tbuckley/cabot-search huggingface dataset:
Myocardial Depressant Factor in Cardiogenic Shock
Authors: Stephen L. Wangensteen
Journal: JAMA (1974)

<h3>To the Editor.—</h3> We read with interest the editorial by Samuel Vaisrub, MD, in the April 22, 1974, issue ofThe Journal, entitled "Myocardial Depressant Factor (MDF) in Cardiogenic Shock" (228:500, 1974). Dr. Vaisrub stated that the most prominent humoral factor shown to play an important part in cardiogenic shock is MDF, a small peptide of molecular weight range between 800 and 1,000. While the hypothesis developed primarily by Drs. Lefer and Glenn is most attractive, we believe it must be interpreted with extreme caution at the present time. Since the turn of the century, toxic factors have been implicated in circulatory shock, but to date, none have had sustained importance as primary factors in the pathogenesis of shock. Using the cat papillary muscle assay system as described by Lefer, we have examined unprocessed plasma, ultrafiltered plasma, dialyzed plasma, column-eluted fractions of plasma, and desalted ultrafiltrates of plasma for MDF activity
DNA methylation of TH1/TH2 cytokine genes affects sensitization and progress of experimental asthma
Authors: Stephanie Brand, Dörthe Andrea Kesper, René Teich, Esma Kilic-Niebergall, Olaf Pinkenburg, Evita Bothur, Michael Lohoff, Holger Garn, Petra Ina Pfefferle, Harald Renz
Journal: Journal of Allergy and Clinical Immunology (2012)
Fat-storing cells of the rat liver synthesize and secrete C1-esterase inhibitor; modulation by cytokines
Authors: Stefan Schwögler, Margarete Odenthal, Thomas Knittel, Karl-Hermann Meyer zum Büschenfelde, Giuliano Ramadori
Journal: Hepatology (1992)

During liver fibrogenesis, fat–storing cells transform into myofibroblast–like cells and produce increasing amounts of extracellular matrix proteins. Because fat–storing cells produce α 2 –macroglobulin, an important serine protease inhibitor (serpin), we investigated whether fat–storing cells also synthesize C1–esterase inhibitor, another important serpin. C1–esterase inhibitor synthesis was studied in rat fatstoring cells at day 0, 3 and 7 after isolation by biosynthetic labeling, immunoprecipitation and sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Messenger RNA was examined by Northern–blot analysis. C1–esterase inhibitor gene expression and synthesis were detectable in freshly isolated fat–storing cells and increased distinctly during the time in culture. The cellular source of C1–esterase inhibitor in fat–storing cell cultures was also identified by in situ hybridization of cells at different times after isolation. By inhibition of the N–glycosylation using tunicamycin, rat C1–esterase inhibitor was identified as a glycoprotein. The time course of C1–esterase inhibitor secretion was determined by pulse–chase experiments. C1–esterase inhibitor synthesis was increased 6–fold to 10–fold by interferon–γ. Specific messenger RNA levels were also raised distinctly by this cytokine. In contrast, interferon–α and dexamethasone did not alter C1–esterase inhibitor gene expression. Because C1–esterase inhibitor synthesis is increased by advancing culture time and by the inflammatory mediator interferon–γ, we suggest that fat–storing cells may enhance the deposition of extracellular matrix proteins by inhibiting their degradation. (Hepatology 1992;16:794-802.)
OBSERVATIONS ON MITOSIS IN PSORIATIC EPIDERMIS
Authors: LIONEL FRY, R. M. H. McMINN
Journal: British Journal of Dermatology (1970)

SUMMARY.— Mitotic counts in psoriatic epidermis removed from (a) the centre and edge of a single plaque in 17 patients, and (b) lesions at 3 different sites—the arm, leg and back—in 16 patients, have been compared. Mitotic counts at the centre and edge of a plaque were similar for an individual patient, although there was variation in the group as a whole. There was no significant difference between the average centre and edge counts. The counts from the arm, leg and back were similar for an individual patient despite variation between patients. There was no evidence of any consistent variation between the 3 sites. These results suggest that the factors influencing mitosis in psoriasis at any given time are similar for all lesions and each part of a lesion in an individual patient, although there are variations between patients.
<i>Mdr</i>P-glycoproteins are not essential for biliary excretion of the hydrophobic heme precursor protoporphyrin in a griseofulvin-induced mouse model of erythropoietic protoporphyria
Authors: Torsten Plösch, Vincent W. Bloks, Juul F. W. Baller, Rick Havinga, Henkjan J. Verkade, Peter L. M. Jansen, Folkert Kuipers
Journal: Hepatology (2002)

