No abstract available.
Bromodeoxyuridine* ; Cervix Uteri* ; Drug Therapy* ; Female

DNA replicating cells were detected in the psoriatic epidermis by anti BrdU antibody after incubating tissue sections biopsied in acute and chronic areas with BrdU. The expression pattern of No. 1 keratin, involucrin. filaggrin, loricrin and transglutaminase E was studied in the paraffin embedded sections of psoriatic specimen which showed various histopathological findings. The results are as follows 1) The labeling index of BrdU in lesional psoriatic skin was significantly greater than that in normal skin. The labeling index was greater in the clinically active lesion of psoriasis than that of the chronic lesion, which suggest that psoriatic lesions are composed of distinct lesions differing in activity. 2) In the epidermis of the psoriatic plaques with extensive parakeratosis or microabscesses at the base of the stratum corneum and absent granular layers, the expression pattern of five epidermal proteins appeared as follows : No. 1 keratin which is found in normal epidermis immediately above the basal layer, appeared several layers higher. Involucrin was detected in most of the suprabasal layers. Fillaggrin, loricrin and transglutaminase E showed negative expression. The results obtained in the present study suggest that the increment of DNA replicating cells and aberrant, maturation pathway of epidermis appear in active psoriatic plaques.
Bromodeoxyuridine ; DNA ; Epidermis ; Paraffin ; Parakeratosis ; Psoriasis ; Skin*

No abstract available.
Bromodeoxyuridine* ; Hep G2 Cells* ; Kinetics* ; Tretinoin*

PURPOSE: We investigated the inhibitory effects of mitomycin-C (MMC) and 5-fluorouracil (5-FU) on the proliferation of the lens epithelial cells (LECs) depending on time and concentration during the epithelial cell culture using capsular bag model. METHODS: We cultured LECs using capsular bag model after exposure to various time and concentration of MMC and 5-FU. We compared the half coverage time and appearance of posterior capsule by LECs. We examined the proliferative and inhibitory effect on LECs using BrdU immune staining. We observed the morphologic change of LECs on histologic section. RESULTS: Half coverage time of posterior capsule by LEC was 18.2 +/- 3.5 days in control group, whereas 27.5 +/- 3.8 days and 26.8 +/- 4.2 days when treated with 0.2 mg/ml MMC, 50 mg/ml 5-FU for 3 minutes, repectively. The increase of concentration and the exposure time of MMC or 5-FU resulted in the delay of coverage time of posterior capsule by LECs and reduction of BrdU incorporation in the nucleus of proliferating cells. On histologic section, reduction of LECs' multilayering and few cytoplasmic organells were observed. CONCLUSIONS: Using capsular bag model, we found the inhibitory effect of MMC and 5-FU on LECs proliferation depending on the concentration and exposure time. Capsular bag model would be contribute to the study about after-cataract.
Bromodeoxyuridine ; Cytoplasm ; Epithelial Cells* ; Fluorouracil* ; Mitomycin*

BACKGROUND: Anesthetics have been suspected of impairing various aspects of the immune function either directly by affecting the function of immunocompetent cells or indirectly by modulating the stress response. Splenocytes play important roles in the cellular host defense against infection. In order to assess the immune modulatory effects of propofol, this study examined the cytotoxic and proliferative effects of propofol on splenocytes. METHODS: Splenocytes, as responders, were isolated from BALB/c mice (n = 10). The cells were pretreated with different propofol concentrations (0micrometer, 30micrometer, 100micrometer, 300micrometer) for 24 hours. The cytotoxic effect was assayed by the NADH dehydrogenase activity and the proliferation was evaluated by the level of 5-bromo-2'-deoxyunridine (BrdU) incorporation during DNA synthesis in the presence or absence of propofol, in addition to lipopolysaccharide (LPS, 1 microgram/ml) for mitogenic stimulation. A cell proliferation enzyme-linked immuno-sorbent assay (ELISA) system was used, and the stimulation index was calculated in the presence or absence of propofol. RESULTS: The percentage of the NADH dehydrogenase activity was changed by the propofol pretreatment (P < 0.001). LPS stimulation significantly decreased the NADH dehydrogenase activity at 100micrometer and 300micrometer compared with the propofol-added or pretreated cells (P < 0.05). The stimulation index to LPS was lower at concentrations of 100micrometer and 300micrometer than at 30micrometer, and proliferative response of splenocytes were completely abrogated by adding toxic concentrations (100micrometer) of propofol (P < 0.05). CONCLUSIONS: Neither cytotoxicity, as defined by the NADH dehydrogenase activity, nor a proliferative effect, as measured by the level of (BrdU) incorporation in the splenocytes, were affected by the clinical concentration of propofol.
Anesthetics ; Animals ; Bromodeoxyuridine ; Cell Proliferation ; DNA ; Mice ; NADH Dehydrogenase ; Propofol

