tbuckley/cabot-search huggingface dataset:
Reaction of human small intestine to an intraluminal tube and its importance in jejunal perfusion studies
Authors: G. C. Cook, R. H. Carruthers
Journal: Gut (1974)

A double-lumen tube with a mercury weight attached to its distal end was positioned in the small intestine of six subjects who were to undergo an elective laparotomy. The tube and the technique for its localization were exactly similar to those used in previous intestinal perfusion experiments. Marked ;concertinaing', or gathering of the small intestine proximal to the mercury weight, was seen at laparotomy in all six subjects. The ratio between the mean intestinal length from the mercury weight to the ligament of Treitz after removal of the tube to that with the tube in situ was 3.0 (2.5-3.8). Mean total jejuno-ileal length was 421 (320-521) cm. In five of the six subjects the distal end of the tube was more than half way between the ligament of Treitz and the ileo-caecal valve although it was only 100-120 (mean 108) cm from the incisor teeth. Segmental perfusion studies of the human jejunum involve a much longer length of small intestine than is generally assumed-by a factor of approximately 3. Such studies assess absorption rates over a substantial proportion of the small intestine and are not confined to a short segment of proximal jejunum. The nutritional significance of such studies in which amino acids, peptides, and carbohydrates are investigated is increased. Studies designed to measure absorption rates from the ileum should be treated with caution as part or all of the perfusion segment may be past the ileo-caecal valve.
Developing and Costing Local Strategies to Improve Maternal and Child Health: The Investment Case Framework
Authors: Eliana Jimenez Soto, Sophie La Vincente, Andrew Clark, Sonja Firth, Alison Morgan, Zoe Dettrick, Prarthna Dayal, Bernardino M. Aldaba, Beena Varghese, Laksono Trisnantoro, Yogendra Prasai
Journal: PLoS Medicine (2012)

Eliana Jimenez Soto and colleagues describe the Investment Case framework, a health systems research approach for planning and budgeting, and detail the implementation of the framework in four Asian countries to improve maternal, newborn and child health.
Recent advances in cardiovascular development: promise for the future
Authors: H Baldwin
Journal: Cardiovascular Research (1998)

Time for primary review 26 days 

Nearly three years ago, an extra issue of Cardiovascular Research was published which spotlighted the developing cardiovascular system (Cardiovascular Research, Vol. 31, February, 1996). The spotlight issue was accompanied by an editorial suggesting that the field of developmental cardiology was entering a period analogous to adolescence [1]. In retrospect, that seems to have been an accurate characterization. The past three years have seen enormous growth, paradigm shifts and exciting new discoveries in the field of cardiovascular development. Applications of new molecular techniques and model systems have provided insights into many of the very basic questions relevant to the control of cardiac morphogenesis. For the first time, the promise of understanding the molecular basis of many forms of congenital heart defects seems within our grasp.

In this review, we will attempt to cover some of the major new advances that have occurred during the past three years in this rapidly expanding field. We were given the task of relating the recent developments to the reviews and papers that were contained in the original spotlight issue. Accordingly, this review will cover the same general subjects presented in the February, 1996 issue. In further keeping with our goal, each contributor to that issue was contacted and given the opportunity to provide a recent update related to their original topic (over half of the authors responded) and we appreciate those who took the time to answer. Because the field is advancing so rapidly, it is impossible to detail all the significant progress that has been made. We apologize to all whose work could not be discussed herein because of space limitations (and our own short-sightedness). Several recent reviews offer more comprehensive coverage of selected aspects of cardiac development which should provide a valuable supplement to this article … 

* Corresponding author. Tel.: +1-212-263-5993; fax: +1-212-263-5808; e-mail: michael.artman@mcfpo.med.nyu.edu
Maternal Immunization Programs Postnatal Immune Responses and Reduces Atherosclerosis in Offspring
Authors: Tomoya Yamashita, Stefan Freigang, Claudia Eberle, Jennifer Pattison, Sachin Gupta, Claudio Napoli, Wulf Palinski
Journal: Circulation Research (2006)

