tbuckley/cabot-search huggingface dataset:
TMOD-12. AN ONCOLYTIC MEASLES VIRUS SENSITIVE GROUP 3 MEDULLOBLASTOMA MODEL IN IMMUNE-COMPETENT MICE
Authors: Sangeet Lal, Corey Raffel
Journal: Neuro-Oncology (2017)

Modified measles virus (MV) has demonstrated oncolytic efficacy in xenograft models of multiple tumor types using human cells in immune-deficient mice. However, MV does not grow in murine cells, thus, no murine tumor cell line that is oncogenic, grows in immune-competent mice, and is infectable by MV exists. The lack of such a model prevents an examination of the effect of anti-MV immunity and other possible effects of the immune system on MV oncotherapy. We have developed a murine Group 3 medulloblastoma cell line that allows replication of, and is killed by, MV in-vivo. Cerebellar stem cells isolated from P6 human CD46-transgenic immune-competent mice were transduced to express Sendai virus C-protein, c-Myc-Td tomato and GFI1B-GFP proteins. The cell line stably expresses higher levels of C-myc and GFI1B proteins but identical levels of N-myc and p53 when compared to unmodified cerebellar stem cells. Measles virus infects and replicates in the cell line, and cells are killed in a dose and time dependent manner with 55%, 85% and 92% cell death at MOI of 0.1, 1 and 10 respectively after 96h of MV infection. The cells express stem cell makers and NPR3, an established marker for the group 3 subtype of medulloblastoma. This cell line is highly tumorigenic when orthotopically implanted into the brain of syngeneic immune-competent mice. A single intratumoral injection of MV results in significant prolongation of median survival compared to mice injected with heat-killed virus (P=0.0027). Sixty percent of MV-treated mice did not die during the period of study and showed no evidence of tumor at autopsy. Autopsy of brains from inactivated virus treated animals revealed tumors resembling group 3 medulloblastoma in all mice. This is the first cell line and tumor model of any type available for testing the effect of an intact immune system on MV therapy.
Mechanisms of Differentiation in Melanoma Cells and Melanocytes
Authors: Dorothy C. Bennett
Journal: Environmental Health Perspectives (1989)

Literature is reviewed on the mechanisms of differentiation in mammalian melanoma cells and normal melanocytes. Pigment cells are particularly useful for studies requiring the observation of differentiation in living cells, for example, studies of commitment. Topics discussed include melanin synthesis and other markers of pigment cell differentiation; stochastic models of differentiation and commitment; the lability of early stages of differentiation; extracellular factors affecting pigment cell differentiation, with implications for intracellular controls; the role of proliferation and the cell cycle in differentiation, and the relative roles of changes in transcription, translation, and posttranslational processes.
Mycoplasma Pneumoniae.
Authors: Robert M. Chanock
Journal: Annals of Internal Medicine (1964)

s1 April 1964Mycoplasma Pneumoniae.Robert M. Chanock, M.D.Robert M. Chanock, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-60-4-733_4 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptNonbacterial pneumonia is a syndrome of multiple etiology. In certain age groups and ecologic settings adenovirus, parainfluenza, and respiratory syncytial viruses may play an important role. A large segment of this syndrome still awaits an etiologic explanation. The viral agents just described are not active in those nonbacterial pneumonia illnesses in which a cold agglutinin response occurs during convalescence.During the past 5 years epidemiologic and volunteer studies have established that the organism originally described by Eaton and associates in 1944, is the etiologic agent in a majority of cold agglutinin positive pneumonia illnesses. Recently the Eaton agent has been... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Bethesda, Maryland PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byDEXTRAN 1 April 1964Volume 60, Issue 4Page: 733-734KeywordsAge groupsAgglutininsConvalescenceEpidemiologyEtiologyMycoplasma pneumoniaePneumonia Issue Published: 1 April 1964 PDF downloadLoading ...
Mortality is high in treated hypertension
Journal: BMJ (1998)

Mortality is high in treated hypertensionAlthough treatment of hypertension reduces cardiovascular complications, the long term prognosis of treated hypertension is virtually unknown.For over 20 years Andersson et al (p 167) studied 686 men treated for hypertension.Compared with controls they showed a significantly increased mortality especially from myocardial infarction.The prognosis was apparent only after 10-12 years.Serum cholesterol concentration was one of the most important risk factors for dying from myocardial infarction.
The utility of quantitative endoscopic ultrasound elastography for the diagnosis of solid pancreatic masses
Authors: M. F. Dawwas, H. Taha, J. Leeds, M. Nayar, K. Oppong
Journal: Gut (2011)

