Cardiovascular diseases represent one of the most notable health problems of the modern civilization. Stroke and heart attack often lead to lethal outcome; essential problem underneath being thrombus formation. Prophylactic approaches include acetylsalicylic acid and clopidogrel therapy on the level of primary hemostasis, i.e., primary clot formation. In the last five years, in the USA, health care expenses related to cardiovascular diseases have increased 50 %, to over 350 billion dollars. Thus, application of plant species and medicinal plants rich in polyphenols in prevention of thrombus formation are of interest. This is supported by the fact that the number of publications on antiaggregatory effect of polyphenols has doubled in the last decade. In this review we focus on antiaggregatory effect of most abundant polyphenols – flavonoids, the effect of plant extracts rich in polyphenols (propolis, species Salvia sp., Calamintha nepeta L., Lavandula angustifolia Mill., Melissa officinalis L, Mentha x piperita L., Ocimum basilicum L., Origanum vulgare L., Rosmarinus officinalis L.) on platelet aggregation, association of chemical composition and antioxidant properties with the observed biological effect, and possible clinical significance of the published results.

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Inflationary mechanisms for generating primordial fluctuations ultimately compute them as the leading contributions in a derivative expansion, with corrections controlled by powers of derivatives like the Hubble scale over Planck mass: H/Mp. At face value this derivative expansion breaks down for models with a small sound speed, cs, to the extent that cs ≪ 1 is obtained by having higher-derivative interactions like Leff ∼ (∂ Φ)4 compete with lower-derivative propagation. This concern arises more generally for models whose lagrangian is given as a function P(X) for X = −∂μ Φ ∂μ Φ—including in particular DBI models for which P(X) ∝ √1−kX—since these keep all orders in ∂ Φ while dropping ∂n Φ for n > 1. We here find a sensible power-counting scheme for DBI models that gives a controlled expansion in powers of three types of small parameters: H/Mp, slow-roll parameters (possibly) and cs ≪ 1. We do not find a similar expansion framework for generic small-cs or P(X) models. Our power-counting result quantifies the theoretical error for any prediction (such as for inflationary correlation functions) by fixing the leading power of these small parameters that is dropped when not computing all graphs (such as by restricting to the classical approximation); a prerequisite for meaningful comparisons with observations. The new power-counting regime arises because small cs alters the kinematics of free fluctuations in a way that changes how interactions scale at low energies, in particular allowing 1−cs to be larger than derivative-measuring quantities like (H/Mp)2.

Dear Sir,The Rh blood group system is determined by the highly homologous RHD and RHCE genes located on the first chromosome, which encode for the RhD and RhCE polypeptides. D antigen is of special clinical relevance in the fields of transfusion medicine and obstetrics. Owing to its high immunogenicity, D antigen can induce the production of alloantibodies and thus cause posttransfusion haemolytic reaction and haemolytic disease of the newborn (Wagner et al., 2000).About 0·2-1% of the European population are carriers of structurally altered RHD alleles encoding for various types of weak D proteins. At the molecular level, point mutations resulting in amino acid substitutions in the intracellular or transmembranous segments of RhD protein are causing weak D phenotypes. More than 170 different RHD alleles closely related to the expression of the respective D phenotype, including more than 70 weak D types, have been discovered to date (Flegel, 2007). Some weak D types (types 1, 2 and 3) are not associated with the development of alloantibodies; however, alloimmunisation in weak D types 4·2, 11 and 15 carriers have been reported (Flegel, 2006). Owing to the extremely small phenotypic variation, particular weak D types are very difficult to differentiate by serology and can only be identified by molecular methods, thus enabling definitive decision on the mode of transfusion treatment and the need of anti-D prophylaxis in pregnant women. The individuals who are carriers of weak D types 1, 2 and 3 can receive transfusion of D+ red blood cell (RBC) units, although such pregnant women do not require anti-D prophylaxis. Thus, the unnecessary utilisation of D− RBC units and RhIg is avoided (Flegel and Wagner, 2002).Particular segments of the RHD gene sequence are multiplied by RHD genotyping using primers specific for the known mutations characterising particular weak D types by use of the polymerase chain reaction with sequence-specific priming (PCR-SSP). This procedure is employed to determine polymorphism of the weak D types.

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