Maternal hypercholesterolemia during pregnancy increases offspring susceptibility to atherosclerosis by an oxidation-dependent mechanism. The present studies investigated whether maternal immunization with oxidized LDL (OxLDL) before pregnancy protects the fetus from atherogenic in utero programming by maternal hypercholesterolemia. Maternal immunization of NZW rabbits and LDL receptor-deficient mice indeed reduced atherosclerosis in adult offspring by up to 56%, but the protective effect could not be attributed to a reduction of fetal exposure to hypercholesterolemia alone, and even nonspecific immune stimulation with adjuvant only provided some protection. Unexpectedly, offspring of immunized mothers developed increased IgM antibodies to selective OxLDL epitopes and increased IgM-LDL immune complexes, compared with offspring of nonimmunized controls. Even naïve offspring of OxLDL-immunized mothers never exposed to postnatal hypercholesterolemia responded to a one-time OxLDL and KLH challenge with greater OxLDL-specific IgM responses, increased OxLDL-specific IgM-secreting B cells, and more IgM-LDL immune complexes. In contrast, maternal immunization with KLH, a T cell-dependent nonmammalian antigen, did not influence postnatal immune responses. Effects of maternal OxLDL-immunization on offspring B cells and selective antibodies were independent of transplacental passage of maternal immunoglobulins. Results show that maternal immunization with antigens prevalent in atherosclerotic lesions reduces atherogenesis in their offspring by mechanisms that include, but are not limited to, reduced fetal exposure to maternal hypercholesterolemia and lipid peroxidation. More importantly, they demonstrate in principle that maternal adaptive immunity to selective antigens influences postnatal B cell and antibody responses in offspring, and that modulation of in utero immune programming may influence immune-modulated diseases later in life.
Sunscreen application by photosensitive patients is inadequate for protection
Authors: None AZURDIA, None PAGLIARO, None DIFFEY, None RHODES
Journal: British Journal of Dermatology (1999)

Photosensitive patients often comment that sunscreen products seem of little benefit. We used fluorescence spectroscopy to assess quantitatively their sunscreen application technique. A dose-response relationship for sunscreen skin surface thickness and fluorescence intensity was determined for an intrinsically fluorescent sunscreen, Neutrogena sun protection factor (SPF) 15. Ten women with long-standing photosensitivity conditions were asked to apply this sunscreen in the manner they would normally on a bright sunny day. Fluorescence measurements were taken from all unclothed body areas, comprising 17 sites of the head, neck, upper and lower limbs. Geometric regression analysis of the dose-response data showed a high level of correlation (r = 0.99) between sunscreen thickness and fluorescence intensity, allowing fluorescence measurements to be converted to an equivalent sunscreen thickness. The overall median sunscreen thickness was 0.5 mg/cm2, with median thicknesses of individual sites ranging from 0 to 1.2 mg/cm2. The most frequently missed sites were the posterior neck, lateral neck, temples and ears, all of which had median thicknesses of 0 mg/cm2. Hence, photosensitive patients fail to apply sunscreen in some prominently exposed sites, and use average thicknesses far less than the manufacturers' recommendation (2 mg/cm2). The level of protection is much lower than anticipated from the stated SPF of the product.
Synergistic interaction between exercise and insulin on peripheral glucose uptake.
Authors: R A DeFronzo, E Ferrannini, Y Sato, P Felig, J Wahren
Journal: Journal of Clinical Investigation (1981)

The interaction of exercise and insulin on glucose metabolism was examined in 10 healthy volunteers. Four study protocols were used: study 1: plasma insulin was raised by approximately 100 microunits/ml while plasma glucose was maintained at basal levels for 2 h (insulin clamp). Study 2: subjects performed 30 min of bicycle exercise at 40% of VO2 max. Study 3: an insulin clamp was performed as per study 1. Following 60 min of sustained hyperinsulinemia, however, subjects exercised for 30 min as per study 2. Study 4: subjects were studied as per study 3 except that catheters were inserted into the femoral artery and vein to quantitate leg glucose uptake. During the 60-90 min period of hyperinsulinemia (study 1), glucose uptake averaged 8.73 +/- 0.10 mg/kg per min. With exercise alone (study 2), the increment in peripheral glucose uptake was 1.43 +/- 0.30 mg/kg per min. When hyperinsulinemia and exercise were combined (study 3), glucose uptake averaged 15.06 +/- 0.98 mg/kg per min (P less than 0.01) and this was significantly (P less than 0.001) greater than the sum of glucose uptake when exercise and the insulin clamp were performed separately. The magnitude of rise in glucose uptake correlated closely with the increase in leg blood flow (r = 0.935, P less than 0.001), suggesting that the synergism is the result of increased blood flow and increased capillary surface area to exercising muscle. More than 85% of total body glucose metabolism during studies 1 and 3 was accounted for by skeletal muscle uptake. These results demonstrate that (a) insulin and exercise act synergistically to enhance glucose disposal in man, and (b) muscle is the primary tissue responsible for the increase in glucose metabolism following hyperinsulinemia and exercise.
Wegener's Granulomatosis: Anti–proteinase 3 Antibodies Are Potent Inductors of Human Endothelial Cell Signaling and Leakage Response
Authors: Ulf Sibelius, Katja Hattar, Angelika Schenkel, Thomas Noll, Elena Csernok, Wolfgang Ludwig Gross, Werner-Johannes Mayet, Hans-Michael Piper, Werner Seeger, Friedrich Grimminger
Journal: The Journal of Experimental Medicine (1998)

