Entity

Time filter

Source Type

Houston, TX, United States

Baylor College of Medicine , located in the Texas Medical Center in Houston, Texas, US, is a health science university. It includes a medical school, Baylor College of Medicine; the Graduate School of Biomedical science; the School of Allied Health science; and the National School of Tropical Medicine. The school, located in the middle of the world's largest medical center, is part owner of Baylor St. Luke's Medical Center, part of the CHI St. Luke's Health system, and has hospital affiliations with: Harris Health System, Texas Children's Hospital, The University of Texas MD Anderson Cancer Center, Memorial Hermann - The Institute for Rehabilitation and Research, Menninger Clinic, the Michael E. DeBakey Veterans Affairs Medical Center and Children's Hospital of San Antonio.The medical school has been consistently considered in the top-tier of programs in the country, and is particularly noted for having the lowest tuition among all private medical schools in the US. Its Graduate School of Biomedical science is among the top 30 graduate schools in the United States. Within the School of Allied Health science, the nurse anesthesia ranks 5th and the physician assistant program ranks 6th. A program in Orthotics and Prosthetics began in 2013, with 18 students in the first class. The National School of Tropical Medicine is the only school in the nation dedicated exclusively to patient care, research, education and policy related to neglected tropical diseases.On June 21, 2010, Dr. Paul Klotman was named as the new President and CEO of the Baylor College of Medicine. In January 2014, the College and CHI St. Luke's became joint owners of Baylor St. Luke's Medical Center. Wikipedia.


An unanticipated and tremendous amount of the noncoding sequence of the human genome is transcribed. Long noncoding RNAs (lncRNAs) constitute a significant fraction of non-protein-coding transcripts; however, their functions remain enigmatic. We demonstrate that deletions of a small noncoding differentially methylated region at 16q24.1, including lncRNA genes, cause a lethal lung developmental disorder, alveolar capillary dysplasia with misalignment of pulmonary veins (ACD/MPV), with parent-of-origin effects. We identify overlapping deletions 250 kb upstream of FOXF1 in nine patients with ACD/MPV that arose de novo specifically on the maternally inherited chromosome and delete lung-specific lncRNA genes. These deletions define a distant cis-regulatory region that harbors, besides lncRNA genes, also a differentially methylated CpG island, binds GLI2 depending on the methylation status of this CpG island, and physically interacts with and up-regulates the FOXF1 promoter. We suggest that lung-transcribed 16q24.1 lncRNAs may contribute to long-range regulation of FOXF1 by GLI2 and other transcription factors. Perturbation of lncRNA-mediated chromatin interactions may, in general, be responsible for position effect phenomena and potentially cause many disorders of human development. Source


El-Serag H.B.,Baylor College of Medicine
Gastroenterology | Year: 2012

Most cases of hepatocellular carcinoma (HCC) are associated with cirrhosis related to chronic hepatitis B virus (HBV) or hepatitis C virus (HCV) infection. Changes in the time trends of HCC and most variations in its age-, sex-, and race-specific rates among different regions are likely to be related to differences in hepatitis viruses that are most prevalent in a population, the timing of their spread, and the ages of the individuals the viruses infect. Environmental, host genetic, and viral factors can affect the risk of HCC in individuals with HBV or HCV infection. This review summarizes the risk factors for HCC among HBV- or HCV-infected individuals, based on findings from epidemiologic studies and meta-analyses, as well as determinants of patient outcome and the HCC disease burden, globally and in the United States. © 2012 AGA Institute. Source


Graham D.Y.,Baylor College of Medicine
Gastroenterology | Year: 2015

Helicobacter pylori infection contributes to the development of diverse gastric and extragastric diseases. The infection is necessary but not sufficient for the development of gastric adenocarcinoma. Its eradication would eliminate a major worldwide cause of cancer death, therefore there is much interest in identifying how, if, and when this can be accomplished. There are several mechanisms by which H pylori contributes to the development of gastric cancer. Gastric adenocarcinoma is one of many cancers associated with inflammation, which is induced by H pylori infection, yet the bacteria also cause genetic and epigenetic changes that lead to genetic instability in gastric epithelial cells. H pylori eradication reduces both. However, many factors must be considered in determining whether treating this bacterial infection will prevent cancer or only reduce its risk - these must be considered in designing reliable and effective eradication therapies. Furthermore, H pylori infection has been proposed to provide some benefits, such as reducing the risks of obesity or childhood asthma. When tested, these hypotheses have not been confirmed and are therefore most likely false. © 2015 by the AGA Institute. Source


Mutations in the transcription factor GATA2 underlie the syndrome of monocytopenia and B- and natural killer (NK)-cell lymphopenia associated with opportunistic infections and cancers. In addition, patients have recurrent and severe viral infections. NK cells play a critical role in mediating antiviral immunity. Human NK cells are thought to mature in a linear fashion, with the CD56(bright) stage preceding terminal maturation to the CD56(dim) stage, considered the most enabled for cytotoxicity. Here we report an NK cell functional defect in GATA2-deficient patients and extend this genetic lesion to what is considered to be the original NK cell-deficient patient. In most cases, GATA2 deficiency is accompanied by a severe reduction in peripheral blood NK cells and marked functional impairment. The NK cells detected in peripheral blood of some GATA2-deficient patients are exclusively of the CD56(dim) subset, which is recapitulated on in vitro NK cell differentiation. In vivo, interferon α treatment increased NK cell number and partially restored function but did not correct the paucity of CD56(bright) cells. Thus, GATA2 is required for the maturation of human NK cells and the maintenance of the CD56(bright) pool in the periphery. Defects in GATA2 are a novel cause of profound NK cell dysfunction. Source


Moyer V.A.,Baylor College of Medicine
Annals of Internal Medicine | Year: 2012

Description: Update of the 2008 U.S. Preventive Services Task Force (USPSTF) recommendation statement on screening for prostate cancer. Methods: The USPSTF reviewed new evidence on the benefits and harms of prostate-specific antigen (PSA)-based screening for prostate cancer, as well as the benefits and harms of treatment of localized prostate cancer. Recommendation: The USPSTF recommends against PSA-based screening for prostate cancer (grade D recommendation). This recommendation applies to men in the general U.S. population, regardless of age. This recommendation does not include the use of the PSA test for surveillance after diagnosis or treatment of prostate cancer; the use of the PSA test for this indication is outside the scope of the USPSTF. © 2012 American College of Physicians. Source

Discover hidden collaborations