tbuckley/cabot-search huggingface dataset:
Cell‐mediated immunity assessed by skin testing (Multitest®)
Authors: F. Moesgaard, M. Lykkegaard Nielsen, P. Nørgaard Larsen, S. Christophersen, H. Mosbech
Journal: Allergy (1987)

The Multitest CMI system consists of a disposable multiple puncture device that simultaneously applies seven standardized recall antigens for assessment of cell-mediated immunity (CMI). The seven antigens included were toxoid from Clostridium tetani and Corynebacterium diphtheriae, tuberculin, plus antigens from streptococcus (group C), Candida albicans, Trichophyton mentagrophytes, and Proteus mirabilis. A population of 352 healthy Danish adults, aged between 17 and 90 years, was tested to determine the incidence and size of delayed-type hypersensitivity (DTH) responses. All but six healthy adults (98%) responded to one or more antigens, the median number of positive responses being four in males and three in females. The incidence of positive responses ranged from 91% for tuberculin to 11% for trichophyton. The number of positive responses declined with age, being somewhat faster in females than males. Six of the seven antigen response rates were significantly lower in the over 65-years-olds, the only exception being trichophyton, and for four of the seven antigens significantly lower in females compared to males. When correlated to age and sex no major differences were found with regard to the size of response to the seven antigens except that the tuberculin response was larger in males. A scoring system based on both number and size of positive responses revealed significant age and sex related differences. The median "score" in 17-65-year-old males and females were, respectively, 17 mm and 14 mm compared to 13 mm and 8 mm in those over 65 years old (P less than 0.001 for both comparisons).
Role of Ubiquitin-proteasome proteolytic pathway in malignant pleural mesothelioma.
Authors: Anil Wali, Ying Wang, Deepa Kanakapalli, Zhandong Liu, Sunita Sharma, Fulvio Lonardo, Arun Rishi, Adhip Majumdar, Q. Ping Dou, Michele Carbone, John Ruckdeschel, Harvey Pass
Journal: Cancer Research (2007)

4406  Malignant Pleural Mesothelioma (MPM) is an aggressive, asbestos-related locally recurrent thoracic cancer with no effective curative options, affecting about 3000 new patients in the United States annually. Despite advances in cancer treatment, the median survival rate remains low and most patients die within two years after diagnosis. We have recently shown that U95 Affymetrix ologonucleotide microarray platform could be used for the identification of markers of survival and progression among series of 21 MPM cases Pass HI. et al. Clin Cancer Res. 10: 849-859, 2004. For this study we wanted to identify the aberrations in ubiquitin-proteasome proteolytic pathway (UPP) regulatory proteins that were critical to the pathogenesis of MPM. 241 genes involved in the UPP pathway were compared based on survival time, tumor stage, and histology using t-test analysis with a ninety five percent confidence interval. The software used for the calculations was “Genesight” from Biodiscovery Inc. Twenty-four genes showed significant difference between designated short- ( 1year) term survivors. We observed proteasome alpha subunits 5 and 7 were predominantly overexpressed among short-survivors whereas ubiquitin-activating enzyme E1 was profoundly overexpressed among long-term MPM patient tumor samples. We observed thirty-three genes were differentially expressed among epithelioid and biphasic histotypes. Ubiquitin carrier protein was expressed at low levels among epithelioid MPMs compared to biphasic histotypes. Fifteen genes were significantly altered among stage I and II combined versus stage III cases. Ubiquitin specific proteases 1, 10, 14 were expressed at low levels amomg majority of stage I and II tumors. Increased chymotryptic activity associated with proteasome subunit beta 5 was also observed among six MPM patient derived cell lines compared to MeT5A immortalized mesothelial cells. Taken together, these results indicate that protein ubiquitination and degradation have important role in mesothelioma tumorigenesis that could be utilized for the development of more effective targeted therapies for this fatal disease.
Abstract #4413: The role of fatty acid desaturation in tumor cell proliferation.
Authors: Justin Cross, Ralph DeBerardinis, Craig Thompson
Journal: Cancer Research (2009)

