tbuckley/cabot-search huggingface dataset:
Reviews and Notes: HIV Medicine: Strong Shadows: Scenes from an Inner City AIDS Clinic
Authors: Susan J. Rehm
Journal: Annals of Internal Medicine (1996)

Literature of Medicine15 October 1996Reviews and Notes: HIV Medicine: Strong Shadows: Scenes from an Inner City AIDS ClinicSusan J. Rehm, MDSusan J. Rehm, MDCleveland Clinic Foundation, Cleveland, OH 44195Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-125-8-199610150-00036 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail A Zuger. 243 pages. New York: WH Freeman; 1995. $22.95. ISBN 0-7167-2916-4. Order phone 800-877-5351.The literature of the acquired immunodeficiency syndrome (AIDS) runs the gamut, from scholarly review to underground newsletter, from textbook to pamphlet. Few medical publications attempt to provide a view of the human side of the epidemic, particularly when the faces of AIDS are those of the poor.Building on pieces published in Discover and The New York Times Magazine, the author uses a series of case vignettes to comprehensively examine the effect of AIDS on individual persons, their families, and their health care teams. The ... Author, Article, and Disclosure InformationAffiliations: Cleveland Clinic Foundation, Cleveland, OH 44195 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 October 1996Volume 125, Issue 8Page: 702-703KeywordsAIDSCase seriesHIVHIV infectionsHealth care Issue Published: 15 October 1996 CopyrightCopyright © 1996 by American College of Physicians. All Rights Reserved.PDF DownloadLoading ...
TCT-81 Long-term Safety and Efficacy of Percutaneous Left Ventricular Transapical Access and Closure for Structural Heart Disease Interventions
Authors: Chad Kliger, Bryce Einhorn, Vladimir Jelnin, Leandro Maranan, Gila Perk, Itzhak Kronzon, Howard Cohen, Carlos Ruiz
Journal: Journal of the American College of Cardiology (2012)
Dangers from dissolution of latex in Celestin endo-oesophageal tube.
Authors: S A Hussain, R Hughes, E Gross
Journal: BMJ (1987)

Above: Renal biopsy specimen at presentation showing dilated tubules, hyaline casts, and.surrounding inflammatory infiltrate but no evidence of amyloid.Below: Biopsy specimen eight months later showing no hyaline casts, reduced ibflammatory infiltrate, and normal tubules.myeloma kidney have been shown to be reversible, and the parallel reduction in urinary light chain excretion supports the role of light chains in the pathogenesis of myeloma kidney.Long term dialysis or even renal transplantation' has been used to treat such patients in the past, but our case demonstrates a well tolerated alternative approach, which we are evaluatig further.
Self-Expandable Metal Stents for Malignant Gastric Outlet Obstruction: A Modified Technique
Authors: R. P. Venu, B. J. Pastika, M. Kini, D. Chua, R. Christian, J. Schlais, R. D. Brown
Journal: Endoscopy (1998)

Background and Study Aims: Endoscopic palliative treatment may be effective in the management of malignant gastric outlet obstruction. However, experience in this area is limited, and the techniques vary widely. In this retrospective study, a uniform technique using nearly identical self-expandable metal stents was employed to assess technical feasibility, safety, and outcome.
THE TREATMENT OF AMBULATORY ADOLESCENT SCHIZOPHRENIA WITH ACETOPHENAZINE
Authors: HARRY F. DARLING
Journal: American Journal of Psychiatry (1963)

Relative remission was obtained in 72% of adolescents and children having ambulatory schizophrenia when treated with acetophenazine. The great majority were early cases. Due to the fact that the drug is chemically a piperazine phenothiazine jaundice and leukopenia were not factors of undue concern. Pharmacologically the drug resembles aliphatic phenothiazines so that the problem of parkinsonism was reduced in comparison with other piperazines, although the percentage of lethargy was considerably higher than in its chemical analogs.
E2FBP1 antagonizes the p16INK4A‐Rb tumor suppressor machinery for growth suppression and cellular senescence by regulating promyelocytic leukemia protein stability
Authors: Yayoi Fukuyo, Akiko Takahashi, Eiji Hara, Nobuo Horikoshi, Tej K Pandita, Takuma Nakajima
Journal: International Journal of Oral Science (2011)

