Recent accolades for our Department

Published: May 4th, 2016

Category: Department News

The last several months have proven to be remarkably significant for the University of Florida Department of Pathology, Immunology and Laboratory Medicine’s doctors and graduate students, some of whom have been recognized for their forward-driving medical research, and others, for their presentations at industry symposia. Please join us in congratulating our brilliant faculty and students on their hard work and accomplishments.

 


 

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The UF Faculty Council honors Drs. Khan and Wilkinson with Lifetime Achievement Awards.

On April 6, 2016, at the UF College of Medicine Faculty Appreciation Ceremony at University House, Experimental Pathologist Saeed R. Khan, Ph.D. and Cytopathologist and Gynecological Pathologist Edward J. Wilkinson, M.D. were both honored with a Lifetime Achievement Award from the UF Faculty Council for their lifelong contributions to their specialties and the medical community at large.

President-elect of the College of Medicine Faculty Council Laurence M. Solberg, M.D., AGSF, authored the award introduction speeches for Drs. Khan and Wilkinson.

On why Dr. Khan was chosen for this award, Dr. Solberg warmly commented, “Dr. Khan has a distinguished history of service to the College of Medicine (COM) and the University of Florida, with three full pages in his CV reserved for his responsibilities in [many] administrations and committees.”

“For all of his incredible service, we are honored to present Dr. Khan with the UF COM Lifetime Achievement Award,” said Solberg.

Dr. Solberg’s remarks on Dr. Wilkinson’s Lifetime Achievement Award were just as heartfelt.

“Dr. Wilkinson is known for his wisdom, kindness, passion, sound judgment, caring, perspective and concern for his colleagues, trainees and patients. For [his] nomination, the UF Faculty Council received so many letters from faculty, current and past fellows, and medical students, that all of the wonderful quotes would take up hours to mention,” said Solberg.

 “[His] years of service are appreciated by all, especially in the COM. He is a role model who demonstrates great credit on his department,” Solberg asserted.

More details on these preeminent faculty members and why they were chosen for these high honors can be found in Dr. Solberg’s complete award introduction speeches for Dr. Khan and Dr. Wilkinson.

Also, learn more about another Lifetime Achievement Award that Dr. Khan will receive from the International Urolithiasis Society in July 2016.


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Stephanie McRae-Robinson, CPC, and Randall L. Chamberlain, MBA, MT(ASCP)DLM, win 2016 UF Divisional Superior Accomplishment Awards.

The University of Florida College of Medicine (COM) Superior Accomplishment Awards recognize faculty and staff at the divisional level who have shown efficiency or economy in their work; have contributed outstanding and meritorious service; or who improve the quality of life provided to students and employees. Each of this year’s 14 winners was nominated by supervisors, peers, clients and other stakeholders who wrote glowing letters of recommendation on their behalf.

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(shown from left to right) 2016 UF College of Medicine Superior Accomplishment Award Winners Stephanie McRae-Robinson, CPC, and Randall L. Chamberlain, MBA, MT(ASCP)DLM, share lunch at the awards banquet on March 28, 2016, along with UF Health Pathology Laboratories Medical Director Robert W. Allan, M.D.

As division-level winners, UF Health Pathology Laboratories Billing Stephanie McRae-Robinson, CPC, and Administrative Director Randall L. Chamberlain, MBA, MT(ASCP)DLM, received cash awards of $200 each and were considered for the university-level awards. All of the COM award winners were recognized on March 28, 2016, at an awards banquet, along with their nominators and supervisors.

The 2016 UF College of Medicine Superior Accomplishment Award winners include:

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The UF Department of Pathology, Immunology and Laboratory Medicine increases its NIH funding by more than $1 million from last year in the 2015 Blue Ridge rankings.

According to the 2015 Blue Ridge Institute for Medical Research (BRIMR) data, which records the grant funding for medical schools across the United States, the UF Department of Pathology, Immunology and Laboratory Medicine now ranks as #20 (up from #21 last year) for National Institutes of Health (NIH)-funded public research pathology departments across the country and remains at #10 for public universities.

