- Vector-borne infectious diseases
- Extracellular vesicles in disease
- Parasites and Host Interactions
- COVID-19 Clinical Research Studies
- Kawasaki Disease and Coronary Complications
- Vasculitis and related conditions
- Mosquito-borne diseases and control
- Bacterial Infections and Vaccines
- Viral Infections and Vectors
The University of Texas Medical Branch at Galveston
2021-2025
National Cancer Institute
2025
National Institutes of Health
2025
Center for Cancer Research
2025
Background/Objectives: 89Zr-oxine is an ex vivo cell labeling agent that enables cells to be tracked in by positron emission tomography (PET) over a period of up two weeks. To better understand where binds within cellular components, factors affecting and intracellular distribution 89Zr were examined. Methods: Mouse primary T cells, natural killer dendritic monocytes, lines EL4 (mouse lymphoma), DC2.4 cell), Kit225K6 (human leukemia) MC38 colon adenocarcinoma) labeled with or 111In-oxine...
Spotted fever group rickettsioses caused by Rickettsia ( R ) are devastating human infections, which mainly target microvascular endothelial cells (ECs) and can induce lethal EC barrier dysfunction in the brain lungs. Our previous evidence reveals that exosomes (Exos) derived from rickettsial - infected ECs, namely -ECExos, disruption of tight junctional (TJ) protein ZO-1 normal recipient (BMECs). However, underlying mechanism remains elusive. Given we have observed microRNA23a (miR23a), a...
Intracellular cAMP receptor exchange proteins directly activated by 1 (EPAC1) regulate obligate intracellular parasitic bacterium rickettsial adherence to and invasion into vascular endothelial cells (ECs). However, underlying precise mechanism(s) remain unclear. The aim of the study is dissect functional role EPAC1-ANXA2 signaling pathway during initial adhesion rickettsiae EC surfaces.In present study, an established system that anatomically based quantifies bacterial ECs in vivo was...
Abstract Spotted fever group rickettsioses caused by Rickettsia ( R ) are devastating human infections, which mainly target microvascular endothelial cells (EC) and can induce lethal EC barrier dysfunction in the brain lungs. Our previous evidence reveals that exosomes (Exos) derived from rickettsial-infected ECs, namely -ECExos, disruption of tight junctional (TJ) protein ZO-1 normal recipient (BMECs). However, underlying mechanism remains elusive. Given we have observed microRNA23a...