Cellular senescence is an irreversible cell cycle arrest triggered by the activation of oncogenes or mitogenic signaling as well as the enforced expression of tumor suppressors such as p53, p16INK4A and promyelocytic leukemia protein (PML) in normal cells. E2F‐binding protein 1 (E2FBP1), a transcription regulator for E2F, induces PML reduction and suppresses the formation of PML‐nuclear bodies, whereas the down‐regulation of E2FBP1 provokes the PML‐dependent premature senescence in human normal fibroblasts. Here we report that the depletion of E2FBP1 induces the accumulation of PML through the Ras‐dependent activation of MAP kinase signaling. The cellular levels of p16INK4A and p53 are elevated during premature senescence induced by depletion of E2FBP1, and the depletion of p16INK4A, but not p53 rescued senescent cells from growth arrest. Therefore, the premature senescence induced by E2FBP1 depletion is achieved through the p16INK4A‐Rb pathway. Similar to human normal fibroblasts, the growth inhibition induced by E2FBP1 depletion is also observed in human tumor cells with intact p16INK4A and Rb. These results suggest that E2FBP1 functions as a critical antagonist to the p16INK4A‐Rb tumor suppressor machinery by regulating PML stability.
Inhibition of FLT3 in MLL
Authors: Scott A Armstrong, Andrew L Kung, Meghann E Mabon, Lewis B Silverman, Ronald W Stam, Monique L Den Boer, Rob Pieters, John H Kersey, Stephen E Sallan, Jonathan A Fletcher, Todd R Golub, James D Griffin, Stanley J Korsmeyer
Journal: Cancer Cell (2003)
Diagnosis of Tuberous Sclerosis
Authors: Charles Steffen
Journal: JAMA (1983)

<h3>To the Editor.—</h3> I would like to comment on the important article by Cassidy et al wherein they studied the families of patients with tuberous sclerosis (1983;249:1302). The term<i>adenoma sebaceum</i>is no longer used to describe the skin papules found in the tuberous sclerosis complex. Pringle, who coined the term, did not appreciate how large normal sebaceous glands can be on the center of the face and misinterpreted these papules as neoplasms of sebaceous glands.<sup>1</sup>The histopathology of the facial and periungual lesions in the tuberous sclerosis complex consists of widely dilated vascular spaces and abnormalities of the fibroblasts. They are called "angiofibromas," not "adenoma sebaceum." Cassidy et al claim that the adenoma sebaceum and periungual fibromas (ie, angiofibromas) are diagnostic of the tuberous sclerosis complex when they state that patients with them have "unequivocal findings demonstrating tuberous sclerosis." However, many authors, including most recently Meigel and Ackerman,
How to support the basic sciences
Authors: Andrew R. Marks
Journal: Journal of Clinical Investigation (2005)

It has become axiomatic that basic science faculty and research programs at medical schools must support themselves. The days when excess clinical revenue was used to support basic research are long gone. With the pressure of managed care and faculty practice programs on medical school budgets, it appears that medical school leaders are looking everywhere but at clinical programs for critical support of biomedical research at their institutions, even as NIH support shrinks.
Nerve gas antidote a possible cause of Gulf war illness
Authors: F. Charatan
Journal: BMJ (1999)

A study conducted over two years by the Rand Corporation, a non-profit organisation financed by the US Department of Defense, suggests that pyridostigmine bromide may cause a number of symptoms affecting more than 100000 Gulf warveterans.

The 385 page report, written by Dr Beatrice Golomb, professor of medicine at the University of California and physician at the Veterans Affairs Medical Center, San Diego, sharply contradicts two earlier studies—by a presidential advisory committee on Gulf war veterans' illnesses and the Institute of Medicine—both of which …
CB-02 * MiRNA EXPRESSION PROFILES OF GLIOMA STEM CELLS AND THEIR ASSOCIATION WITH THE MESENCHYMAL TRANSFORMATION OF THESE CELLS
Authors: A. Bier, S. Finniss, S. Cazacu, C. Xiang, H. K. Lee, D. Rand, M. Yalon, A. Toren, L. Poisson, C. Brodie
Journal: Neuro-Oncology (2014)

