tbuckley/cabot-search huggingface dataset:
Continuous In-vitro Cultivation of the Human Malaria Parasite
Authors: LOUIS H. MILLER
Journal: Annals of Internal Medicine (1978)

Editorial Notes1 September 1978Continuous In-vitro Cultivation of the Human Malaria ParasiteLOUIS H. MILLER, M.D., F.A.C.P.LOUIS H. MILLER, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-89-3-418 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptSometimes an advance in biomedical research deserves to be highlighted in a clinical journal even though the work does not have immediate application to the practice of medicine. One such advance was the continuous in-vitro cultivation of the asexual stages ofPlasmodium falciparumin erythrocytes by Trager and Jensen (1). Bass and Johns (2) first attempted this in 1912 and were able to maintain the parasite through three cycles (6 days). They predicted that within a year their methods would be obsolete and the parasite would be growing continuously in culture. Like the long search by Howard Carter and Lord...References1. TRAGERJENSEN WJ: Human malaria parasites in continuous culture. Science 193:673-675, 1976 CrossrefMedlineGoogle Scholar2. BASSJOHNS CF: The cultivation of malarial plasmodia (Plasmodium vivax and Plasmodium falciparum) in vitro. J Exp Med 16:567-579, 1912 CrossrefMedlineGoogle Scholar3. HAYNESDIGGSHINESDESJARDINS JCFR: Culture of human malaria parasites (Plasmodium falciparum). Nature 263:767-769, 1976. CrossrefMedlineGoogle Scholar4. USAID/WHO workshops on the biology and in-vitro cultivation of malaria parasites. Bull WHO 55:121-430, 1977 Google Scholar5. : Chemoprophylaxis of malaria. Morbid Mortal Weekly Rep 27 (10) (suppl): 81-90, 10 March, 1978 Google Scholar6. THOMPSONWERBEL PL: Antimalarial Agents. Chemistry and Pharmacology. New York, Academic Press, 1972 Google Scholar7. COATNEY G: Pitfalls in a discovery: the chronicle of chloroquine. Am J Trop Med Hyg 12:121-128, 1963 CrossrefMedlineGoogle Scholar8. TRENHOLMEWILLIAMSDESJARDINSFRISCHERCARSONRIECKMANNCANFIELD GRRHPKC: Mefloquine (WR 142, 490) in the treatment of human malaria. Science 190:792-794, 1975 CrossrefMedlineGoogle Scholar9. MILLER L: Current prospects and problems for a malaria vaccine. J Infect Dis 135:855-864, 1977 CrossrefMedlineGoogle Scholar10. CARTERBEACH RR: Gametogenesis in culture by gametocytes of Plasmodium falciparum. Nature 270:240-241, 1977 CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Laboratory of Parasitic Diseases National Institute of Allergy and Infectious Diseases National Institutes of Health Bethesda, Maryland PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 September 1978Volume 89, Issue 3Page: 418-419KeywordsMalariaPlasmodium falciparum Issue Published: 1 September 1978 PDF downloadLoading ...
Cytokine-induced free radicals and their roles in myocardial dysfunctions
Authors: G Bkaily
Journal: Cardiovascular Research (1999)

See article of Cheng et al. [9] ( pages 651 -659) in thisperoxynitrite (ONOO ), could be the element contributing issue.to the development of cardiovascular dysfunction [6].Amazingly, in several animal models, improved hemo-Recent studies dealing with oxygen free radicals and dynamic function were reported after treatment with free nitric oxide (NO) have demonstrated their implications in radicals scavengers, antioxidant vitamins, NO inhibitors or diseases such as inflammation, ischemia-reperfusion in-ACE inhibitors [5,7,8].It seems that one of main sources jury and several other cardiovascular dysfunctions [1][2][3][4].of free radicals is activated neutrophils, which by their Activated oxygen species, such as singlet oxygen, infiltration into the injured cardiac zone, contribute to free 2 superoxide anion (O ), hydrogen peroxide (H O ) and radical dependent pathogenesis of heart diseases in several 2 2 2 2 hydroxyl radical (OH ) are highly unstable, extremely species including man.The study by Cheng et al. [9] in reactive and highly toxic [4].Superoxide anions are this issue provides first hand evidence that intra-coronary 2 usually required for the generation of H O and OH .The administration of microspheres coated with interleukin-1b 2 2
The effect of fluticasone propionate aqueous nasal spray on nasal mucosal inflammation in perennial allergic rhinitis
Authors: T. Godthelp, A. F. Holm, H. Blom, A. Klein‐Jan, E. Rijntjes, W. J. Fokkens
Journal: Allergy (1995)

