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Biomedical subjects

N Yuki

Publications and source records attributed to N Yuki.

At least 289 records · Page 16Linked to original sources
PubMed1991

Renal kinin and kallikrein excretion in cirrhotic patients.

Urinary kinin and urinary kallikrein activity were measured in 33 liver cirrhotics, and the values were correlated with the severity of the liver disease. A significant relationship was observed between urinary kinin excretion and urinary kallikrein excretion (r = 0.53; p less than 0.01). Both urinary kinin and kallikrein excretion were significantly lower in Child's group C than in Child's groups A and B (p less than 0.05) and showed positive correlations with serum albumin (r = 0.47, p less than 0.01 and r = 0.46, p less than 0.01, respectively). Increases in urinary kinin and kallikrein excretion after endoscopic variceal sclerotherapy were observed in 18 patients (p less than 0.01 and p less than 0.05, respectively). These results suggest that the renal kallikrein-kinin system in suppressed in severe liver disease in proportion to the severity of the underlying liver disease. In this study possible activation of this system after sclerotherapy was also demonstrated.

Esophageal and Gastric Varices↗
PubMed1991

[Detection of hepatitis C virus RNA in serum during treatment of chronic hepatitis C with interferon alpha].

We estimated HCV RNA in serum of 20 patients with chronic hepatitis C during interferon therapy using a combination assay of reverse transcription and polymerase chain reaction (RT-PCR). RNA was extracted from 200 microliters of serum. The primers were chosen from the NS3 region of prototype HCV RNA sequence. After 40 cycles of PCR, the products were analyzed by Southern hybridization. HCV RNA was detected in 18 of 20 (90%) patients before therapy. In cases with improvement of serum GPT level, HCV RNA became undetectable at 4 weeks of the therapy. However, HCV RNA reappeared within 4 weeks after the therapy in cases with relapse. In the no response group, HCV RNA did not disappear during the therapy. Interferon therapy is beneficial in improvement of viremia of HCV, and the detection of HCV RNA in serum is useful to evaluate the antiviral effect of interferon.

Adult↗
PubMed1991

[The correlation of consciousness level and the concentration of CSF ammonia in a patient with adult-type citrullinemia].

A 29-year-old man who had a taste for peanuts frequently showed abnormal behaviors. Physical examination revealed consciousness disturbance associated with flapping tremor, hypotonus in the extremities, and hypoactive deep tendon reflexes. Laboratory examination showed hyperammonemia with mild liver injury. A level of serum citrulline was 14 times higher than the upper limit of normal. A diagnosis of type 2 citrullinemia (Seheki et al) was established by the decreased argininosuccinate synthetase (ASS) in liver with low amount of ASS protein and normal kinetic properties. Diurnal fluctuation of consciousness level in this patient was not correlated with the concentration of ammonia in serum, but with that in cerebrospinal fluid. Main metabolic pathway of ammonia in brain is considered to be localized in astrocytes which have receptors for glucocorticoids. Glucocorticoids induce additional glutamine synthetase activity. Circadian rhythm of cortisol level might play a role in diurnal fluctuation of consciousness level in patients with citrullinemia.

Adult↗
PubMed1991

[A case of distal lower motor neuron syndrome associated with IgM anti-GM1 antibodies].

A 34-year-old man had noted progressive weakness in his right hand. On admission at age 39, cranial nerves were not involved. Fasciculations were observed in his upper limb girdles. Neurological examination revealed severe wasting and weakness of arms and the right hand, whereas mild in the left hand. The deep tendon reflexes were absent in the upper extremities, but normal in the lower extremities. No sensory disturbances were observed. Motor and sensory nerve conduction velocities were normal, and multifocal conduction block was not observed. EMG showed neuropathic changes in all 4 limbs and sternocleidomastoideus muscles. Serum immunoelectrophoresis failed to detect an M protein. High-performance thin-layer chromatography with immunostaining revealed that his serum IgM reacted with GM1, but not reacted with GM2, GD1a, GD1b, and asialo-GM1.

Adult↗
PubMed1991

Expression of X protein and hepatitis B virus replication in chronic hepatitis.

