tbuckley/cabot-search huggingface dataset:
Induction of macrophage inflammatory protein 2 gene expression by interleukin 1 beta in rat lung.
Authors: W B Xu, E B Haddad, H Tsukagoshi, I Adcock, P J Barnes, K F Chung
Journal: Thorax (1995)

BACKGROUND--Recruitment of inflammatory cells in the lungs may contribute to tissue injury as a result of mediators released from these cells. Interleukin 1 beta (IL-1 beta) is a potent inducer of neutrophil accumulation, a process that may require local protein biosynthesis. Macrophage inflammatory protein 2 (MIP-2) is a approximately 6 kD heparin binding protein and is a member of the C-X-C superfamily that causes significant neutrophil chemotaxis and activation in vitro. A study was performed to determine whether IL-1 beta could induce the expression of MIP-2 in the lungs of Brown-Norway rats. METHODS--rhIL-1 beta (500 U) or 0.9% NaCl was injected intratracheally and bronchoalveolar lavage (BAL) cells and lung tissues were evaluated for MIP-2 mRNA expression after RNA extraction by Northern blot analysis. MIP-2 probe was prepared from cDNA obtained by reverse transcriptase-polymerase chain reaction (RT-PCR) of BAL cells obtained from a rat treated with lipopolysaccharide. RESULTS--There was no detectable MIP-2 mRNA in the lungs of control rats but a marked enhancement of the expression at four hours with no expression at 12 hours and a slight expression at 24 hours. IL-1 beta induced a significant influx of neutrophils into BAL fluid with a transient increase in macrophages. In situ hybridisation of lungs using MIP-2 cDNA probe labelled with digoxigenin showed expression of MIP-2 mRNA in airway mononuclear cells and airway epithelium at four hours after IL-1 beta; at 24 hours the signal had nearly gone. CONCLUSION--IL-1 beta induces the expression of MIP-2 mRNA in rat lung. MIP-2 may be one chemokine that could contribute to IL-1 beta induced neutrophil influx.
Diagnosis and management of coronary artery disease in patients with end-stage renal disease on hemodialysis.
Authors: J A de Lemos, L D Hillis
Journal: Journal of the American Society of Nephrology (1996)

Cardiovascular disease accounts for almost half of the total mortality in patients with ESRD. Ischemic heart disease is responsible for many cardiovascular deaths, with myocardial infarction accounting for approximately 15% and sudden cardiac death or severe left ventricular dysfunction accounting for much of the remainder. The markedly increased prevalence of atherosclerotic cardiovascular disease in patients with ESRD is influenced, at least in part, by numerous risk factors for atherosclerosis, with hypertension, diabetes mellitus, and hypercholesterolemia being particularly important. Because atherosclerotic coronary artery disease (CAD), whether symptomatic or asymptomatic, is associated with an increased incidence of allograft failure and mortality, the results of this study suggest the need for careful evaluation for the presence of CAD in those persons who are under consideration for renal transplantation. Candidates with angina pectoris, previous myocardial infarction, or congestive heart failure are at particularly high risk of a cardiac event, and, therefore, should routinely undergo pretransplant coronary angiography and subsequent surgical revascularization if angina is refractory to medical therapy or CAD is extensive. In contrast, although young, nondiabetic transplant candidates without symptoms or electrocardiographic evidence of CAD have an increased relative risk of cardiac death when compared with age-matched control subjects, their absolute risk of such an event is very low. As a result, they do not require a cardiac evaluation before transplantation. For the remaining transplant candidates at neither low nor high risk of a fatal or nonfatal cardiac event (i.e., those at intermediate risk), the authors of this study routinely perform (1) thallium imaging with dipyridamole or (2) two-dimensional echocardiography with intravenous dobutamine. If the result of these investigations are normal, transplantation proceeds; if abnormal, coronary angiography is performed, followed by surgical revascularization if CAD is extensive. Percutaneous transluminal coronary angioplasty is not recommended in patients with ESRD because it appears to be accompanied by a high likelihood of acute and chronic complications. Although it is hoped that surgical revascularization before renal transplantation improves allograft and patient survival, prospectively obtained data proving that this, in fact, is true do not exist.
Characteristics of a Large Cohort of Patients with Autoimmune Pulmonary Alveolar Proteinosis in Japan
Authors: Yoshikazu Inoue, Bruce C. Trapnell, Ryushi Tazawa, Toru Arai, Toshinori Takada, Nobuyuki Hizawa, Yasunori Kasahara, Koichiro Tatsumi, Masaaki Hojo, Toshio Ichiwata, Naohiko Tanaka, Etsuro Yamaguchi, Ryosuke Eda, Kazunori Oishi, Yoshiko Tsuchihashi, Chinatsu Kaneko, Toshihiro Nukiwa, Mitsunori Sakatani, Jeffrey P. Krischer, Koh Nakata
Journal: American Journal of Respiratory and Critical Care Medicine (2008)