Mast cell degranulation, and the subsequent recruitment of infiltrating inflammatory cells, such as eosinophils, into the nasal mucosa has long been considered the most important model to explain allergic rhinitis. Several studies show a decrease in the number of eosinophils and possibly also mast cells during local corticosteroid treatment. Over the last decade, a new model to explain allergic inflammation has evolved. In this model, Langerhans’cells and T‐cells play an important role. Langerhans’cells possess a high affinity receptor for IgE. In patients with allergic rhinitis, allergen provocation results in stimulation of T‐cells by the IgE‐positive Langerhans’cells. The T‐cells produce a number of cytokines which stimulate IgE production as well as the inflammatory reaction. The number of T‐cells is not usually influenced by corticosteroid treatment; however, the function of the T‐cells, shown by the spectrum of cytokines produced, is clearly influenced. The cells that are most dramatically affected by local corticosteroid treatment are the Langerhans’cells, which completely disappear during treatment. This decrease suggests that there is a reduction in antigen presentation. The subsequent decrease in T‐cell stimulation may result in a reduction of the reactions that are dependent on T‐cell‐derived mediators.
Abstract 4479: Targeting non-small cell lung cancer cells harboring a PIK3CA mutation by a novel and oral PI3K selective inhibitor, PF-4989216
Authors: Marlena Walls, Pramod P. Mehta, Sangita M. Baxi, Kevin Liu, Chunze Li, Tod Smeal, Min-Jean Yin
Journal: Cancer Research (2011)

Abstract Aberrant phosphatidylinositol 3-kinase (PI3K)/AKT signaling occurs commonly in cancer. Gene mutation, amplification, and copy number gains of the PI3K catalytic subunit p110α have been shown in a variety of human cancers. The tumor suppressor phosphatase and tensin homologue deleted on chromosome 10 (PTEN) dephosphorylates the 3-phosphoinositides and is frequently mutated, deleted, or down-regulated in many cancers to constitutively activate the PI3K pathway. In response to activation, PI3Ks phosphorylate membrane phosphatidylinositides to generate phosphatidylinositol 3,4,5-triphosphate (PIP3); PIP3 serves as an secondary messenger activating AKT and 3’-phosphoinositide-dependent kinase-1 (PDK1). Phosphorylation of AKT at threonine-308 (T308) by PDK1 and serine-473 (S473) by mTORC2 fully activates the AKT pathway to regulate various cellular processes including cell growth, proliferation, survival, and metabolism. Several inhibitors targeting the PI3K pathway have been developed in preclinical discovery or clinical trials; however, a small molecule inhibitor has not yet been approved for cancer treatment. Most inhibitors have inhibitory activity against both PI3Ks and mTOR kinases. The mTORC1 and mTORC2 complexes control critical pathways regulating cell proliferation, apoptosis, angiogenesis, and metabolism through AKT-dependent and AKT-independent mechanisms. Therefore, agents targeting PI3K with additional mTOR kinase inhibitory activities may carry extra toxicity through the disruption of mTOR function in normal cells. To develop a drug selectively targeting PI3K, we have identified PF-4989216 as a novel potent and selective PI3K inhibitor. In this study, we describe the in vitro and in vivo anti-tumor activity of PF-4989216 in human non-small-cell lung cancer cells (NSCLCs). PF-4989216 inhibits the phosphorylation of PI3K downstream molecules and subsequently leads to inhibition in cell proliferation and xenograft tumor growth in NSCLCs harboring a PIK3CA mutation, including an erlotinib resistant line, NCI-H1975. Although PF-4989216 inhibits the phosphorylation of PI3K downstream molecules in the NSCLCs with PTEN loss (NCI-H1650), PF-4989216 does not sufficiently induce anti-tumor efficacy in NCI-H1650. Our results suggest that there may be a different tumorigenesis mechanism between PIK3CA mutation and PTEN loss in NSCLCs, and indicate that PF-4989216 is a potential cancer drug candidate for erlotinib resistant non-small-cell lung cancer patients with PIK3CA mutation. 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 4479. doi:10.1158/1538-7445.AM2011-4479
Micro-RNA-34a Contributes to the Impaired Function of Bone Marrow-Derived Mononuclear Cells From Patients With Cardiovascular Disease
Authors: Quanfu Xu, Florian H. Seeger, Jessica Castillo, Kazuma Iekushi, Reinier A. Boon, Ruxandra Farcas, Yosif Manavski, Yi-Gang Li, Birgit Assmus, Andreas M. Zeiher, Stefanie Dimmeler
Journal: Journal of the American College of Cardiology (2012)
Effect of erythromycin on endotoxin-induced microvascular leakage in the rat trachea and lungs.
Authors: J Tamaoki, E Tagaya, I Yamawaki, N Sakai, A Nagai, K Konno
Journal: American Journal of Respiratory and Critical Care Medicine (1995)

