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Objective: The Cold Intolerance Symptom Severity questionnaire (CISS) is a tool for measuring cold intolerance (CI) in patients with hand injuries. This consists of six questions (Q1-Q6); CI symptoms, frequency, duration, prevention measures, severity, and impact on daily activities. Q1 asks about the[for full text, please go to the a.m. URL], 14th Triennial Congress of the International Federation of Societies for Surgery of the Hand (IFSSH), 11th Triennial Congress of the International Federation of Societies for Hand Therapy (IFSHT), 11th Triennial Congress of the International Federation of Societies for Hand Therapy (IFSHT)

Objective: After digital replantation, patients frequently stop using the replanted digit in their activities of daily living (ADL). The purpose of this study was to investigate the non-use rate of replanted digits in ADL. Materials and Methods: This study included 30 fingers in 28 patients treated[for full text, please go to the a.m. URL], 14th Triennial Congress of the International Federation of Societies for Surgery of the Hand (IFSSH), 11th Triennial Congress of the International Federation of Societies for Hand Therapy (IFSHT), 11th Triennial Congress of the International Federation of Societies for Hand Therapy (IFSHT)

The distorted kagome lattice antiferromagnet Tb3Ru4Al12 with a hexagonal structure has the Néel temperature TN = 22 K. To clarify the 4 f -electronic state and an influence of electric quadrupoles in Tb3Ru4Al12, ultrasonic measurements on a single-crystalline sample at zero magnetic field and under fields were carried. A characteristic elastic softening of the transverse modulus C66 originating from a quadrupole interaction was found. The crystal electric field parameters were determined to reproduce C66, magnetic susceptibilities, and magnetization curves. The obtained level scheme is that the ground and first excited states are singlets, despite the existence of both the magnetic transition and the quadrupole interaction, indicating that Tb3Ru4Al12 is a curious compound. The positive sign of the quadrupole-quadrupole coupling constant for C66 indicates a ferroquadrupolar-type interaction of the electric quadrupole Oxy or O2. The anisotropic magnetic field dependencies of TN in the field along [100] and [001] were also clarified.

We report on the magnetic and elastic properties of Er3Ru4Al12 in static and pulsed magnetic fields up to 58 T. From the ultrasound results, we obtain evidence for a phase transition at 2 K related to magnetic ordering. Furthermore, in the paramagnetic state, Er3Ru4Al12 shows pronounced anomalies in the magnetization and elastic moduli as a function of temperature and magnetic field. We explain our findings using a crystal-electricfield (CEF) model that includes quadrupolar interactions and propose a CEF level scheme for this material. However, the CEF effects cannot explain all field-induced anomalies, which indicates that refined models are needed for explaining these.

The contact width is important design parameter for optimizing the design of new metal gasket for asbestos substitution gasket. The contact width is found have relationship with the helium leak quantity. In the increasing of axial load value, the helium leak quantity is decreasing and the contact width is increasing. This study provides validity method using simulation analysis and the result is compared to experimental using pressure sensitive paper. The results denote similar trend data between simulation and experimental result. Final evaluation is determined by helium leak quantity to check leakage performance of gasket design. Considering the phenomena of position change on the convex contact, it can be developed the optimization of gasket design by increasing contact width., {"references":["Saeed, H.A, Izumi S., Sakai S., Haruyama S., Nagawa M., Noda H.,\n\"Development of New Metallic Gasket and its Optimum Design for\nLeakage Performance\", Journal of Solid Mechanics and Material\nEngineering, Vol. 2, No. 1, pp.105-114, 2008.","Haruyama S., Choiron M.A, Kaminishi K., \"A Study of Design Standard\nand Performance Evaluation on New Metallic Gasket\", Proceeding the\n2nd International Symposium on Digital Manufacturing, Wuhan China,\npp. 107-113, 2009.","C.Y. Lee, C.S. Lin, R.Q. Jian, C.Y. Wen, \"Simulation and\nexperimentation on the contact width and pressure distribution of lip\nseals\", Tribology International Vol. 39, pp. 915-920, 2006.","JIS B2404, Dimensions of gaskets for use with the pipe flanges, Japanese\nStandards Association, 2006.","JIS Z2241, Method of tensile test for metallic materials, Japanese\nStandards Association, 1998.","Pressure measuring film-FUJI prescale film instruction manual.","MSC Marc 2007. User manual.","JIS Z2330, Standard recommended guide for the selection of helium leak\ntesting, Japanese Standards Association, 1992.","JIS Z2331, Method of helium leak testing, Japanese Standards\nAssociation, 2006.\n[10] JIS B2220, Steel pipe flanges, Japanese Standards Association, 2004."]}

