Prediction of outcome in fulminant hepatic failure by serum human hepatocyte growth factor.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to T Arima.
Explore the source record for details and available documents.
Forty-two endometrial carcinomas of various stages of progression were analyzed to search for loss of chromosomal regions and for point mutations of ras genes and amplification of Int-2 gene. This approach is particularly favorable for observation of genetic events and their significance in the process of neoplastic conversion by considering the clinico-pathological characteristics of each tumor. At least 3 genetic events, including 18q, 17p deletions, and point mutations at codon 12 of the K-ras gene, are implicated in the development of endometrial carcinomas. Likely targets for allelic losses on chromosomes 18q and 17p are the DCC gene and the p53 gene sequences, respectively. Overall numbers of allelic losses in individual tumors appeared to increase in case of advanced stage tumors, thereby indicating the association of allelic loss accumulation with tumor progression. The genetic features seen in 2 juvenile-type adenocarcinomas and 2 clear-cell carcinomas suggested the possibility that etiological factors providing selective pressure for particular mutation sub-sets during carcinogenesis are probably heterogeneous.
A new phenylglyoxal-binding protein (31.5 kD) was solubilized from frog skeletal muscle. The monoclonal AB against the 31.5 kD protein inhibited extracellularly E-C coupling process of single-muscle fibers.
Explore the source record for details and available documents.
We assessed the effects of the calcium channel blocker verapamil on postischemic oxidative injury in the rat liver. In the untreated rats, the values of tissue lipid peroxidation products (thiobarbituric acid-reactive substances) remained unchanged during 90 min of warm ischemia. However, the values increased significantly after the next 60 min of reperfusion compared with those in the sham-operated rats (P less than 0.01). Intravenous infusion of verapamil (5 micrograms.kg-1.min-1) significantly reduced the extent of lipid peroxidation during reperfusion compared with that in the untreated rats (P less than 0.02). The percentages of tissue water content and the serum lactate dehydrogenase activities after 60 min of reperfusion were significantly lower in the treated rats than in the untreated rats (P less than 0.02 and P less than 0.01, respectively). We also investigated the influence of verapamil on superoxide-generating activity determined by the superoxide-dependent cytochrome c reduction of peritoneal polymorphonuclear leukocytes (PMNs) harvested from normal, non-ischemic, and non-treated rats in vitro. This demonstrated that there was no apparent effect with the highest verapamil concentration level (8 microM) observed in the rat plasma during our experiment. These findings suggest that verapamil might reduce the postischemic oxidative injury in the rat liver by mechanisms perhaps not related to the suppression of rat PMNs superoxide-generating activity.
The HCV, a single stranded RNA virus belonging to the family of flavivirus, has been identified as the probable cause of the majority of cases of transfusion-associated NANB hepatitis and community-acquired NANB hepatitis in Japan. The hepatitis virus is present in a least 2% of the blood donor population and is extremely common in high risk groups, such as hemophiliacs and hemodialysis patients. The contribution of HCV infection to sporadic, acute and chronic hepatitis, liver cirrhosis and primary liver cancer has been established. Furthermore anti-HCV in 20% of alcoholic patients with liver injury suggest that HCV may be etiologically associated with liver disease previously attributed to other causes. Therapy of acute and chronic liver disease associated with HCV infection is likely to be undertaken with recombinant IFN alpha in the future to prevent the progression of the disease from acute hepatitis to chronic hepatitis, and from chronic hepatitis to liver cirrhosis or primary liver cancer. However the prevention of HCV infection will be the goal, in addition to screening of donor blood and exclusion to a large degree of positive units likely to decrease the incidence of post-transfusion hepatitis.
Thirty-five cases of neonatal hepatitis (20 males and 15 females) were reviewed, 3 of whom were lost during the follow-up, leaving 32 patients for review. There were 10 late deaths and 22 patients survived, 18 of whom with a normal bilirubin level and 4 with a bilirubin level of greater than 1.0 mg/dL. In the 18, jaundice disappeared between the ages of 4 and 7 months. The current lifestyles of the patients include 4 adults aged 19 to 21 who are either working or at university, while the other 18 children are all making good progress at school. Except for moderate growth retardation in 3 children, all are growing well. In all 10 patients who died, liver failure persisted until the time of death. Three died of other causes and 7 died of neonatal hepatitis itself between 4 months and 7 years of age. Four patients ran a fulminating course resulting in death between the ages of 4 and 12 months. All 7 had growth and developmental retardation. A histological examination showed that in those who died, there was significantly more periportal fibrosis, inflammation in the periportal area, and diffuse giant cell transformation. These results indicate that some infants with neonatal hepatitis have a poor prognosis and, therefore, the identification of such a condition requires a careful, long-term follow-up.
