AIM: To investigate the expressions of the cyclin dependent kinase inhibitor (CKI) in human corneal epithelium.METHODS: The expressions of CKI, P27, P21 and proliferating cell nuclear antigen (PCNA) were tested in different regions of corneal epithelium by SP immunohistochemistry.RESULTS: Limbal basal cells stained positively for PCNA while central corneal epithelium cells stained negatively for PCNA, their difference was statistically significant (P＜0.01).Positive staining for P27 and P21 were observed in central epithelium, but there was no positive staining in limbal epithelium. Their difference were also statistically significant (P＜0.01).CONCLUSION: The different expressions of CKI P27, P21and PCNA in different corneal epithelial regions suggest that in limbal basal layer there are a group of cells that have higher proliferative capacity staying in G1 status, namely stem cell.

This paper discussed AIDS epidemic sityation and it's tendency, AIDS harmful-ness to human beings health and social economic development. The dangerous factors of AIDS epidemic in china is pointed out. prsvent and treatment AIDS is urgency.

Adolescent ; Dentigerous Cyst ; pathology ; Humans ; Jaw Cysts ; pathology ; Male

Humans ; Male ; Neurofibromatosis 1 ; Pharyngeal Neoplasms ; Salivary Gland Neoplasms ; Salivary Glands ; Young Adult

BACKGROUND: We can investigate mechanism of endogenous neuroprotection in rat cerebral hypoxic tolerance trial. OBJECTIVE: To observe the characteristics of cerebral hypoxic tolerance in rat models with cerebral hypoxic preconditioning. DESIGN: Randomized controlled observation. SETTING: Department of Neurology, China-Japanese Friendship Hospital, Jilin University. MATERIALS: The experiment was performed in the Basic Animal Experimental Center, China-Japan Friendship Hospital, Jilin University from April 2003 to April 2004. Inbred line healthy Wistar rats, of either sex, with the body mass of 200-300 g, were randomly assigned into normal control group (n=6), sham operation group (n=6), ischemic control group (n=20), hypoxic preconditioning (3 hours, 8% O2 and 92% N2) plus ischemic group (n=60) (according to different hypoxic phases, there were 5 time phases: 30 minutes, 1, 3, 5 and 6 hours with 12 rats in each time phase), hypoxic preconditioning group (n=18) [according to different hypoxic phases, there were 3 time phases: 1, 3 and 5 hours with 6 rats in each time phase, 3 rats received TTC staining and 3 rats received hematoxylin and eosin (HE) staining]. METHODS: ①Hypoxic preconditioning: Firstly, natrica calx was put into closed glass container to absorb CO2 and O2, secondly, mixed gas of 8% O2 and 92% N2 was input, and then animals were put into the container, 3 rats each time. Temperature and humidity were kept steadily. ②Permanent ischemic middle cerebral artery rat models were established. ③The models were determined with a series in procedures: neurological score, infarcted volume evaluation, pathological sample preparation, immunohistochemical staining, imaging analysis and so on. ④The data were compared in groups with variance analysis.MAIN OUTCOME MEASURES: Changes in cerebral infarcted volume, neurological score and pathological morphology in rats of experimental group and control group. RESULTS: Neurological score in the hypoxic preconditioning (8% O2, at hours 1, 3 and 5) plus ischemic group was lower than in the ischemic control group(P＜0.01). Neurological score at minute 30 and hour 6 after hypoxia (8% O2) had insignificant difference in the ischemic control group. Mean cerebral infarcted volume ratio in the hypoxic preconditioning (8% O2, at hours 1, 3 and 5) plus ischemic group was lower than in the ischemic control group(P＜0.01). Mean cerebral infarcted volume ratio after hypoxia (8% O2, at minute 30 and hour 6) had insignificant difference with ischemic control group (P＞0.05). CONCLUSION: Hypoxic preconditioning in rats can effectively release nerve injury induced by focal cerebral ischemia, suggesting that it has protective effect on brain. The procedure of establishing cerebral ischemic tolerance models with hypoxic preconditioning, which is simple and stable, with little injury on experimental animals, is a useful tool for studying cerebral ischemic tolerance.

