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Background: Wear of the polyethylene glenoid component and subsequent particle-induced osteolysis remains one of the most important modes of failure of total shoulder arthroplasty. Vitamin E is added to polyethylene to act as an antioxidant to stabilize free radicals that exist as a byproduct of irradiation used to induce cross-linking. This study was performed to assess the in vitro performance of vitamin E-enhanced polyethylene compared with conventional polyethylene in a shoulder simulator model., Methods: Vitamin E-enhanced, highly cross-linked glenoid components were compared with conventional ultrahigh-molecular-weight polyethylene glenoids, both articulating with a ceramic humeral head component using a shoulder joint simulator over 500,000 cycles. Unaged and artificially aged comparisons were performed. Volumetric wear was assessed by gravimetric measurement, and wear particle analysis was also subsequently performed., Results: Vitamin E-enhanced polyethylene glenoid components were found to have significantly reduced wear rates compared with conventional polyethylene in both unaged (36% reduction) and artificially aged (49% reduction) comparisons. There were no differences detected in wear particle analysis between the 2 groups., Conclusion: Vitamin E-enhanced polyethylene demonstrates improved wear compared with conventional polyethylene in both unaged and artificially aged comparisons and may have clinically relevant benefits., (Copyright © 2019 Journal of Shoulder and Elbow Surgery Board of Trustees. Published by Elsevier Inc. All rights reserved.)

Background: We postulated that the response of vascular smooth muscle cells (SMCs) to oxidized low-density lipoprotein (LDL) may be modulated through calcium and 3', 5' cyclic adenosine monophosphate (Ca+2-cAMP) second-messenger activity., Methods: Changes in cytosolic calcium [Ca+2]i in aortic SMCs exposed to native (N-) and oxidized (Ox-) LDL were measured with a Fura 2-AM indicator. The influence of cAMP on this response was determined by incubating the cells with either forskolin or 8-bromo-cAMP (stimulatory) or galanin (inhibitory). The cells were then activated by an initial preincubation with N- or Ox-LDL, and the subsequent cellular oxidation of N-LDL was measured. The effect of cAMP mediators alone or in conjunction with calcium antagonism was studied., Results: Exposure of SMCs to Ox-LDL resulted in a marked elevation of [Ca+2]i(306 +/- 12 nmol/L) compared with that in the control group (192 +/- 15 nmol/Liter; p < 10(-6)). This response was augmented by cAMP stimulation (406 +/- 8 nmol/L; p < 10(-6)) but reduced by cAMP inhibition (247 +/- 8 nmol/L; p < 10(-6)). The activation of intracellular signaling by initial Ox-LDL priming increased the subsequent oxidation of N-LDL (0.40 +/- 0.02 nmol malondialdehyde versus 0.24 +/- 0.02 nmol MDA control; p < 10(-4)). This response was enhanced by cAMP (0.45 +/- 0.03 nmol MDA; p < 10(-4)) and inhibited by galanin (0.26 +/- 0.02; p < 10(-4)). The cAMP effect was reversed by the blockade of calcium mobilization via membrane channels and reticular release., Conclusions: Oxidized LDL-induced Ca+2-cAMP signaling modulates the cellular oxidation of N-LDL. This finding suggests a mechanism through which the scavenger uptake of modified LDL may potentially be regulated.

Background: This study was undertaken to evaluate the outcome of infrainguinal arterial reconstruction in a high-risk subset of patients with end-stage renal disease., Methods: We reviewed the medical records of 44 patients requiring maintenance dialysis and undergoing 57 infrainguinal bypass procedures for limb salvage from 1986 to 1992. These included 16 (28%) femoropopliteal and 41 (72%) tibial or pedal bypasses with autogenous (82%), prosthetic (12%), or composite (6%) graft materials. The principal indications for operation were ischemic ulceration or gangrene (79%) and rest pain (21%). Angiographic evaluation most frequently showed single-vessel runoff (56%). Risk factors included age (mean, 63 years), diabetes (75%), hypertension (93%), coronary artery disease (52%), smoking (39%), previous myocardial infarction (20%), and contralateral amputation (18%). Infection was present in 22 limbs (39%)., Results: Early (30-day) surgical morbidity rate was 39%, including wound breakdown (19%), graft thrombosis (9%), and major amputation (4%). Perioperative mortality rate was 9%. Cumulative primary graft patency rates were 71% and 63%, secondary patency rates were 80% and 66%, and limb salvage rates were 70% and 52% at 1 and 2 years, respectively. Limb loss correlated most highly with the presence of preoperative infection (p = 0.036; log-rank method). Patient survival rate was 52% at 2 years., Conclusions: Life-table analysis confirms a poor life expectancy for this population but indicates that an acceptable level of limb salvage may be achieved with arterial reconstruction in properly selected patients.

The inhibition of atherosclerosis by estrogen has been shown clinically and experimentally, but the mechanism by which this occurs is unknown. Previous studies have shown that estrogen enhances the uptake of low-density lipoprotein (LDL) by bovine aortic endothelial cells (BAEC) while not altering membrane binding at saturating levels of LDL. In this study the effect of estrogen on LDL binding kinetics has been investigated. Computer-assisted Scatchard analysis of binding data suggests a single-site binding model. Estrogen-treated BAEC showed a lower binding affinity (Ka = 2.47 +/- 0.74 E7 M-1) than control cells (1.95 +/- 0.21 E7 M-1) (p = 0.0012). Estrogen-treated cells, however, had a greater binding capacity (Bmax = 1.26 +/- 0.07 E-10M) than control cells (Bmax = 8.49 +/- 0.44 E-11M) (p = 0.0004). The latter was due primarily to a difference in LDL binding at higher concentrations of LDL (greater than 40 micrograms/ml). These findings are consistent with an estrogen-stimulated increase in low-affinity binding of LDL to BAEC, which may not be directly receptor mediated and which appears to enhance the uptake of LDL at higher lipoprotein concentrations. Such alterations in LDL uptake by endothelial cells could influence the formation of atherosclerotic plaque.

In 1831 James Syme described the unusual occurrence of an aortocaval fistula in a 22-year-old man with luetic aortitis. This initial report was followed by illustration of this phenomenon in Rokitanski's Book of Pathologic Anatomy in 1841 and by Ryle's delineation of an aortocaval fistula on a pathologic specimen placed in Guy's Hospital Museum in 1892. The first series of aortocaval fistulas, cited by Rudolf Matas in 1909, consisted of a collection of 20 cases gathered by Boinet 10 years earlier. Several later reports, including those by Reid in 1925 and by Lehman in 1938, failed to add any additional cases. It was not until 1955 that Boffi presented an additional six patients who had this disorder, none of whom survived. Since that time, more than 100 cases of spontaneous aortocaval fistulas have been documented. This increasing experience has resulted in improved understanding and surgical treatment of these large-vessel arteriovenous communications. Nevertheless, lack of awareness and failure of recognition of this problem continue to impede its successful management. In this review we present two additional illustrative cases, summarize the clinical and pathophysiologic features of aortocaval fistulas, and outline present approaches to treatment.