Energy straggling for medium-energy H+ beams penetrating Cu, Ag, and Pt.
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Biomedical subjects
Publications and source records attributed to Y Kido.
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Three families of tRNA-derived repeated retroposons in the genomes of salmonid species have been isolated and characterized. These three families differ in sequence, but all are derived from a tRNA(Lys) or from a tRNA species structurally related to tRNA(Lys). The salmon Sma I family is present in the genomes of two species of the genus Oncorhynchus but not in other species, including five other species of the same genus. The charr Fok I family is present only in four species and subspecies of the genus Salvelinus. The third family, the salmonid Hpa I family, appears to be present in all salmonid species but is not present in species that are not members of the Salmonidae. Thus, the genome of proto-Salmonidae was originally shaped by amplification and dispersion of the salmonid Hpa I family and then reshaped by amplification of the Sma I and Fok I families in the more recently evolved species of salmon and charr, respectively. We speculate that amplification and dispersion of retroposons may have played a role in salmonid speciation.
Cytophotometric analysis of nuclear DNA content was done in 128 patients with squamous cell carcinoma of the esophagus. The relationship among histopathologic features, DNA distribution pattern, and survival time was investigated from the standpoint of recurrence. Of 128 patients, 77 (60.1%) died of recurrence within 2 years after surgery: 16 (12.5%) from 2 to 5 years and two (1.6%) over 5 years. The rate of death of recurrence within 2 years was higher in patients with T4 or N1 than T1, T2, and T3 or N0 (P less than 0.01). Survivors over 5 years more frequently possessed type II DNA pattern than types III and IV (P less than 0.05). The rate of death of recurrence within 2 years was 34.4% in type II, which was lower than the 59.6% rate in type III (P less than 0.05) and the 76.6% rate in type IV (P less than 0.01). Survivors from 2 to 5 years were higher in type III than in type IV (P less than 0.05), and recurrence over 5 years was found only in type II. This inclination was more apparent in those with curative resection. In the patients with type II, careful follow-up may be needed over 5 years for late recurrence. However, in those with type IV, no recurrence over 2 years could be regarded as healed because most of their recurrences occur within 2 years. These findings suggest that the growth rate of esophageal carcinoma should reflect DNA aneuploidy, and the DNA analysis of esophageal carcinoma should be a valuable parameter for postoperative follow-up planning.
In ongoing reviews of 339 patients with surgically treated primary squamous cell carcinoma, there were 19 (5.6%) with concurrent gastric cancer and 11 (3.2%) with head and neck cancer. The incidences of intra-esophageal multiple occurrence of esophageal cancer are 27.3% and 26.3% in those with associated head and neck cancer and gastric cancer, respectively, and higher than 7.1% in those without such a concurrent cancer. There was no difference in the clinicopathological characteristics of those with concurrent head and neck and gastric cancers, except for the higher incidence of metachronous occurrence in the former. These findings suggest that, in cases of esophageal cancer associated with concurrent head and neck cancer and gastric cancer, intraesophageal multiplicity of the esophageal carcinoma is frequent and that preoperative serial evaluations is most important to design treatment and estimate the prognosis.
We examined the cytotoxic effects of combined low dose and long exposure to 5-fluorouracil (5-FU) and hyperthermia on Chinese hamster V-79 cells with reference to timing and sequence of administration. The survival rate following hyperthermia at 42 degrees C for 2 h alone was 95.4%, and that after exposure to 1.0 micrograms/ml/5-FU alone for 48 hours, 94.2%. With respect to the combination of 5-FU and heat, the survival rate of cells exposed to hyperthermia at 42 degrees C for 2 h followed by 1.0 micrograms/ml 5-FU treatment for 48 h followed by hyperthermia led to a survival rate of 10%. Flow cytometric analysis of V-79 cells after exposure to 1.0 micrograms/ml 5-FU for 48 h revealed an accumulation of cells in the S-phase; the percentage of S-phase exponential growing cells was 65% and the plateau phase was 38%. The former were more sensitive to heat than the latter cells according to the MTT assay. V-79 cells pretreated with 5-FU were more sensitive to hyperthermia than were those not pretreated with 5-FU. Therefore, when 5-FU plus heat is to be used to treat a patient with a malignancy, the sequence of 5-FU followed by hyperthermia may be more effective than the reverse.
