Professor, Anesthesia, Stanford University Medical Center
Anesthesiology
Dr. Rona G. Giffard, MD
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Dr. Rona G. Giffard practices Anesthesiology. He graduated from Stanford University School of Medicine. Stanford University School of Medicine is one of the top medical schools in the US. Stanford University School of Medicine is ranked 2/25 in Research/PrimaryCare. Rona Giffard has written publications. He has 99 publications published with PubMed. The lastest paper is: 'Two tips for users of Bullard Intubating Laryngoscope.'
Publications
- Physiologically normal 5% O2 supports neuronal differentiation and resistance to inflammatory injury in neural stem cell cultures.
- Post-stroke treatment with miR-181 antagomir reduces injury and improves long-term behavioral recovery in mice after focal cerebral ischemia.
- MicroRNA-200c contributes to injury from transient focal cerebral ischemia by targeting Reelin.
- Advances in Astrocyte-targeted Approaches for Stroke Therapy: An Emerging Role for Mitochondria and microRNAS.
- Overexpression of Heat Shock Protein 72 Attenuates NF-κB Activation Using a Combination of Regulatory Mechanisms in Microglia.
- MicroRNAs Regulate the Chaperone Network in Cerebral Ischemia.
- The use of microRNAs to modulate redox and immune response to stroke.
- microRNAs affect BCL-2 family proteins in the setting of cerebral ischemia.
- Mini-review: Neuroprotection by astrocytes in brain ischemia: importance of microRNAs.
- Astrocyte-enriched miR-29a targets PUMA and reduces neuronal vulnerability to forebrain ischemia.
- Inhibition of microRNA-181 reduces forebrain ischemia-induced neuronal loss.
- The future of molecular chaperones and beyond.
- Anaesthetic neurotoxicity and neuroplasticity: an expert group report and statement based on the BJA Salzburg Seminar.
- Mitigation of Murine Focal Cerebral Ischemia by the Hypocretin/Orexin System is Associated With Reduced Inflammation.
- Selective activation of protein kinase C? in mitochondria is neuroprotective in vitro and reduces focal ischemic brain injury in mice.
- Inflammatory response of microglial BV-2 cells includes a glycolytic shift and is modulated by mitochondrial glucose-regulated protein 75/mortalin.
- Effects of heat shock protein 72 (Hsp72) on evolution of astrocyte activation following stroke in the mouse.
- microRNAs: Innovative Targets for Cerebral Ischemia and Stroke.
- MicroRNA-320 induces neurite outgrowth by targeting ARPP-1.
- Stroke-induced activation of the α7 nicotinic receptor increases Pseudomonas aeruginosa lung injury.
- Significance of marrow-derived nicotinamide adenine dinucleotide phosphate oxidase in experimental ischemic stroke.
- miR-181 regulates GRP78 and influences outcome from cerebral ischemia in vitro and in vivo.
- miR-181 targets multiple Bcl-2 family members and influences apoptosis and mitochondrial function in astrocytes.
- Inflammation, mitochondria, and the inhibition of adult neurogenesis.
- Quantitative characterization and analysis of the dynamic NF-kappaB response in microglia.
- Increased Brain Injury and Worsened Neurological Outcome in Interleukin-4 Knockout Mice After Transient Focal Cerebral Ischemia.
- Astrocytes: Targets for Neuroprotection in Stroke.
- Heat shock protein 72 overexpression prevents early postoperative memory decline after orthopedic surgery under general anesthesia in mice.
- Astrocyte proliferation following stroke in the mouse depends on distance from the infarct.
- Mitochondrial protection attenuates inflammation-induced impairment of neurogenesis in vitro and in vivo.
- Astrocyte targeted overexpression of Hsp72 or SOD2 reduces neuronal vulnerability to forebrain ischemia.
- Age-related defects in sensorimotor activity, spatial learning, and memory in C57BL/6 mice.
- Overexpression of mitochondrial Hsp70/Hsp75 in rat brain protects mitochondria, reduces oxidative stress, and protects from focal ischemia.
- Inflammation and NFkappaB activation is decreased by hypothermia following global cerebral ischemia.
- Postischemic brain injury is attenuated in mice lacking the beta2-adrenergic receptor.
- Regulation of apoptotic and inflammatory cell signaling in cerebral ischemia: the complex roles of heat shock protein 70.
- Overexpression of mitochondrial Hsp70/Hsp75 protects astrocytes against ischemic injury in vitro.
- Selective dysfunction of hippocampal CA1 astrocytes contributes to delayed neuronal damage after transient forebrain ischemia.
- Biphasic role of nuclear factor-kappa B on cell survival and COX-2 expression in SOD1 Tg astrocytes after oxygen glucose deprivation.
- The carboxyl-terminal domain of inducible Hsp70 protects from ischemic injury in vivo and in vitro.
- Chaperonin GroEL and its mutant D87K protect from ischemia in vivo and in vitro.
- Microglia potentiate damage to blood-brain barrier constituents: improvement by minocycline in vivo and in vitro.
- Antegrade cerebral perfusion reduces apoptotic neuronal injury in a neonatal piglet model of cardiopulmonary bypass.
- Overexpression of inducible heat shock protein 70 and its mutants in astrocytes is associated with maintenance of mitochondrial physiology during glucose deprivation s...
- Antiapoptotic and anti-inflammatory mechanisms of heat-shock protein protection.
- Ischemia-induced programmed cell death in astrocytes.
