无症状吸烟者的肺功能改变情况分析

目的：探讨烟龄215年,日吸烟量≥15支的无症状男性吸烟者的肺功能改变情况。方法：选择男性无症状吸烟者190人及非吸烟者180人,进行肺功能测定,并比较两组人群的肺功能改变情况。结果：吸烟组与非吸烟组比较,肺活量（VC）、用力肺活量（FVC）、第1秒用力呼气容积（FEV1）、Tiffeneau1秒率（FEV1／VC）结果改变不明显,而Gaensler1秒率（FEV1/FVC）、最大分钟通气量（MVV）、用力呼气50％肺活量的呼气流量（FEF50％）、用力呼气75％肺活量的呼气流量（FEF75％）、呼出25％-75％肺活量时的平均流量（FEF25％～75％）、肺一氧化碳弥散量（DLCO）结果均有显著降低,有统计学意义。结论：通过对无症状吸烟人群肺功能测定结果进行分析。发现有些吸烟者虽无临床症状,但已经出现了小气道及肺弥散功能的损伤,提醒吸烟者应早期戒烟,关爱自身健康,净化生存环境,提高生活质量。     

Increased interleukin-6 receptor expression in the paraventricular nucleus of rats with heart failure

Activation of the hypothalamic-pituitary-adrenal (HPA) axis and augmented plasma and tissue levels of IL-6 are hallmarks of heart failure (HF). Within the forebrain, cardiovascular homeostasis is mediated in part by the paraventricular nucleus (PVN) of the hypothalamus. IL-6, via binding to the IL-6 receptor (IL-6R)/glycoprotein 130 (gp130) complex influences cellular and physiological responses. Thus, in the current study, we hypothesized that PVN IL-6R protein and gene expression are upregulated in HF vs. sham-operated rats, whereas gp130 levels in the same tissues remain stable. Six weeks after coronary ligation surgery, hemodynamic measurements were obtained, and HF rats were divided into moderate noncongestive and severe chronic congestive groups based on cardiac indices. Plasma IL-6 levels were determined and changes in gene and protein expression of IL-6R and gp130 between sham-operated and HF rats were determined via real-time PCR and Western blot analyses, respectively. Plasma levels of IL-6 were elevated in rats with severe, but not moderate, HF compared with sham-operated controls. In both moderate and severe HF rats, protein but not gene expression of IL-6R was significantly increased in PVN tissue but not in non-PVN tissue, compared with sham-operated controls. Gene and protein levels of the gp130 subunit were not altered by HF in either tissue analyzed. Collectively, these data suggest that within the brain of HF rats, IL-6R expression is not a global change. Rather the increased IL-6 levels characteristic of HF may alter PVN-mediated physiological responses via enhanced expression of the IL-6R.     

Intestinal Tissues Induce an SNP Mutation in Pseudomonas aeruginosa That Enhances Its Virulence: Possible Role in Anastomotic Leak

The most feared complication following intestinal resection is anastomotic leakage. In high risk areas (esophagus/rectum) where neoadjuvant chemoradiation is used, the incidence of anastomotic leaks remains unacceptably high (～10%) even when performed by specialist surgeons in high volume centers. The aims of this study were to test the hypothesis that anastomotic leakage develops when pathogens colonizing anastomotic sites become in vivo transformed to express a tissue destroying phenotype. We developed a novel model of anastomotic leak in which rats were exposed to pre-operative radiation as in cancer surgery, underwent distal colon resection and then were intestinally inoculated with Pseudomonas aeruginosa, a common colonizer of the radiated intestine. Results demonstrated that intestinal tissues exposed to preoperative radiation developed a significant incidence of anastomotic leak (>60%; p<0.01) when colonized by P. aeruginosa compared to radiated tissues alone (0%). Phenotype analysis comparing the original inoculating strain (MPAO1- termed P1) and the strain retrieved from leaking anastomotic tissues (termed P2) demonstrated that P2 was altered in pyocyanin production and displayed enhanced collagenase activity, high swarming motility, and a destructive phenotype against cultured intestinal epithelial cells (i.e. apoptosis, barrier function, cytolysis). Comparative genotype analysis between P1 and P2 revealed a single nucleotide polymorphism (SNP) mutation in the mexT gene that led to a stop codon resulting in a non-functional truncated protein. Replacement of the mutated mexT gene in P2 with mexT from the original parental strain P1 led to reversion of P2 to the P1 phenotype. No spontaneous transformation was detected during 20 passages in TSB media. Use of a novel virulence suppressing compound PEG/Pi prevented P. aeruginosa transformation to the tissue destructive phenotype and prevented anastomotic leak in rats. This work demonstrates that in vivo transformation of microbial pathogens to a tissue destroying phenotype may have important implications in the pathogenesis of anastomotic leak.     

