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Biomedical subjects

J Petros

Publications and source records attributed to J Petros.

8 recordsLinked to original sources
PubMed2006

Integrating simulation into a surgical residency program: is voluntary participation effective?

OBJECTIVE: Surgical training programs nationwide are struggling with the integration of simulation training into their curriculum given the constraints of the 80-h work week. We examine the effectiveness of voluntary training in a simulation lab as part of the surgical curriculum. METHODS: The ProMIS simulator was introduced into the general surgery residency at Boston University Medical Center. All categorical residents (28) and non-categorical residents (23) were offered a 2-h training session and curriculum review. After the introductory session, time spent in the lab was encouraged, but voluntary. Use of the simulator was tracked for all residents. Participation in the simulation curriculum was defined as three or more uses of the simulator. After 3 months, all residents completed a survey regarding the simulation lab and their simulator usage. RESULTS: Twenty-six (93%) categorical residents and three (6%) non-categorical residents completed the introductory simulator training session. Over a 3 month period, use of the simulator at least once was 31% among all eligible residents; 80% of postgraduate year (PGY)1, 40% of PGY2, 60% of PGY3, and 0% of PGY4 and PGY5. Four residents (14%) participated in the simulation curriculum. Overall, 70% of simulator usage was during working hours, and 30% was completed post-call or when the resident was off duty. Most residents agreed that the simulator was easy to use and that its use improved their operative skills, but they did not think it was a good substitute for actual operative experience. Reported reasons for not using the simulator included off-site rotation (44%), no time (30%), and no interest (11%). CONCLUSIONS: Voluntary use of a surgical simulation lab leads to minimal participation in a training curriculum. Participation should be mandatory if it is to be an effective part of a residency curriculum.

Boston↗
PubMed2006

Ubiquitin E3 ligase WWP1 as an oncogenic factor in human prostate cancer.

The gene for E3 ubiquitin ligase WWP1 is located at 8q21, a region frequently amplified in human cancers, including prostate cancer. Recent studies have shown that WWP1 negatively regulates the TGFbeta tumor suppressor pathway by inactivating its molecular components, including Smad2, Smad4 and TbetaR1. These findings suggest an oncogenic role of WWP1 in carcinogenesis, but direct supporting evidence has been lacking. In this study, we examined WWP1 for gene dosage, mRNA expression, mutation and functions in a number of human prostate cancer samples. We found that the WWP1 gene had copy number gain in 15 of 34 (44%) xenografts and cell lines from prostate cancer and 15 of 49 (31%) clinical prostate cancer samples. Consistently, WWP1 was overexpressed in 60% of xenografts and cell lines from prostate cancer. Mutation of WWP1 occurred infrequently in prostate cancer. Functionally, WWP1 overexpression promoted colony formation in the 22Rv1 prostate cancer cell line. In PC-3 prostate cancer cells, WWP1 knockdown significantly suppressed cell proliferation and enhanced TGFbeta-mediated growth inhibition. These findings suggest that WWP1 is an oncogene that undergoes genomic amplification at 8q21 in human prostate cancer, and WWP1 overexpression is a common mechanism involved in the inactivation of TGFbeta function in human cancer.

Animals↗
PubMed1998

Opium alkaloid noscapine is an antitumor agent that arrests metaphase and induces apoptosis in dividing cells.

An alkaloid from opium, noscapine, is used as an antitussive drug and has low toxicity in humans and mice. We show that noscapine binds stoichiometrically to tubulin, alters its conformation, affects microtubule assembly, and arrests mammalian cells in mitosis. Furthermore, noscapine causes apoptosis in many cell types and has potent antitumor activity against solid murine lymphoid tumors (even when the drug was administered orally) and against human breast and bladder tumors implanted in nude mice. Because noscapine is water-soluble and absorbed after oral administration, its chemotherapeutic potential in human cancer merits thorough evaluation.

Animals↗
PubMed1997

Loss of heterozygosity on the long arm of human chromosome 7 in sporadic renal cell carcinomas.

Cytogenetic and molecular analysis of DNA sequences with highly polymorphic microsatellite markers have implicated allele loss in several chromosomal regions including 3p, 6p, 6q, 8p, 9p, 9q, 11p and 14q in the pathogenesis of sporadic renal cell carcinomas (RCCs). Deletions involving the long arm of chromosome 7 have not been described in RCCs although they have been seen in several other tumor types. However, there have been no detailed analysis of loss of heterozygosity (LOH) of 7q sequences in sporadic RCCs. We therefore studied LOH for DNA sequences on 7q with 10 highly polymorphic markers in 92 matched normal/tumor samples representing sporadic RCCs including papillary, nonpapillary, and oncocytomas in order to determine whether allelic loss could be detected in a tumor type with no visible 7q rearrangements at the cytogenetic level. We found chromosome 7q allele loss in 59 of 92 cases (64%) involving one, two, or more microsatellite markers. The most common allele loss included loci D7S522 (24%) and D7S649 (30%) at 7q31.1-31.2, a region that contains one of the common fragile sites, FRA7G. By comparative multiplex PCR analysis, we detected a homozygous deletion of one marker in the 7q 31.1-31.2 region in one tumor, RC21. These results support the idea that a tumor suppressor gene in 7q31 is involved in the pathogenesis of sporadic renal cell carcinomas.

Adenoma, Oxyphilic↗
PubMed1997

Frequent breakpoints in the region surrounding FRA3B in sporadic renal cell carcinomas.

The constitutive fragile site at chromosomal band 3p14.2, FRA3B, is the most active common fragile site in the human genome. We have localized aphidicolin-induced breakpoints to two distinct clusters, separated by 200 Kb, in FRA3B (Paradee et al., 1996). Sequence analysis of these regions identified two polymorphic microsatellite markers immediately adjacent to each of these breakpoint clusters. In this report we have used these two new microsatellites and 14 additional 3p microsatellites to analyse chromosome 3p breakage and loss in 94 sporadic RCC samples, including nonpapillary, papillary and oncocytomas. We have found heterozygous loss of 3p14 sequences in >60% of the RCC samples, including both clear cell and papillary renal cell carcinomas. We have found frequent breakage in the region immediately surrounding FRA3B, demonstrating that FRA3B does play a role in chromosome breakage and loss in RCC. In contrast to other reports, >50% of the papillary tumors also showed LOH of 3p markers. We also observed microsatellite instability (MIN) with most of the tested markers in seven of eight oncocytomas and one of 69 clear cell carcinomas. The MIN in some oncocytomas was of the RER+ (replication error) type I phenotype. None of the five 3p14.2 markers detected any homozygous deletions in tumor samples, but 69/94 (73%) of the tumors had LOH for the region, which includes the recently identified FHIT gene.

Adult↗
PubMed1975

Disinfection.

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Antiviral Agents↗