We demonstrated that even a single session of LDL apheresis with the reduction of total LDL and oxidized LDL improved endothelial function. Our results suggest that total LDL and/or oxidized LDL may directly impair endothelial function in the human forearm vessel.

Functional near-infrared spectroscopy (fNIRS) is used to measure cerebral activity because it is simple and portable. However, scalp-hemodynamics often contaminates fNIRS signals, leading to detection of cortical activity in regions that are actually inactive. Methods for removing these artifacts using standard source-detector distance channels (Long-channel) tend to over-estimate the artifacts, while methods using additional short source-detector distance channels (Short-channel) require numerous probes to cover broad cortical areas, which leads to a high cost and prolonged experimental time. Here, we propose a new method that effectively combines the existing techniques, preserving the accuracy of estimating cerebral activity and avoiding the disadvantages inherent when applying the techniques individually. Our new method accomplishes this by estimating a global scalp-hemodynamic component from a small number of Short-channels, and removing its influence from the Long-channels using a general linear model (GLM). To demonstrate the feasibility of this method, we collected fNIRS and functional magnetic resonance imaging (fMRI) measurements during a motor task. First, we measured changes in oxygenated hemoglobin concentration (∆Oxy-Hb) from 18 Short-channels placed over motor-related areas, and confirmed that the majority of scalp-hemodynamics was globally consistent and could be estimated from as few as four Short-channels using principal component analysis. We then measured ∆Oxy-Hb from 4 Short- and 43 Long-channels. The GLM identified cerebral activity comparable to that measured separately by fMRI, even when scalp-hemodynamics exhibited substantial task-related modulation. These results suggest that combining measurements from four Short-channels with a GLM provides robust estimation of cerebral activity at a low cost.

Nc,NG-dimethyl-L-argmme (ADMA) IS an endogenously synthesized mtnc oxide (NO) synthase mhibltor which has potent pressor/vasoconstnctor effects Dimethylargmmase metabolizes ADMA to L-citrullme and plays a key role m deterrmmng the m VIVO levels of ADMA To mvestlgate the role of ADMA m the pathogenesls of hypertension, we measured 24-hour urinary excretion of ADMA (UADMA) and nitrate/nitrite (NOx) m Dahl salt-sensitive hypertensive rats and spontaneously hypertensive rats (SHR) In Dahl salt-resistant rats, high-salt &et (8% NaCI) did not increase blood pressure and increased urinary NOx (P< 01) wlthout changes in UADMA cornpaled with lowsalt diet (0 3% NaCI) In contrast, m Dahl salt-sensitive rats, hlghsalt diet Increased blood pressure (P< Ol), did not change urinary NOx excretion, and Increased UADMA (P< 01) There was a slgmficant (Y= 65, P< 01) correlation between UADMA and the level of blood pressure m Dahl salt-sensltlve rats Plasma levels of NOx and ADMA and renal chmethylargmmase content were comparable among them These results may suggest that m Dahl salt-resistant rats, blood pressure 1s kept constant during high-salt intake, possibly due to the compensatory increased production of NO, and that m Dahl salt-sensitive rats, high-salt intake increases the production of ADMA, attenuates the compensatory Increase\ m NO, and increases blood pressure These results also suggest that the systemic production of ADMA 19 not dependent on renal dlmethylargmmase SHR had significantly greater urinary NOx excretion (P< 05) and smaller UADMA than Wlstar-Kyoto rats nously have suggested that the NO production 1s preserved m SHR * Furthermore, recent evidence demonstrated the increased but not decreased production of NO m the heart9.10 and aorta" of SHR The synthesis of NO can be inhibited experimentally by some analogues of argmme mcludmg L-NMMA and ADMA), both of which have equally potent vasoconstnctor and pressor actions 12 Acute admmlstratlon of ADMA into guinea pigsI and rats'4 causes blood pressure elevation partly via elevation of total peripheral resistance I4 In humans, mtra-arterial admmlstratlon of ADMA lowers forearm blood flow 1~15 Although both L-NMMA and ADMA are synthesized I6 and metabolized I7 endogenously, the plasma concentration of dlmethylargmme 1s ten times greater than that of L-NMMA 13 Since studies m ammals suggest that the kidney may be mvolved m the excretion lx and metabolism 1Y.*O of ADMA, abnormalities of the ADMA production or ehmmatlon have been reported m human kidney diseases 13 21 Although recent evidence demonstrated high accumulation of ADMA m plasma from hypercholesterolexmc ammals**J3 and m balloon-injured vessels,*4 the role of this endogenous NO synthase mhlbltor m the pathogenesls of hypertension has not been elucidated at all Accordmgly, we hypothesized that endogenous ADMA may play a role m salt-sensitive hypertension by competltlve inhibition of NO synthesis. To test this hypothesis, urinary and plasma ADMA and NOx were evaluated m Dahl rats on different salt intakes....

There is an infinity of impedance parameter values, and thus different co-contraction levels, that can produce similar movement kinematics from which the CNS must select one. Although signal-dependent noise (SDN) predicts larger motor-command variability during higher co-contraction, the relationship between impedance and task performance is not theoretically obvious and thus was examined here. Subjects made goal-directed, single-joint elbow movements to either move naturally to different target sizes or voluntarily co-contract at different levels. Stiffness was estimated as the weighted summation of rectified EMG signals through the index of muscle co-contraction around the joint (IMCJ) proposed previously. When subjects made movements to targets of different sizes, IMCJ increased with the accuracy requirements, leading to reduced endpoint deviations. Therefore without the need for great accuracy, subjects accepted worse performance with lower co-contraction. When subjects were asked to increase co-contraction, the variability of EMG and torque both increased, suggesting that noise in the neuromotor command increased with muscle activation. In contrast, the final positional error was smallest for the highest IMCJ level. Although co-contraction increases the motor-command noise, the effect of this noise on the task performance is reduced. Subjects were able to regulate their impedance and control endpoint variance as the task requirements changed, and they did not voluntarily select the high impedance that generated the minimum endpoint error. These data contradict predictions of the SDN-based theory, which postulates minimization of only endpoint variance and thus require its revision.