tbuckley/cabot-search huggingface dataset:
<i>Winter Landscape</i>
Authors: Jeanette M. Smith
Journal: JAMA (2014)

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
Serum Cardiac Troponin T and Creatine Kinase–MB Elevations in Murine Autoimmune Myocarditis
Authors: Kurt Bachmaier, Johannes Mair, Felix Offner, Christian Pummerer, Nikolaus Neu
Journal: Circulation (1995)

Background We used a murine model of autoimmune myocarditis to investigate systematically whether serum markers of myocardial cell injury, that is, cardiac troponin T (TnT) and the MB isoenzyme of creatine kinase (CK-MB) are useful for the diagnosis of inflammatory heart disease. Methods and Results Fifty-two A.SW mice were immunized with cardiac myosin to induce myocarditis. The disease was evident on day 12 after the initial immunization in 14 of 22 immunized mice, on day 16 in 7 of 10 mice, on day 19 in 6 of 10 mice, and on day 23 in 5 of 10. The severity of myocarditis increased between days 12 and 16 and remained constant thereafter. TnT was elevated in a considerable number of mice with myocarditis, resulting in a diagnostic sensitivity (number of marker elevations per number of mice with myocarditis) of 0.43 on day 12, 0.71 on day 16, and 0.50 on day 19. CK-MB elevations were not seen on day 12 but resulted in a diagnostic sensitivity of 0.71 on day 16 and of 0.33 on day 19. No elevations of CK-MB or TnT were observed on day 23. All elevations were specific for the disease, as none of the mice lacking myocarditis showed increased markers. Conclusions In murine autoimmune myocarditis, TnT is a more sensitive marker for the disease than CK-MB. Elevations clearly indicate myocarditis, but negative test results do not exclude the presence of the disease. These data suggest that the determination of CK-MB and, in particular, of TnT, can be useful for the diagnostic evaluation of patients with suspected myocarditis.
Thromboxane and Stable Prostaglandin Endoperoxide Analogs Stimulate Water Permeability in the Toad Urinary Bladder
Authors: Ronald M. Burch, Perry V. Halushka
Journal: Journal of Clinical Investigation (1980)

The effects of thromboxane B2 and the stable prostaglandin endoperoxide analogs (15Z)-hydroxy - 9α - 11α - (epoxymethano)prosta - 5Z,13E - dienoic acid (U44069) and (15Z)-hydroxy -11α,9α-(epoxymethano) prosta-5Z,13E-dienoic acid (U46619) were tested on water flow across the toad urinary bladder. In the presence of indomethacin or meclofenamic acid, inhibitors of prostaglandin and thromboxane A2 synthesis, thromboxane B2 stimulated water flow in a dose-dependent manner. U44069 (1 μM) stimulated water flow from 3.6±0.8 to 12.4±1.2 mg/min per 10 cm2 hemibladder surface area, while U46619 (1 μM) stimulated water flow from 2.8±1.0 to 21.8±2.0 mg/min per 10 cm2. The prostaglandin endoperoxide/thromboxane A2 antagonist trans- 13-azaprostanoic acid, an inhibitor of vasopressin-stimulated water flow, inhibited thromboxane B2- and U46619-stimulated water flow in a dose-dependent manner. The inactive cis-13-azaprostanoic acid did not inhibit vasopressin-stimulated water flow in untreated hemibladders and had no effect on U46619-stimulated water flow in indomethacin or meclofenamic acid pretreated hemibladders. U46619 (1 μM) enhanced vasopressin-stimulated water flow in indomethacin pretreated hemibladders, producing a significant parallel shift (P < 0.001) in the dose-response relationship to submaximal concentrations of vasopressin (0.1-0.6 mU/ml), while not affecting water flow stimulated by supramaximal concentrations of vasopressin (10 mU/ml). trans-13-Azaprostanoic acid abolished the potentiating effects of U46619 on vasopressin-stimulated water flow. These results show that thromboxane A2-like compounds stimulate water flow in the toad urinary bladder.
Para-Aminosalicylic Acid (PAS) in Chronic Pulmonary Tuberculosis
Authors: Alfred S. Dooneief, Abraham Buchberg, M. Maxim Steinbach
Journal: New England Journal of Medicine (1950)

