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  1. Article ; Online: Gene Therapy of the Peripheral Nervous System: Celiac Ganglia.

    Hammond, Bradley / Kreulen, David L

    Methods in molecular biology (Clifton, N.J.)

    2016  Volume 1382, Page(s) 275–283

    Abstract: Gene therapy has played an integral role in advancing our understanding of the central nervous system. However, gene therapy techniques have yet to be widely utilized in the peripheral nervous system. Critical targets for gene therapy within the PNS are ... ...

    Abstract Gene therapy has played an integral role in advancing our understanding of the central nervous system. However, gene therapy techniques have yet to be widely utilized in the peripheral nervous system. Critical targets for gene therapy within the PNS are the neurons in sympathetic ganglia, which are the final pathway to end organs. Thus they are the most specific targets for organ-specific neuron modification. This presents challenges because neurons are not viscerotopically organized within the ganglia and therefore cannot be targeted by their location. However, organ-specific neurons have been identified in sympathetic ganglia of some species and this offers an opportunity for targeting and transducing neurons by way of their target. In fact, alterations in sympathetic neurons have had pathological effects, and transducing organ-specific sympathetic neurons offer an exciting opportunity to selectively modify sympathetic pathology. In this chapter, we describe a method to virally transduce the celiac ganglion (CG), a prevertebral sympathetic ganglion that innervates abdominal organs, with AAV serotypes 1 and 6; thereby, providing a potential avenue to modulate specific subsets of neurons within the celiac ganglion.
    MeSH term(s) Animals ; Dependovirus/genetics ; Ganglia, Sympathetic/pathology ; Ganglia, Sympathetic/virology ; Genetic Therapy ; Genetic Vectors/administration & dosage ; Green Fluorescent Proteins/genetics ; Green Fluorescent Proteins/metabolism ; Injections ; Male ; Rats ; Transduction, Genetic
    Chemical Substances Green Fluorescent Proteins (147336-22-9)
    Language English
    Publishing date 2016
    Publishing country United States
    Document type Journal Article
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-4939-3271-9_20
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Percutaneous cardioplegic arrest before repeat sternotomy in patients with retrosternal aortic aneurysm.

    Mehta, Anand R / Hammond, Bradley / Unai, Shinya / Navia, Jose L / Gillinov, Marc / Pettersson, Gosta B

    The Journal of thoracic and cardiovascular surgery

    2019  Volume 161, Issue 5, Page(s) 1724–1730

    Abstract: Objective: Redo sternotomy in patients with arterial cardiac structures adherent to the sternum carries a risk of catastrophic bleeding. In some of those cases, particularly if they have undergone multiple previous operations, deep hypothermic ... ...

    Abstract Objective: Redo sternotomy in patients with arterial cardiac structures adherent to the sternum carries a risk of catastrophic bleeding. In some of those cases, particularly if they have undergone multiple previous operations, deep hypothermic circulatory arrest alone may not provide sufficient time for a controlled dissection.
    Methods: We present a series of 6 cases at risk for exsanguination during sternal re-entry successfully reoperated using percutaneous cardioplegic cardiac arrest induced before completed sternal re-entry to avoid or minimize the hypothermic circulatory arrest time.
    Results: All patients survived their complex operations.
    Conclusions: Percutaneous cardioplegic arrest allows safer repeat sternotomy in patients with arterial cardiac structures adherent to the sternum.
    MeSH term(s) Adult ; Aged ; Aortic Aneurysm/surgery ; Female ; Heart Arrest, Induced/methods ; Humans ; Male ; Middle Aged ; Reoperation/methods ; Sternotomy/adverse effects ; Sternotomy/methods
    Language English
    Publishing date 2019-11-16
    Publishing country United States
    Document type Case Reports ; Journal Article
    ZDB-ID 3104-5
    ISSN 1097-685X ; 0022-5223
    ISSN (online) 1097-685X
    ISSN 0022-5223
    DOI 10.1016/j.jtcvs.2019.09.191
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Anesthetic Management for Paraesophageal Hernia Repair.

    Kazakova, Tatiana / Hammond, Bradley / Talarek, Chad / Sinha, Ashish C / Brister, Neil W

    Thoracic surgery clinics

    2019  Volume 29, Issue 4, Page(s) 447–455

    Abstract: Paraesophageal hernia repairs are complex surgical cases frequently performed on patients of advanced age with multiple comorbidities, both of which create difficulties in the anesthetic management. Preoperative evaluation is challenging because of ... ...

    Abstract Paraesophageal hernia repairs are complex surgical cases frequently performed on patients of advanced age with multiple comorbidities, both of which create difficulties in the anesthetic management. Preoperative evaluation is challenging because of overlapping cardiopulmonary symptoms. The patient's symptoms and anatomy lead to an increased aspiration risk and the potential need for a rapid sequence induction. Depending on the surgical approach, lung isolation may be required. Communication with the surgeon is vital throughout the case, especially when placing gastric tube and bougies. Multimodal analgesia should include regional and/or neuraxial techniques, in addition to the standard intravenous and oral pain medications.
    MeSH term(s) Airway Management/methods ; Anesthesia, General/methods ; Fluid Therapy/methods ; Hernia, Hiatal/surgery ; Herniorrhaphy/methods ; Humans ; Intubation, Gastrointestinal/methods ; Laparoscopy ; Neuromuscular Blocking Agents/therapeutic use ; Pain, Postoperative/therapy ; Respiration, Artificial/methods ; Risk Assessment
    Chemical Substances Neuromuscular Blocking Agents
    Language English
    Publishing date 2019-09-26
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2149218-9
    ISSN 1558-5069 ; 1547-4127
    ISSN (online) 1558-5069
    ISSN 1547-4127
    DOI 10.1016/j.thorsurg.2019.07.007
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Prenatal stress-immune programming of sex differences in comorbidity of depression and obesity/metabolic syndrome.

