tbuckley/cabot-search huggingface dataset:
An Atlas of Diabetes Mellitus
Authors: Nicholas P. Sauter
Journal: Annals of Internal Medicine (1998)

Medical Writings: Book Notes1 September 1998An Atlas of Diabetes MellitusNicholas P. Sauter, MDNicholas P. Sauter, MDUniversity of Chicago Medical Center, Chicago, IllinoisSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-129-5-199809010-00028 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail An Atlas of Diabetes Mellitus; Scobie IN. 96 pages. New York: Parthenon; 1998. $78.00. ISBN 1850704899. Order phone 800-735-4744.Field of medicine: Endocrinology.Format: Hardcover book.Audience: Medical students, primary care providers, endocrinologists, and other providers of diabetes-related services.Purpose: To provide a brief overview of diabetes mellitus and to convey, through images, the wide spectrum of diabetes and its complications.Content: A concise review of diabetes mellitus is followed and enriched by an extensive section of illustrations. The book covers the diagnosis and classification of diabetes, the pathogenesis of the disease, complications, and treatment.Highlights: The most outstanding feature ... Author, Article, and Disclosure InformationAffiliations: University of Chicago Medical Center, Chicago, Illinois PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 September 1998Volume 129, Issue 5Page: 431-432KeywordsDiabetes mellitusDiabetic retinopathyEndocrinologyExercise therapyGlobal healthInsulinPathogenesisType 2 diabetes ePublished: 15 August 2000 Issue Published: 1 September 1998 Copyright & PermissionsCopyright © 1998 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
A RANDOMIZED CONTROLLED TRIAL OF FRACTIONAL FLOW RESERVE TO OPTIMIZE PERCUTANEOUS CORONARY INTERVENTION
Authors: Eric Durand, Martine Gilard, Alain Furber, Pierre Coste, Michel Slama, Jean Luc Dubois-Randé, Paul Barragan, Patrick Dupouy, Saliha Rahal, Antoine Lafont
Journal: Journal of the American College of Cardiology (2010)
The Malpractice Insurance Crisis: Short-Term and Long-Term Solutions
Authors: William J. Curran
Journal: New England Journal of Medicine (1975)

LAST month's LawMedicine Notes column called attention to the economic crisis in medical malpractice insurance throughout the United States. The major carriers, after asking and receiving huge premium increases in the last three years, are threatening to drop out of the field entirely after July 1, 1975. Medical societies and other medical professional groups are threatening curtailments of certain high-risk procedures and even all-out strikes or "vacations" in mid-summer if something is not done before July 1.Insurance commissioners and governors are in panic all over the country. Legislative bills that seem patently unconstitutional are being seriously proposed and seriously . . .
Targeted pharmacotherapy in progressive familial intrahepatic cholestasis type 2: Evidence for improvement of cholestasis with 4‐phenylbutyrate
Authors: Emmanuel Gonzales, Brigitte Grosse, Brice Schuller, Anne Davit‐Spraul, Filomena Conti, Catherine Guettier, Doris Cassio, Emmanuel Jacquemin
Journal: Hepatology (2015)

Progressive familial intrahepatic cholestasis type 2 (PFIC2) is a result of mutations in ABCB11 encoding bile salt export pump (BSEP), the canalicular bile salt export pump of hepatocyte. In some PFIC2 patients with missense mutations, BSEP is not detected at the canaliculus owing to mistrafficking of BSEP mutants. In vitro, chaperone drugs, such as 4-phenylbutyrate (4-PB), have been shown to partially correct mistrafficking. Four PFIC2 patients harboring at least one missense mutation (p.G982R, p.R1128C, and p.T1210P) were treated orally with 4-PB and followed prospectively. Patient mutations were reproduced in a Bsep/green fluorescent protein plasmid. Cellular localization of the resulting Bsep mutants was studied in a hepatocellular line (Can 10), and effects of treatment with 4-PB and/or ursodeoxycholic acid (UDCA) were assessed. In Can 10 cells, Bsep mutants were detected in the endoplasmic reticulum instead of at the canalicular membrane. Treatment with 4-PB and UDCA partially corrected Bsep mutant targeting. With 4-PB, we observed, in all patients, a decrease of pruritus and serum bile acid concentration (BAC) as well as an improvement of serum liver tests. Pathological liver injuries improved, and BSEP, which was not detected at the canalicular membrane before treatment, appeared at the canalicular membrane. Bile analyses showed an increase in BAC with 4-PB. Patient conditions remained stable with a median follow-up of 40 months (range, 3-53), and treatment tolerance was good.4-PB therapy may be efficient in selected patients with PFIC2 owing to ABCB11 missense mutations affecting BSEP canalicular targeting. Bile secretion improvement may be a result of the ability of 4-PB to retarget mutated BSEP.
Gastrointestinal Problems in the Infant
Authors: Ann Ouyang
Journal: JAMA (1983)