IT HAS been shown that para-aminosalicylic acid (PAS) has a definite bacteriostatic effect on human strains of Mycobacterium tuberculosis in vitro1 2 3 4 and in vivo.3 4 5 6 7 8 9 It is also known that its tuberculostatic potency is considerably less than that of streptomycin.5 , 6 However, the emergence of streptomycin-resistant tubercle bacilli after treatment with streptomycin constitutes an important restriction on its use in the therapy of pulmonary tuberculosis and necessitates careful timing and co-ordination of streptomycin treatment with the total therapeutic attack. Since retreatment with streptomycin for exacerbations and reactivations is often futile, it is frequently necessary to withhold this drug for use at the . . .
California Encephalitis Virus
Authors: DON J. YOUNG
Journal: Annals of Internal Medicine (1966)

Excerpt California encephalitis virus is an ungrouped neurotropic arthropod-borne virus first isolated in Kern County, Calif., in 1943. Only four cases in humans have been described in detail (1, 2). Recently there have been a number of brief reports of human cases in various parts of the world (3-5). In 1964 the first known epidemic of this virus took place in Indiana, involving 9 patients (6),* and in Ohio, involving 34 patients (7). It is the purpose of this paper to report three serologically confirmed cases of California encephalitis virus encephalitis from the Indiana epidemic and to review the literature. CASE
"SODIUM VERSUS POTASSIUM"
Authors: William D. Byrne
Journal: JAMA (1918)

<h3>To the Editor:</h3> —Your editorial in the issue of June 1 on "Sodium Versus Potassium" is both illuminating and suggestive, and illustrates the point that our boche friends have been working the American public in a manner that is shameful in this matter of the potassium salts. As you say, we are creatures of habit, and their clever propagandists have taken advantage of this to persuade us that the K salts are superior to those of the Na group, whereas, quite the contrary, the latter group is every bit as effective and less depressing. In order to obviate this fallacy I would suggest that you keep standing on your editorial page some such brief text as the following: American doctors should <h3>HELP WIN THE WAR</h3> by prescribing sodium salts for the States and let the Prussians prescribe potassium salts for Potsdam! Sodium is produced in America, is less depressing than
Controlled Clinical Trial of Mepiprazole in Irritable Bowel Syndrome
Authors: G. Dotevall, E. Groll
Journal: BMJ (1974)

The effect of a new tranquillizer, mepiprazole, in the treatment of the irritable bowel syndrome has been studied in a double-blind cross-over trial in 19 patients. After examination to exclude organic disease the patients were followed up over two treatment periods of four weeks each under either placebo or the active principle, each patient being his own control. The results indicated that the drug had a beneficial effect (P &lt; 0·05) provided that it was given for a period of at least three weeks.
Ho, Ho, Ho, and a Bottle o' Rum
Authors: G. G. Liddle
Journal: JAMA (1971)

To the Editor.—  Sir, I must thank you for your beautiful Christmas card. It is remarkably like the one I received from you Christmas 1967. On a surfaced paper which would not accept writing or printing, I was able to send it (Christmas 1968) to Charley Waterhouse of Baton Rouge, La. You don't know Charley—at least he denies acquaintance with you. He is a frugal man, yea thrifty. Christmas 1969, it did duty to an intermediate in Cleveland, who claims you as his. A jokester, or equally thrifty, I do not know.  I am happy to see it again. The edges are a little frayed, but the paper cutter solved that problem. It goes back to Charley, Christmas 1971, and I look forward to a third transit of the Christmas sun about Dec 22, 1973.  In Bloomington, Hawaii, we scored 38% passalong presents on the receiving side, but only disposed
The Clinical Recognition of Tinea Capitis From Trichophyton tonsurans
Authors: Andrew H. Rudolph
Journal: JAMA (1979)

