We describe a new chiral tubule-forming lipid in which the C-O-P headgroup/glycerol backbone linkage of the archetypal tubule-forming phospholipid, 1,2-bis(10,12-tricosadiynoyl)-sn-glycero-3-phosphocholine, DC(8,9)PC, is replaced by a C-C-P linkage. Tubule formation from this phosphonate analogue occurs under the same mild conditions as with DC(8,9)PC and produces identical yields, but the phosphonate tubules have cylindrical diameters twice that of DC(8,9)PC tubules. Small-angle X-ray scattering, atomicforce, and optical microscopy reveal the new tubules to consist of fewer coaxially nested cylindrical lamellae than DC(8,9)PC tubules; accordingly, the phosphonate tubules are more fragile. In addition, a small portion of the phosphonate precipitate is in the form of stable open helices, and enantiomerically pure preparations of the new molecule contain significant numbers of helices possessing the unexpected sense of handedness.
We describe a new chiral tubule-forming lipid in which the C-O-P phosphoryl linkage of the archetypal tubule-forming molecule, 1,2-bis(10,12-tricosadiynoyl)-sn-glycero-3-phosphocholine, "DC(8,9)PC", is replaced by a C-P linkage. Tubule formation with this phosphonate analogue proceeds under the same mild conditions as with DC(8,9)PC and produces similar yields, but synchrotron small-angle X-ray scattering, atomic force microscopy, and optical microscopy show the new tubules to have diameters 1.94 times as great, to be significantly shorter, and to be thinner-walled. A significant portion of the enantiomerically pure chiral phosphonate precipitate is in the form of stable open helices, and these helices are divided almost evenly between left- and right-handed members.
In 2007, the Acute Kidney Injury Network (AKIN) developed a modified standard for diagnosing and classifying acute kidney injury (AKI). This classification system is a modification of the previously described risk, injury, failure, loss, and end-stage (RIFLE) criteria. Among other modifications, the AKIN staging requires an absolute serum creatinine change of 0.3 mg/dl in a 48-hour period to establish the diagnosis of AKI. The purpose of this study was to apply these new criteria in the severely burned population and to compare the prevalence, stage, and mortality impact of these criteria to the RIFLE criteria. The authors performed a retrospective analysis of consecutive patients with burns admitted to their burn center for at least 24 hours from June 2003 through December 2008. Each patient was classified by both the AKIN and RIFLE criteria by three referees. Both univariate and multivariate analyses were performed to determine the impact of the various AKI stages on mortality. A total of 1973 patients met inclusion and exclusion criteria and were included in the analysis. The average age, %TBSA, injury severity score, and percent with smoke inhalation injury were 36 ± 16, 16 ± 18, 10 ± 12, and 13%, respectively. Overall, the prevalence of AKI was 33% using the AKIN criteria and 24% using the RIFLE criteria with an associated mortality of 21 and 25%, respectively. Of those meeting criteria for AKIN stage 1 (N = 434), 41% (N = 180) would have been categorized as not having AKI on the basis of the RIFLE criteria. In this cohort of patients, mortality increased by almost 8-fold when compared with those without AKI (odds ratio 7.8 [95% confidence interval (CI) 3.7-16.2], P < .0001). The area under the receiver operator characteristic curve for in-hospital mortality was significantly higher for the AKIN criteria at 0.877 (95% CI 0.848-0.906) when compared to the RIFLE criteria at 0.838 (95% CI 0.801-0.874; P = .0007). Burn patients identified as having AKI by the AKIN criteria missed by RIFLE appear to be an important cohort. On the basis of our study, AKIN criteria may be more precise and are more predictive of death than the RIFLE criteria in this population. Prospective validation is needed.
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