Upon appointment, a postdoctoral scholar is assigned to one of two distinct categories for payroll and taxation purposes:

Status Code 21: A Postdoctoral Employee is an individual who, while pursuing further training, provides services to UAB for compensation. These postdocs receive a salary, usually as part of an NIH-funded grant. Salaries and wages are fully taxable to the individual providing the services. Postdoctoral employees receive benefits as shown under the Benefits section.

Status Code 20: A Postdoctoral Trainee is an individual who is receiving a true fellowship, as defined by the IRS, and receives an amount to aid in the pursuit of research training. This amount cannot represent payment for the performance of any past, present, or future teaching, research, or other services. Postdoctoral trainees are provided health insurance with the opportunity to purchase dental options.

In accordance with IRS regulations, UAB does not withhold federal income taxes on status code 20 postdoc trainees, and the State of Alabama currently excludes fellowships from taxation in their entirety. Therefore, to the extent that a scholarship/fellowship is federally taxable to the individual, that individual will probably have to file federal quarterly estimated income tax returns and pay quarterly taxes in order to comply with individual income tax regulations. (For specific advice on an individual tax situation, a tax professional or the IRS should be contacted. Non-resident aliens should direct their tax questions to the International Scholar and Student Services (ISSS) at (205) 934-3328. Postdoctoral trainees receive benefits as shown under the Benefits section.

In accordance with regulations, federal and state income taxes are not withheld from stipend amount IF YOU ARE A CITIZEN OF THE UNITED STATES. You may be required to file federal quarterly estimated income tax returns and pay quarterly taxes to comply with individual income tax regulations.

It is important to consult an income tax professional or the IRS for advice on this matter.

The IRS booklet, Publication 970, Tax Benefits for Education, can be viewed on-line at http://revenue.alabama.gov/. In the Search For field type: Publication 970 and in the Search Within field choose: IRS site. The booklet can be printed out or you may call (800) 829-3676 for a copy to be sent by mail. Additional publications at this site that may help you include:

Publication 421, Scholarships and Fellowship Grants 
Publication 355, Estimated Tax 
Publication 306, Penalty for Underpayment of Estimated Tax 
Publication 505, Tax Withholding and Estimated Tax

State of Alabama income tax website - http://www.revenue.alabama.gov/incometax 

Financial Affairs webpage on the UAB web site has a Scholarship & Fellowship section which is very helpful. See "Taxability to Individuals" at http://main.uab.edu/show.asp?durki=14627

Postdocs in UAB News

  • UAB researchers work to unravel the complex genetic disease neurofibromatosis type 1
    One major goal is the discovery of new genotype/phenotype correlations — how a particular mutation indicates that some symptoms in patients are unlikely to develop with age.
    Ludwine Messiaen

    It is easy to tell a medical research story that has a simple and dramatic moment. But disease is often much more complex, and the work to understand it can be painstaking.

    A vivid example of that is seen in the UAB Medical Genomics Laboratory, headed by Ludwine Messiaen, Ph.D., professor of genetics. This lab offers clinical genetic testing for a broad array of common and rare genetic disorders. One of the most confounding is neurofibromatosis type 1.

    This can be a heartbreaking disease.

    Changes at puberty

    It usually starts with café-au-lait skin markings, so named because of their distinctive coloring, in an infant. But at puberty — already a challenging time in a person’s life, many patients develop benign skin tumors called neurofibromas that erupt as bumps across the body. Patients vary widely in their symptoms, which can include freckles near skin folds of the body, nodules in the eyes, tumors along the optic nerve, heart defects, anomalies of connective tissue or bones, developmental delay, intellectual disability, and learning problems.

    Patients show a broad clinical variability as they grow, and whether their case will be mild or severe cannot — in most cases — be predicted when the disease first appears. This leaves physicians and families uncertain about what symptoms will appear in a particular child as he or she nears puberty.

    Cafe-au-lait skin markings on the back of a young child

    Profusion of mutations

    This kaleidoscope of clinical signs is mirrored by an abundance of different mutations in the NF1 gene, responsible for the disease. The UAB Medical Genomics Laboratory has collected DNA and identified a pathogenic mutation in more than 7,800 unrelated neurofibromatosis type 1 patients. All have NF1 mutations, but meticulous examination has revealed so far more than 3,000 different mutations. These can be found in every part of the gene, and the mutational spectrum involves microdeletions, deletions or duplications that involve one or more exons, frameshift and nonsense mutations, and splice or missense mutations. Almost half of the NF1 patients carry a unique mutation found only in their specific family. Other mutations have been found in multiple unrelated families.

