![]() Sweat beads up on his brow, on the dusting of hair coating his chest as he throws his head back, filling the condom with a groan, the cords in his neck straining. fuck, don’t stop.” “Fuuuck.” He squeezes my hips while he pounds into me. You ready? Huh? You ready to come all over this cock?” I dig my nails into Paul’s shoulders, arching my back off the bed. ![]() Chronologically, it is set after Sweet Possession and between All I Want and When I Fall.īROOKE “Fuck yeah, baby. Sweet Obsession is a standalone novel in the Sweet Addiction series, and crosses over with the Alabama Summer series. This book is dedicated to my amazing street team, J’s Sweeties. Cover design © Kari March, Kari March Designs Interior design and formatting Christine Borgford, Perfectly Publishable ![]() No part of this book may be reproduced, storied in a retrieval system, or transmitted in any form, or by any means, electronic, mechanical, photocopying, recording, or otherwise, without prior permission of the author. Any resemblance to real persons or events is coincidental. Names, characters, places, events, and other elements portrayed herein are either the product of the author ’s imagination or used fictitiously. All Rights Reserved This book is a work of fiction. Our studies suggest that stimulation of microglial activation may be a viable therapeutic approach for the treatment of WNV neuroinvasive disease.Table of Contents Sweet Obsession Dedication Author ’s Note Chapter One Chapter Two Chapter Three Chapter Four Chapter Five Chapter Six Chapter Seven Chapter Eight Chapter Nine Chapter Ten Chapter Eleven Chapter Twelve Chapter Thirteen Chapter Fourteen Chapter Fifteen Chapter Sixteen Chapter Seventeen Chapter Eighteen Chapter Nineteen Chapter Twenty Chapter Twenty-One Chapter Twenty-Two Epilogue Playlist Acknowledgements About the Author Books by J. WNV-infected ex vivo brain slice cultures (BSCs) treated with GM-CSF also showed reduced viral titers and caspase 3 apoptotic cell death, indicating that GM-CSF specifically targets the CNS and that its actions are not dependent on peripheral immune activity. GM-CSF-induced microglial activation in WNV-infected mice was associated with reduced viral titers and apoptotic activity (caspase 3) in the brains of WNV-infected mice and significantly increased survival. In addition, more microglia adopted an activated morphology as demonstrated by increased sizes and more pronounced processes. ![]() Daily treatment of both uninfected and WNV-infected mice with subcutaneous injections of GM-CSF resulted in microglial proliferation and activation as indicated by the enhanced expression of the microglia activation marker ionized calcium binding adaptor molecule 1 (Iba1) and several microglia-associated inflammatory cytokines, including CCL2 (C-C motif chemokine ligand 2), interleukin 6 (IL-6), and IL-10. Recombinant human GM-CSF (rHuGMCSF) (sargramostim ) is an FDA-approved drug used to increase white blood cells following leukopenia-inducing chemotherapy or bone marrow transplantation. To determine if augmenting microglial activation would provide a potential therapeutic strategy, we administered granulocyte-macrophage colony-stimulating factor (GM-CSF) to WNV-infected mice. In WNV-infected mice, the depletion of microglia leads to enhanced viral replication, increased central nervous system (CNS) tissue injury, and increased mortality, suggesting that microglia play a critical role in protection against WNV neuroinvasive disease. As there are currently no proven antiviral therapies or licensed human vaccines, understanding the neuropathogenesis of WNV is critical for rational therapeutic design. West Nile virus (WNV) is the leading cause of epidemic arboviral encephalitis in the United States. ![]()
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