Jeff Hansen
| This email address is being protected from spambots. You need JavaScript enabled to view it.Research Editor
jeffhans@uab.edu | (205) 209-2355Communicates UAB research discoveries and initiatives from across the university for a variety of audiences.
Specific beats:
- Alabama Drug Discovery Alliance
- Biochemistry and Molecular Genetics
- Biomatrix Engineering and Regenerative Medicine
- Cell biology
- Center for Biophysical Sciences and Engineering
- CCTS
- Center for Metabolic Bone Disease
- Microbiology
- Neurobiology
- Comprehensive Neuroscience Center
- Pathology, research shared with MS2
- Pharmacology and Toxicology
- Physiology and Biophysics
- UAB Research Foundation/IIE
- Research Administration
The vaccine candidate Altimmune’s AdCOVID potently stimulated neutralizing antibody and T cell responses, as well as mucosal immunity in the respiratory tract.
Precision disease modeling involves creation of patient-specific disease models that mimic the molecular character of a condition present in a patient, enabling more precise diagnoses and treatments.
This avenue of basic research will aid understanding of neurodevelopmental disorders in humans.
The exosomes were secreted by cardiac cells derived from human induced pluripotent stem cells. These non-living exosomes may be an easier form of regenerative treatment than living cells.
These molecular insights may foster effective therapies using existing drugs for patients with COVID-19.
This study of ischemic stroke patients is the first to associate the neutrophil-lymphocyte ratio in patients with COVID-19 and ischemic stroke and stroke severity.
These lipids may act as a biomarker for Type 1 diabetes and offer a therapeutic target to prevent the disease.
A drug that inhibits the protease plasmin is hypothesized to reduce the infectivity and virulence of the virus, as measured by reduced need for hospitalization within a week.
These potent CD4+ and CD8+ T-cell responses were stimulated in the lungs following a single intranasal administration.
UAB and Polish researchers propose that the COVID-19 virus acts as a microRNA “sponge” to deplete miRNA levels in ways that aid viral replication and stymie the host immune response.