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Biomedical subjects

K Sugimoto

Publications and source records attributed to K Sugimoto.

At least 55 records · Page 3Linked to original sources
PubMed2001

Covered Gianturco stent for tracheal stricture: application of polychlorovinylidene and polyurethane as covering materials.

The aim of this study was to assess the efficacy and safety of thin membranes of polychlorovinylidene (PCV) or polyurethane (PU) as covering materials for Gianturco stents in the treatment of severe tracheal stricture caused by intraluminal tumor. Manufactured Gianturco stents covered with PCV or PU membrane were used to treat six malignant and one benign tracheal stricture. The initial results, complications, clinical follow-up, bronchoscopic findings, and three autopsy microscopic examinations were reviewed. Informed consent was obtained after the nature of the treatment had been fully explained before every procedure. The stents successfully dilated the tracheal strictures, providing immediate relief of respiratory symptoms in all patients with no major complications. During the follow-up period, the covering materials prevented tumor ingrowth until death or intraluminal granuloma formation. Autopsies proved that no histological change occurs in the tracheal mucosa in response to the presence of PCV or PU; however, ulcer formation occurred in one patient and penetration of the stent struts into the tracheal wall in two. Bloody sputum with ulcer formation, minimal granuloma formation at the distal end of the stent, and abnormal bacterial load in the sputum were long-term complications. The Gianturco stent covered with PCV or PU membrane is a useful option as a palliative treatment for malignant and an emergent salvage for benign tracheal stricture, because both materials are thinner and less voluminous than the others. However, the indications for its use are limited to patients with poor prognoses, because hemoptysis, granuloma formation, and bacterial propagation remain problematic.

Aged↗
PubMed2001

Protein kinase C and phosphatidylinositol 3-kinase independently contribute to P-glycoprotein-mediated drug secretion in the mouse proximal tubule.

We have recently reported that the apical membrane of the proximal tubule S2 segment from wild-type mice (WT mice) has the capacity for P-glycoprotein- (P-gp-) mediated drug efflux, whereas mice in which both mdr1a and mdr1b genes are disrupted (KO mice) do not. To examine the intracellular regulatory mechanisms of drug-transporting P-gp activity, we isolated and perfused proximal tubule S2 segments from WT and KO mice, and measured luminal efflux of the intracellular fluorescence of rhodamine 123, a fluorescent substrate of P-gp. The decay half-time of the intracellular fluorescence (t1/2) was regarded as an index of the drug-transporting P-gp activity. In the WT mice, the t1/2 was 36+/-5 s (n=35) during the basal period, and was significantly increased to 440+/-45 s by the luminal addition of verapamil (an inhibitor of P-gp). The addition of phorbol 12-myristate 13-acetate (PMA) [a protein kinase C (PKC) activator] to the bath increased t1/2, but 4alpha-phorbol (the inactive form of PMA) did not. The PMA-induced increase in t1/2 was further increased by the luminal addition of verapamil, and was partially inhibited by co-treatment with staurosporine or H-7 (inhibitors of PKC). Pretreatment with wortmannin or LY294002 [inhibitors of phosphatidylinositol 3-kinase (PI 3-kinase)] added to the bath also increased t1/2. The wortmannin- and LY294002-induced increase in t1/2 was also further increased by the luminal addition of verapamil. The effects of PMA on t1/2 were additive after cotreatment with wortmannin or LY294002. In the KO mice, t1/2 was 440+/-25 s (n=18) during the basal period, and was no longer affected by the addition of verapamil, staurosporine, H-7, wortmannin, or LY294002. Based on the use of pharmacological agents, we conclude that in the proximal tubule from WT mice, P-gp-mediated drug secretion occurs independently via PKC- and PI 3-kinase-dependent processes, whereas it is not present in KO mice, independently of PKC- and PI 3-kinase.

ATP Binding Cassette Transporter, Subfamily B↗
PubMed2001

Crystal structures of substrate free and complex forms of reactivated BphC, an extradiol type ring-cleavage dioxygenase.

