Breast cancer is one of the leading causes of death attributable to cancer in women. In view of the limitations of conventional predictable factors of the breast cancer, additional second-generation parameters would be valuable in selecting the patients who would be most likely to be beneficial from adjuvant therapy and breast reconstruction. The author investigated the HER2/neu gene amplification and the number of chromosome 17 in 39 cases of paraffin embedded breast cancer tissues, 20 cases without lymph node metastasis and 19 cases with lymph node metastasis, using fluorescent in situ hybridization(FISH) and compared the results with HER2/neu and p 53 protein expression detected by immunohistochemical method. Eleven cases fibroadenoma were used as benign tumor control. Numerical aberrations of chromosome 17 were found in 17 out 39 breast cancer cases (44%)(monosomy in 10 cases, 26%; trisomy in 3 cases, 8%; tetrasomy in 3 cases, 8%; polysomy in 1 case ,3%), and the frequency of each type aberration was not significantly different between the negative and positive groups in lymph node metastasis. Monosomy of chromosome 17 was found in 2 out of 11(12%) fibroadenoma cases. HER2/neu gene amplification was found in 8 out of 39 cases (19%) and other 2 cases revealed HER2/neu gene amplification in lymph node metastatic tumor only, not in original tumor. Fourteen out of 19 cases of breast cancer with lymph metastasis showed HER2/neu protein expression both in original and metastatic tumors. All of the six cases showing HER2/neu gene amplification in original and/or metastatic tumor revealed HER2/neu protein expression. The frequency of HER2/neu gene amplification in the 39 breast cancer cases was not different between metastatic and non-metastatic groups(p= 0.284). However, HER2/neu protein expression was increased significantly in the metastatic group(p=0.028). None of the 11 fibroadenoma cases revealed HER2/neu gene amplification or HER2/ neu protein expression. Nine out of 19 cases of breast cancer with lymph node metastasis showed p 53 protein accumulation in original tumor(47%), but 3 of them revealed p 53 protein accumulation only in original tumor. The frequency of p 53 protein accumulation was not significantly different between metastatic and non-metastatic groups. None of the 11 fibroadenoma cases revealed p 53 protein accumulation. In conclusion, there are no differences between the lymph node metastatic group and non-metastatic groups in numerical aberrations of the chromosome 17 , amplification of the HER2/neu gene expression and accumulation of the p 53 protein in breast cancer. However, the HER2/neu protein expression was increased significantly in lymph node metastatic group, so it could be one of the predictors of the metastasis in breast cancer.
Breast Neoplasms* ; Breast* ; Cause of Death ; Chromosomes, Human, Pair 17* ; Female ; Fibroadenoma ; Gene Amplification* ; Gene Expression ; Humans ; Lymph Nodes ; Mammaplasty ; Monosomy ; Neoplasm Metastasis ; Paraffin ; Tetrasomy ; Trisomy

No abstract available.
Animals ; Burns* ; Rats*

No abstract available.
Animals ; Lymphocyte Subsets* ; Lymphocytes* ; Rats*

No abstract available.
Animals ; Burns* ; Lymphocyte Subsets* ; Lymphocytes* ; Mice* ; Spleen* ; Thymus Gland*

No abstract available.
Burns*

No abstract available.
Silicones* ; Transplants*

No abstract available.
Frontal Sinus*

OBJECTIVE: To evaluate the effects of gabapentin and clonidine on neuropathic pain in an experimental pain model. METHOD: 24 male adult rats were anesthetized and the sciatic nerve was exposed. Each exposed nerve was electrically injured with 10 volts for 10 seconds by two needle electrodes. Rats were divided into three groups by treating with gabapentin, clonidine and sham. Gabapentin and clonidine were given orally from post operation day 3 to 7 in gabapentin and clonidine groups respectively. To evaluate the presence of mechanical allodynia, withdrawal frequency was tested by Von Frey hair in the same days. After post operation day 7, all the medications were discontinued and mechanical allodynia was evaluated at post operation day 14. RESULT: Neuropathic pain was developed after electrical injury in all the rats. Withdrawal frequency is more decreased in gabapentin and clonidine groups than sham group in post operation day 4 to 7. The withdrawal frequency was 2.88+/-0.83, 2.75+/-0.89, 3.13+/-0.99, 3.25+/- 1.28 in gabapentin group and 3.38+/-0.92, 4.50+/-2.20, 3.25+/-1.17, 3.50+/-0.93 in clonidine group in post operation day 4, 5, 6, 7, respectively. In post operation day 14, withdrawal frequency was increased and showed no difference compared to the sham group. CONCLUSION: Gabapentin and clonidine can suppress the neuropathic pain in an experimental pain model. There was no different effect on the neuropathic pain suppression between gabapentin and clonidine.
Adult ; Animals ; Clonidine* ; Electrodes ; Hair ; Humans ; Hyperalgesia ; Male ; Needles ; Neuralgia* ; Rats ; Sciatic Nerve

OBJECTIVE: The purpose of this study is to develop a new neuropathic pain model in the rat. METHOD: Each male adult rat was anesthetized and the sciatic nerve was exposed. Each exposed nerve was injected with 0.03 cc of 1% phenol solution. Normal saline 0.03 cc was injected to the placebo group. Rats were tested for the presence of mechanical allodynia by von Frey hair. Spontaneous pain behavior (paw shaking, paw elevation) was examined for 5 minutes in the cage. RESULTS: Phenol injected group developed allodynia after the second post-injection day for up to 1 month. Allodynia was also observed in the contralateral legs of phenol injected group. The control group did not develop allodynia. Spontaneous pain behavior was not observed in either group. CONCLUSION: Neuropathic pain model was developed by 1% phenol solution injection to the rat sciatic nerve. This study suggests an easier method for making the neuropathic pain model.
Adult ; Animals ; Hair ; Humans ; Hyperalgesia ; Leg ; Male ; Neuralgia* ; Phenol* ; Rats* ; Sciatic Nerve*

OBJECTIVE: The purpose of this study was to develop a new neuropathic pain model in rat. METHOD: Twenty Sprague-Dawley adult male rats, 10 for control and 10 for experimental, were anesthetized and their sciatic nerves were exposed. In an experimental group, exposed nerve was injured with 10 volts electrical current for 10 seconds. The mechanical and thermal allodynia and pain behavior were evaluated in pre-electrical injury and post-injury 1, 2, 3 days, 1, 2, 3, 4, 6 and 8 weeks. The mechanical allodynia was evaluated by the frequency of response to 5 stimulations of von Frey hairs (4.31 and 4.56) and the thermal allodynia was tested by withdrawal latency to stimulation with radiant heat. Spontaneous pain behavior (paw shaking, paw elevation) was observed for 5 minutes in the cage. RESULTS: The experimental group exhibited significantly higher withdrawal frequency to mechanical stimulation: from post-injury 3 days to 6 weeks for von Frey hair 4.31 and from 2 days to 4 weeks for von Frey hair 4.56 (p<0.05). There was no difference between two groups in withdrawal latency to radiant heat stimulation. The experimental group showed spontaneous pain behavior but control group did not. In electron microscopic finding, prominent myelin destruction and axonal sprouting were observed in experimental group. CONCLUSION: These results suggest that a new neuropathic pain model can be made by 10 volts electrical injury for 10 seconds to rat sciatic nerve.
Adult ; Animals ; Axons ; Hair ; Hot Temperature ; Humans ; Hyperalgesia ; Male ; Myelin Sheath ; Neuralgia* ; Rats* ; Rats, Sprague-Dawley ; Sciatic Nerve*