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The BRIMR is a North Carolina-based federal non-profit organization that studies the interfaces of fundamental biological and clinical sciences, as well as clinical care, with an emphasis on targeted cancer therapy. The numbers below are based only on NIH funding with faculty being a principal investigator of a grant (not including subcontracts).

The Blue Ridge Institute for Medical Research’s 2015 Rankings
of NIH Funding for United States Medical Schools
Rank Medical School
NIH Pathology Research Funding
1 JOHNS HOPKINS UNIVERSITY $47,984,237
2 UNIVERSITY OF PENNSYLVANIA $35,320,333
3 WASHINGTON UNIVERSITY $31,462,389
4 EMORY UNIVERSITY $31,319,134
5 UNIVERSITY OF WASHINGTON $26,459,643
6 COLUMBIA UNIVERSITY HEALTH SCIENCES $24,984,709
7 UNIVERSITY OF MICHIGAN $19,105,195
8 NEW YORK UNIVERSITY SCHOOL OF MEDICINE $19,033,130
9 STANFORD UNIVERSITY $16,833,409
10 UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR $15,208,501
11 UNIVERSITY OF ALABAMA AT BIRMINGHAM $15,197,408
12 CASE WESTERN RESERVE UNIVERSITY $13,588,621
13 UNIVERSITY OF CALIFORNIA SAN DIEGO $13,107,650
14 UNIVERSITY OF PITTSBURGH AT PITTSBURGH $10,112,607
15 UNIVERSITY OF MINNESOTA $9,955,582
16 UNIVERSITY OF CALIFORNIA, SAN FRANCISCO $9,726,359
17 UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA $9,479,181
18 UNIVERSITY OF CHICAGO $9,207,968
19 VANDERBILT UNIVERSITY $8,871,695
20 UNIVERSITY OF FLORIDA $8,722,528

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Todd M. Brusko, Ph.D.

Todd M. Brusko, Ph.D.

Todd Brusko, Ph.D. is awarded a $1.25 million grant to to research type 1 diabetes immune pathways.

This year, Assistant Professor and Experimental Pathologist Todd M. Brusko, Ph.D. was awarded a five-year, $1.25 million R01 grant from the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). As the research project’s principal investigator, Principal Investigator Brusko and co-investigators Mark A. Wallet, Ph.D, and Sharon Wallet, Ph.D., will study the genes linked to a genetic risk for developing type 1 diabetes that determine whether a person’s immune system is over-activated or controlled.

According to Dr. Brusko, ““We know that genes control risk for developing autoimmune diseases like type 1 diabetes. What is not well understood is how these small genetic differences between individuals change the immune response and lead to disease. This grant will help us to understand a critical immune checkpoint, making it possible to design targeted therapies for preventing and reversing the disease.”

The primary goal of this research is to improve the lives of those with or at risk of developing type 1 diabetes by studying a key immune checkpoint that is linked with a genetic risk for autoimmune disease. Brusko and his team hope that by better understanding these immune pathways their research will lead to new, more effective therapies that will prevent and possibly reverse the disease process in type one diabetes.

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Research Fellow Jared Taylor wins second place at the 2015 iPSC Retreat.

On December 11, 2015, Research Fellow Jared Taylor of the Wallet Lab, won the second place award for his research poster, iPSC-derived macrophages: A tool for studying HIV-1 persistence, at last year’s second annual UF Clinical and Translational Science-sponsored Induced Pluripotent Stem Cells (iPSC) Retreat. He was recognized for his research and awarded a $50 cash prize.

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(shown, left to right) Santiago Carrasquilla (third place winner) – UF College of Engineering; Clayton Mathews, Ph.D. – poster contest judge; Jared Taylor (second place winner) – UF Department of Pathology, Immunology and Laboratory Medicine; Nihal El Rouby (first place winner) – UF Department of Pharmacotherapy and Translational Research, Center of Pharmacogenomics; Naohiro Terada, M.D., Ph.D. – UF Department of Pathology, Immunology and Laboratory Medicine


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Abstract

Background: Infection by human immunodeficiency virus type 1 [HIV-1] remains incurable because the virus establishes a persistent viral reservoir within host cells. A major gap in our knowledge is a general lack of understanding of how we can eliminate HIV-1 reservoirs that are found in at least two cell types, CD4+ T cells and macrophages. Following infection of macrophages, HIV-1 elicits a biochemical and molecular response that appears to be a partial activation of innate activation pathways including expression of some anti-viral ISGs. This limited host response may provide a basis for persistent infection.