To determine whether the macrolide antibiotic erythromycin prevents microvascular leakage produced by lipopolysaccharide (LPS), we studied tracheae and lungs of pathogen-free rats. Tracheal vascular permeability and neutrophil recruitment were assessed by the percent area occupied by Monastral blue-labeled blood vessels and by myeloperoxidase-containing granulocytes, respectively, in tracheal whole mounts. Pulmonary microvascular leakage was evaluated by lung wet-to-dry (W/D) weight ratio. Inhalation of Escherichia coli LPS (5 mg/kg) caused time-dependent increases in tracheal vascular permeability, neutrophil influx, and lung W/D ratio. These responses were inhibited by pretreatment with oral erythromycin, but not by ampicillin or cefaclor, in a dose-dependent manner: erythromycin at 10 mg/kg daily for 1 wk reduced the area density of Monastral blue-labeled vessels from 6.7 +/- 1.2 to 1.4 +/- 0.3% (p < 0.01), the number of neutrophils (from 365 +/- 51 to 149 +/- 30 cells/mm2, p < 0.01), and lung W/D weight ratio (from 6.76 +/- 0.30 to 5.39 +/- 0.21, p < 0.01). This inhibitory effect of erythromycin was abolished by depletion of circulating neutrophils with cyclophosphamide. These results suggest that LPS causes acute lung injury, microvascular leakage, and neutrophil recruitment in the trachea, and that erythromycin protects against these changes, probably by acting on neutrophils.
Profiling Care Provided by Different Groups of Physicians: Effects of Patient Case-Mix (Bias) and Physician-Level Clustering on Quality Assessment Results
Authors: Sheldon Greenfield, Sherrie H. Kaplan, Richard Kahn, John Ninomiya, John L. Griffith
Journal: Annals of Internal Medicine (2002)

Background: Patient characteristics (case-mix bias) and physician-level variation (clustering) are often overlooked in profiling the quality of care provided by different groups of physicians, such as specialties. Objective: To examine the effect of case-mix bias and physician-level clustering on differences in quality of diabetes care between specialty groups participating in the American Diabetes Association's Provider Recognition Program. Design: Retrospective record review of both process and outcome measures over 1 year and a cross-sectional patient survey. The sample included 29 solo and group practice sites in diverse regions of the United States. Of the 29 sites, 15 were endocrinology sites and 14 were primary care sites. Patients: 1750 adults with diabetes. Measurements: Process measures included frequency of hemoglobin A1c, lipid, and urine protein testing; blood pressure measurement; and foot and eye examinations. Outcome measures included A1clevel, blood pressure, lipid levels, and patient satisfaction. Patient case-mix variables included age, sex, health status, level of education, ethnic minority status, and duration of diabetes. Results: Unadjusted differences between endocrinologists and generalists were statistically significant for most process and outcome measures. Inclusion of patient case-mix variables reduced the statistical significance of specialty differences for some quality measures. After accounting for the substantial physician-level clustering, observed differences between specialties were no longer statistically significant for any of the quality measures except patient satisfaction. Conclusions: The findings underscore the importance of designing physician profiling studies with sufficient power to account for physician-level variation (clustering) as well as patient case-mix. Studies that are not designed with both sufficient numbers of physicians and patients per physician may distort differences in quality of care between physician groups.
PRESSURE VOLUME LOOP ANALYSIS IN PATIENTS WITH SINGLE VENTRICLES: COMPARISON OF PRESSURE-VOLUME LOOP AND NON-INVASIVE MEASURES OF SYSTOLIC FUNCTION
Authors: Shahryar Chowdhury, Ryan Butts, Jason Buckley, Anthony Hlavacek, Sachin Khambadkone, Tain-Yen Hsia, G. Hamilton Baker
Journal: Journal of the American College of Cardiology (2013)
THE SCINTILLATING SCOTOMA OR TRANSIENT FUNCTIONAL HEMIOPIA.
Authors: CHARLES J. KIPP
Journal: JAMA (1905)

