tbuckley/cabot-search huggingface dataset:
PAROXYSMAL VENTRICULAR TACHYCARDIA: REPORT OF A CASE SHOWING THE PHASES OF RECOVERY RECORDED BY ELECTROCARDIOGRAPH
Authors: J A COLLINS
Journal: Annals of Internal Medicine (1946)

Case Reports1 December 1946PAROXYSMAL VENTRICULAR TACHYCARDIA: REPORT OF A CASE SHOWING THE PHASES OF RECOVERY RECORDED BY ELECTROCARDIOGRAPHJAMES A. COLLINS JR., M.D.JAMES A. COLLINS JR., M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-25-6-981 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe uncommon finding of paroxysmal ventricular tachycardia with the phases of recovery recorded by electrocardiograph prompted this communication. The usual prognosis in such a case is quite grave, and since this patient recovered under therapy in spite of serious myocardial damage, it was thought worth while to report it.CASE REPORTW. E., a white male, aged 64, was admitted to the hospital by ambulance. He had suffered from a severe attack of precordial pain two years previously. The pain radiated down the left arm and was accompanied by dyspnea, weakness, and perspiration. Apparently, this was a coronary occlusion, although... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Danville, Pennsylvania*Received for publication August 6, 1945.From the Department of Medicine, Geisinger Memorial Hospital, Danville, Penna. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 December 1946Volume 25, Issue 6Page: 981-985KeywordsAmbulancesDyspneaElectrocardiographyHospital medicineSweatVentricular tachycardia ePublished: 1 December 2008 Issue Published: 1 December 1946 PDF downloadLoading ...
Virus-induced airway obstruction and parasympathetic hyperresponsiveness in adult rats.
Authors: R Sorkness, J J Clough, W L Castleman, R F Lemanske
Journal: American Journal of Respiratory and Critical Care Medicine (1994)

Viral respiratory infections in humans have been associated with exacerbations of late allergic responses and asthma, as well as with airway abnormalities that persist after resolution of the acute infection. We hypothesized that augmented parasympathetic contractile mechanisms may contribute to postviral airway dysfunction. We studied airway physiology in anesthetized rats at 1 to 8 wk after inoculation with Parainfluenza 1 virus or vehicle. The virus groups had airway obstruction (abnormal lung mechanics, gas exchange and residual volume), and increased sensitivity to intravenous methacholine at 1 to 4 wk, although methacholine hypersensitivity was minimal in vagotomized rats; these abnormalities were absent at 7 to 8 wk after inoculation. Airway responses to vagal parasympathetic nerve stimulation were enhanced markedly at 1 to 4 wk, and significantly at 7 to 8 wk, after viral inoculation. Dysfunction of M2 muscarinic autoreceptors during acute viral infection was indicated by a significant attenuation of gallamine-induced augmentation of airway parasympathetic responses; in contrast, gallamine-augmentation of parasympathetic responses at 2 to 8 wk after viral inoculation was not different from noninfected control animals. We conclude that respiratory virus infection in rats produces airway dysfunction that remains for weeks after resolution of the acute infection, and that is caused in part by parasympathetic hyperresponsiveness, associated both with M2 autoreceptor malfunction and with M2-independent mechanism(s).
Analysis of Immune Responses and Serological Cross Reactivities among Vibrio cholerae O1, Shigella flexneri 2a and Haemophilus influenzae b
Authors: Fazle Rabbi, Nasreen Sultana, Tasmina Rahman, H M Al-Emran, M Nizam Uddin, Mahbub Hossain, Kazi Selim Anwar, Mahmuda Yasmin, Jamalun Nessa, Chowdhury R Ahsan
Journal: Cellular and Molecular Immunology (2008)
ONTOGENY OF MACROPHAGE RESISTANCE TO MOUSE HEPATITIS IN VIVO AND IN VITRO
Authors: Ruth Gallily, Anne Warwick, Frederik B. Bang
Journal: The Journal of Experimental Medicine (1967)

