tbuckley/cabot-search huggingface dataset:
Psychological Characteristics of Breast Cancer Patients
Authors: Bruce D. Kirkcaldy, Elzbieta Kobylinska
Journal: Psychotherapy and Psychosomatics (1987)

Two breast cancer groups (mastectomised or chemotherapeutic intervention) and a control group of healthy female nurses were given a demographic questionnaire and the Minnesota Multiphasic Personality Inventory. The personality profiles of all three groups emerged as significantly different from each other on all scales with the exception of social introversion and psychopathic deviance. Both cancer groups displayed inflated scores on the clinical scale Depression. A separate series of univariate F tests revealed that the mastectomised patients were characterised by elevated scores on the clinical scales Hypochondriasis, Depression, Hysteria, Masculinity-Femininity and Schizophrenia compared to normals. The discriminant analysis confirmed that between the clinical groups the mastectomised patients exhibited higher scores (compared to those receiving chemotherapy) along the scales Hypochondriasis, Paranoia, Psychaesthenia, Schizophrenia and Hypomania, the latter 4 scales constituting the psychotic tetrad.
Oncogenetics and minimal residual disease are independent outcome predictors in adult patients with acute lymphoblastic leukemia
Authors: Kheira Beldjord, Sylvie Chevret, Vahid Asnafi, Françoise Huguet, Marie-Laure Boulland, Thibaut Leguay, Xavier Thomas, Jean-Michel Cayuela, Nathalie Grardel, Yves Chalandon, Nicolas Boissel, Beat Schaefer, Eric Delabesse, Hélène Cavé, Patrice Chevallier, Agnès Buzyn, Thierry Fest, Oumedaly Reman, Jean-Paul Vernant, Véronique Lhéritier, Marie C. Béné, Marina Lafage, Elizabeth Macintyre, Norbert Ifrah, Hervé Dombret
Journal: Blood (2014)
The role of purinergic P2X7 receptors in the inflammation and fibrosis of unilateral ureteral obstruction in mice
Authors: R.G. Gonçalves, L. Gabrich, A. Rosário, C.M. Takiya, M. L.L. Ferreira, L.B. Chiarini, P.M. Persechini, R. Coutinho-Silva, M. Leite
Journal: Kidney International (2006)
Abstract SY02-01: Pericellular proteolysis and the regulation of the 3-D cancer invasion program
Authors: Stephen J. Weiss
Journal: Cancer Research (2011)

Abstract To initiate prometastatic programs, carcinoma cells must transmigrate multiple extracellular matrix barriers, including the subtending basement membrane and the underlying interstitial matrix before gaining access to vascular and/or lymphatic beds. Subsequently, the cells extravasate and embed themselves in distant tissues where they must reactivate proliferation programs (Ann Rev Cell Dev Biol 25:567, 2009). Current evidence suggests that proinvasive carcinoma cells engage a reversible epithelial-mesenchymal cell-like transition (EMT) that falls under the regulation of a growing number of transcription factors, including Snail1 or Snail2. In response to multiple stimuli, ranging from growth factors and hypoxia to inflammatory cytokines and loss-of-function p53 mutations, EMT-inducing transcription factors promote the mobilization of a complex mix of proteinases that propagate the proteolytic remodeling of the extracellular matrix in a fashion that supports tissue-invasive activity (PNAS 106:20318, 2009; J Cell Biol 185:11, 2009; Genes &amp; Dev 20:2673, 2006). While the identity of proteases mobilized by invading cells to traverse matrix barriers remains controversial, increasing evidence supports a critical role for a subclass of membrane-anchored matrix metalloproteinases, termed the membrane-type MMPs (MT-MMPs). In an exocyst-regulated fashion, MT-MMP family members decorate the leading edge of migrating cancer and stromal cells alike in order to drive invasion through extracellular matrix barriers. Importantly, MT-MMP function is not restricted to invasion alone as membrane-anchored proteases play additional roles in regulating cell proliferation, survival and differentiation (Cell 114:33, 2003; Cell 125:577, 2006; Genes &amp; Dev 22:1231, 2008; Blood 115:221, 2010). While the range of cellular activities that fall under the MT-MMP umbrella is, in some ways, perplexing, new evidence suggests that MT-MMP-dependent pericellular proteolysis indirectly controls nuclear architecture and function in a 3-D extracellular matrix-specific fashion. Understanding the interplay between EMT-inducing transcription factors, the activation of tissue-remodeling cell programs, and the impact of pericellular proteolysis on gene regulation and function should provide new insights into the control of neoplastic cell trafficking and metastatic activities. 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 SY02-01. doi:10.1158/1538-7445.AM2011-SY02-01
Radiopharmaceutical Reimbursement Rates
Authors: Jack W. Singer
Journal: JAMA (2008)

