200 Years of lice in Glasgow: an index of social deprivation

Who gets lice? Using detailed health records of the citizens of Glasgow over the past couple of centuries, Steve Lindsay shows that lice have in the past been associated with deprivation. This conclusion may be controversial but, with the demise of the nit nurses and their detailed records, we are no longer in a position to say whether or not the same is true today.     

睡眠剥夺对大鼠心肌损伤效应和抗氧化指标的影响

目的：探讨睡眠剥夺对大鼠心肌和抗氧化指标的影响。方法：大鼠随机分为睡眠剥夺2 d组（SD 2 d）、睡眠剥夺4 d组（SD 4 d）、睡眠剥夺6 d组（SD 6 d）、大平台对照组（TC）、正常对照组（CC）,利用＂小平台水环境法＂建立大鼠睡眠剥夺模型,利用BL-410机能实验系统描记体表心电图,采用光镜及透射电镜观察心肌形态学改变,测定心肌线粒体丙二醛含量、超氧化物歧化酶活性。结果：睡眠剥夺组大鼠心率加快,心电图出现缺血性改变;心肌细胞染色质、肌浆网、线粒体、闰盘等亚细胞结构出现损伤性改变,部分心肌纤维溶解、坏死,心肌间质水肿、出血、炎性细胞浸润;心肌线粒体MDA水平升高,SOD活性随睡眠剥夺时间延长有降低趋势。结论：睡眠剥夺能够引起大鼠心肌损伤,其引起的氧化应激可能是心肌损伤的机制。     

Cardiopulmonary regulation after rapid-eye-movement sleep deprivation.

Arterial blood pressure, chest movement, electroencephalogram, and electromyogram were monitored in six normotensive Sprague-Dawley rats for 4 h/day 3 days before and 4 days after 114 h of rapid-eye-movement (REM) sleep deprivation. During recovery sleep immediately after REM sleep deprivation (RD), there was a significant increase in the amount of time spent in REM sleep. During this rebound in REM sleep, there was a significant rise (26%) in heart rate in wakefulness, non-REM sleep, and REM sleep during the first 4 h after RD. Systolic blood pressure was also significantly elevated (14%) but only during wakefulness before recovery sleep. Rats with the greatest waking systolic blood pressure after RD had the lowest REM sleep rebound in the 4 h immediately after RD (r = -0.885, P less than 0.05). The rise in heart rate, systolic blood pressure, and REM sleep time evident on day 1 immediately after RD was absent on recovery days 2-4. The respiratory rate tended to be higher throughout the recovery period in every state of consciousness; however, these values never reached the level of significance. In the initial recovery sleep period, regulation of heart rate was more disrupted by REM sleep deprivation than either arterial blood pressure or respiratory rate.     

CHRNA5 variants moderate the effect of nicotine deprivation on a neural index of cognitive control

Individuals with reduced attention and memory cognitive control‐related processes may be motivated to smoke as a result of the cognitive enhancing effects of nicotine. Further, nicotine deprivation‐induced reductions in cognitive control may negatively reinforce smoking. Minor allele carriers at rs16969968 in the nicotinic acetylcholine receptor α5 subunit gene (CHRNA5) have been shown to exhibit both reduced cognitive control and greater nicotine dependence. It is therefore of interest to see if variants in this gene moderate the influence of nicotine deprivation on cognitive control. P3b and P3a components of the event‐related brain potential waveform evoked by a three‐stimulus visual oddball task are widely viewed as positive indices of cognitive control‐related processes. We tested the hypothesis that individuals possessing at least one minor allele at rs16969968 in CHRNA5 would show greater nicotine deprivation‐induced reductions in P3b and P3a amplitude. The sample included 72 non‐Hispanic, Caucasian heavy smokers (54 men and 18 women) with a mean age of 36.11 years (SD = 11.57). Participants completed the visual oddball task during counterbalanced nicotine and placebo smoking sessions. Findings indicated that rs16969968 status did not moderate nicotine effects on P3b or P3a, whereas variation in other CHRNA5 polymorphisms, which are not as well characterized and are not in linkage disequilibrium with rs16969968, predicted nicotine deprivation‐induced reduction of P3a amplitude: rs588765 (F_1,68 = 7.74, P = 0.007) and rs17408276 (F_1,67 = 7.34, P = 0.009). Findings are interpreted in the context of vulnerability alleles that may predict nicotine effects on cognitive control.     

Moderate glucose deprivation preconditions myocardium against infarction.

Glucose-free perfusion preconditions myocardium against the consequences of subsequent ischemia. We investigated whether mitochondrial ATP-sensitive potassium (mK (ATP)) channels are involved in preconditioning by glucose deprivation, and whether moderate glucose deprivation also preconditions myocardium. Isolated rat hearts underwent 30 min of no-flow ischemia followed by 1 h reperfusion. Controls were not further treated. Three groups were preconditioned by perfusion with 0, 40 or 80 mg/dl (0, 2.22, 4.44 mmol/l) glucose (correction of osmotic pressure by addition of urea) for 10 min followed by 10 min perfusion with normal buffer (150 mg/dl, or 8.33 mmol/l glucose) before the ischemia reperfusion protocol. In one group, 100 micromol/l of the mK (ATP) channel blocker 5-HD was added to the glucose-free perfusate. Two groups were treated with 5-HD or urea before ischemia without preconditioning. Left ventricular developed pressure and maximum ischemic contracture (82 +/- 21 mmHg) were similar in all groups. Mean left ventricular developed pressure was 100 +/- 16 mm Hg under baseline conditions, and poorly recovered to 8 +/- 11 mm Hg during reperfusion. Preconditioning with 0 and 40 mg/dl glucose containing buffer reduced infarct size from 41 +/- 10% (control) to 23 +/- 12% (p = 0.02) and 26 +/- 8% (p = 0.011). The 5-HD blocked preconditioning by glucose deprivation (38 +/- 9%, p = 0.04) while 80 mg/dl glucose, 5-HD and urea had no effect on infarct size (39 +/- 9%; 38 +/- 13%; 37 +/- 8%; p = 1.0 each). We conclude that transient severe glucose deprivation and moderate glucose deprivation preconditions the isolated rat heart. Preconditioning by complete glucose deprivation depends on the opening of mK (ATP) channels.