    Two searches

    From this complicated array of mutations and clinical symptoms, Messiaen and her colleagues have tried to answer two questions.

    First, can a particular mutation be correlated with the symptoms that will develop as the child grows? This is called a genotype/phenotype (DNA/symptoms) correlation, and only two have previously been found for neurofibromatosis type 1.

    “It’s important for people to know what may happen,” Messiaen said. “When a child is born with neurofibromatosis type 1, café-au-lait spots appear very shortly after birth; but other problems, more specifically the development of skin neurofibromas, typically appear around puberty. If a genotype/phenotype correlation exists for a particular mutation, it will help these families have some perspective of what the future will bring, and it will help families cope with the disease. If it is a mutation that takes away the heavy tumor burden at puberty, that information will relieve families, even though learning disabilities may still appear.”

    The second question for Messiaen and UAB postdoctoral trainee Meng-Chang “Jack” Hsiao, UAB Department of Genetics, is whether they could identify the likely mechanism that caused a group of mutations in which the DNA has been rearranged to create mix-ups that make the gene longer or shorter.

    Each question requires meticulous research. One means reaching out to patients, families and referring physicians around the nation and the world. The other is a molecular genetic detective story, pursued in the UAB lab.

    Messiaen and Meng-Chang "Jack" Hsiao are exploring the mechanisms behind the mutations seen in neurofibromatosis type 1.

    Seeking a correlation

    For the first question, Messiaen last year led a group of 74 researchers and clinicians from 58 centers in the discovery of just the third genotype/phenotype correlation ever found for neurofibromatosis type 1. They looked at 136 individuals who all had a missense mutation in the arginine moiety of neurofibromin, the protein encoded by the NF1 gene, at amino acid position 1,809. These mutations are the second-most-frequent ones seen in the UAB collection.

    To look for a correlation, the team had to gather detailed clinical symptomatic information for each of the neurofibromatosis patients, from patients, families, referral physicians and researchers in 24 U.S. states and Australia, Belgium, Brazil, Chile, the United Kingdom, India, Israel and Spain.

    In a paper published in the journal Human Mutation last year, they found that these patients have a distinct phenotype, Messiaen says. They had the café-au-lait marks, with or without the skin-fold freckling and Lisch eye nodules. But the patients did not develop the visible, disfiguring neurofibromas on their skin around puberty. However, there was a higher prevalence of blood flow obstruction from the heart to the lungs and a short stature. More than half had developmental delays and/or learning disabilities.

    Messiaen is calling for international collaboration to expand the study to a total of 250 mutations, which will provide the statistical power needed for patient case management by doctors. And in the next few years, she will focus on finding more genotype/phenotype correlations for other specific mutations.

    "If a genotype/phenotype correlation exists for a particular mutation, it will help these families have some perspective of what the future will bring, and it will help families cope with the disease."

    "If a genotype/phenotype correlation exists for a particular mutation, it will help these families have some perspective of what the future will bring, and it will help families cope with the disease."

    Chasing molecular clues

    For the second question, Hsiao, Messiaen and colleagues looked at NF1 copy-number variations — where the mutant gene is either longer or shorter than a normal NF1 gene — from 85 unrelated neurofibromatosis type 1 patients, along with two previously published copy-number variations. Ten of these were partial duplications within the NF1 gene, and 77 were deletions. Hsiao looked for specific nucleotide breakpoints in these variants — the places where the duplication or deletion begins or ends — that would be clues to how the changes occurred.

    The methods to examine these mutant genes include multiplex ligation-dependent probe amplification, array comparative genomic hybridization, breakpoint-spanning PCR and sequencing.

    “The most difficult challenge is to see how the rearrangements happen,” Hsiao said. “It’s really difficult to decipher.”

    In a paper published in The American Journal of Human Genetics last year, Hsiao found that DNA replication-based mechanisms — such as fork stalling and template switching, and microhomology-mediated break-induced replication — as well as serial replication stalling appear to be the major causes of the NF1 copy-number variants. In one complicated rearrangement, the DNA replication appeared to have stalled five times, with the stalled DNA strand then either invading forward or invading backward into another part of the NF1 gene. Hsiao also found that the mutant genes showed rearrangement hotspots that included one palindromic sequence and four Alu elements. Alu elements are short primate-specific repeats in the DNA; the human genome contains about 1 million copies of various Alu elements that make up almost 11 percent of the genome.

    Two sides to the research

    Messiaen says the two recent papers are “nice companions.”

    “They show two sides of research aspects of this laboratory,” she said. “One digs deeper into the mechanism of specific types of mutation, and one contributes to genotype/phenotype correlation.”