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
Abstract 2475: Effect of mTOR inhibition by rapamycin on promotion of skin tumors in BK5. Aktwt transgenic mice
Authors: Okkyung Rho, Guiyu Jiang, Allyson Sandifer, John DiGiovanni
Journal: Cancer Research (2010)

Abstract Akt is a serine/threonine kinase involved in a variety of cellular responses including cell survival and proliferation. It has been shown that PI3K/Akt signaling is frequently altered (upregulated) in human cancers. mTOR is one of the Akt downstream signaling pathways that regulates protein synthesis, cell growth and proliferation. mTOR exists in two complexes, mTORC1 and mTORC2. Our laboratory previously reported that tumor promoters including TPA, okadaic acid (OA), and chrysarobin (CHRY) activate epidermal Akt after topical treatment of mouse epidermis and mouse primary cultured keratinocytes. Activation of Akt during tumor promoter treatment leads to enhanced downstream signaling including mTORC1 pathways. BK5. Aktwt transgenic mice where Akt is overexpressed in basal epidermis were significantly more sensitive to two-stage carcinogenesis, showing tumors with a much shorter latency, considerably larger in size, and enhanced progression of papillomas to SCCs. Importantly, Akt transgenic mice showed significant elevations in several downstream signaling pathways both in the absence and presence of TPA, including mTORC1 activity. Collectively, the studies with transgenic mice overexpressing Akt in epidermis (BK5.Aktwt) have suggested that activation of mTORC1 signaling may contribute to the process of skin tumor promotion. In this study, we have examined the ability of rapamycin, a known inhibitor of mTOR, on mTORC1 signaling in relation to its effect on TPA-induced epidermal cell proliferation and skin tumor promotion. Rapamycin given at doses of 1 μmol, 100 nmol, 20 nmol, and 5 nmol 30 min prior to 6.8 nmol TPA treatment inhibited mTORC1 activity in a dose-dependent manner. Notably, in a multiple treatment regimen (4 applications of rapamycin and TPA over a two week period) high doses of rapamycin significantly inhibited TPA-induced Akt phosphorylation at serine 473 as well as mTORC1 signaling in a dose dependent way, suggesting mTORC2 inhibition induced by prolonged high dose rapamycin treatment. The ability of rapamycin (at doses of 100, 20, and 5 nmol per mouse) to inhibit skin tumor promotion by TPA in BK5. Aktwt transgenic mice was compared with wild-type mice. Rapamycin significantly reduced TPA promotion in BK5.Aktwt mice, however, it was less effective compared to similar doses used in wild-type mice. The data demonstrate that rapamycin, although less effective, still retained significant inhibitory activity toward TPA promotion even when Akt and mTOR activities were elevated. These data demonstrate an important role for mTOR signaling in skin tumor promotion of TPA. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2475.
STUDIES ON SUSCEPTIBILITY TO INFECTION FOLLOWING IONIZING RADIATION
Authors: Carolyn W. Hammond, Margaret Colling, Dorothy B. Cooper, C. Phillip Miller
Journal: The Journal of Experimental Medicine (1954)

Mice were inoculated by mouth at different times (2 hours, 5 days, and 11 days) after a single exposure to 550 r total body x-irradiation. The inocula contained approximately 10(7)Pseudomonas aeruginosa which was found to be quite harmless for unirradiated mice. Comparison of the cumulative mortality curves and of the incidence of Pseudomonas bacteremia showed their susceptibility to infection by this route to be greatest on the 11th day, somewhat less on the 5th day post irradiation, and least of all directly after irradiation. Since damage to the intestinal mucosa has been found to be maximal within the first few hours after exposure to doses of x-irradiation in this range, it seems reasonable to conclude that the increased susceptibility is not due to increased permeability of the mucosa of the gut, but to impairment of the animal's natural defenses against infection.
Increased plasma adiponectin concentrations in poorly controlled patients with phenylketonuria normalize with a strict diet: evidence for catecholamine-mediated adiponectin regulation and a complex effect of phenylketonuria diet on atherogenesis risk factors
Authors: Kleopatra H. Schulpis, Ioannis Papassotiriou, Stylianos Tsakiris, Maria Vounatsou, George P. Chrousos
Journal: Metabolism (2005)
Hospital admission is a relevant source of hepatitis C virus acquisition in Spain
Authors: Eva Martínez-Bauer, Xavier Forns, Mercé Armelles, Ramon Planas, Ricard Solà, Mercé Vergara, Silvia Fàbregas, Roser Vega, Javier Salmerón, Moisés Diago, Jose María Sánchez-Tapias, Miquel Bruguera
Journal: Journal of Hepatology (2007)
972. HSC-Based Ex Vivo Gene Therapy Prolongs Survival and Improves the Phenotype of Globoid Cell Leukodystrophy Mice
Authors: Alessandra Biffi, Ilaria Visigalli, Letterio S. Politi, Angelo Quattrini, Ubaldo Del Carro, David Wenger, Claudio Bordignon, Luigi Naldini
Journal: Molecular Therapy (2005)

