tbuckley/cabot-search huggingface dataset:
502 High affinity IgE receptor (FcεRI)-bearing cells in bronchial biopsies from atopic and non-atopic asthma
Authors: J BARKANS, J GRANT, L TABORDABARATA, S YING, G MENZ, R PFISTER, S DURHAM, A KAY, M HUMBERT
Journal: Journal of Allergy and Clinical Immunology (1996)
THE INFLUENCE OF TWO SELECTED TRANQUILIZERS ON DRIVING SKILLS
Authors: WARREN J. HUFFMAN, AURELIO E. FLORIO, JOBE L. PAYNE, FLOYD E. BOYS
Journal: American Journal of Psychiatry (1963)

Since this was a multivariable study and some statistically significant differences would be expected by chance, it was concluded that under the conditions of this experiment hydroxyphenamate had no significant effect on the performance of the subjects, neither at the normal nor double the normal dosage.
Transgenic Overexpression of Aldehyde Dehydrogenase-2 Rescues Chronic Alcohol Intake–Induced Myocardial Hypertrophy and Contractile Dysfunction
Authors: Thomas A. Doser, Subat Turdi, D. Paul Thomas, Paul N. Epstein, Shi-Yan Li, Jun Ren
Journal: Circulation (2009)

Chronic alcoholism leads to the onset and progression of alcoholic cardiomyopathy through toxic mechanisms of ethanol and its metabolite, acetaldehyde. This study examined the impact of altered acetaldehyde metabolism through systemic transgenic overexpression of aldehyde dehydrogenase-2 (ALDH2) on chronic alcohol ingestion-induced myocardial damage.ALDH2 transgenic mice were produced with the chicken beta-actin promoter. Wild-type FVB and ALDH2 mice were placed on a 4% alcohol diet or a control diet for 14 weeks. Myocardial and cardiomyocyte contraction, intracellular Ca(2+) handling, histology (hematoxylin and eosin, Masson trichrome), protein damage, and apoptosis were determined. Western blot was used to monitor the expression of NADPH oxidase, calcineurin, apoptosis-stimulated kinase (ASK-1), glycogen synthase kinase-3beta (GSK-3beta), GATA4, and cAMP-response element binding (CREB) protein. ALDH2 reduced the chronic alcohol ingestion-induced elevation in plasma and tissue acetaldehyde levels. Chronic alcohol consumption led to cardiac hypertrophy, reduced fractional shortening, cell shortening, and impaired intracellular Ca(2+) homeostasis, the effect of which was alleviated by ALDH2. In addition, the ALDH2 transgene significantly attenuated chronic alcohol intake-induced myocardial fibrosis, protein carbonyl formation, apoptosis, enhanced NADPH oxidase p47(phox) and calcineurin expression, as well as phosphorylation of ASK-1, GSK-3beta, GATA4, and CREB.The present results suggest that transgenic overexpression of ALDH2 effectively antagonizes chronic alcohol intake-elicited myocardial hypertrophy and contractile defect through a mechanism that is associated, at least in part, with phosphorylation of ASK-1, GSK-3beta, GATA4, and CREB. These data strongly support the notion that acetaldehyde may be an essential contributor to the chronic development of alcoholic cardiomyopathy.
Pulmonary Infiltrates and Eosinophilia From Minocycline
Authors: Manuel Otero
Journal: JAMA (1983)

<h3>To the Editor.—</h3> A variety of drugs has been implicated as causes of pulmonary infiltrates with peripheral eosinophilia. Ho et al<sup>1</sup>described two patients in whom administration of a tetracycline antibiotic was associated with diffuse skin rash and pulmonary infiltrates with eosinophilia. <h3>Report of a Case.—</h3> A 55-year-old woman was given oral minocycline hydrochloride (100 mg twice a day) in December 1982 for treatment of a cutaneous<i>Mycobacterium marinum</i>infection. Approximately four weeks later, the skin lesions had resolved but she experienced fever, chills, night sweats, and fatigue. The minocycline therapy was discontinued and she was admitted to the hospital. Her temperature was 40 °C. On auscultation, breath sounds were decreased and fine crackles were heard over both lung bases. Admission chest x-ray film showed diffuse bilateral fine reticulonodular infiltrates involving all lobes but most prominent in the lung bases. The WBC count was 12,900/cu mm with 22% eosinophils; an
HLA specificities are related to development and prognosis of diffuse large B-cell lymphoma
Authors: Miguel Alcoceba, Elena Sebastián, Luis Marín, Ana Balanzategui, M. Eugenia Sarasquete, M. Carmen Chillón, Cristina Jiménez, Noemí Puig, Rocío Corral, Emilia Pardal, Carlos Grande, José Luis Bello, Carmen Albo, Fátima de la Cruz, Carlos Panizo, Alejandro Martín, Eva González-Barca, M. Dolores Caballero, Jesús F. San Miguel, Ramón García-Sanz, Marcos González
Journal: Blood (2013)
Effective Treatment of Tumors with Strong β-Catenin/T-Cell Factor Activity by Transcriptionally Targeted Oncolytic Herpes Simplex Virus Vector
Authors: Toshihiko Kuroda, Samuel D. Rabkin, Robert L. Martuza
Journal: Cancer Research (2006)

