tbuckley/cabot-search huggingface dataset:
Intravenous Almitrine Combined with Inhaled Nitric Oxide for Acute Respiratory Distress Syndrome
Authors: LLUIS GALLART, QIN LU, LOUIS PUYBASSET, G. S. UMAMAHESWARA RAO, PIERRE CORIAT, JEAN-JACQUES ROUBY
Journal: American Journal of Respiratory and Critical Care Medicine (1998)

Inhaled nitric oxide (iNO), a selective pulmonary vasodilator and intravenously administered almitrine, a selective pulmonary vasoconstrictor, have been shown to increase PaO2 in patients with acute respiratory distress syndrome (ARDS). This prospective study was undertaken to assess the cardiopulmonary effects of combining both drugs. In 48 consecutive patients with early ARDS, cardiorespiratory parameters were measured at control, after iNO 5 ppm, after almitrine 4 μ g · kg− 1 · min− 1, and after the combination of both drugs. In 30 patients, dose response to 2, 4, and 16 μ g · kg− 1 · min− 1 of almitrine with and without NO was determined. Almitrine and lactate plasma concentrations were measured in 17 patients. Using pure O2, PaO2 increased by 75 ± 8 mm Hg after iNO, by 101 ± 12 mm Hg after almitrine 4 μ g · kg− 1 · min− 1, and by 175 ± 18 mm Hg after almitrine combined with iNO (p < 0.001). In 63% of the patients, PaO2 increased by more than 100% with the combination of both drugs. Mean pulmonary artery pressure (Ppa) increased by 1.4 ± 0.2 mm Hg with almitrine 4 μ g/kg/ min (p < 0.001) and decreased by 3.4 ± 0.4 mm Hg with iNO and by 1.5 ± 0.3 mm Hg with the combination (p < 0.001). The maximum increase in PaO2 was obtained at almitrine concentrations ⩽ 4 μ g · kg− 1 · min− 1, whereas almitrine increased Ppa dose-dependently. Almitrine plasma concentrations also increased dose-dependently and returned to values close to zero after 12 h. In many patients with early ARDS, the combination of iNO 5 ppm and almitrine 4 μ g · kg− 1 · min− 1 dramatically increases PaO2 without apparent deleterious effect allowing a rapid reduction in inspired fraction of O2. The long-term consequences of this immediate beneficial effect remain to be determined.
Impact of dental care in the prevention of bisphosphonate-associated osteonecrosis of the jaw: a single-center clinical experience
Authors: A.M. Vandone, M. Donadio, M. Mozzati, M. Ardine, M.A. Polimeni, S. Beatrice, L. Ciuffreda, M. Scoletta
Journal: Annals of Oncology (2011)
Novel alphavirus-based vaccine induces strong immune responses against prostate-specific antigen (PSA) and mediates tumor cell elimination in a mouse model of prostate cancer
Authors: Vladimir Ryabov, Peter Pushko, Irina Tretyakova, Rikka Saito, Richard B Alexander, Elena N Klyushnenkova
Journal: Journal for ImmunoTherapy of Cancer (2013)

Meeting abstracts Prostate cancer is the second most frequently diagnosed cancer in men worldwide and sixth leading cancer-related cause of death in males. Treatments for recurrent prostate cancer are only rarely curative, and the majority of patients eventually demonstrate progressive disease.
Sites of Impulse Formation within the Atrioventricular Junction of the Rabbit
Authors: YOSHIO WATANABE, LEONARD S. DREIFUS
Journal: Circulation Research (1968)

