Search PubMed⌕ Search

Biomedical subjects

T Hada

Publications and source records attributed to T Hada.

At least 145 records · Page 8Linked to original sources
PubMed1990

Analysis of uric acid transport in renal tubules using benzbromarone and pyrazinamide.

Both the benzbromarone loading test alone and the pyrazinamide suppression test combined with the benzbromarone loading test were performed in four healthy male volunteers to examine the renal handling of uric acid and to demonstrate whether benzbromarone selectively blocks postsecretory reabsorption. On the basis of the four-component theory, equations of four states of fractional uric acid clearance were constructed: 1) the control state, the states of 2) benzbromarone loading, 3) pyrazinamide suppression and 4) both pyrazinamide suppression and benzbromarone loading. As a result, presecretory reabsorption, tubular secretion and postsecretory reabsorption of uric acid were calculated to be about 93-98%, 30-44% and 79-92%, respectively. In addition, it was calculated that benzbromarone inhibited postsecretory reabsorption selectively. Because of the selectivity of the action site of benzbromarone in renal tubules, this loading test is considered to reflect uric acid transport more precisely than tests using probenecid.

Benzbromarone↗
PubMed1989

B cell response pathways regulated by IL-5 and IL-2. Secretory microH chain-mRNA and J chain mRNA expression are separately controlled events.

We have examined the effect of IL-5 and/or IL-2 on the expression of the secretory form of microH chain (microsecond) and J chain mRNA in a homogeneous neoplastic B cell clone, in which proliferation, IL-2R up-regulation and entry into the IgM secretory state are separately controlled events. The IL-5 signal triggers a partial induction of CL-3 cells into the IgM secretory state, characterized by a striking increase of microsecond mRNA expression and an increase in the ratio of the secretory to membrane forms of microH chain mRNA, with a modest increase of J chain mRNA. In contrast, amplification of J chain mRNA is accomplished by the late-acting B cell differentiation stimulus, IL-2, acting on IL-5-pretreated CL-3 cells or acting simultaneously with IL-5 on CL-3 cells. Such dually stimulated cells now are fully induced into IgM secreting cells. These results define the relative roles of IL-5 and IL-2 in B cell differentiation by showing important regulatory effects at the mRNA level. In addition, these results substantiate that appearance of mRNA for J chain, a molecule key to the formation of pentameric IgM, is a limiting factor for high level IgM secretion. The separate control of microsecond and J chain mRNA found in CL-3 cells stimulated with IL-5 and IL-2 elucidates a molecular mechanism by which these two lymphokines synergize in the development of CL-3 cells into IgM secreting cells.

B-Lymphocytes↗
PubMed1989

Metabolism of pyrazinamide and allopurinol in hereditary xanthine oxidase deficiency.

The metabolism of pyrazinamide and allopurinol was studied in three xanthinuric patients from two families with hereditary xanthinuria to determine whether both substrates were oxidized only by xanthine oxidase or by other oxidases as well. One xanthinuric patient could neither metabolize pyrazinamide into 5-hydroxypyrazinamide nor allopurinol into oxypurinol. Two xanthinuric patients could metabolize both pyrazinamide into 5-hydroxypyrazinamide and allopurinol into oxypurinol but could not oxidize pyrazinoic acid to 5-hydroxypyrazinoic acid. These findings suggest that xanthinuria comprises at least two subgroups.

Adult↗
PubMed1989

Reduction of 7-ketolithocholic acid by human liver enzyme preparations in vitro.

