tbuckley/cabot-search huggingface dataset:
Oxidation of short and medium chain C2-C8 fatty acids in Sprague-Dawley rat colonocytes.
Authors: J R Jorgensen, M R Clausen, P B Mortensen
Journal: Gut (1997)

BACKGROUND: The predominant colonic short chain fatty acids, acetate, propionate, and butyrate, are oxidised into CO2 in colonocytes from rat and humans in the preferred order of butyrate (C4) &gt; propionate (C3) &gt; acetate (C2)- hence butyrate is considered to be the principal oxidative substrate for colonocytes. AIMS: To compare colonocyte oxidation of valerate (C5), hexanoate (C6), and octanoate (C8) with that of butyrate. METHODS: Isolated rat colonocytes were incubated in the presence of a concentration range of 1-14C labelled C2-C8 fatty acids. Oxidation rates were obtained by quantifying the production of 14CO2, and Vmax (maximum velocity) and K(m) (Michaelis-Menten constant) were calculated by computer fitting of the data to a Michaelis-Menten plot. RESULTS: The K(m) value of acetate (0.56 (SEM 0.02) mmol/l) was about fourfold higher than the K(m) of butyrate (0.13 (0.01) mmol/l), whereas the K(m) values of valerate (0.19 (0.01) mmol/l), hexanoate (0.19 (0.01) mmol/l), and octanoate (0.16 (0.01) mmol/l) were of the same order of magnitude as the K(m) of butyrate. Acetate did not influence butyrate oxidation, whereas butyrate strongly inhibited the oxidation of acetate. By contrast, valerate, hexanoate, and octanoate inhibited colonocyte oxidation of butyrate equally or more than the reverse inhibitory effect of butyrate on valerate, hexanoate, and octanoate oxidation. The maximum rates of ATP production were in the order of valerate &gt; octanoate = hexanoate &gt; butyrate &gt; acetate (28.47 (0.70), 21.78 (0.75), 21.33 (0.78), 16.12 (0.49), 9.09 (0.34) (mumol/min/g) respectively). CONCLUSIONS: Valerate, hexanoate, and octanoate seem to be excellent substrates for colonocyte oxidation, similar to butyrate. These results may influence the choice of fatty acid composition in enemas used for treatment of patients in whom deficient colonocyte oxidation is suspected-for example, patients with ulcerative colitis and diversion colitis.
John Earl Evans
Authors: D. Whittingham
Journal: BMJ (2010)

Protein kinase Cϵ (PKCϵ) plays a pivotal role in cardioprotection during cardiac ischemia and reperfusion injury. Recent studies demonstrated that prenatal cocaine exposure caused a decrease in PKCϵ expression and increased heart susceptibility to ischemic injury in adult offspring, suggesting an in utero programming of PKCϵ gene expression pattern in the heart. The present investigation aimed to elucidate whether an epigenetic mechanism, DNA methylation, accounts for cocaine-mediated repression of the PKCϵ gene in the heart. Pregnant rats were administered either saline or cocaine intraperitoneally (15 mg/kg) twice daily from days 15 to 20 of gestational age, and term fetal hearts were studied. Cocaine treatment significantly decreased PKCϵ mRNA and protein levels in the heart. CpG dinucleotides found in cAMP response element-binding protein (CREB), CREB/c-Jun1, and CREB/c-Jun2 binding sites at the proximal promoter region of the PKCϵ gene were densely methylated and were not affected by cocaine. In contrast, methylation of CpGs in the activator protein 1 (AP-1) binding sites was low but was significantly increased by cocaine. Reporter gene assays showed that the AP-1 binding site played a strong stimulatory role of PKCϵ gene transcription. Methylation of the AP-1 binding sites significantly decreased AP-1 binding to the PKCϵ promoter. Supershift analyses implicated c-Jun homodimers binding to the AP-1 binding sites. Cocaine did not affect nuclear c-Jun levels or the binding of c-Jun to the unmethylated AP-1 binding sites. The results indicate a role for DNA methylation in cocaine-mediated PKCϵ gene repression in the developing heart and suggest an epigenetic mechanism affecting this gene linked with vulnerability of ischemic injury in the heart of adult offspring.
Long-term Outcomes of Patients With Wilson Disease in a Large Austrian Cohort
Authors: Sandra Beinhardt, Waltraud Leiss, Albert Friedrich Stättermayer, Ivo Graziadei, Heinz Zoller, Rudolf Stauber, Andreas Maieron, Christian Datz, Petra Steindl-Munda, Harald Hofer, Wolfgang Vogel, Michael Trauner, Peter Ferenci
Journal: Clinical Gastroenterology and Hepatology (2013)
Quantitation of Precordial Movement
Authors: GEORGE C. SUTTON, ERNEST CRAIGE, JAMES E. GRIZZLE
Journal: Circulation (1967)

