Esophageal stenosis and Graves disease in brittle type 1 diabetes mellitus.
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Blood Glucose↗
Biomedical subjects
T Ando
Publications and source records attributed to T Ando.
Cervical spondylotic amyotrophy. Magnetic resonance imaging demonstration of intrinsic cord pathology.
STUDY DESIGN: Three case reports. OBJECTIVE: To elucidate the pathophysiology of cervical spondylotic amyotrophy. SUMMARY OF BACKGROUND DATA: Cervical spondylotic amyotrophy is the clinical syndrome in cervical spondylosis characterized by severe muscular atrophy in the upper extremities, with an absent or insignificant sensory deficit. Pathophysiology of this particular syndrome has not been well understood. METHODS: Three cases of cervical spondylotic amyotrophy are presented in which magnetic resonance imaging confirmed the intrinsic cord disease as the cause of the syndrome. RESULTS: The patients had segmental muscular atrophy of the proximal upper extremities, with an absent or insignificant sensory deficit. After initial disease progression, the symptoms stabilized for years. Sagittal T2-weighted magnetic resonance images showed multi-segmental linear high-signal intensity within the compressed spinal cord. These high-signal intensity lesions appeared to be located at the anterior horns on axial images. The spinal cord compression was less severe in the neck-neutral position, but spinal canal stenosis increased when the neck was extended. CONCLUSIONS: The results suggest that one pathophysiology of this syndrome may be multisegmental damage to the anterior horns caused by dynamic cord compression, possibly through circulatory insufficiency.
Aged↗
Expression of Bcl-2 and p53 correlates with the morphology of gastric neoplasia.
The growth of a tumour can be determined by an interplay between cell proliferation and loss. The expression of apoptosis-related proteins (Bcl-2 and p53), cell proliferation (Ki-67), and apoptotic cell death were investigated using immunohistochemistry and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labelling in gastric neoplams, to evaluate whether they correlate with the morphology of the tumour. The materials included ten cases of gastric adenoma and 40 cases of early gastric carcinoma consisting of differentiated adenocarcinomas (n = 20) and undifferentiated carcinomas (n = 20). All cases of adenoma and eight cases of differentiated adenocarcinoma were of the elevated type, while 12 differentiated adenocarcinomas and all of the undifferentiated carcinomas were of the depressed type. The diffuse expression of Bcl-2 was observed in all cases of adenoma and seven out of eight (88 per cent) of elevated-type differentiated adenocarcinoma. In contrast, Bcl-2 expression was absent or focal in the depressed type of carcinoma. Overexpression of p53 was found exclusively in the depressed type of carcinoma. Thus, Bcl-2 and p53 expression was associated with tumour morphology. It seemed unlikely that Bcl-2 and p53 expression was involved in the morphogenesis of the gastric tumours through inhibiting apoptotic cell death, since the degree of apoptosis in Bcl-2-positive gastric tumours was rather higher than that in Bcl-2-negative ones and it did not differ significantly between p53-positive and p53-negative tumours. Instead, the diffuse distribution of Bcl-2 correlated with the superficial distribution of Ki-67-positive proliferating cells, and the overexpression of p53 had a tendency to correlate with the diffuse distribution of proliferating cells. These results suggest that diffuse Bcl-2 expression and a superficial distribution of proliferating cells may contribute to the elevated configuration, and that overexpression of p53 and a diffuse distribution of proliferating cells may result in the depressed configuration in the relatively early stages of gastric tumourigenesis.
Adenocarcinoma↗
Effects of Postoperative Pericardial Effusion on Coronary Artery Bypass Grafts: A Study with X-ray Computed Tomography.