Objective: To understand the role of USP18 in HIV-1 persistence in macrophages.

Hypothesis: USP18 is required for HIV-1 replication and persistence in macrophages.

Rationale: Transcriptional profiling of human monocyte derived macrophages [MDMs] showed that ubiquitin specific proteinase 18 [USP18] is highly upregulated during HIV-1 infection. USP18 is a negative regulator of type I interferon [T1-IFN] and nuclear factor kappa B [NFκB] signaling pathways. Partial knockdown of USP18 in the human monocytic leukemia cell line THP-1 results in marked inhibition of HIV-1 replication (Figure 1). However, THP-1 cells as a model for HIV-1 infection are lacking and a better model is needed where full knockout of USP18 can be achieved.

Results and Discussion: HIV-1 infection in macrophages leads to a significant increase in USP18 expression. USP18 negatively regulates signaling pathways that are activated in response to pathogens. Partial knockdown of USP18 in THP-1 cells resulted in a marked inhibition of HIV-1 replication.

We have utilized CRISPR/Cas9 gene editing and iPSC technology to generate USP18-/- macrophages. We have demonstrated that these iMacs support HIV-1 replication and that HIV-1 induces USP18 expression in this model as it does in macrophages derived from healthy donor monocytes.

Future Directions: iMacs will be used to study the effects of total USP18 knockout in the context of HIV-1 infection. This tool will also be used to investigate the effects of USP18 knockout on T1-IFN signaling pathways in macrophages.

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Dr. Morel’s groundbreaking lupus research paper becomes one of the most viewed, downloaded on the Journal of Leukocyte Biology’s website.

Experimental Pathology Division Chief Laurence Marguerite Morel, Ph.D.

Experimental Pathology Division Chief Laurence Marguerite Morel, Ph.D.

Experimental Pathology Division Chief Laurence Marguerite Morel, Ph.D. was recognized this February by the Journal of Leukocyte Biology for having one of the most viewed and downloaded research papers on its website since the date of its publication on the JLB website. The paper, Genetic and cellular dissection of the activation of AM14 rheumatoid factor B cells in a mouse model of lupus, was published on May 8, 2015 and has generated strong interest from researchers and lupus-afflicted patients alike.

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Resident Elham Nasri, M.D.wins first place in the 2016 Florida Society of Pathologists Resident Poster Competition.

Elham Nasri, Pathology resident

Resident Elham Nasri, M.D.

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Robert W. Allan, M.D., accepted the first place award for Elheim Nasri, M.D., at the Annual Business Luncheon during the 2016 FSP Annual Anatomic Pathology Conference on Saturday, Feb. 13.

At this year’s Florida Society of Pathologists 2016 Annual Anatomic Pathology Conference (Feb. 12 – 14), Elham Nasri, M.D. won first place in the Resident Poster Competition, which showcased resident posters on case studies and primary research in anatomic and clinical pathology. Dr. Nasri was awarded a $500 prize for her outstanding poster, Tumorigenic and Non-Tumorigenic Osteosarcoma Cell Subpopulations Exhibit Distinct MiRNA Expression Profiles.

Professor and UF Health Pathology Laboratories Medical Director Robert W. Allan, M.D., accepted the award on Dr. Nasri’s behalf (right).

Abstract

Tumorigenic and Non-Tumorigenic Osteosarcoma Cell Subpopulations
Exhibit Distinct MiRNA Expression Profiles

