University of Texas Medical School

University of, Texas, United States

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(PR NewsChannel) / April 25, 2017 / Winter Park, Florida Mark A. LaGatta, MD, Nephrologist working for Nephrology Associates of Central Florida, and affiliated with Winter Park Memorial Hospital, has been named a 2017 Top Doctor in Winter Park, Florida. Top Doctor Awards is dedicated to selecting and honoring those healthcare practitioners who have demonstrated clinical excellence while delivering the highest standards of patient care. Dr. Mark A. LaGatta is an experienced and respected physician, having been in practice for over 20 years. His career in medicine started in 1996, when he graduated from the University of Texas Medical School at San Antonio. An internship and residency then followed at the Shands Jacksonville Medical Center, prior to completing a fellowship at the Jackson Memorial Hospital. Dr. LaGatta is board certified in Internal Medicine and Nephrology by the American Board of Internal Medicine, and he treats and diagnoses a wide variety of conditions. These include kidney stones, gout, nephritis, vascular disease, hypertension, alkalosis, chronic kidney diseases, and acute kidney failure. Expert treatments undertaken by Dr. LaGatta include hemodialysis and peritoneal dialysis. Dr. LaGatta is known not only for his clinical excellence as a nephrologist, but also for his patient centric approach to medicine. He takes the time to get to know and understand his patients, and provides tailored and effective solutions. This laudable philosophy makes Dr. Mark A. LaGatta a very deserving winner of a 2017 Top Doctor Award. About Top Doctor Awards Top Doctor Awards specializes in recognizing and commemorating the achievements of today’s most influential and respected doctors in medicine. Our selection process considers education, research contributions, patient reviews, and other quality measures to identify top doctors.


(PR NewsChannel) / April 26, 2017 / Winter Park, FloridaMark A. LaGatta, MD, Nephrologist working for Nephrology Associates of Central Florida, and affiliated with Winter Park Memorial Hospital, has been named a 2017 Top Doctor in Winter Park, Florida. Top Doctor Awards is dedicated to selecting and honoring those healthcare practitioners who have demonstrated clinical excellence while delivering the highest standards of patient care. Dr. Mark A. LaGatta is an experienced and respected physician, having been in practice for over 20 years. His career in medicine started in 1996, when he graduated from the University of Texas Medical School at San Antonio. An internship and residency then followed at the Shands Jacksonville Medical Center, prior to completing a fellowship at the Jackson Memorial Hospital. Dr. LaGatta is board certified in Internal Medicine and Nephrology by the American Board of Internal Medicine, and he treats and diagnoses a wide variety of conditions. These include kidney stones, gout, nephritis, vascular disease, hypertension, alkalosis, chronic kidney diseases, and acute kidney failure. Expert treatments undertaken by Dr. LaGatta include hemodialysis and peritoneal dialysis. Dr. LaGatta is known not only for his clinical excellence as a nephrologist, but also for his patient centric approach to medicine. He takes the time to get to know and understand his patients, and provides tailored and effective solutions. This laudable philosophy makes Dr. Mark A. LaGatta a very deserving winner of a 2017 Top Doctor Award. About Top Doctor Awards Top Doctor Awards specializes in recognizing and commemorating the achievements of today’s most influential and respected doctors in medicine. Our selection process considers education, research contributions, patient reviews, and other quality measures to identify top doctors.