AACR Annual Meeting-- Apr 18-22, 2009; Denver, CO

Tumor cells must produce new membrane lipids to grow and proliferate. To do this, they use fatty acids (FAs) acquired from two different pools: extracellular lipids and fatty acids synthesized de novo by the cell. Tumor cell membranes contain a typical mixture of saturated, monounsaturated and polyunsaturated FAs. While the extracellular lipid pool contains all of these, the major end product of de novo synthesis is the saturated fatty acid, palmitate. Therefore, membranes produced during tumor growth are influenced both by FAs available in the tumor environment and by the tumor's intrinsic ability to produce and modify FAs. Preliminary data showed that increasing the extracellular concentration of saturated FAs by palmitate supplementation causes decreased viability in proliferating cells, but that non-proliferating cells are impervious to palmitate-mediated toxicity. This effect can be reversed by increasing the extracellular availability of the monounsaturated FA oleate, thereby restoring the saturated : unsaturated FA ratio. We therefore investigated whether rapidly proliferating tumor cells depend upon up-regulation of the de novo FA desaturation pathway. The rate-limiting step in this process is controlled by Stearoyl-CoA Desaturase (SCD), which introduces the first carbon-carbon double bond into newly synthesized saturated FAs. SCD represents an attractive therapeutic target since its inhibition should both impair new lipid synthesis and also cause a build up of toxic saturated FAs. Disruption of SCD expression by RNA interference increases the saturation index of cellular lipids and reduces cell viability. Supplementation with exogenous oelate, the product of the SCD reaction, rescues this defect. SCD is also an important target of PI3K/Akt signaling and we have built upon these observations, quantifying the proportion of FAs synthesized de novo versus those from extracellular sources, the in vivo requirement for SCD activity and the impact of Akt activation on these processes using a variety of cancer cell lines. Finally, we will present data from mouse xenograft tumor models in which we have manipulated SCD expression to determine whether SCD activity is required for tumor growth in vivo. Because the cellular FA milieu is also influenced by dietary fatty acid composition, we are also testing whether dietary manipulations that increase saturated FA load, or administration of an SCD inhibitor, can impair tumor growth. Such interventions could provide novel strategies to augment current chemotherapy regimes.

Citation Information: In: Proc Am Assoc Cancer Res; 2009 Apr 18-22; Denver, CO. Philadelphia (PA): AACR; 2009. Abstract nr 4413.
Tobacco money, the BMJ, and guilt by association
Authors: Steven H Woolf
Journal: BMJ (2003)

From BMJ USA 2003;July:344 

Bans against smoking in public are ubiquitous. Cigarette smoke is irritating, and passive inhalation increases tobacco-related morbidity and mortality. Or perhaps not, say Enstrom and Kabat ( BMJ USA p 369). Based on an analysis of data from the American Cancer Society, they conclude that the association “may be considerably weaker than generally believed.” A firestorm erupted when the BMJ published this article in May. The American Cancer Society released a stinging press statement. The BMJ received 130 Rapid Responses and was advised to issue a retraction. Two main concerns predominated. First, the authors acknowledged being funded by an organization tied to tobacco …
On Decatur Island
Authors: John L. Wright
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
Gout as a Complication of Bartter's Syndrome
Authors: Walter J. Meyer, John R. Gill, Frederic C. Bartter
Journal: Annals of Internal Medicine (1975)