The phenomenon of scintillating scotoma is well known, though it is not always described in the text-books on diseases of the eye. My interest in this affection dates back many years, when I became more intimately acquainted with it through<i>personal experience</i>. Since then I have talked with many physicians, and especially ophthalmologists, who also had knowledge of it from personal experience, and what I have thus gathered is recorded here. It should be of particular interest to the general practitioner because patients suffering from this disturbance for the first time are greatly alarmed and apply to their family physician for relief. This condition was first described, so far as I know, in a dissertation by Vater and Heinecke,<sup>1</sup>in 1723. Since then many men eminent in medicine and in the natural sciences have described this condition as they have observed it. Various names have been
Disappearance of cyclin A correlates with permanent withdrawal of cardiomyocytes from the cell cycle in human and rat hearts.
Authors: M Yoshizumi, W S Lee, C M Hsieh, J C Tsai, J Li, M A Perrella, C Patterson, W O Endege, R Schlegel, M E Lee
Journal: Journal of Clinical Investigation (1995)

The regulated expression of cyclins controls the cell cycle. Because cardiomyocytes in adult mammals withdraw permanently from the cell cycle and thus cannot regenerate after injury, we examined cyclin expression during development by comparing cyclin A-E mRNA levels in fetal and adult human hearts. Cyclin B mRNA was detectable in adult hearts, although at a level markedly lower than that in fetal hearts. Levels of cyclin C, D1, D2, D3, and E mRNA were essentially identical in the two groups. In contrast, cyclin A mRNA was undetectable in adult hearts whereas cyclin A mRNA and protein were readily detectable in fetal hearts and cardiomyocytes, respectively. We then measured cyclin A mRNA and protein levels in rat hearts at four stages of development (fetal and 2, 14, and 28 d). Cyclin A mRNA and protein levels decreased quickly after birth (to 37% at day 2) and became undetectable within 14 d, an observation consistent with reports that cardiomyocytes stop replicating in rats by the second to third postnatal week. This disappearance of cyclin A gene expression in human and rat hearts at the time cardiomyocytes become terminally differentiated suggests that cyclin A downregulation is important in the permanent withdrawal of cardiomyocytes from the cell cycle.
Persistent hepatitis C viremia after acute self-limiting posttransfusion hepatitis C
Authors: Josep M. Barrera, Miguel Bruguera, Guadalupe M. Ercilla, Cristina Gil, Raquel Celis, Pilar M. Gil, Valle M. Del Onorato, Joan Rodés, Antoni Ordinas
Journal: Hepatology (1995)

Persistent viremia after clinical or subclinical hepatitis C virus (HCV) infection is believed to occur in patients with chronic hepatitis C, but little is known about the duration of HCV replication in patients with acute hepatitis who have recovered or the relation of HCV viremia with the kinetics of antibodies to HCV (anti-HCV). We tested HCV-RNA and anti-HCV in serial serum samples from 41 patients with posttransfusion non-A, non-B hepatitis, followed for an average of 6 years after transfusion. Serum HCV-RNA was measured by nested polymerase chain reaction, which used primers from the 5' untranslated region of the HCV genome. Anti-HCV were tested with first- and second-generation enzyme-linked immunosorbent assays (ELISA 1 and ELISA 2), and with a second-generation recombinant immunoblot assay. Of the 41 patients, 10 recovered and 31 progressed to chronic liver disease. HCV-RNA was detected in serum before or simultaneously with the onset of hepatitis in all cases, and lasted between 2 and 6 weeks in 5 of the 10 patients who recovered, whereas it persisted for the entire follow-up period in every case with chronic hepatitis and in the remaining 5 patients with self-limiting hepatitis. Anti-HCV were detected with ELISA 2 in the first serum sample, with raised serum transaminases in 57% of patients, but in only 6% with ELISA 1. In the sample obtained 1 month after the onset of hepatitis, anti-HCV were detected with ELISA 2 in 94% of patients, but in 34% with the ELISA 1.(ABSTRACT TRUNCATED AT 250 WORDS)
Fibronectin enhances the opsonic and protective activity of monoclonal and polyclonal antibody against group B streptococci.
Authors: H R Hill, A O Shigeoka, N H Augustine, D Pritchard, J L Lundblad, R S Schwartz
Journal: The Journal of Experimental Medicine (1984)