We report herein, the histological observations taken at initial laparotomy from a 55 year old man with unresectable gastric cancer who responded almost completely to chemotherapy with Etoposide/Adriamycin/Cisplatin (EAP). The patient underwent a second operation after 2 cycles of EAP therapy and the stomach and adjacent lymph nodes were successfully resected. Histologic findings showed that cancer cells in the main tumor including the site of direct invasion had completely disappeared and been replaced by regenerated mucosa. The metastatic lymph node tumor was also partially killed, as indicated by a cluster of viable cancer cells which was divided by a strip of necrotic tissue. These findings led us to conclude that EAP therapy was remarkably effective for the patient.
Vascular clearance of chondroitin sulfate iron colloid (CSFe) was evaluated as a test for the reticuloendothelial system (RES) in rabbits. Injected CS59Fe was taken up by the RES in the liver (49%) and bone marrow (41%) after 60 min, suggesting its application for the RES function test. The clearance rate (K-value) of CSFe from the blood was calculated by measuring serum Fe concentrations after releasing iron from CSFe at certain intervals after injection. Depending upon different injected doses, K-values were varied and the phagocytic velocity, computed by multiplying K-values by corresponding injected doses, reached a plateau at high doses, indicating the phagocytosis of CSFe by the RES takes a saturation process. Double-reciprocal plotting of the dose and the phagocytic velocity showed a linear relationship, which provided the data on the maximum phagocytic velocity (Vmax), 0.122 mg/kg/min, and the CSFe concentration producing 1/2 Vmax (Kp), 0.426 mg/kg. Thus, this CSFe clearance test can be used for the evaluation of the RES function.
The disposition and elimination of sulfadimethoxine (SDMX) in the skin of broiler-chickens were investigated. The administration of SDMX, in drinking water, at a concentration of 1,000 ppm for 5 days demonstrated that the SDMX was eliminated much more slowly from the skin than from the other tissues or plasma. These results were duplicated and confirmed in another experiment, in which a single dose of 200 mg/kg BW of SDMX was administered via a stomach tube. No significant difference in the SDMX residue level was observed between the broiler-chickens that had their skin surface sealed versus the non-sealed animals and that had ingested SDMX in their drinking water. This illustrated the higher SDMX residue in the skin was not attributable to external SDMX contamination from the drinking water, feces or urine. In addition, there was no significant difference among the SDMX residue concentrations in the thoracic, dorsal and leg skin samples, following an intravenous injection of SDMX (30 mg/kg BW). This indicated that the SDMX was distributed evenly throughout the entire skin area of the broiler-chickens.
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In an attempt to further characterize non-irradiated contact-inhibited confluent monolayer of BALB/c 3T3 cells (= Contact-Sensitive Plates; CSP) as substrata for in vitro drug sensitivity testing, we compared the efficiency of colony formation with panels of cell lines on CSP with that on plastic dishes or in agar. Tumorigenicity in athymic nude mice was also examined. We found that: (1) HeLa cells, 2 esophageal cancer lines, rat 3Y1 fibroblasts transformed by either adenovirus type 12, mouse polyoma virus, Rous avian sarcoma virus, or plasmid DNA carrying v-Ha-ras oncogene all formed colonies on CSP and in agar and at the same time was tumorigenic. The efficiency of colony formation on CSP proved always to be higher than that in agar. (2) None of the 4 "normal" fibroplastic cell lines formed colonies on CSP or in agar and were tumorigenic. (3) Simian virus 40 and adenovirus E1A gene transformed rat 3Y1 fibroblasts formed colonies on CSP but not in agar, and were not tumorigenic. Therefore, CSP was found to provide selective and efficient growth of neoplastic cells when compared to other substrata and is also helpful in detecting incompletely transformed cells.
We have attempted to develop an in vitro assay system for predicting estradiol sensitivity of clinical cancer cells by measuring the effects of estradiol on the net DNA synthesis of primary culture cells. Superinoculation of neoplastic and normal cells onto confluent monolayers of a contact-sensitive cell line, which have been designated as contact-sensitive plates (CSPs), resulted in both the specific growth of the neoplastic cells and the growth inhibition of contact-sensitive normal cells. The applicability of CSPs to an estradiol sensitivity test was examined in the known estradiol-sensitive, estrogen receptor-possessing cell lines, MCF-7 breast cancer and KSE-1 esophageal cancer cells. The responses of each cancer cell to estradiol were sufficiently evaluated in this assay and clearly demonstrated stimulative and inhibitive growth regulatory effects of the estradiol in MCF-7 and KSE-1 cells, respectively. A total of 38 clinical carcinomas (33 of the breast and 5 of the esophagus) were tested for their estradiol sensitivity. A statistically significant increase of cancer cell growth (P less than 0.1) in nontreated culture from the 48th to the 96th h of the primary culture on CSPs was observed in 28 of 38 overall cases (73.7%), and the evaluable data were obtained within 5 days by a sampling of 5 X 10(3) cancer cells. Most of the breast carcinomas exhibited a positive correlation between the growth-stimulative effect of estradiol in this assay and the estrogen receptor levels in the resected specimens. On the other hand, a clinical case of esophageal cancer with an estrogen receptor showed a growth inhibition of primary carcinoma cells by estradiol treatment. These results therefore indicate the feasibility of predicting individual tumor response to estradiol by using a rapid sensitivity test in vitro.