The aim of this study was to evaluate the effects of pericardial effusion on coronary artery bypass grafts and their patency using X-ray computed tomography (CT). Uncontrasted CT of horizontal sections from the lower margin of the aortic arch to the left ventricle was done at 5-mm intervals. In one cross-section of the pulmonary bifurcation level, 30 ml of a contrast media (lohexol 350) was injected at a rate of 3 ml/second into the antecubital vein. All slices of uncontrasted CT were analyzed for the presence or absence of effusion. The severity was expressed as the maximum value of the thickness of effusion. CT was repeated about every 6 months postoperatively under the same conditions. Selective angiography was also performed 7.1 +/- 3.9 months postoperatively. A total of 46 patients (mean age 57 years) underwent CT and angiography. A total of 95 grafts were implanted: 90 saphenous veins and 5 internal thoracic arteries. Selective angiography revealed that 79 grafts were patent and 16 were occluded. The first postoperative CT (at 2.6 +/- 2.1 months) showed the retention of effusion in all patients. The mean maximum value was 1.0 +/- 0.5 cm; there were no significant differences between patent grafts (1.0 +/- 0.5 cm) and occluded grafts (1.0 +/- 0.5 cm). Occlusion was found in 10 grafts by the first CT (2.9 +/- 2.7 months postoperatively) and another 6 grafts by the second CT (11.3 +/- 4.2 months). Thereafter, all grafts were patent. Previously occluded grafts showed no cross-section images on uncontrasted or contrasted CT. Except for two grafts, all patent grafts could be observed even without contrast enhancement. The remaining two grafts were masked with effusion, but patency was confirmed by a contrast media. In conclusion, retention of effusion does not affect the patency of grafts. Occlusion occurs early after surgery, and grafts cannot be imaged on CT. Patent grafts can be observed by uncontrasted CT, as well as contrasted CT, except where a large amount of effusion is present.
Journal Article↗
Characterization of B16 melanoma-specific cytotoxic T lymphocytes.
A B16 melanoma-specific CD8+ T cell line (AB1) was established from the spleen cells of C57BL/6 mice cured of B16 melanoma with interleukin (IL)-12 treatment. The AB1 line exclusively used T cell receptor Vbeta11. The AB1 cells exhibited a cytolytic activity against both syngeneic B16 melanoma and allogeneic P815 mastocytoma, whereas a cold inhibition assay revealed specificity of the AB1 cells against B16 melanoma. Their lostability to kill a class I loss variant of B16 melanoma was restored by the transfection of H-2Kb gene. In addition, their interferon (IFN)-gamma production was significantly suppressed by the addition of anti-H-2Kb monoclonal antibody, and RT-PCR analysis showed that the AB1 line expressed the mRNA encoding IFN-gamma, but not IL-4 or IL-10. The experiment using synthetic peptides of tyrosinase-related protein-2 (TRP-2) revealed that the AB1 cells could recognize TRP-2(181-188) peptide. Moreover, the AB1 cells showed an in vivo antitumor effect against established pulmonary metastases of B16 melanoma. Overall, these results indicate that the Tc1-type Vbeta11+ AB1 cells exert an antitumor activity against syngeneic B16 melanoma through recognition of TRP-2(181-188) peptide in an H-2Kb-restricted manner.
Animals↗
Carcinoid of the esophagus located in lamina propria.
We report a carcinoid tumor in the mucosal layer of the esophagus of a 63-year-old man. Barium X-ray and endoscopy indicated the tumor to be a polypoid lesion in the lower esophagus. Endoscopic ultrasonography (EUS) demonstrated the lesion to be a sharply demarcated hyperechoic tumor in the mucosal layer. Biopsy yielded a diagnosis carcinoid of the esophagus. In the resected specimen of the esophagus, the tumor was 11 mm in longest dimension with a shallow depression on it smooth surface. Histologically, the tumor was located in the mucosal layer, as shown by EUS, and was composed of small round cells which were positive for argyrophil, but not argentaffine. Carcinoid tumor of the esophagus found at an early stage, and localized in the lamina propria layer, is very rare. The present case is the second report in Japan.
Carcinoid Tumor↗
Interleukin 15 activity in the rectal mucosa of inflammatory bowel disease.
BACKGROUND & AIMS: Interleukin (IL)-15 has been found to share many immunoregulatory activities in lymphocytes with IL-2. The aim of this study was to investigate IL-15 activity in organ cultures, localization of IL-15 messenger RNA (mRNA), and proliferation of lamina propria mononuclear cells (LPMCs) in response to recombinant IL-15 using the mucosal tissues obtained from patients with inflammatory bowel disease (IBD). METHODS: The contents of IL-15, tumor necrosis factor alpha, and IL-2 in the culture supernatant of the rectal mucosal tissues were determined by an enzyme-linked immunosorbent assay. Expression of IL-15 mRNA was analyzed by in situ hybridization, and proliferative response of LPMCs to recombinant IL-15 was determined by [3H]thymidine incorporation into DNA. RESULTS: Significantly greater IL-15 activity was detected in active IBD, and this elevation was also observed in inactive ulcerative colitis. In contrast, greater tumor necrosis factor alpha activity was observed only in active IBD, and IL-2 was not detected in organ cultures. In situ hybridization showed IL-15 mRNA in macrophages and epithelial cells in active IBD specimens, and recombinant IL-15 induced a dose-dependent proliferative response in LPMCs. CONCLUSIONS: Mucosal IL-15 may be involved in the pathogenesis of IBD as one of the important mediators in activation of mucosal immune cells.