Glioblastoma, are characterized by increased infiltration into the surrounding brain tissue, resistance to therapies, and poor prognosis. A major pathway that contributes to these characteristics is the mesenchymal phenotype of these tumors. A small subpopulation of cancer stem cells (GSCs) have been implicated in the enhanced infiltration, radio-resistance and tumor recurrence. GSCs share some similarities with neural stem cells (NSCs) but exhibit deregulated differentiation ability and enhanced oncogenic potential. Recent studies documented miRNAs as important regulators of GSC functions and of the malignant and stemness features of these cells. In this study we performed miRNA and mRNA integrated analysis of GSCs compared to human NSCs and mesenchymal stromal cells (MSCs) to identify significant miRNA-mRNA signatures associated with the mesenchymal signature of GSCs, using miRNA and mRNA microarray analysis. The comparison of GSCs and NSCs identified 79 miRNAs that were upregulated in GSCs and 21 miRNAs that were increased in MSCs. Twenty six miRNAs were downregulated in GSCs compared to NSCs and 21 miRNAs from this group were further downregulated in MSCs. The comparison of mRNA expression of GSCs and NSCs identified gene clusters associated with glioma cell invasiveness, axonal guidance signaling and TGF-b signaling. miR-504 is one of the miRNAs that was significantly downregulated in GSCs compared to NSCs. The expression of miR-504 was also decreased in mesenchymal GBM and highly increased in the G-CIMP subset of GBM. miR-504 promoted the neural differentiation of GSC, inhibited their self-renewal, migration and the mesenchymal signature of these cells, by downregulating CD44, BCAN, ZRB1 and ZEB2. In conclusion, these results reveal novel miRNAs and potential target networks that play a role in the oncogenic potential and stemness of GSCs and in their mesenchymal transformation and may lead to the identification of therapeutic targets for the eradication of GSCs and the treatment of GBM.
1000–37 The “Long Long” Balloon Pilot: Dilatation of Class C Coronary Lesions Using Slow, Oscillating, Prolonged Inflation of 40 mm Balloons
Authors: Mitchell W. Krucoff, Theodore L. Schreiber, Russell E. Raymond, Suzanne W. Crater, Cindy L. Grines, Patrick L. Whitlow, Paul A. Gurbel, Donald F. Fortin, William R. Herzog, Brian H. Annex, Cindy L. Green, Jack T. Cusma, Kenneth G. Morris
Journal: Journal of the American College of Cardiology (1995)
Antibody to Coxsackie B virus in diagnosing postviral fatigue syndrome.
Authors: N A Miller, H A Carmichael, B D Calder, P O Behan, E J Bell, R A McCartney, F C Hall
Journal: BMJ (1991)

OBJECTIVE--To study the association between coxsackie B virus infection and the postviral fatigue syndrome and to assess the immunological abnormalities associated with the syndrome. DESIGN--Case-control study of patients with the postviral fatigue syndrome referred by local general practitioners over one year. SETTING--General practitioner referrals in Dunbartonshire, Scotland. PATIENTS--254 Patients referred with the postviral fatigue syndrome (exhaustion, myalgia, and other symptoms referable to postviral fatigue syndrome of fairly recent onset--that is, several months) and age and sex matched controls obtained from same general practitioner; 11 patients were rejected because of wrong diagnoses, resolution of symptoms, and refusal to participate, leaving 243 patients and matched controls. MAIN OUTCOME MEASURES--Detailed questionnaire (patients and controls) and clinical examination (patients) and blind analysis of blood sample at entry and after six months for determination of coxsackie B virus IgM and IgG antibodies and other variables (including lymphocyte protein synthesis, lymphocyte subsets, and immune complexes). RESULTS--Percentage positive rates for coxsackie B virus IgM at entry were 24.4% for patients and 22.6% for controls and for coxsackie B virus IgG 56.2% and 55.3% respectively; there were no significant differences between different categories of patients according to clinical likelihood of the syndrome nor any predictive value in a fourfold rise or fall in the coxsackie B virus IgG titre in patients between entry and review at six months. The rates of positive antibody test results in patients and controls showed a strong seasonal variation. Of the numerous immunological tests performed, only a few detected significant abnormalities; in particular the mean value for immune complex concentration was much higher in 35 patients and 35 controls compared with the normal range and mean value for total IgM was also raised in 227 patients and 35 controls compared with the normal range. CONCLUSIONS--Serological tests available for detecting coxsackie B virus antibodies do not help diagnose the postviral fatigue syndrome. Percentage positive rates of the antibodies in patients simply reflect the background in the population as probably do the raised concentrations of total IgM and immune complexes.
Personal and Social Psychopathology and the Primary Prevention of Violence
Authors: LEON J. SAUL
Journal: American Journal of Psychiatry (1972)

