tbuckley/cabot-search huggingface dataset:
Noninvasive exploration of cardiac autonomic neuropathy. Four reliable methods for diabetes?
Authors: M Ducher, C Cerutti, M P Gustin, S Abou-Amara, C Thivolet, M Laville, C Z Paultre, J P Fauvel
Journal: Diabetes Care (1999)

The purpose of this work was to assess relevant information that could be provided by various mathematical analyses of spontaneous blood pressure (BP) and heart rate (HR) variabilities in diabetic cardiovascular neuropathy.There were 10 healthy volunteers and 11 diabetic subjects included in the study. Diabetic patients were selected for nonsymptomatic orthostatic hypotension in an assessment of their cardiovascular autonomic impairment. Cardiac autonomic function was scored according to Ewing's methodology adapted to the use of a Finapres device. The spontaneous beat-to-beat BP and HR variabilities were then analyzed on a 1-h recording in supine subjects. The global variabilities were assessed by standard deviation, fractal dimension, and spectral power. The cardiac baroreflex function was estimated by cross-spectral sequences and Z analyses.In diabetic patients, Ewing's scores ranged from 1 to 4.5, confirming cardiovascular autonomic dysfunction. In these diabetic patients, global indices of variabilities were consistently lower than in healthy subjects. Furthermore, some of them (standard deviation and fractal dimension of HR, spectral power of systolic blood pressure and HR) were significantly correlated with the Ewing's scores. The Z methods and the spectral analysis found that the cardiac baroreflex was less effective in diabetic subjects. However, the baroreflex sensitivity could not be reliably assessed in all the patients. The sequence method pointed out a decreased number of baroreflex sequences in diabetic subjects that was correlated to the Ewing's score.Indices of HR spontaneous beat-to-beat variability are consistently related to the degree of cardiac autonomic dysfunction, according to Ewing's methodology. The Z method and spectral analysis confirmed that the cardiac baroreflex was impaired in diabetic patients. These methods might be clinically relevant for use in detecting incipient neuropathy in diabetic patients.
Chronic Homeless in Intervention Spotlight
Authors: Mike Mitka
Journal: JAMA (2006)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Indobufen inhibits tissue factor in human monocytes through a thromboxane-mediated mechanism
Authors: S ELIGINI, F VIOLI, C BANFI, S BARBIERI, M BRAMBILLA, M SALIOLA, E TREMOLI, S COLLI
Journal: Cardiovascular Research (2005)

To assess whether indobufen, a reversible inhibitor of platelet cyclooxygenase (Cox) activity, affects tissue factor (TF) in human monocytes and to investigate the relationship between Cox-derived products and TF.TF was evaluated in isolated adherent monocytes, both resting and lipopolysaccharide (LPS)-stimulated, in terms of procoagulant activity, protein, and mRNA levels. The expression of TF surface antigen was determined in LPS-stimulated whole blood monocytes by flow cytometry. The levels of the stable thromboxane A2 (TxA2) metabolite, TxB2, and of prostaglandin E2 (PGE2) were measured in monocyte supernatant by immunoenzymatic techniques. Cox-1 and Cox-2 protein level, tyrosine phosphorylation, and mitogen-activated protein kinase (MAP-kinase) activation were determined by Western blot analysis.Indobufen prevents TF expression and activity both in isolated and in whole blood monocytes. Reduction of TxA2 synthesis, coupled with a lack of effect on PGE2 levels and prevention of ERK1/2 phosphorylation are highlighted as the mechanisms through which indobufen negatively affects TF.Data show that indobufen down-regulates TF in monocytes. This novel activity, coupled with the antiplatelet effect of the drug, may add benefit for its use in the management of atherothrombosis.
Source of the aeroallergen of soybean dust: A low molecular mass glycopeptide from the soybean tela
Authors: Mark C. Swanson, James T.C. Li, Patricia E. Wentz-Murtha, Walter L. Trudeau, Enrique Fernandez-Caldas, Alice Greife, Maria A.J. Rodrigo, Ferran Morell, Charles E. Reed
Journal: Journal of Allergy and Clinical Immunology (1991)
Mechanisms of protection by the betaine-homocysteine methyltransferase/betaine system in HepG2 cells and primary mouse hepatocytes
Authors: Cheng Ji, Masao Shinohara, John Kuhlenkamp, Christine Chan, Neil Kaplowitz
Journal: Hepatology (2007)