The authors state in the preface that the book is directed primarily toward house officers, practicing pediatricians, and gastroenterologists. It is organized into three sections. The first, "Signs, Symptoms and Evaluation," is actually a group of chapters on a variety of subjects, some of which are specific, such as "Gastroesophageal Reflux," or general, such as "Development and Evaluation of Liver Function." Thus, the initial section does not follow any unified concept or pattern, although the individual chapters are readable. A short section on nutritional support follows. The third section and bulk of the book deals with disease states by organ. Each disease process is treated in a rather superficial manner, but, for the most part, the book is thoroughly referenced. There are instances, however, where the author mentions that a subject has been discussed elsewhere, but fails to provide either a cross-reference or reference. The discussions of treatment are concise
Female Narcotic Addicts: A Follow-up Study of Criminal and Addiction Careers
Authors: P. T. d'Orban
Journal: BMJ (1973)

A sample of 66 female narcotic addicts first examined in prison in 1967-8 was followed-up four years later. At the end of the period of follow-up 36% were off narcotics, 32% were still addicted, and 15% had died. Altogether 62% committed further offences. Drug offences and offences against property were almost equally frequent and accounted for over two-thirds of all convictions. There was no evidence of a link between prostitution and narcotic addiction. A significant association was found between continued delinquency and continued addiction during the period of follow-up. Addiction career and criminal career coincided in over three-quarters of the subjects, who tended either to continue manifesting both forms of deviant behaviour (46%) or to relinquish both (30%). The findings are in keeping with the view that narcotic addiction and crime are not causally related but may be parallel effects of common underlying factors leading to social deviance.
Basal Lamina of Abdominal Skeletal Muscle Capillaries in Diabetics and Nondiabetics
Authors: RUDOLF VRACKO, DONALD E. STRANDNESS
Journal: Circulation (1967)

In a "blind" study, skeletal muscle biopsies were obtained from the trunk of 13 nondiabetics, eight chemical diabetics, and four overt diabetics of comparable age. On electron micrographs of 20 capillaries from each case, the areas of various components of the capillary structure were measured with a planimeter. The area of the basal lamina was expressed as a percentage of the total vessel area. This method for measuring objectively the relative thickness of capillary basal lamina considered the vessel size, plane of sectioning, and the function state of the vessel. The theoretical validity of the method is discussed. The widths of the basal lamina of the capillaries of the trunk skeletal muscles of both diabetics and nondiabetics were identical. Morphological differences between the two groups were not present. The discrepancies in results of investigations concerned with the quantity of basal lamina in capillaries of skeletal muscle may be due to naturally occurring regional differences, or because capillary beds of different organs or tissues may be affected differently in diabetes mellitus.
Activation of Leukemic Pro-Suppressor Cells to Become Suppressor-Effector Cells
Authors: Samuel Broder, Takashi Uchiyama, Linda M. Muul, Carolyn Goldman, Susan Sharrow, David G. Poplack, Thomas A. Waldmann
Journal: New England Journal of Medicine (1981)

We studied the suppressor activity and surface-membrane antigens of immunoregulatory neoplastic T cells from a child with acute lymphoblastic leukemia and hypogammaglobulinemia. The neoplastic T cells were potent inhibitors of immunoglobulin production by pokeweed-mitogen-stimulated normal B cells when radiosensitive cooperating normal T cells were present. Preculturing trie leukemic cells with normal T cells or soluble factors allowed them to mediate suppression without the need for cooperating T cells. While acquiring new functional capabilities, approximately 95 per cent of the leukemic cells displayed an antigen (OKT-3) that is found on mature normal T cells; 77 per cent displayed an antigen (Tac) that is found on normal activated immunoregulatory effector cells but not on thymocytes or circulating T cells that are precursors of these effector cells. The results suggest that a population of leukemic pro-suppressor cells can be induced to undergo both functional and antigenic differentiation by the influence of normal T cells. (N Engl J Med. 1981; 304: 1382–7.)
Abstract 5701: Targeting KRAS lung cancer in vivo by pulmonary surfactant-mediated gene transfer
Authors: Takuya Fukazawa, Yutaka Maeda, Junji Matsuoka, Toshiro Ono, Katsumi Mominoki, Tomoki Yamatsuji, Munenori Takaoka, Ichiro Morita, Ichiro Murakami, Hirotoshi Tanaka, Mary L. Durbin, Yoshio Naomoto
Journal: Cancer Research (2012)

