tbuckley/cabot-search huggingface dataset:
Differential Diagnosis of Cardiovascular Disease by X-Ray
Authors: Donald C. Fyler
Journal: JAMA (1967)

The authors provide an exhaustive discussion of the differential diagnosis of congenital heart disease from the standpoints of conventional radiography, electrocardiography, and phonocardiography. They also present, in small print, additional detailed data of the anatomy and clinical course. Schematized differential diagnostic considerations are given at the end of each chapter, and a final chapter of schemas of the differential diagnosis of all congenital heart disease has been devised. Brief case summaries with illustrations of radiograms, electrocardiograms, and phonocardiograms of excellent quality finish each chapter. Many excellent reproductions of angiograms are presented. The bibliography is extensive.  Pertinent hemodynamic data are interspersed but are not discussed as general topics or as subheadings. The indications for angiocardiography and cardiac catheterization are scarcely noted, and the indications and problems of surgery are superficially covered.  This is not a clinical book. Rather is it a discussion of the diagnosis of congenital heart disease as
Lack of a relationship of elastin peptide level to emphysema assessed by CT scans.
Authors: C Frette, M P Jacob, C Defouilloy, C Atassi, F Kauffmann, Q T Pham, J Bignon
Journal: American Journal of Respiratory and Critical Care Medicine (1996)

Clinical reports suggest that peptide (EP) concentration may be used as a subclinical marker of pulmonary emphysema. This hypothesis was tested in a clinical study by comparing EP concentration in male emphysematous patients with the level in two control groups, and by exploring the relation of elastin peptide level to high-resolution computed tomography (HRCT) scan emphysema score among emphysematous patients. Serum EP level was determined among male emphysematous patients with at least 20% of emphysema (n = 27) and in two populations of male workers, drawn from epidemiologic studies (227 coal miners and 310 policemen). No difference in elastin peptide concentration was observed between emphysematous patients and control subjects (mean +/- SD = 2.39 +/- 1.18 micrograms/ml in patients versus 2.55 +/- 1.34 micrograms/ml in policemen and 2.59 +/- 1.20 micrograms/ml in coal miners). The correlation of elastin peptide concentration with percentage of pulmonary emphysema was negative and of borderline significance (r = -0.36; p = 0.06). These results cast doubts on the usefulness of elastin peptide level as a predictive marker of pulmonary emphysema.
Plasminogen activator inhibitor-1 suppresses endogenous fibrinolysis in a canine model of pulmonary embolism.
Authors: C F Reilly, T Fujita, J E Hutzelmann, E J Mayer, R J Shebuski
Journal: Circulation (1991)

Plasminogen activator inhibitor-1 (PAI-1), the specific, fast-acting inhibitor of tissue-type plasminogen activator (t-PA), binds to fibrin and has been found in high concentrations within arterial thrombi. These findings suggest that the localization of PAI-1 to a thrombus protects that same thrombus from fibrinolysis. In this study, clot-bound PAI-1 was assessed for its ability to suppress clot lysis in vivo.Autologous, canine whole blood clots were formed in the presence of increasing amounts of activated PAI-1 (0-30 micrograms/ml). Approximately 6-8% of the PAI-1 bound to the clots under the experimental conditions. Control and PAI-1-enriched clots containing iodine-125-labeled fibrin (ogen) were homogenized, washed to remove nonbound elements, and delivered to the lungs of anesthetized dogs where the homogenates subsequently underwent lysis by the endogeneous fibrinolytic system. 125I-labeled fibrin degradation products appeared in the blood of control animals within 10 minutes and were maximal by 90 minutes. PAI-1 reduced fibrin degradation product release in a dose-responsive manner at all times between 30 minutes and 5 hours (greater than or equal to 76% inhibition at 30 minutes, PAI-1 greater than or equal to 6 micrograms/ml). PAI-1 also suppressed D-dimer release from clots containing small amounts of human fibrin (ogen). t-PA administration attenuated the effects of PAI-1, whereas latent PAI-1 (20 micrograms/ml) had no effect on clot lysis. Blood levels of PA and PAI activity remained unaltered during these experiments.The results indicate that PAI-1 markedly inhibits endogenous fibrinolysis in vivo and, moreover, suggest that the localization of PAI-1 to a forming thrombus is an important physiological mechanism for subsequent thrombus stabilization.
Th9 cells promote antitumor immune responses in vivo
Authors: Yong Lu, Sungyoul Hong, Haiyan Li, Jungsun Park, Bangxing Hong, Lijuan Wang, Yuhuan Zheng, Zhiqiang Liu, Jingda Xu, Jin He, Jing Yang, Jianfei Qian, Qing Yi
Journal: Journal of Clinical Investigation (2012)

