Effects of body mass index and full body kinematics on tennis serve speed.

Effective training to improve serve speed is important for competitive tennis players. The purposes of this study were to investigate the effects of anthropometric factors and whole body kinematics of elite players on ball speed and to propose possible training strategies for improving the quality of tennis serves. Body and racket kinematics of tennis serves of 12 male elite Hong Kong players were investigated. The tennis serve was divided into four phases: I) Back-Swing Phase, II) Lead-Leg-Drive Phase, III) Forward-Swing Phase, and IV) Follow-Through Phase. It was shown that racket-side knee range of motion during phases II and III (r=0.705; p<0.05), racket-side knee peak extension velocity during phase II (r=0.751; p<0.01), racket-side hip peak extension velocity during phase II (r=0.657; p<0.05), racket-side shoulder range of motion in the coronal plane during phase III (r=0.616; p<0.05), racket-side elbow peak extension velocity during phase III (r=0.708; p<0.01) and body mass index (r=0.577; p<0.05) were significantly correlated with ball speed. Body mass index and the identified kinematic parameters that were significantly correlated with ball speed could be used as training guidelines for coaches and players to improve serve speed. Players should pay particular attention in training to increasing the extension velocity and range of motion of the identified joints.

An image feature approach for computer-aided detection of ischemic stroke.

We present a computer-aided detection (CAD) scheme for early detection of ischemic stroke with small lesions using image feature characteristics. A novel Circular Adaptive Region of Interest (CAROI) method is proposed to analyze the Computed Tomography (CT) images of the brain. Our result indicates that for the emergency physicians and radiology residents, there is a significant improvement in sensitivity and specificity when using CAD (P < 0.005). A mathematical model is established incorporating the weighting of the feature changes. Our CAD scheme is promising for early detection of ischemic stroke and helps improve the efficiency and accuracy of clinical practice.

Elevated platelet angiostatin and circulating endothelial microfragments in idiopathic pulmonary arterial hypertension: a preliminary study.

INTRODUCTION: Idiopathic pulmonary arterial hypertension (IPAH) is characterized by pulmonary arteriolar narrowing and degeneration associated with in situ thrombosis. We hypothesized that microvascular endothelial injury and apoptosis may be an initiating mechanism in IPAH. Endothelial apoptosis generates endothelial microfragments (EMF), which can activate platelets. Platelets release both VEGF and angiostatin, which depending the balance can inhibit or induce endothelial apoptosis, respectively. MATERIALS AND METHODS: We measured EMFs from blood of IPAH patients as index of endothelial cell apoptosis/injury and levels of pro- and anti- EC apoptotic factors found in platelets. EMFs and platelets in blood samples from control subjects and patients with IPAH were measured using a 4-color flow cytometry protocol, and platelet levels of VEGF and angiostatin were determined by ELISAs and immunoblotting. RESULTS: Compared to controls, IPAH patients exhibited higher numbers of circulating EMFs and more activated/apoptotic platelets. IPAH patients also exhibited higher levels of platelet angiostatin; however, no significant difference was detected in platelet VEGF levels between the two groups. CONCLUSIONS: These results are consistent with an increase in EC dysfunction in patients with IPAH, possibly contributing to the progression of IPAH and its associated thrombosis.

A semi-quantitative approach to compare high-sensitivity power Doppler sonography and conventional power Doppler sonography in the assessment of thyroid vascularity.

BACKGROUND: Ultrasound is a useful imaging tool in the assessment of thyroid glands, and Doppler ultrasound helps in the evaluation of thyroid vascularity. This study was undertaken to evaluate the difference in the thyroid vascularity demonstrated on the state-of-the-art high-sensitivity power Doppler sonography (HSPDS) and the conventional power Doppler sonography (PDS), and to investigate the feasibility of using a customized algorithm with image-processing software for semi-quantitative assessment of thyroid vascularity. METHODS: A total of 25 healthy volunteers were included in the study, and each subject had two thyroid ultrasound examinations with HSPDS and PDS, respectively. High sensitivity and conventional power Doppler sonograms of the thyroid glands were taken and recorded. To evaluate the vascularity of thyroid lobes quantitatively, a customized algorithm using the software Matlab was developed and used to analyze the ultrasound images. The vascularity of thyroid lobe (i.e., region of interest, ROI) was expressed as the vascular index (VI), which is the ratio of the number of color pixels to the total number of pixels within the ROI. RESULTS: Results showed that thyroid vascularity was detected in all thyroid lobes on both HSPDS and PDS. The mean VI of the thyroid lobes on HSPDS (right lobe, 0.31 +/- 0.08; left lobe, 0.32 +/- 0.07) was significantly higher than on PDS (right lobe, 0.18 +/- 0.09; left lobe, 0.16 +/- 0.08) (p < 0.05). There was no significant difference in the VI between the right and left thyroid lobes (p >0.05). On HSPDS, 96% of the thyroid lobes showed a VI <0.5, while 96% of thyroid lobes had a VI <0.3 on PDS. CONCLUSIONS: HSPDS is more sensitive than PDS in the detection of thyroid vascularity. The developed algorithm can quantify the color pixels on power Doppler sonograms, which is useful for objective assessment of thyroid vascularity.

Preferential association of serum amyloid P component with fibrillar deposits in familial British and Danish dementias: similarities with Alzheimer's disease.

