Laparoscopic microwave coagulation (LMC) for hepatocellular carcinomas (HCCs) was performed on 26 HCCs in 17 patients. Contrast-enhanced CT (CECT) and MR images (T1-weighted imaging [T1WI], T2WI, gadolinium-diethylenetriamine pentaacetic acid [Gd-DTPA] T1WI) were obtained to determine changes over time. The irradiated center exhibited low to moderate intensity with surrounded high intensity (HI) on T2WI and Gd-DTPA T1WI. On T1WI, lesions showed four patterns of intensity: uniform HI (30.8%), arcuate HI (26.9%), mainly low with spot HI (30.8%), and isointensity to hypointensity (11.5%). Follow-up imaging at more than 170 days revealed isointensity to hypointensity on T1WI (96.2%) and reduced HI on T2-weighted imaging (T2WI) and Gd-DTPA T1WI. All lesions became less conspicuous and were reduced in volume. HCC shows time-related changes in signals and size after LMC. Identifying the irradiated lesion is necessary to estimate the adequacy of treatment by comparison with the pretherapeutic image.

Adult↗

PubMedDate not supplied

Heme-biosynthetic enzyme activities and porphyrin accumulation in normal liver and hepatoma cell lines of rat.

The activities of four heme-biosynthetic enzymes, delta-aminolevulinic acid (ALA) synthase, ALA dehydratase, porphobilogen (PBG) deaminase, and ferrochelatase, were studied in five epithelial cell lines of normal rat liver origin (RL, RLC-10, RLC-24, M, Culb-TC) and five cell lines derived from Yoshida ascites hepatoma (JTC-1, JTC-2, JTC-15, JTC-16, JTC-24). The JTC series of hepatoma-derived cell lines exhibited decreased ALA synthase activity and increased ALA dehydratase activity, although the activities of all four enzymes and the Km values for their respective substrates varied widely from one cell line to another, a finding suggesting that specific regulatory mechanisms for porphyrin metabolism might operate in each cell type. M cells, which were transformed by 4-dimethylaminoazobenzene in vitro, gave the most abnormal Km values of heme-biosynthetic enzymes among all the cell lines studies, and were found to accumulate hematoporphyrin derivative (HpD).

5-Aminolevulinate Synthetase↗

PubMedDate not supplied

Timing of cycloheximide administration and inhibition of the development of analgesic tolerance to morphine.

A single injection of cycloheximide (10 mg/kg, i.p.) partially prevented the development of analgesic tolerance to morphine (10 mg/kg, i.p. daily for 5 days). The inhibitory effect of cycloheximide was strictly dependent on the time of its administration, and only effective when it was administered 2 hrs before or 1 hr after morphine injection. Daily repeated treatment with cycloheximide 2 hrs before and/or 1 hr after morphine also prevented the tolerance development. However, the pre or post treatment with cycloheximide differed in the duration of the effect, and the discrepancies between two treatments suggest the importance of timing of the administration of inhibitor in the underlying mechanisms.

Analgesia↗

PubMedDate not supplied

Mercury uptake in vivo by normal and acatalasemic mice exposed to metallic mercury vapor (203Hg degrees) and injected with metallic mercury or mercuric chloride (203HgCl2).

Levels of mercury in the brain and liver of acatalasemic mice immediately following exposure to metallic mercury vapor or injection of metallic mercury were higher than those found in normal mice. Acatalasemic mice had decreased levels of mercury in the blood and kidneys when the levels were compared with those of normal mice, which indicated that catalase plays a role in oxidizing and taking up mercury. Thus, the brain/blood or liver/blood ratio of mercury concentration in acatalasemic mice was significantly higher than that of normal mice. These results suggest that metallic mercury in the blood easily passed through the blood-brain or blood-liver barrier. The levels of mercury distribution to the kidneys of normal and acatalasemic mice, 1 hr after injection of mercuric chloride solution, were higher than that of normal and acatalasemic mice, respectively, 1 hr after injection of metallic mercury.

Animals↗

PubMedDate not supplied

Reduction of mercuric ion and exhalation of mercury in acatalasemic and normal mice.

A significant difference in the amount of exhaled mercury per hour between normal and acatalasemic mice was observed in 7 of 11 experiments for different periods of time. The total amount of mercury exhaled from acatalasemic mice was significantly higher than those of normal mice. The results confirm that the reduction of mercuric ion to metallic mercury occurs by recycling of mercury in the tissues and reoxidized metallic mercury to mercuric ion by catalase. Mercuric ion was reduced to metallic mercury in the presence of superoxide anion in vitro. The reduction rate of mercuric ion to metallic mercury in the presence of both superoxide anion and cytochrome C or nitro blue tetrazolium was higher than that in the presence of superoxide anion alone, and the reduction of mercuric ion by NADPH or NADH was also observed. The reduction of mercuric ion to metallic mercury by liver homogenates of acatalasemic mice was higher than that of normal mice.

Acatalasia↗

PubMedDate not supplied

Enhanced anti-metastatic efficacy of IL-2 activated NK (A-NK) cells with novel benzothiazoles.