Precordial displacement records of 39 patients with mitral regurgitation have been analyzed using a new method of quantitation. Three groups of patients were studied, and the data from each group have been compared in a number of different ways to those obtained from a control group. The optimal method of discrimination is a graphic representation involving the two variables of the height of the outward movement in systole and the height of the rapid-filling wave. This method allows discrimination between normal persons and patients with mitral regurgitation in a high proportion of cases. It is postulated that the increase of systolic outward movement in patients with mitral regurgitation is related to an increase in stroke volume of the left ventricle, and the increase in the height or the slope of the rapid-filling wave represents increase in flow and rate of flow into the ventricle in early diastole. The importance of consideration of the functional status of the ventricle in the assessment of precordial movement is stressed.
Multitarget inhibition of drug-resistant multiple myeloma cell lines by dimethyl-celecoxib (DMC), a non–COX-2 inhibitory analog of celecoxib
Authors: Adel Kardosh, Nathaniel Soriano, Yen-Ting Liu, Jasim Uddin, Nicos A. Petasis, Florence M. Hofman, Thomas C. Chen, Axel H. Schönthal
Journal: Blood (2005)
Girl is healthy after having donor heart removed
Authors: D. M Henderson
Journal: BMJ (2009)

A 16 year old girl is fit and well three and a half years after the removal of a donor heart that had been transplanted alongside her own. The donor heart had been in place for 10 and a half years, allowing her own heart to recover from advanced cardiomyopathy.

Hannah Clark presented with signs of severe heart failure, secondary to idiopathic dilated cardiomyopathy, at the age of 8 months, a paper in the Lancet has reported (doi:10.1016/S0140-6736(09)61201-0). When she was 2 years old she underwent a heterotopic cardiac transplantation, in which the donor heart was placed in the right pleural cavity and attached to Hannah’s own heart, and …
Iris atrophy and posterior synechiae as a complication of eyebrow laser epilation
Authors: Ioannis Halkiadakis, Sotiris Skouriotis, Christina Stefanaki, Eleni Patsea, Dimitrios Papakonstatndinou, Apostolos Amariotakis, Gerasimos T. Georgopoulos
Journal: Journal of the American Academy of Dermatology (2007)
Where Was the Artificial Liver Machine?
Authors: Martel J. Dailey
Journal: JAMA (1975)

To the Editor.—  Recently, a 5-year-old child was admitted to my service at Martin General Hospital, Williamston, NC, because of advanced liver failure. His body was cadaverous and his features bird-like. Death appeared imminent. Acting out of frustration and futility  left the order: Connect the patient immediately to the artificial liver machine! Before  could leave the hospital, the nurse in charge of the floor came running after me and inquired, Where is the artificial liver   replied, I don't know where it is. A few hours later the patient died.   often wonder: Where was the artificial liver machine? Was it sacrificed for Vietnam? Was it on a space ship headed toward Mars? Did the Russians get it via detente?  concluded: The artificial liver machine's nonexistence could be explained by a thousand different causes.  Liver disease incidence in America is bad and it is getting worse.
Pain control and the World Health Organization analgesic ladder
Authors: M. M. Reidenberg
Journal: JAMA (1996)

To the Editor.  —Drs Jadad and Browman1review literature to evaluate the effectiveness of the World Health Organization (WHO) analgesic ladder approach to treating cancer  They state, Unless there are controlled studies, it would be difficult to know whether the WHO ladder has really  the management of cancer pain. They ignore the real worldwide issue of improved compared to what?  This WHO program had as its major goal making opioid analgesics available to everyone in the world suffering from pain from advanced cancer. The ladder approach was to facilitate the acceptance of opioid use in these patients since historically opioid use was condemned by medical authorities if it [could] possibly be avoided,2and surveys have found inadequate use of opioids to treat cancer pain (references cited in reference 1). One should assess the success of the ladder concept by learning what fraction of dying cancer patients
Platelet interaction with modified articular cartilage. Its possible relevance to joint repair.
Authors: D Zucker-Franklin, L Drosenberg
Journal: Journal of Clinical Investigation (1977)