Betaine-homocysteine methyltransferase (BHMT) regulates homocysteine levels in the liver. We previously reported that the alteration of BHMT is associated with alcoholic liver steatosis and injury. In this study, we tested whether BHMT protects hepatocytes from homocysteine-induced injury and lipid accumulation. Both BHMT transfectants of HepG2 cells and primary mouse hepatocytes with suppressed BHMT were generated. Comparisons were made between the cell models with respect to their response to homocysteine treatments. Homocysteine metabolism was impaired in HepG2 cells, and the expression of BHMT in HepG2 cells ameliorated the impairment and stabilized the levels of intracellular homocysteine after the addition of exogenous homocysteine. BHMT expression inhibited homocysteine-induced glucose-regulated protein 78 (GRP78) and C/EBP-homologous protein (CHOP) and homocysteine-induced cell death. A betaine treatment protected primary mouse hepatocytes from a homocysteine-induced increase in GRP78 and cell death but not a tunicamycin-induced increase. Homocysteine induced greater CHOP expression (2.7-fold) in BHMT small interfering RNA (siRNA)–transfected cells than in a control (1.9-fold). Homocysteine-induced cell death was increased by 40% in the siRNA-treated cells in comparison with the control. Apolipoprotein B (apoB) expression was higher and triglycerides and cholesterol were lower in HepG2 expressing BHMT. In primary mouse hepatocytes, homocysteine induced the accumulation of triglycerides and cholesterol, which was reduced in the presence of betaine. Betaine partially reduced homocysteine-induced sterol regulatory element binding protein 1 expression in HepG2 cells and increased S-adenosylmethionine in primary mouse hepatocytes. Conclusion: The BHMT/betaine system directly protects hepatocytes from homocysteine-induced injury but not tunicamycin-induced injury, including an endoplasmic reticulum stress response, lipid accumulation, and cell death. This system also exhibits a more generalized effect on liver lipids by inducing ApoB expression and increasing S-adenosylmethionine/S-adenosylhomocysteine.
Medical Department, United States Army, Internal Medicine in World War II. Vol. 1: Activities of Medical Consultants
Authors: John H. Talbott
Journal: JAMA (1962)

The first of 3 volumes in the series on Internal Medicine in the U.S. Army history of the medical department concerns the activities of the medical consultants. Under the direction of Brig. Gen. Hugh J. Morgan, Chief Consultant in Medicine to the Surgeon General, the available physicians of first-class talent in this specialty who had not already been assigned to general hospitals, station hospitals, or other armed forces activities, were recruited as consultants. In this category one notes, particularly: William S. Middleton, then of Madison; Benjamin M. Baker of Baltimore; Garfield G. Duncan of Philadelphia; Yale Kneeland, Jr., and Perrin Long of New York; and Walter Bauer, Dennette Adams, and Herrman L. Blumgart of Boston. Although I was never in the pyramid on the way up to a consultant assignment, I had occasion during the years 1942 to 1946 to confer with several consultants in the Zone of the Interior
Abstract 5520: Therapeutic vaccination with epitope-enhanced and wild-type TARP peptides in stage D0 prostate cancer
Authors: Lauren V. Wood, William Dahut, James L. Gulley, Ravi A. Madan, Philip Arlen, Howard L. Parnes, Brenda D. Roberson, Seth M. Steinberg, Masaki Terabe, Jay A. Berzofsky
Journal: Cancer Research (2011)