News Article | December 8, 2016
Site: www.24-7pressrelease.com

HOUSTON, TX, December 08, 2016-- Frank Arnett, MD, has been included in Marquis Who's Who. As in all Marquis Who's Who biographical volumes, individuals profiled are selected on the basis of current reference value. Factors such as position, noteworthy accomplishments, visibility, and prominence in a field are all taken into account during the selection process.Widely regarded for his focus on the genetics of rheumatic disease, Dr. Arnett has taught medical doctors and academic students for nearly four decades. Since entering the field of rheumatology, he has contributed more than 600 publications in his fields of expertise, which includes genome-wide scans, genetics of rheumatic disease, and the mapping of three genes causing Scleroderma. Dr. Arnett has been featured in numerous medical journals, including the Annals of Rheumatic Disease, the Journal of Rheumatology, Arthritis and Rheumatology, Nature Genetics, PLOS Genetics, Science, American Journal of Human Genetics, and Annals of Internal Medicine. As a professor emeritus with the University of Texas Medical School, he is certified in internal medicine, rheumatology and diagnostic immunology.Dr. Arnett began his career upon receiving an MD from the University of Cincinnati in 1968. He completed a residency at Johns Hopkins Hospital before joining the medical team as a fellow of rheumatology in 1970. During the next decade, Dr. Arnett launched a career as a respected doctor, researcher and educator. In 1984, he joined the University of Texas Medical School in Houston as the director of the division of rheumatology, a position he held until 2001. Dr. Arnett also served as chairman of internal medicine (2000-2004) and he retired in 2010.Throughout the course of his career, Dr. Arnett has been continually recognized for his commitment to medicine and education. Between 2000 and 2010, he was the recipient of the Best Doctors in America Award, as well as the TIAA Distinguished Educator Award and President Scholar Teaching and Research Award from the University of Texas Medical School. Since 2011, Dr. Arnett has been honored with inclusion in Who's Who in America and Who's Who in Medicine and Healthcare. Although he is now retired, Dr. Arnett maintains active involvement with the Heritage Society of the University of Texas, the American College of Physicians (Master), the American College of Rheumatology (Master), and the Association of American Physicians.About Marquis Who's Who :Since 1899, when A. N. Marquis printed the First Edition of Who's Who in America , Marquis Who's Who has chronicled the lives of the most accomplished individuals and innovators from every significant field of endeavor, including politics, business, medicine, law, education, art, religion and entertainment. Today, Who's Who in America remains an essential biographical source for thousands of researchers, journalists, librarians and executive search firms around the world. Marquis now publishes many Who's Who titles, including Who's Who in America , Who's Who in the World , Who's Who in American Law , Who's Who in Medicine and Healthcare , Who's Who in Science and Engineering , and Who's Who in Asia . Marquis publications may be visited at the official Marquis Who's Who website at www.marquiswhoswho.com