During studies concerned with the platelet-collagen interaction, it was observed that platelets did not adhere to bovine or human articular cartilage and that cartilage did not induce platelet aggregation in vivo or in vitro. To study the mechanism responsible for this observation, the role of proteoglycans was examined. Purified cartilage collagen proved to be fully active as a platelet aggregant. Addition of small amounts of proteoglycan subunit (PGS) blocked platelet aggregation, whereas chondroitin sulfate, a major glycosaminoglycan component of cartilage matrix, impaired platelet aggregation only at concentrations which resulted in a marked increase in viscosity. Moreover, PGS abolished aggregation of platelets by polylysine but did not prevent aggregation by ADP, suggesting that PGS may block strategically placed lysine sites on the collagen molecule. Treatment of fresh articular cartilage with proteolytic enzymes rendered the tissue active as a platelet aggregant. In vivo experiments demonstrated that surgical scarification of rabbit articular cartilage does not result in adhesion of autologous platelets. Treatment of rabbit knee joints with intraarticular trypsin 1 wk before the injection of blood resulted in adhesion and aggregation of platelets on the surface of the lesions. Since there is evidence from other studies that some degree of cartilage healing may take place after initiation of an inflammatory response, it is postulated that induction of platelet-cartilage interaction may eventuate in cartilage repair.
Abstract 3112: Host MMP-2 impacts tumor survival in the metastatic bone microenvironment through a TGFβ dependent mechanism
Authors: Sophie Thiolloy, James Edwards, Barbara Fingleton, Daniel Rifkin, Herbert S. Schwartz, Gregory Mundy, Lynn M. Matrisian, Conor C. Lynch
Journal: Cancer Research (2011)

Abstract Breast to bone metastases frequently induce a “vicious cycle” in which osteoclast mediated bone resorption and proteolysis results in the release of bone matrix sequestered factors that drive tumor growth. While osteoclasts express numerous proteinases, analysis of human breast to bone metastases unexpectedly revealed that bone forming osteoblasts were consistently positive for the proteinase, MMP-2. In immunocompetent murine models of the lytic tumor-bone microenvironment, we identified that, independent of osteoclast function, osteoblast derived MMP-2 promoted tumor survival by regulating the bioavailability of TGFβ, a factor critical for cell-cell communication in the bone. Collectively, these studies identify a novel interplay between the osteoblast and tumor compartments that is key for tumor survival in the bone microenvironment. 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 3112. doi:10.1158/1538-7445.AM2011-3112
Researchers Praise Drug-Eluting Stents but Appropriate Use Is Still Debated
Authors: Mike Mitka
Journal: JAMA (2011)

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
Pentamidine Isethionate in the Treatment of Pneumocystis carinii Pneumonia
Authors: KARL A. WESTERN
Journal: Annals of Internal Medicine (1970)

In an 18-month period 164 patients with suspected or proved interstitial pneumonia due to Pneumocystis carinii were treated with pentamidine isethionate. Side effects were noted in 69 patients. Local pain, abscess formation, and ulceration were clearly attributable to pentamidine administration. Azotemia, hypoglycemia, and changes in liver function occurred frequently during therapy. Pentamidine may have been responsible for two deaths. Seventy-five of the patients who received pentamidine had documented P. carinii pneumonia; 36 of the 75 patients recovered. All 75 had a serious underlying disease, and 60 were on immunosuppressive therapy.
De novo CCND2 mutations leading to stabilization of cyclin D2 cause megalencephaly-polymicrogyria-polydactyly-hydrocephalus syndrome
Authors: Ghayda M Mirzaa, David A Parry, Andrew E Fry, Kristin A Giamanco, Jeremy Schwartzentruber, Megan Vanstone, Clare V Logan, Nicola Roberts, Colin A Johnson, Shawn Singh, Stanislav S Kholmanskikh, Carissa Adams, Rebecca D Hodge, Robert F Hevner, David T Bonthron, Kees P J Braun, Laurence Faivre, Jean-Baptiste Rivière, Judith St-Onge, Karen W Gripp, Grazia M S Mancini, Ki Pang, Elizabeth Sweeney, Hilde van Esch, Nienke Verbeek, Dagmar Wieczorek, Michelle Steinraths, Jacek Majewski, Kym M Boycott, Daniela T Pilz, M Elizabeth Ross, William B Dobyns, Eamonn G Sheridan
Journal: Nature Genetics (2014)
Bone Scintigraphy in Painful Os Peroneum Syndrome
Authors: Johanne B. Jeppesen, Frank K. Jensen, Bettina Falborg, Jan L. Madsen
Journal: Clinical Nuclear Medicine (2011)

