tbuckley/cabot-search huggingface dataset:
Immunotherapy of tree pollen allergy with a modified alginate conjugated birch pollen extract compared to an aluminium adsorbed extract
Authors: N. P. Boye, O. P. Salo, N. Hyldebrandt, J. A. Wihl, A. Bevan, R. I. Harris, J. R. Lovely
Journal: Allergy (1990)

The safety and efficacy of two birch pollen extracts, one chemically conjugated to alginate (Anjuvac®) the other adsorbed to aluminium hydroxide (Alutard®), were investigated in an open multicentre comparative study of 63 birch pollen allergic patients. Both extracts decreased the nasal symptoms during the birch pollen season. The changes in specific IgE and IgG were much the same in both treatment groups. The adverse reactions recorded were mild in both groups, but more frequent in the Anjtivac group, probably because of a more aggressive dose schedule though there were twice as many asthmatics in the Anjuvac group. The two investigated allergen extracts were useful alternatives for immunotherapy.
AN ANTIVIRAL SUBSTANCE FROM PENICILLIUM FUNICULOSUM
Authors: Richard E. Shope
Journal: The Journal of Experimental Medicine (1966)

1. Helenine injected intraperitoneally 24 hr prior to a regularly fatal dose of Semliki Forest virus saves most of the mice to which it is administered. 2. Mice saved by helenine develop no viral immunity and regularly succumb when rechallenged 2 wk later with the same dose of virus from which they were originally saved. 3. The time during which helenine is optimally effective in protecting mice from death by Semliki Forest virus covers a period of approximately 36 hr beginning after about 12 hr and extending to 48 hr before virus infection. When periods of less than 12 hr, or more than 48 hr, elapse between the time of helenine administration and virus inoculation, its protective effectiveness diminishes progressively. 4. Repeated injections of helenine at 2- or 3-day intervals, if continued long enough, exhaust the capacity of a host to respond favorably to helenine administered 24 hr before virus inoculation. 5. Helenine injections at intervals of 4, 3, and 2 wk before its administration 24 hr prior to infection do not decrease the effectiveness of this final dose in protecting mice from fatal infection by the virus. The experimental results here reported indicate that, as suggested by the findings of earlier work, helenine does not act directly as an antiviral substance, but instead exerts its effect through some substance that it induces the host to elaborate. The nature of this induced antiviral substance is as yet unknown though, to judge from the failure of spared mice to acquire viral immunity, it appears to act at a stage in viral replication prior to that at which antigenic viral protein is produced. The findings with helenine and those thus far reported for interferon afford no factual basis for judging the relationship of the two, if any.
Diagnostic and Prognostic Value of Serial Dobutamine Stress Echocardiography for Noninvasive Assessment of Cardiac Allograft Vasculopathy
Authors: Christoph H. Spes, Volker Klauss, Harald Mudra, Susanne D. Schnaack, Andres R. Tammen, Johannes Rieber, Uwe Siebert, Karl-Heinz Henneke, Peter Überfuhr, Bruno Reichart, Karl Theisen, Christiane E. Angermann
Journal: Circulation (1999)

Background —Routine methods for surveillance of cardiac allograft vasculopathy (CAV) are coronary angiography and intravascular ultrasound (IVUS). This study analyzed the diagnostic and prognostic value of dobutamine stress echocardiography (DSE) for noninvasive assessment of CAV. Methods and Results —In 109 heart transplant recipients, 333 DSEs were compared with 285 coronary angiograms and 199 IVUS analyses. Studies were repeated after 1, 2, 3, 4, and ≥5 years in 88, 74, 37, 18, and 7 patients, respectively. Resting 2D echocardiography detected CAV defined by IVUS and angiography with a sensitivity of 57% (specificity 88%). DSE increased the sensitivity to 72% ( P =0.002). M-mode analysis increased the sensitivity of 2D rest and stress analysis ( P =0.001, 0.004). Cardiac events occurred after 1.9% of normal stress tests by 2D analysis (combined 2D and M-mode: 0%), compared with 6.3% (3.8%) of normal resting studies. Worsening of serial DSE indicated an increased risk of events compared with no deterioration (relative risk 7.26, P =0.0014). Serial deterioration detected by stress only was associated with a higher risk of events than changes evident from resting studies (relative risk 3.06, P =0.0374). Conclusions —DSE identifies patients at risk for events and facilitates monitoring of CAV. A normal DSE predicts an uneventful clinical course and justifies postponement of invasive studies. The prognostic value of DSE is comparable to that of IVUS and angiography.
Calcium supplements reduce risk fracture
Authors: Janice Hopkins Tanne
Journal: BMJ (1997)

Healthy elderly people who took supplements of calcium and vitamin D had less than half the fractures of those in a placebo group in a three year study, even though they fell just as often, according to researchers at the Tufts University Nutrition Center in Boston.