News Article | November 18, 2015
Site: www.nature.com

Twelve years ago, Mary Jane Lapinski had a routine breast-cancer screening mammogram at her local hospital in Baltimore, Maryland. The mammogram showed multiple specks in her left breast. Her physician called it ductal carcinoma in situ (DCIS) — an early-stage, non-invasive cancer of the milk ducts. A surgeon told her he could attempt a lumpectomy to remove the lesions, but he recommended a mastectomy — removal of the entire breast. “I kept thinking, this isn't logical,” says Lapinski, who was 48 at the time. “It was mind-boggling that a non-invasive cancer carried the same or more aggressive treatment than an invasive cancer.” The rogue cells in Lapinski's breast occupied a diagnostic grey area. Some cases of DCIS advance to invasive breast cancer, metastasis and death, but most do not. By current estimates, 20–30% of DCIS tumours will become aggressive within 20 years, says Shelley Hwang, a breast-cancer surgeon and researcher at Duke University School of Medicine in Durham, North Carolina. Still, most oncologists feel that it is best to remove the lesions and offer radiation treatment to stave off their progression. The trouble is that oncologists cannot tell for certain which DCIS lesions will remain idle and which will turn deadly. Identifying breast-cancer biomarkers — molecules that can identify the pre-cancerous cells that are likely to progress to invasive cancer — could lead to better-informed decisions about treatment. Unfortunately, little is known about the natural history of DCIS. It is difficult to track the course of the disease because so many women undergo surgery. “If we can identify a subset of patients that are at risk of developing an invasive cancer and only treat those, we would spare many women unnecessary treatment,” says Eileen Rakovitch, a radiation oncologist at Sunnybrook Health Sciences Center in Toronto, Canada. Before the introduction of widespread screening mammography in the 1980s, DCIS lesions represented about 3% of breast cancers in the United States. They now account for nearly one-third of newly diagnosed breast cancers1. But detecting DCIS does not necessarily add much information about a woman's future or overall health. “It is entirely possible to find cancers that don't matter,” says H. Gilbert Welch, an internist and cancer epidemiologist at the Geisel School of Medicine at Dartmouth in Hanover, New Hampshire. Welch and Archie Bleyer, then at the University of Texas Medical School in Houston, estimated that, in 2008, 70,000 US women received an early-stage breast-cancer diagnosis for lesions that would not have led to clinical symptoms, accounting for 31% of screening-detected breast cancers2. Most women diagnosed with DCIS have a lumpectomy or mastectomy — or a double mastectomy — along with radiation therapy. But the benefits of such treatments are hard to find. A much-discussed observational study of more than 100,000 US women with DCIS found that women who had lumpectomies or mastectomies to treat DCIS had just a 3.3% chance of dying of breast cancer in the next 20 years, not much different than the risk to women in the general population3 (2.7%, according to the American Cancer Society). Ideally, women with DCIS would be tested to assess whether surgery is the best course of action. Although no such test is clinically available, physicians are starting to use biomarkers to predict the future of women who have already had surgery. One test — Oncotype DX DCIS Score, produced by Genomic Health in Redwood City, California — stratifies women who have had breast-conserving surgery for DCIS into low, medium and high risk for future cancer. The test evaluates the expression of seven cancer genes (including those associated with cell proliferation and hormone receptors) in tissue samples taken from breast biopsies. Rakovitch validated DCIS Score in a retrospective study of women diagnosed with DCIS and who'd had breast conserving surgery. In work funded by a research grant from Genomic Health, she and her colleagues applied the test to tissue samples from 718 women4. “Women with an intermediate- or high-risk score had twice the risk of developing local recurrence compared to women with a low-risk score,” says Rakovitch. She says that the assay can pick out some women who are at a high risk of recurrence, but whom doctors might have considered to be low risk based on patient history and tumour characteristics. The search for a reliable measure to prevent surgery in the first place goes on. Any test, Hwang says, would probably involve a large array of markers that could be combined to form a cohesive picture. “We've taken the individual biomarkers as far as they can go and they're not giving us the answers we need,” she says. Thea Tlsty, a molecular pathologist at the University of California, San Francisco, and her colleagues have identified three proteins involved in cell proliferation that are associated with future aggressive breast cancers5. Tlsty's team found that of 1,162 women who had a lumpectomy for DCIS, those whose tissue was positive for all three biomarkers — COX-2, p16 and ki67 — had a 20% risk of developing an invasive cancer within 8 years. If they had none of the proteins, their risk dropped to 4%. “These markers indicate which pre-cancers are the baby, basal-like cancers, which are the most lethal and metastatic,” she says. In unpublished research, Tlsty's group has subsequently identified several other potential biomarkers in proteins that coordinate cell death. Four prospective studies in Australia, the United States and the United Kingdom are further evaluating the trio of markers, Tlsty says. Other biomarkers have also shown promise. Invasive breast cancers often stop the expression of tumour suppressor genes. One of those genes, called SYK, seems to be part of a genetic hub that determines which precancerous cells eventually metastasize. One study found that women who had altered expression of 55 genes that interact with SYK had reduced survival6. The search for circulating markers for early detection has proved frustrating at times, says Jeffrey Marks, a cancer cell biologist at Duke University. Marks and his colleagues selected 90 blood-based biomarkers, but none were useful in distinguishing cases of breast cancer from benign controls7. “They're very difficult to validate in independent populations,” he says. Some researchers are looking for signals that might reveal which DCIS lesions are associated with an increased risk of developing future invasive breast cancer. Andy Beck, a computational biologist at Harvard Medical School in Boston, Massachusetts, and his team are examining patterns of genomic alteration. Using data from DNA profiles of invasive breast cancers catalogued with The Cancer Genome Atlas, the group identified genomic locations that are most frequently copied or deleted in invasive breast cancer lesions. “We're basically saying that if it's not present in invasive cancer then it's not likely to be useful,” says Beck. In this case, the marker proved to be grimly robust. In a study of 271 patients, women with lesions that had extra copies in all three regions had a 17-fold higher risk of having a coincident invasive breast cancer compared with those women who had none8. The group is expanding the study to include about 20 chromosomal regions commonly altered in invasive breast cancer. In collaboration with Stanford University, Washington University and the Nurse's Health Study, the group is launching a study of 1,400 patients to predict the risk of recurrence or a subsequent invasive cancer over time. Researchers have recognized that sheer genetic diversity within precancerous tissues may help to predict cancer formation and progression. As precancerous cells evolve and accumulate genetic and epigenetic alterations, they become more varied. Some studies have shown that diversity can predict progression. Marks is now studying the genetic diversity of the cells within DCIS lesions. In theory, if the DCIS has a more complex mosaic of cells, there is a stronger likelihood that one of them will develop into a more 'fit' cancer cell that can invade the surrounding tissue and metastasize. Until scientists have a fuller understanding of which markers indicate an increased risk of developing invasive cancer, patients with DCIS will lack clarity about their future. For her part, Lapinski never went under the knife. Instead, she tracked down Hwang, who suggested that Lapinski join a three-month clinical study of the oestrogen-blocking drug tamoxifen. Lipinski was supposed to have surgery at the end of the trial, but she opted to forego the operation and continue with the tamoxifen, and, later, raloxifene. She checks in with Hwang twice a year for an examination and a mammogram. Although others see uncertainty in Lapinski's choice, she doesn't see it as a risky move. “Everybody has to make their own decision,” she says. “It has to be comfortable for them.”