Background: Osteosarcoma (OS) is the most common primary malignant bone tumor in children and adolescents. Despite aggressive treatment around 40% of patients still die of their disease, which may be due to the heterogeneous nature of the tumor. Previously in our lab, we were able to identify and isolate tumorigenic and non-tumorigenic cells within the same tumor based on their ability to activate an exogenous Oct-4/GFP human promoter. Oct-4/GFP positive fraction probed to be at least 100-fold more tumorigenic than Oct-4/GFP negative fraction. The global transcription profile of these two populations revealed G2/M, spindle assembly checkpoint override and proliferation pathways more active in GFP positive cells. Stress induced differentiation and reversion pathways were more active in Oct-4/GFP negative cells.There are several molecular mechanisms controlling the expression of genes. One important level of post-transcriptional gene expression regulation is microRNA. MicroRNAs (miRNA, miR) are non-coding small RNAs that regulate gene expression by targeting mRNAs. Accumulating evidence has shown that miRNAs are involved in multiple processes in cancer development and progression; however their role in intra-tumoral heterogeneity remains to be elucidated. In this study we investigated the expression of 95 cancer-related miRNAs in tumorigenic and non-tumorigenic sub-populations isolated from the same tumor in two human osteosarcoma cell lines established from two patient biopsies (OS156, OS521). We believe these studies will help to identify novel targets for treatment, prevent the relapse of the disease and finally improve the patients’ survival.

Objective: To establish miRNA profiles of tumorigenic and non-tumorigenic OS cell populations and identify putative mRNA targets.

Methods: Human OS cell lines, OS156 and OS521, were established from patient biopsies and transfected with the hOct4/GFP reporter. Subcutaneous tumors were generated in NOD/SCID mice by injection of Oct4/GFP+ cells isolated by fluorescence Activating Cell Sorting (FACS). End point (1.5 cm) tumors were harvested and sorted by FACS in to GFP positive and negative. Cell fractions from three different passages (each as one biological replicate) from each cell line were used to extract RNA and perform miRNA expression analysis using the Quantimir RT & PCR system (SBI System Biosciences, Mountain View, California). For each cell line, results were analyzed by t-student test. TargetScan Human 6.2 and DIANNA were utilized for miRNA target prediction analysis.

Results: Analyzed data showed that 22 miRNAs in OS521 and 16 miRNAs in OS156 were up-regulated significantly (p value<0.05) in the GFP positive fraction vs. GFP negative. Of these, a total of 12 miRNAs (miR-7, 20-a, 15b, 18-a, 25, 30a-3p, 106-a, 103, 93, 155, 221, 222) were common to both OS521 and OS156. A total of 4 miRNAs were found to be down-regulated in the GFP+ fraction relative to GFP- in OS156 (miR-134, miR-202, miR-206, miR-153) and one in OS521 (miR-153) (p value<0.05). Thus, only one miRNA, MiR-153, was significantly down-regulated in both cell lines.

To elucidate possible regulatory functions of the differentially expressed miRNAs, TargetScan and DIANNA prediction software were used to identify putative mRNA targets. Further validation was performed by microarray-based mRNA expression profiling to identify mRNA targets that demonstrated corresponding down-regulation within the same OS cell populations. In GFP+ cells, validated mRNA targets of the upregulated miRNAs (miR-15b, 18a, 20a, 93, 106a, 221) included G2-M (ATM, CHEK1 and WEE1) and G1-S checkpoint proteins (TP53, CDKN2A and CDKN2B). Down-regulation of these mRNAs suggests a loss of cell cycle control and deregulated cell proliferation which is consistent with the phenotype of tumorigenic GFP+ cells. Conversely, validated mRNA targets of miR-153 (down-regulated in the GFP+ fraction of both OS cell lines) suggest a possible tumor suppressor function for this miRNA. Among its targets are IRS2, which is known to enhance tumor growth via activation of MAPK signaling. Loss of miR-153-mediated IRS-2 suppression in GFP+ cells is again consistent with their tumorigenic phenotype.

Conclusion: This is the first study to examine the expression of miRNAs in tumorigenic and non-tumorigenic sub-populations of OS. We have identified differentially expressed miRNAs associated with each sub-population and their putative mRNA targets which can be explored further to elucidate the key regulatory mechanisms that drive tumorigenesis in OS.

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Graduate Student Desai’s poster and oral presentation impress, win awards

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Graduate Student Pritesh Desai

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The Statewide Graduate Research Symposium | April 22, 2016 University of Florida – Touchdown Terrace at Ben Hill Griffin Stadium

Scientists from across the globe gather to communicate scientific findings at the annual meetings of the American Association of Immunologists (AAI). It he AAI annually makes a few travel awards available to graduate and postdoctoral students. This year, Shagram Salek-Ardakani Laboratory Graduate Student Pritesh Desai won a 2016 AAI Trainee Abstract Award, for his presentation titled, HVEM Keeps the Memories of a Killer T-Cell Alive. This is the second year in a row that he has received this prestigious honor.