Children reared with love and respect mature adequately and become loving, responsible, and productive spouses, parents, and citizens. Those reared in such a way that they hate their parents will also hate other persons for life. If repressed, this pathological hostility causes neuroses; if it is acted out, it results in crime, tyranny, revolution, and aggressive war. The author believes that this kind of individual is the primary cause of violence in the world today.
Pentraxin 3 Is a New Inflammatory Marker Correlated With Left Ventricular Diastolic Dysfunction and Heart Failure With Normal Ejection Fraction
Authors: Junichi Matsubara, Seigo Sugiyama, Toshimitsu Nozaki, Koichi Sugamura, Masaaki Konishi, Keisuke Ohba, Yasushi Matsuzawa, Eiichi Akiyama, Eiichiro Yamamoto, Kenji Sakamoto, Yasuhiro Nagayoshi, Koichi Kaikita, Hitoshi Sumida, Shokei Kim-Mitsuyama, Hisao Ogawa
Journal: Journal of the American College of Cardiology (2011)
DUSP1 Phosphatase Regulates the Proinflammatory Milieu in Head and Neck Squamous Cell Carcinoma
Authors: Xiaoyi Zhang, J. Madison Hyer, Hong Yu, Nisha J. D'Silva, Keith L. Kirkwood
Journal: Cancer Research (2014)

Abstract DUSP1 is a dual-specificity phosphatase that regulates mitogen-activated protein (MAP) kinase activity. Studies have associated loss of DUSP1 expression with certain cancers, but there has been no report of a mechanism by which this supports tumor progression. In this study, we found DUSP1 mRNA and protein decreased in human head and neck squamous cell carcinoma tissues compared with adjacent nontumor controls. To evaluate the impact of this difference, we compared the susceptibility of Dusp1-deficient mice with oral squamous carcinogenesis induced by 4-nitroquinoline 1-oxide. Dusp1-deficient mice displayed enhanced disease progression, characterized by advanced onset, histologic stage, and tumor burden. In a syngeneic model of tumor progression, subcutaneous injection of EO771 cells formed faster-growing tumors in Dusp1-deficient mice, an effect abrogated by inhibition of p38 MAP kinase with SB203580. Histologic and quantitative assessments demonstrated increased inflammation and deregulated chemokine and cytokine expression in Dusp1-deficient tumor tissues. Specifically, proinflammatory cytokine IL1β was elevated. IL1β production was recapitulated ex vivo in primary bone marrow–derived macrophages from Dusp1-deficient mice. Together, our results clearly establish the role of Dusp1 as a tumor suppressor gene that regulates cancer-associated inflammation. Cancer Res; 74(24); 7191–7. ©2014 AACR.
LOCAL AND REMOTE ISCHEMIC PRECONDITIONING CREATE DIFFERENT PHENOTYPES IN SUBSARCOLEMMAL CARDIAC MITOCHONDRIA PRIOR TO ISCHEMIA/REPERFUSION INJURY
Authors: Michael-Alice Moga, Lixing Wang, Yaqin Yana Fu, Chung Ho Leung, Hideyuki Kato, Zida Li
Journal: Journal of the American College of Cardiology (2011)
Genomic analyses provide insights into the history of tomato breeding
Authors: Tao Lin, Guangtao Zhu, Junhong Zhang, Xiangyang Xu, Qinghui Yu, Zheng Zheng, Zhonghua Zhang, Yaoyao Lun, Shuai Li, Xiaoxuan Wang, Zejun Huang, Junming Li, Chunzhi Zhang, Taotao Wang, Yuyang Zhang, Aoxue Wang, Yancong Zhang, Kui Lin, Chuanyou Li, Guosheng Xiong, Yongbiao Xue, Andrea Mazzucato, Mathilde Causse, Zhangjun Fei, James J Giovannoni, Roger T Chetelat, Dani Zamir, Thomas Städler, Jingfu Li, Zhibiao Ye, Yongchen Du, Sanwen Huang
Journal: Nature Genetics (2014)
Temporal-spatial activation of apoptosis and epithelial injury in murine experimental biliary atresia
Authors: Nissa Erickson, Sujit Kumar Mohanty, Pranavkumar Shivakumar, Gregg Sabla, Ranajit Chakraborty, Jorge A. Bezerra
Journal: Hepatology (2008)