Spontaneous A-V nodal rhythm was observed in 23 isolated, perfused rabbit hearts during electrophysiologic studies of A-V transmission. In 19 of the 23, the earliest point of activation was determined by recording transmembrane potentials from numerous A-V junctional fibers. Most commonly (15 hearts), the earliest depolarization was found in a specific area of the A-V node near the point where the fibrous A-V ring extending into the coronary sinus joins a portion of A-V ring between right atrial and ventricular free walls. Various observations suggested that this area was the NH region. In the remaining four hearts, the origin of nodal beats was in the AN region. Diastolic depolarization was often seen in and around the earliest point of activation. The A-V interval in these nodal rhythms ranged from -38.7 to +71.6 msec, in contrast to the A-V interval of 93.3 to 135.7 msec during sinus rhythm. In the presence of NH rhythm, different retrograde intranodal conduction time (across the N region) was the major cause for the wide variation of the A-V interval. Wandering of the pacemaker between the S-A and A-V nodes and examples of exit block of A-V nodal impulses were observed.
The impact of the hepatitis B mass immunisation campaign on the incidence and risk factors of acute hepatitis B in Italy
Authors: Tommaso Stroffolini, Alfonso Mele, Maria Elena Tosti, Giovanni Gallo, Emanuela Balocchini, Pietro Ragni, Franco Santonastasi, Antonella Marzolini, Massimo Ciccozzi, Angela Moiraghi
Journal: Journal of Hepatology (2000)
Final results of a randomised trial comparing ‘Tomudex’® (raltitrexed) with 5-fluorouracil plus leucovorin in advanced colorectal cancer
Authors: D. Cunningham, J.R. Zalcberg, U. Rath, I. Oliver, E. van Cutsem, C. Svensson, J.F. Seitz, P. Harper, D. Kerr, G. Perez-Manga
Journal: Annals of Oncology (1996)
Addressing the Knowledge Gap in Clinical Recommendations for Management and Complete Excision of Clinically Atypical Nevi/Dysplastic Nevi
Authors: Caroline C. Kim, Susan M. Swetter, Clara Curiel-Lewandrowski, James M. Grichnik, Douglas Grossman, Allan C. Halpern, John M. Kirkwood, Sancy A. Leachman, Ashfaq A. Marghoob, Michael E. Ming, Kelly C. Nelson, Emir Veledar, Suraj S. Venna, Suephy C. Chen
Journal: JAMA Dermatology (2014)

The management of clinically atypical nevi/dysplastic nevi (CAN/DN) is controversial, with few data to guide the process. Management recommendations for DN with positive histologic margins were developed by the Delphi method to achieve consensus among members of the Pigmented Lesion Subcommittee (PLS) of the Melanoma Prevention Working Group (MPWG) after reviewing the current evidence.To outline key issues related to the management of CAN/DN: (1) biopsies of CAN and how positive margins arise, (2) whether incompletely excised DN evolve into melanoma, (3) current data on the outcomes of DN with positive histologic margins, (4) consensus recommendations, and (5) a proposal for future studies, including a large-scale study to help guide the management of DN with positive margins.The literature, including recent studies examining management and outcomes of DN with positive margins between 2009 to 2014, was reviewed.A consensus statement by the PLS of the MPWG following review of the literature, group discussions, and a structured Delphi method consensus.This consensus statement reviews the complexities of management of CAN/DN. A review of the literature and 2 rounds of a structured Delphi consensus resulted in the following recommendations: (1) mildly and moderately DN with clear margins do not need to be reexcised, (2) mildly DN biopsied with positive histologic margins without clinical residual pigmentation may be safely observed rather than reexcised, and (3) observation may be a reasonable option for management of moderately DN with positive histologic margins without clinically apparent residual pigmentation; however, more data are needed to make definitive recommendations in this clinical scenario.
Gap junctional channels in adult mammalian sinus nodal cells. Immunolocalization and electrophysiology.
Authors: J M Anumonwo, H Z Wang, E Trabka-Janik, B Dunham, R D Veenstra, M Delmar, J Jalife
Journal: Circulation Research (1992)

The subcellular mechanism of cell-to-cell communication in the natural pacemaker region of the mammalian heart was studied using electrophysiological and immunofluorescence techniques in isolated pairs of rabbit sinus nodal cells. By measuring whole-cell currents using a double patch-clamp approach, it was demonstrated that communication in the sinus node is mediated through gap junctional channels similar to those in other types of adult cardiac cell pairs. Macroscopic sinus nodal junctional resistance had a mean value of 387.9 +/- 97.1 M omega (mean +/- SEM, n = 10) and was greatly increased by superfusion with alkanols. Single-channel junctional conductance could be resolved in three cell pairs. Given their high membrane resistance (1.16 +/- 0.32 G omega, n = 12), the electrical coupling provided by as few as three gap junctional channels between nodal cells will allow for pacemaker synchronization. Further evidence for the presence of the channels was obtained from immunofluorescent double-labeling of desmin and the gap junction protein (connexin43) in sinus nodal tissue as well as in cultured sinus nodal cells. Using antisera against residues 243-257 of the connexin43 protein, a specific staining at the site of cell-to-cell apposition was demonstrated. These data provide direct evidence in favor of electronic coupling as the means for achieving pacemaker synchronization in the rabbit sinus node.
Blocking the transcription factor E2F/DP by dominant-negative mutants in a normal breast epithelial cell line efficiently inhibits apoptosis and induces tumor growth in SCID mice.
Authors: R C Bargou, C Wagener, K Bommert, W Arnold, P T Daniel, M Y Mapara, E Grinstein, H D Royer, B Dörken
Journal: The Journal of Experimental Medicine (1996)