The finding comes as the American Medical Association makes new recommendations about calcium and warns that “a large percentage of Americans fail to meet the currently recommended guidelines for optimal calcium intake.”

The double blind, placebo controlled study of 176 men and 213 women over 65 found that 26 people in the placebo group had …
Abstract 1517: Pancreatic stellate cells and chemoresistant pancreatic cancer cells induce EMT gene expression in normal pancreatic ductal cells.
Authors: Krishan Kumar, Vaibhav Sahai, Kazumi Ebine, Hidayatullah G. Munshi
Journal: Cancer Research (2013)

Abstract Pancreatic cancer, one of the deadliest of human cancers, is associated with a collagen-rich pronounced stromal reaction. Previously, we showed that the collagen microenvironment increased the motility of human pancreatic ductal epithelial (HPDE) cells (Ottaviano AJ et al, Cancer Research 2006). Since stellate cells are one of the major contributors to the stromal reaction, we examined the effect of stellate cells on HPDE cells. HPDE cells were labeled with cell tracking dye and then co-cultured stellate cells to allow intimate cell-cell contact. HPDE cells were then isolated 72 hours later using FACS and changes in gene expression analyzed by real time PCR. We found that HPDE cells upregulated expression of epithelial-mesenchymal transition (EMT) markers Zeb1, Snail and vimentin. Stellate cells also increased expression of these EMT markers in HPDE cells expression Kras (HPDE-Kras). However, no change in these EMT markers were seen when the HPDE and stellate cells were prevented from direct cell-cell contact using transwell co-culture system. Treatment with TGF-b type I receptor inhibitor SB431542 blocked the effect of stellate cells on HPDE gene expression. Since ductal cells also encounter malignant cells in vivo, we also examined the effect of co-culture of ductal cells with cancer cells. HPDE cells failed to upregulate EMT markers when they were co-cultured with HPAFII/CD18 cell. However, when HPDE cells were co-cultured with chemo-resistant CD18 cells (CD18-CR), HPDE cells upregulated EMT markers. The effect of CD18-CR cells on HPDE gene expression was only observed when there was intimate cell-cell contact. Also, treatment with SB431542 blocked the effect on HPDE gene expression. These results indicate that the tumor microenvironment may affect the behavior of peri-tumoral non-malignant cells and thereby contribute to tumor progression. Citation Format: Krishan Kumar, Vaibhav Sahai, Kazumi Ebine, Hidayatullah G. Munshi. Pancreatic stellate cells and chemoresistant pancreatic cancer cells induce EMT gene expression in normal pancreatic ductal cells. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1517. doi:10.1158/1538-7445.AM2013-1517
FUNCTIONAL ANATOMY OF THE LYMPHOCYTE IN IMMUNOLOGICAL REACTIONS IN VITRO
Authors: William McFarland, Dorothy H. Heilman, John F. Moorhead
Journal: The Journal of Experimental Medicine (1966)

The motile lymphocyte in vitro has a prominent "tail" that becomes a means of "attachment" to other cells and debris during interaction. The term "uropod" is proposed to designate this specialized cytoplasmic projection which appears totally different, anatomically and functionally, from the pseudopods. Observations of lymphoblasts during mitosis indicate that the uropod is formed immediately following mitosis at the point of final cytoplasmic connection between daughter cells, a fact that may prove significant as lymphocyte function is better understood. In the mixed leukocyte reaction the lymphocyte interacts with macrophages, cell debris, and lymphoblasts via the uropod, suggesting that stimulatory material may be acquired through this specialized appendage. Lymphoblast-lymphocyte interaction is noteworthy and implies that immunologically committed cells may be mustered through horizontal as well as vertical processes: horizontally by lymphoblast-lymphocyte interaction and vertically by mitosis of transformed lymphoblasts. The possible relevance of these in vitro observations to lymphocyte functions in vivo is discussed.
160 ONE MONTH POST-OPERATIVE SERUM INSULIN PREDICTS SERUM AMINOTRANSFERASE ELEVATION AND FIBROSIS PROGRESSION DUE TO HCV RECURRENCE AFTER LIVER TRANSPLANTATION
Authors: S. Ginanni Corradini, A. Molinaro, A. Eramo, M. Siciliano, M.A. Burza, A. De Santis, M. Merli, F. Gentili, G. Ferretti, A. Onetti Muda, D. Lilli, G. Mennini, P.B. Berloco, A.F. Attili, M. Rossi
Journal: Journal of Hepatology (2009)
Neuroblastoma — from Genetic Profiles to Clinical Challenge
Authors: Brian H. Kushner, Nai-Kong V. Cheung
Journal: New England Journal of Medicine (2005)

