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Archive for December, 2012

NGMMA Annual Holiday Event

Wednesday, December 12th, 2012

December 12, 2012, Rocky Face, GA. For more information, visit North Georgia Medical Management Association

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Understanding the Immune Response

Tuesday, December 11th, 2012

by Gary E. Myerson, M.D., F.A.C.R.

From ATLANTA Medicine, 2012, Rheumatology, Vol. 83, No. 3

Gary E. Myerson, M.D.

Gary E. Myerson, M.D.

Centuries ago, geography itself served as the primary barrier to disease exposure. But man’s exploration of the planet, enhanced by progressive technological expertise, has permitted both exposure to and expansion of diseases worldwide. However, our increasing knowledge of science overall and the specific components of the immune response has led to numerous diseases either being reduced or eliminated.

The immune response is an ancient system. Certain components, however, have not significantly changed in the millions of years of existence of species with vertebrae. The homo-sapiens and homo-erectus, nearly 250,000 years ago, possessed an immune system similar to ours. Innate immune response has been present throughout this entire period. It has been our “equalizer” in dealing with the microscopic environment that envelops us. We have made” friends” with many microbes, resulting in relationships that are symbiotic, while others are indeed antagonistic or parasitic. It is this inherent, genetically provided, innate response that is our defense against invaders both physically and chemically. The Adaptive or acquired immune response, our body’s ability to develop antibodies, has allowed us to improve or enhance our own innate immune response. Biologic therapy with monoclonal antibodies now allows us to manipulate specific proteins important in the immune response.

Our first line of defense includes the skin and lining surfaces of the internal body organs. There are enzymes in body secretions including lysozymes, phospholipases and defensins, which disrupt cell membranes promoting cell death. Periodically, the anatomical barriers are penetrated and an “acute inflammatory reaction” follows. The release of acute phase reactants: transferrin, CRP, interferon and interleukins, results in the cardinal signs of inflammation: calor/hot, rubor/red, dolor/painful and tumor/swelling.  The phagocytic cells including the neutrophils, macrophages, dendritic cells, natural killer or NK cells and eosinophils are the major players in identifying and responding to microscopic invaders. The phagocytic cells are directed to specific locations via cytokines, protein communicators of inflammation that identify, engulf and destroy pathogens.

These cells are primary players of the innate immune response – the oldest form of the host defense system. The innate immune response is triggered when microbes
(bacteria, virus and fungi) are detected. On or attached to the cell membranes of pathogens are commonly shared patterns (PAMPS). These include lipopolysaccharides(LPS), lipoteichoic acid, flagellin, RNA of viruses, amongst others. These molecules are recognized by receptors on the phagocytic cells called pattern recognition receptors (PRR).

One large group of the PRRs is a specific subgroup entitled Toll-like receptors (TLR). These highly specific receptors, numbered 1 through 13, identify and bind PAMPS, resulting in cytokine production triggering inflammation.

The complement cascade is also a major component of the innate immune response. The Complement system serves as an identifier and clearing house of pathogens by promoting vascular permeability, recruitment of phagocytic cells and ultimately the opsonization of bacteria and immune complexes. Opsonization refers to the coating and subsequent marking of bacteria for future destruction.

A large component of opsonization occurs in the spleen, which is why splenectomized patients particularly need vaccinations. Complement CH50 is a measure of total complement activity. Individuals with active autoimmune disease may have low levels of C3 and C4 due to  overactivity of the complement cascade.  This results in immune complex formation and the consumption of complement.

When the inflammation resolves, complement levels return to the normal range. Therefore, low levels of CH50 and C3 and C4 reflect active autoimmune disease, but higher levels do not.

Innate immune response is a non-antigen specific, immediate reaction. It does not produce immunological memory. For long-term protection, there is our adaptive or acquired immune response. Immunological memory is accomplished by the development of antibodies as our ready reserve defense force. Subsequent encounters with the same organism result in an enhanced response. There is a period of approximately 10-14 days for antigen-specific antibodies to be developed.

All cells of the immune system have their origin in the bone marrow. The myeloid series primarily produces the cells of the innate immune system including the neutrophils, monocytes and dendritic cells.  While the lymphoid series(lymphocytes) produces cells for the acquired or adaptive immune response, the T cells undergo differentiation into their distinct types under the influence of the thymus gland. B cells become mature in the lymph nodes and the spleen.