Adult or weanling C(3)H mice were found to be genetically resistant to a strain of mouse hepatitis virus. Infant C(3)H mice, however, developed infection and died from mouse hepatitis virus when minimal infectious doses of virus were given to them. There was a delay in the time of death compared to that of the genetically susceptible strain, and the virus recovered from these mice had increased pathogenicity for C(3)H mice. The ontogeny of resistance to hepatitis in the C(3)H mice thus progresses from delayed susceptibility to complete resistance as the age of the host increases. It is reflected in increased resistance of macrophages derived in vitro from liver cultures of infant mice of different ages. This increase in resistance with age was reduced by maintaining the cultures for a longer period of time before inoculation, or by increasing the number of explants in a given culture. Resistant cells were uniformly furnished by mice age 16 days, or more. It is concluded that a process of maturation of resistance of the cells takes place after the mice are born, but that this does not continue under in vitro conditions, and that it may be modified by the environment of the cells.
The micro-RNA 199b-5p regulatory circuit involves Hes1, CD15, and epigenetic modifications in medulloblastoma
Authors: Immacolata Andolfo, Lucia Liguori, Pasqualino De Antonellis, Emilio Cusanelli, Federica Marinaro, Francesca Pistollato, Livia Garzia, Gennaro De Vita, Giuseppe Petrosino, Benedetta Accordi, Roberta Migliorati, Giuseppe Basso, Achille Iolascon, Giuseppe Cinalli, Massimo Zollo
Journal: Neuro-Oncology (2012)

Micro-RNA (miR) 199b-5p targets Hes1 in medulloblastoma, one of the downstream effectors of both the canonical Notch and noncanonical Sonic Hedgehog pathways. In medulloblastoma patients, expression of miR-199b-5p is significantly decreased in metastatic cases, thus suggesting a downregulation mechanism. We studied this mechanism, which is mediated mostly by Hes1 and epigenetic promoter modifications. The miR-199b-5p promoter region was characterized, which identified a Hes1 binding site, thus demonstrating a negative feedback loop of regulation. MiR-199b-5p was shown to be downregulated in several medulloblastoma cell lines and in tumors by epigenetic methylation of a cytosine-phosphate-guanine island upstream of the miR-199b-5p promoter. Furthermore, the cluster of differention (CD) carbohydrate antigen CD15, a marker of medulloblastoma tumor-propagating cells, is an additional direct target of miR-199b-5p. Most importantly, regulation of miR-199b-5p expression in these CD15+/CD133+ tumor-propagating cells was influenced by only Hes1 expression and not by any epigenetic mechanism of regulation. Moreover, reverse-phase protein array analysis showed both the Akt and extracellular-signal-regulated kinase pathways as being mainly negatively regulated by miR-199b-5p expression in several medulloblastoma cell lines and in primary cell cultures. We present here the finely tuned regulation of miR-199b-5p in medulloblastoma, underlining its crucial role by its additional targeting of CD15.
Functional Limitations in Elderly Female Cancer Survivors
Authors: Carol Sweeney, Kathryn H. Schmitz, DeAnn Lazovich, Beth A. Virnig, Robert B. Wallace, Aaron R. Folsom
Journal: JNCI Journal of the National Cancer Institute (2006)

The elderly population, including many who are long-term cancer survivors, is increasing. Aspects of quality of life in elderly cancer survivors are not well understood.Subjects were women who enrolled in a population-based cohort study in 1986. At follow-up in 1997, 25,719 women, at a median age of 72 years, reported on functional limitations. We used logistic regression to calculate prevalence odds ratios (ORs) and proportional hazards regression to calculate prevalence ratios (PRs) for associations between cancer survivor status and functional limitations, adjusting for baseline (precancer) characteristics including obesity, smoking, and diabetes.Women who were cancer survivors for less than 2 years reported the most functional limitations, but long-term (5 or more years) cancer survivors remained more likely than cohort members who had not had cancer to report that they were unable to do heavy household work (42% of 1068 5-year survivors, versus 31% of 23 501 who never had cancer, multivariable OR = 1.47, 95% confidence interval [CI] = 1.27 to 1.69; PR = 1.22, 95% CI = 1.10 to 1.34), unable to walk a half mile (26% versus 19%, OR = 1.31, 95% CI = 1.1 to 1.54; PR = 1.16, 95% CI = 1.02 to 1.32), and unable to walk up and down stairs (9% versus 6%, OR = 1.34, 95% CI = 1.05 to 1.72; PR = 1.25, 95% CI = 1.00 to 1.56). The increased prevalence of functional limitations was apparent for 5-year survivors of breast cancer and also certain other cancers.Our findings support the need to target elderly cancer survivors for interventions to maintain or regain physical function.
Systemic Oncolytic Herpes Virus Therapy of Poorly Immunogenic Prostate Cancer Metastatic to Lung
Authors: Susan Varghese, Samuel D. Rabkin, Petur G. Nielsen, Wenzheng Wang, Robert L. Martuza
Journal: Clinical Cancer Research (2006)