Desai was also selected to give an oral presentation in a block symposium at this year’s AAI Annual Meeting, IMMUNOLOGY 2016™, May 13 – 17, 2016, in Seattle, Washington. Additionally, because he has been an AAI Trainee Member in good standing for more than three consecutive years, Desai is also eligible to receive a cash reimbursement prize of up to $750 to help pay for his registration and travel expenses to this event.

His research was so well received, it was handpicked by the dean of the UF Interdisciplinary Program in Biomedical Sciences, Thomas C. Rowe, Ph.D., to compete in the first annual Graduate Student Appreciation Week Research Day oral presentations on March 29, 2016, at the J. Wayne Reitz Union Grand Ballroom.

desai-awardAt this event, Desai’s oral presentation was so impressive that he received a certificate to acknowledge his research, and he was selected to compete in the Statewide Graduate Research Symposium on April 22, 2016, at the Ben Hill Griffin Stadium Touchdown Terrace. UF was one of eight exhibiting universities at the Symposuim. Out of 69 poster’s shown during the presentation session, Desai’s won first place in the Biological Sciences category for his poster presentation. His abstract was also accepted for oral presentation at the International Congress of Immunology 2016 , which takes place August 21 through 26, in Melbourne, Australia.

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Abstract

HVEM Keeps the Memories of a Killer T-Cell Alive
Pritesh Desai, Georges Abboud, Farhad Dastmalchi,
Jessica Stanfield, Tarun E. Hutchinson and Shahram Salek-Ardakani
Department of Pathology, Immunology & Laboratory Medicine,
University of Florida, College of Medicine, Gainesville, FL 32610, USA

CD8 memory T cells (also known as Killer T cells) play a critical role in protection against repeated exposure to respiratory viruses. Memory T cell development in the lung is still not fully understood in terms of the nature and source of the molecular signals that establish and maintain the memory state. HVEM (Herpes Virus Entry Mediator) is a member of tumor necrosis factor receptor superfamily. It serves as a molecular switch facilitating stimulatory and inhibitory signaling by interacting with multiple ligands such as LIGHT and BTLA. Using respiratory vaccinia virus (VACV) infection model, we found that HVEM signaling in CD8 T cells did not affect primary expansion of CD8 T cells in the lungs. In striking contrast, very few effector CD8 T cells that lacked HVEM survived the contraction phase to differentiate into long-lived memory cells in the lungs. Moreover, HVEM-/- memory precursors also showed markedly increased contraction after viral clearance, leading to nearly complete loss of lung resident CD8 memory T cells. Collectively, these results reveal that HVEM expression on memory precursors is critical for development of long-lived memory cells and suggests that strategies targeting HVEM signaling will be crucial in designing novel vaccines that can augment CD8 T cell based immunity against respiratory viruses.

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Terada Laboratory Graduate Assistant Joonseok Cho, MS wins awards at the 41st annual UF Interdisciplinary Programs’ Medical Guild Competition and the Statewide Graduate Research Symposium.

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41st Annual Medical Guild Competition Silver Award Winner Joonseok Cho, MS

Joonseok Cho, MS (left), a graduate assistant at the Naohiro Terada Laboratory, won a silver medal award for his presentation at the 41st annual Medical Guild Competition at the University of Florida Interdisciplinary Programs (IDP) in Biomedical Sciences on Monday, April 4, 2016, at the UF Health Cancer & Genetics Research Complex.

Each IDP nominates a graduate student from each of eight advanced concentrations for participation in this annual competition, which consists of a 15-minute oral research presentation, in addition to a five-minute question and answer session for each participant. Cho was selected to represent the Molecular Cell Biology Concentration at this year’s competition

Participants’ presentations were evaluated by a panel of faculty judges. One gold, two silver and three bronze medals were awarded. Each of the winners were presented with an award certificate, as well as a cash award from the Medical Guild. Additionally, these students’ names will be inscribed on a plaque on permanent display in the Office of Graduate Education.