There is a tremendous amount of interaction between both systems, utilizing the myeloid series innate immune system for stimulation and activation of the acquired immune response. T-cells are involved in the cell-mediated immune response. They have no cytotoxic activity and do not kill infected cells or clear pathogens directly. Instead, they control the immune response by directing other cells to perform these tasks.

The cytokines the T-cells produce are the “protein communicators of inflammation.” Three important cytokines include TNF alpha and interleukins IL-1 and IL-6. These have been identified as primary players in autoimmune diseases including rheumatoid arthritis, psoriasis and psoriatic arthritis, Ankylosing spondylitis and inflammatory bowel disease(specifically Crohn’s disease) as well as Uveitis and Sarcoidosis.The T-cell begins as a “naïve” cell, which requires antigen presentation in order for it to become activated. These antigen-presenting cells (APC) include the macrophage, dendritic cell and the B cell.  The APC presents the antigen to the naive T-cell via its major histocompatibility complex (MHC) T-cell receptor (TCR). Depending on the APC cell type and the predominance of surrounding cytokines, T-cells differentiate in one of four directions:

1. TH 1 cells. APCs include the macrophages and dendritic cells. IL 12 and interferon (INF) gamma are the cytokines that drive differentiation. This type of T-cell usually develops from exposure to intracellular bacteria, fungus or viruses.

2. TH 17 cells. Neutrophils; IL 23, IL-1, IL-6. Usually from exposure of extracellular bacteria and fungi.

3. TH 2 cells. Eosinophils and basophils. IL-4. Usually from exposure to parasites.

4. T reg (regulatory) cells. Response to self-antigens. IL-10 and TGF beta. Down regulates autoimmune response.  There is however cross stimulation and inhibition
depending on which interleukin predominates. For instance, IL6 inhibits TGF beta, therefore driving TH 17 production and reducing T reg production, Alternatively, IL-4 while driving TH2 production inhibits TH 17 production.

Cell membranes of T-cells have cluster differentiation (CD) glycoproteins CD4 and CD8. Cells with the CD4 glycoprotein are referred to as helper cells, and those with
CD8 glycoprotein are referred to as cytotoxic T-cells. CD4 helper cells assist in the maturation of B cells into plasma cells and memory B cells. They also assist in the activation of cytotoxic T-cells and macrophages. Cytotoxic CD8 cells destroy viral-infected and tumor cells and also play a role in transplant rejection.

The humoral immune response is directed by B lymphocytes (B cells) differentiating into plasma cells which produce antibodies. The B cell develops through several stages. A B cell begins as a progenitor cell, then progresses to a pro-B cell and finally a pre-B cell. At this point, it leaves the bone marrow to mature in the lymph nodes and spleen where it becomes exposed to the pathogenic environment. As it matures, it develops three surface receptors – Blys, TACI and the B-cell receptor (BCR). When these receptors are bound, the cell matures and continues to exist. Failure to bind these receptors results in apoptosis or programmed cell death. This has become a recent important discovery since Benlysta, a new drug for the treatment of lupus, works by inhibiting Blys, the cell surface receptor.

These immunoglobulins are a hallmark of our defense system. We’re aware that deficiencies in any one of them or their subtypes results in the development of recurrent infections. Specific types of intravenous and subcutaneous gammaglobulin are available for those deficiency states. Memory B cells are formed from activated B cells that are specific to the antigen encountered during the primary immune response. These cells are capable of living “a long time” and can respond quickly following a second exposure to the same antigen.

B-1 cells and B-2 cells, B-1 cells express high levels of IgM greater than IgG and
are polyspecific – meaning that they have the ability to produce low-level response to many antigens.

Unlike the T cell, the B cell does not need the antigen presented to it. It recognizes the antigen in the blood or lymphatic system and engulfs it. It can then act as an antigen-presenting cell itself by displaying its antigen bound to its unique MHC on the cell surface allowing a T-cell to bind to it. Through a co-stimulatory mechanism necessitating a second binding site to be activated, cytokines can then be released. The cytokines released by that T-cell further propagate the B cell into its mature state, producing plasma cells and more immunoglobulin. Antibodies bind to their specific antigens forming immune-complexes. These complexes are then “cleaved” by the complement system and eliminated through the reticuloendothelial system.

Autoimmune diseases result from aberrant antibody production. These autoantibodies are actually produced on a regular basis by all individuals. Fortunately, more than 90 percent of them undergo spontaneous apoptosis and never progress. Anti-B cell medications predominantly work by interfering with the B cell during its maturation. Examples of these medications are being utilized in both oncology and rheumatology.

