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Highlights: [•] Repeatability of rebound hammer test depends on type of cement, w/c-ratio and age. [•] Repeatability parameter distributions have positive skewness for rebound hammer test. [•] Rebound index coefficient of variation cannot estimate that of compressive strength. [•] Repeatability and precision claims (ACI 228.1R-03; ASTM C 805) need reconsideration. [•] Basic curve and assessment method of EN 13791 need reconsideration for rebound test. [ABSTRACT FROM AUTHOR]

Abstract: Surface hardness testing of concrete is a long established NDT method for in situ strength estimation. Nowadays, the rebound hammer is the surface hardness testing device for concrete of the most widespread use. Based on a comprehensive literature review it was realized that no general theory was developed in the last more than 50years that could describe the relationship between surface hardness and compressive strength of concrete. The diversity of the numerous empirical proposals that can be found in the technical literature needs to be explained. It can be even found in some publications that the method is suitable only for assessing the uniformity of concrete. There is long a time need for a model that can clarify the rebound surface hardness of concrete. Present paper introduces a phenomenological constitutive model (SBZ-model) that can be formulated for the surface hardness of concrete as a time dependent material property. The generating functions of the model are based on the time dependent development of the capillary pore system of the hardened cement paste in concretes that is characterised by the water–cement ratio as a practical simplification. The modelling assumptions and the use of the model would add to the fundamental understanding of the rebound surface hardness of concrete. An extensive experimental verification study clearly demonstrated the reasonable application possibilities of the SBZ-model. [Copyright &y& Elsevier]

Allergen extracts are efficient activators of the complement system trough the classical pathway. Involvement of the lectin pathway was not previously studied. To further examine the mechanism of complement activation by allergens, in vitro experiments, which covered early steps both of classical and lectin pathways, were performed.Two types of allergens were used in these studies: parietaria (PA) and house dust (HD) mite extracts. These allergen extracts bound to the globular head of C1q and interacted with purified mannan-binding lectin (MBL) as measured by solid-phase ELISA. None of the allergen extracts was able to activate human C1 in vitro, as measured by the determination of the split products of C1s in a reconstituted precursor C1 preparation.Neither the HD nor the PA extracts induced C4d generation above background in the serum of three subjects with hypogammaglobulinaemia but normal complement haemolytic activity. After reconstitution to normal level with purified human IgG, allergen extracts induced C4d formation above control at a level comparable to that measured in normal serum incubated with the same amounts of the extracts. HD-induced C4d generation was about the same comparable in MBL-depleted serum and in normal sera. In contrast PA induced no C4d formation in the MBL-depleted serum, whereas reconstitution with purified MBL restored C4d generation.These in vitro findings indicate that although the allergen extracts can bind purified C1q and MBL, they require IgG for efficient complement activation. Depending on the allergens, this activation may be initiated through C1, MBL, or both. [Copyright &y& Elsevier]

To assess concrete strength in a structure, nondestructive technique (NDT) like rebound hammer is combined with destructive technique (coring tests) in order to implement a relationship ‘‘conversion model” between the compressive strength and, NDT measurements. The conversion model is used to estimate the local strength value at each test location using the corresponding NDT value. Then the estimated mean strength and/or estimated strength standard deviation (concrete strength variability) values are calculated. However, the reliability of these estimated values is always a questionable issue because of the uncertainties associated with the strength predictions based upon NDT measurements. To improve the reliability, the uncertainties must be reduced by specifying and controlling their influencing factors. The objective of this paper is to study the reliability of assessment by analyzing the effects of several influencing factors: number of test locations used to identify a conversion model between strength and rebound measurement NC (number of cores), true value of concrete strength variability, within-test variability of rebound measurements, accepted uncertainty level, quantity to be assessed (mean strength, strength variability), model identification approach (like regression) and the way of selection core locations (random or conditional i.e. selection based on NDT measurements from preliminary investigation). To this end, a large campaign of laboratory studies datasets (1700 test results) was considered for the analysis in the present study. Results show that NC , within-test variability of rebound measurements and true concrete strength variability have significant effects on the assessment reliability. Conditional selection of cores has also an important effect on improving the reliability so it is strongly recommended. [ABSTRACT FROM AUTHOR]

Mannan-binding lectin (MBL)-associated serine proteases, MASP-1 and MASP-2, have been thought to autoactivate when MBL/ficolin·MASP complexes bind to pathogens triggering the complement lectin pathway. Autoactivation of MASPs occurs in two steps: 1) zymogen autoactivation, when one proenzyme cleaves another proenzyme molecule of the same protease, and 2) autocatalytic activation, when the activated protease cleaves its own zymogen. Using recombinant catalytic fragments, we demonstrated that a stable proenzyme MASP-1 variant (R448Q) cleaved the inactive, catalytic site Ser-to-Ala variant (S646A). The autoactivation steps of MASP-1 were separately quantified using these mutants and the wild type enzyme. Analogous mutants were made for MASP-2, and rate constants of the autoactivation steps as well as the possible cross-activation steps between MASP-1 and MASP-2 were determined. Based on the rate constants, a kinetic model of lectin pathway activation was outlined. The zymogen autoactivation rate of MASP-1 is ∼3000-fold higher, and the autocatalytic activation of MASP-1 is about 140-fold faster than those of MASP-2. Moreover, both activated and proenzyme MASP-1 can effectively cleave proenzyme MASP-2. MASP-3, which does not autoactivate, is also cleaved by MASP-1 quite efficiently. The structure of the catalytic region of proenzyme MASP-1 R448Q was solved at 2.5 Å. Proenzyme MASP-1 R448Q readily cleaves synthetic substrates, and it is inhibited by a specific canonical inhibitor developed against active MASP-1, indicating that zymogen MASP-1 fluctuates between an inactive and an active-like conformation. The determined structure provides a feasible explanation for this phenomenon. In summary, autoactivation of MASP-1 is crucial for the activation of MBL/ficolin·MASP complexes, and in the proenzymic phase zymogen MASP-1 controls the process. [ABSTRACT FROM AUTHOR]

Abstract: C1r is a modular serine protease which is the autoactivating component of the C1 complex of the classical pathway of the complement system. We have determined the first crystal structure of the entire active catalytic region of human C1r. This fragment contains the C-terminal serine protease (SP) domain and the preceding two complement control protein (CCP) modules. The activated CCP1–CCP2–SP fragment makes up a dimer in a head-to-tail fashion similarly to the previously characterized zymogen. The present structure shows an increased number of stabilizing interactions. Moreover, in the crystal lattice there is an enzyme–product relationship between the C1r molecules of neighboring dimers. This enzyme–product complex exhibits the crucial S1–P1 salt bridge between Asp631 and Arg446 residues, and intermolecular interaction between the CCP2 module and the SP domain. Based on these novel structural information we propose a new split-and-reassembly model for the autoactivation of the C1r. This model is consistent with experimental results that have not been explained adequately by previous models. It allows autoactivation of C1r without large-scale, directed movement of C1q arms. The model is concordant with the stability of the C1 complex during activation of the next complement components. [Copyright &y& Elsevier]