FILE - In this Oct. 10, 1994, file photo, Alfred G. Gilman, 53, poses in a lab at the University of Texas Southwestern Medical School in Dallas. Gilman, a 1994 Nobel Prize-winning scientist and former dean of the University of Texas Southwestern Medical School, has died after a lengthy illness. He was 74. Russell Rian, a spokesman for UT Southwestern in Dallas, said Thursday, Dec. 24, 2015, that the university learned of Gilman's death from his family on Wednesday. (AP Photo/Tim Sharp, File) More AUSTIN, Texas (AP) — Dr. Alfred Gilman, who won a Nobel Prize for his breakthrough research into the inner workings of cells and later left Texas' much-ballyhooed $3 billion cancer-fighting initiative, citing a lack of oversight that led to a scandal, has died. He was 74. Gilman was the former dean of the University of Texas Southwestern Medical School in Dallas, where colleagues said he was dedicated to solid science and an outspoken critic of subpar work. Spokesman Russell Rian said Thursday that the school learned of Gilman's death from his family. The scientist had been fighting pancreatic cancer. Gilman shared a 1994 Nobel Prize in physiology or medicine with Dr. Martin Rodbell of the National Institute of Environmental Health Sciences for their discovery of G proteins. The proteins help in the process of receiving signals from outside the cell and activating responses. "The mechanism that he found explains how many drugs act, it explains how many hormones act and it basically explains how the body responds to its environment," said Dr. Michael Brown, himself a Nobel laureate in 1985, who 35 years ago had the laboratory next to Gilman's at UT Southwestern. Brown said Thursday that, back then, he and Gilman "were drawn together not only by our love of Tanqueray and cigarettes, but because we both shared a passion for rigorous science." Gilman was born July 1, 1941, in New Haven, Connecticut, and discovered G proteins while at the University of Virginia in 1977. He became chairman of pharmacology at UT Southwestern in 1981. In 2009, Gilman became chief scientific officer for the Cancer Prevention and Research Institute of Texas, whose creation was approved by voters two years earlier. It later became the country's second-largest pot of cancer research funding. But Gilman resigned in 2012 and revealed some internal concerns over funding, suggesting there was not enough scrutiny of grants that won approval. He also worried the initiative, known as CPRIT, was more focused on marketable research than sound science. Prosecutors indicted a top state executive the next year on charges related to $11 million in taxpayer funds that the agency awarded to a private company without review, though the executive was later acquitted. "Al Gilman hated sloppy or phony science and he was compelled to speak out whenever he saw it," Brown said. "Sometimes it was very inconvenient for him, but his conscience made him do it." Daniel Podolsky, president of the UT Southwestern Medical Center, called the resignation "an extremely painful period for Al." "Here's someone who had lived his entire life adhering to the integrity of what he did, and that being implicitly questioned by some, when there was nothing about it in terms of self-aggrandizement or self-service," Podolsky said Thursday. "I never doubted he would do anything less than defend what he thought was right in terms of how CPRIT was going to invest in research to really have an impact." Podolsky said Gilman was diagnosed with pancreatic cancer more than two years ago and "was absolutely staunch and courageous in fighting it." Gilman is survived by his wife, Kathryn; daughters Amy Ariagno and Anne Sincovec; and a son, Edward Gilman. This version of the story corrects the spelling of Nobel in paragraph four.