“I was honored to attend the competition as a representative of Molecular Cell Biology Concentration and to have won a silver award,” said Cho.

Later, on, April 21, at the Statewide Graduate Research Symposium, Cho also won the first place award in the Health Sciences category for his presentation, “Targeted Manipulation of Hepatic Mitochondrial Metabolism to Prevent Fatty Liver and Obesity.”

Abstract

Modulation of Adenine Nucleotide Translocase 2 in Liver Prevents Fatty Liver and Obesity

Mitochondria play a critical role in metabolism. Altering overall body metabolism by manipulating mitochondria may be a novel approach to control obesity. ANTs transport ADP and ATP through mitochondrial inner membrane, thus playing an essential role for the energy metabolism. Mice have three ANT paralogs, Ant1, Ant2 and Ant4. While knockout mice have been characterized with Ant1 and Ant4 genes, which resulted in exercise intolerance and male infertility, respectively, the role of the ubiquitously expressed Ant2 gene in organ homeostasis has not been fully demonstrated. Through conditional gene targeting, we generated Ant2 conditional knockout (cKO) mice, in which a majority of ATP transport capacity was impaired in liver mitochondria by deleting the adenine nucleotide translocase 2 (Ant2). Surprisingly, the mice have survived over one year and appeared normal except for a lean phenotype. Mitochondrial number was increased in Ant2 cKO mice liver. Counterintuitively, Ant2-deleted mitochondria were still respiratory but primarily uncoupled, thus wasting nutrients. Liver function was normal but hypoglycemia, hypocholesterolemia, and an increase in ketone bodies were measured in Ant2 cKO mice. In addition, the mice showed less fatty liver changes or obesity under high fat diet feeding conditions. High fat diet induced fatty liver or obesity was ameliorated under administration of the chemical Ant inhibitor. These data imply liver specific deletion of Ant2 or systemic inhibition of Ant can be beneficial for preventing or treating fatty liver diseases such as nonalcoholic fatty liver disease (NAFLD) and obesity.

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Undergraduate Researcher Daniel L. Aldridge

Undergraduate Researcher Daniel L. Aldridge

UF Undergraduate Researcher Daniel Aldridge wins an exclusive Frost Scholarship to study immunology in England this fall.

Wallet Laboratory Undergraduate Researcher Daniel L. Aldridge was recently awarded with a prestigious Frost Scholarship to pursue a Master of Science degree in integrated immunology at the University of Oxford in the United Kingdom, beginning in October 2016. Generously supported by the Phillip and Patricia Frost Philanthropic Foundation, the purpose of the Frost Scholarship Programme is to help students currently enrolled in the State University System of Florida to study yearlong master’s courses in science, technology, engineering and mathematics (so-called STEM subjects).

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Timothy J. Garrett, Ph.D.

Timothy J. Garrett, Ph.D., is appointed to the new Editorial Board of a new journal, Clinical Mass Spectrometry.

On April 18, 2016, Timothy J. Garrett, Ph.D., was appointed the Editorial Board of the upcoming scholarly journal, Clinical Mass Spectrometry, by Chris Herold, Ph.D., MBA, the chief operating officer of Mass Spectrometry: Applications to the Clinical Laboratory (MSACL). In this role, Dr. Garrett will assist the publication’s editors-in-chief in reviewing manuscripts submitted for publication in the journal. He will also promote the journal within the clinical community, as well as solicit the submission of manuscripts from scholastic sources.

According to the MSACL:

Clinical Mass Spectrometry will publish peer-reviewed articles addressing the application of mass spectrometric technologies in laboratory medicine and clinical pathology, with the focus on diagnostic applications. It will be the first journal dedicated specifically to the application of mass spectrometry in the context of diagnostic procedures in medicine. The scope of the journal is not restricted to any particular mass spectrometric technologies but covers the entire methodological range of mass spectrometry and hyphenated technologies.

As a hybrid journal, Clinical Mass Spectrometry will publish both regular and open access articles. It will focus on publishing full papers, short communications, invited critical reviews, reviews and letters to the editor. The online journal will be included in the Elsevier Freedom Collection, to which more than 8,000 universities and other educational institutions subscribe.

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