Section:ChooseTop of pageAbstract <<METHODSRESULTSDISCUSSIONAPPENDIXReferencesCITING ARTICLES
Telomeres and Mitochondria in the Aging Heart
Authors: Javid Moslehi, Ronald A. DePinho, Ergün Sahin
Journal: Circulation Research (2012)

Studies in humans and in mice have highlighted the importance of short telomeres and impaired mitochondrial function in driving age-related functional decline in the heart. Although telomere and mitochondrial dysfunction have been viewed mainly in isolation, recent studies in telomerase-deficient mice have provided evidence for an intimate link between these two processes. Telomere dysfunction induces a profound p53-dependent repression of the master regulators of mitochondrial biogenesis and function, peroxisome proliferator-activated receptor gamma coactivator (PGC)-1α and PGC-1β in the heart, which leads to bioenergetic compromise due to impaired oxidative phosphorylation and ATP generation. This telomere-p53-PGC mitochondrial/metabolic axis integrates many factors linked to heart aging including increased DNA damage, p53 activation, mitochondrial, and metabolic dysfunction and provides a molecular basis of how dysfunctional telomeres can compromise cardiomyocytes and stem cell compartments in the heart to precipitate cardiac aging.
Circulatory Changes during Growth in the Fetal Lamb
Authors: ABRAHAM M. RUDOLPH, MICHAEL A. HEYMANN
Journal: Circulation Research (1970)

The changes in circulation with advancing gestation were investigated in 44 fetal lambs in utero; gestational ages ranged from about 60 days to 150 days. Spinal analgesia was administered to the ewe, polyvinyl catheters were inserted into fetal vessels, and umbilical blood flow was measured by the steady-state diffusion Fick method during antipyrine infusion. Cardiac output, distribution of cardiac output, and actual organ blood flows were calculated from injections of nuclide-labeled microspheres (50µ diam) into a forelimb and into an umbilical or hindlimb vein. Umbilical Po 2 , Pco 2 and pH did not change significantly during gestation. Umbilical blood flow and total cardiac output increased in proportion to fetal weight. The proportion of the combined ventricular output distributed to the placenta decreased from about 50% in the youngest fetuses to about 40% just before term. The proportion of the cardiac output distributed to the lungs, as well as the actual flow in relation to lung weight, increased throughout gestation, with a more rapid rise after about 120 days. There was also a late increase in intestinal flow. Cerebral blood flow increased gradually throughout gestation, both as a proportion of cardiac output and in relation to brain weight. There were no significant changes in percent of cardiac output, or flow related to weight in the kidney, heart, or skin and muscular tissues. The studies suggest that, since lung blood flow is a relatively small proportion of total cardiac output, it is not important in regulating distribution of blood flow, but that the peripheral circulation in skin and muscle, which receives a large percent of fetal cardiac output, is the site where vasomotor responses may effect major redistribution of the fetal circulation.
Different techniques of static/dynamic guided implant surgery: modalities and indications
Authors: Marjolein Vercruyssen, Thomas Fortin, Gerlig Widmann, Reinhilde Jacobs, Marc Quirynen
Journal: Periodontology 2000 (2014)

Abstract For computer‐guided surgery a static surgical guide is used that transfers the virtual implant position from computerized tomographic data to the surgical site. These guides are produced by computer‐aided design/computer‐assisted manufacture technology, such as stereolithography, or manually in a dental laboratory (using mechanical positioning devices or drilling machines). With computer‐navigated surgery the position of the instruments in the surgical area is constantly displayed on a screen with a three‐dimensional image of the patient. In this way, the system allows real‐time transfer of the preoperative planning and visual feedback on the screen. A workflow of the different systems is presented in this review.
Thymosin α1 activates dendritic cell tryptophan catabolism and establishes a regulatory environment for balance of inflammation and tolerance
Authors: Luigina Romani, Francesco Bistoni, Katia Perruccio, Claudia Montagnoli, Roberta Gaziano, Silvia Bozza, Pierluigi Bonifazi, Giovanni Bistoni, Guido Rasi, Andrea Velardi, Francesca Fallarino, Enrico Garaci, Paolo Puccetti
Journal: Blood (2006)
Association between Ia antigens and the Fc receptors of certain T lymphocytes.
Authors: H B Dickler, R D Arbeit, P A Henkart, D H Sachs
Journal: The Journal of Experimental Medicine (1976)