Adolescent↗
An outbreak of viral gastroenteritis associated with consumption of sandwiches: implications for the control of transmission by food handlers.
Although food handlers are often implicated as the source of infection in outbreaks of food-borne viral gastroenteritis, little is known about the timing of infectivity in relation to illness. We investigated a gastroenteritis outbreak among employees of a manufacturing company and found an association (RR = 14.1, 95% CI = 2.0-97.3) between disease and eating sandwiches prepared by 6 food handlers, 1 of whom reported gastroenteritis which had subsided 4 days earlier. Norwalk-like viruses were detected by electron microscopy or reverse transcriptase-polymerase chain reaction (RT-PCR) in stool specimens from several company employees, the sick food handler whose specimen was obtained 10 days after resolution of illness, and an asymptomatic food handler. All RT-PCR product sequences were identical, suggesting a common source of infection. These data support observations from recent volunteer studies that current recommendations to exclude food handlers from work for 48-72 h after recovery from illness may not always prevent transmission of Norwalk-like viruses because virus can be shed up to 10 days after illness or while exhibiting no symptoms.
Caliciviridae Infections↗
Frequency analysis of autosomal dominant cerebellar ataxias in Japanese patients and clinical characterization of spinocerebellar ataxia type 6.
Using a molecular diagnostic approach, we investigated 101 kindreds with autosomal dominant cerebellar ataxias (ADCAs) from the central Honshu island of Japan, including spinocerebellar ataxia type 1 (SCA1), spinocerebellar ataxia type 2 (SCA2), Machado-Joseph disease (MJD), dentatorubral and pallidoluysian atrophy (DRPLA) and spinocerebellar ataxia type 6 (SCA6). In our unselected series, MJD was the most common type of ADCA, accounting for 33.7% followed by DRPLA (19.8%), SCA2 (5.9%) and SCA6 (5.9%). No SCA1 mutations were identified. We analysed the clinical features of six molecular confirmed SCA6 kindreds: in each family, there was an expanded allele in the alpha1A-voltage dependent calcium channel comprising between 23 and 25 CAG repeats. The mean age at onset of symptoms was 43+/-13 years. The clinical features consisted predominantly of cerebellar ataxia, dysarthria and horizontal nystagmus, which was generally consistent with ADCA type 3. However several new clinical features were found in some patients: dramatic anticipation, rapid disease progression, severe ataxia associated with action tremor or action myoclonus, and very early onset, which are not described as the classical features of ADCA type 3.
Adult↗
Bactericidal activity of catechin-copper (II) complexes on Escherichia coli ATCC11775 in the absence of hydrogen peroxide.
Washed Escherichia coli ATCC11775 cells were killed by (-)-epigallocatechin (EGC) in the presence of a non-lethal concentration of Cu2+ (1 mumol l-1) without additional H2O2, but not by (-)-epicatechin (EC). EGC alone (< 0.1 mmol l-1) did not reduce the viability of the cells. The survival curve obtained in the presence of EGC and Cu2+ was similar to that obtained in the presence of (-)-adrenaline (EN) and Cu2+.
Catechin↗
Molecular epidemiology of "Norwalk-like viruses" in outbreaks of gastroenteritis in the United States.
Fecal specimens from 90 outbreaks of nonbacterial gastroenteritis reported to 33 state health departments from January 1996 to June 1997 were examined to determine the importance of and to characterize "Norwalk-like viruses" (NLVs) in these outbreaks. NLVs were detected by reverse transcription-polymerase chain reaction in specimens from 86 (96%) of 90 outbreaks. Outbreaks were most frequent in nursing homes and hospitals (43%), followed by restaurants or events with catered meals (26%); consumption of contaminated food was the most commonly identified mode of transmission (37%). Nucleotide sequence analysis showed great diversity between strains but also provided evidence indicating the emergence of a common, predominant strain. The application of improved molecular techniques to detect NLVs demonstrates that most outbreaks of nonbacterial gastroenteritis in the United States appear to be associated with these viruses and that sequence analysis is a robust tool to help link or differentiate these outbreaks.