A baby’s immune defenses are passively transferred from the mother at birth. The baby’s own immune defenses take approximately three months to begin to function.

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New Studies Reveal Critical Insights to Improve Care of Patients With Sickle Cell Disease

Tuesday, December 11th, 2012

Research unveiling key gaps in continuity of care for sickle cell patients transitioning from pediatric to adult care were presented recently during the 54th Annual Meeting of the American Society of Hematology (ASH).

Sickle cell disease (SCD) is an inherited, chronic blood disorder affecting between 90,000 and 100,000 Americans.[1] Instead of producing healthy red blood cells, individuals with the disease produce abnormal, sickle-shaped cells that cannot easily move through blood vessels and deliver adequate oxygen to the body’s tissues and organs. Blocked blood flow as a result of an accumulation of these sickled cells can cause severe pain and organ damage and increase a patient’s risk for infection.

While SCD was formerly considered a childhood disease because patients rarely lived beyond their teens, thanks to improvements in treatment, an increasing number of SCD patients are living well into adulthood. Although effective treatments are extending life expectancy for these patients, doctors and patients face new challenges to help ensure that the growing adult population of patients with SCD can receive adequate care to manage their disease over the long term.

New research presented at the 2012 ASH Annual Meeting examines a number of factors surrounding care for SCD patients; researchers conclude that SCD patients tend to rely more on emergency departments to manage acute events (e.g., infection, pain, and acute chest syndrome) related to their disease as they transition from childhood to adulthood. Data confirms that these patients are also hospitalized more frequently than the general population, resulting in significantly higher overall costs and burden on the health-care system. The studies identify opportunities to improve the health system, including improving continuity of patient care and education for patients. They also provide evidence to encourage the public health community to continue to develop and refine critical initiatives that will help these patients as they transition from pediatric to adult public and private health insurance coverage.

“While we have made many advances in the treatment of sickle cell disease, this research reveals the important challenge we as physicians continue to face in ensuring that the medical system supports timely access to needed preventive and disease management protocols for our patients,” said ASH President-Elect Janis Abkowitz, MD of the University of Washington School of Medicine in Seattle. “For health-care providers, it is important to consider how we can address the needs of patients transitioning into adulthood and avoid unnecessary trips to the emergency department – steps that will improve the health-care system for everyone.”

Highlights of the SCD-related studies presented during the 2012 ASH Annual Meeting include:

1. Age-Related Emergency Department Reliance and Healthcare Resource Utilization in Patients with Sickle Cell Disease; Presenting Author: Morey A. Blinder, MD

Background: Study investigated age-related patterns of emergency department reliance (EDR) and associated health-care costs by reviewing Medicaid data from more than 3,200 pediatric SCD patients, including those transitioning from pediatric to adult care.

Results: Average ED visits/quarter increased from 0.76 to 2.29 between age 15 and 24, reaching a peak of 2.9 at age 36. Patients were more likely to have high EDR during the post-transition period, incurring higher inpatient and ED costs.

Conclusion: Since advancements in care now allow for SCD patients to live well into adulthood, the study highlights clear areas for improvement to aid in the move to adult care, reduce reliance on ED services, and deliver better long-term support.

 

2. Outpatient Visits, Hospitalizations and Emergency Department Visits Among Patients with Sickle Cell Disease on Medicaid: Trends in 14 USA States, 2006-2007; Presenting Author: Benjamin Ansa, MD

Background: Study examined rates of hospitalizations, outpatient visits (OPV), and emergency department visits (EDV) among 19,168 pediatric and adult patients.

Results: The majority of cases of SCD patients identified were between the ages of 11 and 20 (27.4%), with the highest numbers of cases reported from Florida, Georgia, and Louisiana.
• Patients between 11 and 30 years were the highest utilizers of medical care, with a combined rate of 80/1000 yearly visits for hospital, OPV, and EDV.
• The rate of African Americans (AA) with SCD on Medicaid was highest (1.1/1000) in Louisiana and Mississippi, and lowest in Texas (0.5/1000).
• While patients ages 1-10 had the most OPV (15.1 per 1,000 annual
visits), hospitalization and EDV rates were highest among patients between ages 21 and 30 (8.9 and 22.9 per 1,000 visits yearly, respectively).