Abstract Background: T-cell receptor alternate reading frame protein (TARP) is immunogenic, is expressed in ∼95% of prostate cancer specimens and hence is a good candidate for therapeutic vaccination. The immunogenicity of HLA-A*0201 binding TARP peptides can be improved through epitope-enhancement achieved by amino acid substitutions that result in increased HLA binding affinity and immunogenicity at least in mice. We conducted a pilot study to determine the safety and immunogenicity of TARP peptide vaccination and its impact on PSA doubling time (PSADT) in men with Stage D0 prostate cancer. Methods: HLA-A*0201 positive men were randomized to receive epitope-enhanced (29-37-9V) or wild type (27-35) TARP peptides administered as a peptide emulsion with Montanide ISA 51VG plus GM-CSF (Arm A) or as an autologous peptide-pulsed dendritic cell vaccine (Arm B). Vaccines are administered q 3 weeks for a total of 5 vaccines with an optional 6th dose of vaccine at 36 weeks based on immune response or PSADT criteria and a booster dose of vaccine for all patients at 48 weeks. Results: 26 patients have enrolled in the study to date (n = 14 Arm A, n = 12 Arm B) with a mean on study duration of 7.5 months. Mean baseline cohort characteristics: age 63 yrs, PSA 4.43, PSADT 7.3 months and Gleason Score 6.7 with 19 of 26 s/p radical prostatectomy. TARP vaccination was safe and well tolerated with adverse events limited to local injection site reactions &amp;lt; Grade 2. Nine of 18 patients (50%) reaching 24 weeks on study were documented to have an increase in their PSADT compared to baseline. Mean Percent Increase/Prolongation in PSADT: Surprisingly TARP-specific IFN-γ ELISPOT responses have been detected ex vivo in only 3 of 14 (21%) patients examined to date. Conclusion: Vaccination with wild type and epitope-enhanced TARP peptides results in prolongation of PSADT in a substantial fraction of patients. The immunologic correlates responsible for PSADT lengthening are poorly understood and require additional study. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 5520. doi:10.1158/1538-7445.AM2011-5520
Design and use of conditional MHC class I ligands
Authors: Mireille Toebes, Miriam Coccoris, Adriaan Bins, Boris Rodenko, Raquel Gomez, Nella J Nieuwkoop, Willeke van de Kasteele, Guus F Rimmelzwaan, John B A G Haanen, Huib Ovaa, Ton N M Schumacher
Journal: Nature Medicine (2006)
Long-term treatment with Low-Dose, but not High-Dose, guanethidine improves ventricular function and survival of rats with heart failure after myocardial infarction
Authors: Akihiko Igawa, Takashi Nozawa, Nozomu Fujii, Bun-ichi Kato, Hidetsugu Asanoi, Hiroshi Inoue
Journal: Journal of the American College of Cardiology (2003)
Federated Council of Internal Medicine's Resource Guide for Residency Education
Authors: Jack Ende
Journal: Annals of Internal Medicine (1998)

Letters1 May 1998Federated Council of Internal Medicine's Resource Guide for Residency EducationJack Ende, MD, Mark A. Kelley, MD, and Harold C. Sox, MDJack Ende, MDPresbyterian Medical Center; Philadelphia, PA 19104Hospital of the University of Pennsylvania; Philadelphia, PA 19104 (Kelley).Dartmouth Medical School; Hanover, NH 03756Search for more papers by this author, Mark A. Kelley, MDPresbyterian Medical Center; Philadelphia, PA 19104Hospital of the University of Pennsylvania; Philadelphia, PA 19104 (Kelley).Dartmouth Medical School; Hanover, NH 03756Search for more papers by this author, and Harold C. Sox, MDPresbyterian Medical Center; Philadelphia, PA 19104Hospital of the University of Pennsylvania; Philadelphia, PA 19104 (Kelley).Dartmouth Medical School; Hanover, NH 03756Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-128-9-199805010-00042 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail IN RESPONSE:On behalf of the Federated Council of Internal Medicine's Task Force on Curriculum, we thank Dr. Tachauer for his favorable comments on our recently published report. It has been heartening to see how he and other program directors have viewed this work: not as internal medicine's complete and final curriculum but rather as a base of essential clinical and integrative competencies to which additional curricula can be added. As Dr. Tachauer notes, the resource guide does not include competencies in alternative and complementary medicine, nor does it provide a list of suggested literary and artistic works that will ... Author, Article, and Disclosure InformationAuthors: Jack Ende, MD; Mark A. Kelley, MD; Harold C. Sox, MDAffiliations: Presbyterian Medical Center; Philadelphia, PA 19104Hospital of the University of Pennsylvania; Philadelphia, PA 19104 (Kelley).Dartmouth Medical School; Hanover, NH 03756 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 May 1998Volume 128, Issue 9Page: 787KeywordsComplementary and alternative medicineResidency ePublished: 15 August 2000 Issue Published: 1 May 1998 Copyright & PermissionsCopyright © 1998 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Abstract 5097: Co-targeting of convergent, switchable nucleotide biosynthetic pathways induces synthetic lethality in leukemia
Authors: Caius G. Radu, David A. Nathanson, Johannes Czernin
Journal: Cancer Research (2014)

