The apoptosis, a distinctive type of individual cell necrosis, has been considered to play a complementary but opposite role to mitosis in the regulation of animal cell populations. It can be initiated or inhibited by a variety of environmental stimuli, physiologically and pathologically. Apoptosis seems to appear in either non-neoplastic or neoplastic tissues, even malignant tumors in the state of untreatment or irradiation. This study was carried out to investigate the spontaneous occurrence of apoptosis in squamous carcinomas of the uterine cervix and its mechanisms. Light microscopically, noted were the condensation and fragmentation of individual tumor cells with formation of apoptotic bodies that were frequently phagocytosed by nearby intact tumor cells. They were commonly seen in the neighbourhood of coagulative necrosis. Electron microscopically (TEM and SEM), noted were nuclear condensation, margination toward the nuclear membrane and fragmentation of membrane-bounded apoptotic bodies that were well preserved. The intracellular apoptotic bodies were phagosomes and reduced to electron-dense lysosomal residual bodies. The conclusion obtained was as follow: Apoptosis was found in all cases of squamous carcinoma of the uterine cervix, of which the frequency was higher in tumors of poor differentiation than those of well to moderate differentiation. The process of the apoptosis is considered to pass through the step of formation of the apoptotic bodies, phagocytosis by adjoining tumor cells or histiocytes, and then degradation as lysosmal residual bodies.
Animals

The histogenesis of the myofibroblast continues to be a controversial issue. The most popular view is that the myofibroblast is derived directly from the fibroblast. The important role of myofibroblasts in the synthesis of collagen and in wound contraction was demonstrated initially in granulation tissue in experimental animals. Four settings are recognized in which myofibroblasts are the principal proliferative cells: reparative responses, pseudoneoplastic disorders, stromal response to neoplasia, and true neoplasms, both benign and malignant. To identify of fibroblastic cells with smooth muscle differentiation features in the nonneoplastic and neoplastic lesions, we examined a variety of histological, immunohistochemical and ultrastructural features of 7 cases of granulation tissue, 7 of hypertrophic scar, 10 of chronic persistent hepatitis, 10 of chronic active hepatitis, 7 of liver cirrhosis, 7 of fibromatosis, 42 of cervical intraepithelial neoplasia, 14 of microinvasive carcinoma, 14 of invasive carcinoma, 7 of fibroma, 20 of fibrosarcoma and 72 of malignant fibrous histiocytoma. Antibodies against alpha-smooth muscle actin and desmin were used in a biotin-streptavidin procedures. The results of immunohistochemical and electron microscopical examinations yielded virtually identical findings. The identification of fibroblastic cells with smooth muscle cell differentiation features in the desmoplastic reactions of carcinomas, fibroma, fibrosarcoma and malignant fibrous histiocytoma offers also novel diagnostic and prognostic perspectives, that might help in evaluating preneoplastic lesions and malignant lesions. So degree of proliferative myofibroblasts was helpful diagnostic aid in differentiation of chronic persistent hepatitis, chronic active hepatitis and liver cirrhosis.
Animals

The aim of the present investigation has been to evaluate the depletion pattern of the supercompensated glycogen of hindlimb muscles during strenous exercise in rats. The plan of the maximizing muscle glycogen stores is based on the fact that a glycogen-depleted muscle by exercise will have an increased avidity for glycogen when exposed to a high carbohydrate diet. The glycogen concentration of soleus, red gastrocnemius and plantaris muscle, and liver was measured at 0, 30 and 60 minutes during treadmill exercise. The experimental animals were divided into 5 group - Normal(N), Control(C), 1Hour(1HR:after 1hour of glucose ingestion), 2Hour(2HR:after 2hour of glucose ingestion) and Exercise-1Hour(EX-1HR:glucose ingestion after 1 hour of preloading treadmill exercise)group - for glycogen storage study. The glycogen concentration of soleus, red gastrocnemius and plantaris muscles in N group was 4.57+/-0.34, 5.11+/-0.24 and 6.55+/-0.20 mg/gm wet wt., respectively. The glycogen concentration of soleus and red gastrocnemius in EX-1HR group were about 1.9 and 1.8 times than that of N group, respectively, but the concentration of plantaris was not higher than that of N group. The glycogen concentration of liver in N group was 41.0+/-1.47mg/gm wet wt. and the concentration of the overnight fasted C group wad only 2.9% of the value of N group. The level of glycogen concentration of liver in the other glucose ingested groups(1HR, 2HR, including EX-1HR) was within 19 - 32% of that of N group. The blood glucose concentration of EX-1HR group was higher than that of N group, the plasma free fatty acid concentration of C and 2HR group was higher than that of N group, and the plasma insulin concentration of EX-1HR group was higher than that of N group. The concentration of supercompensated glycogen of soleus and red gastrocnemius were rapidly decreased during 30 minutes of exercise but there was almost no changes of the concentration during the other 30 minutes of continuing exercise. The concentration of N group during 30 minutes of exercise was decreased but more slowly than those of EX-1HR group. The remaining level of glycogen after 60 minutes of exercise in EX-1HR group was higher than that of N group. Taken together, the mobilization of endogenous muscle glycogen at the first stage of exercise was proportioned to the intial level of glycogen concentration, and later on, when exercise continued, the muscle glycogen level was stabilized. And the remaining level of supercompensated muscle glycogen after 60 minutes of exercise was higher than that of normally stored glycogen level. The mobilization of the glycogen stroed in slow and fast oxidative muscle fibers is faster than in the fast glycolytic muscle fibers during strenous exercise.
Animals