A change in the preponderant etiologic agent of tinea capitis in the United States has been occurring during the last 20 to 30 years. Before the 1950s, the<i>Microsporum</i>sp,<i>M audouinii</i>and<i>M canis</i>, were the organisms most commonly isolated in patients with tinea capitis. In the 1950s,<i>Trichophyton tonsurans</i>was introduced into the southern and southwestern states<sup>1,2</sup>from Puerto Rico and Mexico, where epidemics of tinea capitis from this organism previously had occurred. In the early 1960s, the problem of scalp infections caused by<i>T tonsurans</i>also was reported in urban areas in the Midwest and East.<sup>3</sup>In the 1970s, as Prevost reports (p 1765),<i>T tonsurans</i>is now the preponderant organism causing tinea capitis in Charleston, SC, a change also reported in other locations.<sup>4,5</sup> The emergence of<i>T tonsurans</i>as the preponderant cause of tinea capitis is important, for scalp infections caused by this
Uranium Mining and Lung Cancer in Navajo Men
Authors: Jonathan M. Samet, Daniel M. Kutvirt, Richard J. Waxweiler, Charles R. Key
Journal: New England Journal of Medicine (1984)

We performed a population-based case-control study to examine the association between uranium mining and lung cancer in Navajo men, a predominantly nonsmoking population. The 32 cases included all those occurring among Navajo men between 1969 and 1982, as ascertained by the New Mexico Tumor Registry. For each case in a Navajo man, two controls with nonrespiratory cancer were selected. Of the 32 Navajo patients, 72 per cent had been employed as uranium miners, whereas no controls had documented experience in this industry. The lower 95 per cent confidence limit for the relative risk of lung cancer associated with uranium mining was 14.4. Information on cigarette smoking was available for 21 of the 23 affected uranium miners; eight were nonsmokers and median consumption by the remainder was one to three cigarettes daily. These results demonstrate that in a rural nonsmoking population most of the lung cancer may be attributable to one hazardous occupation.
BSC1 inhibition complements effects of vasopressin V2 receptor antagonist on hyponatremia in SIADH rats
Authors: Itsuro Kazama, Ryo Hatano, Mari Michimata, Katsuya Suzuki, Tomohiro Arata, Michiko Suzuki, Noriyuki Miyama, Akira Sato, Susumu Satomi, Yutaka Ejima, Sei Sasaki, Mitsunobu Matsubara
Journal: Kidney International (2005)
Lenalidomide alone or in combination with dexamethasone is highly effective in patients with relapsed multiple myeloma following allogeneic stem cell transplantation and increases the frequency of CD4+Foxp3+ T cells
Authors: M C Minnema, M S van der Veer, T Aarts, M Emmelot, T Mutis, H M Lokhorst
Journal: Leukemia (2008)
Kenneth Arthur Rowley
Authors: P R Duncan
Journal: BMJ (2004)

Former consultant radiologist Victoria Hospital, Blackpool (b 1923; q Manchester 1946; FFR, DMRD), died from lung cancer on 18 January 2004.​2004.




Figure 1




After qualifying he worked at Salford Royal before joining the Royal Army Medical Corps. A six week course in radiology was followed by posting to the Gold Coast, where he found himself command radiologist, west Africa. On return home he trained in radiology at Manchester Royal Infirmary and St Mary's Hospital. In 1954 he became senior consultant radiologist at the Victoria Hospital, Blackpool. As a member of the International Radiological Protection Committee he travelled widely. In his younger days Ken enjoyed dinghy sailing and became a keen salmon fisherman. He leaves a wife, Mary; two sons; and two granddaughters.
Enhancement of 5-Fluorouracil Sensitivity by an <i>rTS</i> Signaling Mimic in H630 Colon Cancer Cells
Authors: Ree Dolnick, Qi Wu, Norman J. Angelino, Lawrence V. Stephanie, Kuan-Chih Chow, Janice R. Sufrin, Bruce J. Dolnick
Journal: Cancer Research (2005)

