[Maldevelopment of teeth caused by traumatic injury].
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Biomedical subjects
Publications and source records attributed to M Takagi.
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An organ-specific alkaline phosphatase inhibitor, L-homoarginine, at 44.5 mM concentration inhibited [3H]thymidine uptake by C3H/He mouse osteosarcoma (OS) cells, while L-arginine, L-phenylalanine, and glycine had little effect on the uptake. This inhibitory effect of L-homoarginine persisted even after the cells were washed free of the amino acid with fresh media. L-Homoarginine did not affect [3H]thymidine uptake by mouse myeloma MOPC 104E cells. In long-term culture, 22.3 mM L-homoarginine inhibited proliferation of OS cells. L-Arginine at the same concentration inhibited the proliferation to a lesser extent. On the other hand, L-phenylalanine and glycine did not affect in vitro proliferation of OS cells. When the same number of viable OS cells was inoculated s.c. after culturing the 24 hr with 44.5 mM L-homoarginine or L-arginine, the tumor growth in mice given injections of L-homoarginine (but not L-arginine)-treated cells was delayed markedly. Electron microscopic studies indicated that the inhibiting effect on OS cell proliferation was associated with a marked increase in lysosomal granules and a decrease in virus-like structures. Similarly, biochemical assay for acid phosphatase of cell homogenates demonstrated a 2-fold increase of activity in L-homoarginine-treated cells when compared to controls and L-arginine-treated cells. Thus, L-homoarginine inhibits proliferation and alkaline phosphatase activity of mouse OS cells and appears to increase acid phosphatase activity in synthesis of lysosomal granules.
The role of osteoclasts or chondroclasts in degradation and synthesis of complex carbohydrates was investigated using the high iron diamine-thiocarbohydrazide-silver proteinate method (HID-TCH-SP) for sulfated glycoconjugates and the periodate-thiocarbohydrazide-silver proteinate (PA-TCH-SP) method for vicinal glycol-containing glycoconjugates. HID-TCH-SP stained the calcified cartilage matrix, the osteoclast ruffled border, vacuoles and heterophagosomes but not the Golgi apparatus and primary lysosomes. The size and number of HID-TCH-SP stain deposits progressively decreased from the calcified cartilage matrix to the ruffled border (p less than 0.001). Enzyme digestion with testicular hyaluronidase removed most HID-TCH-SP stain deposits averaging 13 nm. in diameter in the extracellular matrix, cytoplasmic vacuoles, and heterophagosomes of osteoclasts. Only sparse stain deposits averaging 8 nm. in diameter and presumed to be keratan sulfate remained in these sites after enzyme digestion. Osteoclast heterophagosomes contained the highest concentration of hyaluronidase-resistant material suggesting delayed degradation of keratan sulfate at this site. PA-TCH-SP strongly stained collagen fibrils in the calcified cartilage matrix. Reactive collagen fibrils were also observed in extracellular channels but only rarely were identifiable collagen fibrils observed in cytoplasmic vacuoles. A progressive decrease in the diameter of PA-TCH-SP reactive collagen fibrils was observed between the calcified cartilage matrix and the ruffled border region (p less than 0.001). PA-TCH-SP stained cisternae of rough endoplasmic reticulum, Golgi saccules, and primary lysosomes consistent with the synthesis and packaging of glycoprotein enzymes at these sites. These results indicate that the dissolution of sulfated glycoconjugates requires osteoclastic engulfment of degraded material and subsequent intracellular digestion, whereas the dissolution of collagen fibrils appears to be completed extracellularly.
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The authors have carried out the laboratory and clinical studies of ceftizoxime (CZX), and obtained the following results. 1. The antibacterial activities of CZX were measured by plate dilution method against clinical isolates of S. aureus, E. coli, K. pneumoniae and P. aeruginosa. CZX inhibited the growth of S. aureus at concentrations less than 12.5 micrograms/ml, and the peak of sensitivity distribution was obtained at 3.13 micrograms/ml with an inoculum size of 10(6) cells/ml. And the peak sensitivity distribution of E. coli and K. pneumoniae were obtained at less than 0.1 microgram/ml and that of P. aeruginosa was obtained at 6.25 micrograms/ml. 2. Phagocytosis was determined by Quie's method. Phagocytosis of E. coli and K. pneumoniae by human polymorphonuclear neutrophil was more enhanced in the presence of 1 MIC and 1/2 MIC of CZX than of CEZ at 4 and 6 hours after incubation. 3. As for pharmacokinetic study, CZX was given by intravenous injection and drip infusion for 1 hour at a single dose of 10 mg/kg and 30 mg/kg. After intravenous injection of 10 mg/kg and 30 mg/kg of CZX, the mean peak serum levels were 19.1 +/- 3.4 micrograms/ml and 69.1 micrograms/ml at 30 minutes, and half-life times were 1.20 hours and 1.35 hours, respectively. After 1 hour drip infusion of 10 mg/kg and 30 mg/kg of CZX, the mean peak serum levels were 28.8 +/- 3.6 micrograms/ml and 60.9 +/- 5.9 micrograms/ml at the end of infusion, and half-life times were 1.40 hours and 1.77 hours, respectively. The mean urinary excretion rates were between 75.3% and 101% up to 6 hours after intravenous injection and drip infusion. 4. CZX was given to 4 cases with tonsillitis, 3 with pneumonia, 1 with enteritis, 4 with U.T.I., totaling 21 cases. A daily dose of CZX between 350 mg and 2,000 mg was given for 3 to 5 days. Clinical results obtained were good in all cases. No side effects and abnormal laboratory findings were observed.