Insulin resistance is a prominent feature of diabetic state and has heterogeneous nature. However, the pathogenetic sequence of events leading to the emergence of the defect in insulin action remains controversial. It is well-known that prolonged hyperglycemia and hyperinsulinemia are one of the causes of development of insulin resistance, but both hyperglycemia and hyperinsulinemia stimulate glucose uptake in peripheral tissue. Therefore, it is hypothesized that insulin resistance may be generated by a kind of protective mechanism preventing cellular hypertrophy. In this study, to evaluate whether the acutely increased glucose uptake inhibits further glucose transport stimulated by insulin, insulin sensitivity was measured after preloaded glucose infusion for 2 hours at various conditions in rats. And also, to evaluate the mechanism of decreased insulin sensitivity, insulin receptor binding affinity and glucose transporter 4 (GLUT4) protein of plasma membrane of gastrocnemius muscle were assayed after hyperinsulinemic euglycemic clamp studies. Experimental animals were divided into five groups according to conditions of preloaded glucose infusion: group I, basal insulin (14+/-1.9 micronU/ml) and basal glucose (75+/-0.7 mg/dl), by normal saline infusion; group II, normal insulin (33+/-3.8 micronU/ml) and hyperglycemia (207+/-6.3 mg/dl), by somatostatin and glucose infusion; group III, hyperinsulinemia (134+/-34.8 micronU/ml) and hyperglycemia (204+/-4.6 mg/dl), by glucose infusion; IV, supramaximal insulin (100+/-2.2 mg/dl), by insulin and glucose infusion; group V, supramaximal insulin(4813+/-687.9 micronU/ml) and hyperglycemia (233+/-3.1 mg/dl), by insulin and glucose infusion. Insulin sensitivity was assessed with hyperinsulinemic euglycemic clamp technique. The amounts of preloaded glucose infusion(gm/kg) were 1.88+/-0.151 in group II, 2.69+/-0.239 in group III, 3.54+/-0.198 in groupIV, and 4.32+/-0.621 in group V. Disappearance rates of glucose (Rd, mg/kg/min) at steady state of hyperinsulinemic euglycemic clamp studies were 16.9+/-3.88 in group I, 13.5+/-1.05 in group II, 11.2+/-1.17 in group III, 13.2+/-2.05 in group IV, and 10.4+/-1.01 in group V. A negative correlation was observed between amount of preloaded glucose and Rd )r=-0.701, p<0.001) when all studies were combined. Insulin receptor binding affinity and content of GLUT4 were not significantly different in all experimental groups. These results suggest that increased glucose uptake may inhibit further glucose transport and lead to decreased insulin sensitivity.
Animals

The purpose of this study is to evaluate histologic result of bone substituting material on defects followed tooth extraction. We compare the histologic findings control, DFDBA, Bio-Oss(R), and Regenafil(TM), Briefly, mandibular premolar teeth were extracted available for bone filling. All alveolar sites were checked after extraction and thoroughly debrided with a dental curet to remove the periodontal ligament. Extraction sites were prepared dehiscence on buccal side 7mm height from alveolar crest. The graft materials were filled into the extraction socket and dehiscenc defects. The animals were sacrificed 12 weeks after implantation. Both treated and control mandibular sites were histologically evaluated with light microscopy. Histologic observation at 12 weeks revealed that control and experimental sites were healed uneventfully and directly apposed to new bone without any adverse tissue reaction. DFDBA and Bio-Oss(R) sites maintain width of alveolar crest but were not fully resorbed. Regenafil(TM) sites also maintain width and particles were resorbed more than other graft materials. From this results, it was suggested that Regenafil(TM) is promising boen substituting materials maintaining the width of alveolar crest and height follewed tooth extraction.
Animals