BphC derived from Pseudomonas sp. strain KKS102, an extradiol type catecholic dioxygenase, is a non-heam iron-containing enzyme, playing an important role in the degradation of biphenyl/PCB (Poly Chlorinated Biphenyls) in the microbe. Although we had earlier solved the crystal structure of KKS102 BphC, it was the inactive form with Fe(III) in the active site. In order to determine the active form structure, BphC was re-activated by anaerobic incubation with Fe(II) and ascorbate, and crystallized anaerobically. The crystal structures of activated BphC and its substrate complex (E x S complex) were determined at 2.0 A resolution under cryogenic condition. In addition, crystal structures of unactivated BphC in substrate free and complex forms were also re-determined. Comparison of activated and unactivated E x S complexes reveals that the orientation of the bound substrate in the active site is significantly different between the two. The structural comparison of the substrate free and complex forms of activated BphC show certain small conformational shifts around the active site upon substrate binding. As a result of the conformational shifts, His194, which has been suggested as the catalytic base, takes part in a weak hydrogen bond with hydroxyl group of the substrate.

Anaerobiosis↗
PubMed2001

Enhanced neutrophil superoxide anion production and its modification by beraprost sodium in spontaneously hypertensive rats.

To clarify the function of polymorphonuclear leukocytes (PMN) in spontaneously hypertensive rats (SHR) and the effect of beraprost sodium (BS) on these functions, we examined superoxide anion (O2-) production and adherent activity by PMN, as well as modification of these functions by BS ex vivo and in vitro. In study 1, we measured PMN functions in 4-week-old SHR and Wistar-Kyoto (WKY) rats. In study 2 (ex vivo), 14-week-old SHR received vehicle (n = 6) and BS (30 microg/kg/day [n = 6] and 100 microg/kg/day [n = 7]) once daily for 4 weeks. In study 3 (in vitro), PMN from 18-week-old SHR were incubated with BS (0.1 and 1 micromol/L) and theophylline (200 micromol/L), which is reported to inhibit the PMN O2- production. Systolic blood pressure, platelet counts, and PMN O2- production stimulated by phorbol ester myristate acetate were significantly elevated in 4-week-old SHR compared with WKY (P < .05). Beraprost sodium decreased the ex vivo PMN O2- production, serum superoxide dismutase activity, and platelet counts (P < .05); however, BS did not reduce the in vitro PMN O2- production. These data support our hypothesis that the enhanced PMN function contributes to the cardiovascular damages during the early phase of SHR, and that BS has merit for preventing the O2- related organ damages in this model.

Animals↗
PubMed2001

Alteplase and tenecteplase: applications in the peripheral circulation.

Alteplase (t-PA), a recombinant analogue of human tissue plasminogen activator, became the first genetically engineered thrombolytic approved by the Food and Drug Administration in 1987 for acute myocardial infarction (AMI). In addition to AMI, alteplase is currently approved for the treatment of acute ischemic stroke and pulmonary embolism, and we anticipate approval for catheter clearance in late 2001 in a 2-mg vial configuration. With the withdrawal of human neonatal kidney cell-derived urokinase, alteplase has become an alternative agent in peripheral vascular applications. Because few interventionalists had prior experience with the handling and dosage of alteplase, the Advisory Panel to the Society of Cardiovascular and Interventional Radiology established practice guidelines for use in noncoronary applications. Emerging clinical experience with contemporary dosing regimens shows a safety and efficacy profile similar to urokinase but with significantly reduced drug costs. Tenecteplase (TNK) is a genetically modified version of alteplase. TNK is the only plasminogen activator available that has shown a significantly enhanced safety profile versus alteplase in AMI. Approved for a 5-second, single-bolus injection in AMI, TNK possesses a longer half-life, increased resistance to plasminogen activator inhibitor, and improved fibrin specificity compared with alteplase. Because of its enhanced safety profile, TNK may be a desirable agent for peripheral vascular applications. Initial clinical studies with TNK in acute arterial and venous disease are ongoing. This article outlines the Advisory Panel guidelines for using alteplase and highlights features of tenecteplase.

Blood Circulation↗
PubMed2001

p21WAF1/CTP1 expression and hepatitis virus type.

