No abstract available.
Animals* ; Brain* ; Hypothermia* ; In Situ Nick-End Labeling* ; Models, Animal*

Heat shock protein of 72 kDa (HSP70) has a role in the functional modulation of sex steroid hormone receptors and in p53-associated oncogenesis and inhibits apoptosis associated with bcl-2. However, the exact role of HSP70 in the development of endometrial adenocarcinoma has not been well established. The aim of this study is to evaluate the role of HSP70 in relation with ER, PR, p53 and bcl-2 expressions and apoptosis in benign and malignant endometrial lesions. Immunohistochemical studies for HSP70, ER, PR, p53, bcl-2 and TUNEL method for apoptosis were performed in 30 cases of adenocarcinoma and 30 cases of benign endometrial lesions consisted of each 10 cases of disordered proliferative endometrium (DP), simple or complex hyperplasia (HP), and atypical hyperplasia (AH). There were no significant differences of HSP70 and bcl-2 expression rates and apoptotic index (AI) between DP, HP, AH, and adenocarcinoma. p53 expression rate in adenocarcinoma was 36.7%, but no p53 expression was identified in DP, HP and AH (p<0.05). In adenocarcinoma, HSP70 expression rate was higher in ER and PR negative adenocarcinoma (p<0.05), and p53 expression rate was higher in nonendometrioid type and FIGO grade II and III (p<0.05), but no significant difference of bcl-2 expression rate according to the histological type and FIGO grade. AI was higher in nonendometrioid type (p<0.05). There was no correlation between HSP70, p53 and bcl-2 expressions, and no significant difference of AI according to HSP70, ER, PR, p53, and bcl-2 expressions. In conclusion, higher HSP70 expression rate in poorly differentiated and ER and PR negative adenocarcinoma suggests that HSP70 inhibits ER and PR expression and may be involved in the development of poorly differentiated endometrial adenocarcinoma.
Adenocarcinoma* ; Apoptosis* ; Carcinogenesis ; Endometrium ; Female ; Heat-Shock Proteins ; Hyperplasia ; In Situ Nick-End Labeling

OBJECTIVE: To know whether leiomyomas come from increased proliferation or from decreased apoptosis of uterine muscular cells, and compare the results with the menstrual cycles and expression of ER/PR. METHODS: Between Mar. 2003 to Jun. 2003, the authors got 15 leiomyomatous and normal myometrial tissues from the patients who had undergone hysterectomy transabdominally or laparoscopically. As soon as they were excised, these tissues had been sent to the pathologic department to be stained by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) to determine apoptotic index (A.I.), and immunohistochemistry of Ki-67 to do Ki-67 immunoreactivity index (K.I), and ER/PR. RESULTS: There was no statistically significant difference of A.I. between leiomyoma and normal myometrial tissues But there was a significantly higher Ki-67 immunoreactivity index in leiomyoma rather than normal myometrial tissue. The increase of K.I. in leiomyomas has the reverse correlation with age, but was not statistically correlated with the menstrual cycles. There was no significant different pattern of expressions of ER/PR between in leiomyoma and in normal uterus. CONCLUSION: The main reason the leiomyomas come from may be increased proliferation instead of decreased apoptosis of leiomyoma cells. Although leiomyomas were known to be influenced by sex hormone, there was no solid evidence of increase of K. I. correlated with menstrual cycle or expression status of ER/PR in leiomyomas. Maybe there are another factors such as age that control the pathogenesis of leiomyoma rather than hormones or their receptors.
Apoptosis* ; Cell Proliferation* ; Female ; Humans ; Hysterectomy ; Immunohistochemistry ; In Situ Nick-End Labeling ; Leiomyoma* ; Menstrual Cycle* ; Uterus

BACKGROUND: Recently, the pulse-in-pulse mode of intense pulsed light (IPL) has been used increasingly for the treatment of melasma. OBJECTIVE: To observe the morphologic changes in the melanophore in adult zebrafish after irradiation with conventional and pulse-in-pulse IPL and Q-switched Nd:YAG (QSNY) laser. METHODS: Adult zebrafish were irradiated with conventional and pulse-in-pulse mode of IPL. The conditions for conventional IPL were 3 mJ/cm², 560 nm filter, and pulse widths of 7, 20, and 35 msec. The pulse-in-pulse conditions were 3 mJ/cm² and on-time 1/off-time 2. The QSNY laser was used with the settings of 1,064 nm, 0.4 J/cm², a 7 mm spot size, and one shot. Specimens were observed using a light microscope, a transmission electron microscope (TEM), a scanning electron microscope (SEM) and a confocal microscope. RESULTS: After conventional IPL irradiation with a 7 msec pulse width, melanophore breakage was observed using light microscopy. Under TEM, irradiation with conventional IPL for 7 msec and pulse-in-pulse IPL induced melanophore thermolysis with vacuolization. However, changes in the melanophore were not observed with 35 msec IPL. Under SEM, unlike the control and QSNY groups, IPL-irradiated zebrafish showed finger-like fusion in the protein structure of scales. Specimens examined by a confocal microscope after conventional IPL irradiation showed a larger green-stained area on TUNEL staining than that after pulse-in-pulse mode IPL irradiation. CONCLUSION: Zebrafish irradiated with long pulse-IPL showed no morphologic changes using light microscopy, while morphological changes in melanophores were evident with use of TEM. Pulse-in-pulse mode IPL caused less damage than conventional IPL.
Adult ; Humans ; In Situ Nick-End Labeling ; Melanophores* ; Melanosis ; Microscopy ; Weights and Measures ; Zebrafish*

