On the mechanical ageing of lubricating greases

This thesis focuses on the mechanical degradation of lubricating greases, including the change of thickener micro-structure and rheological properties as well as the influence of the mechanical degradation of grease on the bearing lubricant film thickness. Grease is a multi-phase material, where the base oil is trapped within the thickener network by a combination of Van der Waals and capillary forces. Inside a bearing, grease will act as a reservoir releasing lubricant into the contact area. During bearing operation, mechanical degradation of the grease is observed, reflected by the change of grease consistency, grease bleed, apparent viscosity, etc. This will lead to a loss of lubricant, severe starvation and ultimately the failure of the bearing. The thesis starts with the ageing mechanism for lubricating greases with a fibre-like thickener structure (including lithium-based, lithium-complex-based and polyurea-based greases). Under shear, grease softening is found. The change of the rheological properties of the grease shows a two-phase ageing behaviour. The degradation is initially fast but subsequently slows down. This degradation is closely related to the change of the thickener micro-structure. In addition to shear, high temperatures will accelerate the ageing process following an Arrhenius behaviour. Based on these observations, an Ageing Master Curve is constructed using an energy concept. This model is later validated using a grease worker and applied to the grease ageing process inside a rolling bearing. As a comparison to the fibre-like thickener structure greases, the ageing of calcium sulphonate complex grease is investigated. Different from the greases mentioned above, calcium sulphonate complex grease has a particle-like thickener structure that is difficult to break under shear, hence no shear softening is observed. As a result, the Ageing Master Curve is not applicable for this type of grease. The ultimate goal of grease lubrication is to provide the bearing contacts with a separating film. This is why the influence of grease mechanical ageing on the film thickness is studied as well. The grease film thickness deviates from the calculated elastohydrodynamic film thickness (assuming lubrication by the base oil under fully flooded conditions). The grease film thickness appears to be influenced by churning, channelling, change of grease bleed and rheological properties caused by shear and/or temperature. In addition, the thickener fragments generated by mechanical degradation also contribute to the film thickness. The results from the work described in this thesis give an important contribution to the development of rolling bearing grease life models. These models can then be used for the calculation of maintenance intervals

Type 3 adenylyl cyclase, neuronal primary cilia, and hippocampus-dependent memory formation

Primary cilia are microtubule-based cellular antennae present in most vertebrate cells including neurons. Neuronal primary cilia have abundant expression of G-protein coupled receptors (GPCRs) and downstream cAMP signaling components such as type 3 adenylyl cyclase (AC3). The deflects of neuronal cilia is associated with many memory-related disorders, such as intellectual disability. Thus far, little is known about how neuronal primary cilia regulate neuronal activity and affect hippocampal memory formation. Episodic memory is thought to be encoded by sparsely distributed memory-eligible neurons in the hippocampus and neocortex. However, it is not clear how memory-eligible neurons interact with one another to form and retrieve a memory. The objectives of my dissertation are to determine the roles of AC3 in regulating cortical protein phosphorylation, to examine the cellular mechanism of episodic memory formation, and to examine how neuronal primary cilia regulate trace fear memory formation. Project 1: Compare protein phosphorylation levels in the prefrontal cortex between AC3 knockout (KO) and wildtype (WT) mice. AC3 represents a key enzyme mediating ciliary cAMP signaling in neurons and is genetically associated with major depressive disorder (MDD) and autism spectrum disorders (ASD). The major downstream effector protein of cAMP in cells is protein kinase A (PKA), whose activation leads to the phosphorylation of numerous proteins to propagate the signaling downstream. In my mass spectrometry-based phosphoproteomic study using conditional AC3 KO mice, I identified thousands of peptides from prefrontal cortical tissues, some of which are differentially phosphorylated in AC3 WT and KO samples. In addition, this effort led to identification of over two hundred proteins, whose phosphorylation were sex-biased. Surprisingly, a high percentage of these targets (31%) are autism-associated proteins/genes. Hence, this study provides the first phosphoproteomic evidence suggesting that sex-biased protein phosphorylation may contribute to the sexual dimorphism of autism. Project 2: Investigate how hippocampal neurons are recruited to interact with each other to encode a trace fear memory. Using in vivo calcium imaging in freely behaving mice, I found that a small portion of highly active hippocampal neurons (termed primed neurons) are actively engaged in memory formation and retrieval. I found that induction of activity synchronization among primed neurons from random dynamics is critical for trace memory formation and retrieval. My work has provided direct in vivo evidence to challenge the long-held paradigm that activation and re-activation of memory cells encodes and retrieves memory, respectively. These findings support a new mechanistic model for associative memory formation, in that primed neurons connect with each other to forge a new circuit, bridging a conditional stimulus with an unconditional stimulus. Project 3: Develop an analytical method to identify primed neurons and determine the roles of neuronal primary cilia on hippocampal neuronal priming and trace memory formation. Neuronal primary cilia are “cellular antennae” which sense and transduce extracellular signals into neuronal soma. However, to date little is known about how neuronal primary cilia influence neuronal functions and hippocampal memory. I utilized conditional Ift88 knockout mice (to ablate cilia) as loss-of-function models. I found that inducible conditional Ift88 KOs display more severe learning deficits compared to their littermate controls. Cilia-ablated mice showed reduced overall neuronal activity, decreased number of primed neurons, and failed to form burst synchronization. These data support the conclusion that alteration of neuronal primary cilia impairs trace fear memory by decreasing hippocampal neuronal priming and the formation of burst synchronization. This study also provides evidence to support the importance of burst synchronization among primed neurons on memory formation and retrieval

Situating Asian American Environmental (In)Justices through Radical History Walking Tours

By analyzing two radical history walking tours in Seattle, WA, and Berkeley, CA, this thesis aims to examine how Asian American communities can find their places in the U.S. environmental movement. I argue that these walking tours provide generative pedagogical tools to engage the general public to unpack the complex Asian American history embedded within urban spaces. I also articulate how these walking tours have the capacity to situate environmental struggles and activism within urban spaces, illustrating that various Asian American social and political activism has always been addressing environmental concerns. Furthermore, I argue that these walking tours of Asian American cultural landscapes enable us to recognize the long history of cross-ethnic organizing in Asian American activist movements. Lastly, I advocate for an Asian American environmental movement that incorporates a decolonial/indigenous framework, which could allow all marginalized communities to envision more just practices of spatial organizing and land use in the future