Since p21WAF1/CIP1 (p21) is a universal inhibitor of cyclin-dependent kinases and is regulated transcriptionally by p53, which is activated by DNA stress, its expression reflects DNA stress in chronic hepatitis. Recently an association with both hepatitis B and C virus and the expression of p53 or p21 was reported. We analyzed p21 expression in 18 cases of HBV-associated chronic liver diseases and 32 cases of HCV-associated chronic liver diseases by immunohistochemical analysis, and investigated the possible association between hepatocyte p21 expression and hepatic inflammation, fibrosis, and especially hepatitis virus type. The p21-positive hepatocytes were more numerous in areas of intense inflammation and spotty necrosis and areas close to fibrosis, and they increased according to the degrees of grading and staging. The p21 labeling index (LI) in patients with liver cirrhosis was significantly higher than that in patients with chronic hepatitis of both hepatitis viral types (5.84 +/- 0.61 vs 12.0 +/- 0.83, P < 0.0001 in hepatitis B, 10.28 +/- 0.80 vs 15.6 +/- 1.09, P = 0.0004 in hepatitis C), Furthermore, the p21 LI was significantly higher in HCV-associated liver disease than in HBV-associated liver disease in every group (4.02 +/- 0.48 vs 7.74 +/- 0.96, P = 0.021 in low grade group, 7.35 +/- 0.46 vs 12.8 +/- 0.57, P < 0.0001 in high grade, 12.0 +/- 0.83 vs 15.6 +/- 1.09, P = 0.034 in liver cirrhosis). In, conclusion, p21 expression was up-regulated by the stress of inflammation and fibrosis and might be influenced by viral proteins in human chronic liver disease.

Adult↗
PubMed2001

Diurnal variation in the biliary excretion of flomoxef in patients with percutaneous transhepatic biliary drainage.

AIMS: To examine diurnal variation in biliary excretion of flomoxef. METHODS: Flomoxef (1 g) was injected intravenously in eight patients with percutaneous transhepatic cholangiography with drainage at 09.00 h and 21.00 h by a cross-over design with a 36 h washout period. Drained biliary fluid was collected for 6 h after each dosing. These patients still had mild to moderate hepatic dysfunction. RESULTS: Bile flow and bile acid excretion for 6 h after dosing did not differ significantly between the 09.00 h and 21.00 h treatments. The maximum concentration of biliary flomoxef was significantly greater and its total excretion for 6 h tended to be greater after the 21.00 h dose [maximum concentration (microg ml(-1)): 34.2 +/- 29.9 (09.00 h dose) vs 43.5 +/- 28.3 (21.00 h dose) (95% confidence interval for difference: 2.6 approximately 15.9, P = 0.013); total excretion (mg 6 h(-1)): 1.4 +/- 1.3 (09.00 h dose) vs 1.6 +/- 1.2 (21.00 h dose) (95% confidence interval for difference: -26.8, 313.7, P = 0.087)]. The period that biliary flomoxef remained above the minimal inhibitory concentration did not differ significantly between the two treatment times. CONCLUSIONS: These results suggest that biliary excretion of flomoxef shows diurnal variation. However, as the difference was relatively small, flomoxef could be given at any time of day without any dosage adjustments.

Bile↗
PubMed2001

Linear DNA intermediates of the Tto1 retrotransposon in Gag particles accumulated in stressed tobacco and Arabidopsis thaliana.

The active transcription of some plant retrotransposons under diverse stress conditions suggests active transposition. However, transposition has been demonstrated only during tissue/cell culture. To examine whether transposition is activated under conditions other than tissue/cell culture, DNA intermediates for retrotransposition of the tobacco retrotransposon Tto1 were analysed. Using transgenic Arabidopsis callus expressing high levels of Tto1 RNA in a ddm1 hypomethylation mutant background, the existence of extrachromosomal Tto1 linear DNA molecules in a Gag-particle fraction was demonstrated. By combination with ligation-mediated PCR amplification, we detected Tto1 linear DNA molecules in particle fractions from callus and methyl jasmonate-treated leaves of tobacco, but not from non-stressed leaves. Tto1 DNA intermediates could not be detected in the tobacco corolla where Tto1 is expressed. These results indicate that the transcriptional activation of Tto1 by defence-related stresses leads to the synthesis of DNA intermediates, whereas post-transcriptional suppression of Tto1 activity is suggested in the corolla.

Antigens↗
PubMed2001

Effect of enalapril on diabetic nephropathy in OLETF rats: the role of an anti-oxidative action in its protective properties.