The Fc receptors of thymic and splenic T lymphocytes were detected using indirect immunofluorescence and soluble antigen-antibody complexes. 10-20% of thymocytes and 40-50% of Thy-1-positive splenic lymphocytes bound antigen-complexed Ig. The binding to thymocytes was partially inhibited (45-74%) by antibodies against antigens determined by the I region of the H-2 complex, but not by antibodies against K- or D-region antigens or Thy-1 antigen. The inhibition did not require the Fc portion of the inhibiting antibody. These results provide evidence that Ia antigens and the Fc receptors of some T lymphocytes are associated, and that the populations of T cells which bear these moieties at least partially overlap.
Specific incorporation of penicillamine into the epidermis of mice: an autoradiographic study
Authors: V. RUOCCO, E. ANGELIS, M. LUCA, M. PISANI, G. PROTA
Journal: British Journal of Dermatology (1983)

[3H]-D-penicillamine was injected intra-peritoneally in mice. The highest concentration of the drug was found in the skin, particularly in the epidermis, and a well-defined kinetic sequence of appearance in the epidermis was shown. This finding is consistent with the hypothesis that penicillamine, by virtue of its chemical similarity to cysteine, can replace the latter during keratogenesis by a competition phenomenon, which could provoke acantholytic splitting both biochemically and immunologically.
Studies on the Antigenic Composition of Hamster Tumors Induced by Polyoma Virus, and of Normal Hamster Tissues &lt;italic&gt;In Vivo&lt;/italic&gt; and &lt;italic&gt;In Vitro&lt;/italic&gt;&lt;xref ref-type="fn" rid="fn1"&gt;2&lt;/xref&gt;
Authors: Marian Fogel, Leo Sachs
Journal: JNCI Journal of the National Cancer Institute (1962)

This study, using antiserums produced in rabbits, the complement-fixation reaction, and the agglutination of sheep red blood cells, concerns 1) the antigenic differences between normal hamster kidneys and polyoma-induced hamster kidney tumors and 2) the antigenic changes that occur when normal cells are grown in tissue culture. Kidney tumors induced in vivo by polyoma virus showed, in comparison with normal kidney, a decrease in kidney-specific antigen and an increase in Forssman (F) antigen concentration. No tumor-specific antibodies were detected in these antiserums prepared in a heterologous host. After short-term culturing in vitro, normal hamster kidney cells underwent changes similar to those found in kidney tumors in vivo, and the data suggest that the decrease of kidney-specific antigen in normal cells in culture occurred before the increase of F antigen. With normal embryo cells, an increase of F antigen, after the cells were cultured for short periods in vitro, was found in hamsters and in mice, an F-positive species, but this antigen was not detected in cultures of embryo cells from the rat, an F-negative species. The results suggest that, regarding the kidney-specific and F antigen, the antigenic composition expressed by a cell may change according to physiological conditions.
Thromboendarterectomy for Chronic Thromboembolic Pulmonary Hypertension in Hereditary Hemorrhagic Telangiectasia
Authors: Keith M. Wille, S. Christopher Bellot, Deepak Acharya, Micheal M. Madani, Satinder P. Singh, David C. McGiffin
Journal: American Journal of Respiratory and Critical Care Medicine (2014)
Visualizing Inhibition of Nucleosome Mobility and Transcription by Cisplatin–DNA Interstrand Crosslinks in Live Mammalian Cells
Authors: Guangyu Zhu, Lina Song, Stephen J. Lippard
Journal: Cancer Research (2013)