Lateral foot pain may be caused by various entities including the painful os peroneum syndrome. A case of a 68-year-old man is presented, who experienced a trauma with distortion of the right foot. Nine months later, he still had pain in the lateral part of the right foot. Bone scintigraphy showed uptake in the area where an os peroneum was located and thus confirmed the clinical assumption of painful os peroneum syndrome. Familiarity with the clinical and imaging findings can prevent undiagnosed lateral foot pain.
The 2010 Health Care Reform Act: A Potential Opportunity to Advance Cancer Research by Taking Cancer Personally
Authors: William S. Dalton, Daniel M. Sullivan, Timothy J. Yeatman, David A. Fenstermacher
Journal: Clinical Cancer Research (2010)

Abstract The Patient Protection and Affordable Care Act of 2010 will have a profound influence on health care in the United States, including how we conduct cancer research and cancer care delivery. For this reason, oncologists and researchers must be intimately involved in the implementation and interpretation of this important legislation. A major goal of the Act is to improve access to affordable, quality health care. An important element in achieving this goal will be to learn from patients' experiences and build the foundation for evidence-based personalized medicine. This will require a partnership among researchers, clinicians, policy makers and regulators, and patients to design an integrated information network system that will be the basis for providing the right treatment for the right patient in the right place at the right time. In this review, we will discuss the salient points of the Act that specifically affect cancer research and care, as well as highlight opportunities for oncologists and researchers to play a primary role in developing a health care system that includes personalized medicine approaches that will in turn enhance the likelihood of achieving the goals and objectives of the health care reform act. Clin Cancer Res; 16(24); 5987–96. ©2010 AACR.
Abstract A22: Somatic mutations in DROSHA and DICER1 impair microRNA biogenesis in Wilms tumors
Authors: Dinesh Rakheja, Kenneth S. Chen, Yangjian Liu, Abhay A. Shukla, Sara Hildebrand, Vanessa Schmid, Xiaoyong Sun, Xin Feng, Tsung-Cheng Chang, Shama Khokhar, Nitin J. Karandikar, James S. Malter, Joshua T. Mendell, James F. Amatruda
Journal: Cancer Research (2014)

Abstract Wilms tumor is the most common pediatric kidney cancer and the fourth most common childhood cancer overall. It is treated with a combination of surgery, chemotherapy, and radiation, and while most children are cured, survival remains poor in those with advanced-stage disease. Known driver mutations (in WT1, WTX, and CTNNB1) account for only one-third of Wilms tumor cases. To better define the genomic landscape of Wilms tumor, we performed whole-exome sequencing of 44 Wilms tumors. We also sequenced matched germline DNA by whole-exome sequencing (15 cases) or targeted Sanger sequencing (29 cases) to identify somatic mutations. Through this approach, we identified recurrent somatic mutations in MYCN, DROSHA, and DICER1, which were mutually exclusive with known Wilms tumor mutations in WT1 and CTNNB1. The ribonucleases DROSHA and DICER1 perform two key steps in the biogenesis of microRNAs (miRNAs), which are ∼22-nt non-coding RNAs that regulate the stability and translation of target mRNAs. DROSHA and DICER1 mutations occurred at or near conserved metal-binding residues in their ribonuclease (RNase) IIIB domains. In vitro processing assays modeling these mutations showed that they partially or completely disrupted the ribonuclease activity of DROSHA and DICER1. In addition, next-generation sequencing of small RNAs in these tumors revealed that the DICER1 mutations preferentially impaired processing of miRNAs derived from the 5′ arm of pre-miRNA hairpins, including the let-7 tumor suppressor miRNA family. Processing of 5′-derived miRNAs is specifically dependent on DICER1 RNase IIIB activity. Although DROSHA-mutant tumors did not exhibit skewed expression of 5′ vs. 3′-derived miRNAs, expression of let-7 and other putative tumor suppressor miRNAs was reduced in these tumors as well. While germline and somatic mutations in DICER1 have been reported in some cancers, this is the first report of recurrent DROSHA mutations in any human tumor type. Moreover, these results suggest that impairment of miRNA processing by somatic mutation of DROSHA and DICER1 defines a novel subclass of Wilms tumor. Citation Format: Dinesh Rakheja, Kenneth S. Chen, Yangjian Liu, Abhay A. Shukla, Sara Hildebrand, Vanessa Schmid, Xiaoyong Sun, Xin Feng, Tsung-Cheng Chang, Shama Khokhar, Nitin J. Karandikar, James S. Malter, Joshua T. Mendell, James F. Amatruda. Somatic mutations in DROSHA and DICER1 impair microRNA biogenesis in Wilms tumors. [abstract]. In: Proceedings of the AACR Special Conference on Pediatric Cancer at the Crossroads: Translating Discovery into Improved Outcomes; Nov 3-6, 2013; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2013;74(20 Suppl):Abstract nr A22.
The SDF-1/CXCR4 Axis Is a Novel Driver of Vascular Development of the Glomerulus
Authors: Jürgen Floege, Bart Smeets, Marcus J. Moeller
Journal: Journal of the American Society of Nephrology (2009)

