Citations

Abstract The Nijmegen breakage syndrome 1 (NBS1) gene, which participates in DNA double strand break repair, has been postulated to be a susceptibility factor for a number of cancers, including prostate cancer. Numerous mutations have been identified in NBS1, including the founder mutation 657del5. In this study, a number of analyses were done to determine whether mutations in NBS1 are associated with an increased risk for prostate cancer. The frequency of the 657del5 mutation in both familial prostate cancer cases (1,819 affected men among 909 families) and sporadic prostate cancer cases (1,218 affected men) collected from five centers participating in the International Consortium for Prostate Cancer Genetics were compared with that found in 697 normal controls. Seven individuals were identified to carry the mutation among the 3,037 cases screened: four in the familial group (three from one family and one from another) and three in the sporadic cases. The carrier frequency was 0.22% (2 of 909) for the probands and 0.25% (3 of 1,218) for the sporadic cases of prostate cancer. The 657del5 mutation was not detected in either the 293 unaffected members of the prostate cancer families or in the 697 control samples tested. The entire NBS1 gene was also sequenced in 20 of the youngest affected individuals from the Finnish group of familial cases to identify the presence of possible mutations in this high-risk group. One rare (D95N) and one common (E185Q) missense alteration was identified. More detailed analyses of the E185Q polymorphism, along with a third rare variant (R215W), failed to show an association with prostate cancer. Because the 657del5 mutation was absent from the control population, we are unable to determine if this alteration predisposes to prostate cancer. However, our data does suggest that mutations within NBS1, and in particular, 657del5, do not significantly contribute to the overall prostate cancer burden within our patient samples. (Cancer Epidemiol Biomarkers Prev 2006;15(5):935–8)

Abstract Background: Dietary glycemic index (GI) and glycemic load (GL) affect circulating insulin concentrations. Elevated circulating insulin concentrations can increase insulin-like growth factor-1, and both of these hormones may have growth-promoting effects within the colorectum. Methods: We examined associations of GI and GL with colorectal cancer (CRC) among participants in the Iowa Women's Health Study (n = 35,197; ages 55-69 years at baseline in 1986). Over 15 years of follow-up, we identified 757 cases of colon cancer and 209 cases of rectal cancer (954 CRC cases). Results: Overall, neither GI nor GL were significantly associated with incident CRC. However, among obese women (baseline body mass index ≥30 kg/m2) CRC incidence was increased in the highest versus lowest quintiles of GI (relative risk, 1.66; 95% confidence intervals, 1.13-2.43; P for trend = 0.02) and GL (relative risk, 1.79; 95% confidence intervals, 1.19-2.70; P for trend < 0.01). This pattern of increased risk for obese women with high GI or GL tended to hold for both colon cancer and rectal cancer, and for nondiabetic women as well. No statistically significant associations were observed between GI or GL and CRC among subjects whose baseline body mass index was <30 kg/m2. Conclusion: Our findings suggest that high GI or GL are not major CRC risk factors among older women in general, but may increase CRC risk among women who are obese. (Cancer Epidemiol Biomarkers Prev 2006;15(5):392–6)

Objectives: To review nasal alar support mechanisms, introduce the concept of tractional forces on the nasal ala, and describe a reconstructive technique to correct nasal tip deformities associated with weakened tractional force on the nasal ala. Design: Photographic study and retrospective medical chart review. Results: We noted that patients with weakened support at the dome of the lower lateral cartilage had lateral alar deformities. Strengthening the cartilaginous deficiency improved the nasal appearance and function in 90% of patients. Conclusions: Deformities of the nasal tip are among the most difficult to correct. Tractional forces provided by dome strength help to maintain the ala in its normal anatomical position. Structural tip grafts restore the tractional force and, thereby, help to correct the alar deformity.

Cancer and its treatment are often associated with symptoms such as depression, somnolence, cognitive abnormalities, and fatigue. Methylphenidate, a stimulant medication, is commonly used to treat these symptoms. Several small pilot and a few adequately powered studies have assessed the safety and efficacy of methylphenidate in patients with cancer. Overall, the studies so far suggest that methylphenidate is well-tolerated in patients with cancer. Further, the studies have provided initial evidence of efficacy of this agent in patients with cancer. The present article reviews the evidence base behind the use of methylphenidate in these patients.

ABSTRACT Paramyxovirus V proteins function as host interference factors that inactivate antiviral responses, including interferon. Characterization of cellular proteins that copurify with ectopically expressed measles virus V protein has revealed interactions with DNA binding domains of p53 family proteins, p53 and p73. Specific transcriptional assays reveal that expression of measles virus V cDNA inhibits p73, but not p53. Expression of measles virus V cDNA can delay cell death induced by genotoxic stress and also can decrease the abundance of the proapoptotic factor PUMA, a p73 target. Recombinant measles virus with an engineered deficiency in V protein is capable of inducing more severe cytopathic effects than the wild type, implicating measles virus V protein as an inhibitor of cell death. These findings also suggest that p73-PUMA signaling may be a previously unrecognized arm of cellular innate antiviral immunity.

AbstractAlthough ultrasonic and computed tomographic technology is continuing to evolve, these already sophisticated imaging tests have become the primary methods of evaluating the patients with aortic aneurysms. Both modalities are accurate and noninvasive. The major value of these techniques to the surgeon is in assessing those patients in whom the diagnosis is in doubt and in following patients in whom it has been elected to observe a small stable aneurysm. Changes in an aneurysm can be detected on serial examinations which might indicate the need for surgery in spite of adverse patient risk factors, and these techniques may provide a means of detecting false aneurysms in patients who are difficult to assess accurately by physical examination. Ultrasound and computed tomography are very helpful techniques in the diagnosis and assessment of aortic aneurysms. These diagnostic modalities are not required in every patient and should be used discriminately and when indicated.