Exercise training and muscle microvascular oxygenation: functional role of nitric oxide

Exercise training induces multiple adaptations within skeletal muscle that may improve local O(2) delivery-utilization matching (i.e., Po(2)mv). We tested the hypothesis that increased nitric oxide (NO) function is intrinsic to improved muscle Po(2)mv kinetics from rest to contractions after exercise training. Healthy young Sprague-Dawley rats were assigned to sedentary (n = 18) or progressive treadmill exercise training (n = 10; 5 days/wk, 6-8 wk, final workload of 60 min/day at 35 m/min, -14% grade) groups. Po(2)mv was measured via phosphorescence quenching in the spinotrapezius muscle at rest and during 1-Hz twitch contractions under control (Krebs-Henseleit solution), sodium nitroprusside (SNP, NO donor; 300 μM), and N(G)-nitro-l-arginine methyl ester (l-NAME, nonspecific NO synthase blockade; 1.5 mM) superfusion conditions. Exercise-trained rats had greater peak oxygen uptake (Vo(2peak)) than their sedentary counterparts (81 ± 1 vs. 72 ± 2 ml·kg(-1)·min(-1), respectively; P < 0.05). Exercise-trained rats had significantly slower Po(2)mv fall throughout contractions (τ(1); time constant for the first component) during control (sedentary: 8.1 ± 0.6; trained: 15.2 ± 2.8 s). Compared with control, SNP slowed τ(1) to a greater extent in sedentary rats (sedentary: 38.7 ± 5.6; trained: 26.8 ± 4.1 s; P > 0.05) whereas l-NAME abolished the differences in τ(1) between sedentary and trained rats (sedentary: 12.0 ± 1.7; trained: 11.2 ± 1.4 s; P < 0.05). Our results indicate that endurance exercise training leads to greater muscle microvascular oxygenation across the metabolic transient following the onset of contractions (i.e., slower Po(2)mv kinetics) partly via increased NO-mediated function, which likely constitutes an important mechanism for training-induced metabolic adaptations.     

Topographical distribution of pulmonary perfusion and ventilation, assessed by PET in supine and prone humans.

Using positron emission tomography (PET) and intravenously injected (13)N(2), we assessed the topographical distribution of pulmonary perfusion (Q) and ventilation (V) in six healthy, spontaneously breathing subjects in the supine and prone position. In this technique, the intrapulmonary distribution of (13)N(2), measured during a short apnea, is proportional to regional Q. After resumption of breathing, regional specific alveolar V (sVA, ventilation per unit of alveolar gas volume) can be calculated from the tracer washout rate. The PET scanner imaged 15 contiguous, 6-mm-thick, slices of lung. Vertical gradients of Q and sVA were computed by linear regression, and spatial heterogeneity was assessed from the squared coefficient of variation (CV(2)). Both CV and CV were corrected for the estimated contribution of random imaging noise. We found that 1) both Q and V had vertical gradients favoring dependent lung regions, 2) vertical gradients were similar in the supine and prone position and explained, on average, 24% of Q heterogeneity and 8% of V heterogeneity, 3) CV was similar in the supine and prone position, and 4) CV was lower in the prone position. We conclude that, in recumbent, spontaneously breathing humans, 1) vertical gradients favoring dependent lung regions explain a significant fraction of heterogeneity, especially of Q, and 2) although Q does not seem to be systematically more homogeneous in the prone position, differences in individual behaviors may make the prone position advantageous, in terms of V-to-Q matching, in selected subjects.     

肠系膜上动脉栓塞临床表现及影像特征研究

目的:探讨肠系膜上动脉栓塞(superior mesenteric artery embolism,SMA embolism)临床及影像特征,以及时准确诊断从而改善病人预后。方法:搜集我院2011年7月至2014年8月临床诊断为SMA栓塞的患者24例,回顾性分析其临床及影像资料。结果:24例SMA栓塞发病年龄51~84岁,平均71.9±8.1岁;临床均表现为突发腹痛(24/24,100%),腹痛多持续不缓解(18/24,75%),少有放射痛(1/24,4.17%),多伴有恶心呕吐(16/24,66.67%)、腹泻便血(15/24,62.5%),体格检查多有肠鸣音亢进(19/24,79.17%),少有腹膜刺激征(2/24,8.33%)。多合并高血压(18/24,75%)、房颤(16/24,66.67%)、冠心病(14/24,58.33%)、心脏瓣膜病变(6/24,25%)及其他周围动脉栓塞(9/24,37.5%)。临床上符合SMA栓塞三联征中至少两项特征20例(83.33%),具备典型三联征13例(54.17%)。MSCTA或DSA均表现为SMA主干截断或充盈缺损(24/24,100%),栓塞位置多位于第1空肠动脉起始至回结肠动脉起始水平段(18/24,75%),栓塞远端分支血管多显影不良(23/24,95.83%),少有侧枝循环形成(3/24,12.5%)。MSCTA显示栓塞段血管密度多有增高(12/17,70.59%),少有管径增粗(3/17,17.65%)及脂肪间隙模糊(2/17,11.76%)。肠管多有缺血改变(15/17,88.24%),肠系膜多增粗模糊(15/17,88.24%),腹水少见(1/17,5.82%)。结论:SMA栓塞临床和影像具有一定的特征性,临床怀疑SMA栓塞应及早行MSCTA或DSA明确诊断。