Cisplatin is a widely used anticancer drug that acts by binding DNA and causing the formation of intrastrand and interstrand (ICL) crosslinks, but the precise downstream effects of the latter damage are not well understood. In this study, we investigated the influence of cisplatin ICLs on synthetic nucleosomes that were platinated in a site-specific manner in vitro and on gene transcription in live mammalian cells. Nucleosome core particles that we constructed contained site-specific cisplatin 5'-d(G*pC)/5'-d(G*pC) ICLs, where the asterisk denotes the platinated nucleoside, to examine the influence of platinum lesions on the dynamic behavior of nucleosomes in solution. A cisplatin ICL, but not a 1,2-d(GpG) crosslink, significantly inhibited ATP-independent histone octamer-DNA sliding. We also used a novel linearization-recircularization strategy described here to synthesize mammalian expression vectors containing site-specific cisplatin ICLs. Plasmid vectors were tested in live mammalian cells to study the transcription inhibition effects of cisplatin ICLs in the context of two different repair backgrounds. Cisplatin ICLs inhibit transcription as effectively as 1,2-d(GpG) crosslinks. We determined that nucleotide excision repair plays a key role in the removal of cisplatin ICLs, acting in a replication-independent fashion. We also found that loss of mismatch repair function dramatically attenuates the transcription inhibition effects by cisplatin ICLs but not 1,2-d(GpG) intrastrand crosslinks. Our results revealed the unique properties of cisplatin ICLs on nucleosome mobility and on transcription, and they defined how these adducts act in a manner completely different from that used for cisplatin 1,2-d(GpG) crosslinks. These new findings provide direct support for a role of ICLs in the pharmacologic activities of cisplatin, despite the lower frequency of their formation.
Recruiting male partners for couple HIV testing and counselling in Malawi's option B+ programme: an unblinded randomised controlled trial
Authors: Nora E Rosenberg, Tiwonge K Mtande, Friday Saidi, Christopher Stanley, Edward Jere, Lusubiro Paile, Kondwani Kumwenda, Innocent Mofolo, Wingston Ng'ambi, William C Miller, Irving Hoffman, Mina Hosseinipour
Journal: The Lancet HIV (2015)
Glucocorticoids Regulate the Expression of the Human Osteoblastic Endothelin A Receptor Gene
Authors: Irma Börcsök, Hans U. Schairer, Ulrike Sommer, Glenn K. Wakley, Ulrich Schneider, Florian Geiger, Fritz U. Niethard, Reinhard Ziegler, Christian H. Kasperk
Journal: The Journal of Experimental Medicine (1998)

The endothelial cell–derived peptide endothelin 1 (ET1) stimulates cell proliferation and differentiated functions of human osteoblastic cells (HOC), and HOC constitutively express the endothelin A receptor (ETRA). Therefore, ET1 may play an important role in the regulation of bone cell metabolism. As glucocorticoids (GC) exert a profound influence on bone metabolism and increase the effects of ET1 on bone cell metabolism in vitro, the effects of GC on ETRA expression in HOC were investigated. Dexamethasone (DEX) increased ETRA mRNA levels in a dose- and time-dependent fashion. The effects of dexamethasone, prednisolone, and deflazacort on the increase of ETRA mRNA levels correlate positively with their binding affinity to the GC receptor. Scatchard analysis of ET1 binding data to HOC revealed that DEX increased the binding capacity for ET1 from 25,300 to 62,800 binding sites per osteoblastic cell, leading to an enhanced mitogenic effect of ET1 on HOC after preincubation with DEX. Transiently transfected primary HOC with a reporter gene construct, containing the 5′-flanking region of the ETRA gene fused to luciferase gene, showed a promoter-dependent expression of the reporter gene and the induction of reporter gene expression by DEX treatment. Total RNA extracts of femoral head biopsies with osteonecrotic lesions from GC-treated patients showed threefold higher ETRA mRNA levels compared with extracts of bone biopsies from patients with traumatically induced osteonecrosis and coxarthrosis. Furthermore, GC treatment increased plasma ET1 levels by 50% compared with pretreatment values. These findings suggest that GC induced upregulation of ETRA, and ET1 plasma levels enhance ET1's anabolic action on bone cell metabolism. Increased ET1 concentrations may also impair bone perfusion by vasoconstriction in a metabolically activated skeletal region.
Ascitic fluid analysis in malignancy-related ascites
Authors: Bruce A. Runyon, John C. Hoefs, Timothy R. Morgan
Journal: Hepatology (1988)

