Objective To assess the effect of the gamma knife radiosurgery (GKS) for acoustic neuromas, and to analyze the MRI features of the tumors after GKS. Methods GKS was performed in 309 patients with acoustic neuromas from December 1994 to December 2002 at our center. The Leksell Gamma Knife models B and C were used. 249 cases with 256 tumors were followed up with MRI, which included 107 males and 142 females. The median age of the patients was 48.7?14.2 years (10-77 years). GKS was applied as primary treatment for 189 cases (75.9%), and was an adjunctive management approach for 60 cases (24.1%). The median clinical follow-up period and radiological follow-up period was (26.4?21.3) months (6-101 months) and (22.4?19.0) months (6-93 months), respectively. Results Of the 256 tumors, 79 tumors (30.8%) regressed, 165 tumors (64.5%) remained stable, 12 tumors (4.7%) enlarged, and the overall tumor control rate was 95.3%. Among 30 tumors of NF-Ⅱ , 8 tumors (26.6%) regressed, 19 tumors (63.4) remained stable, and 3 tumors (10.0%) enlarged, and tumor control rate was 90%. The rate of hearing deterioration was 22.7%, the rate of permanent facial paralysis was 0%, the rate of transient facial paralysis was 5.9%, and the incidence of transient trigeminal neuropathies was 19.9%. On the image of follow-up MRI, 79 tumors (30.0%) showed loss of contrast enhancement (LOE). LOE was the imaging property of neuromas on follow-up MRI, which symbolized a chronic decrease in the vascularity of neuromas. The histological findings of LOE demonstrated radiation-induced tumor necrosis. The transient swelling of tumors could not be confounded with the growth of tumors. Conclusion GKS is confirmed to be an effective treatment for acoustic neuromas and plays an important role in the control of NF―Ⅱ, and GKS can prevent cranial nerve from injury to a great extent.

Objective To investigate the effect of As2 O3 in combination with cinobufacini on proliferation and apoptosis of the K562 cells and provide theoretical basis for clinical application.Methods Cell proliferation was assayed by analyzing the growth and viability of the cells.Apoptosis was assayed by performing cell morphology,Annexin-V/PI staining,DNA-PI staining,and DNA gel electrophoresis.Results After exposure to As2O3 and cinobufacini,the growth of K562 cells was inhibited and the viability of K562 cells was decreased. After treated with 1.0μmol/L As2O3,0.125μg/ml cinobufacini,0.25μg/ml cinobufacini,1.0μmol/L As2O3 + 0.125 μg/ml cinobufacini,1.0μmol/L As2O3 + 0.25μg/ml cinobufacini for 24 and 48 hours,the proliferation inhibition rate were(24 ± 1.3)%,(21 ± 1.5)%,(38 ± 3.1)%,(57 ±2.7)%,(66 ±3.3)% and(49 ±2.9)%,(48 ±2.7)%,(61 ±2.1)%,(77 ±3.8)%,(82 ±4.2)%,the apoptosis rate of K562 cells were(4.8 ± 0.5)%,(5.6 ± 0.7)%,(9.8 ± 0.6)%,(11.9 ± 1.2)%,(15.2±1.5)% and(11.0 ±0.9)%,(12.9 ±1.1)%,(18.4 ±1.5)%,(21.0 ±2.0)%,(28.0 ±1.9)%.The percentage of apoptotic cells was a time- and dose-dependent manner.Typical DNA ladder was shown by DNA gel electrophoresis.Conclusions As2O3 combined with cinobufacini inhibited the proliferation of K562 cells and induced apoptosis of the K562 cells,the combination of the two drugs had better effect.

Objective To investigate the histopathological and ultrastructural changes of corneal epithelium induced by erlotinib in mice.Methods Totally 30 6-8 weeks old male BALB/c mice were divided into three groups:Control group (n =12),experimental group (n =12),another 6 mice did nothing as the blank control.Experimental group used erlotinib eye drops and control group used PBS in both eyes,four times per day.At 1 day,7 days and 14 days after the intervention,corneal fluorescence staining (FL) was observed by slit lamp and graded.On the fourteenth day after the intervention,the eye balls of mice were taken,and the histopathological and ultrastructural changes of corneal epithelium and epithelial cells were observed by optical microscope and electron microscope,respectively.And protein of cornea was measured by Western Blot.Results Before the intervention,there was no significant difference in FL scores between the experimental group and control group (P ＞ 0.05).At 1 day,7 days and 14 days,FL score of experimental group was significantly higher than the groups of non-intervention,the difference was statistically significant (all P ＜ 0.05).While FL score of control group was not statistically significant before and after intervention (all P ＞ 0.05);Compared between two groups,there were statistical differences at 7 days,14 days in FL score (all P ＜ 0.05).In the experimental group,the histopathological changes of murine corneal epithelial cells had disorderly arrangement,increased layers of cells,and the inflammatory cells.Under electron microscope,the morphology of corneal epithelial surface cells was irregular and partially detached.The number of microvilli,desmosomes and hemidesmosomes were significantly decreased when compared to the control group.The expression of p-EGFR in experimental group was significantly less than that in control group,the difference was statistically significant (P ＜ 0.05).Conclusion Erlotinib can damage the tissue structure of corneal epithelium and ultrastructure of corneal epithelial cells in mice.And the mechanism is probably that erlotinib influence the corneal epithelium by inhibiting the EGFR activation.

