Pathophysiological Links Between Diabetes and Blood Pressure

Hypertension is highly prevalent among people with diabetes, and the presence of diabetes among those with hypertension portends an increase in cardiovascular risk. In this review we aim to explore the pathophysiological links between diabetes and hypertension. Renal sodium handling differs in diabetes because there is an upregulation of sodium transporters in the kidneys. The renin-angiotensin-aldosterone system may be upregulated in diabetes, leading to hypertension through a direct effect mediated by angiotensin II, as well as indirectly through upregulation of sympathetic activity. Renin-angiotensin-aldosterone system blockade is a mainstay therapy for hypertension, and evidence suggests that it might also reduce the incidence of diabetes. People with diabetes frequently have autonomic dysfunction, which could contribute to hypertension through increased sympathetic tone and through stimulation of renin production in the juxtaglomerular apparatus. Furthermore, people with diabetes also frequently show an abnormality in their circadian blood pressure pattern. Another important link between hypertension and diabetes is the development as well as progression of diabetic kidney disease, the pathophysiology of which is mediated through several pathways including endothelial dysfunction and advanced glycation end products. Finally, obesity and the metabolic syndrome, through their effects on various hormones and inflammation, might also contribute to the pathogenesis of hypertension and diabetes.     

Expressions and inhibitory functions of CD300a receptors on purified human basophils

The inhibitory myeloid immunoglobulin receptor CD300a (IRp60) has been shown to downregulate mast cell and eosinophil activities, thereby serving as a potential target for inhibiting allergic effector cell input in allergy. Our aims were to study the expression and functional properties of this receptor in purified human basophils, cells that crucially contribute to Th2‐type immunity and allergy. Basophils homogeneously expressed CD300a as well as the inhibitory receptor CD200R on their cell surface, and these expressions increased after anti‐IgE stimulation. IgE‐mediated basophil degranulation was also significantly inhibited by crosslinking of either CD200R or CD300a (by 90% and 50%, respectively). Inhibitory SHIP‐1 phosphorylations were also induced by CD200R and CD300a, although they were not noticeably increased by IgE‐dependent activation. We conclude that both CD200R and CD300a play a role in reducing IgE‐mediated basophil function and may crucially govern the known differential activities of these cells in vivo.     

神经心理量表联合事件相关电位对中、重度阻塞性睡眠呼吸

目的 通过神经心理量表和事件相关电位中的P300检测评价中、重度阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者的轻度认知功能障碍(MCI)。 方法 对多导睡眠呼吸监测(PSG)确诊的中重度OSAHS患者30例(患者组)、志愿者20例(对照组),分别以蒙特利尔认知评估量表(MoCA)评分判断参加者是否存在MCI,并行Epworth嗜睡量表(ESS)和事件相关电位中的P300检测,PSG检查记录呼吸暂停低通气指数(AHI)、夜间最低血氧饱和度(LSaO₂)、夜间平均血氧饱和度(MSaO₂)和血氧饱和度低于90%的时间占整个睡眠时间的百分比(CT90%)、氧减指数(ODI)、呼吸性微觉醒指数(RMI)和睡眠结构。分别比较患者组与对照组的各项指标,相关分析MoCA评分与各项指标和P300相关参数的相关性。 结果 与对照组比较,中、重度OSAHS患者年龄和受教育年限差异无统计学意义,BMI和ESS评分明显增加,MoCA总评分明显降低,MoCA亚项分析中记忆/延迟回忆评分明显降低,AHI明显增加,LSaO₂和MSaO₂明显降低,CT90%增加,ODI和RMI指数明显增加,浅睡眠(S1、S2期)延长、深睡眠(S3、S4期)及快动眼睡眠期(REM)减少;在P300检测中,Cz、C3、C4、Pz点P300潜伏期明显延长,直线相关分析MoCA亚项中记忆/延迟回忆评分与ESS、AHI、MSaO₂、Cz、C3、C4点潜伏期无相关性,与LSaO₂正相关,与RMI、ODI、CT90%与Pz点潜伏期和Fz点波幅负相关,Pz点P300潜伏期及Fz点P300波幅对MoCA评分影响较大。 结论 中、重度OSAHS患者存在MCI,OSAHS患者的记忆功能变化是由夜间微觉醒所致。P300检测可作为评价OSAHS患者认知功能障碍的电生理指标之一,结合MoCA评分能对OSAHS患者认知能力及时测评。     

How friendly is a little friendly competition? Evidence of self-interest and empathy during outcome evaluation

Although previous studies have shown that brain potentials recorded from passive observers differ when gambling-task outcomes are delivered to a friend or a stranger, it is unclear how these outcome evaluations are reflected in brain potentials during active competition. The present study recorded event-related potentials (ERP) from 16 normal adults playing an interactive gambling task against both a friend and a stranger. In this task, the P300 was modulated by the feedback valence (gain or loss) and the nature of the interpersonal relationship, such that it was larger when competing against strangers. Regression analyses indicated that empathy to another's personal distress was negatively related to P300 amplitudes when competing against friends. The dFRN, defined as the difference between losses and gains, varied with Perspective-Taking when competing against friends, such that smaller dFRN amplitudes were correlated with increased Perspective-Taking. The modulation of ERP components indicates that interpersonal relationships may influence outcome evaluations in competitive situations. Correlations between ERP components and empathy measures also provide preliminary support of a relationship between one's empathy and the processing of outcomes during competition against a friend.     

Prospect theory does not describe the feedback‐related negativity value function

Humans handle uncertainty poorly. Prospect theory accounts for this with a value function in which possible losses are overweighted compared to possible gains, and the marginal utility of rewards decreases with size. fMRI studies have explored the neural basis of this value function. A separate body of research claims that prediction errors are calculated by midbrain dopamine neurons. We investigated whether the prospect theoretic effects shown in behavioral and fMRI studies were present in midbrain prediction error coding by using the feedback‐related negativity, an ERP component believed to reflect midbrain prediction errors. Participants’ stated satisfaction with outcomes followed prospect theory but their feedback‐related negativity did not, instead showing no effect of marginal utility and greater sensitivity to potential gains than losses.