PURPOSE: We assessed the impact of using a porcine model on the training of laparoscopic partial nephrectomy(LPN) and compared the training effectiveness between surgeons with and without previous laparoscopic experience. MATERIALS AND METHODS: Surgeon A had previous laparoscopic experience, with the exception of LPN, while surgeon B had no prior laparoscopic experience. A tumor model was created by subcapsular injection of liquid plastic(Smooth-Cast 320) in the kidney. We recorded the total operation time, the bowel dissection time, the renal pedicle dissection time, the warm ischemic time, the mass resection time, the suture time, and the presence of major complications for each surgeon. RESULTS: The mean operation time was significantly shorter for surgeon A compared to surgeon B(49.1+/-4.5 and 63.6+/-8.4 minutes, respectively, p<0.001). Although the mass resection time was significantly shorter for surgeon A as well, there were no significant differences between the two surgeons in terms of warm ischemia time and suture time. As the training progressed, surgeon B improved in all surgical steps and surgeon A showed improvement in time for warm ischemia and suturing the defect. Five complications occurred(two cases by surgeon A and three cases by surgeon B). CONCLUSIONS: A porcine model improved the skills needed for LPN, including shortening the warm ischemia and suture times. LPN is a procedure requiring technically-demanding skills that can be improved by training using a animal model, regardless of the previous laparoscopic experiences.
Animals

This study was carried out to visualize lead by Timm sulphide silver method and to define lead-induced change of duodenal absorptive cells of rat after administration of 0.01% lead acetate with drinking water. Sprague-Dawley rats, weighing 250g, were used, and they were orally administered with 0.01% sodium acetate and sacrificed at 0.5, 1, 1.5 hours and 2, 7, 15, 30, 45, 60 days after administration. A portion of duodenal tissue was observed under light microscope, scanning and transmission electron microscopes after development with Danscher method. The blood lead concentration in experimental group began to increase from the 2nd day after administration, and it increased gradually until the 45th day and decreased at the 60th day. On light microscope, many brown lead granules were observed at the villi tip at the 2nd day. There is mild blunting of villi tip at the 45th day. At the 60th day, most of the villi were mildly shortened and showed lymphangiectasia. On scanning electron microscope, the villi tip was mildly blunted and the extrusion zone became irregular at the 45th day. The depth of creases did not change. At the 60th day, the villi tip was moderately blunted and the extrusion zone was markedly irregular. The depth of creases increased. On transmission electron microscope, at 0.5 hour after oral administration, numerous lead granules were diffusely scattered and were not confined to any specific microorganelles. The lead granules decreased with time. At the 7th 15th day, the intercellular spaces were widened and several vacuoles appeared and the condensation of mitochondrial matrix. There was also ribosomal detachment from RER, and there was neither secondary lysosomes or post-lysosomes. At the 30th and 45th day, secondary lysosomes appeared and the condensation of mitochondrial matrix with early formation of myelin figures was noted. At the 60th day, the intercellular space widening extended to the upper most portion of the cells, and nonspeciqic degenerative changes became severe. In view of above mentioned findings, it can be concluded that passive diffusion as well as active transport was partly involved in the absorption of lead. Most of the changes of microorganelle are compatible with nonspecific degenerative changes which could occur due to impairment of oxidative phosphorylation.
Rats ; Animals

This study was performed to investigate the effect of endotoxin to the CCl4-induced liver injury. Twelve Sprague-Dawley rats were intraperitoneally injected 1.6 g/kg CCl4 as control group. Another 24 rats were orally administrated 300 mg/kg of neomycin at 16 and 3 hours prior to CCl4 injection as experimental group. Twelve among them were intraperitoneally infected 1.0 mg/kg of endotoxin(E-Coli, 0111:B4, No L-2630, lipopolysaccharide, Sigma, USA) and CCl4 simultaneously for offsetting neomycin effect. The rats were sacrificed at 1, 4, 10, and 24 hours after CCl4 injection. The liver tissues from all experimental groups were observed by light and electron microscopy. The results obtained were summarized as follows: In the CCl4 only group, the hepatocytes revealed sweling of ER and mitochondria with many lipid droplet in the cytoplasm. Focal cellular necrosis was seen at the later phase. The Kupffer cells were activated and showed many cytoplasmic processes, secondary lysosomes, and vaculoles. The endothelial cells were edematous. Several neutrophils, platelets, and microthrombi were scattered in the sinusoid. In the neomycin-CCl4-endotoxin administrated group, both hepatocytic destruction and intrasinusoidal microthrombi formation were more pronounced. In the neomycin pretreated group, the hepatocytes revealed mild cellular destruction without necrosis. There is no intrasinusoidal microthrombi. According to these results, it would be concluded that the small dosage of gastrointestinal tract-derived endotoxin affects to the liver injury caused by CCl4. The synergistic effects of CCl4 and gastrointestinal tract-derived endotoxin which can not be detoxified by damaged Kupffer cells, may be more important in the pathogenesis of CCl4-induced liver injury.
Rats ; Animals

No abstract available.
Animals ; Lordosis*

No abstract available.
Animals* ; Neurons*