Abstract The rTSβ protein has been hypothesized to synthesize signaling molecules that can down-regulate thymidylate synthase. These molecules share biological and chemical properties with acyl-homoserine lactones (AHL), suggesting some AHLs might act as rTS signaling mimics and down-regulate thymidylate synthase. We have determined that the AHL, 3-oxododecanoyl homoserine lactone (3-oxo-C12-(l)-HSL) can down-regulate thymidylate synthase protein at 10 μmol/L and reduce H630 (human colorectal cancer) growth by 50% at 23 μmol/L (IC50) in cell culture. At its IC50 concentration, 3-oxo-C12-(l)-HSL reduces the apparent IC50 of 5-fluorouracil (5-FU) from 1 μmol/L to 80 nmol/L (12-fold) in a colony formation assay. 3-Oxo-C12-(l)-HSL enhances the activity of 5-fluorodeoxyuridine, tomudex, and taxol but not the activity of 5-fluorouridine, methotrexate or Adriamycin. The unexpected interaction with taxol probably results from effects of the AHL on tubulin expression. Differences in taxol sensitivity, tubulin, and cellular morphology between H630 and the thymidylate synthase and rTSβ-overproducing, 5-FU-resistant H630-1 cell line as determined by colony formation assays, Western analysis of one-dimensional and two-dimensional gels, and photomicroscopy confirm that cytoskeletal changes are induced by the AHL or by rTS signaling. Isozyme differences in thymidylate synthase and rTSβ also exist in the two cell lines. Phosphorylation of rTSβ amino acid S121 is shown to occur and is decreased at least 10-fold in the drug-resistant cells. The data presented provide support for further investigations of rTS signaling mimics as enhancers to thymidylate synthase–directed chemotherapy, evidence that the phosphorylation state of rTSβ may be a marker for 5-FU resistance and a previously unrealized relationship between rTS signaling and the cytoskeleton.
Clinical and Biochemical Aspects of Lactic Acidosis
Authors: George F. Cahill
Journal: JAMA (1977)

This volume is a very well-referenced summation of lactic acidosis, covering the biochemistry and physiology in much detail, but intelligible to clinicians having some current familiarity with metabolism. In fact, even the less academically oriented practitioner could, with a little extra time, derive a clear-cut understanding of the interrelationships of such things as redox potential, state of adenine phosphorylation, and the complicated pathways of pyruvate metabolism, and could relate these to lactate levels in the patient. Important also is the list of more than 500 references covering both pathophysiology and therapy, with welldrawn roadmaps of metabolic pathways and selected patient histories serving as typical examples of the various types and therapies of lactic acidosis. The possible contributory effects of drugs, especially the biguanides, are discussed in detail. Since each clinical form of lactic acidosis is described in toto, there is much repetition between chapters, but the advantage of this is
Impact of Baseline <i>BCR-ABL</i> Mutations on Response to Nilotinib in Patients With Chronic Myeloid Leukemia in Chronic Phase
Authors: Timothy Hughes, Giuseppe Saglio, Susan Branford, Simona Soverini, Dong-Wook Kim, Martin C. Müller, Giovanni Martinelli, Jorge Cortes, Lan Beppu, Enrico Gottardi, Dongho Kim, Philipp Erben, Yaping Shou, Ariful Haque, Neil Gallagher, Jerald Radich, Andreas Hochhaus
Journal: Journal of Clinical Oncology (2009)

Nilotinib is a second-generation tyrosine kinase inhibitor indicated for the treatment of patients with chronic myeloid leukemia (CML) in chronic phase (CP; CML-CP) and accelerated phase (AP; CML-AP) who are resistant to or intolerant of prior imatinib therapy. In this subanalysis of a phase II study of nilotinib in patients with imatinib-resistant or imatinib-intolerant CML-CP, the occurrence and impact of baseline and newly detectable BCR-ABL mutations were assessed.Baseline mutation data were assessed in 281 (88%) of 321 patients with CML-CP in the phase II nilotinib registration trial.Among imatinib-resistant patients, the frequency of mutations at baseline was 55%. After 12 months of therapy, major cytogenetic response (MCyR) was achieved in 60%, complete cytogenetic response (CCyR) in 40%, and major molecular response (MMR) in 29% of patients without baseline mutations versus 49% (P = .145), 32% (P = .285), and 22% (P = .366), respectively, of patients with mutations. Responses in patients who harbored mutations with high in vitro sensitivity to nilotinib (50% inhibitory concentration [IC(50)] <or= 150 nM) or mutations with unknown nilotinib sensitivity were equivalent to those responses for patients without mutations (not significant). Patients with mutations that were less sensitive to nilotinib in vitro (IC(50) > 150 nM; Y253H, E255V/K, F359V/C) had less favorable responses, as 13%, 43%, and 9% of patients with each of these mutations, respectively, achieved MCyR; none achieved CCyR.For most patients with imatinib resistance and with mutations, nilotinib offers a substantial probability of response. However, mutational status at baseline may influence response. Less sensitive mutations that occurred at three residues defined in this study, as well as the T315I mutation, may be associated with less favorable responses to nilotinib.
Abstract 4362: miR-211 is contributive to the progression of oral carcinoma through targeting transcription factor 12 (Tcf12)
Authors: Yi-Fen Chen, Kuo-Wei K. Chang, Shu-Chun Lin
Journal: Cancer Research (2014)

