Formation of abnormal mycelium of Fusarium roseum Link. on a modified Czpek-D-amino acid medium.
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Biomedical subjects
Publications and source records attributed to M Tsuda.
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Seven hundred thirty-nine patients with unresectable hepatocellular carcinoma have been treated by transcatheter arterial chemoembolization using gelatin sponge particles soaked in a solution of Mitomycin C and Adriamycin. This therapy can be equal or superior to surgical resection and serves both as embolic therapy and targeted chemotherapy.
When a mixture of creatinine, glycine and glucose was heated for 2 h at 128 degrees C in diethylene glycol containing 14% water, two mutagens were formed. One of them, responsible for 90% of the mutagenicity, has already been identified as 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx). The other mutagen was purified and characterized. The UV absorption, mass and NMR spectra suggested that this mutagen was 2-amino-3,7,8-trimethylimidazo[4,5-f]quinoxaline (7,8-DiMeIQx). Comparison of the spectral properties of the compound obtained from the heated model mixture with those of synthetic material confirmed this structure. 7,8-DiMeIQx is a newly identified compound which, at a dose of 1 microgram, induced 163 000 and 9900 revertants of Salmonella typhimurium TA98 and TA100, respectively, with S9 mix.
The aim of this study is to analyze the dynamic CT findings after radiofrequency (RF) ablation for hypervascular hepatocellular carcinoma (HCC). RF ablation was used for 22 tumors in 20 patients. Peripheral enhancement was noted in 89% of regions within 1 month in the arterial phase. In 1-3 months, peripheral enhancement remained at 56% and was reduced to 22% by 3-6 months. It is difficult to determine the therapeutic result within 3 months due to continued peripheral enhancement in the arterial phase.
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Protective effects of CV-3611, a free radical scavenger, on retinal ischemic injury in the rat and on glutamate-induced cytotoxicity in a cell line were evaluated. Transient retinal ischemia was induced by raising intraocular pressure of rats to 110 mm Hg for 45 min, and the electroretinogram (ERG) was measured to evaluate retinal function. No ERG could be recorded immediately after reperfusion, and thereafter the ERG gradually recovered. Recovery of the a-wave latency and the amplitudes of the a and b waves in the CV-3611-treated (10 mg/kg, p.o.) group were significantly better than those in the control group up to 24 h after reperfusion. In both the control and CV-3611 group, the b wave showed better recovery than the a wave up to 6 h after reperfusion, while the relationship was reversed after 24-hour reperfusion. Glutamate (10 mM)-induced cytotoxicity in the N18-RE-105 cell, a neural retina-neuroblastoma hybridoma, was quantified by measuring lactate dehydrogenase. Three and 10 microM of CV-3611 significantly attenuated the glutamate-induced cytotoxicity in N18-RE-105 cells. Thus, the radical scavenger (CV-3611) promoted the recovery of retinal function after ischemia-reperfusion injury and ameliorated glutamate-induced cytotoxicity. These results suggest that oxygen free radicals play an important role in the early phase of retinal ischemic injury. Moreover, differential recovery processes of the a and b waves after ischemia suggest that the selective vulnerability of the retina to ischemia could change functionally during the period of reperfusion.
This is a case report on six patients with hyperammonemia that developed while they were receiving total parenteral nutrition (TPN) as a component of renal failure therapy. Clinically, the hyperammonemia presented as mental status changes in all six cases. Four of the six patients with renal failure initially received 400 mL Amiyu in 1400 mL 17% glucose (total = 1800 mL TPN-A) administered over each 24-hour period. Two patients had been placed on 400 mL complete amino acid in 1400 mL 17% glucose (total = 1800 mL TPN-C over each 24-hour period) prior to therapy with TPN-A. Approximately 3 weeks after initiation of TPN therapy with TPN-A, episodes of mental status changes of increasing duration and paroxysms were documented in five of the six patients. In one of the patients receiving TPN-C prior to TPN-A therapy, toxicity was clinically evident only 4 days after initiation of TPN-A. Serum ammonia levels were obtained and found to be elevated in the acute (ie, presenting) stage in all patients. With the discontinuance of TPN-A, ammonia levels normalized uniformly. Mental status also improved in all cases except for the patient with rapid clinical presentation who died 2 weeks after first evidence of clinical toxicity. In cases 1, 2, and 6, serum amino acid analysis in the acute phase showed reduced levels of ornithine and citrulline, the substrate and product, respectively, of condensation with carbamyl phosphate at its entry into the urea cycle. Moreover, levels of arginine, precursor to ornithine, were found to be elevated.(ABSTRACT TRUNCATED AT 250 WORDS)
The effects of in vivo exposure to phenobarbital (PB) on hepatic gap junctional intercellular communication (GJIC) and connexin protein expression in Sprague-Dawley rats were examined by in vivolin vitro dye-transfer assay, immunohistochemical staining, and by Western blot analysis. PB (50 mg/kg) was administered orally once a day for up to 6 wk. The average size of the dye spread after injection of Lucifer Yellow decreased at week 1 and remained at the same level until week 6. The area and number of connexin 32 (Cx32) spots per hepatocyte in the central zone of liver lobules decreased from week 1 to week 6, but no change of Cx32 spots in the peripheral zone was observed. The average area and number of connexin 26 (Cx26) spots per hepatocytes showed no clear change through the experimental periods. The decreased level of Cx32 protein in plasma membranes was observed in the PB group. These results suggest that PB, a liver tumor-promoting agent, inhibits hepatic GJIC in vivo in rats and that aberrant Cx32 protein expression and/or localization may be responsible for this effect.
Thirty-two patients with iliac and femoropopliteal artery occlusions were treated with direct intrathrombotic injection of ultrahigh-dose urokinase (10,000 IU/min). Occlusions ranged from 3 to 25 cm (average 13.3 cm) in length and the total urokinase dose from 120,000 to 1,410,000 IU (average 688,000 IU). The procedure was usually followed by balloon angioplasty to dilate the underlying stenoses. The initial recanalization rate was 96.9%, the two week patency rate 81.3%, and the cumulative one-year patency rate 66.3%. Complications associated with this procedure included three episodes of minimal bleeding, two distal embolisms, one local hematoma, and one low-grade fever. All were well controlled by palliative treatment. Results indicate that this procedure can provide rapid recanalization at a higher success rate and with fewer complications than previously reported.
As a preparative procedure for bone marrow transplantation, intermittent total body irradiation (TBI) has been used in our hospital. The biological significance of this method, in which the instantaneous dose rate is high but the average dose rate is low, has not been evaluated to date. The hematopoietic responses caused by both intermittent and continuous TBI were compared. In the intermittent irradiation, mice in a moving irradiation chamber were exposed under a small field (2 X 35 cm2), and the instantaneous and average dose rates were 1 Gy/min and 0.25-0.12 Gy/min, respectively. The average dose rate was adjusted to the same level in both irradiation methods. LD50/30 and survival of colony-forming units (CFU) in culture and survival of endogenous CFU in the spleen from female BDF1 mice were the same with the two methods. These results show that the response of hematopoietic stem cells depends on the average dose rate, not on the instantaneous dose rate. Our findings suggest that intermittent irradiation, as well as the continuous method, would be useful for preparing patients before bone marrow transplantation.