Molar mass dispersity in polymers affects a wide range of important material properties, yet there are few synthetic methods that systematically generate unimodal distributions with specifically tailored dispersities. Here, we describe a general method for tuning the dispersity of polymers synthesized via atom transfer radical polymerization (ATRP). Addition of varying amounts of phenylhydrazine (PH) to the ATRP of tert -butyl acrylate led to significant deviations in the reaction kinetics, yielding poly( tert -butyl acrylate) with dispersities = 1.08-1.80. ATRP reactions in the presence of the reducing agent tin( ii ) 2-ethylhexanoate, under otherwise comparable reaction conditions, did not drive similar increases in dispersity. We therefore deduced that PH does not function primarily as a reducing agent in these syntheses. Nuclear magnetic resonance analyses revealed the incorporation of aromatic polymer end-groups upon PH addition, suggesting that the ATRP-active halide termini of the growing polymer chains underwent irreversible nucleophilic substitution reactions with PH that led to chain termination. A kinetic model including this irreversible chain termination by PH was in excellent agreement with experimentally measured reaction kinetics. To demonstrate the generality of this approach, we conducted ATRP syntheses of polystyrene in the presence of PH to achieve dispersities of = 1.07-2.30. This study suggests that PH addition is an effective, facile, and flexible method of dispersity control in polymers synthesized by ATRP. Phenylhydrazine is an effective modifier for conventional ATRP syntheses, providing systematic control over the dispersity of polymers with unimodal molecular weight distributions.
Background: The notion that ADHD constitutes a heterogeneous disorder is well accepted. However, this study contributes with new important knowledge by examining independent effects of a large range of neuropsychological deficits. In addition, the study investigated whether deficits in emotional functioning constitute a dissociable component of ADHD. Method: The study included children with ADHD (n = 102; 7–13 years) and a control sample individually matched with regard to age and gender. The administered tasks were designed to tap into three different neuropsychological domains: executive functions (i.e., working memory, inhibition, and shifting), delay aversion, and reaction time variability. Parent ratings of emotion regulation and a test of emotion recognition were also included. Results: Children with ADHD differed significantly from controls on all measures, except for delay aversion and recognition of disgust. No main effects of gender or interaction effects of gender and group were found. More importantly, executive functioning, reaction time variability, and emotional functioning all contributed independently to distinguishing between children with ADHD and controls. Conclusions: The current study supports the view of ADHD as a heterogeneous disorder related to multiple neuropsychological deficits. In addition, emotional functioning appears to be an area of importance for ADHD that needs to be incorporated into future theoretical models.
Aldol reactions with trifluoroacetophenones as acceptors yield chiral α-aryl, α-trifluoromethyl tertiary alcohols, valuable intermediates in organic synthesis. Of the various organocatalysts examined, Singh’s catalyst [(2S)-N-[(1S)-1-hydroxydiphenylmethyl-3-methylbutyl]-2-pyrrolidinecarboxamide] was found to efficiently promote this organocatalytic transformation in a highly enantioselective manner. Detailed reaction monitoring (19F-NMR, HPLC) showed that, up to full conversion, the catalytic transformation proceeds under kinetic control and affords up to 95% ee in a time-independent manner. At longer reaction times, the catalyst effects racemization. For the product aldols, even weak acids (such as ammonium chloride) or protic solvents, can induce racemization, too. Thus, acid-free workup, at carefully chosen reaction time, is crucial for the isolation of the aldols in high (and stable) enantiomeric purity. As evidenced by 19F-NMR, X-ray structural analysis, and independent synthesis of a stable intramolecular variant, Singh’s catalyst reversibly forms a catalytically inactive (“parasitic”) intermediate, namely a N,O-hemiacetal with trifluoroacetophenones. X-ray crystallography also allowed the determination of the product aldols’ absolute configuration (S).
