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ABT-263: a potent and orally bioavailable Bcl-2 family inhibitor.
TLDR
The biological properties and rationale for clinical trials evaluating ABT-263 in small-cell lung cancer and B-cell malignancies are provided and the oral efficacy should provide dosing flexibility to maximize clinical utility both as a single agent and in combination regimens are reported. Expand
Microglia/Macrophage Polarization Dynamics Reveal Novel Mechanism of Injury Expansion After Focal Cerebral Ischemia
TLDR
The results suggest that microglia/macrophages respond dynamically to ischemic injury, experiencing an early “healthy’ M2 phenotype, followed by a transition to a “sick” M1 phenotype, which suggests that stroke therapies should be shifted from simply suppressing microglIA/ Macrophage toward adjusting the balance between beneficial and detrimental microglio-macrophage responses. Expand
Microglial and macrophage polarization—new prospects for brain repair
TLDR
It is argued that therapeutic approaches targeting cerebral inflammation should shift from broad suppression of microglia and macrophages towards subtle adjustment of the balance between their phenotypes, and breakthroughs in the identification of regulatory molecules that control these phenotypic shifts could ultimately accelerate research towards curing brain disorders. Expand
Proinflammatory cytokine expression profile in degenerated and herniated human intervertebral disc tissues.
TLDR
Greater IFNgamma positivity, macrophage presence, and cellularity in herniated IVDs suggests a pattern of Th1 lymphocyte activation in the pathomechanism of disc degeneration. Expand
Trapping of a Methanesulfonanilide by Closure of the Herg Potassium Channel Activation Gate
TLDR
The findings provide direct evidence that the mechanism of slow recovery from HERG channel block by methanesulfonanilides is due to trapping of the compound in the inner vestibule by closure of the activation gate, and suggests that the Vestibule of this channel is larger than the well studied Shaker K+ channel. Expand
Critical Role of Calpain I in Mitochondrial Release of Apoptosis-Inducing Factor in Ischemic Neuronal Injury
TLDR
Calpain I-dependent AIF release is defined as a novel signaling pathway that mediates neuronal cell death after cerebral ischemia and conferred neuroprotection against cell death in neuronal cultures and in hippocampal CA1 neurons after transient global ischemIA. Expand
NMR structure and mutagenesis of the inhibitor-of-apoptosis protein XIAP
TLDR
The nuclear magnetic resonance structure of a region encompassing the second BIR domain (BIR2) of a human IAP family member, XIAP (also called hILP or MIHA), is described and it is indicated that conserved amino acids within the linker region between the BIR1 and BIR2 domains were found to be critical for inhibiting caspase-3. Expand
Microglia/Macrophage Polarization Dynamics in White Matter after Traumatic Brain Injury
TLDR
It is found that microglia/macrophages respond dynamically to TBI, experiencing a transient M2 phenotype followed by a shift to the M1 phenotype, which may propel WMI progression and represents a rational target for TBI treatment. Expand
Neuroprotection against Focal Ischemic Brain Injury by Inhibition of c-Jun N-Terminal Kinase and Attenuation of the Mitochondrial Apoptosis-Signaling Pathway
TLDR
The results confirm the role of JNK as a critical cell death mediator in ischemic brain injury, and suggest that one of the mechanisms by which JNK triggers the mitochondrial apoptosis-signaling pathway is via promoting Bax and Bim translocation. Expand
Rapidly Increased Neuronal Mitochondrial Biogenesis After Hypoxic-Ischemic Brain Injury
TLDR
Neonatal H-I brain injury rapidly induces mitochondrial biogenesis, which may constitute a novel component of the endogenous repair mechanisms of the brain. Expand
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