We have investigated the opsonic and protective effects of fibronectin (FN) against type III group B streptococci. When used by itself, the FN failed to promote actual internalization of group B organisms. The addition of FN to group B streptococci that had been preopsonized in an immunoglobulin preparation modified for intravenous use ( IgIV ) or a type-specific, murine monoclonal antibody of IgG isotype markedly enhanced interaction with human polymorphonuclear leukocytes (PMN). A similar enhanced effect was observed when the FN was combined with type-specific monoclonal antibody preparations of IgM and, surprisingly, IgA isotype. Preincubation experiments indicated that the major effect was upon the PMN rather than directly on the bacteria, but we could not demonstrate an effect of FN on cell surface receptors for the Fc fragment of Ig or C3b using rosetting techniques. In addition to enhancing the in vitro opsonic activity of Ig, the FN significantly increased the protective effect of the polyclonal and monoclonal Ig preparations in an animal model of neonatal group B streptococcal disease. Thus, FN appears to have a critical role in the host defense mechanisms against group B streptococci.
The Pathogenesis of Diffuse Pulmonary Fibrosis: An Ultrastructural Study.
Authors: D. H. Bowden
Journal: Annals of Internal Medicine (1968)

s1 May 1968The Pathogenesis of Diffuse Pulmonary Fibrosis: An Ultrastructural Study.D. H. Bowden, M.D., J. P. Wyatt, M.D.D. H. Bowden, M.D.Search for more papers by this author, J. P. Wyatt, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-68-5-1184_3 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptStudy of the pathology of the end stages of diffuse idiopathic pulmonary fibrosis rarely provides any indication to the pathogenesis of the process.This investigation was directed to the elucidation of the end phases by the ultrastructural study of lung biopsies. In the early stages of pulmonary fibrosis two distinctive tissue responses may be observed. One, which is characterized by a florid alveolar cell proliferation and desquamation, suggests that the injury is primarily of an epithelial nature. The other, exemplified by such clinicopathologic conditions as "alveolar proteinosis" and "diffuse pulmonary hemosiderosis," indicates that the dominant site of injury is in... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Winnipeg, PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 May 1968Volume 68, Issue 5Page: 1184-1185KeywordsBiopsyCell proliferationDesquamationInterstitial lung diseasesLungsPathogenesisProteinsPulmonary fibrosis Issue Published: 1 May 1968 PDF DownloadLoading ...
Antibiotic Dosing—Does One Size Fit All?
Authors: Jerome J. Schentag
Journal: JAMA (1998)

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
The Transcription Factor NFAT Promotes Exhaustion of Activated CD8 + T Cells
Authors: Gustavo J Martinez, Renata M Pereira, Tarmo Äijö, Edward Y Kim, Francesco Marangoni, Matthew E Pipkin, Susan Togher, Vigo Heissmeyer, Yi Chen Zhang, Shane Crotty, Edward D Lamperti, K Mark Ansel, Thorsten R Mempel, Harri Lähdesmäki, Patrick G Hogan, Anjana Rao
Journal: Immunity (2015)
A Mind That Found Itself: An Autobiography
Authors: Leon D. Hankoff
Journal: JAMA (1982)

This account by Clifford Beers of his psychiatric illness and consequent dedication to changing the conditions of care for the mentally ill is well known and established as a classic in its field. Its reprinting now, for the 41st time, is welcome in keeping the work readily available. The wisdom contained in its bare 200 pages for both laymen and professionals cannot be touched on in this review. In 1900, at age 24, Beers experienced his first psychotic depression, beginning a lifelong struggle with manic-depressive illness (now termed bipolar affective disorder). While this catamnesis can be read with great profit by the psychiatrist, Beers' depiction of the inhumanity dealt a mental patient has considerable relevance to the political and social forces shaping the care of the mentally ill today. It is safe to say that the more overt forms of patient abuse experienced by Beers and fellow patients in mental