Abstract Oral squamous cell carcinoma (OSCC) is one of the prevalent malignancies worldwide. MicroRNAs are short RNA molecules that regulate pathogenesis, including OSCC carcinogenesis, by post-transcriptional down-regulation of target genes. Our previous study has identified a relationship between high miR-211 expression and the invasion of OSCC. This study further dissects the molecular mechanisms underlying the progression of OSCC as affected by miR-211. Tcf12 is a helix-loop-helix transcription factor with unclear implications in oral malignancies. MiR-211 was predicted to target the 3′UTR of transcription factor 12 (Tcf12). Reporter assays confirmed the direct targeting of miR-211 on Tcf12. MiR-211 expression decreased both endogenous and exogenous Tcf12 expression. Exogenous Tcf12 expression suppressed proliferation, migration and anchorage-independent colony formation of OECM-1 OSCC cells. On the contrary, knockdown of endogenous Tcf12 expression enhanced these oncogenic phenotypes. Furthermore, in tumor cells with miR-211 overexpression, Tcf12 can reduce its oncogenic potential; whereas miR-211 can also rescue the suppression of Tcf12 to tumor cells. Down-regulation of Tcf12 was identified in 75% (27/36) human OSCC samples. To elucidate the in vivo oncogenic roles of miR-211 in OSCC carcinogenesis, K14 promoter driven murine miR-211 transgenic mouse lines (K14-GFP- miR-211) were established. The Tcf12 expression in squamous epithelium was down-regulated in transgenic mice relative to wild type mice. After tumor induction by 4-nitroquinoline 1-oxide treatment, the transgenic mice exhibited more advanced tongue and esophageal tumorigenesis comparing to wild type mice. In summary, this study reveals that Tcf12 is suppressive to OSCC. MiR-211 regulates OSCC progression by targeting Tcf12. The K14-GFP-miR-211 transgenic mice will help future investigation of the pathogenic mechanisms underlying OSCC progression and the development of therapeutic strategy. Citation Format: Yi-Fen Chen, Kuo-Wei K. Chang, Shu-Chun Lin. miR-211 is contributive to the progression of oral carcinoma through targeting transcription factor 12 (Tcf12). [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 4362. doi:10.1158/1538-7445.AM2014-4362
Skin complications in immunosuppressed patients: follow-up of kidney recipients
Authors: S. HAIM, R. FRIEDMAN-BIRNBAUM, O.S. BETTER, S. TUMA
Journal: British Journal of Dermatology (2006)

Thirth-five patients who received thirty-seven kidney transplants (two patients received live; the rest cadaver kidneys) were followed up for skin complications. There were thirty-nine instances of overt skin infection. In twenty-one instances we encountered fungal, in ten pyogenic and in eight viral infection. The course of these infections was more severe and more protracted than is usual in other patients. In nine instances, the skin infection contributed directly to the death of the patient. One patient developed Kaposi's sarcoma and another pyoderma gangrenosum. This study suggests that immunosuppressive treatment, which all our patients were continuously receiving, enhances their susceptibility to infection and to malignancy and may have been an aetiological factor in pyoderma gangrenosum.
Funding for Biomedical Research
Authors: Michael Seid, Elizabeth A. McGlynn
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
Treatment of Adult T-Cell Leukemia–Lymphoma with a Combination of Interferon Alfa and Zidovudine
Authors: Parkash S. Gill, William Harrington, Mark H. Kaplan, Raul C. Ribeiro, John M. Bennett, Howard A. Liebman, Marjorie Bernstein-Singer, Byron M. Espina, Lisa Cabral, Steven Allen, Steven Kornblau, Malcolm C. Pike, Alexandra M. Levine
Journal: New England Journal of Medicine (1995)

Infection with the human T-cell lymphotropic virus type I, a retrovirus, can cause a distinctive cancer, adult T-cell leukemia–lymphoma. The median survival of patients with the acute and lymphomatous forms of the disease is short, despite the use of cytotoxic chemotherapy.