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Acute sodium fluoride toxicity was studied histologically and histochemically in the rat kidney. The doses given subcutaneously by a single injection were 10, 12.5 and 15 mg/100 gm of body weight and the duration after the administration were 30 minutes, and one, 3, 5 and 7 days. Histologically, coagulation necrosis of the proximal tubules was found at 1 day and the injury was most striking at 3 days. Regeneration was almost complete at 7 days. Among the enzymes studied, e.g., alkaline phosphatase, acid phosphatase, 5'-nucleotidase, adenosine triphosphatase and succinic dehydrogenase, and acid phosphatase of the tubular epithelium was the most severely impaired.
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Sixteen autopsy cases of the primary sarcomas of the mouth and jaws were reviewed, which included 1 chondrosarcoma, 3 osteosarcomas, 1 leiomyosarcoma, 7 rhabdomyosarcomas and 4 histiocytic lymphoma (reticulum cell sarcoma). Although the case materials studied were too small, the pattern of the spread of the sarcomas of the mouth and jaw was likely to be divided into two groups, localized and generalized. The former is comprised of chondrosarcoma osteosarcoma, leiomyosarcoma and pleomorphic rhabdomyosarcoma. The latter is comprised of alveolar rhabdomyosarcoma and histiocytic lymphoma. Embryonal rhabdomyosarcoma belongs to either depending on the case. The former, being resistant to local therapy, tended to recur with a contiguous spread but was slow to metastasize. Metastases were limited to the lung and pleura through the hematogenous route. The primary sarcoma of the latter group were not so extended in local spread and occasionally cured with therapy. However, metastases, both hematogenous and lymphogenous, were generalized.
Unscheduled DNA synthesis (UDS) was investigated by autoradiography in human oral mucosa treated with 10 representative chemical carcinogens. Small sections of gingiva in short-term organ culture were exposed for 2 hours to chemical carcinogens plus [methyl-3H]thymidine. Significant numbers of silver grains, indicating UDS, were detected over the nuclei of both epithelial cells and fibroblasts. All ultimate or proximate carcinogens tested induced UDS. Of five procarcinogens tested, only benzo[a]pyrene (BP) did not induce UDS, but the more activated metabolite of BP, (+/-)-trans-7 beta-8 alpha-dihydroxy-9 alpha, 10 alpha-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene (BPDE I), was very effective in inducing UDS. Ultimate or proximate carcinogens induced higher levels of UDS than did procarcinogens. All the carcinogens that induced UDS showed clear dose-dependent effects. UDS levels were twofold to fivefold higher in the epithelial cells than in the fibroblasts, regardless of the type of carcinogen tested. Comparisons of the levels of UDS induced by 4-(hydroxyamino)quinoline 1-oxide, methyl methanesulfonate, or BPDE I did not reveal any significant differences. These findings indicate that human gingival epithelial UDS assay should be useful for short-term detection of environmental carcinogens that induce cancer in human oral mucosa.
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Two autopsy cases are presented of spindle-cell carcinoma of the oral cavity, which were transformations from the pre-existing well differentiated squamous cell carcinoma in Case 1 and verrucous carcinoma in Case 2, after large doses of irradiation. In Case 2, the conventional squamous cell carcinoma existed at the time of biopsy. Our case study suggests that the spindle-cell carcinoma may develop from the verrucous carcinoma by dedifferentiation through the intermediate stage of conventional squamous cell carcinoma.
Nine cases of fibromatosis occurring in or near the oral cavity are presented here. They are classified as nodular fasciitis (3 cases), aggressive infantile fibromatosis (2 cases), fibrosing myositis (1 case) and fibromatosis (1 case). Of the 5 cases of nodular fasciitis, 3 occurred from the fascia of the masticatory muscle and 2 from the submucous fascia of the palate and tongue. The aggressive infantile fibromatosis showed a prominent infiltrating growth and an alarming histologic appearance. One of the 2 cases showed a recurrence, but the postoperative course of both cases was uneventful for 13 years and 10 years, respectively. The fibrosing myositis is an unusual fibromatosis of the muscle, which arose within the tongue muscle. The lesion was benign and can be cured by conservative surgery.
Sixty-eight cases of benign papillary squamous tumors of the mouth were reviewed to elucidate further their histopathologic variations, as well as to clarify the premalignant nature of these tumors. The cases were classified into five varieties: idiopathic pseudoepitheliomatous hyperplasia (2 cases), papilloma (55 cases), oral florid papilloma (7 cases), inverted papilloma (3 cases) and recurring oral papillomatosis (1 case). The series included very rare cases, to our knowledge, undescribed in the literature. Though a microscopic differentiation between the benign papillary squamous tumors, verrucous carcinoma and well differentiated squamous cell carcinoma is quite difficult, clinical and pathologic recognition of these tumors is imperative, because of the differences in their clinical course and therapeutic requirement. A definite diagnosis should be made after the clinical and microscopic findings have been carefully correlated. Malignant change occurred in the oral florid papilloma and recurring oral papillomatosis.
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The effects of starvation and protein-deficient diet on the acute carbon tetrachloride (CCl4)-induced hepatotoxicity of the mice were studied histologically and histochemically. A total of 69 male mice (C57BL/6) were used and carbon tetrachloride was administered by a single subcutaneous injection at a dose of 0.1 mg/10 g body weight after starvation for 24 hours and feeding with protein-deficient diet for one month. The changes were examined consecutively. It was shown the the CCl4-induced hepatotoxicity was exaggerated by starvation and that the regeneration after centrilobular necrosis due to CCl4 administration was retarded under this condition. In the CCl4-treated group on protein-deficient diet, the centrilobular liver cells seemed to be less responsive to CCl4.