Objective To investigate the mechanism of growth hormone inhibiting IPS-induced apoptosis of alveolar type Ⅱ epithelial cells in rats. Method Isolated and purified AEC Ⅱ cells of SD rats were divided into 5 groups,8 duplicate wells in each group. Group I served as control group; group Ⅱ:LPS 10 ug/ml;group Ⅲ:LPS 10 ug/ml + GH 50 ng/ml;gronp IV :LPS 10 ug/ml + GH 100ng/ml; group V: LPS 10 ug/ml + GH 200 ng/ml. LPS was finally added into wells in group Ⅱ～V . After the cells were incubated for 24 hours, the apoptosis rate and necrosis rate of AEC Ⅱ cells stained with Annexin V/PI were detected by flow cytometry and Fas protein of AEC Ⅱ cells were measured by immunocytochemistry. Results (1) The apoptosis rate and necrosis rate of AECⅡ cells in group Ⅱ,Ⅲ, Ⅳ and V were significantly hitOer than those in group Ⅰ( qapoptosis rate Ⅰ, Ⅱ =12.26,qnecroeis Ⅰ,Ⅱ=18.34, qapoptosisⅠ.Ⅱ=9.63,qnecrosisⅠ,nⅡ=5.75,qapotosisⅠ,Ⅳ= 9.15,qnecrosisⅠ,Ⅳ= 5.39, qapotosisⅠ,Ⅴ = 10.87, qnecrosisⅠ,Ⅴ = 5.91, P 0.05), but lower in group Ⅲ,IV and V than those in group Ⅱ(qapoptosis Ⅱ,Ⅲ= 15.24, qpecrosisⅡ,Ⅲ=16.38, qapoptosisⅡ.Ⅳ = 15.95,qnecrosisⅡ.Ⅳ=16.95, qapoptosis rate Ⅱ,Ⅴ=14.57, qnecrosisⅡ.Ⅴ = 15.61,P<0.05). (2)The positive rate of Fas expression on AEC Ⅱ cells in group Ⅱ,Ⅲ, Ⅳ and V was obviously higher than that in group Ⅰ. ( q Ⅰ.Ⅱ=35.67, qⅠ ,Ⅲ=14.32, qⅠ,Ⅳ = 13.87, qⅠ.Ⅴ=26.16, P<0.05), but lower in gronpⅢ ,Ⅳ and Ⅴ than that in gronp Ⅱ(qⅡ,Ⅲ=12.54, qⅡ,Ⅳ = 13.02, qⅡ,Ⅴ =6.96, P<0.05). Conclusions GH can probably de-crease the apoptosis of AEC Ⅱ cells by inhibiting Fas expression.

1.0 ?mol/L),the toxicity and side effects of MTX increased significantly.The most common drug side effects were gastrointestinal symptoms and leucopenia.The oral mucosal lesions became worse in 12 g/m2 group.Conclusion The monitoring of HD-MTX plasma concentration provides an objective clinical basis for the individualized chemotherapy.

Humans ; Myocardium ; Stem Cell Transplantation ; Stem Cells ; Tissue Engineering

Adult ; Aged ; Aged, 80 and over ; Female ; Guanine Nucleotide Exchange Factors ; genetics ; metabolism ; Humans ; Keratin-18 ; genetics ; metabolism ; Lymph Nodes ; metabolism ; pathology ; Lymphatic Metastasis ; Male ; Middle Aged ; RNA, Messenger ; metabolism ; Stomach Neoplasms ; metabolism ; pathology ; T-Lymphoma Invasion and Metastasis-inducing Protein 1

Animals ; Antigens, CD ; metabolism ; Cell Movement ; Cell Proliferation ; Endoglin ; Genetic Therapy ; Humans ; Mesenchymal Stem Cell Transplantation ; Mesenchymal Stromal Cells ; cytology ; metabolism ; Neoplasms ; pathology ; therapy ; Receptors, Cell Surface ; metabolism ; Thy-1 Antigens ; metabolism ; Vascular Cell Adhesion Molecule-1 ; metabolism