BACKGROUND: We report a heterozygous case of familial qualitative deficiency of antithrombin III associated with cerebral infarction. CASE DESCRIPTION: A 33-year-old man had a history of recurrent transient ischemic attacks from the age of 28. Cerebral computed tomography at age 29 disclosed a low-density area in the left frontal lobe, and an internal carotid angiogram showed branch occlusion of the right anterior cerebral artery and stenosis of the left middle cerebral artery. Occlusion of the right middle cerebral artery developed thereafter. The plasma antithrombin III antigen concentration and progressive antithrombin activity were normal, but plasma heparin cofactor activity was low in the patient and his father. Nucleotide sequence analysis of the proband's deoxyribonucleic acid showed no mutation in exons II and VI of antithrombin III. CONCLUSIONS: We conclude that abnormal antithrombin III with defective heparin binding, even though heterozygous, may cause ischemic stroke in young adults. We named this antithrombin III variant "Antithrombin III Nagasaki."
We investigated changes in serum lipoprotein(a) (Lp(a)) and C4b-binding protein (C4bp) levels following acute myocardial infarction (AMI). Serum lipids, apolipoproteins, C-reactive protein (CRP), sialic acid and haptoglobin (Hp) were also measured and evaluated. The study involved 16 patients (11 men, 5 women, mean age 68.2 +/- 8.4 years) with AMI admitted within 12 h after the onset of illness. CRP rose sharply and immediately after the onset of AMI, reaching its maximum level on the 3rd day of illness. This was followed by temporary increases in sialic acid and Hp, both of which peaked on the 7th day of illness. The Apo A-I level was significantly lower on the 14th day, while the Apo B level was significantly lower on the 3rd day. Serum total cholesterol (T-Ch), HDL-Ch and LDL-Ch showed temporary decreases after the onset of illness. Serial examination of the serum of patients with AMI yielded the following findings; 1) Both Lp(a) and C4bp levels rose temporarily with similar patterns of variation, and 2) they took longer time to peak (around the 14th day) and lasted longer than the increases in the other acute reactive proteins.
We examined serum lipids, lipoproteins, apolipoproteins (Apo), lipoprotein(a) (Lp(a)), C4b-binding protein (C4bp) and lathosterol in 22 normolipidemic (serum total cholesterol less than 220 mg/dl and serum triglycerides less than 150 mg/dl) male patients with coronary artery disease (CAD) and 33 normal male subjects. Many of the patients in the CAD group with normal total cholesterol (T-Ch) and triglycerides (TG) had higher TG, low-density lipoprotein (LDL)-Ch, beta-lipoprotein (Lipo) and Apo B values and lower high-density lipoprotein (HDL)-Ch, Apo A-I and Apo A-II values than those of the control group. Differences were also observed in the beta-Lipo/HDL-Ch, Apo B/Apo A-I, and HDL-Ch ratios and the atherogenic index [A.I. = (T-Ch--HDL-Ch)/HDL-Ch], all of which are generally accepted as indices for atherosclerosis. Even in CAD patients with normolipidemia, the HDL-Ch/T-Ch ratio and A.I. seemed to be important risk factors. In addition, Lp(a) and lathosterol, an accepted indicator of whole-body cholesterol synthesis, were higher in the CAD group. The CAD group also appeared to have a higher C4bp value, suggesting that this parameter is correlated with other lipids.
We report a 57-yr-old woman with severe cardiac failure secondary to postnephrectomy arteriovenous fistula which was successfully removed. A review of the literature shows the rarity of this complication; only 72 cases have been reported in the world literature including 6 cases (including the present case) from Japan. Surgical intervention is generally the treatment of choice from a fistula and provides satisfactory results for cardiac failure which is the major complication of this fistula. A characteristic bruit was observed in all reported cases. Therefore, nonsurgical closure by percutaneous embolization for a small sized shunt may be possible if early diagnosis is obtained by careful auscultation of the loin.