Th9 cells are a subset of CD4+ Th cells that produce the pleiotropic cytokine IL-9. IL-9/Th9 can function as both positive and negative regulators of immune response, but the role of IL-9/Th9 in tumor immunity is unknown. We examined the role of IL-9/Th9 in a model of pulmonary melanoma in mice. Lack of IL-9 enhanced tumor growth, while tumor-specific Th9 cell treatment promoted stronger antitumor responses in both prophylactic and therapeutic models. Th9 cells also elicited strong host antitumor CD8+ CTL responses by promoting Ccl20/Ccr6-dependent recruitment of DCs to the tumor tissues. Subsequent tumor antigen delivery to the draining LN resulted in CD8+ T cell priming. In agreement with this model, Ccr6 deficiency abrogated the Th9 cell–mediated antitumor response. Our data suggest a distinct role for tumor-specific Th9 cells in provoking CD8+ CTL-mediated antitumor immunity and indicate that Th9 cell–based cancer immunotherapy may be a promising therapeutic approach.
Polymorphisms and Promoter Overactivity of the p22 <sup> <i>phox</i> </sup> Gene in Vascular Smooth Muscle Cells From Spontaneously Hypertensive Rats
Authors: Guillermo Zalba, Gorka San José, Francisco J. Beaumont, María A. Fortuño, Ana Fortuño, Javier Díez
Journal: Circulation Research (2001)

In a previous study, we found that the p22(phox) subunit of the NADH/NADPH oxidase is overexpressed in vascular smooth muscle cells (VSMCs) from spontaneously hypertensive rats (SHRs) with enhanced vascular production of superoxide anion ((.)O(2)(-)). Thus, we have investigated whether changes in the sequence or activity of the promoter region of p22(phox) gene are present in SHRs. To carry out this analysis, first of all, we characterized the rat gene structure and promoter region for the p22(phox) subunit. The p22(phox) gene spans approximately 10 kb and contains 6 exons and 5 introns. Primer extension analysis indicated the transcriptional start site 100 bp upstream from the translational start site. The immediate promoter region of the p22(phox) gene does not contain a TATA box, but there are a CCAC box and putative recognition sites for nuclear factors, such as SP1, gamma-interferon, and nuclear factor-kappaB. Using reporter-gene transfection analysis, we found that this promoter was functional in VSMCs. Furthermore, we observed that p22(phox) promoter activity was significantly higher in VSMCs from SHRs than from normotensive Wistar-Kyoto rats. In addition, we found that there were 5 polymorphisms in the sequence of p22(phox) promoter between Wistar-Kyoto rats and SHRs and that they were functional. The results obtained in this study provide a tool to explore the mechanisms that regulate the expression of p22(phox) gene in rat VSMCs. Furthermore, our findings show that changes in the sequence of p22(phox) gene promoter and in the degree of activation of VSMCs are responsible for upregulated expression of p22(phox) in SHRs.
Another reason for opening access to research
Authors: John Wilbanks
Journal: BMJ (2006)

