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Biomedical subjects

T Beppu

Publications and source records attributed to T Beppu.

At least 307 records · Page 17Linked to original sources
PubMed1985

[Transcatheter hepatic arterial embolization therapy using degradable polylactic acid microspheres].

Transcatheter hepatic arterial embolization therapy (TAE) is an established method for the treatment of hepatocellular carcinoma (HCC). We have developed a new embolus consisting of microspheres with a mean diameter of about 200 microns which are composed of biodegradable polymolecular polylactic and the anti-cancer agent, aclarubicin -HCl, in a ratio of 12% w/w. These microspheres were applied to 28 patients with inoperable HCC using the following method microspheres containing 50 mg of aclarubicin-HCl were injected through a catheter placed in the hepatic artery or one of its branches, 2 or 3 times at intervals of 2 to 4 weeks. The effectiveness was confirmed by decreased levels of serum AFP and regression of the tumor size, and the accumulated survival rate for 6 months was 83.3%.

Aclarubicin↗
PubMed1985

Pharmacokinetic study on the hepatic uptake of indocyanine green in cirrhotic patients.

The mechanism by which the mean blood clearance (CLtot,B) of indocyanine green (ICG) was reduced in cirrhotic patients was examined pharmacokinetically. It was demonstrated that the reduction in the CLtot,B of ICG in cirrhosis would be mainly due to the decrease in the hepatic uptake clearance and partly due to the increase in the efflux clearance from the liver to plasma. It is suggested that the decrease in the hepatic uptake clearance in cirrhosis mainly reflects the decrease in the intrinsic clearance of hepatic uptake rather than the decrease in hepatic blood flow.

Adult↗
PubMed1984

Hepatic extraction of chenodeoxycholic acid in dogs chronically intoxicated with dimethylnitrosamine.

The pharmacokinetics of chenodeoxycholic acid (CDCA) in hepatic dysfunction were evaluated by analyzing the plasma disappearance curves after simultaneous administration of [3H]- and [14C]-CDCA through the femoral and portal veins, respectively, in dogs chronically intoxicated with dimethylnitrosamine (DMN). The plasma concentration-time curve of intravenously administered [3H]-CDCA was best fitted to a three-exponential equation, while that of intraportally administered [14C]-CDCA was fitted to either a two- or a three-exponential equation. In the DMN-intoxicated dogs, significant decreases were observed in total body plasma clearance (CLp), hepatic extraction ratio (EH) and apparent intrinsic clearance (CLint) compared to those of the untreated (control) dogs. The hepatic blood flow (QH), calculated from CLp, CLint and blood-to-plasma concentration ratio (RB) according to the equation reported by Wilkinson and Shand [Clin. Pharmac. Ther. 18, 377 (1975)], was reduced to approximately 70% in the DMN-intoxicated dogs compared to the control dogs. The bindings of CDCA to plasma and liver cytosol fraction were determined by equilibrium dialysis; no significant difference was observed in the unbound fraction between the DMN-treated and control dogs. By comparing both pharmacokinetic parameters obtained from intravenous and intraportal administration, the usefulness of the oral bile acid tolerance test was examined. From these findings, it was suggested that the decrease in the CLp of the DMN-intoxicated dogs was due to both the decrease in QH and that in CLint, and that the decrease in CLint may be due not to an alteration of plasma or cytosol binding but to that of a carrier-mediated transport system. It is also suggested that the measurement of fasting plasma bile acid concentration or the oral bile acid tolerance test is more sensitive for the detection of hepatic dysfunction than the intravenous bile acid tolerance test.

Animals↗
PubMed1984

Hepatic transport of indocyanine green in dogs chronically intoxicated with dimethylnitrosamine.

Hepatic transport of indocyanine green (ICG) was examined in dogs chronically intoxicated with dimethylnitrosamine (DMN) (2 mg/kg) intraportally once a week for 6 weeks. In pathophysiological consequences, significant increases (p less than 0.05) were shown in both glutamic-pyruvic transaminase (GPT) and total plasma bile acids, but no significant difference was shown in body weight, liver wet weight, glutamic-oxaloacetic transaminase (GOT), plasma alkaline phosphatase activity, total plasma protein, and total plasma bilirubin. By histologic examination of livers from intoxicated dogs, increased fibrosis in periportal, perisinusoidal, and especially pericentral areas, with loss of normal architecture, was observed. Partial fibrous bridging between periportal and pericentral areas was also demonstrated, but extensive pseudolobulation with regenerative nodules was not observed. The portal venous pressure of the intoxicated dogs was increased by approximately 50% of that of control dogs. In intoxicated dogs, delays were shown in both plasma disappearance and biliary excretion of ICG and significant decreases were observed in the pharmacokinetic parameters k12 (plasma to liver transfer rate constant), V2 (distribution volume of liver compartment), and CLtot (total body-plasma clearance), while a significant increase was observed in k23 (intrahepatic diffusion and transport rate constant); the V1 (distribution volume of plasma compartment) was not altered. From these findings, it is suggested that the decrease in the intrinsic clearance of ICG for the hepatic uptake process might explain the decrease in ICG uptake rate into the liver which was observed in the DMN-intoxicated dogs. Dogs chronically intoxicated with DMN might be a good model for studying hepatic dysfunction.