Conclusion: The study finds that use of public health services changes significantly as children transition into adulthood and utilize outpatient care less and emergency care more. Education programs directed to the emergency department as the most common site of care for young adults with SCD may be valuable in promoting disease management and prevention. More research effort is needed to understand the variation between states in the enrollment of SCD patients in the Medicaid program.

 

3. Acute Healthcare Utilization for Patients with Sickle Cell Disease within a Community-based Hospital System; Presenting Author: Hung Tran, MD

Background: Retrospective chart review conducted among SCD patients at a single center, examining 14- and 30-day readmissions and emergency department (ED) encounters (563 total acute care events).

Results: Acute cases in the 21-30 age group had the highest rate of 14- and 30-day readmissions (41% and 51%, respectively), along with the highest number of acute care encounters per patient annually. Of the few patients who had 11 or more events in a two-year period, the majority (67%) were 21-30 years old.

Conclusion: The study confirms previous studies of the age-related reliance on emergency care for patients with SCD and finds that when treated in the ED, more than half of these patients will return within 30 days. For young adult patients, there is a clear need to understand the reasons for the high rates of acute events and short-term re-hospitalizations to help better manage disease and reduce the
financial burden of care.

For the complete ASH annual meeting program and abstracts, visit www.hematology.org/2012abstracts.

[1] Centers for Disease Control and Prevention, “Sickle Cell Disease Fact Sheet,” http://www.cdc.gov/ncbddd/sicklecell/data.html (Accessed November 2012).

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Fincher Receives Abraham Flexner Award for Distinguished Service to Medical Education

Monday, December 10th, 2012

Dr. Ruth-Marie “Rhee” Fincher, Professor Emeritus and inaugural Vice Dean for Academic Affairs for the Medical College of Georgia at Georgia Health Sciences University, has received the Association of American Medical Colleges’ Abraham Flexner Award for Distinguished Service to Medical Education.

The AAMC established the Flexner award in 1958 to recognize extraordinary individual contributions to medical schools and to the medical education community as a whole. Fincher receivee the award during the AAMC’s recent Annual Meeting.

Over three decades Fincher, who retired from MCG in May 2012, worked to link medical education with the rigor of science, one of Flexner’s most important tenets.

Fincher helped direct the education of more than 5,000 MCG students who have given her more than 20 teaching awards. Fincher also launched a distributed model of medical education in which MCG students learn alongside physicians across the state, enabling growth of the medical school class to help alleviate Georgia’s significant physician shortage.

Early in her career as MCG’s Internal Medicine Clerkship Director, Fincher cofounded the Clerkship Directors in Internal Medicine and the Alliance for Clinical Education to promote excellence in clinical education and create a nationally recognized career development track for faculty to focus on medical education.  At the former, she started and ran for 20 years a training program for faculty new to the clerkship role.  In 2006, that group renamed its annual service award to honor Fincher.  The Alliance for Clinical Education fosters collaboration among clerkship directors across specialties, and Fincher led the organization’s production of two landmark reports to help medical educators understand the role and value of clerkship directors.

In a 25-year volunteer role, Fincher began as an author and reviewer of test questions for assessing medical students’ clinical skills through the National Board of Medical Examiners and ultimately was named to the group’s Executive Board.

In addition to paving a way for medical education scholarship at the national level, Fincher helped develop and implement MCG’s Educator’s Portfolio, which aids in the training and promotion process for faculty educators, as well as the Educational Innovation Institute, a unique resource to develop and disseminate best practices in medical education and support Fincher has served the AAMC in many capacities. She has been highly engaged with its Group on Educational Affairs for 20 years, which she chaired from 1997-98.

Fincher has been a member of the AAMC Board of Directors since 2011 and has participated in 12 accreditation site visits on behalf of the Liaison Committee on Medical Education over the last decade.

Fincher is a 1976 graduate of Emory University School of Medicine. She earned bachelor’s degrees in biology from Colby College and in medical sciences degree from Dartmouth Medical School.

She is the first Georgian and first female recipient of the Flexner Award.

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Larsen Succeeds Lawley as Dean of Emory School of Medicine

Monday, December 10th, 2012

Christian P. Larsen, MD, DPhil, an internationally recognized leader in transplant surgery and immunology, has been named dean of Emory University School of Medicine. He also will serve as vice president for Health Center Integration for the Robert W. Woodruff Health Sciences Center and as chairman of the Board of Directors of The Emory Clinic. Larsen will assume these roles effective January 15, 2013.