PURPOSE: To investigate the effect of low dose radiation on neuronal cell proliferation in diabetic rats. MATERIALS AND METHODS: A group of rats (first group) were divided into three subgroups (nondiabetic control, nondiabetic 0.1 Gy and nondiabetic 10 Gy groups) to determine the effect of radiation on normal hippocampal neuronal cell proliferation. A further group of rats (second group) were divided into six subgroups (nondiabetic control, diabetic control, diabetic 0.01 Gy, diabetic 0.1 Gy, diabetic 1 Gy and diabetic 10 Gy groups) to determine the effect of radiation on hippocampal neuronal cell proliferation under diabetic conditions. Using immunohistochemistry for 5-bromo-2'-deoxyuridine (BrdU), the number of neuronal cells in the dentate gyrus of all the groups was counted. RESULTS: The number of BrdU-positive cells in the dentate Gyrus of the nondiabetic control, nondiabetic 0.1 Gy and nondiabetic 10 Gy subgroups of the first group were 45.96+/-3.42, 59.34+/-5.20 and 19.26+/-2.98/mm2, respectively. The number of BrdU-positive cells in the dentate gyrus of the diabetic control, diabetic 0.01 Gy, diabetic 0.1 Gy, diabetic 1 Gy and diabetic 10 Gy subgroups of the second group were 55.44+/-8.57, 33.33+/-6.46, 67.75+/-10.54, 66.63+/-10.05, 23.59+/-6.37 and 14.34+/-7.22/mm2, respectively. CONCLUSION: Low dose radiation enhances cell proliferation in the dentate gyrus of STZ-induced diabetic rats.
Animals ; Bromodeoxyuridine ; Cell Proliferation* ; Dentate Gyrus ; Hippocampus ; Immunohistochemistry ; Neurons* ; Rats*

PURPOSE: To investigate the effect of low dose radiation on neuronal cell proliferation in diabetic rats. MATERIALS AND METHODS: A group of rats (first group) were divided into three subgroups (nondiabetic control, nondiabetic 0.1 Gy and nondiabetic 10 Gy groups) to determine the effect of radiation on normal hippocampal neuronal cell proliferation. A further group of rats (second group) were divided into six subgroups (nondiabetic control, diabetic control, diabetic 0.01 Gy, diabetic 0.1 Gy, diabetic 1 Gy and diabetic 10 Gy groups) to determine the effect of radiation on hippocampal neuronal cell proliferation under diabetic conditions. Using immunohistochemistry for 5-bromo-2'-deoxyuridine (BrdU), the number of neuronal cells in the dentate gyrus of all the groups was counted. RESULTS: The number of BrdU-positive cells in the dentate Gyrus of the nondiabetic control, nondiabetic 0.1 Gy and nondiabetic 10 Gy subgroups of the first group were 45.96+/-3.42, 59.34+/-5.20 and 19.26+/-2.98/mm2, respectively. The number of BrdU-positive cells in the dentate gyrus of the diabetic control, diabetic 0.01 Gy, diabetic 0.1 Gy, diabetic 1 Gy and diabetic 10 Gy subgroups of the second group were 55.44+/-8.57, 33.33+/-6.46, 67.75+/-10.54, 66.63+/-10.05, 23.59+/-6.37 and 14.34+/-7.22/mm2, respectively. CONCLUSION: Low dose radiation enhances cell proliferation in the dentate gyrus of STZ-induced diabetic rats.
Animals ; Bromodeoxyuridine ; Cell Proliferation* ; Dentate Gyrus ; Hippocampus ; Immunohistochemistry ; Neurons* ; Rats*

