In situ replacement was a safe and durable option in most (64%) patients presenting with prosthetic graft infection. In situ replacement with a rifampin-bonded graft was effective for S epidermidis graft infection, but when the entire prosthesis is involved with either a biofilm or invasive perigraft infection, in situ autogenous vein replacement is preferred. Virulent graft infections presenting with sepsis, anastomotic dehiscence, or graft enteric fistula should continue to be treated with total graft excision, and if feasible, staged ex situ bypass graft.

Werner's syndrome (WS) is a human disease with manifestations resembling premature aging. The gene defective in WS, WRN, encodes a DNA helicase. Here, we describe the generation of mice bearing a mutation that eliminates expression of the C terminus of the helicase domain of the WRN protein. Mutant mice are born at the expected Mendelian frequency and do not show any overt histological signs of accelerated senescence. These mice are capable of living beyond 2 years of age. Cells from these animals do not show elevated susceptibility to the genotoxins camptothecin or 4-NQO. However, mutant fibroblasts senesce approximately one passage earlier than controls. Importantly, WRN ؊/؊ ; p53 ؊/؊ mice show an increased mortality rate relative to WRN ؉/؊ ; p53 ؊/؊ animals. We consider possible models for the synergy between p53 and WRN mutations for the determination of life span.Werner's Syndrome (WS) is a recessive genetic disease which shows premature onset of many pathologies normally associated with old age (18). Patients with WS appear normal during the first decade of life. The first manifestation of this disease is typically growth failure during adolescence. Subsequently, these patients suffer prematurely from a variety of age-related disorders: skin changes, osteoporosis, diabetes, accelerated atherosclerosis, and cancer, particularly sarcomas. Fibroblasts derived from individuals with WS divide many fewer times prior to senescence than do fibroblasts from agematched control individuals (13). Genomic instability has been observed in WS cells, as chromosomal rearrangements (5,19,21) and as mutations within the hypoxanthine phosphoribosyltransferase gene (HPRT); in vivo, an increased frequency of HPRT mutant cells has been observed in patients with WS (2,3,14). The gene defective in WS, WRN, encodes a protein of 1,432 amino acids with similarity to the RecQ subfamily of DNA helicases (26). Although mutations throughout the WRN gene have been observed in the homozygous state, homozygosity for a mutation very near the 3Ј end of the WRN open reading frame is sufficient to lead to the disease (15).A mouse knockout (KO) of the WRN gene has been described (10). Lebel and Leder deleted exons III and IV in the catalytic helicase domain of the WRN locus, a mutation predicted to eliminate catalytic function. Cells containing this mutation express an internally deleted, nearly full-length WRN protein. Homozygous mutant mice are viable, indicating that this particular mutation is not lethal. However Lebel and Leder showed a decreased embryonic survival of their mutant: on a C57BL/6-129/SvEv outbred background and on a 129/ SvEv inbred background, the ratios of ϩ/ϩ:ϩ/Ϫ:Ϫ/Ϫ mice born are 1:2.0:0.8 and 1:1.9:0.6, respectively. Mutant embryonic stem (ES) cells have an approximately sixfold increased mutation rate at the HPRT locus. They are also 10-fold more sensitive to camptothecin, a topoisomerase I inhibitor, and are two-to threefold more sensitive to etoposide, a topoisomerase II inhibitor. Late-passage mutant embryonic fibro...

We measure the threshold accelerations necessary to excite surface waves in a vertically vibrated fluid container (the Faraday instability). Under the proper conditions, the thresholds and onset wavelengths agree with recent theoretical predictions for a laterally infinite, finite-depth container filled with a viscous fluid. Experimentally, we show that by using a viscous, non-polar fluid, the finite-size effects of sidewalls and the effects of surface contamination can be made negligible. We also show that finite-size corrections are of order h/L, where h is the fluid depth and L the container size. Based on these measurements, one can more easily interpret certain unexpected observations from previous experimental studies of the Faraday instability.

Outcomes associated with aortoenteric fistula repair were surprisingly favorable in the absence of preoperative hemodynamic instability.