[A case of gastric mucosal carcinoma with remarkable infiltration of lymphoid cells negative for Epstein-Barr virus].
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Biomedical subjects
Publications and source records attributed to S Ogata.
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BACKGROUND: The clinicopathological features of veno-occlusive lesions (VOL) in the liver were studied in 18 autopsy cases of severe alcoholic hepatitis (sALH). All the cases were heavy drinkers and died of liver failure or variceal rupture. METHODS: We performed histological evaluation by examining stained sections of liver blocks from each case. The severity of VOL was compared with the clinical findings and histopathological changes of alcoholic liver diseases (ALD). RESULTS: Clinically, as the severity of VOL increased, the amount of ascites observed during autopsy increased significantly (p = 0.001) and the time from hospitalization to death was significantly longer (p < 0.05). The peripheral leukocyte count tended to increase and the serum bilirubin level increased significantly (p < 0.05) with increased VOL severity, after we excluded one case that was complicated by acute respiratory distress syndrome and bacterial endocarditis. Histopathologically, the appearance of Mallory bodies increased significantly as VOL became more severe (p < 0.05), but the VOL severity did not correlate with sinusoidal neutrophil infiltration. Fatty degeneration tended to be milder as VOL increased in severity although the difference was not significant, whereas bile retention tended to be more marked. CONCLUSIONS: We conclude that investigation of VOL is clinicopathologically important when assessing the pathophysiology and severity of sALH.
We report two patients in whom hypothyroidism was considered to cause renal dysfunction. Case 1 was a 65-year-old woman who stopped taking levothyroxine sodium for hypothyroidism. After 6 months, she developed proteinuria, edema, weight gain, and renal dysfunction. Renal biopsy revealed focal segmental proliferative glomerulonephritis. After re-administration of levothyroxine sodium, thyroid function and renal function both recovered. Case 2 was a 51-year-old man who presented with edema, difficulty in swallowing, muscular weakness, and fatigue. We diagnosed hypothyroidism, and focal segmental proliferative glomerulonephritis was revealed by renal biopsy. After administration of levothyroxine sodium, his symptoms resolved and his thyroid function and renal function both improved. Our experience suggests that hypothyroidism should be taken into consideration as one of the causes of renal dysfunction.
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We herein describe thallium-201 single photon emission tomography (T1-201 SPECT) findings in three cases with intracranial angioma. One of the lesions which was associated with chronic encapsulated intracerebral hematoma showed moderate accumulation of T1-201, but, others demonstrated no accumulation. The usefulness and limitations of T1-201 SPECT in differential diagnosis of intracranial mass lesions are discussed.
We previously purified a kallikrein-like enzyme from the dog heart and demonstrated that it is not only able to form kinins but can also convert angiotensin (Ang) I to Ang II. The aim of the present study was to clarify the structure and tissue localization of this enzyme. Western blot analysis of various canine tissues was performed with antiserum against the purified dog heart enzyme. The purified enzyme was subjected to a determination of its amino acid composition and a sequence analysis. Western blotting indicated that this enzyme was present in the heart, aorta, kidney, pancreas, lung, liver, spleen, small intestine, and skeletal muscle. The amino acid composition of the enzyme was different from that of dog urinary kallikrein. Amino acid sequence analysis indicated that it is likely to be N-terminally blocked. The present study showed that this kallikrein-like enzyme is different from previously reported kallikrein and is distributed not only in the heart, but also in other tissues such as the aorta, kidney, lung, liver, spleen, small intestine, and skeletal muscle. This enzyme may exert local effects by generating kinins and Ang II.
The rare clinicopathological entity 'disseminated visceral giant cell arteritis' (DVGCA) was first described in 1978. It is characterized by widespread small-vessel giant cell angitis and extravascular granulomas. A normal and healthy 7-month-old boy who presented unexpectedly with sudden infant death syndrome (SIDS) is reported. Histological examination at autopsy revealed giant cell angitis of the aorta, common carotid, coronary, pulmonary, celiac, mesenteric and common iliac arteries. There were also granulomas in the tracheal wall and liver. To our knowledge, this is the first documented case of DVGCA occurring in an infant younger than 12 months of age. A review of the literature on DVGCA is presented in this report, and the differential diagnosis is discussed.
