Molecular analysis of a hospital cafeteria-associated salmonellosis outbreak using modified repetitive element PCR fingerprinting

A hospital cafeteria-associated outbreak of gastroenteritis due to Salmonella enterica serotype Infantis was retrospectively evaluated using modified repetitive element PCR (rep-PCR) fingerprinting with the ERIC2 and BOXA1R primers and computer-assisted gel analysis and dendrogram construction. Rep-PCR yielded objective between-cycler, same-strain similarity values of from 92% (composite fingerprints) to 96% (ERIC2 fingerprints). The 70 Salmonella isolates (which included 19 serotype Infantis isolates from the hospital outbreak, 10 other serotype Infantis isolates, and 41 isolates representing 14 other serotypes) were resolved well to the serotype level with each of the three fingerprint types (ERIC2, BOXA1R, and composite). Rep-PCR typing uncovered several historical serotyping errors and provided presumptive serotype assignments for other isolates with incomplete or undetermined serotypes. Analysis of replicate fingerprints for each isolate, as generated on two different thermal cyclers, indicated that most of the seeming subserotype discrimination noted in single-cycler dendrograms actually represented assay variability, since it was not reproducible in combined-cycler dendrograms. Rep-PCR typing, which would have been able to identify the presence of the hospital-associated serotype Infantis outbreak after the second outbreak isolate, could be used as a simple surrogate for serotyping by clinical microbiology laboratories that are equipped for diagnostic PCR.     

乳腺管状小叶癌

乳腺管状小叶癌（Tubulolobular carcinoma，TLC）最初是被作为小叶癌的管状变型。作者总结了27例TLC的组织学、免疫表型和临床特征，并与纯小管癌和经典型小叶癌进行了比较。此组患者年龄43-79岁（中位年龄60岁）。1例双侧乳腺受累，5例病变为多灶性。肿瘤直径0．5-2．5cm，色灰褐，质硬。组织学观察：TLC的肿瘤细胞形成管状和条索状两种结构模式并相互混杂，且两者比例相当（统称为管状小叶模式）。     

Germline mutations of the CDKN2 gene in UK melanoma families

Germline mutations in CDKN2 on chromosome 9p21, which codes for the cyclin D kinase inhibitor p16, and more rarely, mutations in the gene coding for CDK4, the protein to which p16 binds, underlie susceptibility in some melanoma families. We have sequenced all exons of CDKN2 and analysed the CDK4 gene for mutations in 27 UK families showing evidence of predisposition to melanoma. Five different germline mutations in CDKN2 were found in six families. Three of the mutations (Met53Ile, Arg24Pro and 23ins24) have been reported previously. We have identified two novel CDKN2 mutations (88delG and Ala118Thr) which are likely to be associated with the development of melanoma, because of their co-segregation with the disease and their likely functional effect on the CDKN2 protein. In binding assays the protein expressed from the previously described mutation, Met53Ile, did not bind to CDK4/CDK6, confirming its role as a causal mutation in the development of melanoma. Ala118Thr appeared to be functional in this assay. Arg24Pro appeared to bind to CDK6, but not to CDK4. No mutations were detected in exon 2 of CDK4, suggesting that causal mutations in this gene are uncommon. The penetrance of these mutant CDKN2 genes is not yet established, nor is the risk of non-melanoma cancer to gene carriers.      

Immunohistochemistry of hepatocellular carcinoma associated with cirrhosis

Tumor cell marker antibodies were used to analyze ten cases of hepatocellular carcinoma associated with cirrhosis. Clinically, eight of these cases gave a history of chronic alcoholism and the other two of hepatitis B virus infection. Formalin-fixed, paraffin-embedded sections from these cases were screened with antibodies against alpha fetoprotein (AFP), hepatitis B surface antigen (HBsAg) and carcinoembryonic antigen (CEA) using the peroxidase antiperoxidase and avidin-biotin immunoperoxidase procedures. Three cases were positive for AFP, four for HBsAg, and three for CEA; two cases had both HBsAg and CEA. Alpha fetoprotein was present only in the cytoplasm of tumor cells in three cases. Hepatitis B surface antigen, on the other hand, was present in the cytoplasm of hepatocytes in cirrhotic areas and, in one out of the four cases, was also present in hepatocellular carcinoma cells. Carcinoembryonic antigen was seen in three cases; it was present on the surface and in the cytoplasm of proliferating ducts within the cirrhotic areas and between cell surfaces of individual tumor cells in two cases. The presence of different markers was not related to the microscopic appearance of the tumors. In one case, positivity for AFP was of diagnostic help in a tissue sample obtained by needle biopsy. The avidin-biotin immunoperoxidase procedure was more sensitive than the peroxidase antiperoxidase (PAP technique in the pathological assessment of autopsy specimens. Our findings are in agreement with those of other reports and indicate that AFP and HBsAg are the most commonly found markers in hepatoma associated with cirrhosis, and that CEA staining is variable and hepatoma associated with cirrhosis, and that CEA staining is variable and probably non-contributory.