Neuroblastoma stands out among childhood cancers because of its relative frequency, enigmatic natural history, intriguing biologic features, and daunting therapeutic challenges. Much that is novel and on the cutting edge in oncology comes together in neuroblastoma: preventive screening, biology-driven management, dose-intensive or dose-dense chemotherapy, stem-cell transplantation, targeted therapies (radiation, monoclonal antibodies, drugs), agents that induce differentiation, and monitoring of minimal disease.1 Neuroblastoma is an embryonic neoplasm of the sympathetic nervous system. The histologic composition varies from primitive cells without neuronal features to mature neurons or ganglion cells, often within the same mass. Neuroblastoma is the most common extracranial solid tumor . . .
Polyclonal B Cell Differentiation and Loss of Gastrointestinal Tract Germinal Centers in the Earliest Stages of HIV-1 Infection
Authors: Marc C. Levesque, M. Anthony Moody, Kwan-Ki Hwang, Dawn J. Marshall, John F. Whitesides, Joshua D. Amos, Thaddeus C. Gurley, Sallie Allgood, Benjamin B. Haynes, Nathan A. Vandergrift, Steven Plonk, Daniel C. Parker, Myron S. Cohen, Georgia D. Tomaras, Paul A. Goepfert, George M. Shaw, Jörn E. Schmitz, Joseph J. Eron, Nicholas J. Shaheen, Charles B. Hicks, Hua-Xin Liao, Martin Markowitz, Garnett Kelsoe, David M. Margolis, Barton F. Haynes
Journal: PLoS Medicine (2009)

Studying the effects of early HIV infection on human antibody responses, M. Anthony Moody and colleagues find rapid polyclonal B cell differentiation and structural damage to gut-associated lymphoid tissue.
Educational aspects of medical audit.
Authors: G F Batstone
Journal: BMJ (1990)

Working Paper 6' does not couch medical audit activities in an educational environment.The Royal College of Physicians and Royal College of Surgeons, however, have highlighted the educational aspects of medical audit, stating that "education is the most useful product of audit"2 and that audit "is an important educational process for both seniors and juniors."3Kenneth Clarke in a speech on 10 July stated that in his view, "Medical audit is about quality assurance in clinical work.As it entails a measurement of performance it must be a key part of continuing professional education."This echoes the theme of the report of the Alment Committee: "In our view it is a necessary part of a doctor's professional responsibility to assess his work regularly in association with his colleagues,"4 although in medical audit such reviews are considered educational.The approach of peer review ofpractice creates a "sympathetic environment" for medical audit.This paper aims at highlighting the educational aspects of audit and the framework required to exploit them and at considering the nature of education and of audit. Educational aspectsMedical audit works at two levels: firstly, through individual self assessment and professional develop- ment, and, secondly, through review of performance by the clinical team, leading to enhancement of the quality of activity of that team.Thus audit may be regarded as a process leading to improved clinical care by mechanisms which may be educational or operational, or both.The educational strengths of audit are: * Small group work, which is effective in modifying attitudes and management of clinical conditions * Critical review of current practice, which en- courages learning about new techniques and treatments and when to use them
UK government comes down in favour of making all publicly funded research "open access"
Authors: N. Hawkes
Journal: BMJ (2012)

The government has accepted the recommendations of the Finch report on open access to published research and aims to make all publicly funded research available to everyone.

It agrees with the view of the working group led by Janet Finch,1 professor of sociology at Manchester University, that the “gold model” of open access, where the costs of publication are paid up front by the authors, is the right route. To pay for these changes, Research Councils UK (RCUK) has announced that in future it will make block grants available to universities and other approved organisations, rather than earmarking part of each research grant for this purpose.