The transcription factor E2F is regulated during the cell cycle through interactions with the product of the retinoblastoma susceptibility gene and related proteins. It is thought that E2F-mediated gene regulation at the G1/S boundary and during S phase may be one of the rate-limiting steps in cell proliferation. It was reported that in vivo overexpression of E2F-1 in fibroblasts induces S phase entry and leads to apoptosis. This observation suggests that E2F plays a role in both cell cycle regulation and apoptosis. To further understand the role of E2F in cell cycle progression, cell death, and tumor development, we have blocked endogenous E2F activity in HBL-100 cells, derived from nonmalignant human breast epithelium, using dominant-negative mutants under the control of a tetracycline-dependent expression system. We have shown here that induction of dominant-negative mutants led to strong downregulation of transiently transfected E2F-dependent chloramphenicol acetyl transferase reporter constructs and of endogenous c-myc, which has been described as a target gene of the transcription factor E2F/DP. In addition, we have shown that blocking of E2F could efficiently protect from apoptosis induced by serum starvation within a period of 10 d, whereas control cells started to die after 24 h. Surprisingly, blocking of E2F did not alter the rate of proliferation or of DNA synthesis of these cells; this finding indicates that cell-cycle progression could be driven in an E2F-independent manner. In addition, we have been able to show that blocking of endogenous E2F in HBL-100 cells led to rapid induction of tumor growth in severe combined immunodeficiency mice. No tumor growth could be observed in mice that received mock-transfected clones or tetracycline to block expression of the E2F mutant constructs in vivo. Thus, it appears that E2F has a potential tumor-suppressive function under certain circumstances. Furthermore, we provide evidence that dysregulation of apoptosis may be an important step in tumorigenesis.
Reticulate acropigmentation of Kitamura: pigment specks and pits in unusual locations
Authors: G.G. Lestringant, G.A. Aal, P.M. Frossard, K.I. Qayed
Journal: British Journal of Dermatology (1994)

Journal Article Reticulate acropigmentation of Kitamura: pigment specks and pits in unusual locations Get access G.G. Lestringant, G.G. Lestringant Department of Dermatology, Tawam Hospital and FMHS, Al Ain, United Arab Emirates Search for other works by this author on: Oxford Academic Google Scholar G.A. Aal, G.A. Aal Department of Pathology, Kuwaiti Hospital, Dubai, United Arab Emirates Search for other works by this author on: Oxford Academic Google Scholar P.M. Frossard, P.M. Frossard Department of Pathology, FMHS, Al Ain, United Arab Emirates Search for other works by this author on: Oxford Academic Google Scholar K.I. Qayed K.I. Qayed Department of Dermatology, Kuwaiti Hospital, Dubai, United Arab Emirates Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 131, Issue 1, 1 July 1994, Pages 137–139, https://doi.org/10.1111/j.1365-2133.1994.tb08475.x Published: 01 July 1994
A report with consensus statements of the International Society of Nephrology 2004 Consensus Workshop on Prevention of Progression of Renal Disease, Hong Kong, June 29, 2004
Authors: Philip Kam-Tao Li, Jan J. Weening, John Dirks, Sing Leung Lui, Cheuk Chun Szeto, Sydney Tang, Robert C. Atkins, William E. Mitch, Kai Ming Chow, Giuseppe D'Amico, Barry I. Freedman, David C. Harris, Lai-Seong Hooi, Paul E. de Jong, Priscilla Kincaid-Smith, Kar Neng Lai, Evan Lee, Fu-Keung Li, Shan-Yan Lin, Wai-Kei Lo, M.K. Mani, Timothy Mathew, Mutsumi Murakami, Jia-Qi Qian, Sylvia Ramirez, Thomas Reiser, Yasuhiko Tomino, Matthew K. Tong, Wai-Kay Tsang, Kriang Tungsanga, Haiyan Wang, Andrew K. Wong, K.I.M. Ming Wong, Wu-Chang Yang, Dick D.E. Zeeuw, Alex W. Yu, Giuseppe Remuzzi
Journal: Kidney International (2005)
Short-lived and Long-lived Bone Marrow Plasma Cells Are Derived from a Novel Precursor Population
Authors: Brian P. O'Connor, Marilia Cascalho, Randolph J. Noelle
Journal: The Journal of Experimental Medicine (2002)

