tbuckley/cabot-search huggingface dataset:
The Blood Platelets in Pernicious Anemia After Liver Therapy
Authors: Savas Nittis
Journal: Annals of Internal Medicine (1931)

Article1 February 1931The Blood Platelets in Pernicious Anemia After Liver TherapySAVAS NITTISSAVAS NITTISSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-4-8-931 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptAll morphological constituents of the blood in pernicious anemia show quantitative changes with the onset of a remission.The present study deals with the changes in the numbers of the blood platelets in the relapse and during the development of remissions induced by liver therapy.METHODS OF STUDYIn the beginning of this study different so-called "wet methods" for counting blood platelets were employed. They were soon found to be difficult to execute and inconsistent in their results. A "dry method" was then employed that not only gave fairly satisfactory results but also had the advantage of permitting the counts... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Ann Arbor*From the Thomas Henry Simpson Memorial Institute for Medical Research of the University of Michigan, Ann Arbor, Michigan. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byPhysiologie und Pathologie des Antiperniciosaprinzips 1 February 1931Volume 4, Issue 8Page: 931-938KeywordsBloodLiverPernicious anemiaPlatelets ePublished: 1 December 2008 Issue Published: 1 February 1931 PDF downloadLoading ...
Comparison of the Efficacy of 9-Weeks Versus 52-Weeks of Adjuvant Trastuzumab Treatment in Her-2 Positive Early-Stage Breast Cancer with Axillary Lymph Node Metastases
Authors: M.A. Sendur, S. Aksoy, N. Ozdemir, O. Yazıcı, N. Zengin, M.K. Altundag
Journal: Annals of Oncology (2014)
Sensitivity of renal cell carcinoma (RCC) cell lines to Sorafenib in vitro is dependent upon Akt and GSK3β activity
Authors: Daniel Cho, David Panka, Peter A. Panka, Michael B. Atkins, James Mier
Journal: Cancer Research (2006)

Proc Amer Assoc Cancer Res, Volume 47, 2006

4515 

Introduction: Sorafenib (BAY 43-9006) is a multi-targeted inhibitor of VEGFR2, PDGFR, b-Raf, c-Raf, FLT3, C-KIT, and p38α that has shown promising activity in patients with metastatic RCC (Escudier B, et al, ASCO Proceedings 2005, LBA 4510). Sorafenib is thought to have an anti-angiogenic effect via inhibition of VEGFR and PDGFR in endothelial and perivascular cells as well as a direct anti-proliferative effect on tumor cells (Wilhelm SM, et al, Cancer Res 2004, 64: 7099). In an effort to better characterize this cytotoxic effect, baseline molecular characteristics of RCC cell lines with differential sensitivity to sorafenib were reviewed. We observed that a cell line with high baseline Akt activation, 769-P, was significantly more sensitive to sorafenib in vitro than a cell lines with low Akt activation. Recently, glycogen synthase kinase (GSK) 3β, a protein regulated by Akt, has been shown to have a critical role in tumor proliferation and survival (Shakoori A, et al, Biochem Biophys Res Comm, 334: 1365). In order to assess the dependence of sorafenib sensitivity of RCC cell lines on these signaling elements, the effect of modulating Akt and GSK3β expression on sorafenib-induced apoptosis was investigated. Methods: 769-P, 786-O, and caki-1 RCC cell lines were chosen for study. Akt expression was modulated using an adenovirus containing either a constitutively active or dominant negative Akt. GSK3β expression was altered using an siRNA to GSK3β and by transient transfection with a constitutively active GSK3β construct. GSK3β function was inhibited by treatment with AR-A014418, an inhibitor of GSK3β. RCC cell lines thus modified were treated overnight with sorafenib at 20μM concentration to determine effect on cytotoxic activity. Sorafenib concentration was titrated for suppression of STAT3 phosphorylation. Cells were then stained with propidium iodide (PI) to determine percent viability. Results: Increasing Akt activity by infection with an active Akt adenovirus significantly increased the sensitivity of cell lines with low baseline Akt activity (786-0 and caki-1) to sorafenib, while the dominant negative construct had no effect. Both the siRNA to GSK3β and AR-A014418 increased the cytoxicity of sorafenib treatment as determined by both PI staining and PARP cleavage. Transient transfection with constituitively active GSK3β appeared to have a protective effect on RCC cell lines treated with sorafenib. Conclusions: RCC cell lines demonstrate differential in vitro sensitivity to sorafenib. Higher baseline Akt activity in RCC cell lines correlates with sensitivity to sorafenib in vitro , while higher GSK3β activity correlates with resistance. The effect of Akt in sensitizing RCC cell lines to sorafenib may be mediated through inhibition of GSK3β. GSK3β is a potential novel target for RCC therapy.
SPONTANEOUS HEMOPNEUMOTHORAX: REPORT OF A CASE OCCURRING IN A SOLDIER
Authors: John Franklin
Journal: Annals of Internal Medicine (1945)

