Purpose To compare the macular retinal thickness and macular volume between subjects with high myopia and non-myopia. Methods This prospective nonrandomized, comparative study recruited healthy subjects with high myopia subjects, defined as a spherical equivalence (SE) over À6 dioptres (D) or AXLX26.5 mm and the best corrected visual acuity better than 20/25, and subjects with non-myopia, defined as an with SE between 1.5D and À1.5 D and the BCVA better than 20/25. Optical coherence tomography was performed in each eye. Results Eighty high myopic eyes and 40 non-myopic eyes were included. The mean age of the high myopic group and non-myopia group was 29.6 and 27.5 years old, respectively. The mean refraction was -9.27 D in the high myopia group and -0.22 D in the non-myopia group. The high myopia group had significantly greater mean retinal thickness in the foveola and fovea 1 mm area than the non-myopia group (166 vs 149 lm, Po0.0001, 199 vs 188 lm, P ¼ 0.0063, respectively). However, the mean retinal thickness in the inner and outer macular area (superior, nasal, inferior, or temporal) of the high myopia group was significantly less than in the non-myopia group. In addition, the high myopia group had significantly smaller macular volume than the non-myopia group (Po0.0001). Conclusion This study demonstrated that the retinal thickness in individuals with high myopia is thicker in the foveola and fovea, but thinner in the inner and the outer macular region. The retina of individuals with high myopia had smaller macular volume than those with non-myopia.

AA is related to various psychiatric disorders. Onset age of AA is an important factor in the association with different comorbid psychiatric diseases. In addition to cosmetic impact, which may bring about anxiety or depression, stress neuroendocrine immunology may play an important role in the pathogenesis of both AA and psychiatric disorders.

To identify genes that could potentially serve as molecular therapeutic markers for human head and neck cancer (HNC), we employed differential display analysis to compare the gene expression profiles between HNC and histopathologically normal epithelial tissues. Using reverse transcription-polymerase chain reaction and Western blot analysis, desmoglein 3 (DSG3) was identified as being differentially expressed at both the RNA and protein levels. Of 56 patients assayed, 34 (61%) had overexpression of DSG3, which correlated statistically with T stage (P ¼ 0.009), N stage (P ¼ 0.047), overall stage (P ¼ 0.011), tumor depth (P ¼ 0.009) and extracapsular spread in lymph nodes (P ¼ 0.044), suggesting that DSG3 participates in carcinogenesis of HNC. Consistent with the clinical findings, inhibition of DSG3 by RNA interference (RNAi) significantly reduced cell growth and colony formation to 57-21% in three HNC cell lines. Use of an in vitro wound healing and Matrigel invasion assays, we found that cell migration and invasive ability were also inhibited to 30-48% in three cell lines tested. An in vivo xenograft study showed that administration of DSG3-RNAi plasmid significantly inhibited tumor growth for 2 months in BALB/C nude mice. In conclusion, DSG3 is identified overexpressed in HNC, with the degree of overexpression associated with clinicopathologic features of the tumor. Inhibition of DSG3 significantly suppresses carcinogenic potential in cellular and in vivo animal studies. These findings suggest that DSG3 is a potential molecular target in the development of adjuvant therapy for HNC.

Colorectal cancer is the fourth most frequently diagnosed cancer and the second leading cause of cancer death in the United States. In 2009, an estimated 106,100 new cases of colon and 40,870 cases of rectal cancer will occur. During the same year, it is estimated that 49,920 people will die from colon and rectal cancer. 1 Despite these statistics, mortality from colon cancer has decreased slightly over the past 30 years, possibly due to earlier diagnosis through screening and better treatment modalities. This manuscript summarizes the NCCN Clinical Practice Guidelines in Oncology for managing colon cancer. The guidelines begin with clinical presentation to the primary care physician or gastroenterologist and address diagnosis, patho-The NCCN