Endoscopic treatment of gallstone-impacted choledochocele precisely diagnosed by endoscopic ultrasonography.
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Biomedical subjects
Publications and source records attributed to A Itoh.
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BACKGROUND: Genetic control of serum angiotensin I converting enzyme (SACE) levels has been suggested. A study was undertaken to elucidate the role of this polymorphism in sarcoidosis. METHODS: Three hundred and forty one unrelated healthy controls and 103 consecutive patients with sarcoidosis participated in the study. SACE levels and an insertion/deletion (I/D) polymorphism in intron 16 of the ACE gene were studied in each subject and new reference intervals for SACE activity for each genotype were determined. The difference in genotype and allele frequencies between controls and patients was analysed and odds ratios were calculated to estimate the relative risk. RESULTS: A significant association was seen between ACE gene polymorphism and SACE levels in both patients and controls. The new reference intervals for each genotype discriminated abnormal SACE levels in patients more accurately, especially those with genotype II. In women the frequencies of allele I were 0.68 (allele D 0.32) in controls and 0.58 (allele D 0.42) in patients, and the difference between the two female groups was significant (p < 0.05). Thus, an excess of genotype ID or DD was observed in female patients (odds ratio 2.18; 95% confidence interval 1.18 to 4.01; p = 0.01). CONCLUSIONS: These findings suggest that ACE gene polymorphism is associated with SACE levels in both patients with sarcoidosis and controls. ACE gene polymorphism should be further evaluated as a candidate marker for an increased risk of sarcoidosis.
This study was performed in 37 patients with alcohol dependency. The mean age was 46.3 years and mean duration of heavy drinking was 23.8 years. The mean duration of temperance to the initial examination was 21.4 days and that to the second examination was 82.0 days. The results of the test on body sway in patients with alcohol dependency may summarized as follows. In patients with alcohol dependency the length of and the area covered by the body sway were significantly larger than in the normal group (p < 0.05). This significant difference from the normal group disappeared open eyes, but remained with eyes closed (p < 0.05). The Romberg quotients of both the length and the environmental area tended to be larger than the normal group mean (p < 0.05). The oscillation power spectrum obtained with eyes open and that obtained with eyes closed tended to be low at levels below 0.2Hz and high at range of 0.2Hz to 0.5Hz in the right left direction. The power spectrum in the anterior-posterior direction obtained with eyes closed was lower than that in the normal group at levels less than 0.2Hz, and higher than that in the normal group at range of 2.0Hz to 3.0Hz on the first examination. After temperance on the second examination, these significant differences had disappeared at all levels. The results of the present study on ocular movements in patients with alcohol dependency may be summarized as follows. Using the oculomotor test, abnormalities appeared in more than 40% of the test subjects for ETT, OKN, OKAN, VS and lateral gaze nystagmus test. According to the report of Matsuoka in 1979, some head positional nystagmus was noted in about 30% of patients with alcohol dependency. In the present study, the rate of appearance was as low as 8%. Ataxic pursuit, vertical positioning nystagmus, decrease of VS, disturbance of OKN and abnormalities of OKAN were found. These results suggested lesions between the brain stem and cerebellum, especially around the upper and lower vermis of cerebellum. After about 3 months of temperance, each test revealed a tendency towards some improvement, but the disturbance appeared to be fixed in some cases. It was important that some improvement in the oculomotor and the central vestibular system was found after about 3 months temperance. These results are quite promising for treatment and recovery in patients with alcohol dependency.
Intratympanic dexamethasone infusion was performed as a treatment for cochlear-tinnitus and its efficacy was investigated. This is a Steroid Targeting Therapy (STT) for cochlear-tinnitus. The overall effective rate for the 1214 patients with 1466 affected ears was 71%. In this study, cochlear tinnitus was seen frequently in the age group of 50 - 60 years old, a relatively older population. The results of the treatment for tinnitus in different age groups did not show a correlation between age and efficacy rate of treatment. In the investigation of the treatment results with different underlying ear diseases, the efficacy rate was high for tinnitus accompanying chronic otitis media, Ménière's disease, and labyrinth syphilis. The efficacy rate tended to decrease more with longer disease duration. When the mean hearing level and treatment results were evaluated, a high effective rate was found in patients who had mild deafness. The efficacy rate was high in tinnitus of low tone pitch, and low tinnitus with high tone pitch. On the other hand, different degreees of loudness of tinnitus did not correlate with treatment effects. This treatment method is useful as a local therapy for cochlear-tinnitus in an outpatient setting.
Intravascular ultrasound, performed using a 0.018 in guide wire with a 30 MHz ultrasound transducer, allows to study the acute recoil of Palmaz-Schatz stent. This case showed that the acute recoil of the Palmaz-Schatz stent occurs immediately after stent implantation. The analysis of diameter and lumen cross-sectional area at the stent site was performed at different levels of dilatation. A 20% reduction of cross-sectional area was found immediately after stent expansion and balloon deflation.