Soft tissue related complications are quite frequent in limb lengthening. Muscle fibers may proliferate or regenerate after stretching injury over 10-20% of their original length. However, the cells which are engaged in this phenomenon are not confirmed yet. We chased the S-phase cells (phase for DNA replication) in the posterior leg muscle during limb lengthening by immunohistochemical technique. We lengthened the tibiae of fifteen New Zealand white rabbits. We divided them into three groups and each group is consisted of five rabbits. In group 1, we lengthened the left tibiae by 10% of their original length, in Group 2, 20%, and in group, 3, 25%, respectively, At the end of lengthening posterior muscles of lengthened left side and of controlled right side were fixed and processed for Immunohistochemical staining which could detect the incorporation of bromodeoxyuridine(BDU). Labelling index(LI:% of positively stained S-phase nuclei) of group 1 was zero. LI of groups for more than 20% lengthening (sum of group 2 and 3) was statistically significant. In conclusion, nuclei around or within the muscle tissue are in S-phase during limb lengthening which means proliferation of the muscle fivers or of the certain cells that abut muscle fibers.
Bromodeoxyuridine ; DNA ; Extremities ; Immunohistochemistry ; Leg ; Muscles ; Rabbits ; Tibia

Bone formation by osteoblast may be closely related to the increase in intracellular Ca2+ activity of osteoblast. In order to study the effects of changes in Ca2+ activity of osteoblast-like cell on fracture healing, we changed intracellular Ca2+ activity of osteoblast-like cells by vanadate and verapamil. And the process of fracture healing was observed after injection of the treatment osteoblast-like cells into the fracture site by hematoxylin-eosin (H-E) stain and bromodeoxyuridine (BrdU) stain. The results were as follow: 1) The most effective range of concentration which could facilitate bone formation was 10-6 to 10-5 M. 2) H-E stain showed more abundant osteoblast and osteoid tissues, more active mitotic division of osteoblast, and earlier appearance of chondroblast and chondroid tissue, making the maturation of woven bone faster in the vanadate-treated group than in the control group. The opposite was true in the verapamil-treated group compared with the control group. 3) BrdU labeling index showed more active osteoblastic proliferation in the vanadate-treated than in the control group. The opposite was observed in the verapamil-treated group compared with the control group. From these results, the fracture healing appears to be facilitated and decelerated by vanadate which apparently increase intracellular Ca2+ activity of osteoblast and verapamil which decreases it, repectively. Therefore the change of intracellular Ca2+ activity of osteoblast can be considered to be one of fracture healing mechanisms and expected to be applied for clinical purpose.
Bromodeoxyuridine ; Chondrocytes ; Fracture Healing ; Osteoblasts ; Osteogenesis ; Vanadates ; Verapamil

BACKGROUND: Various aspects of immunological homeostasis are affected by anesthesia and surgery, including the function of immunocompetent cells and the modulation of stress responses. To evaluate immunologic changes that occurred following propofol and enflurane anesthesia, we evaluated the proliferative responsiveness of peripheral blood mononuclear cells (PBMC) in patients undergoing laparoscopic gynecologic surgery. METHODS: PBMC were isolated from patients prior to anesthesia and on the first postoperative day (n = 10). The proliferative response was then evaluated based on the level of 5-bromo-2-deoxyunridine (BrdU) incorporation that occurred during DNA synthesisafter the induction of mitogenic stimulation by treatment with 1 microgram/ml lipopolysaccharides (LPS). To accomplish this, cell proliferation was assayed by enzyme-linked immuno-sorbent assay (ELISA), after which a stimulation index was calculated. RESULTS: Although the calculated stimulation index decreased in response to both propofol and enflurane anesthesia, the stimulation index did not differ significantly between groups. However, following stimulation with LPS, the stimulation index was significantly higher in the enflurane group than in the propofol group (P < 0.05). CONCLUSIONS: Propofol and enflurane anesthesia inhibit the PBMC proliferation. However, the decrease in proliferation that occurred in response to enflurane was attenuated by LPS.
Anesthesia ; Bromodeoxyuridine ; Cell Proliferation ; DNA ; Enflurane ; Homeostasis ; Humans ; Lipopolysaccharides ; Propofol