The X protein can act on the enhancer of hepatitis B virus in an in vitro system and elevate the transcriptional level of hepatitis B virus. However, because no relationship had been reported between X protein expression and hepatitis B virus replication in patients with chronic hepatitis B, we focused on its expression in the liver in comparison with markers of hepatitis B virus replication. Liver biopsy samples and sera from 59 carriers with HBsAg were examined immunohistochemically for X protein using rabbit IgG against recombinant X protein. There was a significant difference in the serum hepatitis B virus DNA level between X protein-positive and -negative patients (p less than 0.001). Serum pre-S1 and pre-S2 antigens were also measured quantitatively by enzyme immunoassay using monoclonal antibodies specific against each antigen. The titers of pre-S1 antigen in patients positive for X protein were significantly higher (p less than 0.001) than those of the X protein-negative patients (3.02 +/- 0.99 vs. 2.00 +/- 0.59, respectively). Similarly, the titers of pre-S2 antigen were 2.98 +/- 0.91 vs. 1.94 +/- 0.54, respectively (p less than 0.001). The rate of positivity of the X protein was higher (38 of 49; 77.6%) in the replicative group (serum HBeAg, serum hepatitis B virus DNA or HBcAg in liver positive) compared with that observed in the nonreplicative group (3 of 10; 30%--serum HBeAg, serum hepatitis B virus DNA and HBcAg in liver negative) (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

Quantitative analysis of pre-S1 and pre-S2 in relation to HBsAg expression.

Sera from four patients with acute hepatitis B and 87 patients with chronic hepatitis B were examined quantitatively for pre-S1 and pre-S2 antigens by solid-phase enzyme immunoassays. Pre-S1 and pre-S2 antigens were detected in HBsAg-positive sera irrespective of the presence of viral replicative markers, and their titers correlated with those of HBsAg (r = 0.74, p less than 0.01; r = 0.74, p less than 0.01, respectively). Sera positive for HBeAg showed higher titers of pre-S1 (p less than 0.01) and pre-S2 (p less than 0.01) antigens than sera negative for HBeAg. The titers of pre-S1 and pre-S2 antigens also correlated with the levels of HBV-associated DNA polymerase activity (r = 0.51, p less than 0.01; r = 0.59, p less than 0.01, respectively) and HBV-DNA (r = 0.50, p less than 0.01; r = 0.46, p less than 0.01, respectively). However, the ratios between the titers of pre-S antigens and HBsAg had no significant relationships with those viral replicative markers. These findings suggest that the expression of pre-S antigens is intimately related to the expression of HBsAg and that they are not useful as markers of viral replication. The ratios between the titers of pre-S antigens and HBsAg tended to be high in patients with chronic active hepatitis and high aminotransferase levels. This finding may have been due to the hepatic release of pre-S antigens, over-production of which may have some relationship to liver injury.

Acute Disease↗
PubMed1990

Detection of antibodies against the polymerase gene product in hepatitis B virus infection.

We have studied antibodies (anti-pol antibody) against the polymerase gene product of hepatitis B virus by solid-phase enzyme immunoassay using synthetic peptides coded for by this gene. Sera from six patients with acute hepatitis B, 112 chronic hepatitis B virus carriers and six healthy individuals with naturally acquired immunity to hepatitis B virus were tested for anti-pol antibody. In acute hepatitis B virus infection, anti-pol antibody was detected in three of six patients. In chronic hepatitis B virus infection, anti-pol antibody was detected in 17 of 29 (59%), in 23 of 33 (70%) of cirrhotic patients and in 18 of 24 (75%) patients with cirrhosis complicated by hepatocellular carcinoma, compared with 4 of 19 (21%) asymptomatic carriers and 2 of 7 (29%) patients with chronic persistent hepatitis. Titers of anti-pol antibody were higher in cirrhotic patients with and without hepatocellular carcinoma than in patients with chronic active hepatitis. The presence of anti-pol antibody, however, had no relationship with hepatitis B virus-associated DNA polymerase activities and other viral replicative markers. As for sera from six healthy individuals with naturally acquired immunity to hepatitis B virus, two (33%) were positive for anti-pol antibody. These results indicate that the immune response toward the polymerase gene product is induced during acute and chronic hepatitis B virus infection. In chronic hepatitis B virus infection, anti-pol antibody may serve as a new marker indicative of a long period of hepatitis B virus-induced hepatitis.

Acute Disease↗
PubMed1990

Effects of endoscopic variceal sclerotherapy using GT XIII on blood coagulation tests and the renal kallikrein-kinin system.

Forty-six sclerotherapy sessions were performed on liver cirrhotics with high-risk esophageal varices using GT XIII, a sclerosant composed of gelatin, thrombin and coagulation factor XIII. GT XIII was effective for the prevention of temporary symptoms and transient hypotension observed in 55 sclerotherapy sessions using thrombin. In 42 (91%) sessions, patients underwent sclerotherapy with no symptoms, and in the other four (9%) sessions, only slight symptoms of general fatigue and headache were observed. Changes in the mean arterial pressure were significantly smaller in sessions using GT XIII than in those using thrombin (-12.3 +/- 13.6 vs. -26.8 +/- 20.7 mmHg, P less than 0.01). Changes in coagulation tests, similar to those of disseminated intravascular coagulation (DIC), were also reduced in sessions using GT XIII. Urinary kallikrein and kinin excretion significantly increased after the procedure (P less than 0.01), indicating activation of the renal kallikrein-kinin system. Increases in urinary kallikrein and kinin excretion showed a significant relationship with the consumed plasma fibrinogen levels (r = -0.51, P less than 0.01 and r = -0.58, P less than 0.01, respectively), and it was suggested that activation of the glandular kallikrein-kinin system caused by abrupt DIC-like changes in the hemostatic system might play a role in manifestations of temporary complications occurring with the use of hemostatic agents containing thrombin.

