Biomedical subjects

Thomas J Fahey

Publications and source records attributed to Thomas J Fahey.

23 records · Page 2Linked to original sources

PubMed2002

Effects of limited work hours on surgical training.

BACKGROUND: Legal mandates to reduce resident work hours have prompted changes in the structure of surgical training programs. Such changes have included modification of on-call schedules and the adoption of "night float" resident coverage. Little is known about the effects of these changes on surgical resident education and perceptions of quality of patient care. STUDY DESIGN: The surgical housestaff and faculty at a single institution completed a 21-point Likert survey. Subjects were asked to compare parameters of resident education, patient care, and resident quality of life before and after institution of a strict 80-hour work week resident training schedule. The number of hours worked per week before and after these changes were reported. American Board of Surgery In-Training Examination (ABSITE) scores were compared for the 2 years before and after implementation of this schedule. Total number of surgical cases performed by graduating chief residents were recorded and compared for the 3 years before and after the schedule changes. RESULTS: Resident work hours reduced significantly after schedule changes were implemented. A majority of surgical residents reported an improvement in quality of life, but residents and faculty perceived changes to have a negative impact on continuity of patient care. Mean ABSITE composite percentile scores significantly improved after the reduction of working hours. ABSITE scores for junior residents improved significantly; no significant differences were noted in scores for senior residents. CONCLUSIONS: Reduction in resident work hours has salutary effects on perception of quality of life and basic education for surgical residents. These benefits may come at the expense of patient care, particularly continuity of care. This study did not directly assess patient outcomes but the perceptions of caregivers suggest that patient care may be compromised. Further research is needed to assess the longterm effects of changes on both residents and patients.

Attitude of Health Personnel↗

PubMed2002

The use of endoscopic ultrasound in the diagnosis of solid pseudopapillary tumors of the pancreas in children.

Since the first description by Frantz in 1959 of a papillary cystic tumor of the pancreas, solid pseudopapillary tumors have been increasing in incidence. However, management of these lesions remains controversial. Patients under the age of 20 years more often undergo local excision than do their older counterparts, resulting in increased recurrence rates. The cause of this discrepancy is not clear but may be related to an inability to make a definitive preoperative diagnosis. The authors report a case of a solid pseudopapillary tumor of the pancreas in a 13-year-old girl in which the diagnosis was established preoperatively by endoscopic ultrasound scan with fine-needle aspiration (EUS-FNA). EUS-FNA represents a diagnostic technique commonly used in adults that may be useful in identifying the rare pediatric patient with pancreatic malignancy.

Adolescent↗

PubMed2002

Expression of cyclooxygenase-2 in the periprosthetic capsule surrounding a silicone shell implant in the rat.

Prosthetic breast implants are used frequently for both aesthetic and reconstructive purposes. Histologically, the normal tissue response to silicone implants typically involves an inflammatory infiltrate that consists initially of macrophages, and later consists of fibroblasts, myofibroblasts, and lymphocytes. To characterize further the nature of the inflammatory response to silicone breast implants, the authors evaluated the expression of the enzyme cyclooxygenase-2 (COX-2) by the tissues and cells of the breast capsule after silicone augmentation in an animal model. COX-2 is an inducible enzyme that is expressed primarily in response to inflammatory stimuli and mediates the production of prostaglandins that support the inflammatory process. Fifty-nine animals at five time points were evaluated. Specifically, on days 4, 7, 14, 28, and 80 the authors identified cytoplasmic COX-2 expression in each of the three cell types of interest, including endothelial cells, macrophages, and fibroblasts. Selective COX-2 inhibiting agents may be an appropriate pharmacological intervention for modulating the formation of periprosthetic capsules.

Animals↗

PubMed2002

Cyclooxygenase-2 expression in thyroid nodules.

Factors contributing to the development of thyroid neoplasia remain poorly understood. Recent evidence indicates that overexpression of the inducible cyclooxygenase, COX-2, is important in the pathogenesis of epithelial carcinomas. These studies were undertaken to evaluate whether COX-2 is up-regulated in human thyroid neoplasia. Benign (n = 14), and malignant (n = 14) thyroid nodules were analyzed for expression of COX-2 mRNA by quantitative RT-PCR. Immunoblotting and immunohistochemistry were performed on representative samples. Three human thyroid cancer cell lines were similarly analyzed for COX-2 expression. Levels of COX-2 mRNA were significantly increased in thyroid nodule samples compared with adjacent thyroid tissue in the malignant specimens but not in the benign specimens. Additionally, COX-2 mRNA levels were significantly increased in malignant nodule samples compared with benign nodule samples. COX-2 protein expression was higher in 8 of 10 thyroid nodules compared with the adjacent tissue. Immunohistochemical analysis localized expression of COX-2 to the malignant epithelial cells. Immunofluorescence demonstrated COX-2 protein expression in all three thyroid cell lines. Finally, COX-2 expression could be detected by RT-PCR in fine needle aspiration specimens of thyroid nodules. These data indicate that COX-2 is up-regulated in human thyroid cancer, but not in benign thyroid nodules, and suggest that COX-2 expression may serve as a marker of malignancy in thyroid nodules.

Biomarkers, Tumor↗

PubMed2002

Can inhibition of telomerase increase pancreatic cancer cell's susceptibility to chemotherapeutic reagents?

OBJECTIVES: To clarify the inhibition of pancreatic cancer cells by interference with the hTR component of the telomerase reverse transcriptase enzymatic complex and evaluate susceptibility of antisense hTR pancreatic cancer cells to chemotherapeutic reagents. METHODS: A 593 bp of full length hTR cDNA was subcloned into a mammalian expression vector pcDNA3.1(-) in antisense orientation to construct an antisense hTR expression plasmid. The plasmids were introduced into Pancl cells, a human pancreatic carcinoma cell line, by lipofectin, and G418-resistant stable transformants were expanded. Resulting stable clones were screened for the presence of hTR insert by PCR with T7 and BGH reverse primers located on the flanks of the multiclonal site of pcDNA3.1 vector. Cell growth rate, hTR expression, telomerase activity, and anchorage-independent growth property were analyzed. Finally, susceptibility of antisense hTR cells to chemotherapeutic reagents was evaluated. RESULTS: Significant downregulation of endogenous hTR was evident in the antisense-hTR transformed cells, and telomerase activity was markedly decreased compared to control cells in standard TRAP assays. Furthermore, the proliferation and the anchorage-independent growth ability in antisense-hTR expressing cells were significantly decreased compared with the control parental cells. However, no crisis or senescence phenomena was observed. Antisense hTR appears to increase Pancl cell's susceptibility to chemotherapeutic reagent cDDP, but not to differentiation reagent DMSO, COX2 inhibitor sulinbac, NS-398, curcumin, and chemotherapeutic reagent adriamycin (ADM). CONCLUSIONS: These data indicate that hTR is probably a critical component of human telomerase activity and that downregulation of the RNA component of human telomerase is an effective target for anticancer strategy and antisense hTR can increase Pancl cell's susceptibility to cDDP.

Adenocarcinoma↗