Clinicopathological features of veno-occlusive lesions in hepatic veins were studied in autopsy cases of severe alcoholic hepatitis (15 cases) and alcoholic liver cirrhosis (15 cases). All the cases were heavy drinkers and died of liver failure or variceal rupture. The frequency and degree of veno-occlusive lesions, and the diameter and number of hepatic veins were studied from stained sections of liver blocks from each case. The hepatic veins observed ranged from 60 to 3000 microm in diameter. The veno-occlusive lesions were found in hepatic veins mainly 60 to 1200 microm in diameter. These findings were recognized in the majority of severe alcoholic hepatitis cases and alcoholic liver cirrhosis cases. Furthermore, more severe veno-occlusive lesions were noted in severe alcoholic hepatitis, compared with alcoholic liver cirrhosis. In the cases with obstruction in hepatic veins of >400 microm, a decrease in the number of hepatic veins and zonal necrosis were noted. In addition, some of the veno-occlusive lesions were recognized focally in the same cases. Clinical findings also indicated that ascites increased with the progression of the veno-occlusive lesions. We conclude that investigation of veno-occlusive lesions in severe alcoholic liver disease has clinicopathological significance.
A 70-year-old woman with a past history of cholecystolithiasis was admitted to a local clinic because of right hypochondralgia with back pain. Since physical examination revealed Murphy's sign, this patient was diagnosed as acute cholecystitis. The ultrasonographic examination of the gallbladder showed a stone of the cystic duct with no definitive wall thickening. CT scan revealed dissection of the abdominal aorta. She was then referred to our hospital for further examinations. She was observed in the cardiac care unit to determine whether the aneurysm and cholecystitis were in an acute or chronic state. Blood examinations and enhanced CT scan showed that her clinical symptoms originated not from cholelithiasis but from acute closing aortic dissection, Stanford classification type B. Close cooperation with a highly developed medical facility is essential when diagnosing elderly patients with symptoms open to a variety of interpretation.
A 51-year-old woman, who had both aortitis syndrome (Takayasu arteritis) and IgA nephropathy, presented with hypertension, fever, a high erythrocyte sedimentation rate, high C-reactive protein and serum IgG levels, proteinuria, and renal dysfunction. Renal arteriography showed stenosis and poststenotic dilatation at the origin of the right renal artery, as well as tortuosity of the left renal artery branches and marked atrophy of the left kidney. Renal biopsy showed IgA nephropathy with deposits of IgA, C3, and fibrinogen in the glomeruli and arteriolosclerosis. The present patient had human leukocyte antigen (HLA)-B 52, which is reported to be related to the aortitis syndrome, as well as HLA-DR 4, which is possibly related to IgA nephropathy, suggesting that HLA status may be involved in the pathogenesis of both diseases.
Mallory bodies, the intra-cytoplasmic inclusions in hepatocytes, are thought to be a pathognomonic feature of alcoholic liver disease, particularly of alcoholic hepatitis. The presence of Mallory bodies is considered as a reflection of serious illness in alcoholic liver disease. Mallory bodies are thought to disappear relatively rapidly with the use of therapeutic agents after giving up alcohol drinking. However, histological vicissitudes of Mallory bodies have not been studied extensively. In the present study, 19 autopsied cases with a history of heavy drinking were clinicopathologically evaluated. All patients were admitted to our hospital, and stopped alcohol drinking. These period of non-drinking ranged from one day to 150 days (group A: 1-7 days, group B: 8-30 days, group C: 31-150 days). Histological evaluation was performed by hematoxylin and eosin staining, Luxol Fast blue staining and chromotrope aniline blue staining of formalin-fixed paraffin-embedded liver sections. Hepatocytes including Mallory bodies were counted. The incidence of Mallory body formation was as follows: Group A (50%), group B (100%), and group C (100%) respectively. Average count of Mallory bodies: Group A (12.3/10 fields), group B (141.4/10 fields), and group C (188.3/10 fields). Fatty change was more significant in group A than in group B or C, and bile stasis was more significant in group B or C than in group A. These findings suggest that Mallory bodies may remain for several months after giving up drinking.
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AIMS: To investigate the potential prognostic factors for myeloperoxidase anti-neutrophil cytoplasmic antibody- (MPO-ANCA) associated glomerulonephritis. MATERIALS: The clinical and pathological findings were reviewed in 17 patients with this type of glomerulonephritis. METHODS: The relationship between the outcome and various clinical and pathological factors were assessed. The relationship between the blood MPO-ANCA level and cellular crescent formation was also investigated. RESULTS: Patients who died had a significantly lower serum albumin and creatinine clearance than those who survived, but there were no differences of age, blood MPO-ANCA, urinary protein, and serum creatinine levels or cellular crescent formation between the two groups. There was a close relationship between blood MPO-ANCA levels and cellular crescent formation. CONCLUSIONS: Hypoalbuminemia and renal dysfunction may be indicators of a poor prognosis in MPO-ANCA-associated glomerulonephritis. Patients with high blood levels of this antibody and increased cellular crescent formation appear to have active disease, but these factors are not statistically associated with a fatal outcome. Therefore, aggressive treatment may be indicated in patients with active disease initially.
pSA1.1 is a 9.1-kb multicopy plasmid originally isolated from Streptomyces cyaneus (formerly S. azureus) ATCC 14921. This plasmid accumulates single-stranded DNA in S. lividans and is therefore considered to replicate by a rolling-circle replication. In the present work, the rep gene encoding the replication initiator protein and the replication origin ori of pSA1.1 were determined. The rep and ori are located on separate regions. The Rep protein of pSA1.1 belongs to superfamily I which includes A proteins of phages. Nucleotide sequence of the surrounding putative nicking site of pSA1.1 shows good agreement with those of the pC194 group plasmids and phages. The direction of replication was also determined.