Spatial and temporal control of developing glomerular capillaries is complex and requires coordinated cross-talk between various cell types. Recent advances in our understanding of the processes that regulate glomerular morphogenesis reveal some mediators are essential for the emerging tuft, particularly vascular endothelial growth factor (VEGF) and PDGF.1–4

In search of additional crucial mediators, Takabatake et al. 5 examine the role of CXC chemokine ligand 12 (CXCL12; stromal cell–derived factor 1 [SDF-1]) and its receptor, CXCR4, in this issue of JASN . Traditional SDF-1 signaling is involved primarily in the homing of hematopoietic stem cells to their niche within the bone marrow and in hematopoietic stem cell quiescence. A role for SDF-1/CXCR4 is also described for chemotaxis of T lymphocytes and monocytes, B cell development, cardiac and cerebellar development, and cancer stem cell migration.6 This study was triggered by a previous report, which analyzed mice deficient in SDF-1 or CXCR4 and the requirement for this ligand-receptor system in vascularization of the gastrointestinal tract.7 In their beautiful study, Takabatake et al. 5 demonstrate the SDF-1/CXCR4 axis is a novel and essential signaling system for blood vessel formation in the kidney, particularly within the glomerulus.

The …
Thrombocytopenic conditions—autoimmunity and hypercoagulability: Commonalities and differences in ITP, TTP, HIT, and APS
Authors: Martine Szyper Kravitz, Yehuda Shoenfeld
Journal: American Journal of Hematology (2005)

Abstract Immune thrombocytopenia purpura (ITP), thrombotic thrombocytopenia purpura (TTP), heparin‐induced thrombocytopenia (HIT), and antiphospholipid syndrome (APS) are clinical conditions associated with significant morbidity and mortality. These well‐defined clinical syndromes have in common several properties: (1) their pathogenesis is immune mediated, specifically by autoantibodies; (2) thrombocytopenia is a hallmark in these four conditions; (3) except for the case of ITP, platelet and endothelial cell activation occurs in TTP, HIT, and APS, resulting in a prothrombotic state and an increased risk of thrombosis. Although these four immune‐mediated syndromes are well‐defined diseases, several case reports and studies have documented the association of two diseases in the same patient, illustrating the concept of the kaleidoscope of autoimmunity. Am. J. Hematol. 80:232–242, 2005. © 2005 Wiley‐Liss, Inc.
Book Review Medical Management of Vulnerable and Underserved Patients: Principles, Practice, and Populations Edited by Talmadge E. King, Jr., Margaret B. Wheeler, and Andrew B. Bindman, with four others. 454 pp., illustrated. New York, McGraw-Hill, 2007. $41.95. 978-0-07-144331-9
Authors: Helen Burstin
Journal: New England Journal of Medicine (2007)
Listen: The Patient — Once Again
Authors: F. J. Ingelfinger
Journal: New England Journal of Medicine (1976)

The March 24, 1966 issue of the Journal contained a paper entitled "Listen: The patient." The author was Eric Hodgins, a well known editor (managing editor of Fortune, vice-president of Time, Inc.) and writer ("Mr. Blandings Builds His Dream House"), who asked — almost plaintively — that the "medical and other health professions...share with the patient... More, much more, of what they so acutely observe."1 In the current issue, somewhat over a decade later, the Journal once again prints what a well known editor and writer has to say about his illness and medical care. Consistent with the temper . . .