<h3>Introduction</h3> Recent data suggests that endoscopic ultrasound elastography, a novel technique that allows real-time quantification of tissue stiffness, can accurately differentiate benign from malignant solid pancreatic masses.1 External validation of the diagnostic utility of this technique has not been reported. <h3>Methods</h3> We carried out quantitative EUSE on 31 consecutive patients with EUS-proven solid pancreatic masses using the linear Hitachi EUB-7500. Multiple quantitative elastographic measurements of the mass lesion (A) and soft tissue references areas (B) were undertaken in each patient and the corresponding strain ratios (B/A) were calculated. Final diagnosis was based on EUS-fine needle aspiration cytology and/or resection specimen histology. The diagnostic accuracy of EUS elastography in detecting malignancy was calculated using receiver operating curve analysis. <h3>Results</h3> The mean lesion size was 27.6 (SD 9.8) mm. The final diagnoses were pancreatic adenocarcinoma (n=24), inflammatory mass (n=5) and neuroendocrine tumour (n=2). Both strain ratio and pancreatic mass elasticity were significantly higher among patients with pancreatic malignant tumours compared with those with inflammatory masses. However, the sensitivity, specificity, accuracy and area under the receiver operating curve of EUSE for correctly diagnosing pancreatic malignancy in our cohort (table 1) were less favourable than those reported recently, with lower mean strain ratio (4.62 vs 6.04) and higher pancreatic mass elasticity cut-offs (0.28 vs 0.05) providing the highest accuracy. <h3>Conclusion</h3> Quantitative EUS elastography is a promising tool for the differential diagnosis of solid pancreatic masses although its accuracy in our experience has been less favourable than recently reported. Further assessment of the utility of this technique in other cohorts is warranted.
Possible genetic consequences of family planning
Authors: E. Matsunaga
Journal: JAMA (1966)

Family planning means to have children in a desired number, each child at a desired time. Although the parental desire in this regard may be different in individual families, a more or less uniform pattern of reproduction would emerge from practicing family planning, since this need is conditioned by life circumstances that are rather common to all members of the society. Thus, if an appreciable fraction of a population practices it, a change in demographic trends, namely, decline in variances would be expected not only in the number of children per family but also in birth order and parental ages in live-birth data. As family planning is usually used to limit family size, a second sign would be decline in the mean number of children and the mean birth order, while the mean of the parental ages may scarcely be affected. The purpose of this paper is to review the
Variability in the Size of Individual Airways Over the Course of One Year
Authors: Robert H. Brown, Elias A. Zerhouni, Wayne Mitzner
Journal: American Journal of Respiratory and Critical Care Medicine (1995)

Several studies have examined the reproducibility over time of standard clinical measurements of pulmonary airways parameters, such as FEV1 and FVC. These studies indicate fairly consistent reproducibility of such measurements over periods of months and years. Although such traditional pulmonary function tests can provide quantitative measures of lung function, they do not provide any insight into the local or regional variation of individual airways. Therefore, in a longitudinal study in dogs, we directly measured the baseline size (cross-sectional area) of the same individual canine airways multiple times over a 1-yr period, using high-resolution computed tomography (HRCT). We compared the variability of individual airway size both within and between subjects to the various sizes of airways and to seasonal differences in size. Five anesthetized, intubated, and ventilated dogs were studied between five and eight times over a 15-mo period. HRCT scans were acquired at end expiration with the dogs at FRC on all occasions. All individual airways showed considerable variability in size over time as measured by the coefficient of variation (CV) (range: 9.2 to 69.3). The sizes of individual airways within a dog were seen to change by as much as twofold over time. Some dogs also showed significantly greater overall variability in airway size than did other dogs (p < 0.01), but this variability was related neither to the size of the airway (p = 0.34) nor to the season. These findings indicate a substantial local and regional variability in airway caliber that would not be detectable with conventional pulmonary function tests. This variability in airway size could contribute to the local pathogenesis of lung disease.
Personal View
Authors: A K Ross
Journal: BMJ (1983)