Hepatic complications in erythropoietic protoporphyria (EPP) have been attributed to toxic actions of accumulated protoporphyrin (PP). PP can only be removed via the bile but transport systems involved have not been defined. The aim of this study was to gain insight in the mode of biliary PP excretion, with emphasis on the potential contribution of the Mdr1 P-glycoprotein export pump and biliary lipids as PP carriers. Control mice and mice homozygous for Mdr1a/b (Abcb1) or Mdr2 (Abcb4) gene disruption, the latter unable to secrete phospholipids and cholesterol into bile, were treated with griseofulvin to chemically induce protoporphyria. All groups showed dramatically increased PP levels in erythrocytes and liver after griseofulvin treatment. Histologically, massive PP deposits were found in livers of control and Mdr1a/b(-/-) mice but not in those of Mdr2(-/-) mice. Serum unesterified cholesterol and phospholipids were increased by griseofulvin because of formation of lipoprotein-X in control and Mdr1a/b(-/-) mice only. Yet, bile flow was not impaired in griseofulvin-treated mice, and biliary bile salt, phospholipid, and cholesterol secretion rates were significantly increased. Surprisingly, biliary PP excretion was similar in all 3 groups of griseofulvin-treated mice: the observed linear relationship between hepatic and biliary PP concentrations and identical liver-to-bile concentration ratios in treated and untreated mice suggest a passive mode of excretion. In conclusion, the data show that Mdr P-glycoproteins are not critically involved in biliary removal of excess PP and indicate that the presence of biliary lipids is required for formation of intrahepatic PP deposits.
Synthetic Consensus HIV-1 DNA Induces Potent Cellular Immune Responses and Synthesis of Granzyme B, Perforin in HIV Infected Individuals
Authors: Matthew P Morrow, Pablo Tebas, Jian Yan, Lorenzo Ramirez, Anna Slager, Kim Kraynyak, Malissa Diehl, Divya Shah, Amir Khan, Jessica Lee, Jean Boyer, J Joseph Kim, Niranjan Y Sardesai, David B Weiner, Mark L Bagarazzi
Journal: Molecular Therapy (2014)

This study evaluated the safety and immunogenicity of PENNVAX-B in 12 HIV infected individuals. PENNVAX-B is a combination of three optimized synthetic plasmids encoding for multiclade HIV Gag and Pol and a consensus CladeB Env delivered by electroporation. HIV infected individuals whose virus was effectively suppressed using highly active antiretroviral therapy (HAART) received PENNVAX-B DNA followed by electroporation with CELLECTRA-5P at study weeks 0, 4, 8, and 16. Local administration site and systemic reactions to PENNVAX-B were recorded after each treatment along with any adverse events. Pain of the treatment procedure was assessed using a Visual Analog Scale. Whole PBMCs were isolated for use in IFN ELISpot and Flow Cytometric assays. PENNVAX-B was generally safe and well tolerated. Overall, the four dose regimen was not associated with any serious adverse events or severe local or systemic reactions. A rise in antigen-specific SFU was detected in the INFγ ELISpot assay in all 12 participants. T cells from 8/12 participants loaded with both granzyme B and perforin in response to HIV antigen, an immune finding characteristic of long-term nonprogressors (LTNPs) and elite controllers (ECs). Thus administration of PENNVAX-B may prove useful adjunctive therapy to ART for treatment and control of HIV infection. This study evaluated the safety and immunogenicity of PENNVAX-B in 12 HIV infected individuals. PENNVAX-B is a combination of three optimized synthetic plasmids encoding for multiclade HIV Gag and Pol and a consensus CladeB Env delivered by electroporation. HIV infected individuals whose virus was effectively suppressed using highly active antiretroviral therapy (HAART) received PENNVAX-B DNA followed by electroporation with CELLECTRA-5P at study weeks 0, 4, 8, and 16. Local administration site and systemic reactions to PENNVAX-B were recorded after each treatment along with any adverse events. Pain of the treatment procedure was assessed using a Visual Analog Scale. Whole PBMCs were isolated for use in IFN ELISpot and Flow Cytometric assays. PENNVAX-B was generally safe and well tolerated. Overall, the four dose regimen was not associated with any serious adverse events or severe local or systemic reactions. A rise in antigen-specific SFU was detected in the INFγ ELISpot assay in all 12 participants. T cells from 8/12 participants loaded with both granzyme B and perforin in response to HIV antigen, an immune finding characteristic of long-term nonprogressors (LTNPs) and elite controllers (ECs). Thus administration of PENNVAX-B may prove useful adjunctive therapy to ART for treatment and control of HIV infection.
Immunohistology in Sweet's syndrome
Authors: R.Schlegel Gomez, P. Driesch, O.P. Hornstein
Journal: British Journal of Dermatology (1991)