We have characterized a murine IgG monoclonal antibody, OP-G2, specific for platelet glycoprotein (GP) IIb-IIIa (alpha IIb beta 3). OP-G2 Fab fragments inhibit fibrinogen-mediated platelet aggregation and competitively inhibit adenosine diphosphate-induced binding of 125I- fibrinogen to washed platelets. OP-G2 binding to GPIIb-IIIa is specifically inhibited by RGD-containing peptides but not the fibrinogen gamma-chain carboxy-terminal peptide, and OP-G2 Fab fragments, like RGD-containing peptides, alter the conformation of GPIIb-IIIa resulting in the expression of a ligand-induced binding site (LIBS) recognized by PMI-1. OP-G2 fails to bind to the recombinant Cam variant of GPIIb-IIIa (alpha III beta 3Cam) wherein an Asp119 to Tyr119 substitution in GPIIIa abrogates the ability to recognize RGD. These data indicate that OP-G2 recognizes an epitope at or in very close proximity to the RGD recognition site of GPIIb-IIIa and that, in every aspect tested, OP-G2 behaves like a macromolecular RGD ligand. Interestingly, two-color flow cytometry shows that OP-G2 IgG can bind to nonactivated platelets. Quantitative binding assays indicate that nonactivated platelets bind approximately 50,000 125I-OP-G2 molecules/platelet. Furthermore, the affinity of OP-G2 for platelets activated with thrombin is roughly fivefold higher (nonactivated, kd = 24.8 nmol/L; activated, kd = 4.9 nmol/L). These results suggest that the RGD recognition site of GPIIb-IIIa is available to macromolecules that contain RGD even on nonactivated platelets, provided that the affinity of the ligand is adequate.

We analyze the lightcurve of the microlensing event OGLE-2003-BLG-175/MOA-2003-BLG-45 and show that it has two properties that, when combined with future high resolution astrometry, could lead to a direct, accurate measurement of the lens mass. First, the lightcurve shows clear signs of distortion due to the Earth's accelerated motion, which yields a measurement of the projected Einstein radius \tilde r_E. Second, from precise astrometric measurements, we show that the blended light in the event is coincident with the microlensed source to within about 15 mas. This argues strongly that this blended light is the lens and hence opens the possibility of directly measuring the lens-source relative proper motion \vec\mu_\rel and so the mass M=(c^2/4G)\mu_\rel t_E \tilde r_E, where t_E is the measured Einstein timescale. While the lightcurve-based measurement of \tilde r_E is, by itself, severely degenerate, we show that this degeneracy can be completely resolved by measuring the direction of proper motion \vec\mu_\rel., Comment: 28 pages including 7 figures. Submitted to ApJ

The platelet integrin IIbbeta3 has become a new target for the treatment of pathological thrombosis. It becomes apparent that the affinity of IIbbeta3 for its ligands is dynamically regulated by inside-out signaling. However, the components that couple diverse intracellular signals to the cytoplasmic domains of IIbbeta3 remain obscure. Employing a chymotrypsin-induced IIbbeta3 activation model, we previously proposed the hypothesis that Na+/Ca2 + exchanger (NCX) may be involved in inside-out signaling (Shiraga et al: Blood 88:2594, 1996). In the present study, employing two unrelated Na+/Ca2+ exchange inhibitors, 3',4'-dichlorobenzamil (DCB) and bepridil, we investigated the role of NCX in platelet activation induced by various agonists in detail. Both inhibitors abolished platelet aggregation induced by all agonists examined via the inhibition of IIbbeta3 activation. Moreover, these inhibitors abolished IIbbeta3 activation induced by phorbol 12-myristate 13-acetate or A23187. On the other hand, neither of these inhibitors showed apparent inhibitory effects on protein phosphorylation of pleckstrin or myosin light chain, or an increase in intracellular calcium ion concentrations evoked by 0.1 U/mL thrombin. These effects of the NCX inhibitors are in striking contrast to those of protein kinase C inhibitor, Ro31-8220. Biochemical and ultrastructural analyses showed that NCX inhibitors, particularly DCB, made platelets "thrombasthenic". These findings suggest that the NCX is involved in the common steps of inside-out signaling through integrin IIbbeta3.