We developed an autoradiographic screening test for hormone sensitivity of single cell suspensions of tumor tissues on cell mats, which inhibited the growth of normal cells alone. We applied this method to our newly established KSE-1 line derived from esophageal carcinoma and compared this method with well-established cytoplasmic and nuclear assays. Our assay, though taking longer to implement and providing only qualitative information, requires significantly smaller specimens than the current biochemical assay and will predict the hormone sensitivity of only viable neoplastic cells.
We investigated the regulatory effect of cholecystokinin (CCK) on subsequent insulin binding to pancreatic acinar cells. Rat isolated acini were preincubated with various concentrations of CCK octapeptide (CCK-8) at 37 degrees C. Acini were then washed, resuspended in the binding buffer, and incubated with 8.3 pM 125I-labeled insulin for 60 min at 37 degrees C. Pretreatment with CCK-8 caused inhibition of subsequent 125I-insulin binding that was time and concentration dependent. Significant inhibition was observed with 3 pM CCK-8. Computer analysis of the competition-inhibition study with a nonlinear least-squares curve-fitting program revealed that CCK-8 pretreatment of acini reduced the receptor affinity of the high-affinity binding site. This inhibitory action of CCK-8 was not due to the alteration in degradation or internalization of the tracer. When acini were pretreated with 100 pM CCK-8 for 120 min at 4 degrees C, a reduction in the receptor affinity of the high-affinity binding site was also observed. In pancreatic membrane prepared from acini preincubated with 100 pM CCK-8 for 120 min at 37 degrees C, displacement of 125I-insulin (83 pM) by unlabeled insulin (24 degrees C, 1 h) revealed that CCK-8 inhibited 125I-insulin binding by altering the receptor affinity of the high-affinity binding site. In acinar preparations the inhibitory effect of CCK-8 on 125I-insulin binding was abolished when acini were preincubated with CCK-8 and CCK receptor antagonist L 374718 at 37 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)
The effect of glucan (lentinan), beta(1----3)-glucan derived from Lentinus edodes, was evaluated in a clinically relevant septic model. Male, Japanese, white rabbits were intravenously injected with lentinan (1 mg/body) just before septic insult, induced by injecting fecal suspension into the ligated choledochus. In septic animals without lentinan treatment, platelet counts dropped serially following the septic insult and a paracoagulation test, measured by protamine gelation, turned positive. Plasma bilirubin and creatinine elevated significantly in comparison with control animals injected with saline, at 9 h and at 6 and 9 h. respectively. In lentinan-treated septic animals, platelet counts did not decrease and a significant difference was found at 9 h, compared to the untreated septic animals. The degree of positive paracoagulation was less prominent. The elevation of plasma bilirubin and creatinine levels was also less prominent and a significant difference was found at 9 h. Plasma endotoxin elevated significantly at 9 h in the untreated septic animals in comparison with lentinan-treated septic and control animals. The findings suggest a modification of the septic processes by the administration of glucan.
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The effect of fructose on glycogen synthesis was examined in the perfused liver of starved rats. With increasing fructose concentration in the perfusate, glycogen synthesis and the % a form of glycogen synthase increased to a maximum at 2 mM and then decreased, progressively. The glucose 6-P level increased with the increase in fructose concentration. On the other hand, the ATP content was unchanged at a concentration of 2 mM or less and decreased at 3 mM or more. We also showed that the stimulation of glycogen synthesis by fructose at a concentration of 2 mM or less was due to activation of glycogen synthase by accumulated glucose 6-P and that ATP depletion at a concentration of 3 mM or more caused an increase in phosphorylase a and a decrease in glycogen synthase activity even in the presence of a high concentration of glucose 6-P.