Anti–neutrophil cytoplasmic antibodies (ANCAs) targeting proteinase 3 (PR3) have a high specifity for Wegener's granulomatosis (WG), and their role in activating leukocytes is well appreciated. In this study, we investigated the influence of PR3-ANCA and murine monoclonal antibodies on human umbilical vascular endothelial cells (HUVECs). Priming of HUVECs with tumor necrosis factor α induced endothelial upregulation of PR3 message and surface expression of this antigen, as measured by Cyto-ELISA, with a maximum occurrence after 2 h. Primed cells responded to low concentrations of both antibodies (25 ng–2.5 μg/ml), but not to control immunoglobulins, with pronounced, dose-dependent phosphoinositide hydrolysis, as assessed by accumulation of inositol phosphates. The signaling response peaked after 20 min, in parallel with the appearance of marked prostacyclin and platelet-activating factor synthesis. The F(ab)2 fragment of ANCA was equally potent as ANCA itself. Disrupture of the endothelial F-actin content by botulinum C2 toxin to avoid antigen–antibody internalization did not affect the response. In addition to the metabolic events, anti-PR3 challenge, in the absence of plasma components, provoked delayed, dose-dependent increase in transendothelial protein leakage. We conclude that anti-PR3 antibodies are potent inductors of the preformed phosphoinositide hydrolysis–related signal tranduction pathway in human endothelial cells. Associated metabolic events and the loss of endothelial barrier properties suggest that anti-PR3–induced activation of endothelial cells may contribute to the pathogenetic sequelae of autoimmune vasculitis characterizing WG.
T cell hybrids with arsonate specificity. I. Initial characterization of antigen-specific T cell products that bear a cross-reactive idiotype and determinants encoded by the murine major histocompatibility complex.
Authors: A Pacifico, J D Capra
Journal: The Journal of Experimental Medicine (1980)

T cell hybrids have been constructed between the BW5147 thymoma cell line and A/J splenocytes from mice suppressed with the p-azophenylarsonte hapten. Three independently derived cloned lines have been chracterized. Each secretes or sheds a 62,000-dalton antigen-specific product bound by rabbit antisera directed against the arsonate cross-reactive idiotype. In addition, each of the antien-specific molecules contains determinants encoded within the I region of the murine major histocompatibility complex. Peptide mapping analysis indictes that, whereas these molecules are remarkably similar, each is individually distinct in primary structure. The availability of cloned T cell lines that produce antigen-specific idiotype-positive I region-containing products should facilitate a more thorough dissection of the interrelationships of T-B interctions in the arsonate idiotypic system.
Role of diet and fuel overabundance in the development and progression of heart failure
Authors: D. J. Chess, W. C. Stanley
Journal: Cardiovascular Research (2008)

Under physiological conditions, the human heart derives energy from glucose, fatty acids, and/or lactate depending upon substrate availability, circulating hormone levels, and nutritional status. Circulating free fatty acid and glucose levels often exceed the normal range, as observed with type 2 diabetes, obesity, or physical inactivity. Chronic exposure of the heart to high plasma levels of free fatty acids may cause accumulation of toxic lipid intermediates within cardiomyocytes. Furthermore, suppression of glucose oxidation by increased fatty acid uptake shunts glucose into the oxidative pentose phosphate and hexosamine biosynthetic pathways, both of which yield potentially harmful products. Noxious derivatives of aberrant glucose and fatty acid oxidation can activate signalling cascades leading to myocyte dysfunction or death, processes termed 'glucotoxicity' and 'lipotoxicity'. This review discusses the effects of dietary extremes (e.g. high fat and high carbohydrate consumption) and substrate overabundance in the context of heart failure (HF) development and progression. Emerging data suggest that substrate excess leads to cardiac dysfunction and HF, which may be prevented or slowed by maintaining low body fat and high insulin sensitivity and consuming a diet of low glycaemic load that is high in mono- and polyunsaturated fatty acids.
Association Between Acetaminophen and Asthma Morbidity in a Latino Population
Authors: Nana Sarkoah Fenny, Elizabeth Nguyen, Joshua Galanter, Sam Oh, Celeste Eng, Fred Lurmann, Rajesh Kumar, Harold J. Farber, Denise Serebrisky, Luisa Borrell, Saunak Sen, William Rodriguez-Cintron, Jose Rodriguez-Santana, Esteban Gonza Burchard, Pedro C. Avila
Journal: Journal of Allergy and Clinical Immunology (2015)
Evidence for the Presence of Disease-Perturbed Networks in Prostate Cancer Cells by Genomic and Proteomic Analyses: A Systems Approach to Disease
Authors: Biaoyang Lin, James T. White, Wei Lu, Tao Xie, Angelita G. Utleg, Xiaowei Yan, Eugene C. Yi, Paul Shannon, Irina Khrebtukova, Paul H. Lange, David R. Goodlett, Daixing Zhou, Thomas J. Vasicek, Leroy Hood
Journal: Cancer Research (2005)

