Biomedical subjects
Publications and source records attributed to Y Tokuriki.
A case of deep Sylvian meningioma in a 35-year-old woman was precisely diagnosed preoperatively with the aid of computed tomography and stereoscopic cerebral angiography. On reviewing the literature, it appears to be the first case that has been accurately diagnosed preoperatively and successfully treated by a total excision without serious complication. We report this case in detail together with another, similar case which we had encountered previously.
During a 6.5-year period from March 1978, 136 patients with brain tumors, which were diagnosed as gliomas or metastatic brain tumors during surgical operation, were treated by the application of sustained release anticancer pellets in seven institutes. Histological diagnosis disclosed that the majority of the tumors were malignant gliomas (61 cases), metastatic brain tumors (35 cases), and benign astrocytoma (17 cases). The anticancer agents (250 mg of 5FU, 1.5 mg of MMC, 250 mg of BUdR and 6,000 iu of urokinase) were sealed in a Silastic silicone tube of 6 mm in diameter, 0.25 mm in wall thickness, and 12 mm in length. The daily delivery of the drugs was (2-3)/10,000 of the original volume. This treatment was combined with surgical and irradiation therapy with or without general chemotherapy. The median survival time of patients with malignant gliomas was 545 days (18 months). The 1-year survival rate was 65.63%, and the 3-year survival rate 16.2%. On the other hand, in patients with benign astrocytomas, the median survival time was 1,500 days (4.1 years), 1-year survival rate 83.75%, and 3-year survival rate 42.84%. In those with metastatic brain tumors, the median survival time was 280 days, 1-year survival rate 43.87%, and 3-year survival rate 24.84%. The present findings revealed that the tube-type anticancer pellets cannot inhibit the growth of the brain tumors located 5 cm from the pellets.
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The effects of prostaglandin D2 (PGD2) on the growth of mouse malignant glioma cells were studied in vitro and in vivo. The in vitro studies consisted of various concentrations of prostaglandins (PG's) being added to cultures of mouse glioma cells. At concentrations above 2.5 micrograms/ml, PGD2 strongly inhibited the proliferation of glioma cells, whereas PGE2 had no effect at the same value. Exposure to 5.0 micrograms/ml PGD2 for more than 2 hours resulted in inhibition of glioma cell proliferation. This growth-inhibitory effect of PGD2 was related to the inhibition of DNA synthesis of the cells. The in vivo studies were performed with a subcutaneously transplanted mouse glioma model. Injection of 0.5 mg/kg PGD2 into the tumor was more effective than the same concentration given by intraperitoneal injection. In mice with intracranially transplanted glioma, daily intraperitoneal injection of 0.5 mg/kg PGD2 had no significant effect on survival time.
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The authors examined the growth rate of mouse 203 glioma cells in vitro and found it to be markedly inhibited after exposure to ACNU for 5 minutes at a drug concentration of 100 micrograms/ml. Rats that had undergone intracranial implantation of T1 neurogenic tumor were treated by 5 mg/kg of ACNU administered either intravenously or intra-arterially. The median survival times for the control animals and the animals undergoing intravenous or intracarotid administration of ACNU were 23, 29, and 46 days, respectively. The difference in survival time between the intravenous and intracarotid administration groups was statistically significant (p less than 0.01) when examined by the Cox-Mantel test. In a clinical trial, 17 patients with glioblastoma were treated by ACNU, eight intravenously and nine by the intra-arterial route. The drug was given in doses of 2 to 3 mg/kg at least twice before and twice after a course of postoperative radiotherapy. Intra-arterial administration was performed over a period of 5 minutes under local anesthesia. The median postoperative survival time for the patients in the intra-arterial group was 12.5 months, compared with 9.0 months for those in the intravenous group. The survival rate for the intra-arterial group was slightly higher, although statistically not significant, probably because the number of cases was small. The degree of thrombocytopenia due to ACNU tended to be less marked in the intra-arterially treated patients. The theoretical advantages of the intra-arterial administration of ACNU are discussed.
We observed a 55 y.o. right-handed woman, who was suspected of splenium tumor (glioblastoma?) by CT scan and presented bilateral crossed visuomotor ataxia proposed by Rondot et al. Left unilateral apraxia and agraphia were not found, but left unilateral hemialexia was evident by tachistoscopic examinations. In regard to bilateral crossed visuomotor ataxia, we suggested that at least there might be three possible hypotheses about its realization mechanism. (1) Callosal lesion might disconnect heterotopical fibers which runs from one occipital lobe to another frontal lobe. (2) Integrated information of visual and proprioceptive inputs in the parieto-occipital regions could not be transferred mutually to other side of the brain. (3) Functional dissociation between visual perception of "moving" and that of "position" might be the cause of this symptom. Former could be transferred via subcallosal pathway, but latter not transferred due to the callosal lesion. Hypothesis (1) could not explain, at least, "positive aspects" of this symptom, and which hypothesis is most probable might not be decided at present, because anatomical evidence and patho-plastic mechanism are not yet clarified.