Excerpt The true incidence of spontaneous hemopneumothorax is unknown. Whereas the literature contains reports of sporadic cases, many cases are not reported, and many cases are misdiagnosed as hydropneumothorax, when roentgen evidence of fluid alone is accepted without the benefit of a diagnostic thoracentesis. In 1937, Hopkins1 collected 43 cases from the literature and reported three cases of his own. Hartzell2 in 1942, reported 40 selected cases from the literature and three cases observed at Cleveland City Hospital during the preceding 10 years. The apparent rarity of this complication of spontaneous pneumothorax prompts me to report the following case. CASE REPORT
Self-portrait After the Spanish Influenza
Authors: M Therese Southgate
Journal: JAMA (2005)

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
Studies of Guinea Pig Tumors II. The Induction of Malignant Tumors in Guinea Pigs by Methylcholanthrene
Authors: Herman T. Blumenthal, James B. Rogers
Journal: Cancer Research (1962)

Summary  More than 50 per cent of guinea pigs of two strains differing in their susceptibility to the development of spontaneous tumors developed sarcomas following the injection of methylcholanthrene into the abdominal wall. The majority of these tumors contained two or more mesenchymal components, including neurogenic, leiomyomatous, fibroblastic, lipoblastic, chondroblastic, osteoblastic, and primitive mesenchymal elements. Slightly less than 20 per cent of animals with tumors developed distant metastases, including lung, liver, heart, spleen, kidney, and adrenal. Metastasis, evidently, was blood-borne in many instances.  The data showed a trend toward a diminishing response with age, although, in animals developing tumors, age appeared to have no influence on the induction time. Survival time measured from the date of appearance of tumor was longest in the youngest group, although the rate of growth was also greatest in this group. The frequency of metastasis was lowest in the senile group.  No differences were noted concerning sex and strain in the induction of tumors or in the frequency of metastases.  The literature on the induction of tumors in guinea pigs by various agents, but particularly by hydrocarbons, has been reviewed and discussed. Guinea pigs appear to be susceptible to a number of types of tumor induction agents, responding by developing carcinomas or sarcomas, although they may be resistant to the development of lymphomas.
Abstract 4377: Novel RNAi agent can control HCV replication
Authors: Masahiko Kuroda, Masakatsu Takanashi, Shinichiro Ohno, Yoshiki Murakami
Journal: Cancer Research (2014)