Alanine Transaminase↗
PubMed1984

Urinary concentrations of bile acid glucuronides and sulfates in hepatobiliary diseases.

Urinary bile acids in normal subjects and patients with obstructive jaundice and liver cirrhosis were quantitated by mass fragmentography after separation into nonglucuronidated-nonsulfated, glucuronidated and sulfated fractions. Mean values of total bile acids in urine were as follows: Control subjects (n = 7), 1.90 +/- 0.67; obstructive jaundice (n = 9), 77.90 +/- 40.39; liver cirrhosis, compensated (n = 6), 15.14 +/- 8.97, and decompensated (n = 6), 11.84 +/- 9.32 (mean +/- SD, mg/day). The percentages of each conjugate was 19-29% in the non-glucuronidated-nonsulfated fraction, 6-14% in the glucuronidated fraction and 60-74% in the sulfated fraction. Bile acids in urine and serum correlated well in each fraction (r = 0.82-0.84, p less than 0.001). The clearance of the three conjugates was the highest in the sulfates, and the clearance of glucuronides was higher than that of non-esterified bile acids. The glucuronidation and sulfation of bile acids play an important role in the detoxication of bile acids by excreting them into urine, especially in patients with elevated serum bile acids.

Bile Acids and Salts↗
PubMed1984

Reversible denaturation of thermophilic malate dehydrogenase by guanidine hydrochloride and acid.

Thermophilic malate dehydrogenase [L-malate:NAD+ oxidoreductase, EC 1.1.1.37] was denatured at pH 2.0 with complete loss of enzyme activity but without dissociation to monomers, suggesting the presence of strong intersubunit contact. On the other hand, the enzyme was completely denatured and dissociated to monomers in the presence of 5 M GdnHCl. Inactivation and denaturation of the enzyme by acid and GdnHCl were reversible. Upon dilution of the denaturants, the inactivated enzyme regained enzyme activity and the native structure with high yield (80-90%). Kinetic analyses of reactivation of the enzyme denatured by GdnHCl and by acid revealed that the reaction obeyed first-order kinetics. The rate constant and Arrhenius activation energy of the reactivation of the acid-inactivated enzyme were almost the same as those of the enzyme inactivated by GdnHCl. These results suggest that the rate-limiting steps in the reactivation processes of the enzyme denatured by GdnHCl and by acid are the same and that a conformational change of the inactive dimer to active dimer is the rate-limiting step in the reactivation reaction.

Circular Dichroism↗
PubMed1984

Unstable genetic determinant of A-factor biosynthesis in streptomycin-producing organisms: cloning and characterization.

We cloned a DNA fragment directing synthesis of A-factor from the total cellular DNA of streptomycin-producing Streptomyces bikiniensis on the plasmid vector pIJ385 . Introduction of the recombinant plasmid ( pAFB1 ) into A-factor-deficient S. bikiniensis and Streptomyces griseus mutants led to A-factor production in the host cells, as a result of which streptomycin production, streptomycin resistance, and spore formation of these mutants were simultaneously restored. The plasmid pAFB1 also complemented both afsA and afsB mutations of Streptomyces coelicolor A3(2). These results indicated that the cloned DNA fragment contained the genetic determinant of A-factor biosynthesis. The cloned fragment, when carried on a multicopy vector plasmid, induced production of a large amount of A-factor in several Streptomyces hosts. In Southern blot DNA/DNA hybridization analyses with a trimmed 5-kilobase fragment containing the intact A-factor determinant as probe, total cellular DNA from A-factor-deficient mutants gave no positive hybridization. The DNA blot experiment also showed a wide distribution of sequences homologous to the S. bikiniensis A-factor determinant among most, but not all, A-factor-producing actinomycetes with a varying extent of homology and the absence of these sequences from most A-factor nonproducers .

4-Butyrolactone↗
PubMed1984

Studies on new antifungal antibiotics, guanidylfungins A and B. II. Structure elucidation and biosynthesis.

The structures of guanidylfungins A and B were elucidated from the physico-chemical properties of these compounds and the structures of the degradation products by ozonolysis and periodate oxidation. The guanidylfungins consist of a 36-membered polyhydroxyl lactone ring, a guanidine and a monoester of malonic acid. The labelling experiments with sodium [1-13C]acetate and sodium [1-13C]propionate revealed that twelve units of acetate and nine of propionate were incorporated into the molecule of guanidylfungin A.

