The paper deals with the punching resistance of flat slabs with openings adjacent to a column. The results of an experimental campaign carried out at a laboratory of the Slovak University of Technology in Bratislava (STU) are presented in the paper. A total of eight slabs with a thickness of 250 mm and without transverse reinforcement were tested under axis‐symmetric conditions. The six slabs had two symmetrically placed openings with different distances measured from the column's periphery and two reference slabs did that not have any openings. The results obtained were compared with punching resistances assessed using the design equations introduced in Eurocode 2, Model Code 2010, ACI 318‐14, and the CSCT model expressed in a closed form. Significant differences in the values of the Vtest/VR,c ratio were observed for the different positions of the openings for each design model. In order to increase the accuracy of the models, some changes in estimating the reduced lengths of the control perimeter were proposed.

Flat slabs are commonly used structures in contemporary architecture. Although their common use there is still problem in design of these structures. The openings adjacent to a column are often used for plumbing and such a position of the openings increases shear stresses in the flat slab near the column. This paper deals with experimental work focused on the punching shear resistance of the flat slab specimens with openings adjacent to column compared to the flat slab specimens without openings. The opening influence is determined experimentally and by using models for the assessment of punching resistance from relevant standards and codes. The material properties of concrete and reinforcing steel were obtained from the laboratory tests.

Alzheimer's disease (AD) is a multifactorial disorder; neurofibrillary pathology composed of tau protein is found side by side with amyloid-β deposits and extensive neuroinflammation. The immune system of the brain is considered as one of the factors that could influence the speed of the progression of AD neuropathology as a potential mediator of the damage induced by AD protein deposits. Alzheimer's disease pathology can be impacted by psychological stress; however, signalling pathways in background are not well known. We have explored possible avenues of how stress could influence the brain's immune system in a rat model of AD. Animals were subjected either to a single or multiple instances of immobilization stress. The analysis of a panel of immunity-related genes was used to evaluate the impact of stress on the immune response in the brain. We have identified 19 stress-responsive genes that are involved in neuroinflammation accompanying tau pathology: Nos2, Ptgs2, IL-8rb, C5, Mmp9, Cx3cr1, CD40lg, Adrb2, IL-6, IL-6r, IL-1r2, Ccl2, Ccl3, Ccl4, Ccl12, TNF-α, IL-1α, IL-1β, IL-10. Most of them are deregulated under the stress conditions also in control animals; however, the magnitude of the response to either acute or chronic stress differs. This can lead to serious influence, most probably to acceleration of neurodegenerative phenotype in diseased animals. Several of the genes (IL-1β, Casp1, Cx3cr1 and C5) are deregulated solely in tauopathic animals. The stress-induced changes in the inflammatory picture of the brain highlight the fact that the brain's immune response is highly responsive to environmental stimuli. The pattern of changes is indicative of an attempt to protect the brain in the short term, while being potentially detrimental to the response against a long-term pathological process such as neurofibrillary degeneration.

The use of photogrammetry during load tests of building components is a common