Journal Article Immunohistology in Sweet's syndrome Get access R.Schlegel Gomez, R.Schlegel Gomez Department of Dermatology, University of Erlangen/Nuremberg, W‐8520 Erlangen, Germany Search for other works by this author on: Oxford Academic Google Scholar P. von den Driesch, P. von den Driesch Department of Dermatology, University of Erlangen/Nuremberg, W‐8520 Erlangen, Germany Search for other works by this author on: Oxford Academic Google Scholar O.P. Hornstein O.P. Hornstein Department of Dermatology, University of Erlangen/Nuremberg, W‐8520 Erlangen, Germany Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 125, Issue 4, 1 October 1991, Pages 402–403, https://doi.org/10.1111/j.1365-2133.1991.tb14184.x Published: 01 October 1991
Approaches to Increase Physical Activity
Authors: Deborah Grady
Journal: JAMA Internal Medicine (2013)

and to show extremely sedentary behavior in this population.Participants spent a negligible amount of time in moderate activity, and the time spent in nonsedentary activity was mostly of very low intensity and short duration.What do these findings mean for safety-net health care providers as they implement the Patient-Centered Medical Home Standards? 4 Clinicians need to assess their patients' levels of PA and subsequent inactivity to tailor counseling.Their focus might need to shift to increasing light PA and the number and lengths of breaks in sedentary behavior.However, this change is unlikely to be addressed effectively in typical primary care office visits or by physicians alone.More intensive strategies need to be developed to address the motivational changes required. 5 In conclusion, results from this study might indicate a new silent epidemic of a supersedentary lifestyle that might contribute significantly to the health disparities seen in poor and minority populations served by FQHCs.These findings highlight the challenges faced by safety-net providers in promoting healthy lifestyles in their patients.
Human bronchus and intestine express the same mucin gene.
Authors: B H Jany, M W Gallup, P S Yan, J R Gum, Y S Kim, C B Basbaum
Journal: Journal of Clinical Investigation (1991)

The amino acid and sugar composition of mucins from various organs is similar but not identical. This could arise by one or more of the following: organ-specific processing of a single core protein, organ-specific splicing of a single mucin mRNA, or organ-specific expression of various mucin genes. To begin to investigate the source of this variability, we examined (a) immunological cross-reactivity and (b) cDNA cross-hybridization, among several mucin-secreting organs of the human body. Peptide-directed antibodies raised against both nondeglycosylated (LS) and deglycosylated (HFB) intestinal mucin strongly stained mucous cells in the bronchial epithelium and submucosal glands, indicating homology between mucins of the bronchus and intestine at the peptide level. By screening a bronchus cDNA library with an intestinal mucin cDNA, SMUC-41, we isolated a bronchus mucin cDNA, HAM-1. This cDNA is 96% homologous to the first repeat of SMUC-41. HAM-1 hybridized to restriction fragments of human genomic DNA identical to those hybridizing to SMUC-41 on Southern blots. SMUC-41 also hybridized to polydisperse transcripts in the bronchus, cervix, gall bladder, and mammary gland, indicating mucin homology among all these organs at the RNA level. We conclude that the bronchus and intestine express a common mucin gene, which is likely co-expressed by at least several other mucin-secreting organs.
Increased chemotactic activity of neutrophil leukocytes in psoriasis
Authors: GERD MICHAELSSON
Journal: British Journal of Dermatology (1980)

The random and active migration of neutrophil leukocytes in agarose was studied in sixty-one patients with psoriasis and in healthy controls. E. coli filtrate was used as chemoattractant. The random as well as the active migration was increased in psoriasis. The increase was most pronounced in those cases with widespread psoriasis. In twenty patients who were followed for 1-3 years, the neutrophil chemotactic activity remained essentially unchanged.
CHANGES IN PLASMA VOLUME AND CARDIAC OUTPUT FOLLOWING THE INTRAVENOUS INJECTION OF GELATIN, SERUM, AND PHYSIOLOGICAL SALINE SOLUTION 1
Authors: J. P. Holt, P. K. Knoefel
Journal: Journal of Clinical Investigation (1944)