Blood Coagulation↗
PubMed1990

Acute axonal polyneuropathy associated with anti-GM1 antibodies following Campylobacter enteritis.

We report 2 patients with Guillain-Barré syndrome (GBS) following Campylobacter jejuni enteritis. Electrophysiologic studies indicated that the predominant process was axonal degeneration of motor nerves, and clinical recovery was poor. Serum testing by thin-layer chromatography and enzyme-linked immunosorbent assay revealed that the sera from both patients contained high titers of IgG antibody against GM1 ganglioside. These cases may represent a subgroup of GBS as acute axonal polyneuropathy following C jejuni enteritis associated with anti-GM1 antibodies.

Adult↗
PubMed1990

[Expression of hepatitis B virus (HBV) markers in chronic liver disease positive for antibody to hepatitis C virus (HCV)].

We investigated expression of HBV markers in chronic liver disease positive for antibody to HCV (anti-HCV). Sera from 107 patients with chronic non-A, non-B liver disease, 65 HBs antigen carriers with chronic liver disease and 14 asymptomatic HBV carriers were tested for the presence of anti-HCV. Anti-HCV was detected in 83 (78%) patients with chronic non-A, non-B liver disease, irrespective of the past history of blood transfusion, and anti-HCV prevalence was similar in each category of chronic liver disease. Fifty-three (64%) out of these 83 sera positive for anti-HCV has also antibodies to HBV. Anti-HBc antibody was detected frequently in liver cirrhotics with hepatocellular carcinoma than in chronic persistent hepatitis, chronic active hepatitis and cirrhotics without hepatocellular carcinoma. In addition, titers of anti-HBc antibody were significantly higher in cirrhotics with hepatocellular carcinoma than in the other groups. On the other hand, anti-HCV was detected in 7 out of 65 patients with HBV-related liver disease. Four out of these 7 were patients with HBV-related hepatocellular carcinoma. Anti-HCV was detected in none of asymptomatic HBV carriers. These findings suggest that infection with both HBV and HCV is likely to cause more serious liver disease than infection with a single agent.

Adult↗
PubMed1990

[An acute axonal form of Guillain-Barré syndrome with antibodies against gangliosides GM1 and GD1b--a case report].

We reported a case of Guillain-Barré syndrome with autoantibodies against gangliosides GM1 and GD1b, which has not been reported yet. A 25-year-old man was admitted with a 7-day history of acute progressive weakness in the extremities. Two weeks before admission he had suffered from an episode of watery diarrhea. Neurological examination revealed areflexia and tetraparesis without any sensory impairment. Respiration and cranial nerves were not involved. The CSF protein level was 157 mg/dl with normal cellularity on the 14th illness day. The maximum M potential amplitude was 0.1 mV, which was 2% of the lower limit of normal, whereas motor and sensory nerve conduction velocities were normal on day 22. Repeated electrophysiological studies suggested that the predominant process was axonal degeneration. Although he received plasmapheresis at the acute phase, four months after onset he continued to have distal dominant limb weakness with wasting. High-performance thin-layer chromatography with immunostaining revealed that his serum IgG reacted with GM1, GD1b, and asialo-GM1. Enzyme-linked immunosorbent assay showed that anti-glycolipids antibodies titers decreased, concurrent with clinical course. Immunoabsorption study demonstrated that antibodies with anti-GM1 activity were absorbed with liposomes containing purified GD1b, indicating that autoantibodies bind to the galactosyl (beta 1-3) N-acetylgalactosaminyl moiety which is shared by GM1, GD1b, and asialo-GM1. There have been several reports of lower motor neuron diseases with monoclonal IgM antibody to GM1, GD1b, and asialo-GM1. This case suggested that the transient rise in these anti-carbohydrate antibodies may be involved in the pathogenesis of acute axonal degeneration of motor nerve as well as paraproteinemic motor neuron diseases.

Acute Disease↗
PubMed1989

[Expression of Pre-S2 antigen and antibody in patients with hepatitis B virus infection].

