[A case of nodular regenerative hyperplasia (NRH) of the liver associated with recurrent hepatic encephalopathy due to splenorenal shunt].
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Publications and source records attributed to H Okubo.
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We report here a case of pulmonary alveolar proteinosis with significantly increased IgE and CEA values, in both serum and bronchoalveolar lavage fluid. A 35-year-old man presented with exertional dyspnea, diffuse abnormal shadows on radiological examination of the chest and physiologic evidence of a restrictive lung disease. Bronchoalveolar lavage and transbronchial lung biopsy proved that the patient was suffering from pulmonary alveolar proteinosis. He had worked as a landscape gardener for the past 2 years, and had been exposed to insecticides. IgE and CEA levels were significantly elevated in both serum and bronchoalveolar lavage fluid. After whole lung lavage, general status improved remarkably and serum CEA fell to the normal range. The serum IgE level was, however, reduced by only half. Proliferating type II epithelial cells in pulmonary alveolar proteinosis have been suggested to produce CEA. However, the cause of the increased IgE level remains unknown. This case report suggests that some abnormal immunological events, leading to hyperproduction of IgE, could play a role in the onset of pulmonary alveolar proteinosis.
We examined the plasma levels of tissue plasminogen activator antigen and plasminogen activator inhibitor activity in 14 patients with non-Q-wave infarction and in 27 patients with Q-wave infarction before the start of thrombolytic therapy and in 34 control subjects. The mean level of plasma tissue plasminogen activator antigen (ng/ml) was higher (P < 0.01) both in the patients with non-Q-wave infarction and in those with Q-wave infarction than in the control subjects (10.3 +/- 1.9, 9.5 +/- 0.8 vs. 5.8 +/- 0.3), and there was no difference in the level between the patients with non-Q-wave infarction and those with Q-wave infarction. The mean level of plasma plasminogen activator inhibitor activity (IU/ml) was lower (P < 0.01) in the patients with non-Q-wave infarction than in those with Q-wave infarction (7.3 +/- 2.0 vs. 17.1 +/- 2.2), and there was no difference in the level between the patients with non-Q-wave infarction and the control subjects (7.3 +/- 2.0 vs. 4.1 +/- 2.6). The patency rate of infarct-related coronary artery before thrombolytic therapy was higher (P < 0.01) in the patients with non-Q-wave infarction than in those with Q-wave infarction (54% vs. 15%). We conclude that plasminogen activator inhibitor activity was lower in non-Q-wave infarction than in Q-wave infarction and this may be related to the higher patency rate of infarct-related coronary artery in non-Q-wave infarction.
HLA-DR gene frequencies in 59 Japanese children with juvenile rheumatoid arthritis (JRA) and 62 Japanese adults with rheumatoid arthritis (RA) were analyzed by oligonucleotide DNA typing. As in other studies, the frequency of DRB1*0405 in RA patients was significantly higher than in the Japanese controls. In a comparison of non-classified JRA patients with Japanese controls, no significant differences were observed in the frequency of DR types. However, when the JRA patients were classified into four clinical types, i.e., a rheumatoid factor-positive [RF(+)] polyarticular type, a rheumatoid factor-negative [RF(-)] polyarticular type, a pauciarticular type, and a systemic onset type, DRB1*0405 was found to be significantly higher in the RF(+) polyarticular JRA patients than in the controls (P < 0.05). Thus, the RF(+) polyarticular type of JRA had the same HLA association as RA. This result is consistent with the fact that both RF(+) polyarticular JRA and RA cases have a similar clinical course.
The General Health Questionnaire (GHQ) with 28 items was tested in Nagasaki city on 138 senior students in a prefectural high school and 685 freshmen in a national university to evaluate the degree of students' mental stress due to the highly competitive entrance examination for university. The average GHQ score tested on high school students was 5.33 for males and 7.07 for females, and 3.99 for males and 4.42 for females on university students. It showed that high school students were under greater pressure than university students and female students were in a higher tension compared with male students. The factor analysis showed that the primary and secondary factor of high school students were "severe depression" and "anxiety and insomnia," while "somatic symptoms" were the primary factor causing stress in university students.