Much of the debate about open access has focused on the principle of access for scientists and the economics of such a change.There is a second principle to consider: the full power of new technological approaches such as text mining, collaborative filtering, and semantic indexing, are not resulting in powerful new public resources.Despite real success in the open access movement, most scholarly research is unavailable, either for study or for processing by software.According to the Budapest open access initiative, "There are many degrees and kinds of wider and easier access to this literature.By 'open access' to this literature, we mean its free availability on the public internet, permitting any users to read, download, copy, distribute, print, search, or link to the full texts of these articles, crawl them for indexing, pass them as data to software, or use them for any other lawful purpose, without financial, legal, or technical barriers other than those inseparable from gaining access to the internet itself.The only constraint on reproduction and distribution, and the only role for copyright in this domain, should be to give authors control over the integrity of their work and the right to be properly acknowledged and cited." 1 Open access journals are entering the mainstream of scholarly publishing. 2 The Directory of Open Access Journals (www.doaj.org), a listing of "free, full text, quality controlled scientific and scholarly journals," includes 2478 journals, with on average more than one journal a day added in 2006 (121 999 articles are tracked). 3Open access journals have earned top impact factors in fields such as biology and bioinformatics, 4 5 as well as high immediacy factors. 6ut most journals are non-open access.Many nonopen access journals and publishers tackle the access problem by allowing authors to post copies of their works on the internet; this is known as "self archiving."Self archiving by authors is also growing rapidly.Between March 2005 and October 2006, the number of institutional archives tracked at the Registry of Open Access Repositories (http://archives.eprints.org)has grown by nearly one every other day, and the number of records in those archives has grown by nearly 600%, to 1.2 million papers.Open access is here to stay, in one form or another.
A case of cutaneous anthrax with toxaemic shock
Authors: M. DOğANAY, M. BAKIR, İ. DOKMETAŞ
Journal: British Journal of Dermatology (1987)

Journal Article A case of cutaneous anthrax with toxaemic shock Get access M. DOğANAY, M. DOğANAY Department of Infectious Diseases, Faculty of Medicine, Cumhuriyet University, 58040‐Sivas, Turkey Dr M.Doğanay. Search for other works by this author on: Oxford Academic Google Scholar M. BAKIR, M. BAKIR Department of Infectious Diseases, Faculty of Medicine, Cumhuriyet University, 58040‐Sivas, Turkey Search for other works by this author on: Oxford Academic Google Scholar İ. DÖKMETAŞ İ. DÖKMETAŞ Department of Infectious Diseases, Faculty of Medicine, Cumhuriyet University, 58040‐Sivas, Turkey Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 117, Issue 5, 1 November 1987, Pages 659–662, https://doi.org/10.1111/j.1365-2133.1987.tb07500.x Published: 01 November 1987
Increased Myocardial Dysfunction After Ischemia-Reperfusion in Mice Lacking Glucose-6-Phosphate Dehydrogenase
Authors: Mohit Jain, Lei Cui, Daniel A. Brenner, Bo Wang, Diane E. Handy, Jane A. Leopold, Joseph Loscalzo, Carl S. Apstein, Ronglih Liao
Journal: Circulation (2004)

Background— Free radical injury contributes to cardiac dysfunction during ischemia-reperfusion. Detoxification of free radicals requires maintenance of reduced glutathione (GSH) by NADPH. The principal mechanism responsible for generating NADPH and maintaining GSH during periods of myocardial ischemia-reperfusion remains unknown. Glucose-6-phosphate dehydrogenase (G6PD), the rate-limiting enzyme in the pentose phosphate pathway, generates NADPH in a reaction linked to the de novo production of ribose. We therefore hypothesized that G6PD is essential for maintaining GSH levels and protecting the heart during ischemia-reperfusion injury. Methods and Results— Susceptibility to myocardial ischemia-reperfusion injury was determined in Langendorff-perfused hearts isolated from wild-type mice (WT) and mice lacking G6PD (G6PD def ) (20% of WT myocardial G6PD activity). During global zero-flow ischemia, cardiac function was similar between WT and G6PD def hearts. On reperfusion, however, cardiac relaxation and contractile performance were greatly impaired in G6PD def myocardium, as demonstrated by elevated end-diastolic pressures and decreased percent recovery of developed pressure relative to WT hearts. Contractile dysfunction in G6PD def hearts was associated with depletion of total glutathione stores and impaired generation of GSH from its oxidized form. Increased ischemia-reperfusion injury in G6PD def hearts was reversed by treatment with the antioxidant MnTMPyP but unaffected by supplementation of ribose stores. Conclusions— These results demonstrate that G6PD is an essential myocardial antioxidant enzyme, required for maintaining cellular glutathione levels and protecting against oxidative stress-induced cardiac dysfunction during ischemia-reperfusion.
Acute Barbiturate Intoxication
Authors: Fred Plum
Journal: JAMA (1961)

