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Abstract Extent of experiment-related variability in fatigue crack propagation is essential to be known while comparing the performance with other materials, for assessment of welds or damage tolerance analysis. Since such a variability can be dependent on material or parameter investigated, and may originate from the size effect, thin sheets of the relatively new airframe alloy AA6056-T6 have been investigated for baseline data using C(T) and M(T) specimens. As a screening step, various parameters such as surface cladding, crack plane orientation, specimen width and thickness, and initial notch length have been varied on C(T) specimens. The material also stems from different heats. The maximum crack opening displacement (CODmax), obtained from a displacement gauge, is calibrated against the optical crack length for the indirect crack length measurement and its precision is increased by acquiring an individual calibration curve for each specimen. The variability in the mid-regime fatigue crack propagation range is found to be relatively low (± 35%). With this range as the tolerance, the alloy is found to exhibit mostly a parametric non-variance, since, except for the specimen type, other parameters investigated are found to be non-influential. M(T) specimens are found to yield conservative fatigue crack propagation data.
Accuracy of indirect fatigue crack length measurement by potential drop method or by compliance technique may be affected at low load ratio due to fracture surface contact, crack closure or mixed mode fracture. As an alternative, the maximum value of crack opening displacement, CODmax from a clip gauge was utilized. Middle crack tension M(T) specimens were used to obtain conservative data at a low load ratio (R = 0.1). Thin sheet specimens (B = 3.2 mm) with different widths (100 mm <= W <= 400 mm) of AA6056-T4 were investigated in the mid-regime (Paris regime), which is of interest for damage tolerance analysis. The use of COD.), is found to provide crack lengths equivalent to those measured optically. Hence, the method is very suitable for indirect crack length measurement. Furthermore, small width specimens provided data equivalent to large width specimens. Insofar, the size effect is found to be absent, and fatigue crack propagation data can be acquired on small width specimens when material availability is limited.
Background: Defined particles carrying tightly bound allergens at high density have been suggested as alternatives in allergy vaccination. Carbohydrate based particles (CBP), sized 2 μm, provide a platform for covalent coupling of allergens. Objective: To investigate the mechanisms of antigen presentation by CBP, as well as cellular and humoral responses after vaccination with the major cat allergen Fel d 1, covalently coupled to CBP. Methods: Mice ( n = 10/group) were subcutaneously vaccinated with CBP‐rFel d 1, CBP or phosphate buffer saline (PBS) before sensitization with rFel d 1 and challenged with cat dander extract. Fluorescent and 75 Se‐radiolabeled tracking of allergens and particles were performed with flow cytometry and whole‐body autoradiography. Humoral, cellular and regulatory immune responses were analyzed by ELISA and flow cytometry. Cytokines were measured in bronchoalveolar lavage fluid and splenocyte cultures. Results: CBP‐rFel d 1 prevented induction of airway inflammation and induced allergen‐specific T‐cell anergy. CBP‐rFel d 1 also induced rapid IgM and IgG1‐responses compared with soluble rFel d 1. Particles were phagocytosed by antigen‐presenting cells and transported to draining lymph nodes and spleen. Moreover, antigen coupled to CBP remained longer at the injection site compared with alum. Conclusions: Covalent coupling of rFel d 1 to CBP induces rapid antibody production, prevents induction of allergic immune responses and systemic allergen spreading. Thus, CBP comprise several attractive adjuvant features for use in allergy vaccination. Clinical Implications: Prolonged allergen exposure through covalent coupling to particles suitable for phagocytosis, provides an adjuvant for safer and efficient allergy vaccination.
Proneural genes are crucial regulators of neurogenesis and subtype specification in many areas of the nervous system; however, their function in dopaminergic neuron development is unknown. We report that proneural genes have an intricate pattern of expression in the ventricular zone of the ventral midbrain, where mesencephalic dopaminergic neurons are generated. Neurogenin 2(Ngn2) and Mash1 are expressed in the ventral midline, while Ngn1, Ngn2 and Mash1 are co-localized more laterally in the ventricular zone. Ngn2 is also expressed in an intermediate zone immediately adjacent to the ventricular zone at the ventral midline. To examine the function of these genes, we analyzed mutant mice in which one or two of these genes were deleted (Ngn1, Ngn2 and Mash1) or substituted (Mash1 in the Ngn2 locus). Our results demonstrate that Ngn2 is required for the differentiation of Sox2+ ventricular zone progenitors into Nurr1+postmitotic dopaminergic neuron precursors in the intermediate zone, and that it is also likely to be required for their subsequent differentiation into tyrosine hydroxylase-positive dopaminergic neurons in the marginal zone. Although Mash1 normally has no detectable function in dopaminergic neuron development, it could partially rescue the generation of dopaminergic neuron precursors in the absence of Ngn2. These results demonstrate that Ngn2 is uniquely required for the development of midbrain dopaminergic neurons.