  • 2016 Darwin Day commemorates Charles Darwin’s birthday, showcases scientific research
    Poster sessions and guest lecturers aim to celebrate Darwin’s legacy.

    To honor the 207th birthday of legendary evolutionary biologist Charles Darwin, the University of Alabama at Birmingham will host its annual Darwin Day on Thursday, Feb. 11, and Friday, Feb. 12. The events will celebrate scientific research in evolutionary biology and other disciplines.

    The event is co-hosted by UAB’s departments of Anthropology and Biology in the College of Arts and Sciences.

    “Charles Darwin’s great discovery, the principle of natural selection, is more relevant to science than ever before,” said Steven Austad, Ph.D., chair of the Department of Biology. “For instance, it underlies our increasing success in cancer chemotherapy, provides guidance in combating new strains of drug-resistant diseases, and will ultimately determine how catastrophic climate change will prove to be for our planet.”

    A panel discussion exploring evolution, belief and education will kick off this year’s Darwin Day events in Lister Hill Library’s Edge of Chaos.The panel, which will be led by guest speakers Elisabetta Palagi, Ph.D., a behavioral biologist from the Natural History Museum University of Pisa in Italy, and Josh Rosenau, an evolutionary biologist from the National Center for Science Education, will take place from 2-3:30 p.m. on Feb. 11. Lee Meadows, Ph.D., from UAB’s School of Education, and Marshall Abrams, Ph.D., a philosophy professor in UAB’s College of Arts and Sciences, will also be panelists for this discussion.

    Following the panel, students and faculty will present a public poster session highlighting exciting new research from 3:30-4:30 p.m. at the Edge of Chaos. Those interested in presenting a poster should send an email to darwinday@uab.edu with their name, department, poster title, and indication of whether they are a student, postdoc or faculty.

    “Anthropologists and other students of science today will be well-served by striving to emulate Darwin’s objectivity, meticulous attention to detail and appreciation for complexity during the practice of science.”

    On Thursday evening, Darwin Day activities will continue with a reception followed by a talk by Rosenau. Rosenau’s lecture, “The Impact of Darwin in Everyday Life,” will begin at 7 p.m. following the 6 p.m. reception at the McWane Science Center and is open to the public.  

    Darwin Day will continue on Friday, Feb. 12, from 4 to 5 p.m., with a lecture from Palagi. Palagi’s talk, “The Strategic Functions of Play: Modality and Communication,” will be held in Heritage Hall, Room 104.

    “The approach of Charles Darwin represents the scientific endeavor at its best wherein data and reasoning interact to elucidate the natural world,” said Doug Fry, Ph.D., chair of the Department of Anthropology. “Anthropologists and other students of science today will be well-served by striving to emulate Darwin’s objectivity, meticulous attention to detail and appreciation for complexity during the practice of science.”

    Refreshments and drinks will be provided at all events, and Darwin Day T-shirts will be on sale as well. For more information about the events, email darwinday@uab.edu.

    Sponsors for the 2016 Darwin Day include the UAB Honors College and the Endowment for the John S. Jemison, Jr., Visiting Professorship in the Humanities.

  • How obesity makes memory go bad
    UAB researchers find that epigenetic changes associated with chronic obesity alter expression of memory-related genes in the brain.

    J. David Sweatt, Ph.D.University of Alabama at Birmingham researchers are probing how obesity makes memory goes bad, and the underlying molecular mechanism that drives this decline.

    They have found that epigenetic changes dysregulate memory-associated genes, and a particular enzyme in brain neurons of the hippocampus appears to be a link between chronic obesity and cognitive decline. Their work is published in the Jan. 27 issue of Journal of Neuroscience.

    Obesity plagues developed nations, and among the numerous negative health outcomes associated with obesity is a memory impairment that is seen in middle-aged and older obese people. The cause of this decline? Experiments with obese rodents have given a clue: altered gene expression in the hippocampus area of the brain. Until now, the reasons gene expression was changed, as well as the mechanism by which obesity leads to pathogenic memory impairment, have not been known.

    There was one suspect: epigenetic dysregulation in neurons of the hippocampus. Foundational experiments over the past decade have linked the creation of long-term memories to changes in DNA methylation and hydroxymethylation — changes caused by epigenetic mechanisms that sit above the level of the genes.

    Such lasting molecular changes to DNA appear to play an important role in promoting or suppressing memory formation through their ability to increase or reduce the expression of genes that help brain neurons create new synaptic connections.