<h3></h3> The outbreak of COVID-19 had substantial impact on trainees. Examinations were cancelled, rotations to other specialties were suspended with little information available regarding the immediate impact and enduring consequences of the pandemic. Trainee morale in AMU dropped during this uncertain period, which this project aimed to address. To identify baseline levels of morale, an anonymous survey was distributed to all AMU trainees at Musgrove Park Hospital via social media, asking to rate level of agreement using a Likert scale with several wellbeing statements such as ‘I feel happy at work’ and ‘I feel part of the AMU team’. The introduction of a cake rota encouraged trainees to pick a date they would provide cake for the team. Every Friday, after AMU ward round had finished, the team could eat together, whilst also offering an opportunity to socialise as a group. The survey was then redistributed to ascertain post-intervention levels of wellbeing. Responses to the question ‘I look forward to coming to work’ were scored more positively post-intervention, with 50% now strongly agreeing with this statement, compared to 0% prior. Similarly, trainees demonstrated an increasingly positive response to the statements ‘I feel part of the AMU team’, ‘there is a spirit of co-operation and teamwork within my team’ and ‘I get along well with my co-workers’, as 100% of trainees now strongly agreed, compared to 43% pre-intervention. This was echoed in the free text comments at the bottom of the survey, where one individual commented this was a ‘great idea to encourage team camaraderie’. Introducing simple measures (such as a weekly cake rota) promoted teamwork, collaboration, and a sense of unity, to help address a decline in trainee morale resulting from the COVID-19 pandemic. Longer term, this could improve individual wellbeing and maintain enthusiasm for a job which can be challenging and unpredictable, attributes which could be valuable as we enter a post-COVID world.
Persisting Learning Deficits in Rats after Exposure to Pfiesteria piscicida
Authors: Edward D. Levin, Donald E. Schmechel, JoAnn M. Burkholder, Howard B. Glasgow, Nora J. Deamer-Melia, Virginia C. Moser, G. Jean Harry
Journal: Environmental Health Perspectives (1997)

Pfiesteria piscicida and other toxic Pfiesteria-like dinoflagellates have been implicated as a cause of fish kills in North Carolina estuaries and elsewhere. Accidental laboratory exposure of humans to P. piscicida has been reported to cause a complex syndrome including cognitive impairment. The current project was conducted to experimentally assess the possibility of cognitive effects of P. piscicida exposure in rats. Samples of water from aquaria in which P. piscicida zoospores were killing fish were frozen, a procedure that has been found to induce encystment. Thawed samples were injected into albino Sprague-Dawley rats. A significant learning impairment was documented in rats administered samples of P. piscicida that were recently frozen. Prolonged storage of Pfiesteria samples diminished the effect. No effect was seen in the recall of a previously learned task, but when the rats were called upon to learn a new task, the Pfiesteria-treated animals showed a significant learning deficit. This effect persisted up to at least 10 weeks after a single injection of Pfiesteria. The Pfiesteria-induced learning deficit did not seem to be associated with any obvious debilitation or health impairment of the exposed rats. Deficits in habituation of arousal and rearing behavior were detected using a functional observational battery. No Pfiesteria-induced effects on blood count and white cell differential or in a standard pathological screening of brain, liver, lung, kidney, and spleen tissue were seen at 2 months after exposure. These studies document a persistent learning impairment in rats after exposure to the dinoflagellate P.piscicida in otherwise physically well-appearing rats. This effect may partially model the symptoms of cognitive impairments that humans have shown after Pfiesteria exposure.
Notes on Books
Journal: BMJ (1887)

service in India, and 84.8 per cent. of the whole had been under four years in that country.It is hardly necessary to dwell on a fact so prominently brought forward by the late Dr. Bryden, as well as by Dr. William Farr, Surgeon-General Balfour, and many others, namely, the close relationship between enteric fever and age in India.We observe that Surgeon-General THOMSON points out that British troops serving in the Bombay Presidency had an admission ratio of 46.50 for men under 20, 42.55 between 20 and 24, and 51.13 between 25 and 29 years of age per mille of strength ; this, however, is only an apparent exception to the usual rule, as the average strength of men for the latter period was much smaller than the other two combined.One half of the cases were in men in their first year of service in India.The Surgeon-General regrets that in the Bombay Presidency there are no hill stations where regiments fresh from England can be located for the first two years of their service in India.The Sanitaria of Aboo, Purandur and Tarugurh are only small invalid or convalescent dep6ts,
Regulation of herpes simplex virus γ134.5 expression and oncolysis of diffuse liver metastases by Myb34.5
Authors: Hideo Nakamura, Hideki Kasuya, John T. Mullen, Sam S. Yoon, Timothy M. Pawlik, Soundararajalu Chandrasekhar, James M. Donahue, E. Antonio Chiocca, Richard Y. Chung, Kenneth K. Tanabe
Journal: Journal of Clinical Investigation (2002)