However, RCUK gave no undertaking that these block grants will be new money, so they are likely to reduce the amount available for supporting research, at least in the short term. The Finch report estimated that the transition costs would be £50m (€64m; $80m) to £60m a year, caused …
Secondary prevention of gastric cancer
Authors: M. Rugge
Journal: Gut (2007)

When I was young(er), my mentor, Pelayo Correa, who taught a generation of researchers orbiting around gastric oncology, encouraged me to spend some sabbatical time at the European Cancer Agency in Lyon “...to gain, among other things, a better perception of the crucial clinical impact that epidemiological data really have in clinical practice”. I did not follow this good piece of advice... and it was a mistake! This was the first thought that came to me as I read the manuscript produced by de Vries et al in this issue of Gut (page 1665)—a well conducted study that will be mentioned by every paper addressing gastric precancerous lesions.1

The paper provides valuable insight on the declining prevalence of gastric precancerous lesions (that is, atrophic gastritis and gastric non‐invasive neoplasia) in the Netherlands between 1991 and 2005: 15 years is a long enough time to give us a historical perception of how fast our world is changing. The abundance of data presented by the authors prompts a few general considerations on our current strategies for dealing with gastric precancerous lesions/conditions, making us look to the near future in the light of a critical review of our recent past.

Let us start from the conclusions: the Dutch data confirm that gastric cancer usually arises in the second half of life and its incidence is declining in the western world—a victory without a battle. Less optimistically, however, we could argue that gastric epithelial malignancies still have a major oncological impact in both Asian and South‐American countries. Even in large areas of southern and eastern Europe, gastric cancer is still a leading oncological problem and surgeons are still faced with advanced gastric tumours in their daily practice (just to give an example, the incidence of gastric cancer in the Russian Federation exceeds 32/100 000 population/year; personal communication from Professor Victor Pasechnikov, Stavropol Medical Academy, Russia). de Vries's prediction of a 24% drop in the worldwide incidence of gastric cancer still seems out of reach (outside the Netherlands, at least).

Assuming that gastric cancer (and the intestinal type in particular) remains a major health problem in more than two‐thirds of the world's population, any efforts to improve the secondary prevention of gastric cancer will have to include each of the following points: non‐invasive tests for selecting high‐risk subjects, gastric endoscopy procedures and biopsy sampling protocols, consistent (internationally validated) histological assessment of gastric precancerous lesions and finally histology reports.

de Vries's data suggest a few concise comments on each of these major points.1
Abstract LB-126: Replication-associated DNA double-strand breaks and checkpoint abrogation promote gene amplification.
Authors: Anna Kondratova, Michael Marotta, Takaaki Watanabe, Hisashi Tanaka
Journal: Cancer Research (2013)

Abstract Gene amplification, a copy number increase of genomic segments through DNA rearrangements, drives cancer progression and acquired resistance to anti-cancer drugs. Understanding the cellular processes involved in gene amplification is important to rationally develop management strategies for cancer patients with such aggressive tumors. DNA double-strand breaks (DSBs) are the most dangerous lesions of DNA and often initiate gene amplification. A main cellular process giving rise to DSBs in cancer cells is DNA replication, as cancer cells are under strong replication stress. We hypothesized that failure to repair replication-associated DSBs would result in DNA rearrangements and gene amplification. To test this hypothesis, we suppressed the expression of DNA repair protein MRE11 in mammalian cells. MRE11 is a component of the MRN (Mre11-Rad50-NBS1) complex that repairs DSBs of different origin including those arising during DNA replication. Indeed, knocking down MRE11 resulted in the 10-fold increase in the frequency of gene amplification. DSBs were markedly increased in the MRE11 knockdown cells in the S phase of the cell cycle, suggesting a DNA replication-associated origin of DSBs. Importantly, DSBs continued to be abundant in the M phase, indicating that MRE11 knockdown cells lack both intra-S and G2/M checkpoints. The possibility that checkpoint abrogation could also promote gene amplification was further tested in the I-SceI endonuclease-induced gene amplification system, where checkpoint abrogation by caffeine resulted in the 4-fold increase in amplification frequency. These results provide a proof-of-concept that pharmacological modulation of cell cycle checkpoints can alternate the gene amplification frequency, and may be used to prevent proliferation of cells with gene amplification. Citation Format: Anna Kondratova, Michael Marotta, Takaaki Watanabe, Hisashi Tanaka. Replication-associated DNA double-strand breaks and checkpoint abrogation promote gene amplification. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr LB-126. doi:10.1158/1538-7445.AM2013-LB-126
Mediation of Drosophila autosomal dosage effects and compensation by network interactions
Authors: John H Malone, Dong-Yeon Cho, Nicolas R Mattiuzzo, Carlo G Artieri, Lichun Jiang, Ryan K Dale, Harold E Smith, Jennifer McDaniel, Sarah Munro, Marc Salit, Justen Andrews, Teresa M Przytycka, Brian Oliver
Journal: Genome biology (2012)