Homocysteine (Hcy) is a sulfur-containing amino acid that is generated during methionine metabolism. It has a physiologic role in DNA metabolism via methylation, a process governed by the presentation of folate, and vitamins B6 and B12. Physiologic Hcy levels are determined primarily by dietary intake and vitamin status. Elevated plasma levels of Hcy (eHcy) can be caused by deficiency of either vitamin B12 or folate, or a combination thereof. Certain genetic factors also cause eHcy, such as C667T substitution of the gene encoding methylenetetrahydrofolate reductase. eHcy has been observed in several medical conditions, such as cardiovascular disorders, atherosclerosis, myocardial infarction, stroke, minimal cognitive impairment, dementia, Parkinson's disease, multiple sclerosis, epilepsy, and eclampsia. There is evidence from laboratory and clinical studies that Hcy, and especially eHcy, exerts direct toxic effects on both the vascular and nervous systems. This article provides a review of the current literature on the possible roles of eHcy relevant to various neurologic disorders.
Atherosclerosis ; Dementia ; DNA ; Eclampsia ; Epilepsy ; Female ; Folic Acid ; Homocysteine ; Hyperhomocysteinemia* ; Metabolism ; Methionine ; Methylation ; Methylenetetrahydrofolate Reductase (NADPH2) ; Multiple Sclerosis ; Myocardial Infarction ; Nervous System ; Nervous System Diseases* ; Parkinson Disease ; Plasma ; Pregnancy ; Stroke ; Vitamin B 12 ; Vitamins

At the request of all of the authors, the corresponding author of this paper was changed to Dr. Jin Jun Luo.

Mastitis is one of the most widespread infectious diseases that adversely affects the profitability of the dairy industry worldwide. Accurate diagnosis and identification of pathogens early to cull infected animals and minimize the spread of infection in herds is critical for improving treatment effects and dairy farm welfare. The major pathogens causing mastitis and pathogenesis are assessed first. The most recent and advanced strategies for detecting mastitis, including genomics and proteomics approaches, are then evaluated .Finally, the advantages and disadvantages of each technique, potential research directions, and future perspectives are reported. This review provides a theoretical basis to help veterinarians select the most sensitive, specific, and cost-effective approach for detecting bovine mastitis early.

Articular cartilage is a connective tissue consisting of a specialized extracellular matrix (ECM) that dominates the bulk of its wet and dry weight. Type II collagen and aggrecan are the main ECM proteins in cartilage. However, little attention has been paid to less abundant molecular components, especially minor collagens, including type IV, VI, IX, X, XI, XII, XIII, and XIV, etc. Although accounting for only a small fraction of the mature matrix, these minor collagens not only play essential structural roles in the mechanical properties, organization, and shape of articular cartilage, but also fulfil specific biological functions. Genetic studies of these minor collagens have revealed that they are associated with multiple connective tissue diseases, especially degenerative joint disease. The progressive destruction of cartilage involves the degradation of matrix constituents including these minor collagens. The generation and release of fragmented molecules could generate novel biochemical markers with the capacity to monitor disease progression, facilitate drug development and add to the existing toolbox for in vitro studies, preclinical research and clinical trials.
Aggrecans ; chemistry ; genetics ; metabolism ; Animals ; Biomarkers ; metabolism ; Cartilage, Articular ; chemistry ; metabolism ; pathology ; Collagen ; chemistry ; classification ; genetics ; metabolism ; Extracellular Matrix Proteins ; chemistry ; genetics ; metabolism ; Gene Expression ; Humans ; Osteoarthritis ; diagnosis ; genetics ; metabolism ; pathology ; Protein Isoforms ; chemistry ; classification ; genetics ; metabolism