- Overexpression of copper/zinc superoxide dismutase decreases ischemia-like astrocyte injury.
- Development of neonatal murine microglia in vitro: changes in response to lipopolysaccharide and ischemia-like injury.
- Many mechanisms for hsp70 protection from cerebral ischemia.
- Overexpression of HDJ-2 protects astrocytes from ischemia-like injury and reduces redistribution of ubiquitin staining in vitro.
- Perinatal brain injury: the role of development in vulnerability.
- Gene therapy and hypothermia for stroke treatment.
- Bcl-XL maintains mitochondrial function in murine astrocytes deprived of glucose.
- Advances in understanding protection from cerebral ischemia.
- Effect of Bcl-x(L) overexpression on reactive oxygen species, intracellular calcium, and mitochondrial membrane potential following injury in astrocytes.
- Gene transfer of HSP72 protects cornu ammonis 1 region of the hippocampus neurons from global ischemia: influence of Bcl-2.
- Influence of mild hypothermia on inducible nitric oxide synthase expression and reactive nitrogen production in experimental stroke and inflammation.
- Mild hypothermia reduces apoptosis of mouse neurons in vitro early in the cascade.
- Role of Astrocytes in Delayed Neuronal Death: GLT-1 and its Novel Regulation by MicroRNAs.
- Intrathecal injection of an alpha seven nicotinic acetylcholine receptor agonist attenuates gp120-induced mechanical allodynia and spinal pro-inflammatory cytokine pro...
- Heat shock protein 72 (Hsp72) improves long term recovery after focal cerebral ischemia in mice.
- Effect of overexpression of protective genes on mitochondrial function of stressed astrocytes.
- Overexpression of HSP72 after induction of experimental stroke protects neurons from ischemic damage.
- Human papilloma virus type 16 E7 genes protect astrocytes against apoptotic and necrotic death induced by hydrogen peroxide.
- Differential neuroprotection from human heat shock protein 70 overexpression in in vitro and in vivo models of ischemia and ischemia-like conditions.
- Differential sensitivity of murine astrocytes and neurons from different brain regions to injury.
- Principles of gene therapy: potential applications in the treatment of cerebral ischaemia.
- Ischemic vulnerability of primary murine microglial cultures.
- An introduction to the changes in gene expression that occur after cerebral ischaemia.
- Cell death in the central nervous system: therapeutic possibilities?
- The electrogenic sodium bicarbonate cotransporter: developmental expression in rat brain and possible role in acid vulnerability.
- Overexpression of bcl-2, bcl-XL or hsp70 in murine cortical astrocytes reduces injury of co-cultured neurons.
- The neuroprotective potential of heat shock protein 70 (HSP70).
- Overexpression of bcl-xL protects astrocytes from glucose deprivation and is associated with higher glutathione, ferritin, and iron levels.
- Two tips for users of Bullard Intubating Laryngoscope.
- Potentiation of murine astrocyte antioxidant defence by bcl-2: protection in part reflects elevated glutathione levels.
- The E6 and E7 genes of human papilloma virus-type 16 protect primary astrocyte cultures from injury.
- Acidosis reduces neuronal apoptosis.
- Increasing vulnerability of astrocytes to oxidative injury with age despite constant antioxidant defenses.
- Selection of human cervical epithelial cells that possess reduced apoptotic potential to low-oxygen conditions.
- HSP70 protects murine astrocytes from glucose deprivation injury.
- Increased production of extracellular glutamate by the mitochondrial glutaminase following neuronal death.
- Vulnerability to glucose deprivation injury correlates with glutathione levels in astrocytes.
- Ultrastructure of excitotoxic neuronal death in murine cortical culture.
- Over-expression of HSP-70 protects astrocytes from combined oxygen-glucose deprivation.
- Mechanism of heat shock protein 72 induction in primary cultured astrocytes after oxygen-glucose deprivation.
- Activation of class II or III metabotropic glutamate receptors protects cultured cortical neurons against excitotoxic degeneration.
- Neuroprotective effects of glutamate antagonists and extracellular acidity.
- Secobarbital attenuates excitotoxicity but potentiates oxygen-glucose deprivation neuronal injury in cortical cell culture.
- Correlation of CGS 19755 neuroprotection against in vitro excitotoxicity and focal cerebral ischemia.
- Neuroprotection by the N-methyl-D-aspartate receptor antagonist CGP 40116: in vivo and in vitro studies.
- Glia modulate the response of murine cortical neurons to excitotoxicity: glia exacerbate AMPA neurotoxicity.
- Neuroprotective effect of hypothermia in cortical cultures exposed to oxygen-glucose deprivation or excitatory amino acids.
- Ca2+-dependent binding of severin to actin: a one-to-one complex is formed.
- Ca2+-sensitive isolation of a cortical actin matrix from Dictyostelium amoebae.
- Selective vulnerability of cultured cortical glia to injury by extracellular acidosis.
- Acute brain injury, NMDA receptors, and hydrogen ions: observations in cortical cell cultures.
- Acidosis reduces NMDA receptor activation, glutamate neurotoxicity, and oxygen-glucose deprivation neuronal injury in cortical cultures.
Schools
Stanford University School Of Medicine
Kaiser Permanente Med Center
Stanford University Med School
Doctors Specialties
- Anesthesiology
Accepted Insurances
- Great West Healthcare-Cigna PPO
Education
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Stanford University -
Kaiser Permanente Medical Center -
Stanford University School of Medicine
Hospital
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Stanford Health Care -
VA Palo Alto Health Care System
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