<h3>To the Editor:—</h3> The paper by Dobos et al., "Acute Barbiturate Intoxication," in the April 29 issue ofThe Journal, pages 268-272, again and rightly emphasizes the excellent results which accrue when patients with barbiturate poisoning are treated carefully with attention to their physiological needs. Dobos et al. cite the conclusion of Shaw et al. (<i>Nature</i><b>174</b>:402-403 [Aug. 28] 1954) that bemegride (β,β-methylethylglutarimide; Megimide, Mikedimide) is a specific barbiturate antagonist. There is evidence that this may be a misleading statement, since in humans (Plum, F., and Swanson, A. G.,<i>JAMA</i><b>163</b>:827-835 [March 9] 1957) and in animals (Lavenson, G. S., Jr.; Plum, F.; and Swanson, A. G.,<i>J Pharmacol Exper Ther</i><b>122</b>:271-280 [Feb.] 1958) bemegride was found to act similarly to other nonspecific analeptics in subjects deeply anesthesized with barbiturates.
Effect of carvedilol and metoprolol on the mode of death in patients with heart failure
Authors: Willem J. Remme, John G. Cleland, Leif Erhardt, Phillip Spark, Christian Torp‐Pedersen, Marco Metra, Michel Komajda, Christine Moullet, Mary Ann Lukas, Philip Poole‐Wilson, Andrea Di Lenarda, Karl Swedberg
Journal: European Journal of Heart Failure (2007)
Abstract 3701: A targeted delivery system for anticancer drugs based on functionalized carbon nanotubes
Authors: Elena Heister, Vera Neves, Ravi P. Silva, Johnjoe McFadden, Helen M. Coley
Journal: Cancer Research (2010)

Abstract Carbon nanotubes have emerged as a promising nanomaterial for the development of customizable drug delivery system due to their ability to penetrate cell membranes and to attach high loads of drugs and targeting agents on their surface. In the field of oncology, this promotes the development of therapies with improved effectivity and fewer side effects by assisting the targeting of therapeutic agents to the desired site of action. Our work focuses on the targeted delivery of the anthracycline and anthracenedione anticancer drugs doxorubicin and mitoxantrone to human colon cancer cells (WiDr) by means of a carbon nanotube-based drug delivery system. The drugs are attached to the nanotube surface in a non-covalent manner, resulting in a weight ratio (drug: CNTs) of 4:1 owing to the high surface area of CNTs. As drug binding is higher at physiological pH than at a slightly acidic pH, this method allows for the release of the drug from the nanotubes in such environments, for example late endosomes and lysosomes. In a previous study, we have shown that doxorubicin-loaded carbon nanotubes are are taken up by WiDr colon cancer cells and release their drug payload upon cellular internalization, which then translocates to the nucleus [1]. Current work is focusing on the targeting aspect: to increase the specificity of our system, we further attach a monoclonal antibody to the nanotube carrier that recognizes/binds to carcinoembryonic antigen (CEA), a target structure overexpressed by WiDr colon cancer cells. In vitro cytotoxicity studies show that the targeted drug-CNT complexes indeed have a greater therapeutic effect on WiDr cells than on MCF7 breast cancer cells, which do not express CEA. Future work will include in vivo studies on mice bearing tumor xenographs to evaluate the feasibility and behavior of our system in a setting of clinical relevance. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3701.
Treatment of Prehypertension in Diabetes and Metabolic Syndrome
Authors: Julian Segura, Luis M. Ruilope
Journal: Diabetes Care (2009)

