A novel method for apoptosis protein subcellular localization prediction combining encoding based on grouped weight and support vector machine.

Apoptosis proteins have a central role in the development and homeostasis of an organism. These proteins are very important for understanding the mechanism of programmed cell death. Based on the idea of coarse-grained description and grouping in physics, a new feature extraction method with grouped weight for protein sequence is presented, and applied to apoptosis protein subcellular localization prediction associated with support vector machine. For the same training dataset and the same predictive algorithm, the overall prediction accuracy of our method in Jackknife test is 13.2% and 15.3% higher than the accuracy based on the amino acid composition and instability index. Especially for the else class apoptosis proteins, the increment of prediction accuracy is 41.7 and 33.3 percentile, respectively. The experiment results show that the new feature extraction method is efficient to extract the structure information implicated in protein sequence and the method has reached a satisfied performance despite its simplicity. The overall prediction accuracy of EBGW_SVM model on dataset ZD98 reach 92.9% in Jackknife test, which is 8.2-20.4 percentile higher than other existing models. For a new dataset ZW225, the overall prediction accuracy of EBGW_SVM achieves 83.1%. Those implied that EBGW_SVM model is a simple but efficient prediction model for apoptosis protein subcellular location prediction.

The progression of CD56+ myeloid sarcoma: A case report and literature review.

The current study presents a case of cluster of differentiation (CD)56+ myeloid sarcoma in a patient that initially presented with skin lesions, and provides evidence for the clinical and differential diagnosis of myeloid sarcoma. The patient of the present case report was a 65-year-old man who was admitted to hospital with a six-month history of bilateral purple-red papules and nodules, which were present on the upper limbs of the patient and had spread over his whole body one month prior to admission to the hospital. Pathological examination demonstrated a diffuse infusion of primitive round cells at the papillary dermis and subcutaneous tissues. The infiltrated cells were 40-60 µm in diameter and morphologically identical. Immunohistochemical examination revealed that the cells expressed myeloperoxidase, CD56, CD43 and T-cell intracytoplasmic antigen. In addition, several cells expressed CD34, and 90% of the cells expressed Ki67. While the majority of cells in myeloid sarcoma do not express CD56, the present case was a myeloid sarcoma that expressed CD56, which is extremely rare. The sarcoma in the present patient progressed rapidly, and the patient died eight months following the onset of disease. Clinicians should be aware of CD56+ myeloid sarcoma, which is easily misdiagnosed and inappropriately treated. Consequently, myeloid sarcoma may have a high malignancy and poor outcome for patients.

Avidin chase reduces side effects of radioimmunotherapy in nude mice bearing human colon carcinoma.

AIM: To evaluate the influence of avidin chase on the side effects of radioimmunotherapy (RIT) in nude mice bearing human colon carcinoma and therapeutic outcome. METHODS: Purified anti-CEA monoclonal antibody (McAb) was biotinylated with NHS-biotin, and then radiolabeled with 188Re by the direct method. 188Re-labeled biotinylated anti-CEA McAb (188Re-CEA McAb-Bt) was intravenously injected followed by intravenous injection of avidin after 24 h. SPECT imaging and biodistribution study were performed at 28-48 h after the injection of 188Re-CEA McAb-Bt. Three groups of nude mice subcutaneously grafted with human colon carcinoma were treated 7 d after the graft. Mice in the avidin chase group received intravenous injection of 188Re-CEA McAb-Bt (11.1 MBq/20 microg) followed by intravenous injection of cold avidin (80 microg) after 24 h. Mice in the control group (treated group without avidin chase) only received the injection of 188Re-CEA McAb-Bt (11.1 MBq/20 microg), another control group (non-treated group) only received 0.1 mL normal saline solution. Toxicity was evaluated on the basis of change of body weight and peripheral WBC counts, and therapy effects were determined by variation in tumor volume. Histological analysis of tumors was also performed. RESULTS: Avidin chase markedly accelerated the clearance of 188Re-CEA McAb-Bt from the blood and normal tissues. The tumor uptakes of 188Re-CEA McAb-Bt at 28 h were 5.90 and 6.42% ID/g, respectively, in chase group and in non-chase group, while the tumor-to-background (T/NT) ratios were 3.19 and 0.56, respectively. The tumor uptake was slightly decreased by avidin chase, but the T/NT ratios were increased. In treated groups the growth rate of body weight and the number of WBC decreased after injection of 188Re-CEA McAb-Bt, and the WBC counts recovered earlier in the group with avidin chase than in the group without avidin chase. Compared to the non-treated group, treated groups with and without avidin chase showed significant anti-tumor effects. CONCLUSION: Avidin chase can effectively reduce the side effects of RIT, and improve therapeutic efficacy.

[Effects of all-trans retinioic acid and tazarotene on MMP-1 and TIMP-1 expression in cultured human fibroblasts after heat shock].

OBJECTIVE: To investigate the molecular mechanism of dermal damage in heat shock-induced skin aging by observing the expressions of metalloproteinase-1 (MMP-1) and tissue inhibitor of MMP-1 (TIMP-1) in retinoic acid-treated cultured human fibroblasts with heat shock. METHODS: Cultured human fibroblasts were treated with tazarotene or all-trans-retinioic acid (at-RA) after heat shock for 30 min in 43 degrees celsius; water bath. Twenty-four hours later, MMP-1 and TIMP-1 contents in the supernatant of the cell culture medium were measured using enzyme-linked immunosorbent assay (ELISA). RESULTS: Both tazarotene and at-RA dose-dependently reduced the expression of MMP-1 and increased the expression of TIMP-1 in cultured human fibroblasts exposed to heat shock, and tazarotene produced stronger effect than at-RA. CONCLUSION: Retinoic acid can reduce the expression of MMP-1 and increase the expression of TIMP-1 in cultured human fibroblasts, suggesting its therapeutic potential for heat shock-induced skin aging.

[188Re-labeled herceptin inhibits proliferation of breast cancer cell line SKBR-3 in vitro].

OBJECTIVE: To investigate the inhibitory effects of (188)Re-labeled herceptin on the proliferation in vitro of breast carcinoma cell line (SKBR-3) overexpressing HER-2/neu proto-oncogene. METHODS: Herceptin was radiolabeled with (188)Re through a direct labeling method. SKBR-3 cells were cultured with (188)Re-Herceptin at different radioactivity doses (3.7x10(4), 18.5x10(4), 37x10(4), 55.5x10(4) and 74x10(4) Bq/ml) or with (188)Re-nmIgG and (188)ReO(4)(-) for comparison. The cell proliferation inhibition was determined with MTT colorimetric assay. RESULTS: (188)Re-Herceptin could markedly inhibit the growth of SKBR-3 cells in a radioactivity dose-dependent fashion, while the effect of (188)Re-nmIgG and (188)ReO(4)(-) showed rather poor inhibitory effect in vitro. The 50% inhibition doses (IC(50)) of (188)Re-Herceptin, (188)Re-nmIgG and (188)ReO(4)(-) were 76.1x10(4) Bq/L, 139.2x10(4) Bq/L and 175x10(4) Bq/L, respectively. CONCLUSION: (188)Re-Herceptin can effectively inhibit the growth of in vitro cultured breast cancer cells overexpressing HER-2/neu, and shows much potential for clinical use in beast cancer radioimmunotherapy.