Abstract Technique of RNA interference (RNAi) is important for investigating functional gene research and drug target. miRNA-122 (miR-122) is expressed abundantly in liver tissue, and it can control the Hepatitis C virus (HCV) replication. Locked Nucleic Acid (LNA)-miR-122 was shown to suppress HCV replication through inhibiting miR-122 function. Recently, anti-HCV therapy for chronic hepatitis C by LNA-miR-122 has been applied for clinical study in phase II. We developed alternative chemically modified sponge oligonucleotides (SO) for inhibition of interest miRNA function. In order to find more effective anti-viral agent, we attempted to compare the inhibition effects for viral replication between LNA-miR-122 and SO for miR-122. SO contained triplicated binding sites to miR-122, composed of either DNA or RNA, which were combined with terephthalate or glycine. We chose three types of sequences complementary to target miR-122: one perfect match sequence and two imperfect match sequences (bubble, and bulge). The effects of SOs on HCV replication were assessed by using HCV replicon cells (OR6), which contained full-genome HCV with genotype 1b and luciferase reporter genes. We compared the luciferase activity, the expression of HCV RNA, and the expression of HCV core protein in OR6 cells treated with LNA-miR-122 and several SO constructions. SO composed of terephthalate-bound RNA sequences with bulge-type imperfect complementarity was most effective in inhibiting HCV replication. By real-time qPCR analysis, the expression level of ISG15 and RIG-I in the OR6 cell treated with SO was not significantly higher than those treated with negative control (NC) or LNA. By XTT incorporation assay, the cell proliferation level in OR6 treated with SO was not also significantly affected as compared that treated with NC or LNA. We investigated novel RNAi agent termed SO that could effectively suppress HCV replication as compared LNA-miR-122. SO treatment did not activate the endogenous IFN pathway nor induce the cell mortality. Therefore SO is promising as a novel anti-vial agent. Citation Format: Masahiko Kuroda, Masakatsu Takanashi, Shinichiro Ohno, Yoshiki Murakami. Novel RNAi agent can control HCV replication. [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 4377. doi:10.1158/1538-7445.AM2014-4377
Treatment of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: A Systematic Review for a National Institutes of Health Pathways to Prevention Workshop
Authors: M.E. Beth Smith, Elizabeth Haney, Marian McDonagh, Miranda Pappas, Monica Daeges, Ngoc Wasson, Rongwei Fu, Heidi D. Nelson
Journal: Annals of Internal Medicine (2015)

Background: Myalgic encephalomyelitis (ME)/chronic fatigue syndrome (CFS) is a debilitating multisystem condition affecting more than 1 million adults in the United States. Purpose: To determine benefits and harms of treatments for adults with ME/CFS and identify future research needs. Data Sources: MEDLINE, PsycINFO, and Cochrane databases (January 1988 to September 2014); clinical trial registries; reference lists; and manufacturer information. Study Selection: English-language randomized trials of the effectiveness and adverse effects of ME/CFS treatments. Data Extraction: Data on participants, study design, analysis, follow-up, and results were extracted and confirmed. Study quality was dual-rated by using prespecified criteria; discrepancies were resolved through consensus. Data Synthesis: Among 35 treatment trials enrolling participants primarily meeting the 1994 Centers for Disease Control and Prevention and Oxford case definitions of CFS, the immune modulator rintatolimod improved some measures of exercise performance compared with placebo in 2 trials (low strength of evidence). Trials of galantamine, hydrocortisone, IgG, valganciclovir, isoprinosine, fluoxetine, and various complementary medicines were inconclusive (insufficient evidence). Counseling therapies and graded exercise therapy compared with no treatment, relaxation, or support improved fatigue, function, global improvement, and work impairment in some trials; counseling therapies also improved quality of life (low to moderate strength of evidence). Harms were rarely reported across studies (insufficient evidence). Limitation: Trials were heterogeneous and were limited by size, number, duration, applicability, and methodological quality. Conclusion: Trials of rintatolimod, counseling therapies, and graded exercise therapy suggest benefit for some patients meeting case definitions for CFS, whereas evidence for other treatments and harms is insufficient. More definitive studies comparing participants meeting different case definitions, including ME, and providing subgroup analysis are needed to fill research gaps. Primary Funding Source: Agency for Healthcare Research and Quality. (PROSPERO: CRD42014009779)
264. Non-Invasive Monitoring of the Response of Orthotopic Bladder Tumors to GM-CSF Gene Therapy Using the Prostate Specific Antigen Gene as a Reporter
Authors: Qinghui Wu, Ratha Mahendran, Kesavan Esuvaranathan
Journal: Molecular Therapy (2004)

