperinsulinemia with marked obesity. Paradoxically, severe insulin resistance also accompanies lipodystrophy. Animal models of these contrasting conditions have enabled us to observe the profound and complicated aspects of the underlying pathologies. In addition, conventional polygenic rodents with known genetic backgrounds, such as the spontaneously hypertensive rat and the Goto-Kakisaki rat, have also been used to investigate these abnormalities.
The acyl-CoA:cholesterol acyltransferase (ACAT) enzyme is thought to be responsible for foam cell formation and the subsequent progression of atherosclerosis. The apolipoprotein E and low density lipoprotein receptor double knockout (apoE/LDLr-DKO) mouse is an animal model that develops severe hyperlipidaemia and atherosclerosis. Here we have examined the effect of oral administration of an ACAT inhibitor, F-1394, on atherosclerosis in apoE/LDLr-DKO mice fed a regular chow diet. In en face analysis, a dose of 10, 30, or 100 mg kg(-1) day(-1) F-1394 for 10 weeks reduced the extent of lesions visible in the aorta by 24, 28 and 38%, respectively, as detected by staining with oil red O, without affecting serum cholesterol level in these mice. At the highest dose 100 mg kg(-1) day(-1) of F-1394, the reduction was statistically significant. For quantitative analysis of the cellular and non-cellular components comprising the lesions at the aortic sinus, the effects of an oral dose of 100 mg kg(-1) day(-1) F-1394 for 15 weeks were studied. There was a significant reduction (31.9%) in the oil-red O-stained area in cross-sections of the aortic sinus. In addition, the neointimal area, as well as levels of ACAT-1 protein tended to be decreased (15.2 and 25.8%, respectively, not significant). However, the areas containing macrophages, smooth muscle cells, and collagen were not affected by F-1394. In vitro, F-1394 attenuated foam cell formation in mouse peritoneal macrophages. These results indicate that ACAT may be primarily responsible for lipid accumulation in atherosclerotic lesions, and that its inhibition diminishes the lipid deposition via a direct effect on macrophages in the arterial wall.
Gene manipulation in order to artificially express a particular gene in neurons in the central nervous system is a powerful tool for the analysis of brain function. Sindbis viral vectors have been developed to express high levels of foreign genes in postmitotic brain neurons with little transfection of glial cells. In this study, we expressed the gene encoding the unedited GluR2 (GluR-B) subunit of the AMPA-type glutamate receptor that forms inwardly rectifying and Ca2+-permeable channels, in rat CA1 hippocampal neurons in slice cultures using Sindbis viral vectors. The pyramidal cell layer of the CA1 region was injected with recombinant Sindbis viruses encoding both enhanced green fluorescent protein (GFP) and unedited GluR2. The GFP fluorescence from CA1 neurons could be detected as early as 6 h and reached a maximal level about 48 h postinfection. The inwardly rectifying and Ca2+-permeable AMPA receptors were expressed in most CA1 pyramidal cells expressing GFP. These AMPA receptors expressed by gene transfer were involved in fast excitatory neurotransmission elicited by electrical stimulation of the Schaffer collaterals in the stratum radiatum. Tetanic stimulation of Schaffer collaterals induced NMDA receptor-independent, long-term potentiation due to Ca2+ influx through the newly expressed AMPA receptors in the area densely stained with GFP. Thus, the combined use of Sindbis viral vectors with the GFP reporter allowed physiological examination of the roles of a specific gene product in synaptic function in well-characterized brain neurons.
To clarify the mechanism of vascular invasion (VI) and capsular invasion (CI) in thyroid follicular carcinoma (FC), 3-D reconstruction of tumor tissues, vessels and capsules was performed from serial sections in five FC and three follicular adenomas (FA). Outflow veins in the lesions were well developed under the capsule, narrowed just beneath the capsule, and dilated within the capsule. Both VI and CI were observed at the poststenotic intracapsular dilated part of outflow veins. The tumor tissue extended along the intracapsular horizontal veins which flowed in parallel with the capsule in VI, or along the vertical veins which directly flowed outside the capsule in CI. There was tumor tissue in the subendothelial layer of the outflow veins within the capsule. Intravascular tumor nests and nodular lesions within the capsule continued from the main tumors. It can be concluded from these results that most VI and CI may not be true invasions but pre-invasive lesions.