28 research outputs found
Nash points, Ky Fan inequality and equilibria of abstract economies in Max-Plus and B-convexity
AbstractB-convexity was introduced in [W. Briec, C. Horvath, B-convexity, Optimization 53 (2004) 103–127]. Separation and Hahn–Banach like theorems can be found in [G. Adilov, A.M. Rubinov, B-convex sets and functions, Numer. Funct. Anal. Optim. 27 (2006) 237–257] and [W. Briec, C.D. Horvath, A. Rubinov, Separation in B-convexity, Pacific J. Optim. 1 (2005) 13–30]. We show here that all the basic results related to fixed point theorems are available in B-convexity. Ky Fan inequality, existence of Nash equilibria and existence of equilibria for abstract economies are established in the framework of B-convexity. Monotone analysis, or analysis on Maslov semimodules [V.N. Kolokoltsov, V.P. Maslov, Idempotent Analysis and Its Applications, Math. Appl., vol. 401, Kluwer Academic, 1997; V.P. Litvinov, V.P. Maslov, G.B. Shpitz, Idempotent functional analysis: An algebraic approach, Math. Notes 69 (2001) 696–729; V.P. Maslov, S.N. Samborski (Eds.), Idempotent Analysis, Advances in Soviet Mathematics, Amer. Math. Soc., Providence, RI, 1992], is the natural framework for these results. From this point of view Max-Plus convexity and B-convexity are isomorphic Maslov semimodules structures over isomorphic semirings. Therefore all the results of this paper hold in the context of Max-Plus convexity
Should peritoneal tears be routinely closed during laparoscopic total extraperitoneal repair of inguinal hernias? A reappraisal
Evaluation of putative molecular biomarkers in abdominal and retroperitoneal leiomyosarcomas
Altered Expression of the Dna Mismatch Repair Proteins Hmlh1 and Hmsh2 in Cutaneous Dysplastic Nevi and Malignant Melanoma
Molecular alterations in the mismatch repair system suggest that this mechanism may be important in the evolution of cutaneous melanoma. Our current study evaluated the expression of two mismatch repair proteins, hMLH1 and hMSH2, in dysplastic nevi (DN) and cutaneous melanoma (CM). Immunohistochemical staining of these proteins was performed on 55 CM and 30 DN specimens. The staining results were divided into three groups: negative, partially positive and strongly positive. Normal adjacent skin cells served as an internal control for positive immunostaining. Altered immunoreactivity of one of the proteins was found in four (13.4%) DN and seven (12.7%) CM. Lack of staining for hMLH1 was observed in two (6.7%) cases of DN and five (9.1%) cases of CM; staining for hMSH2 was absent in two (6.7%) of the DN and two (3.6%) of the CM specimens. Partially positive staining was found in 33.3% and 53.3% for hMLH1 and hMSH2, respectively, in DN, and in 54.5% and 69.1%, respectively, in CMM. Our study shows that complete or partial loss of MMR protein expression occurs in a subset of both DN and CM and may represent a distinct pathway in the development of some DN and CM. </jats:p
Clinicopathologic and immunohistochemical characteristics of male breast cancer: A single center experience
Male breast cancer (MaleBC) is a rare tumor that has been insufficiently described in the Middle East. The purpose of this study is to report the first MaleBC series in Lebanon, describing its clinicopathologic and immunohistochemical phenotype, and how it compares with MaleBC in the West and with female breast cancer in Lebanon and the Middle East. Forty-seven cases of MaleBC were reviewed. Results showed younger ages at presentation (62 years versus 67 years), higher incidence of lobular carcinoma (6percent versus 1percent), and more frequent p53 positivity and axillary node metastases in our series than in those reported about MaleBC. Other results such as higher estrogen receptor (ER) positivity and lower HER-2-neu over-expression were comparable to the literature. These findings suggest that MaleBC in our region may represent a biologically different tumor with potentially distinct prognostic and therapeutic implications. © 2011 Wiley Periodicals, Inc.Anderson WF, 2010, J CLIN ONCOL, V28, P232, DOI 10.1200-JCO.2009.23.8162; Clarke M, 1998, LANCET, V351, P1451; Bodey B, 1997, ANTICANCER RES, V17, P2577; Donegan WL, 1998, CANCER, V83, P498, DOI 10.1002-(SICI)1097-0142(19980801)83:3498::AID-CNCR193.0.CO;2-R; El Saghir NS, 2006, BMC CANCER, V6, DOI 10.1186-1471-2407-6-194; El-Habbash MM, 2009, SAUDI MED J, V30, P1060; ENGIN K, 1993, J SURG ONCOL, V53, P128, DOI 10.1002-jso.2930530216; Giordano SH, 2004, CANCER, V101, P51, DOI 10.1002-cncr.20312; Koc M, 2001, EUR J CANCER PREV, V10, P531, DOI 10.1097-00008469-200112000-00008; Lakkis NA, 2010, CANCER EPIDEMIOL, V34, P221, DOI 10.1016-j.canep.2010.02.013; Nahleh ZA, 2007, CANCER, V109, P1471, DOI 10.1002-cncr.22589; O'Malley FP, 2010, MODERN PATHOL, V23, pS14, DOI 10.1038-modpathol.2010.35; Ottini L, 2010, CRIT REV ONCOL HEMAT, V73, P141, DOI 10.1016-j.critrevonc.2009.04.003; Pich A, 1996, HUM PATHOL, V27, P676, DOI 10.1016-S0046-8177(96)90397-4; Pich A, 1999, BRIT J CANCER, V79, P959, DOI 10.1038-sj.bjc.6690153; PRECHTEL K, 2003, WHO CLASSIFICATION T, P110; El Saghir Nagi S, 2002, J Med Liban, V50, P3; Rudlowski C, 2004, BREAST CANCER RES TR, V84, P215, DOI 10.1023-B:BREA.0000019953.92921.7e; SALVADORI B, 1994, EUR J CANCER, V30A, P930, DOI 10.1016-0959-8049(94)90117-1; SESHADRI R, 1993, J CLIN ONCOL, V11, P1936; Shamseddine A, 2004, ANN EPIDEMIOL, V14, P663, DOI 10.1016-j.annepidem.2003.12.002; Shpitz B, 2000, J SURG ONCOL, V75, P252, DOI 10.1002-1096-9098(200012)75:4252::AID-JSO53.0.CO;2-2; SLAMON DJ, 1987, SCIENCE, V235, P177, DOI 10.1126-science.3798106; Sorlie T, 2001, P NATL ACAD SCI USA, V98, P10869, DOI 10.1073-pnas.191367098; Willsher PC, 1997, ANTICANCER RES, V17, P233545