1. We have evaluated the effects of the angiotensin-converting enzyme inhibitor enalapril on renal function and oxidative status in the kidney of Otsuka Long-Evans Tokushima Fatty (OLETF) rats, an animal model of spontaneous onset of type 2 diabetes mellitus. 2. Enalapril (5 mg/kg) or vehicle (distilled water) was given once daily by gavage to 22-week-old male OLETF rats for 32 weeks. Long-Evans Tokushima Otsuka (LETO) rats, the control animals for OLETF rats, received vehicle alone (n = 10 in each group). 3. Enalapril attenuated the rise in blood pressure mildly, but significantly. Enalapril significantly blunted the development of proteinuria without a significant effect on creatinine clearance. At the end of the study period, the lipid peroxide content in the renal cortex was significantly increased in OLETF compared with LETO rats, in which enalapril had no effect on lipid peroxide content. Enalapril enhanced the activity of catalase in the renal cortex of OLETF rats, but had no effect on the activity of either superoxide dismutase or glutathione peroxidase. 4. These results suggest that oxidative stress may be involved in the development of nephropathy in type 2 diabetes. Enalapril exhibited renoprotective effects without changing lipid peroxides in the kidney, suggesting that the beneficial effects of the compound on diabetic renal damage in OLETF rats may not be mediated through an anti-oxidative action.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2001

High expression of CD34-positive sinusoidal endothelial cells is a risk factor for hepatocellular carcinoma in patients with HCV-associated chronic liver diseases.

CD34 has been widely used for the assessment of sinusoid-like neoangiogenesis in hepatocellular carcinoma (HCC). Recently, it was demonstrated that CD34-positive cells isolated from human peripheral blood differentiate into endothelial cells and contribute to neoangiogenesis in adults. We investigated the localization and the substantial role of CD34-positive endothelial cells in the liver with hepatitis C virus (HCV)--associated chronic liver diseases. Liver tissue sections obtained by biopsy from 56 patients with HCV-associated chronic liver diseases by were examined immunohistochemically using anti-CD34, anti-von Willebrand factor (vWF), and anti-vascular endothelial growth factor (VEGF) antibodies. CD34 was stained in the sinusoid, showing dotty, linear, semicircular, or circular patterns. However, sinusoidal expression of vWF was not substantially identified in the same specimens, indicating the existence of sinusoidal CD34-positive but vWF-negative endothelial cells. We classified these cells as CD34 LI and found that CD34 LI was correlated with the expression of VEGF. Among 34 patients with advanced-stage disease, the cumulative incidence of HCC was significantly higher in patients with CD34 LI >or= 12 (n = 16) than in those with CD34 LI < 12 (n = 18; P = .009). Moreover, among several clinicopathologic risk factors, CD34 LI could be recognized as an independently significant factor for development of HCC (relative risk, 7.36; P = .019). We conclude that CD34-positive endothelial cells are regulated by several factors, such as VEGF, and might play a substantial role in hepatocarcinogenesis. Furthermore, high expression of CD34-positive sinusoidal endothelial cells is a risk factor for HCC in patients with HCV-associated chronic liver diseases.

Adult↗
PubMed2001

Effect of angiotensin II on venodilator response to nitroglycerin.

OBJECTIVE: An enhanced circulatory angiotensin II level that results from the administration of nitroglycerin may contribute to the development of nitrate tolerance. Using human hand veins, we investigated whether a subconstricting dose of angiotensin II attenuates the venodilator effect of nitroglycerin, whether pretreatment with losartan influences this effect, and whether angiotensin II also attenuates the venodilator effect of diltiazem. METHODS: In 9 healthy male subjects, increasing doses (0.5-128 ng/min) of nitroglycerin were infused into the dorsal hand vein pretreated with 0 (control), 0.3, or 1 ng/min of angiotensin II. In 8 healthy male subjects, angiotensin II (0.3 and 1 ng/min) was infused into the vein dilated by nitroglycerin with and without pretreatment with losartan and with diltiazem. The diameter of the vein was measured with a linear variable differential transformer. RESULTS: The venodilator response of nitroglycerin was significantly suppressed by the pretreatment with angiotensin II; The maximum venodilator effect was dose-dependently decreased, and the infusion rate producing half-maximum response was dose-dependently increased. The venodilation caused by nitroglycerin was decreased by angiotensin II, and this effect was attenuated by pretreatment with losartan. The venodilation caused by diltiazem was also attenuated by angiotensin II, but this attenuating effect was smaller compared with that caused by nitroglycerin. CONCLUSIONS: These findings suggest that an enhanced angiotensin II level might attenuate the venodilation caused by nitroglycerin and diltiazem, and pretreatment with losartan might decrease the attenuating effect of angiotensin II.