The Wnt/beta-catenin/T-cell factor (Tcf) pathway is aberrantly up-regulated in the majority of colorectal cancers (CRC) and hepatoblastomas due to either an APC or beta-catenin gene mutation. We constructed synthetic promoters, T and TE, which contain tandem repeats of a Tcf responsive element without and with the human 4F2 gene intronic enhancer, respectively. Although the T and TE promoters showed higher transcriptional activity than a control promoter in all CRC and hepatoblastoma cell lines tested, with low activities in most other tumor cell lines, the level of transcription varied considerably among the CRC and hepatoblastoma cell lines. In some CRC cell lines, the TE promoter displayed higher levels of transcription than even the human CMV(IE) promoter. In those CRC cells, the APC gene mutations were located within a small segment between the first and second 20-amino-acid repeats in the mutation cluster region of the APC protein. We created a transcriptionally targeted oncolytic herpes simplex virus vector (bM24-TE) in which replication is driven by the TE promoter. This vector efficiently and specifically replicated in and killed tumor cells with strong beta-catenin/Tcf signaling. Intratumoral injection of bM24-TE significantly reduced the growth of highly beta-catenin active SW480 CRC tumors and induced a complete response in half of them, whereas it had no effect on the growth of beta-catenin-inactive A549 tumors. Our results suggest that a transcriptionally regulated oncolytic herpes vector targeting beta-catenin/Tcf signal is very efficacious against CRC tumors carrying an APC gene mutation between the first and second 20-amino-acid repeats.
Cardiac myocytes express multiple gap junction proteins.
Authors: H L Kanter, J E Saffitz, E C Beyer
Journal: Circulation Research (1992)

Electrical propagation in the normal heart occurs via intercellular transfer of current at gap junctions. Alterations in intercellular coupling in the diseased heart are critical in the pathogenesis of reentrant ventricular arrhythmias. Until recently only a single gap junction protein was known to couple cardiac myocytes. We have now identified and sequenced two additional distinct gap junction proteins (connexins) expressed in the mammalian heart. The sequences differ in their predicted cytoplasmic regulatory domains. Expression of all three connexins by canine ventricular myocytes has been confirmed by Northern blotting and by immunohistochemistry with connexin-specific antisera. Immunoelectron microscopy confirmed that all three connexins are localized to myocyte gap junctions. The presence of multiple connexins in myocyte gap junctions suggests novel mechanisms for regulating cardiac electrical coupling.
Axonal BACE1 dynamics and targeting in hippocampal neurons: a role for Rab11 GTPase
Authors: Virginie Buggia-Prévot, Celia G Fernandez, Sean Riordan, Kulandaivelu S Vetrivel, Jelita Roseman, Jack Waters, Vytautas P Bindokas, Robert Vassar, Gopal Thinakaran
Journal: Molecular Neurodegeneration (2014)

