Head–torso–hand coordination in children with and without developmental coordination disorder

Aim This study investigated the nature of coordination and control problems in children with developmental coordination disorder (DCD). Method Seven adults (two males, five females, age range 20–28y; mean 23y, SD 2y 8mo) and eight children with DCD (six males, two females, age range 7–9y; mean 8y, SD 8mo), and 10 without DCD (seven males, three females, age range 7–9y; mean 8y, SD 7mo) sat in a swivel chair and looked at or pointed to targets. Optoelectronic apparatus recorded head, torso, and hand movements, and the spatial and temporal characteristics of the movements were computed. Results Head movement times were longer (p<0.05) in children with DCD than in the comparison group, even in the looking task, suggesting that these children experience problems at the lowest level of coordination (the coupling of synergistic muscle groups within a single degree of freedom). Increasing the task demands with the pointing condition affected the performance of children with DCD to a much greater extent than the other groups, most noticeably in key feedforward kinematic landmarks. Temporal coordination data indicated that all three groups attempted to produce similar movement patterns to each other, but that the children with DCD were much less successful than age‐matched children in the comparison group. Interpretation Children with DCD have difficulty coordinating and controlling single degree‐of‐freedom movements; this problem makes more complex tasks disproportionately difficult for them. Quantitative analysis of kinematics provides key insights into the nature of the problems faced by children with DCD.     

Modeling the direction of causation between cross‐sectional measures of disrupted sleep,anxiety and depression in a sample of male and female Australian twins

The direction of causation between measures of disrupted sleep, anxiety and depression is not well understood. Under certain conditions, cross‐sectional analysis based on genetically informative data can provide important information about the direction of causation between variables. Two community‐based samples of 7235 Australian twins aged 18–87 years were mailed an extensive questionnaire that covered a wide range of personality and behavioral measures. Included were self‐report measures of disrupted sleep, as well as symptoms of anxiety and depression. Among all females, modeling the direction of causation did not support the hypothesis of sleep having a direct causal impact on risk of anxiety or depression. Among older females, we found evidence that both anxiety and depression interact reciprocally with disrupted sleep, whereas among younger women both anxiety and depression appear to have a causal impact on sleep. Results for males were equivocal. The nosological implications of our findings are discussed.     

Purified A2 domain of von Willebrand factor binds to the active conformation of von Willebrand factor and blocks the interaction with platelet glycoprotein Ibα

BACKGROUND: von Willebrand factor (VWF) does not interact with circulating platelets unless it is induced to expose the binding site for platelet glycoprotein (GP)Ibalpha in the A1 domain by high shear stress, immobilization, and/or a modulator. Previous studies have implied indirectly that the A2 domain may be involved in regulating A1-GPIbalpha binding. OBJECTIVE AND METHODS: Because the relationship between the A1 and A2 domains has not been defined, we have investigated the effect of the A2 domain on the binding activity of the A1 domain using recombinant A domain polypeptides, multimeric VWF, and monoclonal antibodies (mAb). RESULTS: The A2 domain polypeptide bound specifically to the immobilized A1 domain polypeptide or full-length VWF, with half-maximal binding being obtained at 60 or 168 nm, respectively. This A1-A2 interaction was inhibited by mAb against the A2 or A1 domain and by the A1 domain polypeptide. The A2 domain polypeptide effectively blocked GPIbalpha-mediated platelet adhesion under high flow conditions. The A2 domain polypeptide specifically recognizes the GPIbalpha-binding conformation in the A1 domain, as it only interacted with VWF activated by the modulator ristocetin or immobilized VWF. Furthermore, in contrast to plasma VWF, the ultra-large (UL)VWF multimers or a recombinant VWF-A1A2A3 polypeptide containing a gain-of-function mutation (R1308 L) of type 2B von Willebrand disease bound to the A2 domain polypeptide without the need for ristocetin. CONCLUSIONS: The recombinant A2 domain polypeptide specifically binds to the active conformation of the A1 domain in VWF and effectively blocks the interaction with platelet GPIbalpha under high-flow conditions.     

Simultaneous Assessment of Coronary Flow Reserve and Fractional Flow Reserve with a Novel Pressure-Based Method

Coronary flow reserve (CFR) and fractional flow reserve (FFR_myo) are two guidewire‐based methods currently used to assess the functional severity of coronary artery lesions. Acquiring both measurements simultaneously may provide complementary information, but would require the passage of two different guidewires and complex instrumentation for their calculation. This study assessed the procedural safety and performance of a novel personal computer‐based algorithm, the SmartFlow Intravascular Processor (SFIP), which utilizes a single conventional pressure wire for obtaining simultaneous CFR and FFR_myo measurements for the assessment of coronary artery lesion severity. In 20 consecutive patients with 21 lesions, pressure‐derived CFR, FFR_myo and SFIP‐FFR_myo measurements were obtained during adenosine‐induced hyperemia. Intravascular ultrasound and quantitative coronary angiography lesion analysis was done off‐line at the Washington Core Laboratory. Mean FFR_myo was 0.83 ± 0.11, SFIP‐FFR_myo was 0.86 ± 0.06, and CFR was 1.74 ± 0.46. Pairwise correlation analysis showed excellent correlation between the FFR_myo and the FFR_myo‐SFIP (r²= 0.83, P < 0.0001) and a fair degree of relationship between the CFR and minimal lumen diameter (r²= 0.43, P = 0.07). We could not find a correlation between CFR and FFR_myo (r²= 0.22, P = 0.37), between CFR and FFR‐SFIP (r²= 0.05, P = 0.86), or between the hemodynamic measurements and any of the IVUS‐derived measurements. In conclusion, the SFIP is u novel algorithm for obtaining simultaneous CFR and FFR_myo that may provide valuable information for the assessment of lesion severity and clinical decision making.     

The porcine bronchial artery. Anastomoses with oesophageal, coronary and intercostal arteries

Information abut the existence and anatomy of arterial anastomoses with the porcine bronchial artery is lacking in the literature. Prior to basic physiological investigations in a porcine model related to lung transplantation with bronchial artery revascularisation, this study was designed to examine the anatomy of systemic arterial anastomoses with the bronchial artery system. Twenty pigs were studied in 3 groups. In 2 groups the heart–lung block was removed with all mediastinal structures. One group served for investigation of coronary–bronchial artery anastomoses and one for investigation of oesophageal–bronchial artery anastomoses. The systemic arteries to be examined were cannulated. The inflated heart–lung block was examined macroscopically with Evans blue, and radiographically after contrast injection. In the 3rd group intercostobronchial artery anastomoses were studied radiographically with the heart–lung block in situ. Coronary–bronchial artery anastomoses were demonstrated in 3 of the 5 pigs with an aortic 'pouch' technique, but contrast was very limited in 2 of these 3. Oesophageal arterial anastomoses with bronchial arterial branches and/or the pulmonary veins were demonstrated in 6 of the 7 pigs and more markedly than the coronary–bronchial anastomoses. Intercostobronchial artery anastomoses could not be demonstrated angiographically. It was concluded that the existence of coronary–bronchial and oesophageal–bronchial artery anastomoses in the pig appear to establish an arterial net between the base of the heart and the distal oesophagus. The resemblance to human oesophageal–bronchial artery anastomoses supports use of a porcine model for experimental studies.