Prostate cancer is initially responsive to androgen ablation therapy and progresses to androgen-unresponsive states that are refractory to treatment. The mechanism of this transition is unknown. A systems approach to disease begins with the quantitative delineation of the informational elements (mRNAs and proteins) in various disease states. We employed two recently developed high-throughput technologies, massively parallel signature sequencing (MPSS) and isotope-coded affinity tag, to gain a comprehensive picture of the changes in mRNA levels and more restricted analysis of protein levels, respectively, during the transition from androgen-dependent LNCaP (model for early-stage prostate cancer) to androgen-independent CL1 cells (model for late-stage prostate cancer). We sequenced >5 million MPSS signatures, obtained >142,000 tandem mass spectra, and built comprehensive MPSS and proteomic databases. The integrated mRNA and protein expression data revealed underlying functional differences between androgen-dependent and androgen-independent prostate cancer cells. The high sensitivity of MPSS enabled us to identify virtually all of the expressed transcripts and to quantify the changes in gene expression between these two cell states, including functionally important low-abundance mRNAs, such as those encoding transcription factors and signal transduction molecules. These data enable us to map the differences onto extant physiologic networks, creating perturbation networks that reflect prostate cancer progression. We found 37 BioCarta and 14 Kyoto Encyclopedia of Genes and Genomes pathways that are up-regulated and 23 BioCarta and 22 Kyoto Encyclopedia of Genes and Genomes pathways that are down-regulated in LNCaP cells versus CL1 cells. Our efforts represent a significant step toward a systems approach to understanding prostate cancer progression.
Provocation testing in polymorphic light eruption using fluorescent ultraviolet (UV) A and UVB lamps
Authors: S. Das, J.J. Lloyd, D. Walshaw, P.M. Farr
Journal: British Journal of Dermatology (2004)

Journal Article Provocation testing in polymorphic light eruption using fluorescent ultraviolet (UV) A and UVB lamps Get access S. Das, S. Das Department of Dermatology and Regional Medical Physics Department, Royal Victoria Infirmary, Newcastle upon Tyne, NE1 4LP, U.K Search for other works by this author on: Oxford Academic Google Scholar J.J. Lloyd, J.J. Lloyd Department of Dermatology and Regional Medical Physics Department, Royal Victoria Infirmary, Newcastle upon Tyne, NE1 4LP, U.K Search for other works by this author on: Oxford Academic Google Scholar D. Walshaw, D. Walshaw Department of Statistics, University of Newcastle upon Tyne, U.K Search for other works by this author on: Oxford Academic Google Scholar P.M. Farr P.M. Farr Department of Dermatology and Regional Medical Physics Department, Royal Victoria Infirmary, Newcastle upon Tyne, NE1 4LP, U.K Professor P. M. Farr. E‐mail: peter.farr@ncl.ac.uk Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 151, Issue 5, 1 November 2004, Pages 1066–1070, https://doi.org/10.1111/j.1365-2133.2004.06235.x Published: 01 November 2004 Article history Accepted: 07 April 2004 Published: 01 November 2004
Serum response of hepatocyte growth factor, insulin-like growth factor-I, interleukin-6, and acute phase proteins in patients with colorectal liver metastases treated with partial hepatectomy or cryosurgery
Authors: Koert P de Jong, Boudewijn Alting von Geusau, Cees A Rottier, Johan Bijzet, Pieter C Limburg, Elisabeth G.E de Vries, Vaclav Fidler, Maarten J.H Slooff
Journal: Journal of Hepatology (2001)
Treatment of cutaneous lymphoid hyperplasia with thalidomide: Report of two cases
Authors: Hakima Benchikhi, Christine Bodemer, Sylvie Fraitag, Janine Wechsler, Marie-Hélène Delfau-Larue, Nicolas Gounod, Yves de Prost, Jean Revuz, Martine Bagot
Journal: Journal of the American Academy of Dermatology (1999)
Cabozantinib in Progressive Medullary Thyroid Cancer
Authors: Rossella Elisei, Martin J. Schlumberger, Stefan P. Müller, Patrick Schöffski, Marcia S. Brose, Manisha H. Shah, Lisa Licitra, Barbara Jarzab, Viktor Medvedev, Michael C. Kreissl, Bruno Niederle, Ezra E.W. Cohen, Lori J. Wirth, Haythem Ali, Colin Hessel, Yifah Yaron, Douglas Ball, Barry Nelkin, Steven I. Sherman
Journal: Journal of Clinical Oncology (2013)