Adult↗
PubMed2001

Furosemide-probenecid interaction as a laboratory exercise for undergraduate education in clinical pharmacology.

OBJECTIVE: The aim of this study was to determine the easiness, reproducibility, and safety of a laboratory exercise for a drug interaction between furosemide and probenecid. METHODS: From 1995 to 1999 approximately 100 medical students participated in the exercise each year after they gave written informed consent. The students were randomly assigned to one of the three groups in a double-blind fashion: group 1, placebo plus 20 mg of furosemide; group 2, 250 mg of probenecid plus 20 mg of furosemide; and group 3, 1000 mg of probenecid plus 20 mg of furosemide. The students took probenecid or its placebo 1 hour before furosemide. Urine volume and urinary sodium excretion were measured for 3 hours after furosemide. At the end of the exercise in 1999, students responded to several questionnaires concerning the utility of furosemide. RESULTS: The entire course of the exercise was completed within half a day. The following findings were obtained every year. (1) Probenecid dose dependently blunted the diuretic effects of furosemide. (2) Time courses of the diuretic effects were altered by probenecid. Ten to twenty percent of the students had slight complaints but completed the exercise without any medications. Finally, more than 80% of the students considered the exercise to be useful. CONCLUSIONS: The data suggest that the exercise of the drug interaction between furosemide and probenecid is easy to perform, reproducible, and safe. Through the experience of the laboratory exercise, students will develop an attitude to assess and estimate potential drug interactions before they prescribe drugs.

Diuresis↗
PubMed2001

Removal of digoxin by column for specific adsorption of beta(2)-microglobulin: a potential use for digoxin intoxication.

BACKGROUND: A beta(2)-microglobulin adsorption column used for the treatment of dialysis-related amyloidosis removes serum beta(2)-microglobulin by recognition of lipophilic residue in the protein. No data are available for the adsorption of the highly lipophilic drug digoxin. METHODS: In vivo clearance of digoxin with the beta(2)-microglobulin column was measured by a single use of the column in 8 patients receiving hemodialysis with a therapeutic level of digoxin. In vitro adsorption was evaluated by use of incubation with adsorbent of the column and digoxin or ranitidine, a hydrophilic drug. Clearance with the beta(2)-microglobulin column was further compared with that obtained by use of activated charcoal in the dogs intoxicated with digoxin. RESULTS: Digoxin concentration was reduced from 1.11 +/- 0.25 ng/mL to 0.57 +/- 0.15 ng/mL at 240 minutes after initiation of hemoperfusion with the column in the patients. Digoxin clearance with the beta(2)-microglobulin column was about 145 +/- 20 mL/min, with a blood flow rate of 160 to 220 mL/min (80% of plasma flow rate). Eighty-five percent of digoxin was adsorbed in vitro, and the capacity of the beta(2)-microglobulin column was not saturated until a toxic level was reached (50 ng/mL). This value was higher than that obtained with use of charcoal. In dogs with digoxin intoxication, digoxin clearance was 38.9 +/- 1.5 mL/min, with a blood flow rate of 50 mL/min (95% of plasma flow rate), which was almost twice as that achieved with charcoal. The degree of thrombocytopenia and leukopenia was small with use of the beta(2)-microglobulin column. CONCLUSION: These data suggested that the beta(2)-microglobulin column selectively adsorbs digoxin. This column is a promising tool for the treatment of digoxin intoxication, especially in patients undergoing hemodialysis.

Adsorption↗
PubMed2001

Different effects of St John's wort on the pharmacokinetics of simvastatin and pravastatin.

