[Management of congenital mediastinal cysts: especially for mediastinal bronchogenic cyst].
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Biomedical subjects
Publications and source records attributed to S Tanaka.
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STUDY OBJECTIVES: Circadian rhythmicity of cysteinyl leukotrienes (LTs) and thromboxane (TX)-A(2) in healthy subjects and nocturnal asthmatic patients remains a subject of controversy. The aim of this study was to investigate the contribution of these mediators to the pathogenesis of nocturnal asthma. METHODS: We measured peak expiratory flow rate, urinary concentration of LTE(4), 11-dehydro-TXB(2), and creatinine eight times every 3 h in three groups: healthy control subjects (n = 5, group A), nocturnal asthmatic patients (n = 9, group B), and nonnocturnal asthmatic subjects (n = 9, group C). To evaluate the reproducibility of the measurement of urinary LTE(4), we measured urinary LTE(4) in group A for 3 separate days. RESULTS: The urinary LTE(4) concentrations from 3 to 6 AM were significantly (p < 0.05) higher than from 3 to 6 PM in both group A and group B, but not in group C. The mean levels of LTE(4) in group B and group C were significantly higher (p < 0.05) than those in group A. In group B, another small peak was observed from 6 to 9 PM. No significant day-to-day variation was observed in group A. Urinary 11-dehydro-TXB(2) values from 3 to 6 AM were significantly (p < 0.001) higher than those levels from 3 to 6 PM in all groups, and the mean levels in group B and group C were significantly higher than those in group A (p < 0.05). CONCLUSIONS: Circadian rhythmicity of urinary LTE(4) with a morning peak was found in healthy control subjects and nocturnal asthmatic subjects, but not in nonnocturnal asthmatic patients. It was suggested that cysteinyl LTs rather than TXA(2) might contribute to the nocturnal worsening of asthma.
We performed a genome-wide quantitative trait locus (QTL) analysis of body weight at 10 weeks of age in a population of 321 intercross offspring from SM/J and A/J mice, progenitor strains of SMXA recombinant inbred strains. Interval mapping revealed two significant QTLs, Bwq3 (body weight QTL3) and Bwq4, on Chromosomes (Chrs) 8 and 18 respectively, and five suggestive QTLs on Chrs 2, 6, 7, 15 and 19. Bwq3 and Bwq4 explained 6% of the phenotypic variance. The SM/J alleles at both QTLs increased body weight, though the SM/J mouse was smaller than the A/J mouse. On the other hand, four of the five suggestive QTLs detected had male-specific effects on body weight and the remainder was female-specific. These suggestive QTLs explained 5-6% of the phenotypic variance and all the SM/J alleles decreased body weight.
The EDS (early-onset diabetes in suncus) colony was developed as a new laboratory colony of the musk shrew and is characterized by a high incidence of early-onset spontaneous non-insulin dependent diabetes mellitus (NIDDM). We examined blood lipid (triglyceride [TG], total cholesterol [TC], phospholipid [PL], free fatty acid [FFA]) and liver lipid (TG, TC, PL) concentrations to investigate the features of lipid metabolism in these animals. All lipid concentrations examined both in blood and liver of the diabetic shrews had a tendency toward higher values than those in non-diabetic shrews. The PL concentration was the only parameter that barely showed a significant difference. Values for all blood lipid concentrations in diabetic shrews at 7-9 months tended to be higher than those of 2-month-old diabetic shrews, although the difference was not significant. These findings indicate that diabetic EDS shrews exhibit a much milder defect of lipid metabolism induced by NIDDM than other rodent models.
The EDS colony, developed as a new laboratory colony of the musk shrew, is characterized by a high incidence of early-onset spontaneous non-insulin dependent diabetes mellitus (NIDDM). In this colony, a few diabetic shrews exhibited a cataract at 1 month after the onset of diabetes, and all diabetic shrews had bilateral cataracts at 5 months after the onset of diabetes. In contrast, cataractous animals were never observed among non-diabetic shrews. These results suggest that the cataract in the EDS colony is a diabetic complication.
Adrenal glands of small smooth-tailed tree shrews (Dendrogale murina), four males and two females, caught and fixed in Thailand were observed macroscopically and histologically. They were located at the cranio-medial sides of the kidney. They were elongated in shape and consisted of a cortex and medulla. The cortex could be subdivided into three zones by the cell arrangement and the morphology of nuclei, cytoplasm and cell strands, like in other mammalian species. The tree shrew seemed to share more morphological characteristics with some laboratory rodents than some of non-human primates.
