Most Popular Books by Erik Larson

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As the market-leading textbook on the subject, Project Management: The Managerial Process, 5e is distinguished by its balanced treatment of both the technical and behavioral issues in project management as well as by its coverage of a broad range of industries to which project management principles can be applied. It focuses on how project management is integral to the organization as a whole. The 5th edition reflects the latest changes found in the practice. Other texts discuss the topics covered in this text but they do not view oversight as the project manager''s operating environment, as does Larson/Gray. Resumes of managers will soon be primarily a description of participation in and contributions to projects.

This is a compelling story about how a series of events led the author to stop letting circumstances control his life. He gained a purpose and a plan to take charge and strive to improve and be successful in every area of his life. Although this story is about the authors journey of intentional personal development, the most important thing is your journey. As you read, you will be inspired to take on your own journey of personal development to reach for your highest potential. This is a book not just to read but to use. Through evaluation exercises you will gain your own life''s purpose statement that you will use to put together a specific and deliberate plan to improve in every are of your life.Whatever the outcome, I can promise you will a more successful person after reading this book.

"Synaptic neurotransmission is a fundamental process which enables signaling between neurons. All voluntary animal behaviour relies on proper synaptic function, and many neurological diseases have their origins in synaptic disruptions. In particular, the neurodevelopmental disease fragile-X syndrome (FXS) has notable defects in synaptic transmission across the brain. FXS is the most common single gene cause of intellectual disability and autism, and is caused by interruptions in the expression or function of the protein FMRP. Like many neurodevelopmental diseases, FXS is characterized in part by an imbalance in excitation and inhibition in the brain. While there is a general consensus regarding the defects in FXS excitatory signaling, there is considerably less known about defects to inhibitory neurotransmission. In particular, there has been no comprehensive study on the synapses of the inhibitory cerebellar molecular layer interneurons (MLIs) in the pathophysiology of FXS. Accordingly, this thesis addresses this gap in our understanding FXS, while also uncovering novel plasticity mechanisms in MLI inhibitory neurotransmission. Neurotransmission is very dynamic and synapses regularly change their efficacy in a process known as synaptic plasticity. Most research into synaptic plasticity has focused on excitatory synapses, but there is a new interest in studying the mechanisms that lead to long term changes of inhibitory synaptic signaling. One of these mechanisms includes a novel role for reactive oxygen species (ROS) to potentiate inhibitory GABAergic signaling of MLIs. Given this, the first objective of this thesis was to identify the physiological signaling pathways of ROS-dependent inhibitory plasticity using an approach involving both pharmacological and genetic manipulations. I found that NMDA receptor activation generates physiological ROS through a nNOS-cGMP-NOX2 pathway. Furthermore, this pathway recruited [alpha]3-containing GABAA receptors to the synapse following PKC activation and GABARAP trafficking. The second half of this thesis was a study on the role of MLIs in the neurodevelopmental disease, FXS. In these chapters, I start by describing a novel defect in MLI NMDA receptor signaling. Consequently, this impacts multiple plasticity mechanisms which regulate inhibition in the CNS. First, MLIs are unable to modulate their firing properties in response to NMDA receptor activation. Second, there is an inability to potentiate inhibitory signaling onto MLIs. Inhibitory plasticity can be restored by the inclusion of a small molecule which potentiates the intracellular signaling pathway. Third, there is a significant impact on the regulation of blood flow through the cerebellum. Together, the lack of these plasticity mechanisms likely impacts the cerebellar circuit which I predict would have downstream consequences on motor learning. Finally, I have also found a defect in dendritic filtering of cerebellar MLIs in FXS. MLIs from FXS mice fire more action potentials following afferent stimulation, which is linked to a larger evoked postsynaptic potential (ePSP) amplitude. Moreover, acute reintroduction of the N-terminal fragment of FMRP reduces the ePSP amplitude in FXS mice. Taken together, this thesis presents original findings on GABAergic plasticity and multiple defects in inhibitory signaling of FXS mice in the cerebellum. Based on our new understanding of inhibitory signaling, this thesis also demonstrates mechanisms to overcome these defects in FXS which could lead to therapeutics in a future clinical setting"--