OBJECTIVE: St John's Wort, a widely used herbal product, is an inducer of CYP3A4 and it decreases blood concentrations of CYP3A4 substrates. The effects of St John's Wort on the pharmacokinetics of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors simvastatin (an inactive lactone pro-drug) and pravastatin were determined in this study. METHODS: Sixteen healthy male subjects (n = 8 in group 1 and n = 8 in group 2) took a St John's Wort caplet (300 mg) or matching placebo three times a day for 14 days in a double-blind, crossover study. On day 14, a single oral dose of 10 mg simvastatin and 20 mg pravastatin was given to subjects in group 1 and group 2, respectively. Blood samples were obtained during a 24-hour period after the administration of each drug. RESULTS: Repeated St John's Wort treatment tended to lower plasma simvastatin concentration and significantly (P <.05) lowered concentrations of simvastatin hydroxy acid, its active metabolite. The peak concentration in plasma (ratio, 0.72 of placebo) of simvastatin hydroxy acid tended to be decreased and its area under the plasma concentration-time curve between time zero and 24 hours after administration (ratio, 0.48 of placebo) was significantly decreased (P <.05) by St John's Wort. On the other hand, St John's Wort did not influence plasma pravastatin concentration. No significant differences were observed in the elimination half-life of simvastatin or pravastatin between the placebo and St John's Wort trials. CONCLUSIONS: This study showed that St John's Wort decreases plasma concentrations of simvastatin but not of pravastatin. Because simvastatin is extensively metabolized by CYP3A4 in the intestinal wall and liver, which are induced by St John's Wort, it is likely that this interaction is partly caused by the enhancement of the CYP3A4-mediated first-pass metabolism of simvastatin in the small intestine and liver.

Adult↗
PubMed2001

Metabolic activation of 1alpha-hydroxyvitamin D3 in human liver microsomes.

1. 1Alpha-hydroxyvitamin D3 (1alpha-OH-D3) is a synthetic prodrug of the active form of vitamin D3, and requires the hydroxylation at the C-25 position before eliciting its biological activity. 2. 25-Hydroxylation activities for 1alpha-OH-D3 were present in both microsomal and mitochondrial fractions of human liver. 3. To determine the P450 enzyme(s) involved in microsomal 25-hydroxylation, 14 P450s (CYP1A1, 1A2, 1B1, 2A6, 2B6, 2C8, 2C9-Arg, 2C9-Cys, 2C19, 2D6-Val, 2D6-Met, 2E1, 3A4, 4A11) were tested for their 25-hydroxylation activity of 1alpha-OH-D3. None catalysed the 25-hydroxylation reaction. 4. 1Alpha-OH-D3 in a high concentration (2.5 ng ml(-1)) showed small but significant inhibition of the catalytic activities of CYP2C8, 2C9-Cys, 2C19, 2D6-Val and 2E1 for their typical substrates. However, 1alpha-OH-D3 in a clinically used low concentration will not significantly affect drug metabolism catalysed by the 14 P450s tested. 5. In summary, the 25-hydroxylation activity of 1alpha-OH-D3 that localizes in the microsomal fraction appears to be attributable to a cytochrome P450 other than the microsomal forms tested in this study.

Biotransformation↗
PubMed2001

Pilot study of local radiotherapy for portal vein tumor thrombus in patients with unresectable hepatocellular carcinoma.

BACKGROUND: Patients suffering from hepatocellular carcinoma (HCC) with portal vein tumor thrombus (PVTT) generally have a poor prognosis. We therefore conducted a prospective pilot trial of combined transcatheter arterial chemoembolization (TACE) and local radiotherapy (RT) for PVTT in unresectable HCC. The aim of the study was to investigate the efficacy and toxicity of this preliminary trial regime and to explore RT guidelines for cirrhosis. METHODS: Eight patients with unresectable HCC accompanied by first branch PVTT were entered into the study from February 1998 to December 1999. TACE was performed using Lipiodol, epirubicin hydrochloride and mytomycin followed by gelatin sponge cubes. RT was started 10-14 days following TACE. A total delivered dose of 60 Gy was given as daily 2 Gy fractions, with the clinical target volume defined as PVTT only. We observed a relationship between deterioration of liver function and the percent volume of the total liver receiving a dose exceeding 30 Gy (V30). RESULTS: An objective response was observed in three of the eight patients. However, on follow-up angiograms the protrusion of PVTT into the main portal trunk was decreased in all cases. Deterioration of liver function was observed in all patients with V30 >40%. CONCLUSION: It is possible that this combined therapy prevents PVTT from spreading to the main trunk and that indicates a further benefit of TACE. Our results indicate that V30 constitutes a predictive test for the development of liver failure. More detailed evaluations of liver function and determination of the safe irradiation volume are necessary.

Aged↗