A prevalence of hyperuricemia of 50% and of acute gouty arthritis of 20% has been observed in a group of patients with Bartter's syndrome. All patients except one presented initially with complaints unrelated to uric acid metabolism. The cause of their hyperuricemia and subnormal clearance of uric acid is unexplained. Systemic alkalosis, a prominent feature of Bartter's syndrome, can decrease the clearance of uric acid and may contribute to the hyperuricemia and gout that have been observed. Physicians should be aware of the possibility of gout as a clinical complication of Bartter's syndrome and of the inhibitory effects of alkalosis on urate clearance.
Clinical and microbiological characteristics of Nocardiosis including those caused by emerging Nocardia species in Taiwan, 1998–2008
Authors: C.-K. Tan, C.-C. Lai, S.-H. Lin, C.-H. Liao, C.-H. Chou, H.-L. Hsu, Y.-T. Huang, P.-R. Hsueh
Journal: Clinical Microbiology and Infection (2009)
A SOURCE OF ERROR IN THE DETERMINATION OF BASAL METABOLIC RATES BY THE CLOSED-CIRCUIT TECHNIC
Authors: H N WILLARD, G A WOLF
Journal: Annals of Internal Medicine (1951)

Article1 January 1951A SOURCE OF ERROR IN THE DETERMINATION OF BASAL METABOLIC RATES BY THE CLOSED-CIRCUIT TECHNICHAROLD N. WILLARD, GEORGE A. WOLF JR.HAROLD N. WILLARD, GEORGE A. WOLF JR.Author, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-34-1-148 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptIn the course of studying mechanisms of dyspnea with the closed-circuit Benedict-Roth type spirometer, we were impressed with the effect which changes in the midposition of the chest had upon the slope of the spirogram. This possible source of error attracted the attention of Greene and Coggeshall1and was also mentioned by Buckingham and Roth.3Further work by Greene,2however, minimized its clinical importance by showing that when changes in the midposition of the chest did occur during the tracing, they could be detected in most instances by observing the subject's respirations or by noting irregularities in the base line...Bibliography1. GreeneCoggeshall JAHC: Clinical studies of respiration, influence of determination of basal metabolism on respiratory movements in man, and effect of these alterations on calculated basal metabolic rate, Arch. Int. Med. 52: 226, 1933. CrossrefGoogle Scholar2. Greene JA: Frequency and significance of changes of expiratory chest volume during routine measurement of basal oxygen consumption, J. Lab. and Clin. Med. 21: 1231 (Sept.) 1936. Google Scholar3. RothBuckingham PPE: The criteria of a dependable basal metabolic report, Am. J. Clin. Path. 9: 79, 1939. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: *Received for publication December 2, 1948.From The Department of Medicine, Cornell University Medical College and The New York Hospital. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byBasal metabolic rate studies in humans: measurement and development of new equationsDiagnosis of Occult and Borderline Disorders of the ThyroidMethoden zur Untersuchung der Ventilation 1 January 1951Volume 34, Issue 1Page: 148-162KeywordsDyspneaHospital medicineRespirationThorax Issue Published: 1 January 1951 PDF downloadLoading ...
1050. Autoimmune Anemia in Macaques Following Erythropoietin Gene Therapy
Authors: Pierre Chenuaud, Thibaut Larcher, Joe Rabinowitz, Nathalie Provost, Yan Cherel, Nicole Casadevall, Jude Samulski, Philippe Moullier
Journal: Molecular Therapy (2004)

