Carrying capacity

The carrying capacity of an environment is the maximum population size of a biological species that can be sustained by that specific environment, given the food, habitat, water, and other resources available. The carrying capacity is defined as the environment's maximal load, which in population ecology corresponds to the population equilibrium, when the number of deaths in a population equals the number of births (as well as immigration and emigration). The effect of carrying capacity on population dynamics is modelled with a logistic function. Carrying capacity is applied to the maximum population an environment can support in ecology, agriculture and fisheries. The term carrying capacity has been applied to a few different processes in the past before finally being applied to population limits in the 1950s. The notion of carrying capacity for humans is covered by the notion of sustainable population. At the global scale, scientific data indicates that humans are living beyond the

Test and lower bound modeling of keyed shear connections in RC shear walls

Cao Linh Hoang, Aurelio Muttoni, Jesper Harrild Sorensen

This paper presents an investigation into the ultimate behavior of a recently developed design for keyed shear connections. The influence of the key depth on the failure mode and ductility of the connection has been studied by push-off tests. The tests showed that connections with larger key indentations failed by complete key cut-off. In contrast, connections with smaller key indentations were more prone to suffer local crushing failure at the key corners. The local key corner crushing has an effect on the load-displacement response, which is relatively more ductile. In addition to the tests, the paper also presents lower bound modeling of the load carrying capacity of the connections. The main purpose of the lower bound model is to supplement an already published upper bound model of the same problem and thereby provide a more complete theoretical basis for practical design. The two models display the same overall tendencies although identical results are not possible to obtain, due to differences in the basic assumptions usually made for upper and lower bound analysis of connections. It is found that the test results, consistent with the extremum theorems of plasticity, are all lying within the gap between the upper and the lower bound solution. The obtained results finally lead to a discussion of how the two models can be used in practice. The primary merit of the upper bound model lies in its simplicity (a closed-form equation). On the other hand, the lower bound model provides safe results, but is more complicated to apply. It is therefore argued that the upper bound model may be used in cases, where calibration with tests has been carried out. The lower bound model should be applied in situations, where the design deviates significantly from the configurations of the available tests.

Engineering Structures2018

Required growth facilitators propel axon regeneration across complete spinal cord injury

Mark Andrew Anderson, Sabry Leonardo Barlatey, Grégoire Courtine, Zhigang He, Nicholas David James, Michael V. Sofroniew, Cheng Wang

Transected axons fail to regrow across anatomically complete spinal cord injuries (SCI) in adults. Diverse molecules can partially facilitate or attenuate axon growth during development or after injury1,2,3, but efficient reversal of this regrowth failure remains elusive4. Here we show that three factors that are essential for axon growth during development but are attenuated or lacking in adults—(i) neuron intrinsic growth capacity2,5,6,7,8,9, (ii) growth-supportive substrate10,11 and (iii) chemoattraction12,13—are all individually required and, in combination, are sufficient to stimulate robust axon regrowth across anatomically complete SCI lesions in adult rodents. We reactivated the growth capacity of mature descending propriospinal neurons with osteopontin, insulin-like growth factor 1 and ciliary-derived neurotrophic factor before SCI14,15; induced growth-supportive substrates with fibroblast growth factor 2 and epidermal growth factor; and chemoattracted propriospinal axons with glial-derived neurotrophic factor16,17 delivered via spatially and temporally controlled release from biomaterial depots18,19, placed sequentially after SCI. We show in both mice and rats that providing these three mechanisms in combination, but not individually, stimulated robust propriospinal axon regrowth through astrocyte scar borders and across lesion cores of non-neural tissue that was over 100-fold greater than controls. Stimulated, supported and chemoattracted propriospinal axons regrew a full spinal segment beyond lesion centres, passed well into spared neural tissue, formed terminal-like contacts exhibiting synaptic markers and conveyed a significant return of electrophysiological conduction capacity across lesions. Thus, overcoming the failure of axon regrowth across anatomically complete SCI lesions after maturity required the combined sequential reinstatement of several developmentally essential mechanisms that facilitate axon growth. These findings identify a mechanism-based biological repair strategy for complete SCI lesions that could be suitable to use with rehabilitation models designed to augment the functional recovery of remodelling circuits

2018

Effects of Tissue-Level Ductility on Trabecular Bone Strength

Frédéric Edouard Juillard

Osteoporosis is one of the most common skeletal diseases that lead to an accelerated bone loss due to an imbalance in bone turnover. This low bone mass and degraded bone microarchitecture cause a reduction in mechanical properties and an associated increase in fracture risk. If individual trabeculae become more brittle with aging, disease, or drug treatment, how does that influence the strength of the overall trabecular bone? This multi-scale issue, which relates energy absorption or tissue ductility at one scale to load-carrying capacity or strength at a higher scale, is particularly relevant in osteoporosis applications since it is well known that aging and drug treatments can influence tissue-level ductility. However, the link between tissue ductility and apparent-level strength for trabecular bone is poorly understood and thus is it not currently possible to infer how known changes in tissue ductility translate into the higher scale and more clinically relevant changes in trabecular strength. To provide insight into this issue, our goal in this study was to determine how trabecular strength is altered when the tissue is changed from perfectly brittle to perfectly ductile – the two extremes of possible tissue-level ductility. The results show that overall trabecular strength can vary two-fold if the tissue is entirely brittle compared to entirely ductile. The comparison with the experimental data suggests that at low bone volume fraction, real variations in tissue ductility could be important since the real behavior is situated between the ductile and brittle behaviors. If so, this implies that future studies assessing the structural consequence of changes in tissue-level ductility need to consider the bone volume fraction. Our analyses are unique since they are the first to account for the complex 3D geometric detail of real trabecular microarchitecture and this study is the first to mechanistically link tissue-level ductility, a potentially important aspect of tissue material behavior, to the apparent-level strength, which is relevant clinically.

2011

Required growth facilitators propel axon regeneration across complete spinal cord injury

Mark Andrew Anderson, Sabry Leonardo Barlatey, Grégoire Courtine, Zhigang He, Nicholas David James, Michael V. Sofroniew, Cheng Wang

2018

Effects of Tissue-Level Ductility on Trabecular Bone Strength

Frédéric Edouard Juillard

2011

Test and lower bound modeling of keyed shear connections in RC shear walls

Required growth facilitators propel axon regeneration across complete spinal cord injury

Effects of Tissue-­Level Ductility on Trabecular Bone Strength

Test and lower bound modeling of keyed shear connections in RC shear walls

Required growth facilitators propel axon regeneration across complete spinal cord injury

Effects of Tissue-­Level Ductility on Trabecular Bone Strength

Effects of Tissue-Level Ductility on Trabecular Bone Strength

Effects of Tissue-Level Ductility on Trabecular Bone Strength