Our goal was to evaluate whether systemic administration of NV1042, an interleukin-12 (IL-12)-expressing oncolytic herpes simplex virus, and its noncytokine parental vector NV1023 are effective against preexisting metastatic prostate cancer in an immunocompetent mice model.Metastatic TRAMP-C2 lung tumors established in C57Bl/6 or nude mice were treated on day 21 with four i.v. administrations of NV1042 or NV1023 and sacrificed on day 42 to assess virus efficacy and the potential mechanism of efficacy.NV1042 or NV1023 treatment was similarly effective in eliminating extrapleural and hemorrhagic tumors present in mock-treated mice. However, NV1042 was further effective compared with NV1023 in controlling the growth of lung tumors (as determined by mean surface tumor nodule number, lung weights, and surface tumor burden) and in extending survival. NV1042-treated mice exhibited a transient increase of serum IL-12 1 day posttreatment, whereas IL-12 levels in tumor bearing lungs persisted a further 2 days at least. Only splenocytes from NV1042-treated mice secreted IFN-gamma in response to TRAMP-C2 stimulation and displayed natural killer activity. The IL-12-mediated enhancement observed with NV1042 in the syngeneic model was abrogated in athymic mice treated in a similar manner, thus indicating a role for T cells in the augmented efficacy of NV1042 virus.Systemic administration of the IL-12-expressing NV1042 virus is more effective than its noncytokine parent, NV1023, against preestablished metastatic lung tumors. Given the clinical safety profile of NV1020, the parental vector of NV1023, and NV1042's enhanced efficacy and ability to activate the host immune system, NV1042 merits clinical consideration for treating metastatic prostate cancers.
t-Darpp Promotes Cancer Cell Survival by Up-regulation of Bcl2 through Akt-Dependent Mechanism
Authors: Abbes Belkhiri, Altaf A. Dar, Alexander Zaika, Mark Kelley, Wael El-Rifai
Journal: Cancer Research (2008)

Abstract t-Darpp is a cancer-related truncated isoform of Darpp-32 (dopamine and cyclic-AMP–regulated phosphoprotein of Mr 32,000). We detected overexpression of t-Darpp mRNA in two thirds of gastric cancers compared with normal samples (P = 0.004). Using 20 μmol/L ceramide treatment as a model for induction of apoptosis in AGS cancer cells, we found that expression of t-Darpp led to an increase in Bcl2 protein levels and blocked the activation of caspase-3 and caspase-9. The MitoCapture mitochondrial apoptosis and cytochrome c release assays indicated that t-Darpp expression enforces the mitochondrial transmembrane potential and protects against ceramide-induced apoptosis. Interestingly, the expression of t-Darpp in AGS cells led to ≥2-fold increase in Akt kinase activity with an increase in protein levels of p-Ser473 Akt and p-Ser9 GSK3β. These findings were further confirmed using tetracycline-inducible AGS cells stably expressing t-Darpp. We also showed transcriptional up-regulation of Bcl2 using the luciferase assay with Bcl2 reporter containing P1 full promoter, quantitative reverse transcription-PCR, and t-Darpp small interfering RNA. The Bcl2 promoter contains binding sites for cyclic AMP–responsive element binding protein CREB/ATF1 transcription factors and using the electrophoretic mobility shift assay with a CREB response element, we detected a stronger binding in t-Darpp–expressing cells. The t-Darpp expression led to an increase in expression and phosphorylation of CREB and ATF-1 transcription factors that were required for up-regulating Bcl2 levels. Indeed, knockdown of Akt, CREB, or ATF1 in t-Darpp–expressing cells reduced Bcl2 protein levels. In conclusion, the t-Darpp/Akt axis underscores a novel oncogenic potential of t-Darpp in gastric carcinogenesis and resistance to drug-induced apoptosis. [Cancer Res 2008;68(2):395–403]
Is Cocaine Desire Reduced by <i>N</i> -Acetylcysteine?
Authors: Steven D. LaRowe, Hugh Myrick, Sarra Hedden, Pascale Mardikian, Michael Saladin, Aimee McRae, Kathleen Brady, Peter W. Kalivas, Robert Malcolm
Journal: American Journal of Psychiatry (2007)