There has recently been a renewed interest in the use of gelatin as a substitute for blood plasma (1 to 5).The purpose of the present study is to determine, in normal dogs, the degree to which a single large intravenous injection of gelatin solu- tion, physiological saline solution, or serum re- mains in the vascular bed and to determine the effect of these injections on cardiac output.METHODS Dogs were anesthetized with an intravenous injection of sodium barbital, 250 mgm.per kgm.body weight.A tracheotomy was performed and a tracheal cannula inserted.A cephalic vein, carotid artery, and a small branch of the right and left femoral arteries were exposed and cannulated.Arterial blood pressure was recorded by means of a Hg manometer that was connected to the carotid cannula.The cardiac output, right auricular pressure, and hematocrit were determined and, at the same time, 10 to 40 mgm. of the dye, T-1824, were injected intravenously to determine the plasma volume.One hour later, 50 cc.per kgm.body weight of warmed gelatin solution, physiological saline solution, or serum were injected into the cephalic vein at the rate of 5 cc.per kgm.per minute.Twenty minutes after the completion of the fluid injection, the cardiac output was determined, an "indirect" determination of plasma volume was made, and the hematocrit was determined.At 40 minutes after the completion of the injection, an "indirect" determination of plasma volume was made and the hematocrit was determined.At 60 minutes after the completion of the injection, the right auricular pressure, hematocrit, -and cardiac output were determined, and an "indirect" deter- mination of plasma volume was made.At the same time, 10 to 20 mgm. of dye were injected for a second "direct" determination of plasma volume.Two hundred and forty minutes after the completion of the injection, the hematocrit, right auricular pressure, and cardiac output were determined.At the same time, 10 mgm. of dye were injected intravenously for a third "direct" plasma volume determination.
Size-Segregated Particle Number Concentrations and Respiratory Emergency Room Visits in Beijing, China
Authors: Arne Marian Leitte, Uwe Schlink, Olf Herbarth, Alfred Wiedensohler, Xiao-Chuan Pan, Min Hu, Matthia Richter, Birgit Wehner, Thomas Tuch, Zhijun Wu, Minjuan Yang, Liqun Liu, Susanne Breitner, Josef Cyrys, Annette Peters, H.-Erich Wichmann, Ulrich Franck
Journal: Environmental Health Perspectives (2010)

The link between concentrations of particulate matter (PM) and respiratory morbidity has been investigated in numerous studies.The aim of this study was to analyze the role of different particle size fractions with respect to respiratory health in Beijing, China.Data on particle size distributions from 3 nm to 1 µm; PM10 (PM ≤ 10 µm), nitrogen dioxide (NO(2)), and sulfur dioxide concentrations; and meteorologic variables were collected daily from March 2004 to December 2006. Concurrently, daily counts of emergency room visits (ERV) for respiratory diseases were obtained from the Peking University Third Hospital. We estimated pollutant effects in single- and two-pollutant generalized additive models, controlling for meteorologic and other time-varying covariates. Time-delayed associations were estimated using polynomial distributed lag, cumulative effects, and single lag models.Associations of respiratory ERV with NO(2) concentrations and 100-1,000 nm particle number or surface area concentrations were of similar magnitude-that is, approximately 5% increase in respiratory ERV with an interquartile range increase in air pollution concentration. In general, particles < 50 nm were not positively associated with ERV, whereas particles 50-100 nm were adversely associated with respiratory ERV, both being fractions of ultrafine particles. Effect estimates from two-pollutant models were most consistent for NO(2).Present levels of air pollution in Beijing were adversely associated with respiratory ERV. NO(2) concentrations seemed to be a better surrogate for evaluating overall respiratory health effects of ambient air pollution than PM(10) or particle number concentrations in Beijing.
Continuous recruitment of naive T cells contributes to heterogeneity of antiviral CD8 T cells during persistent infection
Authors: Vaiva Vezys, David Masopust, Christopher C. Kemball, Daniel L. Barber, Leigh A. O'Mara, Christian P. Larsen, Thomas C. Pearson, Rafi Ahmed, Aron E. Lukacher
Journal: The Journal of Experimental Medicine (2006)