Liver histology was compared in patients with chronic hepatitis C to note the differences between responders and non-responders to interferon treatment. Fifty-eight patients were administered interferon in varying doses and over various periods, and were then followed up for 1 year. According to the improvement status of serum alanine aminotransferase (ALT) levels during this period, the patients were classified into complete responders who showed complete normalization of ALT; partial responders who exhibited a significant decrease, but not complete normalization of ALT; and non-responders who did not reveal any significant decrease of ALT. Before application of the interferon treatment, liver biopsies were analyzed in four parameters and given scores from 0 to 5 for three groups in cord with no prior knowledge of the efficacy. The parameters included necroinflammation, fibrosis/lobular distortion, portal lymphocytic reaction and portal (or fibrous septal) outline destruction. Results indicated that there were no significant differences in the score of necroinflammation and portal lymphocytic reaction between the complete responder group and the non-responder group. In contrast, the complete responder group exhibited weaker fibrosis/lobular distortion and less portal outline destruction than the non-responder group. The partial responder group was more akin to the former group in these parameters. Thus, it is safe to conclude that liver histology may predict the efficacy of interferon treatment.
The prognosis in 52 patients with juvenile rheumatoid arthritis (JRA) was studied. There were 35 cases of systemic onset, 12 of polyarticular onset and 5 of pauciarticular onset. Thirteen systemic cases developed a polycyclic course with chronic polyarthritis. Many monocyclic JRA in systemic cases subsided within 1 year. There were no instances of polyarticular cases or pauciarticular cases that shifted to other type. However, there were many cases with a long active polyarticular JRA and with remission at an early stage in the pauciarticular type. The stage and class were I or II in 90% of cases with a good prognosis for the joints, but there were some serious cases. Transient carditis or iritis which developed at an early stage subsided later. The intractable systemic cases had drug-induced complications. The cases with steroid-induced complications tended to be chronic. One death in a systemic case was caused by hepatic failure.
The relationship between plasma Lipoprotein(a) (Lp(a)) levels and plasminogen activator inhibitor (PAI) activity and tissue plasminogen activator (t-PA) antigen levels were studied in 15 patients with unstable angina. Plasma levels of Lp(a) (mg/dl) were significantly higher in patients with unstable angina after treatment 2 weeks than on admission (19.7 +/- 2.8 vs 14.6 +/- 2.3, p < 0.01). On the other hand, the plasma levels of PAI activity (IU/ml) and t-PA antigen (ng/ml) in patients with unstable angina were significantly higher on admission than after treatment (PAI activity: 11.4 +/- 1.4 vs 7.7 +/- 1.5, t-PA antigen: 8.7 +/- 0.9 vs 7.0 +/- 0.9, p < 0.01). We conclude that patients with unstable antigen have reduced fibrinolytic capacity, as indicated by increased PAI activity, and that the plasma Lp(a) level may be decreased due to binding with fibrin during the acute stage of unstable angina.
Plasminogen activator inhibitor (PAI) activity and tissue plasminogen activator (TPA) antigen were measured in venous samples in 14 patients with unstable angina consisting of eight patients with organic stenosed coronary arteries and six patients with coronary spastic angina (unstable angina group); in 14 patients with stable exertional angina (stable exertional angina group); and in 14 patients with chest pain syndrome (chest pain syndrome group). The plasma levels of PAI activity were higher (p less than 0.01) in the unstable angina group than in the stable exertional angina group and the chest pain syndrome group (12.3 +/- 1.0 versus 5.1 +/- 0.7 and 4.8 +/- 0.6 IU/ml). The plasma levels of TPA antigen were also higher (p less than 0.05) in the unstable angina group than in the stable exertional angina group and the chest pain syndrome group (10.2 +/- 1.3 versus 6.5 +/- 0.8 and 6.0 +/- 0.7 ng/ml). There were no significant differences in PAI activity and TPA antigen levels between the stable exertional angina group and the chest pain syndrome group. Furthermore, both PAI activity and TPA antigen levels in the unstable angina group decreased to the levels in the stable exertional angina group and the chest pain syndrome group after treatment (p less than 0.01). In conclusion, the increased plasma PAI activity in patients with unstable angina and in those with coronary spastic angina indicates that the fibrinolytic system is impaired in these patients.