The contribution that long-lived bone marrow (BM) plasma cells (PCs) provide to enduring humoral immunity has been underscored by a number of recent studies. However, little is known about the immediate precursors that give rise to long-lived PCs in the BM of immune individuals. We have identified subsets of antigen-experienced B cells within the immune BM that are precursors to PCs. These PC precursors arise in the BM 14 days after immunization and persist for greater than 9 months. Phenotypically distinct subsets of PC precursors give rise to short-lived or long-lived PCs. The differentiation of PC precursors to PCs occurs in the absence of antigen and requires cell division. The functional significance of these newly identified PC precursors in the persistence and quality of the humoral immune response is discussed.
Hereditary hepatic and systemic amyloidosis caused by a new deletion/insertion mutation in the apolipoprotein AI gene.
Authors: D R Booth, S Y Tan, S E Booth, G A Tennent, W L Hutchinson, J J Hsuan, N F Totty, O Truong, A K Soutar, P N Hawkins, M Bruguera, J Caballería, M Solé, J M Campistol, M B Pepys
Journal: Journal of Clinical Investigation (1996)

We report a Spanish family with autosomal-dominant non-neuropathic hereditary amyloidosis with a unique hepatic presentation and death from liver failure, usually by the sixth decade. The disease is caused by a previously unreported deletion/insertion mutation in exon 4 of the apolipoprotein AI (apoAI) gene encoding loss of residues 60-71 of normal mature apoAI and insertion at that position of two new residues, ValThr. Affected individuals are heterozygous for this mutation and have both normal apoAI and variant molecules bearing one extra positive charge, as predicted from the DNA sequence. The amyloid fibrils are composed exclusively of NH2-terminal fragments of the variant, ending mainly at positions corresponding to residues 83 and 92 in the mature wild-type sequence. Amyloid fibrils derived from the other three known amyloidogenic apoAI variants are also composed of similar NH2-terminal fragments. All known amyloidogenic apoAI variants carry one extra positive charge in this region, suggesting that it may be responsible for their enhanced amyloidogenicity. In addition to causing a new phenotype, this is the first deletion mutation to be described in association with hereditary amyloidosis and it significantly extends the value of the apoAI model for investigation of molecular mechanisms of amyloid fibrillogenesis.
Anomalous Origin of the Left Coronary Artery
Authors: ROBERT B. CASE, ANDREW G. MORROW, WENDELL STAINSBY, JOHN O. NESTOR
Journal: Circulation (1958)

Anomalous origin of the left coronary artery from the pulmonary artery is a rare and almost universally fatal form of congenital heart disease. It has usually been assumed that flow in the aberrant artery is from the pulmonary artery toward the myocardium and efforts at surgical correction have been directed at increasing the perfusion pressure or the oxygen content of pulmonary artery blood. Evidence is presented, that flow in the aberrant artery is into the pulmonary artery and that ligation of the vessel at its origin should be carried out before irreversible myocardial damage has occurred.
Validity of spirometric testing in a general practice population of patients with chronic obstructive pulmonary disease (COPD)
Authors: T R Schermer
Journal: Thorax (2003)