AAV vectors are in phase I/II gene therapy trials. Therapeutic proteins are currently secreted from ectopic sites (i.e. the factor IX from muscle). The AAV vector encoding for the cynomolgus macaque Epo cDNA (cmEpo) under the control of the reverse Dox-dependent transactivator M2 was packaged in serotype −1 (n=4 cynomolgus macaques) or −2 (n=4) AAV capsids. Epo induction started 2 months after vector administration in the tibialis anterior muscle and consisted of a 5-day Dox pulse given intravenously and repeated once every month. Within 3 to 4 induction cycles, most animals mounted a humoral and cytotoxic T cell immune response against the Dox-dependent transactivator-expressing cells resulting in the loss of Epo secretion from genetically-modified muscles. However, animals that secreted less than 100 mIU/ml of Epo initially, maintained normal hematocrits (44±5 %). Strikingly, except for one, animals that exhibited Epo levels of 100, 162, and 1159 mIU/ml at peak 1, respectively, could precipitate, 1.1×103, 1.2×105, and 6.7×104 cpm of 3H-labeled recombinant human Epo (rhuEpo) respectively, by the second induction cycle. The unexpected presence of neutralizing antibodies against Epo resulted in profound anemia for 2 individuals. Importantly, while the two animals were developing this phenotype, we found cellular infiltrates made of T and B lymphocytes and macrophages at the site of vector injection. Both, endogenous Epo and vector Epo sequences were found to be identical, and Epo secreted from in vitro rAAV-transduced cells had a similar molecular weight as the rhuEpo. This finding emphasizes the requirement for extensive preclinical studies to understand the mechanism(s) involved, in particular when a therapeutic protein is produce at high levels from an ectopic site.
A Phase II Study of BTI-322, a Monoclonal Anti-CD2 Antibody, for Treatment of Steroid-Resistant Acute Graft-Versus-Host Disease
Authors: Donna Przepiorka, Gordon L. Phillips, Voravit Ratanatharathorn, Michele Cottler-Fox, Laurie H. Sehn, Joseph H. Antin, Donna LeBherz, Michel Awwad, James Hope, J. Bruce McClain
Journal: Blood (1998)
The Vine and the Branches
Authors: Derek Economy
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
A Novel Localization of the G-Protein-Coupled CysLT1 Receptor in the Nucleus of Colorectal Adenocarcinoma Cells
Authors: Christian Kamp Nielsen, Joan I.A. Campbell, John F. Öhd, Matthias Mörgelin, Kristian Riesbeck, Göran Landberg, Anita Sjölander
Journal: Cancer Research (2005)

Searching for a link between inflammation and colon cancer, we have found that the inflammatory mediator leukotriene D(4) (LTD(4)), via its receptor CysLT(1), induces cyclooxygenase-2 expression, survival, and proliferation in intestinal epithelial cells. In conjunction with our previous observation that CysLT(1) receptor expression is increased in colorectal adenocarcinomas, we here found an increased nuclear localization of the CysLT(1) receptor in colorectal adenocarcinomas. This novel discovery of CysLT(1) receptors in the nucleus was further analyzed. It was found to be located in the outer nuclear membrane in colon cancer cells and in the nontransformed epithelial cell line Int 407 cells by Western blot and electron microscopy. Cancer cells displayed higher amounts of the nuclear CysLT(1) receptor, but prolonged LTD(4) exposure induced its nuclear translocation in nontransformed cells. Truncation of a nuclear localization sequence abrogated this translocation as well as the LTD(4)-induced proliferative response. In accordance, nuclear CysLT(1) receptors exhibited proliferative extracellular signal-regulated kinase 1/2 signaling. The significance of these experimental findings is supported by the observed correlation between the proliferative marker Ki-67 and nuclear CysLT(1) receptor localization in colorectal adenocarcinomas. The present findings indicate that LTD(4) cannot only be synthesized but also signal proliferation through nuclear CysLT(1) receptors, stressing the importance of leukotrienes in inflammation-induced colon carcinogenesis.
Secondary attack rate of pandemic influenza A(H1N1)2009 in Western Australian households, 29 May–7 August 2009
Authors: D Carcione, C M Giele, L S Goggin, K SH Kwan, D W Smith, G K Dowse, D B Mak, P Effler
Journal: Eurosurveillance (2011)

