ECG 300 - "Strategies for Effective Career Development"
2 credit hours

  • Learn key concepts of successful career development through practical assignments
  • Articulate a career goal by conducting research and participating in field experiences
  • Produce job search documents necessary to accomplish career goals

For more information, contact Career Services at (205) 934-4324 or email careerservices@uab.edu.


School and Department Courses:
Most of these courses are only open to freshmen as part of a First Year Experience (FYE).

School/Dept. Course Title

Course
Number

Art FYE in Art & Art History ARS 160
Business Intro. to Business BUS 101
Communication FYE in Comm. CM 160
Engineering Intro. to Engineering EGR 110
For. Languages FYE in Foreign Lang. FLL 160
Health Professions Survey of Health Prof. LCHP 101
Humanities FYE in Hum. HUM 160
Music FYE in Music MU 160
Nursing Student Success in Nursing NUR 100
Sciences Succeeding in the Sciences NS 101
Soc. & Behav. Sciences Intro. to SBS SBS 101
Theatre FYE in Theatre THR 160

UAB News

  • UAB to begin renovations on Alys Stephens Performing Arts Center
    Renovations to the University of Alabama at Birmingham's Alys Stephens Performing Arts Center have begun as the center prepares to celebrate its 20th anniversary.
  • Parkinson’s disease pathogenesis is reduced in a rat model using a cell-signaling inhibitor drug
    Results show that JAK/STAT pathway inhibitors may be a new class of therapeutic treatments for patients with Parkinson’s disease. Acting by reducing inflammation, they prevent neurodegeneration in animal models and may be an important new approach to slow progression of the disease.

    Etty “Tika” BenvenisteUniversity of Alabama at Birmingham researchers report the first documentation that suppressing a key cell-signaling pathway in a rat model of Parkinson’s disease reduces pathogenesis. Oral administration of AZD1480 — one of the JAK/STAT pathway inhibitors generally known as Jakinibs — lessened the destructive inflammation and nerve cell degradation in the area of the brain affected by Parkinson’s.

    At present, there are no therapies available to patients to prevent progression of Parkinson’s disease, the chronic neurodegenerative movement disorder marked by profound loss of dopamine-producing neurons in the brain.

    “We believe Jakinibs may become a viable therapeutic option for Parkinson’s disease patients,” said Etty “Tika” Benveniste, Ph.D., professor in the Department of Cell, Developmental and Integrative Biology and lead author of a paper published May 4 in The Journal of Neuroscience. “They are already being studied for other conditions, are orally bioavailable, seem to be well-tolerated, and do not promote troublesome immunosuppression. Furthermore, there may also be other ways of targeting the JAK/STAT pathway as a neuroprotective therapy for neurodegenerative disease.”

    A variety of Jakinibs are in Phase I, II or III clinical trials for several other diseases. The current UAB study, funded by the Michael J. Fox Foundation for Parkinson Research and the National Institutes of Health, is the first to show that disrupting the JAK/STAT pathway prevents the neuroinflammation and neurodegradation specific to Parkinson’s disease.

    “This is a very important advance,” said David Standaert, M.D., Ph.D., professor and chair of the UAB Department of Neurology and a collaborator on the project. “It shows that anti-inflammatory strategies have real potential. The next steps will be to validate some of the inflammatory changes seen in the animals in patients with Parkinson’s disease, which in turn will enable planning of clinical studies of anti-inflammatory therapies in patients with Parkinson’s.”

    “This is a very important advance. It shows that anti-inflammatory strategies have real potential. The next steps will be to validate some of the inflammatory changes seen in the animals in patients with Parkinson’s disease, which in turn will enable planning of clinical studies of anti-inflammatory therapies in patients with Parkinson’s.” — David Standaert, M.D., Ph.D.
    Benveniste and Standaert are part of an interdisciplinary UAB team focusing on neuroinflammatory mechanisms in Parkinson’s disease. The group — co-led by Benveniste, Standaert and Andrew West, Ph.D., associate professor of neurology — seeks to understand how the body’s immune system contributes to the pathology seen in the brains of Parkinson’s disease patients and to the development and progression of the disease. Only recently have researchers begun to suspect an important role for inflammation in the disease, and this is still largely uncharted territory.

    For the current paper, UAB researchers, led by Hongwei Qin, Ph.D., associate professor of cell, developmental and integrative biology, either challenged rat immune cells in vitro with aggregated human α-synuclein, or induced overexpression of α-synuclein carried by a virus vector in brains of rats. Untreated, this in vivo model leads to neuroinflammation in the brain and degradation of dopamine-producing neurons in the substantia nigra, the portion of the midbrain marked by cell death in Parkinson’s patients. Accumulation of α-synuclein in the brains of patients is a core feature of Parkinson’s disease, and this leads to the activation of the brain immune cells called microglia, the production of inflammatory signaling chemicals, and ultimately, neurodegradation.

    In vitro and in vivo experiments showed AZD1480 inhibited JAK/STAT activation and downstream gene induction after a challenge by α-synuclein. The genes that are induced by α-synuclein, but not induced in the presence of α-synuclein and AZD1480, are associated with the proinflammatory phenotype. The inhibition by AZD1480 dampened both innate and adaptive immune responses.

