PCGEM1 is a novel, highly prostate tissue-specific, androgen-regulated gene. Here, we demonstrate that PCGEM1 expression is significantly higher in prostate cancer (CaP) cells of African-American men than in Caucasian-American men (P ¼ 0.0002). Further, increased PCGEM1 expression associates with normal prostate epithelial cells of CaP patients with a family history of CaP (P ¼ 0.0400). PCGEM1 overexpression in LNCaP and in NIH3T3 cells promotes cell proliferation and a dramatic increase in colony formation, suggesting a biological role of PCGEM1 in cell growth regulation. Taken together, the cell proliferation/colony formationpromoting functions of PCGEM1 and the association of its increased expression with high-risk CaP patients suggest the potential roles of PCGEM1 in CaP onset/ progression, especially in these high-risk groups.

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PSGR is a novel member of the G-protein-coupled olfactory receptor family. Our initial report showed predominant expression of the PSGR in human prostate gland and significant alterations of PSGR expression in primary prostate cancer (CaP) specimens. The aim of this study was to provide in-depth evaluations of the expression profile of PSGR in prostatic epithelial cells of CaP patients and to evaluate the association of PSGR expression characteristics with clinico-pathologic features. In total, 220 RNA specimens, from laser capture microdissected paired benign and malignant prostatic epithelial cells of 110 CaP patients, were analyzed for PSGR expression by quantitative real-time PCR. The differential expression of PSGR between the prostatic epithelial cells of malignant and benign glands was statistically significant (Po0.0001). Comparison of PSGR expression between paired benign and tumor cells revealed prostate tumor cell-specific overexpression in 67.2% of tumor specimens (74 of 110), decreased expression in 20.9% of tumor specimens (23 of 110) and no difference of PSGR expression between tumor and normal cells in 11.8% of specimens (13 of 110). In representative cases, PSGR expression patterns were independently confirmed by in situ RNA hybridization. The PSGR overexpression associated with higher percentage of pathologic stage, pT3, and a higher level of preoperative serum PSA. CaP cells of African-American CaP patients exhibited about two-fold increase of PSGR expression in comparison to the Caucasian American CaP patients. Strikingly high-percentage CaP cells overexpress PSGR warrants further studies of PSGR expression alterations to define subsets of CaPs.

Aims: To explore associations between work status and multidimensional health indices in a sample of urban Lebanese children. Methods: A cross-sectional survey was used to compare 78 male children (aged 10-17 years) working full time in small industrial shops, and a comparison group of 60 non-working male schoolchildren. All children lived and worked or studied in the poor neighbourhoods of three main Lebanese cities. Results: Working children reported frequent abuses. They smoked and dated more than the comparison group. They also reported a higher number of injuries (last 12 months) and recent skin, eye, and ear complaints (last two weeks). Physical examination revealed more changes in their skin and nails, but no differences in height or weight compared to non-working group. A higher blood lead concentration was detected among working children, but no differences in haemoglobin and ferritin. No differences were noted between the two groups of children regarding anxiety, hopelessness, and self-esteem. The drawings of the working children, however, revealed a higher tendency to place themselves outside home and a wider deficit in developmental age when compared to non-working children. Conclusion: Significant differences were found between working and non-working children with respect to physical and social health parameters, but differences were less with regard to mental health. Future research should focus on (1) more sensitive and early predictors of health effects, and (2) long term health effects. The generality of findings to other work settings in the developing world should also be tested.

Background: Deletion of chromosome 16q is frequently associated with diverse tumors. Numerous studies strongly suggest the presence of one or more tumor suppressor genes on chromosome 16q22 to 16qter including the widely studied cadherin gene family. However, the specific tumor suppressor genes residing in this region need better definition and characterization. Material and Methods: Standard molecular biology approaches have been used to clone and characterize the DERPC cDNA and its protein product on chromosome 16q22.1. Northern blotting was used to define the expression pattern in a multiple human tissue blots. DERPC expression was examined in multi-tumor array (Clontech, CA, USA) dot blot as well as in laser capture microdissection (LCM) derived prostate cancer (CaP) specimens by quantitative RT-PCR. Western blot analysis and a fluorescent microscopy were used to characterize the molecular size and the cellular location of green