BACE1 is one of the two enzymes that cleave amyloid precursor protein to generate Alzheimer's disease (AD) beta amyloid peptides. It is widely believed that BACE1 initiates APP processing in endosomes, and in the brain this cleavage is known to occur during axonal transport of APP. In addition, BACE1 accumulates in dystrophic neurites surrounding brain senile plaques in individuals with AD, suggesting that abnormal accumulation of BACE1 at presynaptic terminals contributes to pathogenesis in AD. However, only limited information is available on BACE1 axonal transport and targeting. By visualizing BACE1-YFP dynamics using live imaging, we demonstrate that BACE1 undergoes bi-directional transport in dynamic tubulo-vesicular carriers along axons in cultured hippocampal neurons and in acute hippocampal slices of transgenic mice. In addition, a subset of BACE1 is present in larger stationary structures, which are active presynaptic sites. In cultured neurons, BACE1-YFP is preferentially targeted to axons over time, consistent with predominant in vivo localization of BACE1 in presynaptic terminals. Confocal analysis and dual-color live imaging revealed a localization and dynamic transport of BACE1 along dendrites and axons in Rab11-positive recycling endosomes. Impairment of Rab11 function leads to a diminution of total and endocytosed BACE1 in axons, concomitant with an increase in the soma. Together, these results suggest that BACE1 is sorted to axons in endosomes in a Rab11-dependent manner. Our results reveal novel information on dynamic BACE1 transport in neurons, and demonstrate that Rab11-GTPase function is critical for axonal sorting of BACE1. Thus, we suggest that BACE1 transcytosis in endosomes contributes to presynaptic BACE1 localization.
Capacity to Provide Informed Consent for Participation in Schizophrenia and HIV Research
Authors: David J. Moser, Susan K. Schultz, Stephan Arndt, Michelle L. Benjamin, Frank W. Fleming, Colleen S. Brems, Jane S. Paulsen, Paul S. Appelbaum, Nancy C. Andreasen
Journal: American Journal of Psychiatry (2002)

OBJECTIVE: The degree to which people with psychiatric symptoms and cognitive dysfunction can provide informed consent to participate in research is a controversial issue. This study was designed to examine the capacity of subjects with schizophrenia and subjects with HIV to provide informed consent for research participation and to determine the relationships among cognitive dysfunction, psychiatric symptoms, and decisional capacity. METHOD: Twenty-five men and women with a DSM-IV diagnosis of schizophrenia and 25 men and women with HIV were recruited. The groups were compared in terms of neuropsychological functioning, psychiatric symptoms, and ability to provide informed consent to a hypothetical drug trial. RESULTS: Eighty percent of the subjects with schizophrenia and 96% of the HIV-positive subjects demonstrated adequate capacity to consent to the hypothetical drug trial, but subjects in the schizophrenia group had significantly lower scores on two of the four aspects of decisional capacity. For the subjects with schizophrenia, neuropsychological functioning and psychiatric symptoms (e.g., apathy and avolition), but not psychotic symptoms (e.g., hallucinations and delusions), were significantly associated with decisional capacity. CONCLUSIONS: The majority of subjects who are recruited and willing to participate in schizophrenia or HIV research will have adequate capacity to provide consent. Cognitive dysfunction and the symptoms shown to be associated with impaired decisional capacity are not unique to schizophrenia and may occur with many other forms of illness. These findings underscore the importance of considering how decisional capacity will be assessed in all types of research, regardless of the specific condition being studied.
Comparison of relative frequency of HFE gene mutations in minor beta-thalassemia and healthy population in Tehran
Authors: M. Jazayeri, V. Bakayev, M.R. Zali, H.R. Mohaghegh, A. Esmaeili, F. Haghighirad, H. Zakeri, E. Kalantar, S. Shahraz, P. Adibi
Journal: Journal of Hepatology (2003)
Screening for lung cancer using low dose CT scanning
Authors: R MacRedmond
Journal: Thorax (2004)

Lung cancer is the most common cause of cancer related death in Ireland. The majority of lung cancers are inoperable at the time of diagnosis and consequently the overall 5 year survival is less than 10%. The objective of the ProActive Lung Cancer Detection (PALCAD) study was to evaluate whether low dose chest computed tomographic scanning (LDCCT) can detect early stage asymptomatic lung cancer in a high risk urban population.Four hundred and forty nine subjects of median age 55 years (range 50-74) with a median pack year smoking history of 45 years (range 10-160), with no previous cancer history and medically fit to undergo thoracic surgery were recruited. After informed consent, LDCCT was performed on all subjects. Non-calcified nodules (NCNs) of >/=10 mm in diameter were referred for biopsy. Follow up with interval LDCCT at 6, 12 and 24 months to exclude growth was recommended for NCNs <10 mm in diameter.Six (1.3%) NCNs of >/=10 mm were detected of which one (0.23%) had non-small cell lung cancer stage 1; 145 NCNs of <10 mm were detected in 87 (19.4%) subjects. Mediastinal masses were detected in three subjects (0.7%)-one small cell lung cancer and two benign duplication cysts. Incidental pathology was noted in 276 patients (61.5%), most commonly emphysema and coronary artery calcification.The prevalence of resectable lung cancer detected by LDCCT at baseline screening was low at 0.23%, but there was a high rate of significant incidental pathology.
Fatal haemoptysis in a case of lymphomatoid granulomatosis treated with rituximab
Authors: S. Jaffre, F. Jardin, S. Dominique, E. Duet, Ph. Hubscher, A. Genevois, F. Corne, S. Bota, G. Nouvet, L. Thiberville
Journal: European Respiratory Journal (2006)