Understanding household transmission of the pandemic influenza A(H1N1)2009 virus, including risk factors for transmission, is important for refining public health strategies to reduce the burden of the disease. During the influenza season of 2009 we investigated transmission of the emerging virus in 595 households in which the index case was the first symptomatic case of influenza A(H1N1)2009. Secondary cases were defined as household contacts with influenza-like illness (ILI) or laboratory-confirmed influenza A(H1N1)2009, occurring at least one day after but within seven days following symptom onset in the index case. ILI developed in 231 of the 1,589 household contacts, a secondary attack rate of 14.5% (95% confidence interval (CI): 12.9–16.4). At least one secondary case occurred in 166 of the 595 households (a household transmission rate of 27.9%; 95% CI: 24.5–31.6).Of these, 127 (76.5%) households reported one secondary case and 39 (23.5%) households reported two or more secondary cases. Secondary attack rates were highest in children younger than five years (p=0.001), and young children were also more efficient transmitters (p=0.01). Individual risk was not associated with household size. Prophylactic antiviral therapy was associated with reduced transmission (p=0.03). The secondary attack rate of ILI in households with a confirmed pandemic influenza A(H1N1)2009 index case was comparable to that described previously for seasonal influenza.
Abstract 15515: Sexual Dimorphism in Cardiac Response to Intrauterine Growth Restriction (IUGR)
Authors: Alina Maloyan, Sribalasubashini Muralimanoharan, Mark Nijland, Peter W Nathanielsz
Journal: Circulation (2014)

Background: Poor fetal nutrient availability predisposes to adult cardiovascular disease (CVD). We have developed a fetal baboon model of maternal undernutrition resulting in Intrauterine Growth Restriction (IUGR) in both male and female fetuses (Li, et al, J Endocrinol, 2013). MicroRNAs are small non-coding RNAs that regulate gene expression through mRNA degradation and translational repression. Hypothesis: We hypothesized that IUGR is accompanied by cardiac dysfunction and dysregulation of cardiac miRNAs. Methods: Six control pregnant baboons ate ad libitum, and six nutrient restricted pregnant baboons ate a globally reduced diet (70% of control feed) from 0.16 gestation (G) through pregnancy resulting in fetal IUGR compared to controls (p&lt;0.05). No differences in heart weight were observed. Fetuses (3 males and 3 females per group) were euthanized at C-section at 0.9G. Cardiac sections were studied for morphological changes and fibrosis using H&amp;E and Masson’s trichrome staining respectively. Total left ventricular RNA was isolated and miRNA array was performed. Results: While no differences in myofiber orientation were observed, IUGR male but not female fetuses showed a reverse correlation between birth weight and accumulation of fibrotic tissue in the heart (r=-0.831, p=0.01). We next investigated the expression of the extracellular matrix proteins thrombospondin-1 (TSP-1) and connective tissue growth factor (CTGF). A reverse correlation between birth weight and cardiac TSP-1 levels (r=-0.77, p=0.03) was found in male but not female fetuses. No changes in CTGF were observed. Sexual dimorphism was observed in fetal cardiac miRNA expression within both IUGR and control groups. In male IUGR group, the increase in levels of TSP-1 was associated with more than 50% reduction in expression of its targeting miRNA-19a, reduction in which has been implicated in CVD. Other CVD-related and differentially expressed miRNAs in male IUGR included miRNA-23b, 27b, 99b, 143, 181a, and 378-3p. Summary: IUGR resulting from decreased maternal nutrition is associated with sexual dimorphism in cardiac structure and miRNA expression. If the changes observed in male IUGR fetuses persists postnatally they may program offspring for higher CVD risk later in life.
Natural alleles of a proteasome α2 subunit gene contribute to thermotolerance and adaptation of African rice
Authors: Xin-Min Li, Dai-Yin Chao, Yuan Wu, Xuehui Huang, Ke Chen, Long-Gang Cui, Lei Su, Wang-Wei Ye, Hao Chen, Hua-Chang Chen, Nai-Qian Dong, Tao Guo, Min Shi, Qi Feng, Peng Zhang, Bin Han, Jun-Xiang Shan, Ji-Ping Gao, Hong-Xuan Lin
Journal: Nature Genetics (2015)
Inhibition of smoothened decreases proliferation of synoviocytes in rheumatoid arthritis
Authors: Shang-ling Zhu, Jian-lin Huang, Wei-xiang Peng, Dan-chun Wu, Min-qi Luo, Qiu-xia Li, Zhao-xia Li, Xiao-xue Feng, Fang Liu, Ming-xia Wang, Wei-qian Chen, Nancy Olsen, Song Guo Zheng
Journal: Cellular and Molecular Immunology (2015)