Mucin production by human colon cancer cells correlates with liver metastasis in animal models, but it is not known which steps in metastasis depend on specific alterations in mucin synthesis. Clonal variants of cell line LS174T selected for differences in mucin core carbohydrate expression have been further characterized biochemically, and tested for their ability to participate in metastasis-related events. LS-C mucin contains truncated carbohydrates enriched for sialyl Tn and these cells bind to basement membrane matrix to a greater extent than LS-B cells. This binding is partially inhibitable by antibody to sialyl Tn. LS-B produces more fully glycosylated mucin and preferentially binds to hepatic sinusoidal endothelial cells and E-selectin through sialylated peripheral mucin-associated carbohydrate structures. Adhesion of LS-B to endothelial cells is inhibited by neutralizing antibody to E-selectin, and inhibition of glycosylation or desialylation of LS-B mucin abrogates binding to E-selectin in vitro. LS-B cells spontaneously metastasized from cecum to liver and colonized the liver of athymic mice after splenic-portal injection to a significantly greater extent than LS-C, suggesting that expression of peripheral mucin carbohydrate structures is most important for metastasis of human colon cancer cells.
Small bowel allograft rejection in large animals has yet to be well defined. There are no specific early signs of graft rejection. The present experiments were undertaken to compare acute small bowel allograft rejection in pigs with and without FK506 and also to examine the usefulness of mucosal biopsies. Thirty-six outbred Large-White pigs were divided into (1) group 1 (n = 9): nonimmunosuppressed recipients; (2) group 2 (n = 8): FK506-immunosuppressed recipients; (3) group 3 (n = 2): autotransplant controls; and (4) donors (n = 17). Orthotopic small bowel transplantations were performed with Thiry-Vella loops for daily biopsies. The survival rate of group 2 was significantly longer than that of group 1 (P < 0.05). One best survivor in group 2 was killed at postoperative day (POD) 365. Treatment by FK506 prevented rejection, but most of the pigs died of pneumonia. In group 1, rejection began on POD 3 and progressed to severe rejection rapidly within 7 days. In group 2, rejection began from POD 6 to POD 8, but either remained mild or spontaneously improved. The differences in the routine laboratory data and the tumor necrosis factor-alpha level were not evident between the groups. Histological studies of repeated graft biopsies are thus considered to be essential for detecting signs of graft rejection.
Electron spin resonance (ESR) spectroscopic study was undertaken to explore the nature of any remaining radicals in ultra-high molecular weight polyethylene (UHMWPE) after irradiation with gamma-rays and electron beams to a dose of 25 KGy in air or N2 environment. The decay of radicals was studied by observing the ESR intensity change as a function of time. The following post-irradiation conditions were employed: (1) storage in air or N2 at 25 degrees C, and (2) heat treatment in air or N2 at 80, 100, and 120 degrees C for time intervals up to 8 h. The study suggests that radicals remaining trapped in the matrix of UHMWPE could be dramatically scavenged by heat treatment, independently of the atmosphere during irradiation and the heating process. The melting temperature and mechanical properties of irradiated UHMWPE under the experimental conditions employed were shown not to alter significantly by heat treatment, except in the presence of air.
Monoclonal antibodies TKH2 and B72.3, which react with the mucin-associated sialyl-Tn(STn) antigen, preferentially bind to cancerous but not normal colonic tissues. If O-acetyl groups are removed by saponification of tissues, MAb TKH2 will react with normal colonocytes, whereas MAb B72.3 remains non-reactive. To explain this difference in binding specificity, we tested both MAbs against synthetic constructs of single (monomeric) or clustered (trimeric) STn epitopes by enzyme immunoassay. Both MAb TKH2 and MAb B72.3 reacted with trimeric STn, but MAb TKH2 demonstrated greater binding than MAb B72.3 to monomeric STn. This suggests that normal colonic mucosa expresses monomeric STn epitopes, but that with transformation to malignancy, clustered STn epitopes appear. The appearance of clustered STn epitopes during colonic carcinogenesis represents a novel pattern of carbohydrate antigen expression and implicates alterations at the level of apomucins and/or glycosyltransferases responsible for cluster epitope formation.