Abstract Pulmonary surfactant has been used as a carrier to deliver a therapeutic virus to dysfunctional lung cells that reside within an intricate lung structure. To investigate whether pulmonary surfactant enhances the efficacy of intratracheal instillation of a therapeutic virus to target KRAS lung cancer in vivo, we developed a recombinant adenovirus that induces cell death only in lung cancer cells and injected the adenovirus into a KRAS lung cancer model mouse intratracheally with or without surfactant. A therapeutic adenovirus that induces cell death only in lung cancer cells was constructed by combining a cancer specific hTERT promoter fused to CEBPα with a modified lung specific CC10 promoter fused to cytotoxic E1A. CEBPα is induced only in cancer cells and activates the CC10 promoter, which in turn induces cytotoxic E1A, and causes cell death only in lung cancer cells in vitro. This adenovirus was intratracheally injected into the KRAS lung cancer model mice (CCSP-rtTA/Tet-op-K-Ras4bG12D bitransgenic mice) in the presence/absence of pulmonary surfactant. Intratracheally-injected therapeutic adenovirus with pulmonary surfactant spread to airways as well as to the alveolar region of the lung and caused reduction of lung tumors developed in the KRAS lung cancer model mouse. The therapeutic adenovirus without pulmonary surfactant spread only to airways and had ten times less effectiveness in tumor reduction. Here, we demonstrate that pulmonary surfactant is an efficient tool to intratracheally deliver a therapeutic virus to treat KRAS lung cancer in vivo. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 5701. doi:1538-7445.AM2012-5701
Abstract B16: Expression of genes involved in PI3K/Akt signaling pathway in arsenic trioxide resistant clones derived from Jurkat cell line
Authors: Joanna Arkusz, Anna Smok-Pieniazek, Magdalena Komorowska, Maciej Stepnik
Journal: Clinical Cancer Research (2010)

Abstract Arsenic trioxide (ATO) is a well-known carcinogen but also an effective cancer therapeutic drug for acute promyelocytic leukemia. Despite intensive research efforts, the molecular mechanisms underlying antileukemic effect of ATO as well as resistance to arsenic therapy appearing during treatment are not well understood. There are data showing that dysregulation of the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway, a central integrating point of survival signals, may be the reason of apoptosis resistance in leukemic cells. The aim of the present study was to assess expression of 84 genes involved in PI3K/Akt signaling pathway in Jurkat cells exposed to ATO at 1, 2.5 and 5 μM for 16 hrs as well as in ATO resistant clones derived from the cells. First screening of genes was performed using the Human PI3K-AKT Signaling Pathway RT2 ProfilerTM PCR Array (Superarray) and then selected genes were verified in a standard real-time PCR. Results of our study showed that ATO induced more intensive changes in expression of PI3K/Akt pathway genes in ATO resistant clones than in Jurkat cells exposed to arsenic. Among genes differently regulated in both cell types were these playing a key role in regulating cell growth e.g. GRB10 (growth factor receptor-bound protein 10), FASLG (Fas ligand), CCND1 (cyclin D1). Interestingly, the level of FASLG mRNA was strongly down-regulated in ATO treated Jurkat cells and up-regulated in ATO resistant clones. Expression of CCND1 and GRB10 varied between resistant clones in a concentration-dependent manner. Moreover, concentration-dependent up-regulation of JUN (jun oncogene) was the most characteristic effect induced by ATO in Jurkat cells. Comparing to untreated Jurkat cells, we identified several genes differently regulated in ATO resistant clones (but not in Jurkat ATO exposed cells) that were mainly involved in anti-apoptotic pathways (e.g. IRS1 (Insulin receptor substrate 1), MAP2K1 (Mitogen-activated protein kinase kinase 1), MAPK3 (Mitogen-activated protein kinase 3), RPS6KA1 (Ribosomal protein S6 kinase, 90kDa, polypeptide 1), PRKCB (Protein kinase C, beta 1), PRKCZ (Protein kinase C, zeta) or Akt activation and growth regulation (e.g. PDK1 (Pyruvate dehydrogenase kinase, isozyme 1), MTOR (Mechanistic target of rapamycin), MTCP1 (Mature T-cell proliferation 1)). In conclusion, our in vitro study identified several targets of ATO that may mediate cytotoxic effects in Jurkat cells. Moreover, the data suggest that the PI3K/Akt signaling pathway plays an important role in the ATO resistance in Jurkat leukemic cells. The work was supported by the Polish State Committee for Scientific Research (grant No PB 2806/B/PO1/2007/33). Citation Information: Clin Cancer Res 2010;16(7 Suppl):B16
on moral intuitions and moral heuristics: a response
Authors: cass r. sunstein
Journal: Behavioral and Brain Sciences (2005)