Abstract Objective To determine whether physical activity may affect cognitive performance in patients with Parkinson's disease by measuring reaction times in patients participating in the Berlin BIG study. Design Randomized controlled trial, rater-blinded. Setting Ambulatory care. Participants Patients with mild to moderate Parkinson's disease (N=60) were randomly allocated to 3 treatment arms. Outcome was measured at the termination of training and at follow-up 16 weeks after baseline in 58 patients (completers). Interventions Patients received 16 hours of individual Lee Silverman Voice Treatment-BIG training (BIG; duration of treatment, 4wk), 16 hours of group training with Nordic Walking (WALK; duration of treatment, 8wk), or nonsupervised domestic exercise (HOME; duration of instruction, 1hr). Main Outcome Measures Cued reaction time (cRT) and noncued reaction time (nRT). Results Differences between treatment groups in improvement in reaction times from baseline to intermediate and baseline to follow-up assessments were observed for cRT but not for nRT. Pairwise t test comparisons revealed differences in change in cRT at both measurements between BIG and HOME groups (intermediate: −52ms; 95% confidence interval [CI], −84/−20; P =.002; follow-up: 55ms; CI, −105/−6; P =.030) and between WALK and HOME groups (intermediate: −61ms; CI, −120/−2; P =.042; follow-up: −78ms; CI, −136/−20; P =.010). There was no difference between BIG and WALK groups (intermediate: 9ms; CI, −49/67; P =.742; follow-up: 23ms; CI, −27/72; P =.361). Conclusion Supervised physical exercise with Lee Silverman Voice Treatment-BIG or Nordic Walking is associated with improvement in cognitive aspects of movement preparation.
Background Minimal hepatic encephalopathy (MHE) is clinically undetectable and the diagnosis requires psychometric tests. However, a lack of clarity exists as to whether the tests are in fact able to detect changes in cognition. Aim To examine if the continuous reaction time test (CRT) can detect changes in cognition with anti-HE intervention in patients with cirrhosis and without clinically manifest hepatic encephalopathy (HE). Methods Firstly, we conducted a reproducibility analysis and secondly measured change in CRT induced by anti-HE treatment in a randomized controlled pilot study: We stratified 44 patients with liver cirrhosis and without clinically manifest HE according to a normal (n = 22) or abnormal (n = 22) CRT. Each stratum was then block randomized to receive multimodal anti-HE intervention (lactulose+branched-chain amino acids+rifaximin) or triple placebos for 3 months in a double-blinded fashion. The CRT is a simple PC-based test and the test result, the CRT index (normal threshold > 1.9), describes the patient's stability of alertness during the 10-minute test. Our study outcome was the change in CRT index in each group at study exit. The portosystemic encephalopathy (PSE) test, a paper-and-pencil test battery (normal threshold above -5), was used as a comparator test according to international guidelines. Results The patients with an abnormal CRT index who were randomized to receive the active intervention normalized or improved their CRT index (mean change 0.92 +/- 0.29, p = 0.01). Additionally, their PSE improved (change 3.85 +/- 1.83, p = 0.03). There was no such effect in any of the other study groups. Conclusion In this cohort of patients with liver cirrhosis and no manifest HE, the CRT identified a group in whom cognition improved with intensive anti-HE intervention. This finding infers that the CRT can detect a response to treatment and might help in selecting patients for treatment.
Manual and saccadic reaction times (SRTs) have been used to determine the minimum time required for different types of visual categorizations. Such studies have demonstrated extremely rapid detection of faces within natural scenes, whereas increasingly complex decisions (i.e. levels of processing) require longer processing times. We reasoned that visual categorization speed is not only dependent on the processing level, but is further affected by decisional space constraints. In the context of two different tasks, observers performed choice saccades towards female (gender categorization) or personally familiar (familiarity categorization) faces. Additionally, familiarity categorizations were completed with stimulus sets that differed in the number of individuals presented (3 vs. 7 identities) to investigate the effect of decisional space constraints. We observe an inverse relationship between visual categorization proficiency and decisional space. Observers were most accurate for categorization of gender, which could be achieved in as little as 140 ms. Categorization of highly predictable targets was more error-prone and required an additional ∼100 ms processing time. Our findings add to an increasing body of evidence demonstraing that pre-activation of identity-information can modulate early visual processing in a top-down manner. They also emphasize the importance of considering procedural aspects, as well as terminology when aiming to characterize cognitive processes.
