Hepatocellular carcinoma (HCC) seldom invades the gallbladder. We report a case of HCC invading the gallbladder that resembled gallbladder carcinoma invading the liver. The diagnosis was confirmed by surgical biopsy. The arteriographic, computed tomography and magnetic resonance imaging findings are presented.

Adult↗

PubMedDate not supplied

Renal tubular function after reduction of environmental cadmium exposure: a ten-year follow-up.

A prospective follow-up study was carried out to assess the prognosis of renal tubular function after reduction of environmental cadmium exposure. Time-related changes in urinary beta 2-microglobulin and cadmium excretion were followed from 1979 to 1989 in 102 residents of a cadmium-polluted area in Nagasaki, Japan. The average dietary cadmium intake among the study population was more than 200 micrograms/d in 1969, which decreased to approximately half that amount in 1983 because cadmium-polluted paddy fields were replaced with new soil in 1981. The geometric mean urinary beta 2-microglobulin concentration for 28 subjects aged 40 y or older in 1979 increased from 1,135.8 micrograms/g creatinine in 1979 to 1,999.7 micrograms/g creatinine in 1989. A similar tendency was also observed in 16 subjects with urinary beta 2-microglobulin concentrations greater than 1,000 micrograms/g creatinine in 1979, although the statistical significance of the difference did not reach the 5% level, probably because of the small sample size. In 48 persons examined in 1982, 1986, and 1989, the geometric mean of urinary cadmium concentration decreased from 8.49 micrograms/g creatinine in 1982 to 6.03 micrograms/g creatinine in 1989. The tendency for increasing beta 2-microglobulin excretion observed in the present study could not be explained by aging alone. Thus, it was concluded that renal tubular dysfunction caused by environmental cadmium was irreversible and slowly progressive, even after reduction of exposure. Six of 8 subjects who had severe renal dysfunction and who were included in the study died before 1986 and could not be followed. The implication of loss of subjects because of death is also discussed.

Adolescent↗

PubMedDate not supplied

Computed tomography of liver sarcoidosis.

A case of sarcoidosis revealed multiple low density areas in the liver on CT. One of these lesions was confirmed by laparoscopic liver biopsy to be a mass of noncaseating granulomas surrounded by necrotic or fibrotic tissues. These lesions disappeared rapidly after steroid therapy.

Adult↗

PubMedDate not supplied

Hyperthermic effects on cell killing in Dictyostelium discoideum amoebae treated with DNA-damaging agents.

Hyperthermic effects on cell killing of amoeboid cells treated with DNA-damaging agents of Dictyostelium (D). discoideum were studied. Though the amoeboid cells are usually cultured at 23 degrees C, heat treatment at 30 degrees C for 15 min immediately after UV irradiation markedly enhanced cell killing, while not observed in the case of heat treatment immediately before UV irradiation. Similar effects were observed in the case of heat treatment after treatment with 4-nitroquinoline 1-oxide, cis-platinum(II) diamminedichloride or 8-methoxypsoralen photoaddition, while not observed when heat was applied before these treatments. On the contrary, little enhancement by heat treatment was observed even after treatment with N-methyl-N'-nitro-N-nitrosoguanidine or methylmethanesulphonate. The hyperthermic mechanisms in D. discoideum are discussed, based on a diverse set of DNA lesions caused by chemicals and DNA repair mechanisms for them.

4-Nitroquinoline-1-oxide↗

PubMedDate not supplied

Influence of pre-treatment with DNA-damaging agents on hyperthermic potentiation in cell killing of ultraviolet light-irradiated Dictyostelium discoideum.

Heat treatment at 30 degrees C for 15 min immediately after ultraviolet (UV) irradiation enhanced cell killing of Dictyostelium discoideum. However, when the cells were UV-irradiated and cultured at 23 degrees C for 30 min before giving UV irradiation and heat treatment, the enhancement of cell killing by heat treatment immediately after post-UV irradiation was depressed. Similar depressions in the heat enhancement of cell killing of UV-irradiated cells were also observed in the case of the cells cultured after pretreatment with 4-nitroquinoline 1-oxide, cis-platinum(II) diaminedichloride or 8-methoxypsoralen photoaddition, but not with N-methyl-N'-nitro-N-nitrosoguanidine or methylmethanesulphonate. These results suggest that the depression in heat enhancement in cell killing of UV-irradiated cells may be deeply related with kinds of DNA lesions or DNA repair processes for them.

4-Nitroquinoline-1-oxide↗

PubMedDate not supplied

Tumour oxygenation is increased by hyperthermia at mild temperatures.

The effects of hyperthermia on the oxygenation status in R3230 AC tumours of Fischer rats were measured using a polarographic oxygen electrode system. The median pO2 in about 10 mm diameter tumours grown s.c. in the leg of rats was 3.7 +/- 0.3 mm Hg and it significantly increased upon heating at modest temperatures. For example, the tumour pO(2) measured within 10-15 min after heating for 30 min at 42.5 degrees C was about three-fold greater than that in the control tumours. About 62% of PO(2) values measured in control tumours were < 5 mm Hg. After heating at 42.5 degrees C for 30 min, 37% of PO(2) values were < 5 mm Hg. Such an increase in tumour oxygenation or reoxygenation of hypoxic cells appeared to result from an increase in tumour blood flow caused by the mild temperature hyperthermia. The presence of hypoxic cells in tumours is believed to be a major factor in limiting the effectiveness of radiotherapy, certain chemotherapy drugs and phototherapy. Hyperthermia at mild temperatures easily achievable with the use of presently available clinical hyperthermia devices may be an effective means to overcome the hypoxic protection in the treatment of human tumours.

Adenocarcinoma↗