Abstract Pharmacological targeting of metabolic processes in cancer must overcome redundancy in biosynthetic pathways. Deoxycytidine triphosphate (dCTP) can be produced by the de novo pathway (DNP) via ribonucleotide reductase, and/or by the nucleoside salvage pathway (NSP) via deoxycytidine kinase (dCK). The NSP's role in supporting tumor DNA replication is unknown. Here we show that survival of acute lymphoblastic leukemia cells upon inhibition of DNP-dependent dCTP production requires a functional NSP. Thus, DNP inhibition triggers a compensatory switch to NSP-mediated dCTP production. This metabolic switch can be imaged by positron emission tomography, thereby providing a non-invasive method for monitoring pharmacological targeting of the DNP. Blocking both DNP dCTP production using thymidine and the switch to NSP using a new dCK inhibitor induces replication stress overload and synthetic lethality in leukemia cells, without significant host toxicity. This co-targeting therapy may be broadly applicable against other malignancies characterized by high levels of replication stress. Citation Format: Caius G. Radu, David A. Nathanson, Johannes Czernin. Co-targeting of convergent, switchable nucleotide biosynthetic pathways induces synthetic lethality in leukemia. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 5097. doi:10.1158/1538-7445.AM2014-5097
SOME DIFFICULTIES IN GROUP PSYCHOTHERAPY WITH PSYCHOTICS
Authors: CHRISTOPHER T. STANDISH, JOSE GURRI, ELVIN V. SEMRAD, MAX DAY
Journal: American Journal of Psychiatry (1952)

1 The difficulty in making a clear working agreement is described. 2. It is suggested that this difficulty is related to the therapist's lack of experience and reluctance to take responsibility. 3. An adequate working agreement is outlined. 4. The difficulty in focusing on the interaction and the associated belief that the patient is helpless in his current regressed state are described. 5. It is suggested that these deprive both the therapist and the patients of constructive experiences. 6. It is further suggested that they may be defensive maneuvers on the part of the therapist. 7. Some other manifestations of defensive behavior in the therapist are mentioned. 8. The specific role of the therapist in overcoming resistances is outlined.
A novel prognostic model in myeloma based on co-segregating adverse FISH lesions and the ISS: analysis of patients treated in the MRC Myeloma IX trial
Authors: K D Boyd, F M Ross, L Chiecchio, G P Dagrada, Z J Konn, W J Tapper, B A Walker, C P Wardell, W M Gregory, A J Szubert, S E Bell, J A Child, G H Jackson, F E Davies, G J Morgan
Journal: Leukemia (2011)
Legumain Expression in Relation to Clinicopathologic and Biological Variables in Colorectal Cancer
Authors: Raghavendra Vasudeva Murthy, Gunnar Arbman, Jingfang Gao, G. David Roodman, Xiao-Feng Sun
Journal: Clinical Cancer Research (2005)

Abstract Purpose: Legumain, a novel asparaginyl endopeptidase, has been observed to be highly expressed in several types of tumors including colorectal cancer. However, there is no study examining the relationship of legumain expression to clinocopathologic and biological variables in colorectal cancers. Experimental Design: We investigated legumain expression in 164 primary colorectal cancers, 34 corresponding distant normal mucosa samples, 89 adjacent normal mucosa samples, and 33 lymph node metastases using immunohistochemistry. We also did Western blotting analysis on three additional colorectal cancers and three colonic cell lines. Results: Legumain expression was increased in primary tumors compared with distant or adjacent normal mucosa (P &amp;lt; 0.05), but there was no significant change between primary tumors and metastases (P &amp;gt; 0.05). Legumain expression was positively related to poorer differentiation/mucinous carcinoma (P = 0.04), higher degree of necrosis (P = 0.03) and apoptosis (P &amp;lt; 0.0001), positive proliferating cell nuclear antigen (P &amp;lt; 0.0001) and p53 expression (P = 0.049), and had a positive tendency towards stromelysin 3 (P = 0.058) and PINCH positivity (P = 0.05). The patients with tumors that showed both weak and lower percentage of the legumain expression, either in tumor (P = 0.01) or in stroma (P = 0.04), had a better prognosis. Conclusions: The legumain expression may be involved in colorectal cancer development and have a prognostic value in the patients.
Drugs and the blood-testis barrier
Authors: B. P. Setchell, S. J. Main
Journal: Environmental Health Perspectives (1978)