Larsen is currently chair of the Department of Surgery at Emory University School of Medicine, director of Surgical Services for Emory Healthcare and executive director of the Emory Transplant Center. He also is an affiliate scientist at Yerkes National Primate Research Center. He holds endowed positions as the Joseph Brown Whitehead Professor of Surgery and the Carlos and Marguerite Mason Professor in the Emory School of Medicine.

Larsen succeeds Thomas J. Lawley, MD, who retired from the deanship this year after 16 years in that position and will remain a medical faculty member.

Larsen joined the Emory School of Medicine faculty in 1991 and was appointed chair of surgery in the medical school and director of surgical services for Emory Healthcare in 2009. His clinical practice is focused on kidney, pancreas and islet transplantation at Emory University Hospital and Children’s Healthcare of Atlanta.

Larsen became founding director of the Emory Transplant Center (ETC) in 2001, building and directing one of the foremost research and clinical transplantation programs in the world. The center is most noteworthy for its leadership in the early integration of clinical care and research.

Under Larsen, the ETC has been a national pacesetter in establishing new standards to ensure reliable, patient-centered care, focusing on multidisciplinary care a full decade before its recognition as an essential attribute in patient care. In addition, the ETC has been one of the nation’s leading centers for NIH research funding in basic immunology, in translational studies in non-human primates and in large, multi-center clinical trials.

Together with long-time collaborator Thomas Pearson, MD, DPhil, Larsen has played a pivotal role in discovering a new class of immunosuppressive drugs known as co-stimulation blockers. Larsen and Pearson helped drive the development of the co-stimulation blocker belatacept, approved in June 2011 by the U.S. Food and Drug Administration for kidney transplant recipients – the first time a new class of drug had been approved for transplant since the 1990s.

In 2012 Larsen received a new NIH grant for nearly $20 million to lead a research team continuing development of more effective co-stimulation blockers for near-term treatment of transplant patients and better strategies for the “holy grail” of transplantation – long-term, true immune tolerance of transplanted organs.

Larsen has been continuously funded by the NIH for the past 16 years. The recipient of a prestigious NIH MERIT award, he has directed program project grants, center awards, and multi-institutional consortia funded by the NIH and Juvenile Diabetes Research Foundation.

After receiving his bachelor of arts in chemistry from Emory College, Larsen received his medical degree from Emory University School of Medicine in 1984. He was a Livingston Surgical Research Fellow at the University of Oxford, England, and he received his doctor of philosophy in transplantation immunology from Oxford in 1990. He completed general and transplantation surgery training at Stanford University and Emory, where he was chief surgical resident and a fellow in transplantation surgery.

Larsen is a Fellow of the American College of Surgeons and an elected member of the American Society for Clinical Investigation, chair of the NIH NIAID Non-Human Primate Tolerance Network and a member of the NIH Clinical Islet Transplant Consortium Steering Committee.

He is the recipient of both national and international research awards, including the Basic Science Award of the American Society of Transplant Physicians (1997), the Roche Award (2001), the Roche Basic Science Established Investigator Award (2004), the Roche Award for Excellence in Translational Research from the American Society of Transplantation (2006), the Thomas E. Starzl Prize in Surgery and Immunology (2007), and the Emory School of Medicine’s Distinguished Faculty Lecture and Award (2009).

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Breast Surgery Symposium to Focus on New Shaped Breast Implants

Monday, December 10th, 2012

The Southeastern Society of Plastic and Reconstructive Surgeons (SESPRS) will hold its 29th Annual Breast Surgery Symposium, January 11-13, 2013, at the Intercontinental Hotel in Atlanta. Titled “Balance without Bias,” the Symposium will feature faculty who will share their knowledge, insight and experiences, covering the full range of aesthetic and reconstructive breast surgery. Approximately 400 participants are expected to attend.

“This is the world’s finest meeting devoted exclusively to breast surgery,” says symposium chair Mark Codner, M.D. “There’s no other meeting that includes live surgical demonstration with state-of-the-art techniques, performed by world leaders in plastic surgery of the breast.”

This year’s Symposium will include live surgery events and a panel discussion, focusing on the use of new shaped implants, approved by the FDA for aesthetic and reconstructive breast surgery. Attendees will have an opportunity to hear some of the most experienced breast surgeons in the country discuss their approaches to device selection for their patients. Another panel will discuss the art of fat grafting for cosmetic and reconstructive breast surgery. Topics relevant to all plastic surgeons will be discussed, with an emphasis on practical solutions including analysis, decision making and treatment options for common problems.