Antifungal Agents↗
PubMed1984

B-factor, an essential regulatory substance inducing the production of rifamycin in a Nocardia sp.

"Curing" treatment of a rifamycin-producing Nocardia sp. resulted in a mutant deficient in the synthesis of antibiotics. This deficiency was reversed in a medium containing yeast extract. The active substance, named B-factor, which induced rifamycin production in the mutant was purified from yeast extract, and its structure, 3'-(1-butylphosphoryl) adenosine, was determined by structural analysis and chemical synthesis. An extremely low concentration of B-factor (10 ng/ml) caused recovery of rifamycin B synthesis in the mutant and stimulated synthesis of the antibiotic in the parental strain.

Adenosine Monophosphate↗
PubMed1984

Isolation and characterization of a pock-forming plasmid pTA4001 from Streptomyces lavendulae.

A covalently closed circular (ccc) DNA with a size of 5.9 kb was isolated from a strain producing streptothricins , Streptomyces lavendulae No. 1080, and its restriction map was determined. Colonies of the plasmid-carrying strain formed pocks on the lawn of the plasmid-free derivatives of the same organism. The pock-forming ability of pTA4001 was confirmed by transformation of S. lividans with the plasmid DNA. Insertion of the chromosomal streptothricin resistance gene of S. lavendulae No. 1080 into pTA4001 gave various composite plasmids with marked deletion in S. lividans as a host. By analyzing these derivatives, a 2.2 kb region essential for replication and a possible region for pock formation were determined in the map of pTA4001 . A cloning vector, pKST2 (4.3 kb) containing resistance genes to streptothricin and thiostrepton with several unique cloning sites was constructed from pTA4001 .

Base Sequence↗
PubMed1984

[Diabetes insipidus following the rupture of cerebral aneurysms--with special reference to preoperative cases].

The authors reported 4 cases with preoperative diabetes insipidus (DI) following the rupture of cerebral aneurysms. In addition, the incidence of preoperative DI and the mechanisms as the cause of DI in cases with the ruptured cerebral aneurysms were also discussed. In the 114 cases underwent clipping of the ruptured cerebral aneurysms more than 14 days after the bleed, only 4 cases (3.5%) developed DI preoperatively. The time period between last subarachnoid hemorrhage and the onset of DI ranged from 23 to 35 days. This delayed onset of DI after subarachnoid hemorrhage was different from previous reports. A few of mechanisms had been suggested through which DI could be brought about in cases with cerebral aneurysm. That is; direct compression to the hypothalamo-hypophysial system by a giant aneurysm. compression and destruction of the hypothalamus by a hematoma or hemorrhage, ischemic changes in the hypothalamo-hypophysial system caused by vasospasm. In the present 4 cases, no had giant aneurysms. Although CT scan revealed subarachnoid clot in all cases, it did not show apparent hypothalamic lesion except case 1 who had small hematoma in the region of the basal frontal interhemispheric fissure. Symptomatic vasospasm was recognized in 3 cases. However, one of them had mild vasospasm restricting in M1 portion and case 3 was free of any vasospasm. Furthermore, the time period from the identification of vasospasm until the onset of DI ranged from 2 to 3 weeks. These results suggest that another mechanism in addition to a hemorrhage, hematoma and/or vasospasm may exist.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1984

[Etiology of water and electrolyte metabolism imbalance following the rupture of cerebral aneurysms--with special reference to preoperative condition].

One hundred fourteen patients with ruptured cerebral aneurysms were reviewed in regard to the incidence and etiological factors of preoperative disturbances of water and electrolyte metabolism. Patients with inadequate salt intake, evidence of renal disease, cardiac failure or excessive diuretic therapy were excluded. Twenty-five (21.9%) patients developed water and electrolyte disturbances. Hyponatremia (less than 130 mEq/l) occurred in 18 (15.8%) of 114 patients. The majority of those patients with hyponatremia showed laboratory findings and/or clinical features suggesting the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). The mean interval between the last subarachnoid hemorrhage (SAH) and the development of hyponatremia was 13.5 days (range 6 to 26 days). No patients developed hypernatremia (more than 155 mEq/l). Preoperative diabetes insipidus (DI) occurred in 7 (6.1%) of 114 patients. The mean interval between the last SAH and the onset of DI was 26.5 days (range 15 to 35 days). When compared with the onset of hyponatremia following SAH, the development of DI was significantly delayed. The present study showed that the following five types of patients significantly related to the development of preoperative water and electrolyte disturbances after SAH due to cerebral aneurysms. The patients with ruptured aneurysms of anterior communicating, anterior cerebral artery or internal carotid artery. The patients in grade III, IV according to Hunt & Hess. The patients with high density in the basal subarachnoid space on the CT scan. The patients with a small hematoma in the region of the basal frontal interhemispheric fissure in cases with aneurysms of the anterior communicating or anterior cerebral artery.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