In 2003, the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VII) published its ultimate guidelines for hypertension prevention and management (1). One of the key messages was the definition of a new category of blood pressure (BP) levels, i.e., prehypertension, that included individuals with a systolic BP of 120–139 mmHg or a diastolic BP of 80–89 mmHg. Patients with prehypertension were considered at increased risk for progression to hypertension and individuals in the 130/80 to 139/89 mmHg range were at twice the risk of developing hypertension than subjects with lower values (2). In the same year, the European Society of Hypertension and the European Society of Cardiology (ESH-ESC) published their guidelines for the management of arterial hypertension and, for the same range of BP, two different categories of BP were defined: normal BP (systolic BP of 120–129 mmHg, or diastolic BP of 80–84 mmHg) and high-normal BP (systolic BP of 130–139 mmHg, or diastolic BP of 85–89 mmHg) (3).

In 2007, the ESH-ESC committee decided against using the term “prehypertension” for several reasons (4). First, even in the Framingham study, the risk of developing hypertension was definitely higher in subjects with high-normal BP than in patients with normal BP (2,5), and therefore there is little reason to combine the two groups. Second, given the ominous significance of the word “hypertension” for the layman, the term “prehypertension” may, in many subjects, create anxiety and a request for unnecessary medical visits and examinations. Finally, although lifestyle changes recommended by the 2003 JNC VII guidelines for all prehypertensive individuals may be a valuable population strategy (1), in practice, this category is a highly differentiated one, with the extremes consisting of subjects with no need of any intervention (e.g., an …
DDW Report 2004 New Orleans: Reflux Disease and Barrett’s Esophagus
Authors: T. Rösch
Journal: Endoscopy (2004)

Gastroesophageal reflux disease (GERD) and Barrett’s esophagus (BE) are still major topics in the field of clinical research. More data are accumulating concerning the endoscopic diagnosis of subtle abnormalities, to allow better classification of patients into those who are endoscopy-positive or endoscopy-negative (nonerosive reflux disease). The situation with regard to endoscopic antireflux techniques has not become much clearer, although evidence appears to be gathering to show that they are not objectively effective. In Barrett’s esophagus (BE), many abstracts dealt with diagnostic techniques, as well as resection and ablation methods, without there being any substantial breakthroughs. As with the other Digestive Disease Week reports, only the most relevant studies are reported in detail here. The remaining abstracts are summarized in the tables.
Morbidity in diabetic and non-diabetic patients after major vascular surgery.
Authors: A Hjortrup, B F Rasmussen, H Kehlet
Journal: BMJ (1983)

In our study five of six index children (380% of families) who pre- sented with motor or psychomotor delay could have been diagnosed if all children who had not walked by the age of 18 months had had their creatine kinase activity estimated, as suggested by Gardner- Medwin.3A further seven (44% of families) presented with clum- siness of gait or excessive falling.Diagnosis in such cases requires familiarity with the typical Duchenne waddle and abnormal con- sistency of the calf muscles.Finally, no doctor should do or recom- mend Achilles tendon lengthening operations until the aetiology is firmly established.Against a background of a relatively rare but important disease-whose prevalence of 3/100 000 means that a considerable number of family practitioners will have no case on their panels-a series of well designed circulars sent to all relevant practitioners, together with financial support for attendance at clinical demonstrations, could provide a real and inexpensive alternative to a newborn screening programme.Such a programme would also circumvent the problem of causing unnecessary distress to parents by diagnosing an incurable disease in the neonatal period.3We thank the Muscular Dystrophy Group of Great Britain for their support.