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B7-H1 participates in T-cell costimulation functioning as a negative regulator of immunity. Recent observations suggest that B7-H1 is expressed by renal cell carcinoma (RCC) tumor cells and is associated with poor prognosis. However, outcome analyses have been restricted to patients with fresh-frozen tissue and limited follow-up. We report the clinical effect of B7-H1 in RCC patients with a median of 10 years of follow-up. Between 1990 and 1994, 306 patients underwent nephrectomy for clear cell RCC and had paraffin tissue available for review. We did immunohistochemistry with anti-B7-H1 and conducted outcome analyses. Among the 306 patients, 73 (23.9%) harbored tumors with B7-H1 expression. Patients with tumor B7-H1 were at a significantly increased risk of both death from RCC [risk ratio (RR), 3.92; P < 0.001] and overall mortality (RR, 2.37; P < 0.001). The 5-year cancer-specific survival rates were 41.9% and 82.9% for patients with and without tumor B7-H1, respectively. In a multivariate model, tumor B7-H1 remained associated with cancer-specific death even after adjusting for tumor-node-metastasis stage, grade, and performance status (RR, 2.00; P = 0.003). In the subset of 268 patients with localized RCC, tumor B7-H1 was significantly associated with metastatic cancer progression (RR, 3.46; P < 0.001) and death from RCC (RR, 4.13; P < 0.001) even after adjusting for stage, grade, and performance status (RR, 1.78, P = 0.036). RCC patients with tumor B7-H1 are at significant risk of rapid cancer progression and accelerated rates of mortality. B7-H1 may function as a key determinant in RCC, abrogating immune responses directed against this immunogenic tumor. (Cancer Res 2006; 66(7): 3381-5)

bioMérieux.

Expression of B7-H1, a costimulating glycoprotein in the B7 family, is normally restricted to macrophage-lineage cells, providing a potential costimulatory signal source for regulation of T cell activation. In contrast, aberrant expression of B7-H1 by tumor cells has been implicated in impairment of T cell function and survival, resulting in defective host antitumoral immunity. The relationship between tumor-associated B7-H1 and clinical cancer progression is unknown. Herein, we report B7-H1 expression by both renal cell carcinoma (RCC) tumors of the kidney and RCC tumor-infiltrating lymphocytes. In addition, our analysis of 196 clinical specimens reveals that patients harboring high intratumoral expression levels of B7-H1, contributed by tumor cells alone, lymphocytes alone, or tumor and͞or lymphocytes combined, exhibit aggressive tumors and are at markedly increased risk of death from RCC. In fact, patients with high tumor and͞or lymphocyte B7-H1 levels are 4.5 times more likely to die from their cancer than patients exhibiting low levels of B7-H1 expression (risk ratio 4.53; 95% confidence interval 1.94 -10.56; P < 0.001.) Thus, our study suggests a previously undescribed mechanism whereby RCC may impair host immunity to foster tumor progression. B7-H1 may prove useful as a prognostic variable for RCC patients both pre-and posttreatment. In addition, B7-H1 may represent a promising target to facilitate more favorable responses in patients who require immunotherapy for treatment of advanced RCC.costimulation ͉ immunotherapy ͉ T lymphocyte ͉ tumor biomarker

We have collected a new face data set that will facilitate research in the problem of frontal to profile face verification 'in the wild'. The aim of this data set is to isolate the factor of pose variation in terms of extreme poses like profile, where many features are occluded, along with other 'in the wild' variations. We call this data set the Celebrities in Frontal-Profile (CFP) data set. We find that human performance on Frontal-Profile verification in this data set is only slightly worse (94.57% accuracy) than that on FrontalFrontal verification (96.24% accuracy). However we evaluated many state-of-the-art algorithms, including Fisher Vector, Sub-SML and a Deep learning algorithm. We observe that all of them degrade more than 10% from FrontalFrontal to Frontal-Profile verification. The Deep learning implementation, which performs comparable to humans on Frontal-Frontal, performs significantly worse (84.91% accuracy) on Frontal-Profile. This suggests that there is a gap between human performance and automatic face recognition methods for large pose variation in unconstrained images.

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Objectives: Intergenerational “mismatch” and/or growth conditions may be relevant to the epidemic of diabetes in developing populations. In a rapidly developing southern Chinese population, we tested whether maternal environment, proxied by maternal literacy, or family socio‐economic position (SEP), proxied by paternal literacy, were associated with fasting glucose and diabetes. To assess if intergenerational mismatch contributed, we tested whether the associations varied by life course SEP. Methods: In 19,818 older (≥50 years) adults from the Guangzhou Biobank Cohort Study (phases 2 and 3), we used censored and logistic regression to assess the associations of maternal and paternal literacy with fasting glucose, elevated fasting glucose and diabetes and whether these associations varied by sex, age or life course SEP. Results: Maternal, but not paternal, literacy was negatively associated with fasting plasma glucose (β‐coefficient −0.06 mmol/l, 95% confidence interval (CI) −0.11 to −0.01) and elevated fasting glucose (odds ratio (OR) 0.92, 95% CI 0.86–0.99) adjusted for age, sex, study phase, life course SEP, childhood growth, adiposity, number of offspring, and birth order. Associations of maternal and paternal literacy with fasting glucose, elevated fasting glucose and diabetes did not vary by sex, age or life course SEP. Conclusion: Offspring of literate mothers had lower risk for impaired glucose tolerance than offspring of illiterate mothers. Being raised by literate mothers may increase the likelihood of children with higher SEP and lower long‐term disease risk, or better maternal conditions over generations may be associated with lower fasting glucose. Am. J. Hum. Biol., 2011. © 2011 Wiley‐Liss, Inc.