We have proved that HSC-based ex vivo gene therapy provides a unique therapeutic option and corrects Metachromatic Leukodystrophy (MLD) in the mouse model (A. Biffi et al., J. Clin. Invest 2004, 113(8): 1118-29). Since the mouse model of MLD is characterized by a mild phenotype, it will be paramount to prove the efficacy of ex vivo gene therapy in more severe LSD models, which better reproduce the human manifestations of LSD, like the mouse models of Globoid Cell Leukodystrophy (GLD), before starting clinical translation of this strategy. Thus, to further evaluate the therapeutic impact of the ex vivo gene therapy approach, we challenged it with the acute and devastating evolution of GLD in its mouse models. GLD is an inborn lipidosis, similar to MLD, caused by the deficiency of the lysosomal enzyme galactocerebrosidase. It is characterized by intracellular storage of psycosine, produced by an alternative metabolic pathway, in the CNS and PNS, leading to severe progressive demyelination and early death. No effective treatment is currently available for these devastating diseases. Different mouse models of GLD are currently available, comprising the Twitcher mouse, carrying a spontaneous stop mutation in the mGALC gene, in the original C57Bl/6 and in a newly generated FVB backgrounds, and the so-called GLD mouse, a knock in mouse carrying a missense mutation in the mGALC gene. These mice differ for disease onset and severity, being the phenotype of the FVB Twitcher and of the GLD mice slightly milder than the one of C57Bl/6 Twitcher. Neonate C57Bl/6 Twitcher mice were transplanted with HSC transduced with the GALC gene, supplemented with accessory Sca1- cells to reduce short-term toxicity of lethal conditioning and allow mice survival. We observed a significant improvement in long-term survival of transplanted mice, and in their phenotype (absence of leg palsy and delayed, minor twitching) and prevention of mayor histopathological signs of the disease (demyelination, axonal loss). Brain MR imaging confirmed these findings, showing clear improvements of the massive CNS demyelination of the Twitcher mouse, upon treatment. To evaluate the need for transplantation of committed progenitors (Sca1- cells) in association to HSC, and to better study the therapeutic potential of ex vivo gene therapy for GLD, we are applying a protocol based on HSC alone to the other two mouse models available. Preliminary results indicate that in these slightly less severe models HSC alone are sufficient for rescue from both lethal conditioning and early disease manifestations. Long-term studies are currently on going in these mice to assess the long-term therapeutic effect of this gene therapy strategy. However, these results are providing evidence, in a severe disease setting, of the therapeutic potential of ex vivo gene therapy for lysosomal storage disorders.
Postconcussion Syndrome After Mild Traumatic Brain Injury in Children and Adolescents Requires Further Detailed Study
Authors: Ian J. Butler
Journal: JAMA Neurology (2013)

<h3>Objective: </h3>To determine the acute predictors associated with the development of postconcussion syndrome (PCS) in children and adolescents after mild traumatic brain injury.<h3>Design: </h3>Retrospective analysis of a prospective observational study.<h3>Setting: </h3>Pediatric emergency department (ED) in a children's hospital.<h3>Participants: </h3>Four hundred six children and adolescents aged 5 to 18 years.<h3>Main Exposure: </h3>Closed head trauma.<h3>Main Outcome Measures: </h3>The Rivermead Post Concussion Symptoms Questionnaire administered 3 months after the injury.<h3>Results: </h3>Of the patients presenting to the ED with mild traumatic brain injury, 29.3% developed PCS. The most frequent PCS symptom was headache. Predictors of PCS, while controlling for other factors, were being of adolescent age, headache on presentation to the ED, and admission to the hospital. Patients who developed PCS missed a mean (SD) of 7.4 (13.9) days of school.<h3>Conclusions: </h3>Adolescents who have headache on ED presentation and require hospital admission at the ED encounter are at elevated risk for PCS after mild traumatic brain injury. Interventions to identify this population and begin early treatment may improve outcomes and reduce the burden of disease.
Levels of non-ortho-substituted (coplanar), mono- and di-ortho-substituted polychlorinated biphenyls, dibenzo-p-dioxins, and dibenzofurans in human serum and adipose tissue.
Authors: D G Patterson, G D Todd, W E Turner, V Maggio, L R Alexander, L L Needham
Journal: Environmental Health Perspectives (1994)

