Thus, the three intermediate structures of insulin including oligomer, proto-fibril and fibril forms can affect the function of PC12 cells via decreasing neuronal dendritic branches. The accumulation of Ab and tau-induced changes are shown to be pathological hallmarks of Alzheimer Disease, and are believed to contribute to many of the alterations in neuronal structures. Thus, the oligomeric structure of insulin has characteristic similar to Ab here. In our experiments, differentiated PC12 cells were used since they are well characterized and exhibit unique sensitivity to neurotoxicity. They have been widely used as an experimental model for this purpose. The current study provides, to the best of our knowledge, the first detailed analysis of the effects of different structural forms of insulin on neuronal morphology. However, the intracellular mechanism of this effect is not clear and needs to be further studied. The studies presented here indicate that there is a correlation between surface tension and neurotoxicity of various aggregated species in the course of insulin fibrillation. Decreased surface tension, when oligomeric aggregates form, was accompanied with increased neurotoxic effects of these forms. In the case of protofibrils and mature fibrils, the increasing surface tension was accompanied with decreased neurotoxic effects. Thus, the quantity of surface tension is an indicator of the intensity of the neurotoxic effects of aggregated species. Oligomeric early aggregates are disorganized structures which expose to the outside hydrophobic surfaces of the protein that are normally buried in the core of globular state. Amphiphilic, detergent-like structure and hydrophobicity of oligomers provide them the capacity to adsorb at the air-water interface, subsequently causing a decrease in surface tension. Moreover, due to hydrophobicity and by a nonspecific detergent-like mechanism, oligomers interact with membranes, trigger destabilization and permeabilizition that can be the reason for toxic responses of neuron-like PC12 cells and subsequent WY 14643 moa morphological alterations. Detergent-like characteristic of aggregates, their effect on the surface tension of solution and perturbation features on morphology of neuron-like PC12 cells, diminished by formation of proto-fibrils and mature fibrils. Thus, here, formation of mature fibrils and lower relative neurotoxicity than their oligomeric early aggregates is a protective mechanism. Dystocia has a major economic impact on the dairy cattle industry. One study estimated that the cost of dystocia with extremely difficult labor was nearly $400 per incident. Selective breeding has resulted in larger cows that have a higher milk production potential, but these larger cows also tend to induce dystocia in the calving female. The probability of dystocia increases by 13% for each kg increase in birth weight. Moreover, high milk production in the dam predisposes it to give birth to a smaller calf, and a lower birth size does not have any subsequent adverse effects on milk productivity. Therefore, selecting for cows with a smaller birth size would prevent dystocia and be beneficial for farmers. Whole-genome scans for quantitative trait loci associated with birth weight or dystocia have been previously conducted. However, this method has identified only one gene, which encodes for non-SMC condensin I complex, subunit G, as a genetic factor that modulates fetal growth in cattle. Birth weight is a quantitative trait that is controlled by many genes, and an additional whole-genome scan is warranted. Choline is a component of the major phospholipids of cell membranes.