To clarify a molecular defect responsible for moderate alphaIIb beta3 deficiency, we examined two unrelated patients, MT and MS, suffering from type II and type I Glanzmann thrombasthenia (GT), respectively. Sequence analysis of polymerase chain reaction (PCR) fragments derived from platelet mRNA showed a single A--C substitution at nucleotide (nt) 2334 leading to a Gln747--Pro in alphaIIb in both patients. Allele-specific restriction enzyme analysis (ASRA) of genomic DNA demonstrated that patient MT was homozygous for the Gln747--Pro substitution and patient MS was compound heterozygous for this substitution and for an RNA splice mutation at the consensus sequence of the splice acceptor site of exon 18 (AG--AA). Furthermore, ASRA showed that, among 17 unrelated Japanese GT patients, this Gln747--Pro substitution was detected in 4 patients, including MT and MS (homozygous, 2 patients; heterozygous, 2 patients). Cotransfection of Pro747alphaIIb and beta3 constructs into 293 cells resulted in moderate reduction in the amount of alphaIIb beta3 within the transfected cells as well as on the cell surface. However, Pro747alphaIIb beta3 bound the ligand mimetic monoclonal antibody (MoAb) PAC-1 after activation of alphaIIb beta3 by the MoAb PT25-2, suggesting that the mutant alphaIIb beta3 possesses the ligand-binding function. The association between the mutant proalphaIIb and beta3 was not disturbed. Surface labeling and pulse chase study showed that the Gln747--Pro substitution moderately impaired both intracellular transport of the alphaIIb beta3 heterodimers to the Golgi apparatus and endoproteolytic cleavage of proalphaIIb into heavy and light chains. By contrast, replacement of Gln747 with Ala by mutagenesis did not impair alphaIIbbeta3 expression on the cell surface. These results suggest that the presence of Pro, rather than the absence of Gln, at amino acid residue 747 on alphaIIb is responsible for moderate alphaIIbbeta3 deficiency.

In the present study, we have investigated the mechanism of affinity modulation of alpha IIb beta 3 by chymotrypsin. We first confirmed that alpha-chymotrypsin could activate alpha IIb beta 3 (approximately 7,000 molecules per platelet) without major intracellular signaling. However, we unexpectedly found that high concentrations of amiloride dose-dependently inhibited 125I-fibrinogen binding to the chymotrypsin-treated platelets, as well as the platelet aggregation (IC50 [50% inhibitory concentration] for fibrinogen binding, 530 mumol/L). In contrast, amiloride did not inhibit alpha IIb beta 3 activation induced by anti-alpha IIb beta 3 monoclonal antibody PT25-2 or AP5. To identify the pathway involved, the effects of alteration of Na+ gradient in platelets were examined. Lowering Na+ gradient by replacing extracellular Na+ with tetramethylammonium (TMA) increased the number of activated alpha IIb beta 3 by twofold, as assessed by fibrinogen-binding assay. The incubation of platelets with ouabain, a Na+/K(+)-adenosine triphosphatase (ATPase) inhibitor, further augmented alpha IIb beta 3 activation. These data suggested that a likely candidate for the pathway was Na+/Ca2+ exchanger. At 140 mmol/L [Na+]o, 45Ca2+ influx to the chymotrypsin-treated platelets was twofold greater than that to non-treated platelets. Replacement of Na+ with TMA further increased the Ca2+ influx, and the increase was inhibited by amiloride dose-dependently. 3',4'-Dichlorobenzamil (DCB) and bepridil, relatively specific inhibitors of Na+/Ca2+ exchanger, also inhibited the chymotrypsin-induced alpha IIb beta 3 activation, and the IC50 values of these inhibitors for fibrinogen binding were 25 mumol/L and 52 mumol/L, respectively. Moreover, platelet aggregation induced by various physiologic agonists was inhibited by DCB or bepridil, while platelet agglutination by ristocetin was not. Our data newly suggest that Na+/Ca2+ exchanger operating in reverse mode may be directly involved in inside-out signaling that activates alpha IIb beta 3.