    UAB researchers have now shown that epigenetic changes are indeed associated with changes in the expression of memory-associated genes within the hippocampus of obese mice, and these epigenetic changes correlate with diminished object location spatial memory in the obese mice. The UAB researchers have also implicated reduced amounts of one particular memory-associated gene product — SIRT1 — as the principal pathogenic cause of obesity-induced memory impairment. The hippocampus subregion of the brain is important for consolidation of long-term memory.

    Obesity and cognitive decline

    Evidence that suggests a link between the two includes:

    • People aged 40-45 who were obese had a 74 percent increased risk of dementia 21 years later; and those who were overweight had a 35 percent greater risk. This study cohort had 10,276 men and women. Whitmer, RA, et al., BMJ 2005.
    • A study of 2,223 healthy workers found that a higher body-mass index was associated with lower cognitive scores, after adjustment for age, sex, educational level, blood pressure, diabetes and other co-variables. Also, a higher BMI at baseline was associated with higher cognitive decline at a follow-up five years later. Cournot, M., et al., Neurology 2006.
    • Metabolic syndrome in 73 people with an average age of 60 was associated with significant reductions in recall and overall intellectual functioning, compared with age- and education-matched controls. Hassenstab, J.J., et al., Dementia and Geriatric Cognitive Disorders 2010.
    • A study of 8,534 twin individuals who were 65 or older showed that being overweight or obese at mid-life, with an average age of 43, was related to later dementia at the older age. Xu, W.L., et al., Neurology 2011.

    Corresponding author J. David Sweatt, Ph.D., first author Frankie D. Heyward, Ph.D., and colleagues in the UAB Department of Neurobiology, Evelyn F. McKnight Brain Institute, write that these data “provide the first evidence that high-fat-diet-induced obesity leads to the time-dependent development of aberrant epigenetic modifications within the hippocampus, as well as corresponding reduction in the expression of various memory-related genes.”

    Sweatt noted, “We feel this is a very exciting finding that identifies a new linkage between diet, epigenetics and cognitive function, especially in light of the burgeoning obesity epidemic in the U.S. and elsewhere.”

    This work, they write, “offers a novel working model that may serve as a conceptual basis for the development of therapeutic interventions for obesity-induced memory impairment.”

    In details about the cause of altered gene expression, the UAB researchers found that:

    • Mice with diet-induced obesity at 20 weeks had impaired performance in object location memory tests, and their hippocampus had impaired synaptic plasticity, as measured by long-term potentiation.
    • Four memory-associated genes — Ppargc1a, Ppp1cb, Reln and Sirt1 — showed significantly decreased gene expression at 23 weeks of diet-induced obesity, as has been seen before, and the latter three had significantly increased DNA methylation in their gene promoter regions. Increased methylation is known to decrease gene expression. Furthermore, the Sirt1 promoter region also had significantly decreased DNA hydroxymethylation. Gene expression increases or decreases as DNA hydroxymethylation increases or decreases.
    • Obesity-induced memory impairment develops over time. At just 13 weeks of diet-induced obesity, seven weeks earlier than the experiments above, mice did not have significant object location memory impairment, and at 16 weeks of diet-induced obesity, also seven weeks earlier than above, none of the genes showed significant increases in DNA methylation. Only one gene at 16 weeks — Ppargc1a — showed significant decreases in gene expression and DNA hydroxymethylation.

    To probe the mechanism by which obesity leads to pathogenic memory impairment, the UAB researchers focused on the gene Sirt1, which makes an enzyme that is active in the neuron during energy expenditure and fat mobilization. This enzyme appears to be depleted and dysfunctional in obesity, and the deletion of the Sirt1 gene in the brain shortly after birth is known to impair memory and the ability to form new neural synapses. These roles for the SIRT1 gene product — in both high-fat-diet-induced molecular pathology and in memory impairment — suggest that it might be a link between chronic obesity and cognitive decline.

    Frankie Heyward, Ph.D.Heyward, Sweatt and colleagues found that the hippocampus of obese mice had significantly diminished protein expression of SIRT1, and a substrate of the enzyme, acetlylated-p53, was significantly increased, suggesting reduced enzymatic activity. Also, a targeted deletion of Sirt1 in the forebrain region that includes the hippocampus at age 8-12 weeks showed decreased Sirt1 mRNA and protein in the hippocampus, and these mice showed impaired object-location memory when tested two weeks later.

    Furthermore, chemical activation of SIRT1 in diet-induced obese mice by feeding them resveratrol showed decreased levels of acetylated-p53, suggesting increased SIRT1 enzymatic activity, and the resveratrol-fed obese mice had a normal object-location memory, as compared with the control obese mice. The resveratrol-fed obese mice did not show an enhanced memory compared with normal mice. This suggests that resveratrol preserved their hippocampus-dependent spatial memory and SIRT1 function in the hippocampus.