The presence and possible physiological roles of alpha-melanocyte-stimulating hormone (alpha-MSH) in the peripheral tissues of birds have not been established. By a combination of RT-PCR, immunocytochemistry and in situ hybridization, we have examined alpha-MSH expression in the eye of the chicken during development. In the 1-day-old chick, alpha-MSH was expressed in the retinal pigment epithelial (RPE) cells, and also at a lower level in the cone cells. The melanocortin receptor subtypes, CMC1, CMC4 and CMC5, were expressed in the layers of the choroid and the neural retina, but not in the RPE cells. It is probable that the RPE cells secrete alpha-MSH to exert paracrine effects on the choroid and neural retina. During embryonic development, alpha-MSH immunoreactivity in the RPE cells was initially detected at embryonic day 10, and increased in intensity as development proceeded. No cone cells were stained with anti-alpha-MSH antiserum in any of the embryonic stages tested. The immunoreactivities for two prohormone convertases, PC1 and PC2, were co-localized to the RPE cells with a pattern of staining similar to that of alpha-MSH. Despite containing alpha-MSH immunoreactivity, the RPE cells in 1-day-old chicks expressed no immunoreactivity for the endoproteases. Furthermore, in a 3-day-old chick, pro-opiomelanocortin mRNA was detectable by in situ hybridization only in the photoreceptor layer and not in the RPE cells. These results suggest that the RPE cells and the cone cells are intraocular sources of alpha-MSH in the embryonic and postnatal life of the chicken respectively. Embryonic expression of alpha-MSH in the RPE cells implies a possible role for the peptide in ocular development.
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The voltammetric detection of soybean agglutinin (SBA) was investigated on the basis of an interaction between the lectin and a sugar. Because galactose and lactose combined with SBA, the sugars were labeled by a Schiff base with an electroactive daunomycin. After the labeled sugar and SBA were mixed, measurements were carried out by voltammetry. When SBA-sugar binding occurs, a part of daunomycin of the labeled sugar is taken to the binding sites. As a result, SBA is detected by a change in the peak current of daunomycin, and the SBA-sugar interaction is evaluated. The length of the alkyl chain between daunomycin and the sugar was also considered. The electrode response to the concentration of SBA was linear over the range of 0.04-0.8 microg min(-1). The merits of this procedure are the convenient preparation of labeled sugar and a rapid measurement without separation. On the other hand, the detection of sugar at the 10(-9) mol dm(-3) level was achieved by a competitive reaction to limited binding sites of the lectin between the sugar and the labeled sugar.
Normal-phase HPLC conditions have been developed for separating the C17(3) isoprenoid isomers, which are expected to be formed as biosynthetic intermediates of chlorophyll (Chl) a, Chl a' (C13(2)-epimer of Chl a), pheophytin (Pheo) a and protochlorophyll (PChl). The application of these conditions to pigment composition analysis of greening etiolated barley leaves allowed us to detect, for the first time, the C17(3) isomers of Chl a', a possible constituent of the primary electron donor of photosystem (PS) I, P700, and those of Pheo a, the primary electron acceptor of PS II, in the very early stage of greening. The C17(3) isomer distribution patterns were approximately the same between Chl a and Chl a', but significantly different between Pheo a and Chl a', probably reflecting the similarity and difference, respectively, in the biosynthetic pathways of these pigment pairs.
A capillary electrophoretic method for a high-sensitivity analysis of cyanide has been developed. Cyanide was derivatized with 2,3-naphthalenedialdehyde and taurine to give a fluorescent product of 1-cyanobenz[f]isoindole. This compound was detected with high sensitivity by fluorescence detection. The detection limit was 0.1 ng/mL, and the calibration curve was linear over the range 0.1-200 ng/mL. The precision of the migration time of within-run assays (n = 6) of 1 ng/mL cyanide standard solution was 0.14%. The precision of the peak area for the same runs was 1.0%. This method was applicable to blood analysis. Detection of the cyanide derivative by UV was also examined.
An application of capillary electrophoresis (CE) using sulfated beta-cyclodextrin (SCD) has been investigated for separating alkylphenols with different chain lengths, as well as bisphenol A and bisphenol S. In the absence of SCD in running buffer, all the phenols migrated at the same velocity as the electroosmotic flow (EOF), whereas the addition of SCD effectively led to the baseline separation of alkylphenols on the basis of the difference in the abilities to bind into the hydrophobic cavity of CD. The host-guest binding constants between analyte phenols and SCD were evaluated from Benesi-Hildebrand plots of the data obtained by two independent methods, CE and UV-visible measurements, demonstrating that the greater the hydrophobicity of the phenols, the larger the binding constants. The effects of organic solvents on the resolution for alkylphenols and bisphenols were also examined. This system using SCD was effective for the separation of 4-octylphenol and 4-nonylphenol isomers having longer alkyl chains.
