A5101964252- Cardiac Arrest and Resuscitation
- Traumatic Brain Injury and Neurovascular Disturbances
- Thermal Regulation in Medicine
- Mitochondrial Function and Pathology
- Adenosine and Purinergic Signaling
- Neuroscience of respiration and sleep
- Neonatal Respiratory Health Research
- S100 Proteins and Annexins
- Neonatal and fetal brain pathology
- Adipose Tissue and Metabolism
- Anesthesia and Neurotoxicity Research
- Cardiac Ischemia and Reperfusion
- GDF15 and Related Biomarkers
- RNA modifications and cancer
- Neuroinflammation and Neurodegeneration Mechanisms
- Traumatic Brain Injury Research
- Respiratory Support and Mechanisms
- Ion Transport and Channel Regulation
- RNA Research and Splicing
- Fibroblast Growth Factor Research
- Sepsis Diagnosis and Treatment
- Nitric Oxide and Endothelin Effects
- Congenital Diaphragmatic Hernia Studies
- Protein Kinase Regulation and GTPase Signaling
- ATP Synthase and ATPases Research
University of South Florida
2019-2025
University of Uyo
2024
Jackson Memorial Hospital
2013-2023
University of Pittsburgh
2006-2019
Children's Hospital of Pittsburgh
2014-2019
University of Pittsburgh Medical Center
2017
Merck & Co., Inc., Rahway, NJ, USA (United States)
2015
University of Nebraska–Lincoln
2013-2015
University of Florida
2007-2010
Estradiol rapidly modulates hippocampal synaptic plasticity and transmission; however, the contribution of various estrogen receptors to rapid changes in function is unclear. This study examined effect receptor selective agonists on transmission slices obtained from 3–5-month-old wild type (WT), alpha (ERαKO), beta (ERβKO) knockout female ovariectomized mice. Hippocampal were prepared 10–16 days following ovariectomy extracellular excitatory postsynaptic field potentials recorded CA3-CA1...
Extremely mild hypothermia to 36.0 °C is not thought appreciably differ clinically from 37.0 °C. However, it possible that stimulates highly sensitive hypothermic signaling mechanism(s) and alters biochemistry. To the best of our knowledge, no such ultra-sensitive pathway/mechanisms have been described. Here we show cold stress protein RNA binding motif 3 (RBM3) increases in neuron astrocyte cultures maintained at 33 or 36 for 24 48 h, compared 37 controls. Neurons cultured also had...
Anthraquinone derivatives such as emodin have recently been shown to protect in models of beta amyloid β (Aβ) and tau aggregation-induced cell death. The mechanisms action possibly involve preconditioning effects, anti-aggregation properties, and/or enhancing the phosphatidylinositol-3-kinase (PI3K)/AKT survival mechanism. We studied several natural (emodin, rhein, aloin) synthetic (AQ2S) anthraquinones, screen for post-treatment therapeutic benefit two neuronal death, namely hydrogen...
Although multiple biochemical pathways produce adenosine, studies suggest that the 2',3'-cAMP-adenosine pathway (2',3'-cAMP→2'-AMP/3'-AMP→adenosine) contributes to adenosine production in some cells/tissues/organs. To determine whether exists vivo brain, we delivered brain (gray matter and white separately) via inflow perfusate of a microdialysis probe either 2',3'-cAMP, 3',5'-cAMP, 2'-AMP, 3'-AMP, or 5'-AMP measured recovered metabolites outflow with mass spectrometry. In both gray matter,...
Secondary insults, such as hemorrhagic shock (HS), worsen outcome from traumatic brain injury (TBI). Both TBI and HS modulate levels of inflammatory mediators. We evaluated the addition on response to TBI. Adult male C57BL6J mice were randomized into five groups (n=4 [naïve] or 8/group): naïve; sham; (through mild-to-moderate controlled cortical impact [CCI] at 5 m/sec, 1-mm depth), HS; CCI+HS. All non-naïve underwent identical monitoring anesthesia. CCI+HS a 35-min period...