moral heuristics are pervasive, and they produce moral errors. we can identify those errors as such even if we do not endorse any contentious moral view. to accept this point, it is also unnecessary to make controversial claims about moral truth. but the notion of moral heuristics can be understood in diverse ways, and a great deal of work remains to be done in understanding the nature of moral intuitions, especially those that operate automatically and nonreflectively, and in exploring the possibility of altering such intuitions through modest changes in context and narrative.
1170 IL28B C/C POLYMORPHISM IS PREDICTIVE OF SPONTANEOUS HCV RNA CLEARANCE IN PATIENTS WITH THALASSEMIA MAJOR
Authors: A. Mangia, R. Santoro, L. Mottola, V. Piazzolla, D. Bacca, R. Sarli, R. Clemente, M. Sacco, A. Andriulli, I. Stefano, P. Violi
Journal: Journal of Hepatology (2010)
Book Review A Clinician's Guide to Medical and Surgical Abortion Edited by Maureen Paul, E. Steven Lichtenberg, Lynn Borgatta, David A. Grimes, and Phillip G. Stubblefield. 336 pp., illustrated. New York, Churchill Livingstone, 1999. $95. 0-443-07529-8
Authors: Anne Davis
Journal: New England Journal of Medicine (2000)
Pemphigus foliaceus developing after metastasis of cutaneous squamous cell carcinoma to regional lymph nodes
Authors: Makoto Inaoki, Kenzo Kaji, Shinobu Furuse, Akihide Fujimoto, Nahoko Komatsu, Minoru Takata, Kazuhiko Takehara
Journal: Journal of the American Academy of Dermatology (2001)
Dexamethasone and oxytetracycline reverse the potentiation of neurogenic inflammation in airways of rats with Mycoplasma pulmonis infection.
Authors: J J Bowden, T R Schoeb, J R Lindsey, D M McDonald
Journal: American Journal of Respiratory and Critical Care Medicine (1994)

Mycoplasma pulmonis infection in rats causes a chronic inflammatory airway disease. Along with extensive remodeling of the airway mucosa, lymphocytic infiltrates, angiogenesis, and mucosal thickening, there is an abnormal sensitivity of the blood vessels to mediators that evoke "neurogenic inflammation". As a result, substance P, a peptide released from sensory nerves, produces an unusually large amount of plasma leakage. These changes can be prevented or reduced by prophylactic treatment with antibiotics, but it is unknown whether the extensive remodeling of the airway mucosa and potentiation of neurogenic inflammation can be reversed once they are established. We addressed this issue in F344 rats that were infected with M. pulmonis at 8 wk of age. Six weeks later, the rats were treated daily with an antibiotic (oxytetracycline, 20 mg/kg intramuscularly), to reduce the number of infecting organisms, or with an antiinflammatory steroid (dexamethasone, 0.5 mg/kg intraperitoneally), to reduce the inflammatory and immunologic response to the infection. Sham-treated infected rats received daily injections of 0.9% NaCl. After 1, 2, or 4 wk of treatment the rats were anesthetized and then challenged with substance P (5 micrograms/kg intravenously). The sham-treated rats had pathologic changes in their airways typical of severe M. pulmonis infection, and had as much as a threefold increase in substance P-induced plasma leakage. By comparison, after 4 wk of treatment with oxytetracycline or dexamethasone, the chronic inflammation was nearly resolved and the response to substance P was in the normal range. Unexpectedly, dexamethasone, like oxytetracycline, reduced the number of infecting organisms.(ABSTRACT TRUNCATED AT 250 WORDS)
Abstract 2533: A novel approach to generate anti-Tn antibody for cancer diagnosis and immunotherapy
Authors: Hsiao-Ling Chiang, Chi-Yu Lin, Fan-Dan Jan, Chiao-En Chen, Chia Cheng Wu, Shin Nieh, Chun-Cheng Lin, Jaulang Hwang
Journal: Cancer Research (2012)

