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Nicolas W. Villelli, Rohit Das, Hong Yan, Wei Huff, Jian Zou and Nicholas M. Barbaro

OBJECTIVE

The Massachusetts health care insurance reform law passed in 2006 has many similarities to the federal Affordable Care Act (ACA). To address concerns that the ACA might negatively impact case volume and reimbursement for physicians, the authors analyzed trends in the number of neurosurgical procedures by type and patient insurance status in Massachusetts before and after the implementation of the state's health care insurance reform. The results can provide insight into the future of neurosurgery in the American health care system.

METHODS

The authors analyzed data from the Massachusetts State Inpatient Database on patients who underwent neurosurgical procedures in Massachusetts from 2001 through 2012. These data included patients' insurance status (insured or uninsured) and the numbers of procedures performed classified by neurosurgical procedural codes of the International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM). Each neurosurgical procedure was grouped into 1 of 4 categories based on ICD-9-CM codes: 1) tumor, 2) other cranial/vascular, 3) shunts, and 4) spine. Comparisons were performed of the numbers of procedures performed and uninsured patients, before and after the implementation of the reform law. Data from the state of New York were used as a control. All data were controlled for population differences.

RESULTS

After 2008, there were declines in the numbers of uninsured patients who underwent neurosurgical procedures in Massachusetts in all 4 categories. The number of procedures performed for tumor and spine were unchanged, whereas other cranial/vascular procedures increased. Shunt procedures decreased after implementation of the reform law but exhibited a similar trend to the control group. In New York, the number of spine surgeries increased, as did the percentage of procedures performed on uninsured patients. Other cranial/vascular procedures decreased.

CONCLUSIONS

After the Massachusetts health care insurance reform, the number of uninsured individuals undergoing neurosurgical procedures significantly decreased for all categories, but more importantly, the total number of surgeries performed did not change dramatically. To the extent that trends in Massachusetts can predict the overall US experience, we can expect that some aspects of reimbursement may be positively impacted by the ACA. Neurosurgeons, who often treat patients with urgent conditions, may be affected differently than other specialists.

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Fengming Lan, Xiao Yue, Lei Han, Xubo Yuan, Zhendong Shi, Kai Huang, Yang Yang, Jian Zou, Junxia Zhang, Tao Jiang, Peiyu Pu and Chunsheng Kang

Object

The goal in this study was to investigate the antitumor effect of aspirin in glioblastoma cells and the molecular mechanism involved in its antineoplastic activities.

Methods

The authors used the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide method, flow cytometry, the annexin V method, and Transwell cell invasion test to detect the proliferation and invasive activity of U87 and A172 glioma cells before and after being treated with aspirin. To determine the effects of aspirin on β-catenin/T-cell factor (TCF) transcription activity, reporter constructs containing 3 repeats of the wild-type (TOPflash) or mutant (FOPflash) TCF-binding sites were used. Reverse transcriptase polymerase chain reaction and Western blot analyses were used to detect the expression of multiple β-catenin/TCF target genes following aspirin treatment.

Results

The transcriptional activity of the β-catenin/TCF complex was strongly inhibited by aspirin. Increasing the concentration of aspirin resulted in decreased expression of c-myc, cyclin D1, and fra-1 mRNA and protein in U87 and A172 cells in a dose-dependent manner. Aspirin inhibited glioma cell proliferation and invasive ability, and induced apoptotic cell death.

Conclusions

The results suggest that aspirin is a potent antitumor agent, and that it exerts its antineoplastic action by inhibition of the β-catenin/TCF signaling pathway in glioma cells.