We have measured non-ortho-substituted (coplanar) polychlorinated biphenyl (PCB) levels as well as polychlorinated dibenzo-p-dioxin (PCDD) and polychlorinated dibenzofuran (PCDF) levels in human adipose tissue and serum collected in Atlanta, Georgia. The results show that the concentrations of the coplanar PCBs can be more than an order of magnitude higher than the concentrations of 2,3,7,8-tetrachlorodibenzo-p-dioxin. Our measurements in pooled serum collected in 1982, 1988, and 1989 show a decrease in coplanar PCB levels from 1982 to 1989. We found that the pattern of relative amounts of coplanar PCBs in adipose tissue varied greatly from person to person unlike the PCDD and PCDF patterns, which were more nearly the same. Age was significantly correlated with the concentrations of 2,3,7,8-TCDD,3,3'4,4'-PCB, 3,3',4,4',5-PCB, and 3,3'4,4',5,5'-PCB in adipose tissue. We also measured levels of the mono- and di-ortho chlorine-substituted PCBs in human serum. The levels for some of these PCB congeners were three orders of magnitude higher than the coplanar PCBs, PCDDs, and PCDFs. We used the international toxicity equivalency factors (TEFs) for PCDDs and PCDFs and the TEFs proposed by Safe for PCBs to calculate the 2,3,7,8-TCDD equivalents. Four PCBs (3,3',4,4',5-; 2,3',4,4',5-;2,3,3',4,4'-;2,3,3',4,4',5-) make a larger contribution than 2,3,7,8-TCDD, while four other PCBs (3,3',4,4'5,5'-; 2,2',3,4,4',5'-;2,2',4,4',5,5'-;2,2',3,4,4',5,5'-) make nearly the same contribution as 2,3,7,8-TCDD. The mono-ortho-chlorine-substituted 2,3',4,4',5-PCB, however, is the major contributor to the total 2,3,7,8-TCDD equivalents in general population samples from the United States, Sweden, and Japan.(ABSTRACT TRUNCATED AT 250 WORDS)
Doctors renew call for "obstinate government" to abandon health bill
Authors: Z. Kmietowicz
Journal: BMJ (2012)

Doctors at the BMA’s annual conference for hospital consultants on 7 March renewed their call for the government to abandon the Health and Social Care Bill, which their leader described as “447 pages of unintelligible red tape.”

In a call to arms Mark Porter, chair of the consultants committee, attacked the “belligerent and obstinate government” for pushing consultants into conflicts over the health bill and pensions “when we would far rather be planning improvement in …
Should Tests for<i>Chlamydia trachomatis</i>Cervical Infection Be Done During Routine Gynecologic Visits?
Authors: RUSSELL S. PHILLIPS
Journal: Annals of Internal Medicine (1987)

We used decision analysis to estimate the clinical and economic implications of testing for cervical infection caused by Chlamydia trachomatis in women during routine gynecologic visits. We compared a strategy of no routine testing with a strategy involving the use of routine cultures or the use of less expensive rapid tests for chlamydial infection (the direct fluorescent assay or the enzyme immunoassay). We used different assumptions for the costs and operating characteristics of the diagnostic tests, complications of undetected infection, and the cost of false-positive test results. We found that using one of the rapid tests would reduce overall costs if the prevalence of infection was 7% or greater. The use of routine cultures would reduce costs if the frequency of infection was 14% or greater. We conclude that testing for cervical infection with C. trachomatis in women seeking routine gynecologic care may reduce overall costs. The choice of diagnostic test should depend on the expected prevalence of infection, local cost considerations, and laboratory expertise in the execution of these tests.
HIV Prevalence Among Washington, DC, Residents Having Abortions
Authors: Christian Wolter
Journal: JAMA (1993)