Our purpose was to determine the feasibility and accuracy of modifying the murine bladder cancer cell line MB49 to secrete the prostate specific antigen (PSA) as a biomarker for monitoring orthotopic bladder tumor growth and to further evaluate the effectiveness of GM-CSF gene therapy in this model. The modified MB49-PSA cells behaved similarly to the parental cell line and produced high levels of PSA both in vitro and in vivo. In a subcutaneous model the level of PSA produced correlated with tumor volume (r=0.96). To test the model, MB49-PSA cells were implanted orthotopically into C57BL/6 mice. On the fourth day after implantation, small tumors measuring as small as 0.2–0.3mm in diameter were identified and these were sufficient to produce measurable PSA in both serum and urine. Mice with confirmed tumors were given liposome-mediated GM-CSF gene therapy on the fifth day after implantation. Therapy was administrated twice a week for 3 weeks intravesically. Tumor growth and response to treatment was monitored at 2–3 day intervals by measuring PSA level in mouse serum and urine samples by ELISA. Measurement of serum PSA level over the treatment period showed that tumor growth was inhibited by GM-CSF gene therapy. Up to 50% of the treated mice were cured. Cytokine array analysis revealed that GM-CSF gene therapy appeared to act by inducing the production of other cytokines and chemokines. Our results demonstrate that the PSA marker protein is constitutively expressed by MB49-PSA cells implanted in mice and changes in its serum levels reflect the tumor burden in vivo. Our results also indicated that liposome-mediated GM-CSF gene therapy is effective in treating murine bladder cancer. The study provides a simple, reliable and non-invasive method to evaluate therapeutic modalities such as gene therapy for bladder cancer Figure 1.
Reply
Authors: Farhan Haq, Sung‐Min Ahn
Journal: Hepatology (2015)

Potential conflict of interest: Nothing to report. Author names in bold designate shared co‐first authorship. We thank Panera and colleagues for their noteworthy comments on our article.1 They highlighted the role of the fibroblast growth factor 19 gene (FGF19) in hepatocellular carcinoma (HCC) using our data set and previously published studies. Moreover, they suggested the potential implication of FGF21 in FGF19‐related HCCs because FGF19 and FGF21 belong to the same family of ligands, which regulates glucose metabolism and bile acid synthesis in the liver. The FGF19 gene mainly functions through the FGFR4–KLB complex in hepatocyte tissues, whereas FGF21 mainly functions through the FGFR1–KLB complex in adipocyte tissues, suggesting a hepatocyte–adipocyte crosstalk in metabolic homeostasis.2 Despite the complementary roles of FGF19 and FGF21 in metabolic homeostasis, the relationship of these two genes in somatic changes has not been reported. Amplifications of FGF19 in HCC have been reported in several genomics studies.1 Recent studies have demonstrated that FGF19 plays key roles in hepatocarcinogenesis.5 Genetic aberrations in FGF21 have not been reported in liver cancer genomics studies. Up‐regulation of FGF21 in transgenic mouse models delayed or hampered HCC proliferation.6 When we investigated FGF21 in our data set upon the suggestion of Panera and colleagues, we found only one case with high copy amplification and two cases with missense mutations in FGF21 out of 231 HCC cases we analyzed. We could not find any relationship between the genetic aberrations of FGF19 and FGF21. Based on the observation from our data sets and previous reports, our conclusions are as follows: 1) the frequency of somatic changes in FGF21 is very low, 2) the somatic changes of FGF19 and FGF21 do not have any meaningful relationship, and 3) it may not be worth considering genetic aberrations in FGF19 and FGF21 together for alternative targeted strategies.
Abstract 20510: Aortic Valve Calcium Score for Paravalvular Aortic Insufficiency (AVCS II) Study in Transapical Aortic Valve Implantation
Authors: Martin Haensig, Lukas Lehmkuhl, Borek Foldyna, Axel Linke, Chirojit Mukherjee, Gerhard Schuler, Matthias Gutberlet, Friedrich W Mohr, David Holzhey
Journal: Circulation (2014)