Women appear to be protected, until the menopause, from the development of coronary artery disease. The incidence of acute myocardial infarction in young women is very low, so there is little information on the etiology, clinical features, and prognosis for such patients. We studied 24 young female patients with acute myocardial infarction (< 50 years) among 2,457 consecutive patients with acute myocardial infarction admitted to the coronary care unit of the National Cardiovascular Center from December 1977 through August 1994. Their clinical features and in-hospital mortality were compared with 100 consecutive young male patients (< 50 years) with acute myocardial infarction. The fraction of patients of age younger than 50 years among all age groups was lower in female than in male acute myocardial infarction patients (5% vs 13%, p < 0.01). The increase of the coronary risk factors, hypercholesterolemia (25% vs 55%, p < 0.05) and cigarette smoking (17% vs 96%, p < 0.05) were less common in women. In female patients, the serum total cholesterol level was lower (195 +/- 50 vs 216 +/- 48 mg/dl, p = 0.06), and the serum high-density lipoprotein cholesterol level was higher (50 +/- 12 vs 39 +/- 12 mg/dl, p < 0.05) than in male patients. Other risk factors did not differ significantly between the two groups. Angiography 1 month after myocardial infarction showed fewer diseased coronary arteries (> 75% stenosis) in female than male patients (0.8 +/- 0.9 vs 1.8 +/- 1.0, p < 0.01), and normal coronary arteries were seen in 35% of female patients (male 6%, p < 0.05). Ten female patients (42%) had obviously non-atherosclerotic causes of acute myocardial infarction: Takayasu aortitis in three patients, coronary embolism in two, acute dissection of the aorta in two, and idiopathic coronary artery dissection, Kawasaki disease, and systemic lupus erythematosus in one each. In contrast, among male patients, only one had coronary embolism (1%). In-hospital mortality was higher in women (17%) than in men (2%, p < 0.05). Young female patients (< 50 years) with acute myocardial infarction have a low incidence of hyperlipidemia and normal coronary arteries or involvement of the left main trunk are more common compared with male patients (< 50 years). Although 42% of female patients had obvious non-atherosclerotic etiology of acute myocardial infarction, the causes varied widely.
To investigate the clinical application of gadolinium diethylenetriaminepentaacetic acid (Gd-DTPA)-enhanced magnetic resonance imaging (MRI) in the management of acute myocardial infarction (AMI), we examined 44 patients with AMI within 1 month after onset. Enhanced images were classified into 4 types: nontransmural (type 1), transmural and homogeneous (type 2), transmural and marginal (type 3), and no enhancement (type 4). Each enhancement pattern was correlated with angiographic and thallium-201 imaging results. The redistribution images of thallium were graded on a 4-point scale from 0 (normal) to 3 (markedly reduced or absent activity). The percentage of the perimeter affected by asynergy was obtained from the left ventriculogram. Peak creatine kinase and the percentage of asynergic perimeter were significantly higher in type 3 than in other type patients. End-diastolic volume index was significantly higher in type 3 than in type 2 patients. Left ventricular ejection fraction was lowest, and end-systolic volume index, thallium-201 score, and incidence of wall thinning on MRI were highest in type 3 patients. Therefore, the transmural and marginal enhancement pattern (type 3) was compatible with extensive myocardial infarction with infarct expansion and less viable myocardium. In the other types, the infarction was small to moderate in size and left ventricular function was well preserved. Thus, Gd-DTPA-enhanced MRI may be useful in the evaluation of left ventricular function and myocardial viability of the infarct region after AMI.
BACKGROUND: Coronary angiography has been used to assess the anatomy of coronary artery and intraluminal pathological changes. However, it has several limitations in its diagnostic quality and sensitivity in the detection of intraluminal details. Angioscopy has enabled coronary artery lumens to be visualized directly and fine intraluminal morphological changes to be detected. The information obtained by angioscopy is expected to provide new insights into the mechanisms and pathophysiology of transluminal coronary angioplasty. METHODS AND RESULTS: Forty-seven patients (39 men and 8 women) with stable angina were enrolled in the present study. Angioscopy was performed before and after angioplasty with a 0.68-mm angioscope with a double-guiding catheter system. The patients who were successfully evaluated by angioscopy were divided into two groups according to the color of the lesion: group 1, mainly yellow; and group 2, white. Angiographic, angioscopic, and clinical parameters in the two groups were compared. Detailed angioscopic findings were obtained in 36 of the 47 patients (77%) before percutaneous transluminal coronary angioplasty (PTCA) and in 24 of the 47 (51%) after PTCA. Yellow plaque were found in 13 of 36 (36%). Age, sex, presence of coronary risk factors, serum cholesterol level, and duration of angina showed no correlation with plaque color. The incidence rates of dissection and thrombi after angioplasty also were not different. Successful dilatation was achieved in 13 of 13 patients (100%) in group 1 and in 21 of 23 (91%) in group 2. The restenosis rate of group 1 was significantly lower than that in group 2 (16.7% versus 57.9%, P < .05). Cox proportional hazards model revealed that plaque color was the independent variable associated with restenosis after PTCA (P = .03). CONCLUSIONS: The restenosis rate after successful balloon angioplasty differs, with the color of the target lesion being significantly higher in patients with solely white plaque. Therefore, angioscopic findings are highly predictive of restenosis.
