Neural sensitivity to social rejection is associated with inflammatory responses to social stress

Although stress-induced increases in inflammation have been implicated in several major disorders, including cardiovascular disease and depression, the neurocognitive pathways that underlie inflammatory responses to stress remain largely unknown. To examine these processes, we recruited 124 healthy young adult participants to complete a laboratory-based social stressor while markers of inflammatory activity were obtained from oral fluids. A subset of participants (n = 31) later completed an fMRI session in which their neural responses to social rejection were assessed. As predicted, exposure to the laboratory-based social stressor was associated with significant increases in two markers of inflammatory activity, namely a soluble receptor for tumor necrosis factor-α (sTNFαRII) and interleukin-6 (IL-6). In the neuroimaging subsample, greater increases in sTNFαRII (but not IL-6) were associated with greater activity in the dorsal anterior cingulate cortex and anterior insula, brain regions that have previously been associated with processing rejection-related distress and negative affect. These data thus elucidate a neurocognitive pathway that may be involved in potentiated inflammatory responses to acute social stress. As such, they have implications for understanding how social stressors may promote susceptibility to diseases with an inflammatory component.     

The influence of muscle load on tibiofemoral knee kinematics

A comparative kinematics study was conducted on six cadaver limbs, comparing tibiofemoral kinematics in five conditions: unloaded, under a constant 130 N ankle load with a variable quadriceps load, with and without a simultaneous constant 50 N medial and lateral hamstrings load. Kinematics were described as translation of the projected centers of the medial (MFT) and lateral femoral condyles (LFT) in the horizontal plane of the tibia, and tibial axial rotation (TR) as a function of flexion angle. In passive conditions, the tibia rotated internally with increasing flexion to an average of −16° (range: −12/−20°, SD = 3.0°). Between 0 and 40° flexion, the medial condyle translated forwards 4 mm (range: 0.8/5.5 mm, SD = 2.5 mm), followed by a gradual posterior translation, totaling −9 mm (range: −5.8/−18.5 mm, SD = 4.9 mm) between 40–140° flexion. The lateral femoral condyle translated posteriorly with increasing flexion completing −25 mm (range: −22.6 to −28.2 mm, SD = 2.5 mm). Dynamic, loaded measurements simulating a deep knee bend were carried out in a knee rig. Under a fixed ankle load of 130 N and variable quadriceps loading, tibial rotation was inverted, mean TR = 4.7° (range: −3.3°/11.8° SD = 5.4°), MFT = −0.5 mm (range: = −4.3/2.4 mm, SD = 2.4 mm), LFT = 3.3 mm (range: = −3.6/10.6 mm, SD = 5.1 mm). Compared to the passive condition, all these excursions were significantly different (p ≤ 0.015). Adding medial and lateral hamstrings force of 50 N each reduced TR, MFT, and LFT significantly compared to the passive condition. In general, loading the knee with hamstrings and quadriceps reduces rotation and translation compared to the passive condition. Lateral hamstring action is more influential on knee kinematics than medial hamstrings action. © 2009 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 28:419–428, 2010     

双轴旋转刺激后模拟失重大鼠前扣带回皮质内Fos表达(英文)

目的:研究动物接受不同实验方式重力刺激后,前扣带回皮质(ACC)这一可能与空间飞行后心血管功能紊乱有关的前庭功能区中神经元活动变化。方法:该研究采用卵白素-生物素复合物(ABC)、3,3’-二氨基联苯胺四盐酸盐水合物(DAB)为呈色剂的免疫组织化学方法。大鼠随机分为三组:正常对照组(Con);后肢去负荷(HU)组(动物吊尾7d)和后肢去负荷-旋转组(HU-R)(动物后肢去负荷7d后进行2h双轴旋转刺激)。结果:(1)HU组动物ACC内Fos阳性神经元的数目(199.8±44.8)比Con组(365.0±135.6)显著降低(P0.05);(2)双轴旋转刺激显著可增加7d吊尾大鼠ACC内Fos免疫阳性神经元数量(491.6±229.3,P0.05)。这些结果提示模拟失重和双轴旋转都可影响ACC神经元活动。结论:ACC受模拟失重的影响,7d吊尾刺激使ACC内Fos表达水平下降可能是一种适应的表现。     

‘Twin’ familial aneurysms of the anterior communicating artery

Abstract

Two sisters harbouringan intracranial aneurysm are described. Rather than merely adding new cases to the records of familial aneurysms, this communication reports clinical and radiological findings supporting the hypothesis of inheritance: (1) same anatomical location with involvement of the anterior communicating artery (ACoA), which is uncommon when dealing with familial aneurysms, and similar morphology of the lesions; (2) identical haemodynamic pattern; (3) similar timing of haemorrhage, occuring in both cases during the sixth decade.     

Cognitive vs. affective listening modes and judgments of music - An ERP study

The neural correlates of processing deviations from Western music rules are relatively well known. Less is known of the neural dynamics of top-down listening modes and affective liking judgments in relation with judgments of tonal correctness. In this study, subjects determined if tonal chord sequences sounded correct or incorrect, or if they liked them or not, while their electroencephalogram (EEG) was measured. The last chord of the sequences could be congruous with the previous context, ambiguous (unusual but still enjoyable) or harmonically inappropriate. The cognitive vs. affective listening modes were differentiated in the event-related potential (ERP) responses already before the ending chord, indicating different preparation for the judgment tasks. Furthermore, three neural events tagged the decision process preceding the behavioral responses. First, an early negativity, peaking at about 280 ms, was elicited by chord incorrectness and by disliking judgments only over the right hemisphere. Second, at about 500 ms from the end of the sequence a positive brain response was elicited by the negative answers of both tasks. Third, at about 1200 ms, a late positive potential (LPP) was elicited by the liking judgment task whereas a large negative brain response was elicited by the correctness judgment task, indexing that only at that late latency preceding the button press subjects decided how to judge the cadences. This is the first study to reveal the dissociation between neural processes occurring during affective vs. cognitive listening modes and judgments of music.     

Black sheep get the blues: A psychobiological model of social rejection and depression

Major life events involving social rejection are strongly associated with onset of depression. To account for this relation, we propose a psychobiological model in which rejection-related stressors elicit a distinct and integrated set of cognitive, emotional, and biological changes that may evoke depression. In this model, social rejection events activate brain regions involved in processing negative affect and rejection-related distress (e.g., anterior insula, dorsal anterior cingulate cortex). They also elicit negative self-referential cognitions (e.g., “I’m undesirable,” “Other people don’t like me”) and related self-conscious emotions (e.g., shame, humiliation). Downstream biological consequences include upregulation of the hypothalamic-pituitary-adrenal axis, sympathetic-adrenal-medullary axis, and inflammatory response. Pro-inflammatory cytokines play an important role in this process because they induce a constellation of depressotypic behaviors called sickness behaviors. Although these changes can be short-lived, sustained inflammation may occur via glucocorticoid resistance, catecholamines, sympathetic innervation of immune organs, and immune cell aging. This response also may be moderated by several factors, including prior life stress, prior depression, and genes implicated in stress reactivity.