We investigated the expression of Pre-S2 antigen (Ag) and antibody (Ab) in sera quantitatively using ELISA. Four patients with acute hepatitis B and 87 chronic HBV carriers were included in this study. We also investigated the expression of Pre-S2Ag in the liver tissues obtained from 26 chronic HBV carriers by direct fluorescent antibody method. There was a significant correlation between Pre-S2Ag titers and HBsAg titers in sera. Pre-S2Ag titers were higher in sera positive for HBeAg, HBV-related DNA polymerase or HBV-DNA than in sera negative for those markers. The ratio of Pre-S2Ag titers to HBsAg titers, however, was constant irrespective of virus replicative markers. Pre-S2Ag in the liver had almost same intracellular localization with HBsAg in the liver. It was suggested that Pre-S2Ag was expressed with an intimate relation to the expression of HBsAg and was not useful as a virus replicative marker. Pre-S2Ag titers/HBsAg titers tended to be high in patients with chronic active hepatitis and high serum GPT levels compared to patients with chronic inactive hepatitis. This may be explained by the release of Pre-S2Ag in the liver. In addition, all patients positive for Pre-S2Ag on the membrane of hepatocytes had chronic active hepatitis. The overproduction of Pre-S2-containing surface proteins in the liver may have some implication related to cell injury via the immune response to Pre-S2Ag etc. Pre-S2Ab was detected only in few cases of chronic HBV infected patients. The lack of immune response to Pre-S2 region may play a role in the persistence of HBV infection.

Enzyme-Linked Immunosorbent Assay↗
PubMed1989

[Expression of pre-S1 antigen and pre-S1 antibody in sera obtained from HBV infected patients].

We investigated the expression of Pre-S1 antigen and Pre-S1 antibody using a synthetic peptide and the monoclonal antibody against it. Four patients with acute hepatitis B and 87 chronic HBsAg carriers were included in this study. There was a significant correlation between Pre-S1 antigen titers and HBsAg titers. Pre-S1 antigen showed higher titers in patients with active viral replication, positive for HBeAg, HBV-DNA or HBV-related DNA polymerase. The ratio of Pre-S1 antigen titers to HBsAg titers, however, had no significant relationship with those replicative markers. It was suggested that Pre-S1 antigen was expressed with an intimate relation to the expression of HBsAg and was not so useful as a new replicative marker. Pre-S1Ag titers/HBsAg titers tended to be high in patients with chronic active hepatitis and high serum GPT levels. This may be due to the release of overproduced intracellular Pre-S1 antigen. Pre-S1 antibody was detected only in few cases of chronic HBsAg carriers. This result shows that the immune tolerance to Pre-S1 region may play a role in the persistence of HBV infection.

Carrier State↗
PubMed1987

Differentiation therapy of a myelomonocytic leukemia (c-WRT-7) in rats by injection of lipopolysaccharide and daunomycin.

We examined the therapeutic effect of lipopolysaccharide (LPS), a differentiation inducer, in combination with daunomycin, an antileukemia drug possessing differentiation-inducing potential, on a rat myelomonocytic leukemia (c-WRT-7). c-WRT-7 cells were found to differentiate into macrophage-like cells and to lose their growth capacity both in vitro and in vivo after incubation with LPS. Morphological differentiation of c-WRT-7 cells was observed in diffusion chambers which had been inserted into the abdominal cavity of syngeneic WKA rats given injections of LPS. A series of i.p. injections of LPS resulted in the complete inhibition of the leukemia development in about 60% of the rats while the remaining rats showed a significant prolongation of survival time when they were given i.p. injections of LPS-sensitive c-WRT-7 cells. The effect of LPS was minimal, however, in those rats which had been given i.p. injections of LPS-hyporesponsive c-WRT-7 cells. Although an i.v. injection of 100 untreated c-WRT-7 cells was enough to kill the syngeneic rats, combination treatment with LPS and daunomycin was able to inhibit completely the development of leukemia in those rats which had been given i.v. injections of LPS-sensitive c-WRT-7 cells, whereas the same treatments were only partially effective in the prolongation of survival among those rats which had been given i.v. injections of LPS-hyporesponsive c-WRT-7 cells. Our studies show that LPS was capable of curing a proportion of rats and that it significantly prolonged the survival of the remainder who had received a transplantation of the differentiation-sensitive leukemia cells; this action was significantly enhanced by the associated administration of daunomycin.

Animals↗
PubMedDate not supplied

Computed tomographic findings of progressive supranuclear palsy compared with Parkinson's disease.

We investigated computed tomographic (CT) films of 4 pathologically documented cases of progressive supranuclear palsy (PSP) in which the clinical presentations were atypical and compared the findings with those of 15 patients with Parkinson's disease (PD). Dilatation of the third ventricle, atrophy of the midbrain tegmentum, and enlargement of the interpeduncular cistern toward the aqueduct were found to be the characteristic findings in PSP. Thus, radiological findings can be useful when the differential diagnosis between PSP and PD is clinically difficult.

Aged↗