    Altogether, the researchers say, the results show the potential of Jakinibs to protect against the degradation of dopamine-producing neurons.

    Details

    For the in vivo neuroinflammation experiments, α-synuclein overexpression was induced, and two weeks later rats were given AZD1480 by oral gavage for 14 days. Then the researchers analyzed the inflammatory response in the substantia nigra of the midbrain for AZD1480-treated and -untreated animals. AZD1480 prevented the increased numbers of microglia and macrophages seen after α-synuclein overexpression. AZD1480 also prevented inflammatory activation of the microglia, as measured by Iba1-positive cells, and it prevented upregulation of genes for the proinflammatory markers TNF-α, iNOS, IL-6 and CCL2.

    AZD1480 also prevented neurodegradation. For the in vivo neurodegradation experiments, α-synuclein overexpression was induced, and four weeks later — at the peak of neuroinflammation — rats were given a four-week treatment of AZD1480 oral gavage. At 12 weeks, the brains were analyzed for nigral neurons of the substantia nigra. Benveniste and colleagues found that overexpression of α-synuclein caused a 50 percent loss of nigral neurons at three months. But when the α-synuclein rats were also treated with AZD1480, that loss was prevented, and the numbers of nigral cells were similar to those of the controls.

    In Parkinson’s disease, chronic inflammation in the brain makes the blood-brain barrier more permeable, allowing immune system T-cells to infiltrate into the brain from the bloodstream, potentially adding to neuroinflammation. In the rat model, α-synuclein overexpression increased the infiltration of CD4+ T-helper cells and induced activation of the STAT3 signaling protein. AZD1480 treatment inhibited both of these immune responses. AZD1480 also inhibited induction of two genes for proinflammatory markers, CIITA and MHC Class II.

    The UAB researchers further found that α-synuclein overexpression significantly upregulated 186 genes in the midbrains of rats, while AZD1480 treatment of α-synuclein-overexpression rats inhibited the expression levels of 59 genes, the majority being genes that were induced by α-synuclein. Genes induced by α-synuclein overexpression include many that are implicated in cell signaling, inflammatory and neurological diseases, and antigen presentation (a step in the adaptive immune response).

    Besides Benveniste, Qin and Standaert, authors of the paper, “Inhibition of the JAK/STAT pathway protects against α-synuclein-induced neuroinflammation and dopaminergic neurodegeneration,” are Jessica A. Buckley, Yudong Liu, Thomas H. Fox III, Gordon P. Meares, Hao Yu and Zhaoqi Yan, all of the UAB Department of Cell, Developmental and Integrative Biology; Xinru Li and Ashley S. Harms, UAB Department of Neurology; and Yufeng Li, UAB Department of Medicine.

    At UAB, Benveniste holds the Charlene A. Jones Endowed Chair in Neuroimmunology, and Standaert holds the John N. Whitaker Endowed Chair in Neurology. West holds the John A. and Ruth R. Jurenko Endowed Professorship in Neurology.

    Research support came from the M.J. Fox Foundation, and from NIH grants RO1 NS57563-05, P20 NS095230, P30 AR48311, P30 NS47466, P30 CA13148 and P30 AI027767.

  • UAB students win public health scholar bowl in St. Louis
    The undergraduates answered questions on everything from disease outbreaks to community health as they competed against 13 teams from across the country.

    Aarin Palomares, Claire Finney, Sean McMahon, Katherine Hymel and Beenish KamranFive students from the UAB School of Public Health competed against 13 teams from across the United States in the St. Louis University Public Health Scholar Bowl, winning first place in the bowl and tying for second place in the case competition.

    Beenish Kamran, Katherine Hymel, Sean McMahon, Claire Finney and Aarin Palomares won the quiz-bowl-style tournament focused on current public health topics ranging from disease outbreaks to global and community health. The group of undergraduate students competed against teams including Johns Hopkins, George Washington University and Washington University.

    “Beyond academic success in the classroom — which this group has in spades — these students have always pushed the envelope to identify opportunities to practice and display their public health skills in the community,” said Suzanne Judd, Ph.D., assistant dean for undergraduate education in the School of Public Health. “The public health scholars bowl was a natural extension of their commitment to seek out these new opportunities. Competing against students from other universities only enhanced their drive to succeed. I am so proud of the passion and drive within each of these talented undergraduates that led to the success they achieved at the scholars bowl.” 

    During the case competition, UAB’s team worked collaboratively to tackle a current issue causing health problems in a community, sleep deprivation on campus. The team developed a promotional campaign and identified policies that may impact sleep, which landed them in second place.

    “These students have participated in our Wicked Problem Case Competition and the Global Case Competition, and this year a couple of them assisted in writing the case for our wicked competition,” said Max Michael, M.D., dean of the UAB School of Public Health. “Because the cases we use are so complex, our students are well-prepared in thinking through the process of dealing with complicated issues. I’m not at all surprised at their success and how well they represented our school at a national competition.”

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