Introduction: Transapical-aortic valve implantation (TA-AVI) has evolved into a routine procedure in selected elderly high-risk patients. However, more-than-mild paravalvular leaks remain a significant drawback of current TAVI systems. The aim was to study the impact of native aortic valve calcification on paravalvular leaks in cardiac contrast-enhanced computed tomography (CT). Methods: The degree and distribution of native valve calcification were quantified using an Aortic Valve Calcium Score (AVCS) for each cusp separately (3mensio Valves™ workstation, version 7.0, 3mensio Medical Imaging B.V., Netherlands). To exclude an artificial increase of the AVCS due to the presence of contrast material, we used a threshold for density [mean aortic density + 2*D] and volume [0, 3, 5, 25 and 50 mm 3 ] of calcification. AVCS was compared to the rate of paravalvular leaks, assessed intraoperatively by echocardiography and root angiography. Results: Eighty-eight consecutive patients prior to TA-AVI with preoperative CT aged 80.0 ± 5.7 years, 51.1 % female were included. Three prosthesis sizes were used for annular diameters up to 23 mm (n = 29), 26 mm (n = 45) and 29 mm (n = 14). Mean log. EuroSCORE was 24.6 ± 15.4 % and mean STS-Score was 8.4 ± 8.3 %. The mean AVCS in patients without paravalvular leaks (n = 42) was 606.4 ± 374.3; with mild paravalvular leaks (n = 39) was 761.2 ± 530.4; and with moderate paravalvular leaks (n = 5) was 792.4 ± 515.3 with the highest calcification in the non-coronary cusp. There was no significant association between the total AVCS and paravalvular leaks (χ 2 -statistic = 2.9; P = 0.13, 551 hounsfield units). The additional use of the volume-based threshold did not lead to an increase of the association between the AVCS and paravalvular leakages. Paravalvular leaks were significantly associated with the degree (r Spearman = 0.34; χ 2 -statistic = 10.0; P = 0.02) and location of eccentric calcified plaques. Conclusions: Quantification of aortic valve calcification in contrast enhanced computed tomography shows only a weak correlation with paravalvular leakage and is therefore not reliable as a predictor, respectively. The degree of eccentric cusp calcification was significantly associated with the occurrence and location of paravalvular leaks.
Identification of the naturally occurring genes encoding carbapenem-hydrolysing oxacillinases from Acinetobacter haemolyticus, Acinetobacter johnsonii, and Acinetobacter calcoaceticus
Authors: S. Figueiredo, R.A. Bonnin, L. Poirel, J. Duranteau, P. Nordmann
Journal: Clinical Microbiology and Infection (2011)
Vaginal delivery after caesarean section
Authors: B.-A. Daviss, K. C Johnson, I. M. Gaskin
Journal: BMJ (2001)

Medical Council is flawed as he assumes that Worcestershire Health Authority has power in managing its responsibility for a successful public health immunisation campaign. 1It is precisely because the authority is impotent as a public statutory public body that it asked the GMC to intervene.The continuing debate about measles, mumps, and rubella vaccine dents the confidence of many public and professional people, not least because of the assumption that there is no smoke without fire.Majeed's third reference indicates his anxiety despite his initial position statement on the safety of the vaccine.Patients and the media take heed of these different emphases.Maintaining a high level of vaccination cover against diseases that are seen rarely or not at all poses serious difficulties.Majeed's role as an educationalist-a position of power and responsibility-could provide a forum where these difficulties are debated.The role of medical journals and the media should not be ignored in that debate.Their keenness for headlines containing bad news, however misguided or ill informed, while
Starlings in the Rain, Wellesville, Ohio
Authors: James E. Lasry
Journal: JAMA (1999)

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