Tyrosinase is the rate limiting enzyme critically associated with melanin synthesis. The melanosomes are specialized membrane-bound organelles within melanocytic cells in which melanin polymers are ultimately deposited. To determine whether tyrosinase correlates with the number of melanosomes, we examined the relationship between tyrosinase activity, tyrosinase mRNA levels, and the number of melanosomes in B16 murine melanoma cells, using melanogenesis regulatory agents. 12-O-Tetradecanoylphorbol-13-acetate (TPA) or linoleic acid decreased tyrosinase activity, while dibutyryl cyclic adenosine monophosphate (dbcAMP) or palmitic acid increased it. The tyrosinase mRNA levels were not always correlated with tyrosinase activity, i.e., TPA down-regulated, dbcAMP upregulated, while linoleic acid or palmitic acid did not alter the message levels, indicating that fatty acid regulation of melanogenesis was due to post-transcriptional events. The number of melanosomes changed when agents which modulate the tyrosinase gene expression were added, since TPA decreased, dbcAMP increased, and linoleic acid or palmitic acid did not alter their number. These results suggest that the number of melanosomes changed in relation to tyrosinase mRNA level but not to tyrosinase activity in response to melanogenesis regulatory agents.
A total of 14 infrainguinal revascularizations in 11 patients with end-stage renal disease resulting from diabetes mellitus were reviewed. Indications for surgery comprised gangrene or non-healing ulcerations in eight patients (11 limbs), ischaemic rest pain in two (two limbs) and disabling claudication in one (one limb). No graft failures occurred during the period of observation. There were two immediate postoperative deaths, one amputation, and four persistent non-healing foot ulcers. The remaining four patients showed improvement. Six deaths occurred, including two perioperative deaths. Four patients with non-healing ulcers died within 1 year and 10 months after revascularization, but their deaths were not associated with the foot ulcers. The cumulative patient survival rate was 42% at 1 year. Infrainguinal revascularization in patients with end-stage renal disease caused by diabetes mellitus is feasible when meticulous preoperative assessment and careful perioperative management are employed to minimize operative risk.
The regulation of gene expression of glucokinase (GK) and L-type pyruvate kinase (L-PK) in rat liver was investigated and compared with the previously reported regulation of lipogenic enzymes. Experiments were conducted in which the time courses and responses to diet quantity of mRNA concentrations and enzyme activities after refeeding a carbohydrate/protein diet (CP) to food-deprived rats were measured. The effects of dietary nutrients on the gene expression were investigated in rats refed either the CP diet, a carbohydrate diet without protein (C), a protein diet without carbohydrate (P), or a carbohydrate/protein/corn oil diet (CPF). The effects of the CPF diet on the gene expression after insulin treatment to diabetic rats were also investigated. After refeeding the CP diet, GK mRNA concentration and enzyme activity reached maximum levels in 2 h and 16-24 h, respectively, whereas those of L-PK peaked in 16 h and 48 h, respectively, similar timecourse to lipogenic enzymes. Moreover, GK mRNA concentrations were maximal in rats fed 20% of the ad libitum diet intake, and L-PK mRNA concentrations, like lipogenic enzyme mRNA, were maximal in rats fed approximately 50% of ad libitum intake. GK mRNA concentrations were significantly increased in parallel with an increase in plasma insulin and glucose concentrations. GK and L-PK mRNA and enzyme levels in rats fed the C diet were comparably induced to the levels in those fed the CP diet. L-PK mRNA induction by the CP diet was significantly reduced by dietary polyunsaturated fatty acids (CPF diet), whereas the GK mRNA induction was not significantly reduced.(ABSTRACT TRUNCATED AT 250 WORDS)
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BACKGROUND: Beta 2 adrenergic dysfunction may be one of the underlying mechanisms responsible for atopy and bronchial asthma. The gene encoding the human beta 2 adrenergic receptor (beta 2ADR) has recently been isolated and sequenced. In addition, a two allele polymorphism of this receptor gene has been identified in white people. A study was carried out to determine whether this polymorphism is functionally important and has any relation to airways responsiveness, atopy, or asthma. METHODS: The subjects studied were 58 family members of four patients with atopic asthma. Restriction fragment length polymorphism (RFLP) with Ban-I digestion of the beta 2ADR gene was detected by a specific DNA probe with Southern blot analysis. Airways responses to inhaled methacholine and the beta 2 agonist salbutamol, the skin prick test, and serum IgE levels were also examined and correlated to the beta 2ADR gene RFLP. In addition, measurements of cAMP responses to isoproterenol in peripheral mononuclear cells were performed in 22 healthy subjects whose genotype for beta 2ADR was known. RESULTS: A two allele polymorphism (2.3 kb and 2.1 kb) of the beta 2ADR gene was detected in the Japanese population. Family members without allele 2.3 kb (homozygote of allele 2.1 kb) had lower airways responses to inhaled salbutamol than those with allele 2.3 kb. The incidence of asthma was higher in those without allele 2.3 kb than in those with allele 2.3 kb. The beta 2ADR gene RFLP had no relation to airways responses to methacholine and atopic status. cAMP responses in peripheral mononuclear cells of the subjects without allele 2.3 kb tended to be lower than those of the subjects with allele 2.3 kb. CONCLUSIONS: These results suggest that Ban-I RFLP of the beta 2ADR gene may have some association with the airways responses to beta 2 agonists and the incidence of bronchial asthma.