Extracellular adenosine 3',5'-cyclic monophosphate (3',5'-cAMP) is an endogenous source of localized production in many organs. Recent studies suggest that extracellular 2',3'-cAMP (positional isomer 3',5'-cAMP) also a adenosine, particularly the brain vivo post-injury. Moreover, vitro show both microglia and astrocytes can convert to adenosine. Here, we examined ability primary mouse oligodendrocytes neurons metabolize their respective monophosphates (2'-AMP 3'-AMP). Cells were isolated...
Cerebral edema is critical to morbidity/mortality in traumatic brain injury (TBI) and worsened by hypotension. Glibenclamide may reduce cerebral inhibiting sulfonylurea receptor-1 (Sur1); its effect on diffuse exacerbated hypotension/resuscitation unknown. We aimed determine if glibenclamide improves pericontusional and/or controlled cortical impact (CCI) (5m/sec, 1 mm depth) plus hemorrhagic shock (HS) (35 min), compare effects CCI alone. C57BL/6 mice were divided into five groups (n =...
The aim of this investigation was to test the hypothesis that extracellular guanosine regulates adenosine levels. Rat preglomerular vascular smooth muscle cells were incubated with adenosine, guanosine, or both. Guanosine (30 μmol/l) per se had little effect on Extracellular levels 1 h after addition (3 0.125 ± 0.020 μmol/l, indicating rapid disposition adenosine. plus 1.173 0.061 slow Cell injury increased endogenous and effects cell modulated by altering exogenous purine nucleoside...
Abstract Nitrite acts as an ischemic reservoir of nitric oxide ( NO ) and a potent S‐nitrosating agent which reduced histologic brain injury after rat asphyxial cardiac arrest ACA ). The mechanism(s) nitrite‐mediated neuroprotection remain to be defined. We hypothesized that mitochondrial S‐nitrosation accounts for by reducing reperfusion reactive oxygen species ROS generation. (4 μmol) or placebo was infused IV normothermic (37°C) in randomized, blinded fashion with evaluation neurologic...
Introduction: Neuroinflammation plays a critical role in tissue injury and repair after neonatal hypoxic-ischemic (HI) brain varies by sex. Growth differentiation factor-15 (GDF-15) is cytokine released macrophages during inflammation upregulated ischemia. We examined the impact of GDF-15 knockout (KO) on volume loss combined microglia/macrophage response Rice Vannucci model HI injury. Methods: Male female wild-type (WT) Gdf15+/+, heterozygous Gdf15nuGFP-CE/+ (Het), homozygous...
Many organs express the extracellular 3',5'-cAMP-adenosine pathway (conversion of 3',5'-cAMP to 5'-AMP and adenosine). Some release 2',3'-cAMP (isomer 3',5'-cAMP) convert 2'- 3'-AMP these AMPs adenosine (extracellular 2',3'-cAMP-adenosine pathway). As astrocytes microglia are important participants in response brain injury is an endogenous neuroprotectant, we investigated whether cAMP-adenosine pathways exist cell types. 2',3'-, 3',5'-cAMP, 5'-, 3'-, 2'-AMP were incubated with mouse primary...
Splicing factors (SFs) coordinate nuclear intron/exon splicing of RNA. factor disturbances can cause cell death. RNA binding motif 5 (RBM5) and 10 (RBM10) promote apoptosis in cancer cells by activating detrimental alternative key death/survival genes. The role(s) RBM5/10 neurons has not been established. Here, we report that RBM5 knockdown human neuronal decreases caspase activation staurosporine. In contrast, RBM10 augments activation. To determine whether brain injury alters RBM...
Activated cardiac fibroblasts (CFs), preglomerular vascular smooth muscle cells (PGVSMCs), and glomerular mesangial (GMCs) proliferate, cause hypertrophy, produce collagen; in this way, activated CFs contribute to fibrosis, PGVSMCs GMCs promote renal fibrosis. In heart kidney diseases, SDF-1α (stromal cell-derived factor 1α; endogenous CXCR4 [C-X-C motif chemokine receptor 4] agonist) levels are often elevated; therefore, it is important know whether how the SDF-1α/CXCR4 axis activates CFs,...