Two hereditary forms of cerebrovascular amyloidosis, familial British and Danish dementias (FBD and FDD), share striking similarities with Alzheimer's disease (AD) despite structural differences among their amyloid subunits (ABri in FBD, ADan in FDD, and Abeta in AD). Neuropathological lesions in these disorders include neurofibrillary tangles, parenchymal amyloid and pre-amyloid deposits and overwhelming cerebral amyloid angiopathy co-localizing with reactive microglia and multiple amyloid associated proteins including activation products of the complement cascade. Immunohistochemical analysis of FBD and FDD brain lesions unveiled the presence of serum amyloid P-component (SAP) primarily associated with thioflavin positive amyloid deposits in spite of the significant pre-amyloid burden existing in both disorders. Using affinity chromatography and ELISA binding assays we demonstrated specific, calcium-dependent, saturable, high affinity binding interactions between SAP and ABri/ADan peptides, with dissociation constant values in the sub-nanomolar range and within the same order of magnitude as those resulting from the interaction of SAP with Alzheimer's Abeta1-40 and Abeta1-42. The preferential association of SAP with fibrillar amyloid lesions and not with non-fibrillar pre-amyloid deposits is puzzling, suggesting that SAP modulates the assembly and stability of the final fibril rather than participating in the early steps of protein misfolding and oligomerization.

Amyloid ion channels: a common structural link for protein-misfolding disease.

Protein conformational diseases, including Alzheimer's, Huntington's, and Parkinson's diseases, result from protein misfolding, giving a distinct fibrillar feature termed amyloid. Recent studies show that only the globular (not fibrillar) conformation of amyloid proteins is sufficient to induce cellular pathophysiology. However, the 3D structural conformations of these globular structures, a key missing link in designing effective prevention and treatment, remain undefined as of yet. By using atomic force microscopy, circular dichroism, gel electrophoresis, and electrophysiological recordings, we show here that an array of amyloid molecules, including amyloid-beta(1-40), alpha-synuclein, ABri, ADan, serum amyloid A, and amylin undergo supramolecular conformational change. In reconstituted membranes, they form morphologically compatible ion-channel-like structures and elicit single ion-channel currents. These ion channels would destabilize cellular ionic homeostasis and hence induce cell pathophysiology and degeneration in amyloid diseases.

Systemic catabolism of Alzheimer's Abeta40 and Abeta42.

To better understand the physiologic excretion and/or catabolism of circulating peripheral amyloid beta (Abeta), we labeled human Abeta40 (monomeric, with predominant unordered structure) and Abeta42 (mixture of monomers and oligomers in approximately 50:50 ratio, rich in beta-sheet conformation) with either Na(125)I or (125)I-tyramine cellobiose, also known as the cell-trapping ligand procedure, testing their blood clearance and organ uptake in B6SJLF1/J mice. Irrespective of the labeling protocol, the peptide conformation, and the degree of oligomerization, both Abeta40 and Abeta42 showed a short half-life of 2.5-3.0 min. The liver was the major organ responsible for plasma clearance, accounting for >60% of the peptide uptake, followed by the kidney. In vivo, hepatocytes captured >90% of the radiolabeled peptides which, after endocytosis, were preferentially catabolized and excreted into the bile. Biliary excretion of intact as well as partially degraded Abeta species became obviously relevant at doses above 10 microg. The use of biotin-labeled Abeta allowed the visualization of the interaction with HepG2 cells in culture, whereas competitive inhibition experiments with unlabeled Abeta demonstrated the specificity of the binding. The capability of the liver to uptake, catabolize, and excrete large doses of Abeta, several orders of magnitude above its physiologic concentration, may explain not only the femtomolar plasma levels of Abeta but the little fluctuation observed with age and disease stages.

Protective role of angiopoietin-1 in experimental pulmonary hypertension.

Angiopoietin-1 (Ang-1), a newly discovered ligand of the endothelial-specific tyrosine kinase receptor Tie-2, has been found to promote cell survival, vascular maturation, and stabilization. We hypothesized that Ang-1 gene transfer to the pulmonary microcirculation would improve pulmonary hemodynamics and vascular remodeling in experimental pulmonary hypertension. Rat pulmonary artery smooth muscle cells were transfected with Ang-1 cDNA or null (pFLAG-CMV-1) vector. Syngeneic Fisher 344 rats were treated with monocrotaline (MCT) (75 mg/kg IP) with or without delivery of 5x10(5) Ang-1-transfected cells into the right jugular vein. After 28 days, plasmid-derived Ang-1 mRNA was consistently and robustly detected by reverse transcriptase-polymerase chain reaction in lungs from all animals receiving Ang-1 gene therapy. Tie-2 receptor expression was markedly downregulated in rats treated with MCT, and this was partially restored by gene therapy with Ang-1. Animals receiving MCT exhibited 77% mortality by 28 days. In contrast, in pAng-1-treated animals, the 28-day mortality was only 14% (P<0.0001). In addition, right ventricular systolic pressure was reduced from 52+/-1.3 mm Hg in the MCT-treated group to 38+/-1.3 mm Hg by Ang-1 gene transfer (P<0.01), whereas the measurement of right to left ventricular plus septal weight ratio was also reduced from 0.41+/-0.03 to 0.31+/-0.01 (P<0.05). Moreover, MCT resulted in increased apoptosis, mainly in the microvasculature, and reduced endothelial NO synthase mRNA expression, both of which were prevented by Ang-1 gene transfer. Thus, cell-based gene transfer with Ang-1 improved survival and pulmonary hemodynamics in experimental pulmonary hypertension by a mechanism involving the inhibition of apoptosis and protection of the pulmonary microvasculature.