Clot Waveform Analysis Demonstrates Low Blood Coagulation Ability in Patients with Idiopathic Thrombocytopenic Purpura

Background: Although platelets, which contain large amounts of phospholipids, play an important role in blood coagulation, there is still no routine assay to examine the effects of platelets in blood coagulation. Methods: Hemostatic abnormalities in patients with thrombocytopenia, including those with idiopathic thrombocytopenic purpura (ITP), were examined using clot wave analysis (CWA)–small-amount tissue-factor-induced FIX activation (sTF/FIXa) and thrombin time (TT). Results: Although there were no marked differences in the three parameters of activated partial thromboplastin time (APTT) between normal healthy volunteers and typical patients with ITP, the peak heights of the CWA-sTF/FIXa were markedly low in patients with ITP. The three peak times of the CWA-sTF/FIXa in patients with a platelet count of ≤8.0 × 1010/L were significantly longer than those in patients with a platelet count > 8.0 × 1010/L and the peak heights of the CWA-sTF/FIXa in patients with a platelet count of ≤8.0 × 1010/L were significantly lower than those in patients with >8.0 × 1010/L. The peak heights of the CWA-APTT in patients with ITP were significantly lower than in patients with other types of thrombocytopenia. The three peak heights of the CWA-sTF/FIXa in ITP patients were significantly lower than those in patients with other types of thrombocytopenia. The CWA-TT showed lower peak heights and longer peak times in patients with ITP in comparison to patients with other types of thrombocytopenia. Conclusions: The CWA-sTF/FIXa and CWA-TT results showed that blood coagulation is enhanced by platelets and that the blood coagulation ability in ITP patients was low in comparison to healthy volunteers and patients with other types of thrombocytopenia.

General Properties of Higher-Spin Fermion Interaction Currents and Their Test in πN-Scattering

The currents of higher-spin fermion interactions with zero- and half-spin particles are derived. They can be used for the N*(J) ↔ Nπ-transitions (N*(J) is thenucleon resonance with the J spin). In accordance with the theorem on currents and fields, the spin-tensors of these currents are traceless, and their products with the γ-matrices and the higher-spin fermion momentum vanish, similarly to the field spin-tensors. Such currents are derived explicitly for J=3/2and 5/2. It is shown that, in the present approach, the scale dimension of a higher spin fermion propagator equals to –1 for any J ≥ 1/2. The calculations indicate that the off-mass-shell N* contributions to the s-channel amplitudes correspond to J = JπN only ( JπN is the total angular momentum of the πN-system). As contrast, in the usually exploited approaches, such non-zero amplitudes correspond to 1/2 ≤ JπN ≤ J. In particular, the usually exploited approaches give non-zero off-mass-shell contributions of the ∆(1232)-resonance to the amplitudes S31, P31( JπN = 1/2) and P33, D33(JπN = 3/2), but our approach – to P33 and D33 only. The comparison of these results with the data of the partial wave analysis on the S31-amplitude in the ∆(1232)-region shows the better agreement for the present approach.

Travelling-wave analysis of a model of tumour invasion with degenerate, cross-dependent diffusion

In this paper, we carry out a travelling-wave analysis of a model of tumour invasion with degenerate, cross-dependent diffusion. We consider two types of invasive fronts of tumour tissue into extracellular matrix (ECM), which represents healthy tissue. These types differ according to whether the density of ECM far ahead of the wave front is maximal or not. In the former case, we use a shooting argument to prove that there exists a unique travelling-wave solution for any positive propagation speed. In the latter case, we further develop this argument to prove that there exists a unique travelling-wave solution for any propagation speed greater than or equal to a strictly positive minimal wave speed. Using a combination of analytical and numerical results, we conjecture that the minimal wave speed depends monotonically on the degradation rate of ECM by tumour cells and the ECM density far ahead of the front.