Myb34.5 is a herpes simplex virus 1 (HSV-1) mutant deleted in the gene for ribonucleotide reductase (ICP6). It also carries a version of γ134.5 (a viral gene product that promotes the dephosphorylation of eIF-2α) that is under control of the E2F-responsive cellular B-myb promoter, rather than of its endogenous promoter. Myb34.5 replication in tumor cells results in their destruction (oncolysis). γ134.5 expression by HSV-1 subverts an important cell defense mechanism against viral replication by preventing shutoff of protein synthesis after viral infection. Infection of colon carcinoma cells with Myb34.5 results in greater eIF-2α dephosphorylation and viral replication compared with infection with HSV-1 mutants completely defective in γ134.5 expression. In contrast, infection of normal hepatocytes with Myb34.5 results in low levels of eIF-2α dephosphorylation and viral replication that are similar to those observed with HSV-1 mutants completely defective in γ134.5 and ICP6. When administered intravascularly into mice with diffuse liver metastases, Myb34.5 has greater antineoplastic activity than HSV-1 mutants with completely defective γ134.5 expression and more restricted biodistribution compared with HSV-1 mutants with wild-type γ134.5 expression. Myb34.5 displays reduced virulence and toxicity compared to HSV-1 mutants with wild-type γ134.5 expression. Portal venous administration of Myb34.5 significantly reduces liver tumor burden in and prolongs the life of mice with diffuse liver metastases. Preexisting Ab’s to HSV-1 do not reduce the antitumor efficacy of Myb34.5 in vivo.
Fever Therapy of Neurosyphilis
Journal: JAMA (1934)

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
Incorrect Value
Journal: JAMA (1984)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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 journal
Abstract 1008: A Protective Role for Cardiac Specific Muscle Ring Finger-1 (MuRF1) in Ischemia/Reperfusion Injury In Vivo
Authors: Monte S Willis, Mauricio Rojas, Pamela Lockyer, Thomas G Hampton, Luge Li, Dane Meredith, Cam Patterson
Journal: Circulation (2007)

We previously identified a critical role for MuRF1 in suppressing pathologic cardiac hypertrophy. To extend these observations to other pathologic processes, we tested the role of MuRF1 in cardiac ischemia reperfusion (I/R) injury. We challenged MuRF1 transgenic (Tg) mice to I/R injury both ex situ and in vivo. First, we examined isolated MuRF1 Tg and age-matched sibling wild-type (WT) hearts after global ischemia (15 min) followed by reperfusion (20 min) in a Langendorff apparatus. Baseline function of MuRF1 Tg hearts did not significantly differ from WT hearts (mean left ventricular developed pressure (LVDP) 88.5 +/− 18 vs. 82.5 +/− 6.7, respectively; n = 4/group). Mean LVDP of hearts from MuRF1 Tg mice after reperfusion was 76.0 +/− 22.9% of baseline function compared to 27.2 +/− 13.3% in WT hearts (N = 5/group, P&lt; 0.05)). To confirm that MuRF1 is cardioprotective in vivo, we subjected MuRF1 Tg and WT mice to a 30 minute ligation of the left anterior descending coronary artery, followed by 24 hours reperfusion. Mice underwent conscious echocardiography at baseline and after 24 hours; cardiac function was further interrogated by Millar pressure volume catheterization at 24 hours. Additionally, hearts underwent a histological evaluation of area at risk and infarct size. By echocardiography, a ~7% decrease in fractional shortening was identified in MuRF1 Tg mice after 24 hours reperfusion compared to baseline. This was in striking contrast to WT mice, which exhibited ~48% decrease in fractional shortening. Steady state catheterization measurements showed a significantly higher ejection fraction in MuRF1 Tg compared to WT mice after I/R injury (81.6 ± 2.3% vs. 49.0 +/− 4.0%, P &lt; 0.05). Contractility reflected by +dP/dt max was better preserved in MuRF1 Tg compared to WT mice after I/R injury (12,614 +/− 776 vs. 7,448 +/−752, N = 3–12/group, P &lt; 0.05). Histologically, the area of infarct in MuRF1 Tg mice was significantly smaller (10.0 +/− 0.8%) than in WT mice (25.5 +/− 2.5%, N = 4/group, P &lt; 0.05). We demonstrate here for the first time that cardiac MuRF1 expression preserves function after I/R injury in vivo. Since MuRF1 is known to interact with metabolic and structural targets, this model will allow us to identify mechanisms by which MuRF1 modifies cardiac pathophysiology.