Aged↗
A viral gastroenteritis outbreak associated with person-to-person spread among hospital staff.
OBJECTIVE: To identify the etiologic agent and risk factors associated with a hospital ward outbreak of gastroenteritis. SETTING: A regional referral hospital in upstate South Carolina. METHODS: We reviewed patient charts, surveyed staff, and tested stool from acutely ill persons. A case was defined as diarrhea and vomiting in a staff member or patient from January 5 to 13, 1996. RESULTS: The initial case occurred on January 5 in a staff nurse who subsequently was hospitalized on the ward and visited by many staff colleagues. The staff were at a significantly greater risk for gastroenteritis than were patients (28/89 [31%] vs 10/91 [11%]; relative risk [RR], 2.9; 95% confidence interval [CI95], 1.5-5.5). All 10 case-patients had been exposed to case-nurses (assigned nurses who were primary caretakers), and eight had documented exposure to case-nurses 1 to 2 days before their illness. Patients exposed to case-nurses had a significantly increased risk of illness (8/57 [14%] vs 0/32; RR, >4.5; CI95, undefined). Neither staff nor patients had significantly increased risk from food, water, ice, or exposure to case-patients. Electron microscopy identified small round-structured viruses (SRSVs) in nine of nine stool samples. CONCLUSION: This nosocomial outbreak of gastroenteritis was likely caused by SRSVs introduced by a staff member and spread via person-to-person transmission from and among staff. The potential for spread of SRSV-associated gastroenteritis from and among staff should be considered in developing strategies to prevent similar outbreaks in hospital settings.
Adult↗
Mucosal macrophage inflammatory protein-1alpha levels are increased in Helicobacter pylori infection.
We examined the relationship between the levels of macrophage inflammatory protein 1alpha (MIP-1alpha) and interleukin-8 (IL-8) in organ cultures of antral mucosal tissues, background gastroduodenal diseases, and grades of histologic gastritis. Significantly higher levels of MIP-1alpha and IL-8 were detected in patients with H. pylori infection than in those without infection. In H. pylori-positive patients, mucosal specimens from patients with peptic ulcer disease showed higher levels of MIP-1alpha and IL-8 than the specimens obtained from patients with erosive gastritis or those from endoscopically normal mucosa, and this was particularly pronounced in patients with duodenal ulcer. There were positive correlations between MIP-1alpha and IL-8 levels and histologic grades of activity, inflammation, and H. pylori density as defined by the Sydney system. However, the degree of association with the inflammatory cell count was different between these two chemokines. MIP-1alpha levels had a stronger association with mononuclear cells than with neutrophils, whereas IL-8 levels showed an association with neutrophils and mononuclear cells to an almost equal degree. These results suggest that MIP-1alpha and IL-8 may play important roles as inflammatory mediators in the pathogenesis of histologically proven H. pylori-associated gastritis.
Adult↗
EAT/mcl-1, a member of the bcl-2 related genes, confers resistance to apoptosis induced by cis-diammine dichloroplatinum (II) via a p53-independent pathway.
EAT/mcl-1 showed increased expression during the differentiation of a multipotent human embryonic carcinoma cell line, NCR-G3, and of myeloblastic cells "ML-1," and has sequence similarity to Bcl-2. In this present study, we determined whether the apoptotic cell death induced by chemotherapeutic agents could be inhibited by EAT/mcl-1, as has been found with Bcl-2. Cells transfected with EAT/mcl-1 showed higher resistance to cis-diammine dichloroplatinum (II) (CDDP) and carboplatin compared with the parental line (10)1 and neomycin-resistance gene-transfected clone, (10)1/neo. There was, however, no difference in sensitivity to etoposide, N,N-bis-(2-chloroethyl)-N'-(3-hydroxypropyl) phosphordiamidic acid cyclic ester monohydrate, adriamycin or other chemotherapeutic agents tested. DNA fragmentation of the parental cells following treatment with CDDP and carboplatin was observed in a concentration-dependent manner. In contrast, cells transfected with EAT/mcl-1 did not show DNA fragmentation following treatment with the same concentration of these drugs. EAT/mcl-1 was capable of delaying the onset of p53-independent apoptosis, although it could not inhibit apoptosis completely. Since CDDP and carboplatin damage DNA and then activate c-abl and the JNK/SAPK pathway, EAT/mcl-1 may inhibit p53-independent apoptosis through a c-abl/JNK (SAPK)-dependent mechanism. EAT/mcl-1 has functional homology to Bcl-2 in that it can enhance cell viability under conditions which otherwise cause apoptosis and increase resistance to chemotherapeutic agents.