Abstract Alterations in carbohydrate epitopes present on the cell surface are often hallmark of the transition from normal to neoplastic tissue. The concept of using carbohydrate antigens as cancer marker has thus spurred intense research interests into exploiting TACAs for the development of anticancer vaccines. This study presents a novel carrier protein containing a binding domain to the receptor of antigen presenting cells (APC) and cysteine-rich repeat peptide to serve as docking sites for conjugating tumor associated carbohydrate antigens (TACAs) or haptens. This novel carrier protein after conjugation with Tn, (GalNAcα1-O-Ser/Thr), can effectively elicit high titer of IgG1 antibody rather than IgM against Tn with high specificity in immunized mice. We then performed immunohistochemical (IHC) staining of twenty-six prostate cancer samples by staining with anti-Tn antibody, and we observed that the IHC staining with anti-Tn antibody is proportional to the malignancy of prostate cancer. Furthermore, we have examined the anti-Tn vaccine potency in Transgenic Adenocarcinoma of the Mouse Prostate (TRAMP) mice. TRMAP mice, which were treated with anti-Tn vaccine, showed longer survival rate and delayed tumor growth. We also successfully constructed the cDNA of mouse anti-Tn antibody from hybridoma cell line, and engineer this mouse cDNA as single-chain anti-Tn mouse antibody and anti-Tn immunotoxin. Our preliminary results showed that anti-Tn single-chain antibody can as a diagnostic antibody to distinguish normal prostatic tissue and prostate cancer, and anti-Tn immunotoxin can inhibit tumor cell growth. This study presents that our carrier protein can offer a platform for designing vaccine against tumor-associated weak immunogen and applies a new strategy in cancer immunotherapy in future. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2533. doi:1538-7445.AM2012-2533
Epigenetic Profiles Distinguish Malignant Pleural Mesothelioma from Lung Adenocarcinoma
Authors: Yasuhiro Goto, Keiko Shinjo, Yutaka Kondo, Lanlan Shen, Minoru Toyota, Hiromu Suzuki, Wentao Gao, Byonggu An, Makiko Fujii, Hideki Murakami, Hirotaka Osada, Tetsuo Taniguchi, Noriyasu Usami, Masashi Kondo, Yoshinori Hasegawa, Kaoru Shimokata, Keitaro Matsuo, Toyoaki Hida, Nobukazu Fujimoto, Takumi Kishimoto, Jean-Pierre J. Issa, Yoshitaka Sekido
Journal: Cancer Research (2009)

Malignant pleural mesothelioma (MPM) is a fatal thoracic malignancy, the epigenetics of which are poorly defined. We performed high-throughput methylation analysis covering 6,157 CpG islands in 20 MPMs and 20 lung adenocarcinomas. Newly identified genes were further analyzed in 50 MPMs and 56 adenocarcinomas via quantitative methylation-specific PCR. Targets of histone H3 lysine 27 trimethylation (H3K27me3) and genetic alterations were also assessed in MPM cells by chromatin immunoprecipitation arrays and comparative genomic hybridization arrays. An average of 387 genes (6.3%) and 544 genes (8.8%) were hypermethylated in MPM and adenocarcinoma, respectively. Hierarchical cluster analysis showed that the two malignancies have characteristic DNA methylation patterns, likely a result of different pathologic processes. In MPM, a separate subset of genes was silenced by H3K27me3 and could be reactivated by treatment with a histone deacetylase inhibitor alone. Integrated analysis of these epigenetic and genetic alterations revealed that only 11% of heterozygously deleted genes were affected by DNA methylation and/or H3K27me3 in MPMs. Among the DNA hypermethylated genes, three (TMEM30B, KAZALD1, and MAPK13) were specifically methylated only in MPM and could serve as potential diagnostic markers. Interestingly, a subset of MPM cases (4 cases, 20%) had very low levels of DNA methylation and substantially longer survival, suggesting that the epigenetic alterations are one mechanism affecting progression of this disease. Our findings show a characteristic epigenetic profile of MPM and uncover multiple distinct epigenetic abnormalities that lead to the silencing of tumor suppressor genes in MPM and could serve as diagnostic or prognostic targets.
Chronic, Recurrent Small-Vessel Cutaneous Vasculitis
Authors: Jeffrey P. Callen
Journal: JAMA (1982)

To the Editor.—  Recently, Cupps et al summarized their clinical experience with chronic vasculitis in 13 patients (1982;247:1994). In an accompanying editorial, Ehrlich (1982;247:2010) has lauded the study for its methods, which allow prognostic and therapeutic clinical information to be gained. Although I agree with the conclusions that therapy is difficult, and that patients have few or no laboratory or systemic abnormalities, the way in which the conclusions have been reached is not logical. This study lumps together patients with leukocytoclastic vasculitis and those with lymphocytic or mixed-cell vasculitis. Thus, with this hetergeneous histological picture, it is not surprising that few systemic symptoms are found. Lymphocytic perivasculitis is rarely if ever complicated by internal disease, whereas leukocytoclastic vasculitis is more frequently associated with laboratory and systemic abnormalities. 1 Also, this is a small sample size from which to draw conclusions. A larger sample size, containing patients with a uniform histological