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Experimental and numerical investigations were conducted on impact performance and deflection of precast, portable concrete construction barrier, referred to as a portable concrete barrier (PCB), with a free-standing and a box-beam stiffened configuration. A 61-m long PCB system, consisting of ten 6.1-m long PCBs, was initially evaluated with two full-scale crash tests in a free-standing configuration and a box-beam stiffened configuration according to safety performance guidelines in Manual for Assessing Safety Hardware (MASH) 2016 for Test Level 3 (TL-3). Finite element models were developed using LS-DYNA and validated with these crash tests to ensure their feasibility to estimate barrier deflections and evaluate safety performance. The validated numerical models were used to conduct numerical simulations and investigate effects of concrete constitutive models and barrier length on the performance of PCB system with a box–beam stiffened configuration. Numerical results provided information on the selection and use of concrete constitutive models for evaluation of reinforced concrete barrier impact performance. Furthermore, the reduced-length analysis demonstrated that a reduction in the total system length resulted in decreased dynamic barrier deflection during impact events, as the ends of each system were pinned. This reduced-length analysis provided useful guideline on PCB system design and application for traffic control plan.

Analysis of indenting, buckling and piercing of aluminum beverage cans using both physical testing and computer simulation was performed in order to develop a better understanding of the sidewall structural strength of the cans. This understanding can be used to help design better cans and/or improve manufacturing processes.Simulation of the sidewall indentation was done with an impacting sphere. Parameters investigated included the sphere size and velocity, and the impact height along the sidewall. Buckling simulation of the dented can was then performed. Results from the deformed can buckling model compared well with physical testing based on buckled geometry, buckling load, and external work to buckle. Severe damage to a can that might occur during the manufacturing process was investigated by studying piercing of the can sidewall. Impacts of 5 and 10 m/s were performed with both blunt (flat) and sharp (45° tip) steel rods. It was found that separated elements with tied nodal constraints more accurately represent the failure behavior of the can subjected to a piercing load than merged element nodes. It was also found that the more crushing a can undergoes before piercing occurs, the more energy the can material absorbs. However, there is an upper limit to the crushing based on the speed and shape of the impactor.

The effects of the calcium channel blocker nimodipine and the non-competitive NMDA-antagonists MK-801 and phencyclidine (PCP) on infarct size 48 h after occlusion of the middle cerebral artery (MCA-O) were evaluated in the rat. Nimodipine was given at a dose of 0.3 mg/kg s.c. 30 min prior and 8, 16, and 24 h after MCA-O. MK-801 (1 mg/kg i.p. or 10 mg/kg i.p.) or PCP (0.3, 1.0, 3.0, 10, or 30 mg/kg i.p.) were administered 30 min prior to ischemia. In additional experiments 30 mg/kg PCP was given 1, 3, or 5 h post ischemia. Nimodipine and 1 mg/kg MK-801 reduced cortical infarct volumes significantly by 50% and 55%, respectively, while cortical infarct size fell by 32% and total infarct volume was not altered significantly after administration of 10 mg/kg MK-801. Pretreatment with 10 or 30 mg/kg PCP reduced cortical infarction by 47–53% and total infarct volumes by 39–42%. Posttreatment with PCP was effective if started at 1 or 3 h post ischemia.

The effects of different cerebro-protective agents on selected key enzymes of the energy metabolism of rat primary glial cultures and rat cerebral cortex were studied. As indicators for the capacity of the most important pathways of energy metabolism the following enzyme activities were determined: hexokinase (HK), phosphofructokinase (PFK), pyruvate kinase (PK), lactate dehydrogenase (LDH), glucose-6-phosphate dehydrogenase (G-6-P-DH), malate dehydrogenase (MDH), glutamate dehydrogenase (GDH), and cytochrome-c-reductase (CCR). After a one week growth period, rat glial cultures were incubated for 3 or 4 weeks with the substances to be tested. Bencyclane (5 X 10(-5) mol/l) increased the activities of HK, G-6-P-DH, and LDH, whereas PFK and CCR were reduced. Pyritinol (10(-4) mol/l) led to a higher G-6-P-DH activity, simultaneously lowering the values for PFK, CCR, PK, LDH, and MDH. Under the influence of an extract of the leaves of Ginkgo bilobae (EGB; 100 mg/l) PFK, LDH, and MDH activities were reduced. All these alterations in enzyme activities went along with simultaneous reductions in protein content, therefore not allowing to exclude toxic effects with regard to the doses used. Moreover, direct interference with the analytical procedure was demonstrable for bencyclane and EGB. Piracetam (10(-3) mol/l), flunarizine (10(-6) mol/l), dihydroergocristine (5 X 10(-6) mol/l), and nicergoline (5 X 10(-6) mol/l) failed to induce any alteration in the employed doses. The most striking effects were obtained with meclofenoxate which was tested at 10(-3) and 10(-4) mol/l. The higher dose caused an elevation of HK, PFK, CCR, G-6-P-DH, GDH and MDH activities, while slightly reducing PK. With the lower dose of meclofenoxate CCR and G-6-P-DH activities were increased. Short-term incubation of the cultures with 10(-3) mol/l meclofenoxate for 24 hr led to an increase in LDH, G-6-P-DH, and GDH activities. Chronic incubation with meclofenoxate (10(-3) mol/l) followed by 48 hr deprivation of the drug resulted in elevated HK, PFK, CCR, G-6-P-DH, GDH, and MDH activities. These changes were accompanied by alterations in related metabolite levels. These include elevations in the concentration of creatine phosphate and fructose-1,6-bisphosphate, whereas glucose-6-phosphate levels were reduced. After one week of meclofenoxate deprivation the activities of CCR and G-6-P-DH were still elevated. The metabolites of meclofenoxate dimethylaminoethanol (DMAE; 10(-3) mol/l) and p-chlorophenoxyacetic acid (10(-3) mol/l) were also investigated.(ABSTRACT TRUNCATED AT 400 WORDS)

In this report the effects of phencyclidine (PCP) on physiologic variables, local cerebral blood flow (LCBF), and on hippocampal cell damage were measured in a rat model of forebrain ischemia (2-vessel occlusion and hypotension). Ischemia was induced for 10 min. LCBF was determined after 2 min of recirculation, using the [14C]iodoantipyrine technique. Hippocampal cell loss was quantified histologically 7 days postischemia as the percentage of acidic stainable neurons. Intravenous application of PCP (2 mg/kg) at 15 min prior to ischemia left postischemic LCBF unchanged, but neuronal damage was significantly reduced in hippocampal CA1 sector from 46 to 15.7%. PCP is concluded to reduce ischemic damage of neurons mainly via a direct effect on brain tissue.

Summary Two models of experimental cerebral ischemia in rats were developed and used. The first model was permanent occlusion of both carotids up to 3 weeks, the second model the temporal occlusion of both carotids and systemic hypotension for 10 min. Rats treated by the first experimental set were investigated after one, 2 and 3 weeks. In all groups, about 40% of so treated animals had territorial infarcts, often more than one in the animal in question. These infarcts developed from necrotic, pale areas to ischemic cysts and this copied the evolution of human territorial infarction. Astroglial reaction was only seen in the border zone. In the second model, rats preferentially developed, as known, the so called delayed ganglion cell necrosis in the field CA 1 of the hippocampus. Cells were not altered on the second, but damaged on the sixth day after experimental ischemia. In both models the hippocampus was damaged, however in the first the damages were morphologically distinct from the damage in carotid occlusion in systemic hypotension. The first experimental model suits better for human territorial infarction, the second is highly reproducible and thus provides a much better experimental tool.