Animal models suggest that N-acetylcysteine inhibits cocaine-seeking. The present pilot study evaluated whether N-acetylcysteine would suppress reactivity to cocaine-related cues in cocaine-dependent humans.In this double-blind, placebo-controlled trial, 15 participants received N-acetylcysteine or placebo during a 3-day hospitalization. Participants were crossed over to receive the opposite condition on a second, identical 3-day stay occurring 4 days later. During each hospital stay, participants completed a cue-reactivity procedure that involved collecting psychophysical and subjective data in response to slides depicting cocaine and cocaine use.While taking N-acetylcysteine, participants reported less desire to use and less interest in response to cocaine slides and watched cocaine slides for less time.The inhibition of cocaine cue reactivity is consistent with existing preclinical data and supports the use of N-acetylcysteine as a treatment for cocaine dependence.
Long-term (37 years) clinical outcome of older women with early operable primary breast cancer managed in a dedicated clinic
Authors: B.M. Syed, S.J. Johnston, D.W.M. Wong, A.R. Green, L. Winterbottom, H. Kennedy, N. Simpson, D.A.L. Morgan, I.O. Ellis, K.L. Cheung
Journal: Annals of Oncology (2011)
OTX2 Is Critical for the Maintenance and Progression of Shh-Independent Medulloblastomas
Authors: David C. Adamson, Qun Shi, Matthew Wortham, Paul A. Northcott, Chunhui Di, Christopher G. Duncan, Jianjun Li, Roger E. McLendon, Darell D. Bigner, Michael D. Taylor, Hai Yan
Journal: Cancer Research (2009)

Abstract OTX2 is a developmentally regulated transcription factor involved in early morphogenesis of the central nervous system. This gene is amplified and overexpressed in medulloblastoma cell lines, but the nature and extent of its genetic alterations in primary tumors have not been evaluated. Analysis of a large cohort of primary medulloblastomas revealed frequent focal copy number gain of a region minimally containing OTX2 as a single gene. OTX2 copy number gain was restricted to tumor subtypes that did not express a molecular signature of Wnt or Shh pathway activation. FISH analysis revealed copy number gain in a subset of cells within medulloblastoma samples, suggesting a late event in tumor progression. Gain of OTX2 copy number was associated with the presence of anaplastic histologic features and shorter survival in medulloblastoma patients. In support of a functional role, ectopic OTX2 expression enhanced proliferation and tumorigenicity of immortalized primary cells, whereas OTX2 knockdown in medulloblastoma cells prolonged the survival of animals bearing xenograft tumors. Mechanistic investigations revealed upregulation of MYC as a potential mechanism whereby OTX2 promotes tumor progression. Our findings define OTX2 as an important oncogenic driver in medulloblastoma. Cancer Res; 70(1); 181–91
Ernest
Authors: J P B O'Connor
Journal: BMJ (2002)

I first met Ernest at the end of a busy surgical clinic. From his pallor and gaunt features I suspected that he might be terminally ill. He looked about 80 years old rather than his real age of 60. He complained of an inability to swallow food, breathlessness, and weight loss. I admitted him for urgent investigation, and an abdominal computed tomogram revealed inoperable gastric cancer with multiple metastases. He deteriorated and was referred for palliative care.

Ernest was an old fashioned sort, well mannered and courteous, quietly spoken, and above all a gentleman. He was single, had lived alone for most of his life, and had no surviving family. His main interests were attending his increasingly rare Air Force reunions and keeping up with old friends—a man content with simple pleasures. We quickly established a rapport, and it fell to me to tell him his diagnosis.

The change was extraordinary. He became confused and aggressive, unaware of his surroundings, confrontational and obstructive at every opportunity. Hypoxia, opiate analgesia, infection, and cerebral metastases were all considered as explanations for his altered behaviour.

On one morning ward round, as we left his cubicle, Ernest asked me to stay. He seemed more lucid and wanted to talk. He realised that his behaviour had changed and was frightened. He accepted death, but one fear remained. He was terrified at the idea of a postmortem examination and wanted his body to be left alone after he died. I explained that I would issue his death certificate, and a postmortem examination was not required for diagnosis and would therefore not be requested. Ernest was relieved. He became his old self again, a favourite of the staff, and two days later he died.