Hypercalcemia in hematological malignancy is frequently encountered in lymphoid malignancies such as adult T-cell leukemia (ATL) and multiple myeloma and is difficult to manage. As a causative agent of hypercalcemia in ATL, tumor necrosis factor-beta (TNF-beta), previously known as lymphotoxin, has been carefully studied and reviewed here. Bone resorption studies showed the presence of activity in culture supernatants of HTLV-I infected cells. Enzyme linked immunosorbent assays (ELISA) for TNF-beta detected elevated TNF-beta in the sera of ATL patients with hypercalcemia. Immunostaining by monoclonal anti-TNF-beta antibody demonstrated the presence of TNF-beta in both HTLV-I infected cell lines and freshly isolated ATL cells. Furthermore biological TNF-beta activity assay including inhibition of anti-TNF-beta antibody confirmed the conventional documentation of TNF-beta activity in the sera and culture supernatants of HTLV-I infected cell lines. These studies showed that the TNF-beta secreted from ATL cells might be one of the factors contributing to the hypercalcemia in patients with ATL functioning as an osteoclast activating factor (OAF).
A quick-freeze, freeze-substitution method was applied to the guinea pig organ of Corti. Many similarities were apparent between the conventionally fixed samples and the freeze-substituted samples, including the lateral membrane system of the cochlear outer hair cells consisting of the lateral plasma membrane, pillars, cytoskeletal lattice and subsurface cysternae. However, some ultrastructural differences were found in the cells prepared by the freeze-substitution method. Electron-dense mosaic structures were found in the lumen of the tubules of the subsurface cysternae. Tangential sections of the tubules of the subsurface cysternae showed spirally wound parallel rows of electron-dense materials. In a rectangularly cut membrane with a trilaminar structure, the electron-dense materials appeared to be triangular protrusions from the outer leaflet of the unit membrane. These structures suggest that the subsurface cysternae may play an important role in the contraction of cochlear outer hair cells.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
We studied left ventricular (LV) volume decrease, namely, the downward displacement of the LV volume curve, during the isovolumic relaxation period on the time-activity curves obtained from gated blood pool scintigraphy in patients with old myocardial infarction (OMI). To evaluate the mechanism and clinical significance of this phenomenon, 113 consecutive patients with OMI undergoing gated blood pool scintigraphy, left ventriculography, and Doppler echocardiography were studied. 1. This phenomenon was observed only in patients with anterior OMI (13 of 51 patients: 25%). Presence (Group I) or absence (Group II) of this phenomenon was examined. 2. On left ventriculography, dyskinetic or aneurysmal wall motion was observed in the anterior or apical region more frequently in Group I (11 of 13 patients: 85%) than in Group II (20 of 51 patients: 39%) (p < 0.001). 3. Doppler echocardiography showed that the presence of abnormal LV reversed flow over 20 cm/sec from the apex to the base during the isovolumic relaxation period is more frequent in Group I (7 of 13: 54%) than in Group II (4 of 51: 8%) (p < 0.001). These results suggested that this blood shift in the left ventricle is attributed to asynchronous LV relaxation occurring simultaneously with LV volume decrease on gated blood pool scintigraphy. In conclusion, this phenomenon suggests the presence of asynchronous LV relaxation.
A 64-year-old man was admitted to our hospital complaining of fever and edema in February, 1990. Lymph node biopsy revealed diffuse lymphoma pleomorphic type according to the LSG classification. On hematological examination, leukocyte count was 23,500/microliters, of which 36% abnormal lymphocytes expressing CD2, CD3, CD4 and CD25 as same as the lymph node cells. Anti-HTLV-I antibody in serum was positive. From these data, the diagnosis of adult T-cell leukemia (ATL) was made. ATL cells in the blood and lymph node expressed CD30 (Ki-1). CD30 positive ATL cells derived from the blood was increased after short-term culture. The induction of Ki-1 antigen in cell lines and short-term cultured cells from ATL patients was accompanied by the appearance of the HTLV-I related antigen. Then, we suggest that there was some relation between expression of the Ki-1 antigen and activation by HTLV-I in ATL cells.
Gastric mucosal lesions in 13 patients with adult T-cell leukemia (ATL) were endoscopically studied at least at 2 occasions during chemotherapy for these patients. X-ray examinations by using barium meal showed deformities in 10 patients and abnormal mucosal pattern in 11 out of 13 patients with ATL. The endoscopic examinations revealed gastric ulcers in 5 patients, erosion in 8, diffuse bleeding in 2, tumorous mucosal folds in one, and submucosal tumor in one patient. In 9 out of 12 ATL patients, pathological study revealed that ATL cells had invaded the mucosal area of the stomach. The ulcers and erosions were improved by chemotherapy in 3 out of 5 and 5 out of 8 patients, respectively, whereas the erosion was not reduced in 2 and even aggravated in one patient. Interestingly, the gastric lesions formed by ATL cell invasion were improved by the administration of anticancer agents in 5 out of 9 patients. However, these lesions reappeared together with systemic lesions of ATL.