Etchegaray J.M.,University of Houston | Ottosen M.J.,Healthcare Quality and Safety | Burress L.,University of Texas Medical School | Sage W.M.,University of Texas at Austin | And 3 more authors.
Health Affairs | Year: 2014

The study of adverse event disclosure has typically focused on the words that are said to the patient and family members after an event. But there is also growing interest in determining how patients and their families can be involved in the analysis of the adverse events that harmed them.We conducted a two-phase study to understand whether patients and families who have experienced an adverse event should be involved in the postevent analysis following the disclosure of a medical error. We first conducted twenty-eight interviews with patients, family members, clinicians, and administrators to determine the extent to which patients and family members are included in event analysis processes and to learn how their experiences might be improved. Then we reviewed our interview findings with patients and health care experts at a one-day national conference in October 2011. After evaluating the findings, conference participants concluded that increasing the involvement of patients and their families in the event analysis process was desirable but needed to be structured in a patient-centered way to be successful. We conclude by describing when and how information from patients might be incorporated into the event analysis process and by offering recommendations on how this might be accomplished. © 2014 Project HOPE-The People-to-People Health Foundation, Inc.


News Article | February 16, 2017
Site: www.businesswire.com

MONTEREY PARK, Calif.--(BUSINESS WIRE)--SynerMed, a market-leading healthcare platform for government-sponsored healthcare programs in Monterey Park, California, announced today that Jorge Weingarten, MD, has joined the organization as the new Chief Medical Officer. Reporting directly to President and Chief Executive Officer James Mason, Dr. Weingarten will oversee the company’s medical affairs and clinical operations. Dr. Weingarten is board certified in Internal Medicine and brings with him a wealth of experience in population health management, government-sponsored healthcare delivery, value-based care and quality improvement. He joins SynerMed from Care1st, a health plan where he oversaw all clinical operations as the company grew from a single line of Medi-Cal business with 40,000 members to more than 500,000 members in Medi-Cal and Medicare throughout California, Arizona and Texas. “We have worked with Dr. Weingarten for many years and have grown to appreciate his capabilities and knowledge, especially in the government-sponsored arena,” said James Mason, President and Chief Executive Officer of SynerMed. “We are excited to have him as part of our team at SynerMed.” During Dr. Weingarten’s 17-year tenure at Care1st, he spearheaded the recruitment and development of high-performance healthcare teams that managed all aspects of medical and quality standards, social services and pharmacy operations. He was instrumental in improving quality metrics, including attaining a Four-Star rating for Care1st’s Medicare plan, and maintaining NCQA accreditation over the last 10 years. Dr. Weingarten’s efforts in both utilization and quality activities led to the successful sale of Care1st to Blue Shield in 2015 for $1.3 billion. “I look forward to working with James and his entire team at SynerMed to ensure the continued delivery of high-quality care that is both innovative and affordable,” said Dr. Weingarten, Chief Medical Officer at SynerMed. Dr. Weingarten received his medical degree from University of Texas Medical School in Houston, Texas, and he completed his residency in internal medicine at Los Angeles County + University of Southern California Medical Center. He is a Diplomate of the Board of Internal Medicine. SynerMed is a market-leading healthcare organization specializing in government-sponsored programs headquartered in Monterey Park, California. SynerMed is dedicated to innovating healthcare through an integrated system of tools, purpose-built web platforms, and professional services that connect physicians, members, hospitals and health plans. SynerMed’s mission is to transform the healthcare system by rewarding high-quality and cost-effective care. For more information about SynerMed, visit www.synermed.com and www.synermedconnect.com.


Ganguly A.,University of Calgary | Yang H.,University of Texas Medical School | Yang H.,University of Houston | Zhang H.,University of Calgary | And 2 more authors.
Molecular Cancer Therapeutics | Year: 2013

Drugs that target microtubules are potent inhibitors of angiogenesis, but their mechanism of action is not well understood. To explore this, we treated human umbilical vein endothelial cells with paclitaxel, vinblastine,and colchicine and measured the effects on microtubule dynamics and cell motility. In general, lower drug concentrations suppressed microtubule dynamics and inhibited cell migration whereas higher concentrations were needed to inhibit cell division; however, surprisingly, large drug-dependent differences were seen in the relative concentrations needed to inhibit these two processes. Suppression of microtubule dynamics did not significantly affect excursions of lamellipodia away from the nucleus or prevent cells from elongating; but, it did inhibit retraction of the trailing edges that are normally enriched in dynamic microtubules, thereby limiting cell locomotion. Complete removal of microtubules with a high vinblastine concentration caused a loss of polarity that resulted in roundish, rather than elongated, cells, rapid but nondirectional membrane activity, and little cell movement. The results are consistent with a model in which more static microtubules stabilize the leading edge of migrating cells, whereas more dynamic microtubules locate to the rear where they can remodel and allow tail retraction. Suppressing microtubule dynamics interferes with tail retraction, but removal of microtubules destroys the asymmetry needed for cell elongation and directional motility. The prediction that suppressing microtubule dynamics might be sufficient to prevent angiogenesis was supported by showing that low concentrations of paclitaxel could prevent the formation of capillary-like structures in an in vitro tube formation assay. Mol Cancer Ther; 12(12); 2837-46. © 2013 American Association for Cancer Research.