Lymphomatoid granulomatosis is a rare angiocentric and angiodestructive disease, which commonly involves the lungs but also the brain, kidneys, liver and skin. This report describes the case of a 33-yr-old female with an aggressive form of lymphoid granulomatosis treated with an anti-CD20 antibody. Dramatic radiological improvement was seen at the fourth week. However, the patient died at home 1 month after the last rituximab administration from a massive haemoptysis.
Digitized Mammography: a Clinical Trial of Postmenopausal Women Randomly Assigned to Receive Raloxifene, Estrogen, or Placebo
Authors: M. Freedman, J. S. Martin, J. O'Gorman, S. Eckert, M. E. Lippman, S.-C. B. Lo, E. L. Walls, J. Zeng
Journal: JNCI Journal of the National Cancer Institute (2001)

Background: High mammographic density is associated with increased breast cancer risk. Previous studies have shown that estrogens increase breast density on mammograms, but the effect on mammographic density of selective estrogen receptor modulators, such as raloxifene, is unknown. We assessed changes in mammographic density among women receiving placebo, raloxifene, or conjugated equine estrogens in an osteoporosis prevention trial. Methods: In a 5-year multicenter, double-blind, randomized, placebo-controlled osteoporosis prevention trial, healthy postmenopausal women who had undergone hysterectomy less than 15 years before the study and had no history of breast cancer received placebo, raloxifene (at one of two doses), or conjugated estrogens (ERT). Women from English-speaking investigative sites who had baseline and 2-year craniocaudal mammograms with comparable positioning (n = 168) were eligible for this analysis. Changes in mammographic density were determined by digital scanning and computer-assisted segmentation of mammograms and were analyzed with the use of analysis of variance. All statistical tests were two-sided. Results: Among the four treatment groups after 2 years on study, the mean breast density (craniocaudal view) was statistically significantly greater in the ERT group than it was in the other three groups (P<.01 for all three comparisons). Within treatment groups, the mean breast density from baseline to 2 years decreased statistically significantly in women receiving the placebo or either the higher or lower raloxifene dose (P = .003, P = .002, and P<.001, respectively) and showed a nonstatistically significant increase in women receiving ERT. Conclusions: In an osteoporosis prevention trial, raloxifene did not increase breast density after 2 years of treatment. Raloxifene administration should not interfere with, and could even enhance, mammographic detection of new breast cancers.
In vivo ANA is a fixation artifact
Authors: K Kramers, M C van Bruggen, T P Rijke-Schilder, H B Dijkman, M N Hylkema, H J Croes, J A Fransen, K J Assmann, W J Tax, R J Smeenk, J H Berden
Journal: Journal of the American Society of Nephrology (1996)

It has been suggested that binding of anti-double-standed DNA antibodies to cell surfaces, followed by internalization and nuclear binding (so called in vivo ANA) is of pathophysiological significance for tissue damage in systemic lupus erythematosus. We have shown before that pathogenic antinuclear antibodies complexed to nucleosomal antigens can bind to heparan sulfate in the glomerular basement membrane in vivo. Because nucleosomes are also reported to bind to the cell surface, we hypothesized that in vivo ANA is a property of antinuclear antibodies bound to nucleosomal antigens. Therefore, we studied three antinucleosome monoclonal antibodies (mAb) that exhibit in vivo ANA as seen by immunofluorescence in mice inoculated intraperitoneally with the hybridoma producing the mAb. The same mAb complexed to nucleosomal antigens after intravenous injection into mice induced in vivo ANA, in contrast to purified noncomplexed mAb. To study this in more detail, we incubated complexed mAb with various cell lines and found binding to the cell surface and subsequent internalization into cytoplasmic vesicles. However, no binding to the nucleus was observed by immunoelectron microscopy (IEM) and confocal laser microscopy. Noncomplexed mAb did not bind to the cell surface. Next, from mice bearing the hybridomas producing the mAb intraperitoneally, a small part of the kidney was snap frozen in liquid N2, fixed with acetone, and studied in immunofluorescence, whereas the remaining part of the kidney was fixed in vivo by renal perfusion with a mixture of 0.01 M sodium periodate, 0.075 M lysine HCl, 0.0375 M Na2HPO4, and 2% paraformaldehyde (PLP) and studied in both immunofluorescence and IEM. In the acetone-fixed kidney sections obtained without in vivo fixation we again observed in vivo ANA. However, after in vivo PLP perfusion fixation, no nuclear binding was found. In IEM, localization in cytoplasmic vesicles was seen. In conclusion, antinucleosome antibodies complexed to nucleosomal antigens can bind to the cell surface and are transported into the cytoplasm, but do not bind to the nucleus. The reported nuclear localization of antinuclear antibodies is caused by a fixation artifact.
Abstract 4955: Role of Angiotensin II in prostate cancer metastasis
Authors: Debanjan Chakroborty, Chandrani Sarkar
Journal: Cancer Research (2014)