It is often difficult in clinical practice to identify the foremost concerns of our patients. After his diagnosis, Ernest feared one thing more than death itself. He worried that his body would be cut up after he died, and that he could do nothing to stop it. In my short career, I cannot recall giving a greater consolation to any patient than the guarantee that I gave Ernest, that when he died he could truly rest in peace.
Recruitment of histone deacetylases HDAC1 and HDAC2 by the transcriptional repressor ZEB1 downregulates E-cadherin expression in pancreatic cancer
Authors: Ali Aghdassi, Matthias Sendler, Annett Guenther, Julia Mayerle, Claas-Olsen Behn, Claus-Dieter Heidecke, Helmut Friess, Markus Büchler, Matthias Evert, Markus M Lerch, Frank Ulrich Weiss
Journal: Gut (2011)

<h3>Objective</h3> Pancreatic cancer is characterised by invasive tumour spread and early metastasis formation. During epithelial–mesenchymal transition, loss of the cell adhesion molecule E-cadherin is frequent and can be caused by genetic or epigenetic modifications, recruitment of transcriptional activators/repressors or post-translational modifications. A study was undertaken to investigate how E-cadherin expression in human pancreatic adenocarcinoma and pancreatic cancer cell lines is regulated. <h3>Methods</h3> In 25 human pancreatic cancer resection specimens, the coding region of the E-cadherin gene (CDH1) was sequenced for somatic mutations. The tumour samples and 11 established human pancreatic cancer cell lines were analysed by immunohistochemistry, western blot analysis, chromatin immunoprecipitation and methylation-specific PCR. The role of specific histone deacetylase inhibitors (HDACi) on pancreatic tumour cell migration and proliferation was studied in vitro. <h3>Results</h3> Neither somatic mutations nor CDH1 promoter hypermethylation were found to be responsible for downregulation of E-cadherin in pancreatic cancer. In the transcriptionally active CDH1 promoter, acetylation of histones H3 and H4 was detected whereas HDAC1 and HDAC2 were found attached only to a silent promoter. Expression of ZEB1, a transcription factor known to recruit HDACs, was seen in E-cadherin-deficient cell lines in which ZEB1/HDAC complexes were found attached to the CDH1 promoter. Moreover, knockdown of ZEB1 prevented HDAC from binding to the CDH1 promoter, resulting in histone acetylation and expression of E-cadherin. HDACi treatment attenuated tumour cell migration and proliferation. <h3>Conclusions</h3> These findings imply an important role for histone deacetylation in the downregulation of E-cadherin in human pancreatic cancer. Recruitment of HDACs to the CDH1 promoter is regulated by the transcription factor ZEB1, and inhibition of HDACs may be a promising antitumour therapy for pancreatic cancer.
Improving the Success of Treating Tobacco Smokers
Authors: Nancy A. Rigotti
Journal: JAMA Internal Medicine (2014)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Internal Medicine HomeNew OnlineCurrent IssueFor Authors Podcast 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) 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 Internal Medicine journal
A new family of genes coding for an antigen recognized by autologous cytolytic T lymphocytes on a human melanoma.
Authors: B Van den Eynde, O Peeters, O De Backer, B Gaugler, S Lucas, T Boon
Journal: The Journal of Experimental Medicine (1995)

Human melanoma MZ2-MEL expresses several distinct antigens that are recognized by autologous cytolytic T lymphocytes (CTL). Some of these antigens are encoded by genes MAGE-1, MAGE-3, and BAGE, which are expressed in a large fraction of tumors of various histological types but are silent in normal adult tissues with the exception of testis. We report here the identification of the gene coding for MZ2-F, another antigen recognized by autologous CTL on MZ2-MEL cells. This gene, which was named GAGE-1, is not related to any presently known gene. It belongs to a family of genes that are expressed in a variety of tumors but not in normal tissues, except for the testis. Antigenic peptide YRPRPRRY, which is encoded by GAGE-1, is recognized by anti-MZ2-F CTL on class I molecule HLA-Cw6. The two genes of the GAGE family that code for this peptide, namely GAGE-1 and GAGE-2, are expressed in a significant proportion of melanomas (24%), sarcomas (25%), non-small cell lung cancers (19%), head and neck tumors (19%), and bladder tumors (12%). About 50% of melanoma patients carry on their tumor at least one of the presently defined antigens encoded by the MAGE, BAGE, and GAGE genes.