Laser Doppler flowmetry (LDF) measures the flux of red blood cells in a vascular network embedded in tissue. In the present report, choroidal and ciliary body blood flow was measured continuously using an LDF technique in pentobarbital anesthetized cats. Blood flow measurements were made from the choroid beneath the lateral and superior rectus muscles and from the surface above the ciliary body 2-3 mm posterior to the limbus. In some experiments, the sympathetic nerve to the eye was stimulated; in others, intraocular pressure (IOP) was monitored manometrically with a controlled saline infusion delivered into the anterior chamber to gradually elevate IOP. Norepinephrine (NE) and methacholine (MC) also were tested for their effects on choroidal blood flow when given intravenously and intra-arterially. Transient bilateral carotid artery occlusions produced a significant drop in blood flow, but flow did not decrease to zero probably due to collateral contribution of the vertebral circulation. Sympathetic nerve stimulation produced a frequency-dependent decrease in both choroidal and ciliary body blood flow with the latter exhibiting a lower threshold and a greater magnitude of effect. Gradual elevation of IOP produced a proportional decrease in choroidal blood flow. The level of intraocular pressure required to decrease blood flow was dependent on the existing ocular perfusion pressure. Both intravenous and intra-arterially administered NE produced dose-dependent decreases of choroidal blood flow despite graded increases of systemic arterial blood pressure. In contrast, MC produced dose-dependent increases of choroidal blood flow in conjunction with graded decreases of systemic blood pressure. The results of the present report demonstrate the validity of the LDF technique for performing continuous reading of blood flow changes in the choroid and ciliary body of experimental animals.(ABSTRACT TRUNCATED AT 250 WORDS)
The purpose of the current study was to investigate the relationship between systemic blood pressure (BP) and long posterior ciliary arterial (LPCA) blood flow (BF) in response to autonomic drugs, and to determine the types of receptors involved. LPCA BF was measured in anesthetized rabbits at the retrobulbar region using laser Doppler flowmetry. The observation that most of the short posterior ciliary arteries diverge from two LPCAs in rabbits was confirmed using a vascular casting technique. Therefore, the LPCA BF at the retrobulbar region should be representative of total uveal BF. Norepinephrine (IV) increased systemic BP and decreased LPCA BF. These responses were suppressed only slightly by yohimbine, but were inhibited markedly by prazosin and by the combination of yohimbine and prazosin. B-HT 920 (IV), a selective alpha-2 adrenoceptor agonist, increased systemic BP and decreased LPCA BF. B-HT 920 (IA) also decreased LPCA BF, with all effects of B-HT 920 antagonized by yohimbine. Methacholine (IV) decreased systemic BP and increased LPCA BF whether administered IV or IA. These effects were blocked uniformly by atropine. The current results suggest that LPCA BF is controlled both by systemic BP and local ocular vascular tone. There are vasoconstrictive alpha-1 and alpha-2 adrenoceptors and vasodilative muscarinic receptors in the rabbit ocular vascular tree.
Condensation reactions between some SH-amino acids (L-and D-cysteine 1%) and acetaldehyde (50 microM) were studied in vitro experiment. In the aqueous solution, free acetaldehyde was reduced to 41.3% by L-cysteine and to 36.4% by D-cysteine. In the reaction with human blood medium, after the medium was deproteinized with perchloric acid reagent, acetaldehyde was reduced to 47.0% by L-cysteine and to 43.8% by D-cysteine. D-Cysteine appears to have great stability of reacting acetaldehyde. In vitro experiment reactability for D-cysteine exhibited 3-8% higher than that for L-cysteine. Next, effects of some amino acids on alcohol metabolism were studied in male ICR mice. The animals were given ethanol through a gastric catheter at a dose of 2 g/kg and they were intraperitoneally injected L-cysteine (300 mg/kg), D-cysteine (300 mg/kg), L-alanine (300 mg/kg) and control (saline), respectively in the period of one hour before the injection of ethanol. Blood and tissues samples were analyzed for ethanol, acetaldehyde, acetate and acetone during alcohol intoxication in mice by head space gas chromatography. In the groups administered D-cysteine and L-cysteine, the mice showed a definitely faster oxidation and disappearance of ethanol. Especially in the D-cysteine group, ethanol levels in blood, liver and brain remained lower than that in the other groups (p less than 0.01). Acetaldehyde levels in blood, liver and brain remained low by L-cysteine. Ethanol metabolites during alcohol oxidation by chemical reactabilities of L- and D-cysteine showed different distribution in the mice, respectively. In the mice received L-alanine, acetate and acetone levels in blood, liver and brain were distinctly reduced (p less than 0.01). L-Alanine is reported to supply an abundance of pyruvic acid that performs the NAD-generating system. NAD produced is introduced to alcohol metabolism and the TCA cycle. It was thus presumed that the L- or/and D-cysteine, and L-alanine was effective in acute alcohol intoxication by heavy drinking.