<h3>To the Editor.</h3> —In their recent article, Rosenberg et al<sup>1</sup>used backcalculation methods to reconstruct human immunodeficiency virus (HIV) incidence from acquired immunodeficiency syndrome (AIDS) incidence in subgroups of the population, and then compared the results with directly measured seroprevalence in selected sentinel populations. In this context, it should be noted that both techniques, ie, backcalculation and direct serosurveys, have different shortcomings. These must be addressed before comparing results of the techniques for the purpose of cross-validation. Forecasts based exclusively on AIDS incidence data cannot produce good estimates of recent HIV incidence because of the virus' long and variable incubation period. On the other hand, direct serosurveys based on unlinked testing allow the assessing of trends in recent HIV prevalence but are restricted to readily accessible sentinel populations, which may be subject to selection bias (eg, patients of sexually transmitted disease clinics, pregnant women, or hospitalized patients). Rosenberg et
The restoration of full-thickness cartilage defects with BMSCs and TGF-beta 1 loaded PLGA/fibrin gel constructs
Authors: Wei Wang, Bo Li, Junzhou Yang, Long Xin, Yanglin Li, Hongpin Yin, Yiying Qi, Yangzi Jiang, Hongwei Ouyang, Changyou Gao
Journal: Biomaterials (2010)
Over-expression of the ribosomal protein L36a gene is associated with cellular proliferation in hepatocellular carcinoma
Authors: Jong-Hyun Kim, Kyung-Ran You, In Hee Kim, Baik-Hwan Cho, Chan-Young Kim, Dae-Ghon Kim
Journal: Hepatology (2004)

Using messenger RNA (mRNA) differential display, we identified a single complementary DNA (cDNA) fragment (HG23T1) that was over-expressed in a hepatocellular carcinoma (HCC) specimen. We cloned the full-length HG23T1 gene by the rapid amplification of cDNA end (RACE) polymerase chain reaction (PCR) method. It perfectly matched the gene encoding human ribosomal protein L36a (RPL36A also referred to as RPL44). RPL36A mRNA was preferentially over-expressed in 34 of 40 HCC cases (85%, P <.001) and in all of 8 HCC cell lines. Ectopically over-expressed L36a ribosomal protein localized in the nucleoli of cells, and this localization seemed to be controlled by the N-terminal or the internal tetrapeptide consensus with its adjacent N-terminal domain. Over-expression of L36a led to enhanced colony formation and cell proliferation, which may have resulted from rapid cell cycling, and an antisense cDNA effectively reversed these alterations. In conclusion, RPL36A plays a role in tumor cell proliferation and may be a potential target for anticancer therapy of HCC.
Increased F-18 FDG Uptake on Positron Emission Tomography/Computed Tomography Imaging Caused by Plantar Fibromatosis
Authors: Jennifer Scheler, Bhavya Rehani, Thomas Percy, Richard Pelstring, Ankur Bharija, Donald Ames, Joseph Mantil
Journal: Clinical Nuclear Medicine (2008)

We detail the history and evaluation of a 68-year-old man who had head-to-toe PET/CT scanning that showed a focal area of increased FDG uptake in the left medial foot. This was thought to be recurrence of his melanoma. The patient was asymptomatic. He had a history of malignant melanoma of the right ear, which was removed in 2001. On biopsy, the foot lesion was diagnosed as plantar fibromatosis. Plantar fibromatosis is a benign fibroblastic condition, which can be indistinguishable from malignancy in head-to-toe PET/CT scans. Awareness of their potential appearance on PET and PET/CT will aid in the appropriate staging of oncology patients.
True Origin of the Epidemic of Yellow Fever.
Authors: Edmond Souchon
Journal: JAMA (1900)

New Orleans, La., July 21, 1900. <h3>To the Editor:</h3> —"True Origin of the Epidemic of 1897 (Yellow Fever)", is the title of a well-written and very interesting article, in which Dr. J. H. White, of the United States Marine-Hospital Service, shows to his thorough satisfaction that yellow fever was introduced into Ocean Springs, Miss., in 1897, by a man named Thomas Shannahan. Dr. White says (report of U. S. M.-H. Service for 1898, page 536): Thomas Shannahan came from Guatemala, where he spent a short time prior to sailing, at a hotel in Port Barrios, at which hotel yellow fever is said to have existed. He sailed from Port Barrios, on April 8, on the steamship<i>Breakwater</i>and arrived at quarantine at Port Eads on April 12, and the quarantine season not being at hand, he suffered neither detention nor disinfection of his effects. He arrived at Ocean Springs, Miss.,