Objective: To discuss the expression of heme oxygenase-1 (HO-1) protein around ischemic focus after focal cerebral ischemia-reperfusion in rats and the effect after naloxone intervention. Methods: Forty-five Sprague-Dawley rats were randomly allocated into three groups (n = 15, each): sham operation group, ischemia-reperfusion group, and naloxone group. A focal cerebral ischemia-reperfusion model was built by the suture method for middle cerebral artery occlusion (MCAO) in rats. After the successful reperfusion by inserting and withdrawing sutures, naloxone (3 mg/kg) was injected intraperitoneally into the rats of naloxone group, and isotonic saline was injected intraperitoneally into the rats of sham operation group and ischemia-reperfusion group. The expression of HO-1 was assayed by immunohistochemistry. In situ terminal deoxynucleotidyl transferase (TUNEL) assay was used to observe the numbers of brain apoptosis. Results: The numbers of HO-1 positive cell in the ischemia-reperfusion group were significantly higher than those in the sham operation group with an average of 51.6 ± 10.8 vs 9.8 ± 2.8/high-power field (HP) (P < 0.05). The numbers of HO-1 positive cell around the ischemic foci in the naloxone group were higher than those in the ischemia-reperfusion group averaged 63.5 ± 10.0 vs 51.6 ± 10.8/HP (P < 0.05). The numbers of TUNEL positive cell in the naloxone group were significantly lower than those in the ischemia-reperfusion group (20.5 ± 3.5 vs 29.8 ± 4.0/ HP,), but were higher than those in the sham operation group (4.2 ± 2.0/ HP), and there were significant differences between the groups (P < 0.05). Conclusion: Naloxone may reduce neuronal apoptosis caused by focal cerebral ischemia-reperfusion injury after MCAO, and its mechanism may be associated with the increase of naloxone-induced HO-1 expression.

Janus kinase 2,myeloproliferative leukemia virus and tet encogene family member2 mutations affect a variety of cytokines signal transduction pathway in BCR/ABL-negative myeloproliferative neoplasms (MPN). In the influence of mutation load,co-mutation and genetic susceptibility,these mutations can induce different MPN phenotypes,and affect the characteristics of patients,the distribution of peripheral blood cells and prognosis. But how these mutations contribute to disease initiation,development,and transformation needs further reseach.

The in vivo tumorigenicity of murine B16 melanoma cells engineered to secret TNF-a was observed. The retrovirus containing mouse TNF-a cDNA was generated by the virus-packing cell PA317 transfected with plasmid pXT-TNF. The B16 cell clone secreting the highest TNF-a level was obtained after G418 resistance selection, limiting dilution and the assay of TNF-a activity. After the mice were inoculated subcutaneously with the cell clone, we found the tumor growth was inhibited and the survival period of the mice extended when compared with the mice inoculated with the wild-type B16 cells . We also found that the tuinorigenicity of B16-TNF-a+ cell was associated with the cell number inoculated. At or above the 1.25? 104 cells, the percentage of the mice with detectable tumor correlated negatively with the cell number inoculated: however, at the 6.25 ? 103 cells, the percentage was higher than that at 2.5?10~(4) cells. These results encourage us to do further experiments on the following tumor cell-targeted TNF-a gene therapy.

Abdominal Neoplasms ; metabolism ; pathology ; surgery ; Actins ; metabolism ; Angiomyolipoma ; metabolism ; pathology ; Desmin ; metabolism ; Diagnosis, Differential ; Humans ; Leiomyosarcoma ; metabolism ; pathology ; surgery ; Liposarcoma ; metabolism ; pathology ; surgery ; Male ; Middle Aged ; Neoplasms, Multiple Primary ; metabolism ; pathology ; surgery ; Retroperitoneal Neoplasms ; metabolism ; pathology ; surgery ; S100 Proteins ; metabolism

Chromosome Banding ; Colorectal Neoplasms ; genetics ; Comparative Genomic Hybridization ; methods ; standards ; DNA Probes ; DNA, Neoplasm ; genetics ; Humans ; Karyotyping ; Quality Control ; Reproducibility of Results

Adult ; Cholesteatoma, Middle Ear ; Humans ; Male

AC133 Antigen ; Animals ; Antigens, CD ; metabolism ; Cell Differentiation ; Cell Proliferation ; Drug Resistance, Neoplasm ; Glioma ; pathology ; Glycoproteins ; metabolism ; Humans ; Neoplastic Stem Cells ; metabolism ; pathology ; physiology ; Neovascularization, Pathologic ; etiology ; pathology ; Peptides ; metabolism ; Radiation Tolerance

Aged ; Aged, 80 and over ; Cross Infection ; etiology ; Diabetes Mellitus, Type 2 ; complications ; microbiology ; Humans ; Male ; Middle Aged ; Pneumoconiosis ; complications ; microbiology ; Retrospective Studies

This study was aimed to clone the full-length cDNA sequence of actin gene of Eleutherococcus sentico-sus. And bioinformatics analysis was used. The total RNA was isolated from leaves of E. senticosus , and cDNA was synthesized by reverse transcription of total RNA. Primers were designed according to the conserved se-quence that had been cloned of Actin of E. senticosus . Then, the 3'and 5' cDNA fragments were cloned by nested PCR . The full-length gene was obtained by gene splicing method . Sequencing results were compared and treated with similarity analysis by blast analysis in the GenBank. Protein secondary structure and tertiary struc-ture of Actin of E. senticosus was predicted by online software. The results showed that the full-length cDNA of Actin of E. senticosus is 1507 bp, which named EsActin1, GenBank accession No. KC469585. The conserved sequence, which contained a 1134 bp open reading frame that encoding a 377 amino acid residues, a 5'-UTR of 140 bp and a 3'-UTR of 233 bp. Homologous alignment showed that it shared over 75% nucleotide se-quence similarity and over 94% amino acid sequences similarity with Actins in other plants. It was concluded that this study first isolated and reported the full-length cDNA sequence of actin gene of E. senticosus , and laid a foundation for the molecular biology research of E. senticosus .

The existent problems of medical insurance specialty core course system currently are tallied up on the foundation of definition of core course system. The strategy and measure for adjustment are put forward,providing a basis for this professional course reform.