Citations

Background The prevalence of cigarette smoking in China is high. Surgery provides an excellent opportunity for patients to quit smoking, and anesthesiologists can play an important role in tobacco control. However, little is known about the practices, knowledge, and attitudes of Chinese anesthesiologists regarding perioperative tobacco interventions. Methods Chinese anesthesiologists were surveyed at a national meeting in 2009, with written questionnaires distributed to 800 practicing anesthesiologists. Results The survey response rate was 60.3%, and 10% of respondents themselves smoked cigarettes. Most (73%) of them frequently or almost always asked about smoking status; 51% advised about the health risk of tobacco use; and 60% advised patients to quit. Compared with nonsmokers, smokers were significantly less likely to advise about the health risks of smoking and quitting. A high proportion of respondents had accurate perceptions of perioperative and long-term health risks of smoking. Although most respondents agreed that advising patients to quit is the responsibility of anesthesiologists and the perioperative period is a good time to help patients quit smoking, few knew how to counsel about smoking or help patients get the help they needed to quit. Nonetheless, most of the respondents were willing to learn about perioperative interventions and spend an extra 5 min to help patients quit smoking. Conclusions Given their adequate knowledge of health risks of smoking, strong perception of responsibilities, and willingness to participate in tobacco control, Chinese anesthesiologists are poised to play a significant role in tobacco control in China that could improve perioperative outcomes and promote long-term health.

AbstractCarnitine plays an essential role in fatty acid metabolism, as well as modulation of intracellular concentrations of free coenzyme A by esterification of acyl residues. Acylcarnitine analysis of various biological fluids is a sensitive method to detect >20 inborn errors of metabolism that result in abnormal accumulation of acylcarnitine species due to several organic acidemias and most fatty acid β‐oxidation disorders. In addition, acylcarnitine analysis may aid in monitoring treatment of known patients affected with these inborn errors of metabolism. This unit describes protocols that can be used to measure acylcarnitine species of various carbon chain lengths in several biological specimen types including plasma, dried blood and bile spots, and urine, by derivatization to butylesters and flow‐injection electrospray ionization tandem mass spectrometry (ESI‐MS/MS). Curr. Protoc. Hum. Genet. 64:17.8.1‐17.8.20. © 2010 by John Wiley & Sons, Inc.

As our understanding of the importance of individualized medicine continues to grow, the clinical relevance of interindividual variability in hemodynamic variables is receiving increasing attention. However, it is not known whether the rat, which is often used for studies of cardiovascular regulation, exhibits similar interindividual variability. In the present study, we evaluated whether the magnitude of interindividual variability in cardiac output (CO) and total peripheral resistance (TPR) was similar in humans and in rats. We assessed interindividual variability of mean arterial pressure (MAP), CO, and TPR during control conditions in normotensive humans ( n = 40) and during normotension and deoxycorticosterone acetate-salt hypertension in Sprague-Dawley rats ( n = 16). Humans and rats showed marked interindividual variability in CO and TPR but low variability in MAP. During deoxycorticosterone acetate-salt hypertension, CO was maintained, but TPR was elevated compared with the baseline period. We conclude that the magnitudes of interindividual variability of MAP, CO, and TPR are quantitatively similar in humans and rats, providing support for the relevance of this variability in both species and suggesting that studies in rats could be designed to address questions specific to individualized medicine in hypertension.

ABSTRACTThe signaling lymphocytic activation molecule (SLAM; CD150) is the immune cell receptor for measles virus (MV). To assess the importance of the SLAM-MV interactions for virus spread and pathogenesis, we generated a wild-type IC-B MV selectively unable to recognize human SLAM (SLAM-blind). This virus differs from the fully virulent wild-type IC-B strain by a single arginine-to-alanine substitution at amino acid 533 of the attachment protein hemagglutinin and infects cells through SLAM about 40 times less efficiently than the isogenic wild-type strain.Ex vivo, this virus infects primary lymphocytes at low levels regardless of SLAM expression. When a group of six rhesus monkeys (Macaca mulatta) was inoculated intranasally with the SLAM-blind virus, no clinical symptoms were documented. Only one monkey had low-level viremia early after infection, whereas all the hosts in the control group had high viremia levels. Despite minimal, if any, viremia, all six hosts generated neutralizing antibody titers close to those of the control monkeys while MV-directed cellular immunity reached levels at least as high as in wild-type-infected monkeys. These findings prove formally that efficient SLAM recognition is necessary for MV virulence and pathogenesis. They also suggest that the selectively SLAM-blind wild-type MV can be developed into a vaccine vector.

Abstract Philadelphia chromosome–negative myeloproliferative neoplasms (MPNs) including polycythemia vera, essential thrombocythemia, and primary myelofibrosis show an inherent tendency for transformation into leukemia (MPN-blast phase), which is hypothesized to be accompanied by acquisition of additional genomic lesions. We, therefore, examined chromosomal abnormalities by high-resolution single nucleotide polymorphism (SNP) array in 88 MPN patients, as well as 71 cases with MPN-blast phase, and correlated these findings with their clinical parameters. Frequent genomic alterations were found in MPN after leukemic transformation with up to 3-fold more genomic changes per sample compared with samples in chronic phase (P < .001). We identified commonly altered regions involved in disease progression including not only established targets (ETV6, TP53, and RUNX1) but also new candidate genes on 7q, 16q, 19p, and 21q. Moreover, trisomy 8 or amplification of 8q24 (MYC) was almost exclusively detected in JAK2V617F− cases with MPN-blast phase. Remarkably, copy number–neutral loss of heterozygosity (CNN-LOH) on either 7q or 9p including homozygous JAK2V617F was related to decreased survival after leukemic transformation (P = .01 and P = .016, respectively). Our high-density SNP-array analysis of MPN genomes in the chronic compared with leukemic stage identified novel target genes and provided prognostic insights associated with the evolution to leukemia.