The study of ion chemistry involving the NO2+ is currently the focus of considerable fundamental interest and is relevant in diverse fields ranging from mechanistic organic chemistry to atmospheric chemistry. A very intense source of NO2+ was generated by injecting the products from the dielectric barrier discharge of a nitrogen and oxygen mixture upstream into the drift tube of a proton transfer reaction time‐of‐flight mass spectrometry (PTR‐TOF‐MS) apparatus with H3O+ as the reagent ion. The NO2+ intensity is controllable and related to the dielectric barrier discharge operation conditions and ratio of oxygen to nitrogen. The purity of NO2+ can reach more than 99% after optimization. Using NO2+ as the chemical reagent ion, the gas‐phase reactions of NO2+ with 11 aromatic compounds were studied by PTR‐TOF‐MS. The reaction rate coefficients for these reactions were measured, and the product ions and their formation mechanisms were analyzed. All the samples reacted with NO2+ rapidly with reaction rate coefficients being close to the corresponding capture ones. In addition to electron transfer producing [M]+, oxygen ion transfer forming [MO]+, and 3‐body association forming [M·NO2]+, a new product ion [M−C]+ was also formed owing to the loss of C═O from [MO]+.This work not only developed a new chemical reagent ion NO2+ based on PTR‐MS but also provided significant interesting fundamental data on reactions involving aromatic compounds, which will probably broaden the applications of PTR‐MS to measure these compounds in the atmosphere in real time.
The stop-signal reaction-time (SSRT) task measures inhibition of a response that has already been initiated, that is, the ability to stop. Human subjects classified as "impulsive," for example, those with attention deficit and hyperactivity disorder, are slower to respond to the stop signal. Although functional and structural imaging studies in humans have implicated frontal and basal ganglia circuitry in the mediation of this form of response control, the precise roles of the cortex and basal ganglia in SSRT performance are far from understood. We describe effects of excitotoxic fiber-sparing lesions of the orbitofrontal cortex (OF), infralimbic cortex (IL), and subthalamic nucleus (STN) in rats performing a SSRT task. Lesions to the OF slowed SSRT, whereas lesions to the IL or the STN had no effect. On the go-signal trials, neither cortical lesion affected go-trial reaction time (GoRT), but STN lesions speeded such latencies. The STN lesion also significantly reduced accuracy of stopping at all stop-signal delays, indicative of a generalized stopping impairment that was independent of the SSRT itself.
Background: Docosahexaenoic acid (DHA) is important for brain function, and its status is dependent on dietary intakes. Therefore, individuals who consume diets low in omega-3 (n-3) polyunsaturated fatty acids may cognitively benefit from DHA supplementation. Sex and apolipoprotein E genotype (APOE) affect cognition and may modulate the response to DHA supplementation. Objectives: We investigated whether a DHA supplement improves cognitive performance in healthy young adults and whether sex and APOE modulate the response. Design: Healthy adults (n=176; age range: 18-45 y; nonsmoking and with a low intake of DHA) completed a 6-mo randomized, placebo-controlled, double-blind intervention in which they consumed 1.16 g DHA/d or a placebo. Cognitive performance was assessed by using a computerized cognitive test battery. For all tests, z scores were calculated and clustered into cognitive domains as follows: episodic and working memory, attention, reaction time (RT) of episodic and working memory, and attention and processing speed. ANCOVA was conducted with sex and APOE as independent variables. Results: RTs of episodic and working memory improved with DHA compared with placebo [mean difference (95% CI): -0.18 SD (-0.33, -0.03 SD) (P = 0.02) and -0.36 SD (-0.58, -0.14 SD) (P = 0.002), respectively]. Sex x treatment interactions occurred for episodic memory (P = 0.006) and the RT of working memory (P = 0.03). Compared with the placebo, DHA improved episodic memory in women [0.28 SD (0.08, 0.48 SD); P=0.006] and RTs of working memory in men [-0.60 SD (-0.95, -0.25 SD); P = 0.001]. APOE did not affect cognitive function, but there were some indications of APOE X sex X treatment interactions. Conclusions: DHA supplementation improved memory and the RT of memory in healthy, young adults whose habitual diets were low in DHA. The response was modulated by sex. This trial was registered at the New Zealand Clinical Trials Registry (http://www.anzctr.org.au/default.aspx) as ACTRN12610000212055. Am J Clinical Nutr 2013;97:1134-43.