Anti-apoptotic gene transcription signature of salivary gland neoplasms

Background  

Development of accurate therapeutic approaches to salivary gland neoplasms depends on better understanding of their molecular pathogenesis. Tumour growth is regulated by the balance between proliferation and apoptosis. Few studies have investigated apoptosis in salivary tumours relying almost exclusively on immunohistochemistry or TUNEL assay. Furthermore, there is no information regarding the mRNA expression profile of apoptotic genes in salivary tumors. Our objective was to investigate the quantitative expression of BCL-2 (anti-apoptotic), BAX and Caspase3 (pro-apoptotic genes) mRNAs in salivary gland neoplasms and examine the association of these data with tumour size, proliferative activity and p53 staining (parameters associated with a poor prognosis of salivary tumours patients).     

Effects of transforming growth factor-beta deficiency on bone development: a Fourier transform-infrared imaging analysis

Transforming growth factor-beta 1 (TGF-β1) is a cytokine member of the TGF-β superfamily involved in the control of proliferation and differentiation of various cell types. TGF-β1 plays an important role in bone formation and resorption. To determine the effect of TGF-β1 deficiency on bone mineral and matrix, tibias from mice in which TGF-β1 expression had been ablated (TGF-β1 null) were analyzed and compared with background- and age-matched wild-type (WT) control animals by Fourier transform-infrared imaging (FTIRI) and histochemistry. FTIRI allows the characterization of nondemineralized thin tissue sections at the ultrastructural level with a spatial resolution of 7 μm. The spectroscopic parameters calculated were: mineral-to-matrix ratio (previously shown to correspond to ash weight); mineral crystallinity (related to the crystallographically determined crystallite size and perfection in the apatite c-axis direction); and collagen maturity (related to the ratio of pyridinoline:deH-DHLNL collagen cross-links). Several fields were selected to represent different stages of bone development within the same specimen from the secondary ossification center to the distal diaphysis. Anatomically equivalent areas were compared as a function of age and genotype. The spectroscopic results were expressed both as color-coded images and as pixel population distributions for each of the three parameters monitored. Based on comparisons of histochemistry and FTIRI, there were distinctive age and genotype variations. At all ages examined, in the TGF-β1 null mice growth plates, alkaline phosphatase (ALP) activity and collagen maturity were reduced, but no effect on mineral content or crystallinity was noted. In the TGF-β1 null mice metaphyses, there was a persistence of trabeculae, but no significant alterations in mineral content or crystallinity. In contrast, mineral content, mineral crystallinity, and collagen maturity were reduced in the secondary ossification center and cortical bone of the TGF-β1 null mice. These results, consistent with a mechanism of impaired bone maturation in the TGF-β1 null mice, may be directly related to TGF-β1 deficiency and indirectly to increased expression of inflammatory cytokines in the TGFβ1 null mice.     

Preoperative Neutrophil-to-Lymphocyte Ratio as a Prognostic Predictor after Curative Resection for Hepatocellular Carcinoma

BACKGROUND: This study was designed to evaluate the impact of an elevated preoperative neutrophil-to-lymphocyte ratio (NLR) on outcome after curative resection for hepatocellular carcinoma (HCC). METHODS: Patients undergoing resection for HCC from January 1994 to May 2007 were identified from the hepatobiliary database. Demographics, laboratory analyses, and histopathology data were analyzed. RESULTS: A total of 96 patients were identified with a median age at diagnosis of 65 (range, 15-85) years. The 1-, 3-, and 5-year overall survival rates were 80%, 58%, and 52%, respectively. Although the presence of microvascular invasion, NLR >or=5, and R1 resection margin were adverse predictors of overall survival, there were no independent predictors identified on multivariate analysis. The 1-, 3-, and 5-year disease-free survival rates were 74%, 63%, and 57%, respectively. Preoperative tumor biopsy, NLR >or= 5, multiple liver tumors, microvascular invasion, and R1 resection margin were all predictors of poorer disease-free survival. Multivariate analysis showed that a NLR >or= 5 and R1 resection margin were independent predictors of poorer disease-free survival. The median disease-free survival of those with a NLR >or= 5 was 8 months compared with 18 months for those with a NLR < 5. CONCLUSION: Preoperative NLR >or= 5 was an adverse predictor of disease-free and overall survival.     

Public hospital-based level I trauma centers: financial survival in the new millennium

BACKGROUND: The medical benefits of trauma centers have been well documented; studies have reported substantial financial losses attributed to trauma care. This study demonstrates the dependence of Level I trauma centers on Disproportionate Share Hospital (DSH) governmental funds and tax dollars. Furthermore, specific injury groups have greater dependence on these funds. METHODS: Records of 553 trauma patients admitted to a public urban Level I trauma center during a 6-month period were reviewed. Patients were grouped according to blunt, penetrating, and thermal injuries. Data for each group included charges, costs, payments, and the source of reimbursement. Profit and loss margins were compared with and without government funds. RESULTS: With diminished DSH funds and tax dollars, a net loss over $2.1 million was incurred. The greatest disparity originates from Medicaid, self-pay, and prisoner patient groups. Inclusion of government funds provided a positive return of over $600,000. CONCLUSION: The financial stability of urban public Level I trauma centers without additional funding is tenuous because of a high proportion of uninsured and underinsured patients. Government tax dollars and DSH funds are required for their continued solvency.