    Goldstein, Jill M / Holsen, Laura / Huang, Grace / Hammond, Bradley D / James-Todd, Tamarra / Cherkerzian, Sara / Hale, Taben M / Handa, Robert J

    Dialogues in clinical neuroscience

    2012  Volume 18, Issue 4, Page(s) 425–436

    Abstract: Major depressive disorder (MDD) is the number one cause of disability worldwide and is comorbid with many chronic diseases, including obesity/metabolic syndrome (MetS). Women have twice as much risk for MDD and comorbidity with obesity/MetS as men, ... ...

    Abstract Major depressive disorder (MDD) is the number one cause of disability worldwide and is comorbid with many chronic diseases, including obesity/metabolic syndrome (MetS). Women have twice as much risk for MDD and comorbidity with obesity/MetS as men, although pathways for understanding this association remain unclear. On the basis of clinical and preclinical studies, we argue that prenatal maternal stress (ie, excess glucocorticoid expression and associated immune responses) that occurs during the sexual differentiation of the fetal brain has sex-dependent effects on brain development within highly sexually dimorphic regions that regulate mood, stress, metabolic function, the autonomic nervous system, and the vasculature. Furthermore, these effects have lifelong consequences for shared sex-dependent risk of MDD and obesity/MetS. Thus, we propose that there are shared biologic substrates at the anatomical, molecular, and/or genetic levels that produce the comorbid risk for MDD-MetS through sex-dependent fetal origins.
    MeSH term(s) Comorbidity ; Depressive Disorder, Major/epidemiology ; Depressive Disorder, Major/physiopathology ; Female ; Gonads/physiology ; Gonads/physiopathology ; Humans ; Hypothalamo-Hypophyseal System/physiology ; Hypothalamo-Hypophyseal System/physiopathology ; Male ; Metabolic Syndrome/epidemiology ; Metabolic Syndrome/physiopathology ; Obesity/epidemiology ; Obesity/physiopathology ; Pituitary-Adrenal System/physiology ; Pituitary-Adrenal System/physiopathology ; Pregnancy ; Prenatal Exposure Delayed Effects/immunology ; Prenatal Exposure Delayed Effects/physiopathology ; Sex Characteristics ; Stress, Physiological/immunology ; Stress, Physiological/physiology ; Stress, Psychological/immunology ; Stress, Psychological/physiopathology
    Language English
    Publishing date 2012-04-26
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2188781-0
    ISSN 1958-5969 ; 1294-8322
    ISSN (online) 1958-5969
    ISSN 1294-8322
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 6188: Show issues Location:
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  5. Article ; Online: Disruption of mitochondrial DNA replication in Drosophila increases mitochondrial fast axonal transport in vivo.

    Baqri, Rehan M / Turner, Brittany A / Rheuben, Mary B / Hammond, Bradley D / Kaguni, Laurie S / Miller, Kyle E

    PloS one

    2009  Volume 4, Issue 11, Page(s) e7874

    Abstract: Mutations in mitochondrial DNA polymerase (pol gamma) cause several progressive human diseases including Parkinson's disease, Alper's syndrome, and progressive external ophthalmoplegia. At the cellular level, disruption of pol gamma leads to depletion of ...

    Abstract Mutations in mitochondrial DNA polymerase (pol gamma) cause several progressive human diseases including Parkinson's disease, Alper's syndrome, and progressive external ophthalmoplegia. At the cellular level, disruption of pol gamma leads to depletion of mtDNA, disrupts the mitochondrial respiratory chain, and increases susceptibility to oxidative stress. Although recent studies have intensified focus on the role of mtDNA in neuronal diseases, the changes that take place in mitochondrial biogenesis and mitochondrial axonal transport when mtDNA replication is disrupted are unknown. Using high-speed confocal microscopy, electron microscopy and biochemical approaches, we report that mutations in pol gamma deplete mtDNA levels and lead to an increase in mitochondrial density in Drosophila proximal nerves and muscles, without a noticeable increase in mitochondrial fragmentation. Furthermore, there is a rise in flux of bidirectional mitochondrial axonal transport, albeit with slower kinesin-based anterograde transport. In contrast, flux of synaptic vesicle precursors was modestly decreased in pol gamma-alpha mutants. Our data indicate that disruption of mtDNA replication does not hinder mitochondrial biogenesis, increases mitochondrial axonal transport, and raises the question of whether high levels of circulating mtDNA-deficient mitochondria are beneficial or deleterious in mtDNA diseases.
    MeSH term(s) Animals ; Axons/metabolism ; DNA/chemistry ; DNA Replication ; DNA, Mitochondrial/genetics ; Drosophila/genetics ; Green Fluorescent Proteins/chemistry ; Image Processing, Computer-Assisted ; Immunohistochemistry/methods ; Kinesin/chemistry ; Microscopy, Confocal/methods ; Microscopy, Electron/methods ; Mutation ; Organic Chemicals/pharmacology
    Chemical Substances DNA, Mitochondrial ; Organic Chemicals ; PicoGreen ; Green Fluorescent Proteins (147336-22-9) ; DNA (9007-49-2) ; Kinesin (EC 3.6.4.4)
    Language English
    Publishing date 2009-11-17
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0007874
    Database MEDical Literature Analysis and Retrieval System OnLINE

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