This experiment was designed to explore the correlation between the mechanism of immobilization-induced skeletal muscle atrophy and the apoptosis of muscular cells. The models of skeletal muscle atrophy induced by immobilization for different length of time were established according to Sievanen II methods. 24 rabbits, each of them having one hind leg fixed by the tubal plaster and the other one free as control, were randomly divided into four groups depending on time of fixation (3, 7, 14, and 28 days respectively). The animals were sacrificed by the end of fixation. TdT-mediated d-UTP nick end labeling (TUNEL) was used to investigate the apoptotic muscle cells in the animal's bone. By comparing the apoptotic muscle cells with the morphology of the skeletal muscle, the correlation between cell apoptosis and skeletal muscle atrophy were analyzed. Apoptotic muscle cells did appear after immobilization in the atrophied skeletal muscle. In various groups, some cells with false positive stained TUNEL were found in the atrophic muscle, which could be distinguished from apoptotic cells by their characteristics. In conclusion, cell apoptosis participates in the process of skeletal muscle atrophy induced by immobilization; the amount of apoptotic cells is strongly associated with the time of immobilization, its peak appears on the 14th day of immobilization; the distribution of apoptotic skeletal muscle cell varies with the time of fixation. The severity of skeletal muscle atrophy is associated with the degree of the muscle cell apoptosis.
Animals ; Apoptosis ; physiology ; Immobilization ; In Situ Nick-End Labeling ; Muscle, Skeletal ; pathology ; Muscular Atrophy ; etiology ; Rabbits

We have studied morphologic characteristics and apoptosis on the fetal brain of the trisomy 16 mouse, a model for human trisomy 21 syndrome. This study was based on serial sections of the whole brain from a sample of sixteen trisomy 16 mice and forty-six age-matched control littermates from embryonic day (ED) 12 to ED 18. Trisomy 16 brains showed a reduction of telencephalic size and abnormal cortical development. At ED 13 trisomy 16 and control brains appeared similar. By ED 14 difference in the cortical thickness and telencephalic growth became evident, and by ED 16 a marked size difference had developed between the trisomy 16 and control brains. By ED 18, however, the thickness of the trisomy 16 cortex had increased considerably and was not significantly different with respect to the thickness and cross-sectional areas of the pallium and its constituent cortical layers. The cell density of the trisomy 16 cortex had persistently decreased before ED 17, when the cell density of control and trisomy 16 corteces was similar within each layer. At ED 18 cell density of trisomy 16 cortex in each layer increased. There was inverse relationship between a number of TUNEL positive apoptotic cells and cell density in the trisomy 16 brains. Our results suggest that developmental abnormalities of the trisomy 16 brain indicated developmental delay of the telencephalon growth, which may be caused by apoptosis rather than by a proliferation defect.
Animals ; Apoptosis* ; Brain* ; Cell Count ; Down Syndrome ; Humans ; In Situ Nick-End Labeling ; Mice* ; Telencephalon ; Trisomy*

PURPOSE: This study was aimed to evaluate changes in the stromal keratocyte after ablation of 50 micrometer and 100 micrometer with use of photorefractive keratectomy(PRK). METHODS: At 4 hours, 24 hours, 72 hours, 7 days and 1 month after PRK, each group of rabbits including normal control group was treated with terminal deoxyribonucleotidyl transferase-mediated dUTP-digoxigenin nick-end labeling(TUNEL) staining using ApopTag(R) kit in vivo, then apoptotic keratocytes were evaluated with light microscope. RESULTS: There was no response with TUNEL staining of the epithelial cells, stromal keratocyte, and endothelium in normal cornea. In the ablation group, however, regardless of the depth of photorefractive ablation, the TUNEL signal was maximal after 4 hours, and it decreased with time. The signal was more intense in 100 micrometer ablation group than 50 micrometer ablation group, although the signal was not observed at the endothelial cells in both groups. The number of apoptotic stromal keratocytes at each time point of 4 hr, 24 hr, 72 hr, and 1 week was 57+/-8.9, 49+/-7.5, 36+/-5.1, and 12+/-1.3 cells/field in 100 micrometer ablation group, and 31+/-4.4, 28+/-4.6, 21+/-3.9, and 5+/-1.1 cells/field in 50 micrometer ablation group, and the difference between the two groups was statistically significant(P<0.05). CONCLUSION: The more the amount of ablation with photorefractive keratectomy, the stronger the apoptotic response. The postoperative apoptotic response was observed especially within 1 week. These findings suggest that early suppression of postoperative apoptosis within 1 week will influence on the prognosis of visual quality after photorefractive keratectomy, and more studies will be needed in the future.
Apoptosis* ; Cornea ; Endothelial Cells ; Endothelium ; Epithelial Cells ; In Situ Nick-End Labeling ; Photorefractive Keratectomy* ; Prognosis ; Rabbits