The formation of chenodeoxycholic and ursodeoxycholic acids from 7-ketolithocholic acid by human liver preparations was examined in vitro. Liver preparations were incubated with 7-ketolithocholic acid at pH 5.5 in a sodium-potassium-phosphate buffer containing NADPH or NADH. The products formed were analyzed by gas chromatography and gas chromatography-mass spectrometry. Results showed that chenodeoxycholic and ursodeoxycholic acids could be formed from 7-ketolithocholic acid by human liver enzyme(s). The enzyme(s) required NADPH but not NADH as coenzyme and was localized largely in the microsomes. The conjugated 7-ketolithocholic acid, especially the taurine conjugated, was predominantly reduced to chenodeoxycholic acid, whereas the unconjugated 7-ketolithocholic acid was not reduced well to either chenodeoxycholic acid or ursodeoxycholic acid. Thus the reduction of 7-ketolithocholic acid by human liver enzyme(s) was found to be dependent on whether the substrate was conjugated or not.

Chenodeoxycholic Acid↗
PubMed1989

Effect of probenecid on oxypurines in plasma.

Probenecid decreased the plasma concentration of oxypurines (hypoxanthine and xanthine) but did not increase the renal excretion of oxypurines. However, the concentrations of hypoxanthine and nucleotides (inosine monophosphate, adenosine monophosphate, adenosine diphosphate, adenosine triphosphate, guanosine diphosphate and guanosine triphosphate) in red blood cells did not change after the administration of probenecid. In addition, the drug did not inhibit adenosine deaminase, purine nucleoside phosphorylase, hypoxanthine guanine phosphoribosyl transferase and xanthine oxidase in vitro. These results suggested that the rapid fall of plasma concentration of uric acid due to the potent uricosuric action of probenecid resulted in the fall of plasma concentration of oxypurines.

Adenosine Deaminase↗
PubMed1989

[A case of multiple cavities on chest film with high titer of serum cryptococcal antigen].

A 26-year-old man admitted to Nishinomiya Municipal Hospital for further evaluation for abnormal shadows on the chest film in a mass examination. He had no subjective complaints; for example, cough, sputum or dyspnea. His past history and physical examinations yielded no significant findings. The chest film revealed the multiple cavities accompanied with a little infiltration throughout several lobes bilaterally. The inflammatory reactions; such as, CRP and ESR, were all intact, but the titer of the serum cryptococcal antigen was high. He was not immunocompromised. Although bronchoscopy and transbronchial lung biopsy were performed twice during admission, they revealed no pathogenic findings both bacteriologically and histologically. The elevation of the serum cryptococcal antigen titer suggested that this disease is the primary pulmonary cryptococcosis. The titer decreased with spontaneous disappearance of the abnormal shadows on the chest film. This test has a sensitivity of 90% for cryptococcal infection, but in rheumatoid arthritis, a small percentage of false positive results have been reported. Therefore, if the rheumatoid factor is eliminated, the test is more specific for cryptococcal infection. On the other hand, some authors have reported the false positive results in Trichosporon beigelii infection by this method. But this disease is negligible for its frequency in clinical features in our country. We emphasized that this non-invasive test is more useful for the diagnosis of the primary pulmonary cryptococcosis.

Adult↗
PubMed1989

Pancreatitis in the annulus of annular pancreas demonstrated by the combined use of computed tomography and endoscopic retrograde cholangiopancreatography.

Annular pancreas, an uncommon condition, is often hard to diagnose before operation. We report a case of annular pancreas with pancreatitis of the annulus that was diagnosed by the use of computed tomography followed by endoscopic retrograde cholangiopancreatography. An upper gastrointestinal series and duodenoscopy revealed stenosis of the second portion of the duodenum. Computed tomography revealed enlargement of the annulus of the pancreas. Two years later, follow-up computed tomography demonstrated calcifications of the annulus, although the remaining pancreas seemed to be normal.

Adult↗
PubMed1989

The effect of phenobarbital on human plasma lipids.