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Cefotiam (1 g) was administered by one-shot intravenous injection to the patients proceeding a brain surgery. The cerebrospinal fluid (CSF) and serum were taken as a specimen, and the concentration CTM was assayed by agar-well method using Proteus mirabilis ATCC 21100. The most high concentration of CTM was 2,273 micrograms/ml in serum, and 2.3 micrograms/ml in CSF, respectively. The concentration of CTM in serum, CSF, and CSF/serum ration were determined at the indicated time. It appears likely that CTM can pass into CSF more easily than other cephalosporins.
Eighty three patients suffering from brain tumors have been treated by anticancer pellets containing 5-FU, urokinase, mitomycin and BUdR in dimethylsiloxan (Silastic) for three years. Constant and prolonged release of the chemicals from the anticancer pellet had already been proved in vitro. The amount of daily release were 1-3/1,000 of original volume. Tissue concentration of 5-FU was measured by bioassay system using staphylococcus 209 P strain with plate dilution method. In spite of the rapid disappearance of serum 5-FU, the local high accumulation of 5-FU was demonstrated in vivo. In rat neurogenic tumor, 1.104 microgram/g was detected on 60 days after the application of anticancer pellet containing 500 mg of 5-FU. The growth of tumor was also suppressed. The clinical study consists of 83 patients, 30 of glioblastoma, 19 of metastatic brain tumor, 13 of astrocytoma, 7 of oligodendroglioma, 4 of ependymoblastoma, 4 of malignant lymphoma and 6 of others. The median survival time of gliblastoma was prolonged to 71.5 weeks by the implantation of anticancer pellet from 40 weeks of control group. However, the median survival time of astrocytoma and metastatic brain tumor were 24 and 6 months, respectively, which have no significant difference from control groups. In the patients of metastatic brain tumor, the regrowth of metastatic foci in the brain was completely suppressed. However, most of them were succumbed from the original tumors. The concentration of 5-FU in several human tissue was measured in ten patients with different time intervals after the implantation of the anticancer pellet. Although they have different histologic patterns, the concentrations of 5-FU in human brain tumors were ranged from 0.05 to 0.67 microgram/g by 14 months after the implantation of the anticancer pellet. The adjacent cystic fluids also contain from 0.62 to 4.9 microgram/ml of 5-FU for two years. These results mean that they are keeping higher level of 5-FU than the tumoricidal level of 5-FU (0.056 microgram/g) for more than two years. On the other hand, no respective accumulation was demonstrated in other tissues. None of the patients showed any adverse reactions except a continuous slight fever up to 38 degrees C.
Penicillin-free-Picibanil was injected into the brain of Wistar/Fibiger strain rat to investigate the histological changes. Its effect on the growth of rat schwannoma inoculated in the brain was also examined histologically. Picibanil caused the most prominent but focal lymphoreticular cell reaction around the injected site in the brain 24 to 48 hours after injection. The cells infiltrating from the blood vessels were neutrophils, monocytes, lymphocyte-like cells, histiocyte-like cells and unidentified cells. This lympho-reticular cell reaction gradually subsided in the next 4 to 5 days. Neutrophils and monocytes (macrophages)stayed till the later phase. Two weeks later, the lesion was minimal with only mild glial changes. Picibanil was however, considered to exert at the site of injection neurotoxic and glia-toxic activity at a concentration of 0.1 KE/10 microliters. The rat schwannoma (T1) cells, when inoculated without any treatment, showed vivid growth in the brain and no lympho-reticular cell reaction was observed. When the T1 tumor cells, suspended in the Picibanil solution, were inoculated into the brain, no lymph-reticular cell reaction was observed 7 and 14 days after inoculation. However, when the rat was pretreated with Picibanil into the brain 7 days before inoculation, only a mild lymphoreticular cell reaction was observed around the T1 cells till 7 days after inoculation. Accordingly, Picibanil was considered to induce nonspecific immunological in the rat brain even around the glioma.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The leukocyte reactions of 106 neurosurgical cases, including 63 brain tumors, 10 intracerebral hematomas, 10 cerebral infarctions, 10 subarachnoidal hemorrhages, 8 cerebral injuries and 5 chronic subdural hematomas, against the extracts of gliomas and normal brain tissues were tested by capillary migration (LMI) and adherence inhibition (LAI) assays. Both tests showed specific responses with autochthonous and allogeneic glioma extracts in glioma patients. The sensitivity of LAI was superior to that of LMI, although LAI also showed adherence enhancement in the presence of weakly sensitized leukocytes or weak antigenic stimuli. Leukocytes from glioma patients showed positive inhibition with normal brain tissues from patients with glioma and intracerebral hematoma. Positive leukocyte reactions with normal brain tissues were also confirmed in patients with intracerebral hematomas, cerebral infarctions and severe cerebral lacerations, but not in those with subarachnoidal hemorrhages, minor cerebral contusions and chronic subdural hematomas. These results suggest that the leukocytes of patients with destructive brain lesions were autosensitized by normal brain antigens. The autosensitization has some advantages in that destroyed brain tissues are eliminated, but the hyperimmune state might cause postictal brain edema and should be properly controlled by steroids.