Morey A.F.,Southwestern Medical School |
Watkin N.,St. Georges Hospital |
Shenfeld O.,Shaare Zedek Medical Center |
Eltahawy E.,Ain Shams University |
Giudice C.,Hospital Italiano
Urology | Year: 2014
The management of primary and recurrent bulbar urethral stricture disease has been a source of controversy with the choice being between endoscopic urethrotomy and open urethroplasty. Further debate exists with regard to the choice of urethroplasty - either excision and primary anastomosis (EPA) or augmentation with a graft or flap. Using PubMed, a 35-year literature search was conducted (1975-2010) for peer-reviewed articles on bulbar strictures treated using EPA. Exclusions included articles with <10 patients, duplications, reviews, or in which the cohort was mixed and the data could not be separately analyzed. Seventeen articles fulfilled the criteria with a total of 1234 patients. Overall success was 93.8%. Reported complications were <5%, and there was no evidence of persistent loss of sexual function. The authors conclude that EPA is associated with a high success rate with low complication rate. Our recommendation is that it should be performed in patients with short isolated bulbar strictures, when expected success rates of other procedures are <90%. © 2014 Elsevier Inc. Source
Young E.J.,Michael bakey Veterans Affairs Medical Center |
Young E.J.,Baylor College of Medicine |
Hasanjani Roushan M.R.,Babol Medical University |
Shafae S.,Babol Medical University |
And 2 more authors.
Human Pathology | Year: 2014
As a major organ of the mononuclear phagocytic system, the liver is probably involved in all cases of brucellosis. In this prospective study, liver slides prepared from percutaneous liver biopsy samples of 20 patients with clinical and laboratory evidence of acute brucellosis due to Brucella melitensis were examined for the presence or absence of granulomas by pathologists in Iran and the United States. Nineteen men and one woman ranging in age from 14 to 62 years were studied. All patients had clinical signs and symptoms compatible with acute brucellosis, and all had significantly elevated titers of antibodies to Brucella in their serum. Liver function tests were mildly elevated in 11 (55%) cases, and C-reactive protein was positive in 15 (65%) patients. Thirteen (65%) patients had blood cultures positive for B melitensis. Iranian and American pathologists reported granulomas in 3 (15%) and in 4 (20%) cases, respectively. There was agreement between Iranian and American pathologists in 17 (85%) cases. The most prevalent findings were mild portal or lobular lymphocytic inflammation (16 cases). Two cases revealed noncaseating epithelioid granulomas, and 2 had microgranulomas. The results show that all patients had microscopic evidence of liver involvement. The predominant histologic finding was mild portal or lobular inflammation with lymphocytes. Granulomas were present in only 4 cases. © 2014 Elsevier Inc. Source
Roland C.L.,Southwestern Medical School |
Roland C.L.,University of Texas at Dallas |
Dineen S.P.,Southwestern Medical School |
Dineen S.P.,University of Texas at Dallas |
And 9 more authors.
Experimental Biology and Medicine | Year: 2010
Tumor infiltration of immune cells (polymorphonuclear cells [PMNs] and macrophages) was initially thought to be an attempt by the host organism to combat malignancy. It appears, however, that certain subsets of chronically activated immune cells likely promote tumor growth, facilitate tumor cell survival and aid in metastasis. The association between tumor cells and tumor-associated PMNs has been demonstrated in several types of cancer, but the presence of tumor-associated PMNs in pancreatic cancer has not been well studied in vivo. Intercellular adhesion molecule-1 (ICAM-1) functions in cell-cell and cell-extracellular matrix adhesion and has a physiological role in PMN tight adhesion of leukocytes via interaction with the ligands LFA-1 and Mac-1. Increased ICAM-1 expression correlates with poor prognosis in pancreatic cancer. Therefore, the aim of this study was to investigate the function of ICAM-1 and tumor-associated PMNs in pancreatic cancer progression using ICAM-1-null (ICAM-1-/-) mice. We hypothesize that ICAM-1 null mice have decreased pancreatic cancer progression. Surprisingly, there is no significant difference in pancreatic cancer progression in wild-type versus ICAM-1 null mice. Interestingly, we found that tumor-derived ICAM-1 co-localizes with host PMNs at the leading edge of the tumor in ICAM-1 null mice. These results suggest that tumor-derived ICAM-1 is a sufficient ligand for tumorassociated PMNs and may play a role in subsequent tumor growth and metastasis. Copyright © 2010 by the Society for Experimental Biology and Medicine. Source