Study of the conrod deformation during piston interaction with liquid in the internal combustion engine cylinder

The paper analyzes the deformation of the connecting rod stem with buckling due to water ingress into the internal combustion engine cylinder (the so-called hydrolock). A method is presented that has been developed to perform calculations of stem deformation in the process of compressing air with liquid in an internal combustion engine cylinder. The method is based on solving a system of differential equations for pressure and temperature in the cylinder, followed by calculating the compression force acting on the connecting rod. A carried-out simulation of the compression process demonstrates the dependence of the air pressure in the cylinder, the stress and the strain of the connecting rod on the fill ratio of the combustion chamber with liquid. The calculations performed according to the classical theory of resistance of materials have shown that the connecting rod with the buckling of the stem begins to deform when the liquid fills the combustion chamber to a minimum of 80%. With the increase in the amount of liquid, the deformation of the conrod increases, and when the level of liquid filling is so significant that it exceeds the volume of the combustion chamber, the conrod stem deformation reaches extreme values. It is shown that under these conditions after the hydrolock occurs the engine may fail due to the piston wedging the crankshaft in the bottom dead center position

Evoked axonal oxytocin release in the central amygdala attenuates fear response.

The hypothalamic neuropeptide oxytocin (OT), which controls childbirth and lactation, receives increasing attention for its effects on social behaviors, but how it reaches central brain regions is still unclear. Here we gained by recombinant viruses selective genetic access to hypothalamic OT neurons to study their connectivity and control their activity by optogenetic means. We found axons of hypothalamic OT neurons in the majority of forebrain regions, including the central amygdala (CeA), a structure critically involved in OT-mediated fear suppression. In vitro, exposure to blue light of channelrhodopsin-2-expressing OT axons activated a local GABAergic circuit that inhibited neurons in the output region of the CeA. Remarkably, in vivo, local blue-light-induced endogenous OT release robustly decreased freezing responses in fear-conditioned rats. Our results thus show widespread central projections of hypothalamic OT neurons and demonstrate that OT release from local axonal endings can specifically control region-associated behaviors

The neural EGF family member CALEB/NGC mediates dendritic tree and spine complexity

The development of dendritic arborizations and spines is essential for neuronal information processing, and abnormal dendritic structures and/or alterations in spine morphology are consistent features of neurons in patients with mental retardation. We identify the neural EGF family member CALEB/NGC as a critical mediator of dendritic tree complexity and spine formation. Overexpression of CALEB/NGC enhances dendritic branching and increases the complexity of dendritic spines and filopodia. Genetic and functional inactivation of CALEB/NGC impairs dendritic arborization and spine formation. Genetic manipulations of individual neurons in an otherwise unaffected microenvironment in the intact mouse cortex by in utero electroporation confirm these results. The EGF-like domain of CALEB/NGC drives both dendritic branching and spine morphogenesis. The phosphatidylinositide 3-kinase (PI3K)-Akt-mammalian target of rapamycin (mTOR) signaling pathway and protein kinase C (PKC) are important for CALEB/NGC-induced stimulation of dendritic branching. In contrast, CALEB/NGC-induced spine morphogenesis is independent of PI3K but depends on PKC. Thus, our findings reveal a novel switch of specificity in signaling leading to neuronal process differentiation in consecutive developmental events