We have previously shown that A-NK cells when locoregionally administered accumulate within established cancer metastases and establish direct contact with both tumor cells and microvascular endothelial cells. Nevertheless, the accumulation of adoptively transferred A-NK cells into established cancer metastases is not sufficient for therapeutic efficacy in the B16 melanoma model. We have therefore attempted to enhance the anti-metastatic therapeutic efficacy of adoptively transferred A-NK cells with standard anticancer chemotherapeutic agents. We have found that chemoimmunotherapy with A-NK cells plus cyclophosphamide to be more effective than A-NK cell adoptive immunotherapy alone. We have now built on these findings, by examining the ability of novel biologic response modifiers (low molecular weight benzothiazole compounds) to augment adoptive immunotherapy with A-NK cells. Two compounds KB-R4107 (4-methoxy-2-(4-t-butylphenyl)benzothiazole) and KB-R4250 (4-methoxy-2-(4-trifluoromethylphenyl)benzothiazole) enhanced reduction of B16 melanoma pulmonary metastases mediated by A-NK cell adoptive immunotherapy. Both compounds were administered for 5 days prior to administration of A-NK cells at 100 mg/kg p.o. All experimental groups initially contained at least 7 animals and were examined for tumor burden on day 10. With B16 melanoma cells administered on day 0 and A-NK cells administered on Day 4, KB-R4107 and KB-R4250 yielded on average a 64% and 52% reduction in metastatic burden, respectively compared to an average 17% reduction using A-NK cells alone. In contrast these compounds did not diminish metastatic burden when administered alone. KB-R4107 and KB-R4250 are therefore low molecular weight, heterocyclic, biological response modifiers which can augment the anti-metastatic therapeutic effect of adoptively transferred A-NK cells.

Animals↗

PubMedDate not supplied

Targeted killing of squamous carcinoma cells by a monoclonal antibody-peplomycin conjugate which recognizes the EGF receptor.

We determined in vitro the antitumor activity of a conjugate prepared by binding a monoclonal antibody (B4G7), which recognizes the human epidermal growth factor (EGF) receptor, with peplomycin (PEP), which is an antitumor agent effective against squamous cell carcinoma. This B4G7-PEP conjugate was prepared by coupling of B4G7 and carboxymethylpeplomycin active ester. The conjugate killed A431 cells of squamous cell carcinoma which overexpress EGF receptors at lower concentrations than PEP alone. On the basis of its IC50, the conjugate was six times more potent than PEP alone. A simple mixture of B4G7 and PEP was as effective as PEP alone in cytotoxicity. The addition of ten times the amounts of B4G7 to this conjugate decreased its cytotoxicity. When other squamous cell carcinoma cell lines with different levels of EGF receptors (NA, Ca9-22, TE-1, TE-8) were treated with the conjugate, cells were killed dose-dependently and the cytotoxicity was dependent on the number of EGF receptors. When each squamous cell carcinoma cell line was treated with a control conjugate prepared by combining PEP with mouse IgG instead of B4G7, no cytotoxicity was observed. These results indicate that B4G7-PEP will be a useful weapon in multidisciplinary treatment which utilizes the EGF receptor, as these receptors are detected in a higher incidence in squamous cell carcinoma.

Antibiotics, Antineoplastic↗

PubMedDate not supplied

Study of response to naproxen in patients with hepatocellular carcinoma who developed fever following transcatheter arterial embolization.

Good antipyretic response was obtained when naproxen was given at 600 mg/day for about one week to patients who developed fever after transcatheter arterial embolization (TAE). Fever recurred in several patients, but subsided again when naproxen was given at 300 mg/day. No patients developed gastric mucosal lesions of clinical concern that seemed to be related to naproxen.

Aged↗

PubMedDate not supplied

Effect of the type of serum in the medium on sodium ascorbate-induced cytotoxicity.

Sodium ascorbate induced cytotoxicity against human glioblastoma T98G cells in RPMI1640 medium supplemented with fetal bovine serum or human serum samples was studied. Several human serum samples significantly reduced the cytotoxic activity of sodium ascorbate, regardless of sex, age or the disease of the serum donor with or without heat-inactivation of the serum. ESR spectroscopy revealed that this serum effect was not simply due to the alteration of the ascorbyl radical intensity, produced from sodium ascorbate. The present study suggests that the apoptosis-inducing activity of sodium ascorbate might be significantly affected by human serum.

Adult↗

PubMedDate not supplied

Effect of methionine depletion on growth and apoptosis in various tumor cell lines.

Sodium ascorbate, sodium 5,6-benzylidene-L-ascorbate (SBA), gallic acid and caffeic acid induced apoptotic cell death in human myelogenous leukemic cell lines, and stimulated oxidation of methionine into methionine sulfoxide in the culture medium. When various tumor cell lines were cultured in methionine-free medium, their growth was nearly terminated at G1 phase of the cell cycle, producing much smaller number of apoptotic cells. Addition of methionine sulfoxide to the methionine-free medium did not stimulate the apoptosis induction. These data suggest that induction of apoptosis by ascorbates, gallate or by caffeate cannot be simply explained by methionine oxidation.

Antioxidants↗