Abstract Background Gene dosage change is a mild perturbation that is a valuable tool for pathway reconstruction in Drosophila . While it is often assumed that reducing gene dose by half leads to two-fold less expression, there is partial autosomal dosage compensation in Drosophila , which may be mediated by feedback or buffering in expression networks. Results We profiled expression in engineered flies where gene dose was reduced from two to one. While expression of most one-dose genes was reduced, the gene-specific dose responses were heterogeneous. Expression of two-dose genes that are first-degree neighbors of one-dose genes in novel network models also changed, and the directionality of change depended on the response of one-dose genes. Conclusions Our data indicate that expression perturbation propagates in network space. Autosomal compensation, or the lack thereof, is a gene-specific response, largely mediated by interactions with the rest of the transcriptome.
Primary Hyperparathyroidism Presenting as Fever of Unknown Origin with Unremitting Headache
Authors: Donald C. Blair, F. Robert Fekety
Journal: Annals of Internal Medicine (1979)

Brief Reports1 October 1979Primary Hyperparathyroidism Presenting as Fever of Unknown Origin with Unremitting HeadacheDONALD C. BLAIR, M.D., F. ROBERT FEKETY JR., M.D.DONALD C. BLAIR, M.D.Search for more papers by this author, F. ROBERT FEKETY JR., M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-91-4-575 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptHyperparathyroidism, classically characterized by hypercalcemia, bone demineralization, and nephrolithiasis, is increasingly associated with more protean manifestations (1). We describe a patient with a parathyroid adenoma who presented with fever and intractable headache persisting for over a year before hyperparathyroidism was diagnosed. Headache as a major manifestation of hyperparathyroidism is rare, and, to our knowledge, presentation of the disease as fever of unknown origin has not been reported previously (1-4).A 29-year-old white woman presented to the clinic of the University of Michigan Medical Center in March 1972 with bilateral, dull, nonpulsatile temporal and frontal headaches dating from an upper respiratory...References1. AURBACHMALLETTEPATTENHEATHDOPPMANBILEZIKIAN GLBDJJ. Hyperparathyroidism: recent studies. Ann Intern Med. 1973;79:566-81. LinkGoogle Scholar2. PETERSDORFBEESON RP. Fever of unexplained origin: report on 100 cases. Medicine (Baltimore). 1961;40:1-30. CrossrefMedlineGoogle Scholar3. JACOBYSWARTZ GM. Fever of undetermined origin. N Engl J Med. 1973;289:1407-10. CrossrefMedlineGoogle Scholar4. SIMONDANIELS HG. Hormonal hyperthermia: endocrinologic causes of fever. Am J Med. 1979;66:257-63. CrossrefMedlineGoogle Scholar5. ARNAUDTSAOLITTLEDIKE CHT. Radioimmunoassay of human parathyroid hormone in serum. J Clin Invest. 1971;50:21-34. CrossrefMedlineGoogle Scholar6. HAWKER C. Parathyroid hormone: radioimmunoassay and clinical interpretation. Ann Clin Lab Sci. 1975;5:383-98. MedlineGoogle Scholar7. ALBRIGHTAUBBAUER FJW. Hyperparathyroidism: a common and polymorphic condition as illustrated by 17 proved cases from one clinic. JAMA. 1934;102:1276-87. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByMusculoskeletal manifestations of primary hyperparathyroidismAReferencesSevere neurological disease associated with hyperparathyroidismCase 21-1981 1 October 1979Volume 91, Issue 4Page: 575-576KeywordsBoneFever of unknown originFeversHeadachesHypercalcemiaHyperparathyroidismParathyroid tumors Issue Published: 1 October 1979 PDF DownloadLoading ...