Numerous microbes establish persistent infections, accompanied by antigen-specific CD8 T cell activation. Pathogen-specific T cells in chronically infected hosts are often phenotypically and functionally variable, as well as distinct from T cells responding to nonpersistent infections; this phenotypic heterogeneity has been attributed to an ongoing reencounter with antigen. Paradoxically, maintenance of memory CD8 T cells to acutely resolved infections is antigen independent, whereas there is a dependence on antigen for T cell survival in chronically infected hosts. Using two chronic viral infections, we demonstrate that new naive antigen-specific CD8 T cells are primed after the acute phase of infection. These newly recruited T cells are phenotypically distinct from those primed earlier. Long-lived antiviral CD8 T cells are defective in self-renewal, and lack of thymic output results in the decline of virus-specific CD8 T cells, indicating that newly generated T cells preserve antiviral CD8 T cell populations during chronic infection. These findings reveal a novel role for antigen in maintaining virus-specific CD8 T cells during persistent infection and provide insight toward understanding T cell differentiation in chronic infection.
Increased blood manganese in cirrhotic patients: Relationship to pallidal magnetic resonance signal hyperintensity and neurological symptoms
Authors: L Spahr, R F Butterworth, S Fontaine, L Bui, G Therrien, P C Milette, L H Lebrun, J Zayed, A Leblanc, G Pomier-Layrargues
Journal: Hepatology (1996)

Increasing evidence suggests that manganese deposition is responsible for the T1–weighted magnetic resonance imaging (MRI) signal hyperintensity consistently observed in pallidum of cirrhotic patients. However, the relationship between blood manganese and the etiology or severity of liver disease, as well as the neurological symptomatology in these patients, has not been well established. In the present study, blood manganese concentrations were measured by atomic absorption spectrometry together with MRI and neurological evaluation in 57 cirrhotic patients with various etiologies and severity of liver disease. Blood manganese concentrations were elevated in 67% of cirrhotic patients and were significantly higher in patients with previous portacaval anastomoses or transjugular intrahepatic portosystemic shunt (TIPS). Pallidal signal hyperintensity was observed in 88% of patients, and significant correlations were demonstrated between blood manganese and pallidal index (PI) (a measure of pallidal signal hyperintensity), as well as Child–Pugh score. Assessment of extrapyramidal symptoms using the Columbia rating scale revealed a significant incidence of tremor, rigidity, or akinesia in up to 89% of cirrhotic patients. However, there was no significant correlation between blood manganese and extrapyramidal symptoms, although severity of akinesia was significantly greater in Child–Pugh C patients. Extrapyramidal symptoms could result from a toxic effect of manganese on basal ganglia dopaminergic function. These findings further support a role for manganese in the etiology of pallidal MRI signal hyperintensity in patients with chronic liver disease.
Combined treatment of portal hypertension with ritanserin and propranolol in conscious and unrestrained cirrhotic rats
Authors: Gilles Pomier-Layrargues, Lise Giroux, Bernard Rocheleau, Pierre-Michel Huet
Journal: Hepatology (1992)

We recently reported that ritanserin, a 5-hydroxytryptamine receptor antagonist, induced significant reduction of portal pressure in cirrhotic rats. In this study, we investigated the hemodynamic effects of a combination of propranolol and ritanserin in conscious and unrestrained cirrhotic rats. Heparinized catheters exiting from the neck were placed into the portal vein, inferior vena cava, aorta and left ventricle. Cardiac output and regional blood flows were measured with radiolabeled microspheres and the reference-sample method. Serial hemodynamic studies were performed 4 hr after rats awakened (basal), 1 hr after administration of ritanserin (0.63 mg/kg body wt, intravenously) and after intravenous propranolol infusion (0.33 mg/kg/min for 15 min) in nine cirrhotic rats. Similar measurements were obtained in a control group of eight cirrhotic rats treated with the solvents of ritanserin and propranolol. Ritanserin caused significant reduction of portal pressure (−19%). Portal-venous inflow and splanchnic arteriolar resistances remained unchanged, whereas portal-venous resistances were slightly but significantly lowered (−17%); and ritanserin had no effects on systemic hemodynamics. The addition of propranolol resulted in further reduction of portal pressure (−24%); the final reduction after combined therapy was −38%. Propranolol induced a marked decrease in cardiac output (−31%) and portalvenous inflow (−30%). It also caused a significant increase in splanchnic arteriolar resistance (+39%), but did not magnify the ritanserin-induced decrease of portal-venous resistance. The combined therapy did not modify the mean arterial pressure. Our results show that the effects of ritanserin on portal pressure - probably mediated by a reduction of intrahepatic and/or portocollateral resistances - can be potentiated by propranolol, which lowers the portalvenous inflow. (HEPATOLOGY 1992;15:878–882).