The cytogenetical etiology of partial mole (PM) was studied by means of the Q-banding technique in 49 cases during the period between Sep. 1976 and Nov. 1986. Moreover, histological examinations were performed in 39 cases concentrating on the existence of fetal components and trophoblastic hyperplasia, etc. The results were as follows. 1. Karyotype analysis showed triploidy (24 cases), normal diploidy (10 cases), trisomy (9 cases) and other anomalies (mosaic, translocation etc.) (6 cases). These results are quite different from those of many western authors, who reported that most cases of PM are triploidy. 2. The criteria of PM in Japan differ from those of WHO Scientific Group in regard to trophoblastic hyperplasia. 3. Our cases were reclassified on the basis of the definition drawn up by the WHO Scientific Group. Nevertheless, the rate of triploidy was only 54.5%, which is lower than that reported by many western authors. These results show that the development of PM cannot be explained cytogenetically at present, in contrast with complete mole.
We investigated the kinetics of production of the hepatocyte stimulating factor (HSF) by peritoneal exudate- and peripheral circulating blood-polymorphonuclear leukocytes (PMNLs). Effects of the HSFs on alpha-2-macroglobulin (a2M) synthesis and a2M specific gene expression in primary cultured adult rat hepatocytes were also examined. Peritoneal exudate-PMNLs were collected 3 hr after the injection of alkaline-denatured casein into the peritoneal cavity of rats. Secretion of HSF into the culture medium began within 15 min after the start of incubation and practically a full secretion was noted within 3 hr. Lipopolysaccharide or other agents were not required to induce HSF from the PMNLs. Inhibitors of protein or DNA synthesis, cycloheximide, actinomycin D or puromycin, did not inhibit the secretion of HSF by rat PMNLs thereby suggesting that preformed and pooled HSF in the PMNLs was secreted during incubation. Peripheral circulating blood-PMNLs collected from a healthy man did not secrete HSF, in the absence of stimulation but did secrete HSF after vigorous agitation during incubation at 37 degrees C. The PMNL-HSF induced the synthesis of a2M and the accumulation of a2M mRNA in primary cultured rat hepatocytes. However, the effect was evident only with dexamethasone present in the culture medium. Furthermore, the effects of the PMNL-HSFs on a2M and albumin protein synthesis were reciprocal: The PMNL-HSF induced a2M synthesis, whereas it suppressed albumin synthesis.
A 68-year-old male was admitted to hospital for treatment of a hepatocellular carcinoma with a bone metastasis. By TAE and the administration of PSK, the tumor was necrotized and the AFP level returned to normal range. We presume that this combination therapy of TAE and PSK was able to maintain normal cellular immunity and bring about this good result.
A case of non-functional adrenocortical adenoma is reported. The patient was a 62-year-old woman with the chief complaint of right hypochondoralgia. The small right adrenal tumor was found incidentally by ultrasonography on examination for cholecystolithiasis. Since there was no evidence of malignancy from biochemical data, observation of the tumor was performed for 3 months. However, the lesion was gradually increased in size. Therefore, right adrenalectomy was performed. Histological findings revealed benign adrenocortical adenoma. In the Japanese literature this case seems to be the 36th case of non-functional adrenocortical adenoma.
The effect of Kupffer cells on natural killer (NK) cell-mediated cytotoxicity was examined. Kupffer cells prepared from rat liver suppressed NK activity against K562 cells and other tumor cell lines through a soluble factor secreted into the culture supernatant. When human peripheral blood mononuclear cells were incubated with the Kupffer cell-culture supernatant, a significant reduction of the cytotoxic activity was observed in the 6-hr chromium-release assay. This activity was dose dependent and was evident at various effector/target cell ratios. Lipopolysaccharide stimulated generation of the suppressive factor released from Kupffer cells in a dose-dependent manner. Suppression of the NK activity was observed when the Kupffer cell-culture supernatant was present in the assay system, whereas pretreatment of effector/target cells with the supernatant had minimal inhibitory effects. Autologous monocytes in human peripheral mononuclear cells were not related to this suppression. The suppressive factor in the fraction had a molecular weight below 10,000. Indomethacin, an inhibitor of prostaglandin synthesis, ameliorated the suppressive effects. These results suggest that Kupffer cells may modulate NK activity by producing PGs (E1, E2, and F2 alpha).