As part of the SESPRS Foreign Scholarship Program, a group of young surgeons from South Korea will attend the meeting to learn from the Symposium’s faculty. The international participants will translate the information they gather into improved patient care and surgical outcomes in their native country.

The event is sponsored by Northside Hospital.

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Northeast Georgia Medical Center Performs Robotic Angioplasty

Sunday, December 9th, 2012

Northeast Georgia Medical Center (NGMC) is performing robotic angioplasty, thanks to the recent installation of a new CorPath 200 System.

“Robotic angioplasty may open the doors to new possibilities and more complex procedures as the technology evolves,” says Mark Leimbach, MD, Chair of the Department of Cardiology at NGMC and an interventional cardiologist with NGHC.  “Coronary artery disease is the leading cause of death in the United States, but the implementation of this new technology shows we are thinking outside the box, pushing the boundaries and doing everything we can to try to save the lives of heart patients.”

Interventional cardiologists sit behind a lead-shielded cockpit during robotic angioplasty, versus standing at the procedure table during traditional angioplasty, and use digital controls to operate the CorPath System as it guides stents and balloons through the catheter and into the patient’s arteries.  Robotic angioplasty offers several benefits versus traditional procedures:
•    Improved precision when placing stents in arteries
•    Provides an extra set of “hands,” which don’t get tired, during longer procedures
•    Less radiation exposure for physicians and staff

“It’s remarkable to be the first hospital in the state for this groundbreaking advancement in heart care, and, since we were part of the clinical trial for the robotic equipment, we already have more than a year of experience with these procedures,” says J. Jeffrey Marshall, MD, Medical Director of Cardiac Catheterization Labs at NGMC; interventional cardiologist with Northeast Georgia Heart Center (NGHC); and President of the Society for Cardiac Angiography and Interventions.

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Emory Transplant Center Names Pearson as New Executive Director

Saturday, December 8th, 2012

Thomas C. Pearson, MD, DPhil, has been named executive director of the Emory Transplant Center, effective Jan. 15, 2013. Pearson currently is associate director of the Emory Transplant Center, a position he has held since the center’s founding in 2001. He is surgical director of the kidney and pancreas transplant program and Livingston Professor of Surgery in Emory University School of Medicine. He also is an affiliate scientist at Yerkes National Primate Research Center.

Pearson succeeds Christian P. Larsen, MD, DPhil, recently named dean of Emory University School of Medicine, vice president for Health Center Integration for the Robert W. Woodruff Health Sciences Center and chairman of the Board of Directors of The Emory Clinic.

Pearson is associate medical director of LifeLink of Georgia, a role he has had for 12 years, and he serves on the executive committee of its board of directors. He also has served as chair of the kidney pancreas committee of the American Society of Transplantation and as the UNOS (United Network of Organ Sharing) Region 3 representative to key national committees. He currently is on the board of directors of the American Society of Transplantation and is an associate editor of the American Journal of Transplantation.

Pearson’s clinical specialties include islet, kidney and pancreas transplantation. Together with long-time collaborator Chris Larsen, Pearson has played a pivotal role in discovering a new class of immunosuppressive drugs known as co-stimulation blockers. Larsen and Pearson helped drive the development of the co-stimulation blocker belatacept, approved in June 2011 by the U.S. Food and Drug Administration for kidney transplant recipients — the first time a new class of drug had been approved for transplant since the 1990s.

Pearson joined the Emory faculty in 1991. He received his medical degree from Emory in 1982 and was a Livingston Surgical Research Fellow at the University of Oxford, England, where he received his doctor of philosophy in transplantation immunology in 1990. He completed a general surgery residency at Emory, where he served as chief resident, and a fellowship in transplantation surgery and in portal hypertension.

He was named to Emory University’s Alpha Omega Alpha National Honor Medical Society in 2004, and he received the NIH Basic Science Award from the American Society of Transplant Physicians in 1997 and the Dean’s Clinical Investigator award at Emory in 1999 and 2002.

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CPT Coding for OBGyn Practices Seminar

Friday, December 7th, 2012

December 7, 2012, Atlanta. For more information, visit OBGyn Practices Seminar

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GAMMA Meeting & Gala

Friday, December 7th, 2012

December 7, 2012. For more information, visit Greater Atlanta Medical Management Association

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