OBJECTIVE: Our objectives were to propose and evaluate a dynamic sonography protocol for the characterization of hepatic tumors. SUBJECTS AND METHODS: The subjects were 107 patients with focal liver lesions that initially had been found on conventional sonograms. The final diagnoses for the lesions were hepatocellular carcinoma in 60 patients, cholangiocellular carcinoma in six, metastatic carcinoma in 24, hemangioma in 10, and focal fat-spared region in seven. The pulse inversion harmonic imaging mode and a galactose-based contrast agent (Levovist) were used. Dynamic sonography was designed to obtain vascular-phase (composed of the arterial phase and the portal phase) images of the focal lesion and liver-parenchymal-phase images of the whole liver in a series obtained after a bolus injection of the contrast agent. RESULTS: If the whole-tumor or mosaic enhancement patterns (arterial phase) and/or the reticular enhancement (parenchymal phase) are regarded as positive findings for hepatocellular carcinoma, the sensitivity, specificity, and positive predictive value of dynamic sonography in our study were 92%, 96%, and 96%, respectively. If a ring enhancement (arterial to portal phase) or a clear defect (parenchymal phase) or both are regarded as positive findings for cholangiocellular carcinoma or metastasis, the sensitivity, specificity, and positive predictive value were 90%, 95%, and 88%, respectively. If puddle enhancement (portal phase) is regarded as a positive finding for hemangioma, the figures for sensitivity, specificity, and positive predictive value were 60%, 100%, and 100%, respectively. Also, the tumors that showed no focal sign in the liver parenchymal phase were all benign lesions, such as hemangiomas or focal fat-spared regions. CONCLUSION: Dynamic sonography in a protocol combining pulse inversion harmonic imaging and an IV bolus injection of the contrast agent proved to be an effective tool in characterizing liver tumors.
OBJECTIVE: To find whether sodium sensitivity of blood pressure appears before hypertension and whether the sensitivity is related to diabetic nephropathy, we examined type 2 diabetic patients with normal levels of serum creatinine. RESEARCH DESIGN AND METHODS: A total of 32 patients were divided into three age-matched groups: 11 patients had normoalbuminuria, 12 had microalbuminuria, and 9 had macroalbuminuria. Patients stayed on a diet with ordinary sodium levels for 1 week and a sodium-restricted diet for 1 week, in random order. Urinary excretion of sodium and albumin and systemic blood pressure were measured daily. A pressure-natriuresis curve was drawn by linkage of the two datum points obtained in the steady state during the different diets. We calculated the sodium sensitivity index as the reciprocal of the slope of this curve. RESULTS: The median sodium sensitivity index and the mean blood pressure were higher in micro- and macroalbuminuric patients than in normoalbuminuric patients. Eighteen patients were without hypertension (<140/90 mmHg); of these, 10 had blood pressure readings <130/85 mmHg with ordinary sodium levels. Urinary albumin was correlated with the index but not with blood pressure. For these 10 patients, the index in those with albuminuria was higher than in those with normoalbuminuria. In such patients with albuminuria, sodium restriction decreased albuminuria and blood pressure. CONCLUSIONS: In type 2 diabetic patients with albuminuria but normal levels of serum creatinine, sodium sensitivity of blood pressure appears before hypertension and is related to albuminuria; sodium restriction is one treatment for diabetic nephropath, even without hypertension.
OBJECTIVE: Diabetes associated with autoimmune chronic pancreatitis (ACP) is a subtype of diabetes that is responsive to corticosteroid treatment of progressive endocrine and exocrine dysfunction. However, little is known about pathological changes of islet and exocrine pancreas in ACP. RESEARCH DESIGN AND METHODS: We examined pancreatic specimens obtained on biopsy from four diabetic men with ACP (mean [range]: age 62 years [48-78], duration of ACP 3 months [1-5], duration of diabetes 1 month [0-3]) morphologically, immunohistochemically, and morphometrically. RESULTS: The pancreatic specimens in all cases exhibited inflammatory cell infiltration surrounding ductal cells and extensive fibrosis. Some islets were infiltrated with mononuclear cells with disrupted beta-cells. The subsets of T-cells infiltrated to the islets were mainly CD8(+). Islet beta-cell volume was decreased; the mean percentage area of beta-cells in the islets in four cases with ACP were 16% (range 13-20) (P = 0.0015 vs. type 2 diabetic patients, 48% [27-73], n = 8; P = 0.0002 vs. nondiabetic control subjects, 58% [39-77], n = 7). Preserved ductal cells were surrounded predominantly by CD8(+) or CD4(+) T-cells. Some cytokeratin 19-positive ductal cells contained insulin and glucagon, representing upregulated differentiation of islet cells from ductal cells. Insulin promoter factor-1 (IPF-1) was hyperexpressed in insulin-containing ductal cells. CONCLUSIONS: Diabetes associated with ACP is caused by T-cell-mediated mechanisms primarily involving islet beta-cells as well as pancreatic ductal cells. In ACP, ductal islet precursor cells were associated with IPF-1 hyperexpression, suggesting a critical role of IPF-1 on islet cell differentiation and eventual beta-cell restoration.