Abstract Introduction: At the initial stages prostate cancer development depends on a crucial level of androgenic stimulation but at later stages when it becomes androgen independent the perturbation from androgen receptor axis leads to the development of more aggressive phenotypes with greater metastatic potential. At this stage the growth and progression of prostate cancer is regulated by various local growth factors and neuro-hormones which are altered in prostate cancer microenvironment. Therefore, identifying these factors which are aberrantly expressed in the tumor microenvironment and understanding how these factors are involved in regulating the tumor progression are essential for developing better targeted therapeutic strategy for the treatment of advanced stages of prostate cancer. Objective: As emerging reports suggest the importance of tissue based renin angiotensin system (RAS) in pathophysiology of the prostate and as studies indicate a lower incidence of cancer and cancer related deaths in patients taking angiotensin receptor blockers (ARBs) (as medication for hypertension), we intend to study the role played by this system in the progression of prostate cancer. Methods and Results: Our results show that there is limited expression of RAS components, Angiotensin II (AT II), the main bioactive effector peptide of RAS and its receptors, and its receptor Angiotensin receptor type 1( AT1R) and Angiotensin receptor type 2 (AT2R) , in mouse prostate tissues. However, RAS becomes activated in prostate cancer. The expressions of ATII and AT1R are significantly higher in androgen independent orthotopic PC3 prostate tumor tissues. The expression of AT2R remains unaltered during the development of tumor. Therefore to evaluate the role of ATII in prostate cancer progression, in vitro experiments using two androgen independent orthotopic cell lines, PC3 and C4-2 were performed. Both these cell lines express AT1R. Our results indicate that ATII acting through AT1R promotes metastatic behavior such as invasion and migration of prostate cancer cells and inhibition of ATII by blocking AT1R receptor abrogates this action of ATII. Conclusions: This study identifies a new role of local RAS in the metastatic progression of prostate cancer and will eventually help to develop newer and effective therapeutic strategies in treatment of androgen independent prostate cancer by targeting ATII or AT1R. This strategy can be used either alone or in combination with existing therapeutic strategies in treatment of the disease. Citation Format: Debanjan Chakroborty, Chandrani Sarkar. Role of Angiotensin II in prostate cancer metastasis. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4955. doi:10.1158/1538-7445.AM2014-4955
The Effect of Imported Fire Ant Whole-Body Extract on the Degradation of Timothy, Ragweed, Cat, and House Dust Mite Allergens
Authors: T RANS, T HRABAK, B WHISMAN, T GRIER, D LEFEVRE, E DUNCAN, K WHITAKER, P KWON, M TANKERSLEY
Journal: Journal of Allergy and Clinical Immunology (2008)
The lung cancer patient, the pneumologist and palliative care: a developing alliance
Authors: Torsten Blum, Nicolas Schönfeld
Journal: European Respiratory Journal (2014)

Considerable evidence is now available on the value of palliative care for lung cancer patients in all stages and at all times during the course of the disease. However, pneumologists and their institutions seem to be widely in arrears with the implementation of palliative care concepts and the development of integrated structures. This review focuses on the available evidence and experience of various frequently unmet needs of lung cancer patients, especially psychological, social, spiritual and cultural ones. A PubMed search for evidence on these aspects of palliative care as well as on barriers to the implementation, on outcome parameters and effectiveness, and on structure and process quality was performed with a special focus on lung cancer patients. As a consequence, this review particularly draws pneumologists’ attention to improving their skills in communication with the patients, their relatives and among themselves, and to establish team structures with more far-reaching competences and continuity than existing multilateral cooperations and conferences can provide. Ideally, any process of structural and procedural improvement should be accompanied by scientific evaluation and measures for quality optimisation.