Imatinib mesylate is a selective tyrosine kinase inhibitor used in the treatment of chronic myelogenous leukemia. Ocular side effects of imatinib include periorbital edema, which may become so severe as to obstruct the visual field. The purpose of this case study is to describe the clinical characteristics of imatinib- induced postoperative periorbital purpura. We retrospectively reviewed the medical literature using PubMed, searching the terms edema, Gleevec, imatinib, periorbital, postoperative and purpura. Patient reports and previous reviews of the subject were critically assessed and the salient features are presented. Three patients have undergone surgery to reduce the imatinib-induced periorbital edema; two of these individuals have developed imatinib-induced postoperative periorbital purpura. We recommend discontinuing imatinib usage one week prior to periorbital surgery and not resuming therapy until the eighth postoperative day.


Abrams J.L.,University of Texas Medical School
Journal of visualized experiments : JoVE | Year: 2013

Proteostasis, defined as the combined processes of protein folding/biogenesis, refolding/repair, and degradation, is a delicate cellular balance that must be maintained to avoid deleterious consequences (1). External or internal factors that disrupt this balance can lead to protein aggregation, toxicity and cell death. In humans this is a major contributing factor to the symptoms associated with neurodegenerative disorders such as Huntington's, Parkinson's, and Alzheimer's diseases (10). It is therefore essential that the proteins involved in maintenance of proteostasis be identified in order to develop treatments for these debilitating diseases. This article describes techniques for monitoring in vivo protein folding at near-real time resolution using the model protein firefly luciferase fused to green fluorescent protein (FFL-GFP). FFL-GFP is a unique model chimeric protein as the FFL moiety is extremely sensitive to stress-induced misfolding and aggregation, which inactivates the enzyme (12). Luciferase activity is monitored using an enzymatic assay, and the GFP moiety provides a method of visualizing soluble or aggregated FFL using automated microscopy. These coupled methods incorporate two parallel and technically independent approaches to analyze both refolding and functional reactivation of an enzyme after stress. Activity recovery can be directly correlated with kinetics of disaggregation and re-solubilization to better understand how protein quality control factors such as protein chaperones collaborate to perform these functions. In addition, gene deletions or mutations can be used to test contributions of specific proteins or protein subunits to this process. In this article we examine the contributions of the protein disaggregase Hsp104 (13), known to partner with the Hsp40/70/nucleotide exchange factor (NEF) refolding system (5), to protein refolding to validate this approach.


Abrams J.L.,University of Texas Medical School | Morano K.A.,University of Texas Medical School
Journal of Visualized Experiments | Year: 2013

Proteostasis, defined as the combined processes of protein folding/biogenesis, refolding/repair, and degradation, is a delicate cellular balance that must be maintained to avoid deleterious consequences 1. External or internal factors that disrupt this balance can lead to protein aggregation, toxicity and cell death. In humans this is a major contributing factor to the symptoms associated with neurodegenerative disorders such as Huntington's, Parkinson's, and Alzheimer's diseases 10. It is therefore essential that the proteins involved in maintenance of proteostasis be identified in order to develop treatments for these debilitating diseases. This article describes techniques for monitoring in vivo protein folding at near-real time resolution using the model protein firefly luciferase fused to green fluorescent protein (FFL-GFP). FFL-GFP is a unique model chimeric protein as the FFL moiety is extremely sensitive to stress-induced misfolding and aggregation, which inactivates the enzyme 12. Luciferase activity is monitored using an enzymatic assay, and the GFP moiety provides a method of visualizing soluble or aggregated FFL using automated microscopy. These coupled methods incorporate two parallel and technically independent approaches to analyze both refolding and functional reactivation of an enzyme after stress. Activity recovery can be directly correlated with kinetics of disaggregation and re-solubilization to better understand how protein quality control factors such as protein chaperones collaborate to perform these functions. In addition, gene deletions or mutations can be used to test contributions of specific proteins or protein subunits to this process. In this article we examine the contributions of the protein disaggregase Hsp104 13, known to partner with the Hsp40/70/nucleotide exchange factor (NEF) refolding system 5, to protein refolding to validate this approach.

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