A5034378543- Neuroinflammation and Neurodegeneration Mechanisms
- Spinal Cord Injury Research
- Neurogenesis and neuroplasticity mechanisms
- Aortic Disease and Treatment Approaches
- Traumatic Brain Injury and Neurovascular Disturbances
- Sirtuins and Resveratrol in Medicine
- Pressure Ulcer Prevention and Management
- Traumatic Brain Injury Research
- Advanced biosensing and bioanalysis techniques
- Antimicrobial Peptides and Activities
- Spinal Dysraphism and Malformations
- RNA Interference and Gene Delivery
- Adenosine and Purinergic Signaling
- Diabetic Foot Ulcer Assessment and Management
- Adipose Tissue and Metabolism
Rutgers, The State University of New Jersey
2021-2025
University of Washington
2023
Rutgers Sexual and Reproductive Health and Rights
2022
The young mammalian central nervous system regenerates after spinal cord injury and recovers locomotion, whereas adult mice only show limited recovery that depends on the severity, genetic background, physical therapy. At molecular level, key regulators contribute to are cell adhesion molecules, such as L1CAM (L1). surface, L1 functions a homotypic receptor signal-transduces crucial in neuronal migration survival, neurite outgrowth, myelination, formation of synapses, synaptic plasticity. In...
ABSTRACT Uncovering the intricacies of recovery trajectory following spinal cord injury (SCI) has remained a critical exploration for researchers and clinicians, fostering need innovative approaches to offer insight into underlying dynamics this complex phenomenon. Existing methods, such as Basso Mouse Scale (BMS) kinematic analyses, have provided valuable insights, yet limitations in their ability comprehensively capture behavioral nuances call more sophisticated approaches. This study...
CHL1 is a close homolog of L1, cell adhesion molecule that plays major roles in neural and tumor functions. We had found young adult female mice deficient recovered better than their wild-type littermates after thoracic Spinal Cord Injury (SCI). This observation was surprising, because increases neurite outgrowth vitro. mouse central peripheral nervous systems upregulate expression neurons astrocytes, consistent with CHL1's pro-active, homophilic interaction between surface molecules mice....
Myristoylated alanine-rich C-kinase substrate (MARCKS) is a critical member of signaling cascade that influences disease-relevant neural functions such as growth and plasticity. The effector domain (ED) MARCKS interacts with the extracellular glycan polysialic acid (PSA) through cell membrane to stimulate neurite outgrowth in culture. We have shown synthetic ED peptide improves functional recovery after spinal cord injury female but not male mice. However, peptides themselves are unstable...
Abstract STUDY DESIGNAnimal studyOBJECTIVESFemale mice deficient in the adhesion molecule CHL1 recovered better than their wild-type female littermates after spinal cord injury (SCI). This observation was unexpected, because increases neurite outgrowth vitro a homophilic, neuron-dependent manner. Yet, SCI, is upregulated glial scar which reduces axonal regrowth, showing that on glia can block regrowth of positive axons. notion verified co-cultures astrocytes and neurons. Since these SCI...
Like other conditions affecting the central nervous system, spinal cord injury (SCI) is difficult to treat with molecular therapies because blood-brain barrier makes intravenous treatments largely ineffective. For example, a synthetic peptide chain derived from effector domain (ED) of myristoylated alanine-rich C-kinase substrate (MARCKS) has been found improve functional recovery after SCI in female mice; however, peptides do not always pass and are easily degraded due natural proteases...