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  • Book
    edited by Alexzander A.A. Asea, Punit Kaur.
    Summary: The book Heat Shock Proteins in Neuroscience provides the most comprehensive review on contemporary knowledge on the role of HSP in signaling pathways relevant to a number of diseases. Using an integrative approach, the contributors provide a synopsis of novel mechanisms, signal transduction pathways. To enhance the ease of reading and comprehension, this book has been subdivided into various section including; Section I, reviews current progress on our understanding of Neurological Aspects of HSP; Section II, focuses on Aspects of HSP in Neurodegenerative Diseases and Disorders, Section III, emphasizes the importance of HSP in Multiple Sclerosis; Section IV, reviews critical Aspects of HSP in Alzheimer's Disease and Section V, gives a comprehensive update of the Development of HSP-Based Therapies for Neurological Disorders. Key basic and clinical research laboratories from major universities, academic medical hospitals, biotechnology and pharmaceutical laboratories around the world have contributed chapters that review present research activity and importantly project the field into the future. The book is a must read for starters and professionals in the fields of Neurology and Neurosciences, Translational Medicine, Clinical Research, Human Physiology, Biotechnology, Cell & Molecular Medicine, Pharmaceutical Scientists and Researchers involved in Drug Discovery.

    Contents:
    Section I: Neurological Aspects of HSP
    Chapter 1. Hsp60 Friend and Foe of the Nervous System
    Chapter 2. Role of Heat Shock Proteins in Brain Tumors
    Chapter 3. Body Temperature Regulation Determines Immune Reactions and Species Longevity
    Chapter 4. Interaction between Heat Shock Proteins and Components of the Plasminogen Activator System in the Central Nervous System
    Chapter 5. Role of HSP70 in Plasticity and Mem
    Chapter 6. Role of Heat Shock Proteins (HSP) in Neuroprotection for Ischemic Stroke
    Section II: Aspects of HSP in Neurodegenerative Diseases and Disorders
    Chapter 7. Dysregulation of Heat Shock Proteins in Neurodegenerative Diseases: Restorative Roles of Small Molecules and Natural Compounds
    Chapter 8. Molecular Chaperones and Protein Quality Control System in the Canine Model of Brain Aging and Neurodegenerative Diseases
    Chapter 9. Role of Hsp90 Interacting Molecular Chaperones on Tau And Ass Processing in Alzheimer's Disease
    Section III: Aspects of HSP in Multiple Sclerosis
    Chapter 10. Role of Hsp70 in Multiple Sclerosis: An Overview
    Chapter 11. Protective Role of Glial Heat Shock Proteins in Amyotrophic Lateral Sclerosis
    Section IV: Development of HSP-Based Therapies for Neurological Disorders
    Chapter 12. Therapeutic Drugs and Natural Products: The Effect of Suppressing Hsps in Brain Tumors
    Chapter 13. Can HSP Targeted Gene Therapy be a New Hope for Gliomas?
    Chapter 14. Therapeutic Aspects of Heat Shock Proteins in Glioma: Cementing the Crevasses between Bench and Bedside
    Chapter 15. Engineering Chaperones for Alzheimer's Disease: Insights from Drosophila Models
    Chapter 16. Role of HSP in the Treatment of Internal Dıseases.
    Digital Access Springer 2019
  • Journal
    Digital Access Full text via HathiTrust, Vol. 1, no. 1 (Mar. 25, 1877)-v. 138, no. 4214 (spring 1994)
  • Article
    Bredenberg CE, Kazui T, Webb WR.
    Ann Thorac Surg. 1978 Jul;26(1):62-7.
    The effect of 10 cm of positive end-expiratory pressure (PEEP) on lung water was studied during pulmonary edema induced in dogs by inflating a Foley balloon placed in the left atrium. Colloid oncotic pressure (COP) was measured directly. Intrapleural pressure (IPP) was measured after surgical closure of the chest. Transmural left atrial (LA) pressure (LA minus IPP) minus COP was considered to be the net force driving water out of the capillaries. LA pressure was elevated so that transmural LA pressure minus COP averaged +7.5 mm Hg. Water accumulation was expressed as the ratio of wet to dry weight. The control ratio of wet to dry lung weight was 4.30 +/- 0.10 (+/- SE). After 2 hours of standardized pulmonary edema and ventilation without PEEP, wet-to-dry lung weight was 5.63 +/- 0.24. In animals ventilated with 10 cm of PEEP through 2 hours of pulmonary edema the ratio was 5.36 +/- 0.14. Animals ventilated with 10 cm of PEEP showed a significant increase in functional residual capacity and decreased intrapulmonary shunt. Ten centimeters of PEEP, however, had no statistically significant effect on water accumulation during experimental pulmonary edema.
    Digital Access Access Options