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Prostate cancer is a complex, multifactorial disease with genetic and environmental factors involved in its etiology. The search for genetic determinants involved in the disease has proven to be challenging, in part because such complex diseases are often not amenable to characterization by linkage analysis and positional cloning as is the case for diseases with simple Mendelian genetic inheritance. Prostate cancer susceptibility loci that have been reported so far include HPC1 (1q24-q25), PCAP (1q42-q43), HPCX (Xq27-q28), CAPB (1p36), HPC20 (20q13), HPC2/ELAC2 (17p11) and 16q23. Prostate cancer aggressiveness loci have also been reported (5q31-q33, 7q32 and 19q12). Further complicating the process is the existence of polymorphisms in several genes associated with prostate cancer including, AR, PSA, SRD5A2, VDR and CYP isoforms. These polymorphisms, however, are not thought to be highly penetrant alleles in families at high risk for prostate cancer. It is clear that prostate cancer etiology involves several genetic loci with no major gene accounting for a large proportion of susceptibility to the disease.

Routine glaucoma screening for middle-aged African American individuals is potentially clinically effective but its impact on visual impairment and blindness may be modest. However, we did not assess the impact on visual field loss.

IntroductionNonsteroidal anti-inflammatory drugs (NSAID) have been associated with reduced risks of colon cancer, breast cancer, and other cancer sites (1, 2). We previously reported a strong inverse relationship between NSAID use and breast cancer in a North Carolina study, with a suggestion of stronger associations among African Americans (3). One hypothesized mechanism for the reduction in cancer risk by NSAIDs is the inhibition of cyclooxygenase 2 (COX2), which is overexpressed in various cancer types and is thought to stimulate angiogenesis and inhibit apoptosis (1).A polymorphism in the COX2 gene [valine to alanine at residue 511 (Val 511 Ala)] has been identified in African Americans that results in a conformation change in the enzyme near its active site, and it has been hypothesized this polymorphism could modify biochemical function or change the response to NSAIDs (4, 5). In a recent paper, carriers of this polymorphism seemed to be at reduced risk for colon adenomas [odds ratio (OR), 0.56; 95% confidence interval (95% CI), 0.25-1.27] and colon cancer (OR, 0.67; 95% CI, ref. 5). In this report, we describe the relationship between the COX2 Val 511 Ala polymorphism, NSAIDs, and breast cancer in a case-control study in North Carolina. Materials and MethodsThese analyses were based on 1,441 African American participants in the Carolina Breast Cancer Study, a population-based, case-control study conducted between 1993 to 2001 (3, 6). Cases were 20 to 74 years old and had either invasive breast cancer or carcinoma in situ. Control women were selected from Division of Motor Vehicle and Health Care Financing Administration lists and matched by race and age to cases.Genotyping was done according to previously described procedures using the Taqman system (6). The Ala 511 (C) allelespecific probe was labeled on the 5Vend with the VIC reporter dye and contained the nucleotide sequence 5V-TGCTCCAgCTTCTAC-3Vwith a melting temperature of 68.5jC and a G-C content of 53.3%. The Val 511 (T) allele-specific probe was labeled on the 5V end with the 6-FAM reporter dye and contained the nucleotide sequence 5V-TGCTCCAaCTTCTAC3Vwith a melting temperature of 67.5jC and a G-C content of 46.7%. Both probes were minor groove binding and used a nonfluorescing quencher on the 3V end. Forward and reverse primers were used to amplify the region surrounding the Val 511 Ala polymorphism. The nucleotide sequences for the forward and reverse primers were 5V-AGAAAAGCCTCGGC-CAGATG-3V and 5V-GGCAGGAGAACATATAACATTACC-CATAA-3V, respectively.Logistic regression analyses were done using the GENMOD procedure in SAS (Cary, NC). We calculated ORs and 95% CIs to evaluate the association between breast cancer and the Val 511 Ala polymorphism and the joint effects of NSAIDs and genotype. ResultsGenotyping results were available for 763 cases (673 invasive and 90 in situ) and 678 controls. The frequency of the Ala allele was 4.3% in cases and 4.0% in controls (Table 1), which is very similar to the allele frequency of 4.5% reported by Lin et al. (5)...

Bacteria isolates belonging to the genera Bacillus, Corynebacterium, Aeromonas, and Enterobacter were isolated from a municipal waste landfill in Durham, NC. Bacterial counts obtained with three general purpose media were log(10) colony-forming units (cfu)/g of 9.30, 9. 26, and 9.20 respectively for Plate Count Agar, Brain Heart Infusion Agar, and Nutrient Agar. Coliform count from MacConkey agar was log(10) 7.28/g sample. Isolates were generally sensitive to tetracycline and chloramphenicol (13 of 14 isolates) and generally resistant to ampicillin (9 of 9), erythromycin (10 of 14), streptomycin (8 of 14), with 3 of 14 isolates having multiple resistance to the last three antibiotics. A dose-independent growth response to ampicillin was observed for two isolates. The detection of a 22,000-bp plasmid in one but not in the second ampicillin-resistant isolate suggests more than one mechanism of antibiotic resistance.