Biliary atresia is a fibro-inflammatory cholangiopathy that obstructs the extrahepatic bile ducts in young infants. Although the pathogenesis of the disease is undefined, studies in livers from affected children and neonatal mice with experimental biliary atresia have shown increased expression of proapoptosis molecules. Therefore, we hypothesized that apoptosis is a significant mechanism of injury to duct epithelium. To test this hypothesis, we quantified apoptosis using terminal transferase dUTP nick end labeling and active caspase-3 staining in livers and extrahepatic bile ducts from Balb/c mice infected with Rhesus rotavirus (RRV) within 24 hours of birth. RRV induced a significant increase in labeled cells in the portal tracts and in epithelial and subepithelial compartments of extrahepatic bile ducts, with onset within 3 days and peaks at 5–10 days. Exploring mechanisms of injury, we found increased biliary expression of caspases 1 and 4 and of interferon-gamma (IFNγ)–related and tumor necrosis factor-alpha (TNFα)–related genes. Using a cholangiocyte cell line, we found that neither IFNγ nor TNFα alone affected cell viability; however, simultaneous exposure to IFNγ and TNFα activated caspase-3 and decreased cell viability. Inhibition of caspase activity blocked apoptosis and restored viability to cultured cholangiocytes. In vivo, administration of the caspase inhibitor IDN-8050 decreased apoptosis in the duct epithelium and the extent of epithelial injury after RRV challenge. Conclusion: The biliary epithelium undergoes early activation of apoptosis in a mouse model of biliary atresia. The synergistic role of IFNγ and TNFα in activating caspase-3 in cholangiocytes and the decreased apoptosis following pharmacologic inhibition of caspases support a prominent role for apoptosis in the pathogenesis of experimental biliary atresia.
Perturbation of Defense Pathways by Low-Dose Arsenic Exposure in Zebrafish Embryos
Authors: Carolyn J. Mattingly, Thomas H. Hampton, Kimberly M. Brothers, Nina E. Griffin, Antonio Planchart
Journal: Environmental Health Perspectives (2009)

Exposure to arsenic is a critical risk factor in the complex interplay among genetics, the environment, and human disease. Despite the potential for in utero exposure, the mechanism of arsenic action on vertebrate development and disease is unknown.The objective of this study was to identify genes and gene networks perturbed by arsenic during development in order to enhance understanding of the molecular mechanisms of arsenic action.We exposed zebrafish embryos at 0.25-1.25 hr postfertilization to 10 or 100 ppb arsenic for 24 or 48 hr. We then used total RNA to interrogate genome microarrays and to test levels of gene expression changes by quantitative real-time polymerase chain reaction (QPCR). Computational analysis was used to identify gene expression networks perturbed by arsenic during vertebrate development.We identified a set of 99 genes that responded to low levels of arsenic. Nineteen of these genes were predicted to function in a common regulatory network that was significantly associated with immune response and cancer (p < 10(-41)). Arsenic-mediated expression changes were validated by QPCR.In this study we demonstrated that arsenic significantly down-regulates expression levels of multiple genes potentially critical for regulating the establishment of an immune response. The data also provide molecular evidence consistent with phenotypic observations reported in other model systems. Additional mechanistic studies will help explain molecular events regulating early stages of the immune system and long-term consequences of arsenic-mediated perturbation of this system during development.
Geographic variability of hemophilia‐associated aids in the United States: Effect of population characteristics
Authors: Jeanette K. Stehr‐Green, Janine M. Jason, Bruce L. Evatt
Journal: American Journal of Hematology (1989)

Abstract National AIDS surveillance suggests that approximately 3.5% of all hemophilic patients in the United States have developed AIDS as of February 1988; however, the cumulative incidence of AIDS among seropositive patients at individual hemophilia treatment centers (HTCs) has been reported to be as high as 12%. The purpose of this study was to examine the reported excess risk of AIDS at selected HTCs. Between July 13 and November 6, 1987, we reviewed medical charts from the 598 hemophilia A and hemophilia B patients receiving comprehensive care as of 1980 at six U.S. hemophilia treatment centers (three identified as low AIDS risk and three identified as high AIDS risk using national hemophilia‐associated AIDS surveillance data). The risk of AIDS among all patients was 8% and among seropositive patients was 18%. At the individual HTCs, the risk ranged from 0% to 14% among all patients and 0% to 25% among seropositive patients. Overall incidence rates were higher than those derived from national surveillance data because national estimates include all hemophilic patients (regardless of severity) whereas this study included only patients receiving comprehensive care (who are more likely to be severely affected by their coagulation disorder and receive concentrated clotting factors). The higher incidence of AIDS in the high‐risk centers was attributable to the older age of the patients in these HTCs, a factor previously associated with an increased risk of AIDS in seropositive patients. These findings do not support geographic variability in the incidence of AIDS and emphasize the importance of patient characteristics when comparing the incidence of hemophilia‐associated AIDS between populations.