BACKGROUND: Genistein and daidzein are two major soybean isoflavones. They have received increasing attention because of their possible roles for cancer prevention. However, their mechanisms of action and molecular targets on the human colon cancer cells are not fully understood. METHODS: Human colon cancer HCT-116 cells were treated with genistein and daidzein to investigate their effects on the cell growth and this was analyzed with MTT assay. TUNEL assay and Hoechst33342 stain were carried out to identify apotosis. RESULTS: Daidzein was able to inhibit cell proliferation and induce apoptosis of the HCT-116 cells, but genistein didn't affect the cell growth. The ER antagonist ICI182780 didn't attenuate the antiproliferative and proapoptotic effects of daidzein: this means the effect of daidzein on the HCT-116 cells may not be dependent on the ER pathway. The other soybean isoflavone, genistein, attenuated the effects of daidzein on the HCT-116 cells and its mechanism should be elucidated. CONCLUSIONS: These data suggest that daidzein may act as a preventive agent on human colon cancer, and its mechanism of action doesn't involve the ER-dependent pathway.
Apoptosis ; Cell Proliferation ; Colon* ; Colonic Neoplasms* ; Genistein* ; HCT116 Cells* ; Humans* ; In Situ Nick-End Labeling ; Isoflavones ; Soybeans

OBJECTIVETo observe the change of quantitative distribution,apoptosis and proliferation of T and B cells in the skin of KM mutant mice.

METHODSWe chose 1-,3-,6-,9-,22-day,3-,6-month-old KM mutant and wild-type mice to detect the changes of T and B lymphocytes using blood routine tests and immunohistochemical staining. Apoptosis was detected by TUNEL staining and proliferation by proliferating cell nuclear antigen (PCNA) staining.

RESULTST cells on KM mutant mice skin were mainly seen in epidermis and dermis. They increased on the first day to 6(th) day after birth and decreased on the 9(th) and 22(nd) day,but after 3-month-old,their number began to increase;at the time of 6 months,the number of B cells also increased. The apoptosis of the skin hair follicle and sebaceous gland cells were more obvious in KM mutant mice than in wild-type mice,with the maximal apoptosis occurred at the age of 22-day-old in both groups. The proliferation of epidermal basal cells in KM mutant mice between 1 to 9-day-old was not significantly different from that in the wild-type mice,but decreasing on the 22(nd) day and 3(rd) month and increasing in the 6(th) month. The proliferation in hair follicle and sebaceous glands decreased on 9(th) day,increased on 22(nd) day,and deceased on the 3(rd) month again.

CONCLUSIONSThe quantitative distribution,apoptosis,and proliferation of T and B lymphocytes abnormally change in the skin tissue of KM spontaneous mutant mice. They may lead to immune and hair growth disorders and promote the inflammatory responses.

OBJECTIVETo explore the influences of Mycobacterium tuberculosis on the levels of human acute monocytic leukemia cell line THP-1 apoptosis and death.

METHODSHuman acute monocytic leukemia cell line THP-1 were infected with Mycobacterium tuberculosis strains H37Ra, H37Rv, or Beijing genotype (BJTB), respectively, to construct the infection models. Cell apoptosis was detected using flow cytometry. The distribution of the apoptotic proteins was detected using immunofluorescent staining assays. The cells late apoptosis was detected using terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling staining assays. The change of cell death was determined by Tyrpan blue staining assays.

RESULTSTHP-1 apoptosis was induced by Mycobacterium tuberculosis strains H37Ra, H37Rv, and BJTB. H37Ra strongly induced THP-1 apoptosis, H37Rv weakly induced THP-1 apoptosis, and BJTB induced THP-1 apoptosis at the lowest level among these three Mycobacterium tuberculosis strains. On the contrary, BJTB strongly induced THP-1 death, H37Rv weakly induced THP-1 death, and H37Ra induced THP-1 death at the lowest level.

CONCLUSIONSMycobacterial strains with different virulence induce different levels of apoptosis and death of THP-1 cells. Compared with highly virulent strains, attenuated strains induce more apoptosis and less death.