A5080599420- Neonatal and fetal brain pathology
- Neonatal Respiratory Health Research
- Anesthesia and Neurotoxicity Research
- Neuroinflammation and Neurodegeneration Mechanisms
- Immune Response and Inflammation
- Birth, Development, and Health
- Neurogenesis and neuroplasticity mechanisms
- Cancer, Hypoxia, and Metabolism
- Congenital Diaphragmatic Hernia Studies
- Pregnancy and preeclampsia studies
- Emergency and Acute Care Studies
- Congenital heart defects research
- Preterm Birth and Chorioamnionitis
- Infant Development and Preterm Care
- Mitochondrial Function and Pathology
- Alzheimer's disease research and treatments
- Extracellular vesicles in disease
- Nitric Oxide and Endothelin Effects
- MicroRNA in disease regulation
- Chaos control and synchronization
- Cancer, Lipids, and Metabolism
- Medical Coding and Health Information
- Immune cells in cancer
- Thermal Regulation in Medicine
- Angiogenesis and VEGF in Cancer
University of Mississippi Medical Center
2014-2024
Jackson Memorial Hospital
2007-2024
University of Mississippi
2013
State Street (United States)
2008-2011
McGill University
2009
University of Rochester
1999-2002
Golisano Children's Hospital
2001
An abnormal pulmonary vasculature may be an important component of bronchopulmonary dysplasia (BPD). We examined human infant lung for the endothelial cell marker PECAM-1 and angiogenic factors their receptors. Lung specimens were collected prospectively at ∼ 6 h after death. The right middle lobe was inflation fixed part lower flash frozen. compared lungs from infants dying with BPD (n = 5) nonpulmonary causes 5). group significantly more premature had days ventilator supplemental oxygen...
Proper formation of the pulmonary microvasculature is essential for normal lung development and gas exchange. Lung microvascular may be disrupted by chronic injury developing lungs in clinical diseases such as bronchopulmonary dysplasia. We examined development, angiogenic growth factors, endothelial cell receptors a fetal baboon model disease (CLD). In last third gestation, marker platelet adhesion molecule (PECAM)-1 increased 7.5-fold, capillaries immunostained PECAM-1 changed from central...
Oligodendrocyte (OL) development relies on many extracellular cues, most of which are secreted cytokines from neighboring neural cells. Although it is generally accepted that both astrocytes and microglia beneficial for OL development, there a lack understanding regarding whether play similar or distinct roles. The current study examined the effects developmental phenotypes including cell survival, proliferation, differentiation, myelination in vitro. Our data reveal that, although...
Serotonin (5-hydroxytryptamine, 5-HT) has been implicated to play critical roles in early neural development. Recent reports have suggested that perinatal exposure selective serotonin reuptake inhibitors (SSRIs) resulted cortical network miswiring, abnormal social behavior, callosal myelin malformation, as well oligodendrocyte (OL) pathology rats. To gain further insight into the cellular and molecular mechanisms underlying SSRIs-induced OL abnormalities, we investigated effect of 5-HT on...
Abstract Background Cyclooxygenase-2 (COX-2) is induced in inflammatory cells response to cytokines and pro-inflammatory molecules, suggesting that COX-2 has a role the process. The objective of current study was examine whether celecoxib, selective inhibitor, could ameliorate lipopolysaccharide (LPS)-induced brain inflammation, dopaminergic neuronal dysfunction sensorimotor behavioral impairments. Methods Intraperitoneal (i.p.) injection LPS (2 mg/kg) performed rat pups on postnatal Day 5...
Perinatal infection is a well-identified risk factor for number of neurodevelopmental disorders, including brain white matter injury (WMI) and Autism Spectrum Disorders (ASD). The underlying mechanisms by which early life inflammatory events cause aberrant neural, cytoarchitectural, network organization, remain elusive. This study aimed to investigate how systemic lipopolysaccharide (LPS)-induced neuroinflammation affects microglia phenotypes neural developmental in rats. We show here that...
We previously reported that intranasal insulin protects substantia nigra dopaminergic neurons against 6-hydroxydopamine neurotoxicity in rats. This study aimed to assess pharmacokinetics the rat brain following application. Recombinant human (rh-Ins) or phosphate buffer solution was administered both nostrils of Animals were sacrificed at 15 minutes, 1, 2, and 6 hours determine levels different regions by an ultrasensitive, human-specific enzyme-linked immunosorbent assay kit. For...
The hematopoietic growth factor erythropoietin (EPO) has been shown to be neuroprotective against hypoxia-ischemia (HI) in Postnatal Day 7 (P7)–P10 or adult animal models. current study was aimed determine whether EPO also provides long-lasting neuroprotection HI P5 rats, which is relevant immature human infants. Sprague-Dawley rats at were subjected right common carotid artery ligation followed by an exposure 6% oxygen with balanced nitrogen for 1.5 h. Human recombinant (rEPO, a dose of 5...
The use of dexamethasone in premature infants to prevent and/or treat bronchopulmonary dysplasia adversely affects neurocognitive development and is associated with cerebral palsy. underlying mechanisms these effects are multifactorial likely include apoptosis. objective this study was confirm whether causes apoptosis different regions the developing rat brain. On postnatal day 2, pups each litter were randomly divided into dexamethasone-treated (n = 91) or vehicle-treated 92) groups. Rat...
Neonatal lipopolysaccharide (LPS) exposure-induced brain inflammation resulted in motor dysfunction and dopaminergic neuronal injury, increased the risks of neurodegenerative disorders adult rats. Our previous studies showed that intranasal administration insulin-like growth factor-1 (IGF-1) protects against LPS-induced white matter injury developing rat brain. To further examine whether IGF-1 neurobehavioral dysfunction, recombinant human (rhIGF-1) at a dose 50 µg/pup was administered...
Our previous study showed that a single lipopolysaccharide (LPS) treatment to neonatal rats could induce long-lasting neuroinflammatory response and dopaminergic system injury late in life. This is evidenced by sustained activation of microglia elevated interleukin-1β (IL-1β) levels, as well reduced tyrosine hydroxylase (TH) expression the substantia nigra (SN) P70 rat brain. The object current was test whether co-administration IL-1 receptor antagonist (IL-1ra) protects against LPS-induced...