Animals↗
Using polymerase chain reaction to detect the etiological virus of serologically non-A, non-B, non-C fulminant hepatitis in Japanese children.
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Child↗
Differential normalization of mucosal interleukin-8 and interleukin-6 activity after Helicobacter pylori eradication.
There is differential resolution of mucosal infiltration with neutrophils and mononuclear cells following successful Helicobacter pylori eradication. We investigated the effects of H. pylori eradication on mucosal interleukin-8 (IL-8) and IL-6 activity in relation to the resolution of H. pylori-associated gastritis. Eighty-one duodenal ulcer patients with H. pylori infection received dual- or triple-treatment eradication therapy, and mucosal biopsy specimens obtained at the initial and follow-up endoscopic examinations were cultured in vitro for 24 h. The levels of IL-8 and IL-6 were measured by enzyme-linked immunosorbent assays. In the 42 patients in whom H. pylori eradication failed, there was little change in the numbers of neutrophils and mononuclear cells infiltrating the mucosa and in IL-8 and IL-6 activity. In the 39 patients in whom H. pylori was eradicated, there was normalization both in the numbers of infiltrating neutrophils and in mucosal IL-8 activity, which was evident within 1 month following therapy. In contrast, there was a gradual resolution of mononuclear cell infiltration over a 6-month period, accompanied by a gradual normalization in IL-6 levels. Addition of H. pylori to cultures of mucosal tissues induced a significant increase in IL-8 activity in both uninfected control subjects and patients from whom H. pylori was eradicated. However, this introduction yielded a significant increase in IL-6 activity only in the latter group. This study indicates a dichotomy in the changes of mucosal IL-8 and IL-6 activity after H. pylori eradication. The rapid normalization of IL-8 after H. pylori eradication and the ability of H. pylori cells to stimulate IL-8 in control tissues indicate that IL-8 induction is a part of the innate (nonimmune) responses to this organism. In contrast, the results of experiments analyzing IL-6 activity in cultured mucosal tissues suggest that the gradual resolution of mucosal IL-6 activity and mononuclear infiltration after successful eradication observed in vivo may reflect gradually diminishing residual immune responses against H. pylori.
Adult↗
Peripheral corticotropin-releasing factor mediates the elevation of plasma IL-6 by immobilization stress in rats.
We previously reported the elevation of plasma interleukin (IL)-6 activity in response to immobilization stress in rats. To investigate the role of peripheral corticotropin-releasing factor (CRF) in this response, we examined the effects of CRF antagonists on immobilization-induced IL-6 response. Intravenous pretreatment with either [D-Phe12,Nle21,38,CalphaMeLeu37]-anti-human rat (h/r) CRF12-41 (1.5 mg/kg) or cyclo(30-33)[D-Phe12, Nle21,38,Glu30, Lys33]-h/rCRF12-41 (Astressin, 0.5 mg/kg) attenuated the IL-6 response to immobilization, which confirmed our previous finding that systemic administration of an antiserum against CRF blocked this response. In addition, an intraperitoneal injection of h/rCRF (100 micrograms/kg) or rat urocortin (10 and 100 micrograms/kg) increased the plasma IL-6 activity, mimicking the response to immobilization. An intravenous injection of h/rCRF (100 micrograms/kg) also elevated plasma IL-6 in adrenalectomized rats. These findings suggest that peripheral CRF mediates the plasma IL-6 elevation in response to immobilization.
Animals↗
Localization of TGF-beta and its receptors in the kidney.
This paper reviews the expression and localization of proteins of the TGF-beta system in the kidney, i.e. TGF-beta isoforms, latent TGF-beta binding protein, and receptors. There is heterogeneity of TGF-beta isoforms, binding proteins and receptors. TGF-betas are more evenly distributed among different segments of the nephron than TGF-beta receptors, and are expressed by almost all cell types in the kidney. The spatial distribution of TGF-beta and its signaling receptor may help to better understand the biologic function of TGF-beta in the kidney.
Animals↗