A 19-year-old man suffered hepatic dysfunction after 5 months of exposure to N,N-dimethylformamide (DMF) at his job in the synthetic resins industry. Laboratory data revealed elevated levels of AST (578 IU/l), ALT (1193 IU/l), and gamma-GTP (107 IU/l), no viral infection with HAV, HBV, or HCV, and no history or evidence of hepatic injury, although he did have a slight abdominal abnormality and swelling which was detected by palpation. His urinary N-methylformamide level, as a biological exposure index of DMF, was 42.8 mg/l, indicating 10-30 ppm of DMF exposure. After 2 months he was reinstated in two workplaces, the former where he worked in the morning and the other in the afternoon where environmental DMF concentrations were less than those in the former workplace. On the 18th day after his reinstatement, his liver function became exasperated again. After the second period of medication and one month of rest from work, he had fully recovered and was reinstated, but to a workshop without DMF exposure.
To reveal the significance of genetic abnormalities of the c-myc gene, 56 colorectal tumors (43 colorectal carcinomas, 5 recurrent or metastatic tumors, and 8 adenomatous polyps) were analyzed using fluorescence in situ hybridization (FISH). Two probes specific for c-myc and the chromosome 8 centromere were used for dual color FISH. In each case, 100-200 nuclei were observed for signals from the probes. The percent of nuclei with c-myc amplification (PMA) was defined as the proportion of nuclei representing the ratio of c-myc/chromosome 8 >1.0, and the percent of nuclei with the greater number of c-myc (PGNM) was defined as the proportion of nuclei representing the ratio of c-myc/chromosome 8 > or =2.0. Low level amplification was defined as a case with PMA > or =10% and PGNM <10%. High level amplification was defined as a case with PGNM > or =10%. While adenomatous polyps and in situ carcinomas showed no c-myc amplification, the low level amplification and high level amplification of c-myc were observed in 48.8% (21/43) and 20.9% (9/43) of primary colorectal carcinomas. In addition, the group including cases of stage IIIb and IV exhibited significantly higher average copy numbers of c-myc (CN-myc), PMA and PGNM than the other group of earlier stages. FISH was thought a useful cytogenetic method to detect genetic abnormalities in solid tumors. It was shown that the c-myc gene amplification identified using FISH was associated with the aggressiveness of colorectal carcinoma.
Recent studies have shown that 70-80% of low-grade mucosa-associated lymphoid tissue (MALT) lymphomas regress in response to eradication of Helicobacter pylori (H. pylori). However, there are no reports on whether gastric high-grade MALT lymphomas regress after H. pylori eradication. We performed H. pylori eradication therapy in 4 patients with stage I, high-grade MALT lymphoma after obtaining their informed consent. H. pylori infection was observed in all 4 patients. The patients were treated with proton-pump inhibitor-based eradication therapy for 1 or 2 weeks, and then underwent endoscopic examination and biopsy sampling. H. pylori eradication was achieved in all 4 patients. Six months after eradication treatment, 2 patients showed complete regression of the lymphoma and 2 patients showed no change. The 2 patients with non-responding lymphoma were then treated with an additional chemotherapy (CHOP regimen), whereupon the tumors completely regressed. These patients, followed-up at least 18 months after eradication treatment, showed no recurrence. We also examined genetic alteration of the p53 and K-ras genes and microsatellite instability in these high-grade MALT lymphomas. One patient with a tumor that showed no change after H. pylori eradication, had a loss of heterozygosity of the p53 gene. No other genetic alterations were detected among the patients. Our results indicate that the eradication of H. pylori may be effective not only for patients with low-grade MALT lymphoma but also for patients with high-grade MALT lymphoma. The treatment may be efficacious as a first-line therapy for patients with high-grade MALT lymphoma. However, our sample size was limited and further studies are needed to clarify the issue.