The functional and morphological evidence for the blood-testis barrier is discussed, together with evidence for the various processes (simple diffusion and facilitated diffusion) by which various substances enter the seminiferous tubule. Data are presented to show that methylmethane-sulfonate (MMS) and dimethylnitrosamine (DMNA) both enter the seminiferous tubules rapidly, although from the published rates of methylation of testicular DNA, by these two compounds, it might be expected that the entry of DMNA would be slower than that of MMS. It appears, however, that DMNA in blood is gradually converted to some nonpermeant compound. The possibility, as yet unsubstantiated, is discussed that a nontoxic permeant precursor may be converted into a nonpermeant toxic substance inside the tubules, thereby effectively concentrating the toxic compound inside the tubules.
Polycystic Liver Disease
Authors: Charles J. Sanner
Journal: JAMA (1976)

POLYCYSTIC liver disease is a relatively rare condition with a reported autopsy incidence varying from 1/687 autopsies to 8/11, 245 autopsies.<sup>1-3</sup>Ante-mortem diagnosis is usually made at surgery.<sup>4,5</sup>It is the purpose of this report to discuss the noninvasive approach to the diagnosis of polycystic liver disease and to emphasize the role of abdominal sonography in evaluating selected cases of unexplained hepatomegaly. <h3>Report of a Case</h3> A 53-year-old woman was admitted to a hospital for a whiplash injury in 1971 and was told that she had an enlarged liver. Liver function tests were normal. Liver biopsy was done and reportedly showed cirrhosis. On Dec 3, 1974, the patient was again admitted to another hospital with an acute onset of right upper quadrant pain and with an enlarging mass in that area. Physical examination showed a large, tender liver with an irregular margin. Laboratory studies disclosed normal values for complete blood
Abstract P5-07-08: Restoration of APC decreases tumorigenic potential in breast cancer cells
Authors: JM Cole, JR Prosperi
Journal: Cancer Research (2013)

Abstract Mutations of the Adenomatous Polyposis Coli (APC) tumor suppressor gene have been reported in 5-70% of human breast cancers. APC is most well known for its role as a negative regulator of the Wnt/b-catenin pathway, where APC sequesters β-catenin and targets it for degradation via the proteasome. The breast cancer cell line, DU4475, has a single point mutation in the mutation cluster region of APC, coding for an early stop and subsequent truncated protein, lacking the β-catenin binding domain. Preliminary data using a TOPFlash reporter assay suggested that Wnt/β-catenin pathway was active, which was validated with immunofluorescence (IF) showing nuclear localization of β-catenin. Our overall hypothesis is that restoration of APC will decrease tumorigenic potential in DU4475 breast cancer cells. To test our hypothesis, we have generated DU4475 cells stably expressing GFP (control) (DU4475-GFP), a GFP-tagged internal fragment of APC that includes the β-catenin binding domain (DU4475-APCmid), and a GFP-tagged C-terminal fragment of APC that includes the microtubule binding domain of APC (DU4475-APCC-ter). After selection using G418, the GFP positive cells were sorted using a cell sorter. Results from TOPFlash reporter assay and IF demonstrated a modest decrease in Wnt/β-catenin activity in DU4475-APCmid cells. In addition, we observed decreased proliferation as measured in a growth assay in DU4475-APCmid cells compared to the control cells. We also observed a 17% increase in cleaved caspase-3 and only a minimal decrease in cell proliferation as measured by phospho-Histone H3 using IF in 3D cultures upon APCmid re-introduction. We also observed decreases in Cyclin D1, Cyclin B1, Early Growth Response 1, and HIF1α in DU4475-APCmid using real time PCR. These changes suggest that the re-introduction of the central domain of the APC tumor suppressor results in alterations in cell growth and gene expression changes indicative of an increased tumorigenic phenotype in vitro. Ongoing studies in the laboratory are dissecting the signaling pathways downstream of APC restoration to identify therapeutic targets that may be used to restore the functional alterations of mutant APC. These studies have generated a system to be utilized for in vivo tumor and metastasis formation under the control of APC mutation in a human cell culture model. Citation Information: Cancer Res 2013;73(24 Suppl): Abstract nr P5-07-08.