Serum troponin T, a myocardial contractile protein, has been reported to be a sensitive marker for the diagnosis of acute myocardial infarction. However, there have been few reports on its ability to detect coronary reperfusion and to predict left ventricular function in the chronic stage. Twenty two patients (20 males and 2 females, 61 +/- 10 y.o.) with acute myocardial infarction were enrolled in this study. They were divided into 2 groups, one with successful reperfusion (group A: n = 13) and one without reperfusion (Group B: n = 9) and the serial changes of their serum troponin T levels were evaluated. Serum myosin light chain was measured in another group of patients with acute myocardial infarction without history of old myocardial infarction (group C: n = 8). The slope of the logarithm of serum troponin T on a time-value curve was calculated from the time of admission to the first peak within 24 hours of the onset of acute myocardial infarction. The correlation coefficient between the late peak of serum troponin T and the left ventricular ejection fraction in 11 patients with first Q wave acute myocardial infarction was compared with that between the serum myosin light chain peak and the left ventricular ejection fraction in group C. 1) The slope of the logarithm of serum troponin T on the time-value curve in group A was greater than that in group B (0.57 +/- 0.45 vs. 0.22 +/- 0.16) (p < 0.05). 2) There was a good correlation between the late peak level of serum troponin T (78 +/- 10 hours after the onset) and the left ventricular ejection fraction in 11 patients with first Q wave acute myocardial infarction (r = -0.84, p < 0.01), which was similar to that of the serum myosin light chain peak and the left ventricular ejection fraction (r = -0.72, p < 0.05). On the other hand, there was no correlation between the peak level of serum creatine phosphokinase and the left ventricular ejection fraction (r = -0.55, NS). The serum troponin T levels 24, 36, 48 and 60 hours after the onset also correlated well with the left ventricular ejection fraction (r = -0.65, -0.7, -0.65 and -0.89, respectively). We conclude that the serial measurement of serum troponin T in patients with acute myocardial infarction is useful in the evaluation of left ventricular function in the chronic stage and that it is a potential non-invasive predictor of coronary reperfusion.
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201T1C1 SPECT and 123I-MIBG SPECT were performed in two patients with familial amyloid polyneuropathy (FAP). Both patients showed normal accumulation of 201T1C1 and no accumulation of 123I-MIBG in the myocardium at the early and delayed images. These results indicate that the patient with FAP-related myocardial change accompanies sympathetic nerve dysfunction. The dysfunction is supposed to be caused by disturbance of re-uptake of MIBG by the terminal ending of the sympathetic nerve (uptake-1) through the amyloid-deposited connective tissue.
Members of the E2F gene family are transcription factors that have been implicated in the control of genes essential for cell cycle progression. Regulation of E2F function is finely tuned by the retinoblastoma tumor suppressor gene product and a small family of related "pocket proteins," with the participation of a number of cyclins and cyclin-dependent kinases. Perturbations of this regulatory network can lead to oncogenic transformation and, in certain systems, to the loss of the ability to maintain terminal differentiation. We describe here the cloning, structural characterization, and tissue expression pattern of a new member of the E2F family, E2F-5. We show that this protein is highly conserved between human and rat but exhibits considerable divergence from E2F-1, E2F-2, or E2F3. Together with the recently reported E2F-4, E2F-5 defines a new branch of the E2F family. The distribution of E2F-5 mRNA among adult rat tissues and the temporal pattern of its expression during the cell cycle of vascular smooth muscle cells are distinctly different from that of E2F-1. The structural divergence between the two branches of the E2F family may thus reflect participation in different regulatory networks.
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