Cabozantinib, a tyrosine kinase inhibitor (TKI) of hepatocyte growth factor receptor (MET), vascular endothelial growth factor receptor 2, and rearranged during transfection (RET), demonstrated clinical activity in patients with medullary thyroid cancer (MTC) in phase I.We conducted a double-blind, phase III trial comparing cabozantinib with placebo in 330 patients with documented radiographic progression of metastatic MTC. Patients were randomly assigned (2:1) to cabozantinib (140 mg per day) or placebo. The primary end point was progression-free survival (PFS). Additional outcome measures included tumor response rate, overall survival, and safety.The estimated median PFS was 11.2 months for cabozantinib versus 4.0 months for placebo (hazard ratio, 0.28; 95% CI, 0.19 to 0.40; P < .001). Prolonged PFS with cabozantinib was observed across all subgroups including by age, prior TKI treatment, and RET mutation status (hereditary or sporadic). Response rate was 28% for cabozantinib and 0% for placebo; responses were seen regardless of RET mutation status. Kaplan-Meier estimates of patients alive and progression-free at 1 year are 47.3% for cabozantinib and 7.2% for placebo. Common cabozantinib-associated adverse events included diarrhea, palmar-plantar erythrodysesthesia, decreased weight and appetite, nausea, and fatigue and resulted in dose reductions in 79% and holds in 65% of patients. Adverse events led to treatment discontinuation in 16% of cabozantinib-treated patients and in 8% of placebo-treated patients.Cabozantinib (140 mg per day) achieved a statistically significant improvement of PFS in patients with progressive metastatic MTC and represents an important new treatment option for patients with this rare disease. This dose of cabozantinib was associated with significant but manageable toxicity.
Ontogeny of human natural killer (NK) cells: fetal NK cells mediate cytolytic function and express cytoplasmic CD3 epsilon,delta proteins.
Authors: J H Phillips, T Hori, A Nagler, N Bhat, H Spits, L L Lanier
Journal: The Journal of Experimental Medicine (1992)

Natural killer (NK) cells have been defined as CD3 epsilon-, CD16+ and/or CD56+ lymphocytes that mediate major histocompatibility complex (MHC)-unrestricted cytotoxicity against certain tumors and virus-infected cells. Unlike T lymphocytes, NK cells do not rearrange or productively express T cell antigen receptor genes. Moreover, NK cells from adults have been reported to not express CD3 gamma, delta, or epsilon proteins on the cell surface or in the cytoplasm. Nonetheless, NK cells have been shown to share a number of antigenic and functional similarities to T cells that suggest the possibility of common origins. In this report, we demonstrate that functional NK cells exist in liver at early stages of human embryonic development. Freshly isolated fetal NK cells mediated MHC-unrestricted cytotoxicity against NK-sensitive targets and acquired the ability to lyse NK-resistant tumors after overnight culture in interleukin 2. Unlike adult NK cells, freshly isolated fetal liver NK cells and clones derived from these cells, as well as a subset of cord blood NK cells, express substantial levels of CD3 delta and CD3 epsilon proteins in the cytoplasm. Expression of CD3 epsilon and CD3 delta transcripts and cytoplasmic proteins in fetal NK clones was confirmed by polymerase chain reaction and Western blot analysis. These findings support the concept that NK and T cells may arise from a common progenitor that expresses components of the CD3 complex. Alternatively, it is possible that the cytoplasmic CD3 delta, epsilon+ fetal NK cells represent a distinct subpopulation of NK cells that is predominant in the fetus, but replaced by the cytoplasmic CD3 delta,epsilon- adult NK cell population after embryogenesis.