The effect of phenobarbital to increase the activity of hepatic microsomal enzyme system, resulting in an increase in high density lipoprotein (HDL)-cholesterol, is well known. However, it remains uncertain whether phenobarbital increases plasma concentrations of cholesterol and triglyceride, and which subfractions of the high density lipoprotein fractions phenobarbital increases. The present study was therefore, conducted to investigate these points. Long-term treatment of phenobarbital increased the plasma concentrations of HDL2-cholesterol, HDL3-cholesterol and HDL3-phospholipid, and decreased the plasma concentrations of low density lipoprotein + very low density lipoprotein-cholesterol. On the other hand, its long-term treatment did not affect the plasma concentrations of cholesterol, triglyceride and phospholipid. In addition, phenobarbital increased the plasma concentration of apolipoprotein A-I, decreased the plasma concentration of apolipoprotein B, but did not affect the plasma concentration of apolipoprotein A-II. These results indicate the possibility that phenobarbital has an antiatherogenic effect.

Adult↗
PubMed1988

Serum pseudouridine as a biochemical marker in patients with hepatocellular carcinoma.

The concentration of serum pseudouridine, a degradation product of transfer ribonucleic acid, was determined by high-performance liquid chromatography in patients with hepatocellular carcinoma, liver cirrhosis, other benign hepatobiliary diseases, and healthy controls. The serum pseudouridine concentration in patients with hepatocellular carcinoma was significantly higher than that in patients with cirrhosis or the controls. Twenty-seven (51.9%) of 52 patients with hepatocellular carcinoma had serum pseudouridine concentrations higher than the mean value for healthy controls plus 2 SD. Fourteen of the 36 patients who had serum alpha-fetoprotein levels below 400 ng/ml, had elevated serum pseudouridine concentration. In total, 36 of the 52 patients (69.2%) could be detected by combination of these two markers. Two patients who had developed hepatocellular carcinoma during the course of cirrhosis and were continuously negative for alpha-fetoprotein, had higher levels of the pseudouridine concentration when hepatocellular carcinoma occurred. Furthermore, 4 of the 7 patients who had a very small cancer and were negative for alpha-fetoprotein, had elevated serum pseudouridine concentration. These results indicate that serum pseudouridine is a useful biochemical marker and that serum pseudouridine and alpha-fetoprotein in combination are considered to serve as complementary markers, for the diagnosis of hepatocellular carcinoma.

Aged↗
PubMed1988

Direct determination of urinary pseudouridine by high-performance liquid chromatography.

A reversed-phase high-performance liquid chromatographic method was developed for the determination of pseudouridine in urine. This method does not need pretreatment by boronate affinity gel. Therefore, it can be used in screening patients with malignant disease and for monitoring clinical response to chemotherapy with other tumor markers.

Biomarkers, Tumor↗
PubMed1988

Tumor markers in pleural effusion diagnosis.

In order to discriminate between malignant and benign effusions, the values of carcinoembryonic antigen (CEA), ferritin, beta2-microglobulin (BMG), acid-soluble glycoprotein (ASP), tissue polypeptide antigen (TPA), adenosine deaminase (ADA), and immunosuppressive acidic protein (IAP) were measured in the pleural fluid of 54 patients with lung cancer, 20 with malignancies other than lung cancer, 18 with tuberculous pleurisy, and 22 with benign diseases other than tuberculosis. CEA levels in malignant effusions were significantly higher than those in benign effusions. At a cutoff level of 5 ng/ml, 68% of the patients with lung cancer and 44% of the patients with other malignancies showed elevated pleural fluid CEA levels. In 13 lung cancer cases with negative pleural fluid cytology, nine cases had elevated pleural fluid CEA levels. The mean pleural fluid BMG level of patients with benign diseases was significantly higher than that of patients with malignant diseases, but there was a marked overlap between those with malignant and benign diseases. No significant differences were found in the pleural fluid ferritin, ASP, TPA, and IAP levels between malignant and benign conditions. ASP and IAP pleural fluid levels showed significant correlations with the pleural fluid C-reactive protein (CRP) concentrations suggesting that they also reflect inflammatory activity. The mean ADA activity in tuberculous effusion was significantly higher than that resulting from other causes of pleural effusion.

Adult↗