A prospective study identified 45 patients with malignancy-related ascites among 448 ascites patients (10% of the total). Patients were categorized into five subgroups based on the pathophysiology of ascites formation. Each subgroup had a distinctive ascitic fluid analysis. Patients with peritoneal carcinomatosis but without massive liver metastases (53.3% of the patients with malignancy-related ascites) had a uniformly positive ascitic fluid cytology, high ascitic fluid protein concentration and low serum-ascites albumin gradient. Patients with massive liver metastases and no other cause for ascites formation (13.3% of the series) had a negative cytology, low ascitic fluid protein concentration, high serum-ascites albumin gradient and markedly elevated serum alkaline phosphatase. Those with peritoneal carcinomatosis and massive liver metastases (13.3% of the series) had a nearly uniformly positive ascitic fluid cytology, variable protein concentration, high serum-ascites albumin gradient and markedly elevated serum alkaline phosphatase. Chylous ascites (6.7%) was characterized by a milky appearance, negative cytology and an elevated ascitic fluid triglyceride concentration. Patients with hepatocellular carcinoma superimposed on cirrhosis (13.3%) had negative ascitic fluid cytology, low ascitic fluid protein concentration, high serum-ascites albumin gradient and elevated serum and ascitic fluid α-fetoprotein concentration. Two-thirds of patients with malignancy-related ascites had peritoneal carcinomatosis; 96.7% of patients with peritoneal carcinomatosis had positive ascitic fluid cytology. Ascitic fluid analysis is helpful in identifying and distinguishing the subgroups of malignancy-related ascites.
End Points and Outcomes in Castration-Resistant Prostate Cancer: From Clinical Trials to Clinical Practice
Authors: Howard I. Scher, Michael J. Morris, Ethan Basch, Glenn Heller
Journal: Journal of Clinical Oncology (2011)

New therapeutic approaches for castration-resistant prostate cancer (CRPC) introduce new treatment dilemmas: how best to sequence these options to maximally benefit patients, what tests to perform before and after treatment to assess disease status, and how to interpret the test results and use them to guide treatment. New and specific end points for different classes of drugs are needed to provide the information to guide these treatment decisions. In 2008, the Prostate Cancer Working Group 2 consensus criteria for early-phase clinical trials redefined clinical trial end points as first, to control, relieve, or eliminate disease manifestations present when treatment is started and second, to prevent or delay future disease manifestations. Disease manifestations include prostate-specific antigen (PSA), soft-tissue disease (nodes and/or viscera), bone disease (most common site of spread), and symptoms. Recent US Food and Drug Administration (FDA) approvals for CRPC therapies have been based on the prevent/delay end points that reflect unequivocal benefit to a patient: prolongation of life or reduction in skeletal-related events (SREs). For the practicing oncologist, the control/relieve/eliminate outcomes should serve primarily to inform the decision of whether to continue therapy. In this review, we consider individual end points such as PSA, imaging, and patient-reported outcomes in the context of the control/relieve/eliminate and prevent/delay framework. We address the time-to-event end points of metastasis prevention, SRE, time to progression, and overall survival in the context of regulatory approvals. We also discuss circulating tumor cells measured with the CellSearch assay, recently cleared by the FDA for monitoring CRPC.
Exposure to indoor combustion and adult asthma outcomes: environmental tobacco smoke, gas stoves, and woodsmoke
Authors: M D Eisner
Journal: Thorax (2002)

<b>Background:</b> Because they have chronic airway inflammation, adults with asthma may be particularly susceptible to indoor air pollution. Despite widespread exposure to environmental tobacco smoke (ETS), gas stoves, and woodsmoke, the impact of these exposures on adult asthma has not been well characterised. <b>Methods:</b> Data were used from a prospective cohort study of 349 adults with asthma who underwent structured telephone interviews at baseline and 18 month follow up. The prospective impact of ETS, gas stove, and woodsmoke exposure on health outcomes was examined. <b>Results:</b> ETS exposure at baseline interview was associated with impaired health status at longitudinal follow up. Compared with respondents with no baseline self-reported exposure to ETS, higher level exposure (≥7 hours/week) was associated with worse severity of asthma scores at follow up, controlling for baseline asthma severity, age, sex, race, income, and educational attainment (mean score increment 1.5 points; 95% CI 0.4 to 2.6). Higher level baseline exposure to ETS was also related to poorer physical health status (mean decrement –4.9 points; 95% CI –8.4 to –1.3) and asthma specific quality of life (mean increase 4.4 points; 95% CI –0.2 to 9.0) at longitudinal follow up. Higher level baseline ETS exposure was associated with a greater risk of emergency department visits (OR 3.4; 95% CI 1.1 to 10.3) and hospital admissions for asthma at prospective follow up (OR 12.2; 95% CI 1.5 to 102). There was no clear relationship between gas stove use or woodstove exposure and asthma health outcomes. <b>Conclusion:</b> Although gas stove and woodstove exposure do not appear negatively to affect adults with asthma, ETS is associated with a clear impairment in health status.