To investigate the validity of spirometric tests performed in general practice.A repeated within subject comparison of spirometric tests with a "gold standard" (spirometric tests performed in a pulmonary function laboratory) was performed in 388 subjects with chronic obstructive pulmonary disease (COPD) from 61 general practices and four laboratories. General practitioners and practice assistants undertook a spirometry training programme. Within subject differences in forced expiratory volume in 1 second and forced vital capacity (DeltaFEV1 and DeltaFVC) between laboratory and general practice tests were measured (practice minus laboratory value). The proportion of tests with FEV1 reproducibility <5% or <200 ml served as a quality marker.Mean DeltaFEV1 was 0.069 l (95% CI 0.054 to 0.084) and DeltaFVC 0.081 l (95% CI 0.053 to 0.109) in the first year evaluation, indicating consistently higher values for general practice measurements. Second year results were similar. Laboratory and general practice FEV1 values differed by up to 0.5 l, FVC values by up to 1.0 l. The proportion of non-reproducible tests was 16% for laboratory tests and 18% for general practice tests (p=0.302) in the first year, and 18% for both in the second year evaluation (p=1.000).Relevant spirometric indices measured by trained general practice staff were marginally but statistically significantly higher than those measured in pulmonary function laboratories. Because of the limited agreement between laboratory and general practice values, use of these measurements interchangeably should probably be avoided. With sufficient training of practice staff the current practice of performing spirometric tests in the primary care setting seems justifiable.
Cross-talk between HER2 and MED1 Regulates Tamoxifen Resistance of Human Breast Cancer Cells
Authors: Jiajun Cui, Katherine Germer, Tianying Wu, Jiang Wang, Jia Luo, Shao-chun Wang, Qianben Wang, Xiaoting Zhang
Journal: Cancer Research (2012)

Despite the fact that most breast cancer patients have estrogen receptor (ER) α-positive tumors, up to 50% of the patients are or soon develop resistance to endocrine therapy. It is recognized that HER2 activation is one of the major mechanisms contributing to endocrine resistance. In this study, we report that the ER coactivator MED1 is a novel cross-talk point for the HER2 and ERα pathways. Tissue microarray analysis of human breast cancers revealed that MED1 expression positively correlates most strongly with HER2 status of the tumors. MED1 was highly phosphorylated, in a HER2-dependent manner, at the site known to be critical for its activation. Importantly, RNAi-mediated attenuation of MED1 sensitized HER2-overexpressing cells to tamoxifen treatment. MED1 and its phosphorylated form, but not the corepressors N-CoR and SMRT, were recruited to the ERα target gene promoter by tamoxifen in HER2-overexpressing cells. Significantly, MED1 attenuation or mutation of MED1 phosphorylation sites was sufficient to restore the promoter recruitment of N-CoR and SMRT. Notably, we found that MED1 is required for the expression of not only traditional E2-ERα target genes but also the newly described EGF-ERα target genes. Our results additionally indicated that MED1 is recruited to the HER2 gene and required for its expression. Taken together, these findings support a key role for MED1 in HER2-mediated tamoxifen resistance and suggest its potential usage as a therapeutic target to simultaneously block both ERα and HER2 pathways for the treatment of this type of endocrine resistant breast cancer.
Systematic Analysis of MicroRNAs Targeting the Androgen Receptor in Prostate Cancer Cells
Authors: Päivi Östling, Suvi-Katri Leivonen, Anna Aakula, Pekka Kohonen, Rami Mäkelä, Zandra Hagman, Anders Edsjö, Sara Kangaspeska, Henrik Edgren, Daniel Nicorici, Anders Bjartell, Yvonne Ceder, Merja Perälä, Olli Kallioniemi
Journal: Cancer Research (2011)

Androgen receptor (AR) is expressed in all stages of prostate cancer progression, including in castration-resistant tumors. Eliminating AR function continues to represent a focus of therapeutic investigation, but AR regulatory mechanisms remain poorly understood. To systematically characterize mechanisms involving microRNAs (miRNAs), we conducted a gain-of function screen of 1129 miRNA molecules in a panel of human prostate cancer cell lines and quantified changes in AR protein content using protein lysate microarrays. In this way, we defined 71 unique miRNAs that influenced the level of AR in human prostate cancer cells. RNA sequencing data revealed that the 3'UTR of AR (and other genes) is much longer than currently used in miRNA target prediction programs. Our own analyses predicted that most of the miRNA regulation of AR would target an extended 6 kb 3'UTR. 3'UTR-binding assays validated 13 miRNAs that are able to regulate this long AR 3'UTR (miR-135b, miR-185, miR-297, miR-299-3p, miR-34a, miR-34c, miR-371-3p, miR-421, miR-449a, miR-449b, miR-634, miR-654-5p, and miR-9). Fifteen AR downregulating miRNAs decreased androgen-induced proliferation of prostate cancer cells. In particular, analysis of clinical prostate cancers confirmed a negative correlation of miR-34a and miR-34c expression with AR levels. Our findings establish that miRNAs interacting with the long 3'UTR of the AR gene are important regulators of AR protein levels, with implications for developing new therapeutic strategies to inhibit AR function and androgen-dependent cell growth.