    Besides Heyward and Sweatt, co-authors of the paper, “Obesity weighs down memory through a mechanism involving the neuroepigenetic dysregulation of Sirt1,” are Daniel Gilliam, Mark Coleman, Cristin Gavin, Ph.D., Jing Wang, Ph.D., Garrett Kaas, Ph.D., Richard Trieu, John Lewis and Jerome Moulden, all of the UAB Department of Neurobiology.

    Heyward is now a postdoctoral fellow at Harvard Medical School, the Broad Institute and Beth Israel Deaconess Medical Center. While at UAB, Heyward was supported by a UNCF/Merck Graduate Science Research Dissertation Fellowship that helps train and develop African-American biomedical scientists.

    About 10 years ago, Sweatt’s lab made the seminal discovery that everyday experiences tap into epigenetic mechanisms in subregions of the brain, and the resulting epigenetic changes in DNA are critically important for long-term memory formation and the stable storage of long-term memory. The 2007 Neuron paper “Covalent modification of DNA regulates memory formation,” by Courtney Miller, Ph.D., and Sweatt, was the first to show that active regulation of the chemical structure of DNA is involved in learning and experience-driven changes in the brain.

    This work was supported by National Institutes of Health grants T32HL105349, MH57014, P60DK079626 and P30DK56336. The T32 pre-doctoral fellow grant to Heyward from the UAB Nutrition and Obesity Research Center supported his training in the biological basis of obesity.

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  • Spain Rehab Women’s Committee hosts ‘Firefly’ fundraiser
    The Women’s Committee of the Spain Rehabilitation Center will host its signature benefit and Valentine’s Day celebration, “The Firefly,” on Saturday, Feb. 13, at The Florentine at 6 p.m.

    The Women’s Committee of the Spain Rehabilitation Center will host its signature benefit and Valentine’s Day celebration, “The Firefly,” on Saturday, Feb. 13, at The Florentine at 6 p.m.

    This year, the committee will honor former patients Kelly Garner and Ryan Robinett.

    Garner is an author, inspirational speaker and community leader. Following a near-death experience and extraordinary recovery, he wrote the book “The Night That Changed Our Lives.” Garner’s book was inspired primarily by his experience during the massive January 2014 snowstorm in Birmingham.

    Garner became familiar to many in the Birmingham area as the Good Samaritan during the storm when he offered assistance to stranded motorists and was injured after falling 40 feet off a cliff into a ravine. He spent over 12 hours in single-digit temperatures before a neighborhood rescue party located him early the next morning. He survived the fall but suffered shattered vertebrae and fell into a severe diabetic hypoglycemic state. Some doubted  he would ever walk again; but after numerous surgeries and rigorous rehabilitation at the Spain Rehabilitation Center, he has beaten the odds. Just a year after this incident, he completed the Mercedes half marathon. His surgical team was so inspired by his story that they ran the race with him.

    A native of Birmingham, Robinett serves as the managing director of Computer Technology Solutions’ Birmingham Operations. Ryan received his MBA from the UAB.

    Robinett was introduced to Spain’s Research and Rehabilitation programs in 2014 after experiencing a sudden onset of neurologic issues. Over the course of 16 months, his ability to walk deteriorated significantly. He has since made a full recovery following intense physical rehabilitation at Spain, is medicine-free and has been granted full medical release.

    Throughout his medical trials, Robinett has been an advocate and partner of UAB research, especially focusing on demyelinating diseases. He is an advocate of innovative ways to improve current rehabilitation methods, particularly involving neuro-physical rehabilitation. 

    To make a donation, please contact Catherine Newhouse.

  • Raise some dough for Pediatric Heart Transplant Study Foundation
    Enjoy great pizza and help raise some dough for the Pediatric Heart Transplant Study Foundation at Slice Birmingham.

    On Tuesday, Feb. 9, the Pediatric Heart Transplant Study Foundation will host a fundraiser at Slice Birmingham.

    Dine in or take out for lunch, dinner or anytime in between and 10 percent of the proceeds will be donated to the PHTS Foundation to help improve the outcomes and quality of life for children who are awaiting or have received a heart transplant.

    Participants must print or display this ticket at the time of purchase for the PHTS Foundation to receive credit.

    The goals of the PHTS are to establish and maintain an international database for heart transplantation, to use the database to encourage and stimulate basic and clinical research

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