tbuckley/cabot-search huggingface dataset:
Murine erythroid short-term radioprotection requires a BMP4-dependent, self-renewing population of stress erythroid progenitors
Authors: Omid F. Harandi, Shailaja Hedge, Dai-Chen Wu, Daniel Mckeone, Robert F. Paulson
Journal: Journal of Clinical Investigation (2010)

Acute anemic stress induces a systemic response designed to increase oxygen delivery to hypoxic tissues. Increased erythropoiesis is a key component of this response. Recovery from acute anemia relies on stress erythropoiesis, which is distinct from steady-state erythropoiesis. In this study we found that the bone morphogenetic protein 4-dependent (BMP4-dependent) stress erythropoiesis pathway was required and specific for erythroid short-term radioprotection following bone marrow transplantation. BMP4 signaling promoted the development of three populations of stress erythroid progenitors, which expanded in the spleen subsequent to bone marrow transplantation in mice. These progenitors did not correspond to previously identified bone marrow steady-state progenitors. The most immature population of stress progenitors was capable of self renewal while maintaining erythropoiesis without contribution to other lineages when serially transplanted into irradiated secondary and tertiary recipients. These data suggest that during the immediate post-transplant period, the microenvironment of the spleen is altered, which allows donor bone marrow cells to adopt a stress erythropoietic fate and promotes the rapid expansion and differentiation of stress erythroid progenitors. Our results also suggest that stress erythropoiesis may be manipulated through targeting the BMP4 signaling pathway to improve survival after injury.
Prevention of LPS-Induced Acute Lung Injury in Mice by Mesenchymal Stem Cells Overexpressing Angiopoietin 1
Authors: Shirley H. J Mei, Sarah D McCarter, Yupu Deng, Colleen H Parker, W. Conrad Liles, Duncan J Stewart
Journal: PLoS Medicine (2007)

The acute respiratory distress syndrome (ARDS), a clinical complication of severe acute lung injury (ALI) in humans, is a leading cause of morbidity and mortality in critically ill patients. ALI is characterized by disruption of the lung alveolar-capillary membrane barrier and resultant pulmonary edema associated with a proteinaceous alveolar exudate. Current specific treatment strategies for ALI/ARDS are lacking. We hypothesized that mesenchymal stem cells (MSCs), with or without transfection with the vasculoprotective gene angiopoietin 1 (ANGPT1) would have beneficial effects in experimental ALI in mice.Syngeneic MSCs with or without transfection with plasmid containing the human ANGPT1 gene (pANGPT1) were delivered through the right jugular vein of mice 30 min after intratracheal instillation of lipopolysaccharide (LPS) to induce lung injury. Administration of MSCs significantly reduced LPS-induced pulmonary inflammation, as reflected by reductions in total cell and neutrophil counts in bronchoalveolar lavage (BAL) fluid (53%, 95% confidence interval [CI] 7%-101%; and 60%, CI 4%-116%, respectively) as well as reducing levels of proinflammatory cytokines in both BAL fluid and lung parenchymal homogenates. Furthermore, administration of MSCs transfected with pANGPT1 resulted in nearly complete reversal of LPS-induced increases in lung permeability as assessed by reductions in IgM and albumin levels in BAL (96%, CI 6%-185%; and 74%, CI 23%-126%, respectively). Fluorescently tagged MSCs were detected in the lung tissues by confocal microscopy and flow cytometry in both naïve and LPS-injured animals up to 3 d.Treatment with MSCs alone significantly reduced LPS-induced acute pulmonary inflammation in mice, while administration of pANGPT1-transfected MSCs resulted in a further improvement in both alveolar inflammation and permeability. These results suggest a potential role for cell-based ANGPT1 gene therapy to treat clinical ALI/ARDS.
Value of ascitic lipids in the differentiation between cirrhotic and malignant ascites
Authors: Dieter Jüngst, Alexander L. Gerbes, Robert Martin, Gustav Paumgartner
Journal: Hepatology (1986)

Ascitic fluid concentrations of cholesterol, triglycerides and phospholipids, were compared with ascitic fluid total protein in 40 patients with chronic liver disease, 51patients with various neoplasms and 1 patient with cardiac failure. Seven patients withboth chronic liver disease and malignancy were considered separately. The first 54 patients (23 cirrhotic and 31 with malignancy) were used to determine median values and ranges and to define the most suitable cutoff concentrations between both groups. Median values for cholesterol (75 mg per dl), phospholipids (0.79 mmole per liter), triglycerides (75 mg per dl) and protein (3.8 gm per dl)were higher in malignant ascites compared to ascitic fluid concentrations of cholesterol (20 mg per dl), phospholipids (0.33 mmole per liter), triglycerides (51 mg per dl) and protein (1.9 gm per dl) in patients withcirrhosis. The best discrimination values were 48 mg per dl for cholesterol, 0.6 mmole per liter for phospholipids, 65 mg per dl for triglycerides and 2.5 gm per dl for protein. Application of these cutoff points to 38 subsequent patients (17 cirrhotic, 1 with cardiac failure and 20 with malignancy) revealed an efficiency of 86.8% for cholesterol, 86.8% for phospholipids, 68.4% for triglycerides and 79.0% for protein. From the data of all 92 patients, an efficiency of 92.3% forcholesterol, 79.4% for phospholipids, 72.8% for triglycerides and 79.4% for protein was calculated. We conclude that ascitic fluid cholesterol determination offers an excellent, cost–effective discrimination of ascites due to cirrhosis vs. ascites caused by malignancies.
THE RESULTS OF THE USE OF THE ELECTRO-MAGNET FOR THE EXTRACTION OF FOREIGN BODIES FROM THE EYE, WITH A REPORT OF TEN CASES.Read in the Section on Ophthalmology, at the Forty-fourth Annual Meeting of the American Medical Association.
Authors: C. BARCK
Journal: JAMA (1893)

In the history of the use of the magnet on the eye we can distinguish two phases: 1, the use of the common magnet; 2, of the electro-magnet. The first one dates back as far as two hundred and fifty years ago, when Dr. Fabry of Cologne, used a magnet to remove a piece of iron from the superficial layers of the cornea. In 1842 Dr. Meyer from Minden (Germany), used a magnet, carrying thirty-two pounds, to remove a piece of steel out of the interior through the scleral wound. The first one who made a section through the sclera in order to remove a piece of steel with a magnet from the vitreous was Dr. McKeown of Belfast in 1874. In 1875 Hirschberg of Berlin, made a similar trial without result. These are the instances of the use of the common magnet we find in literature. The second phase
Regulation of Microtubule-Dependent Protein Transport by the TSC2/Mammalian Target of Rapamycin Pathway
Authors: Xiuyun Jiang, Raymond S. Yeung
Journal: Cancer Research (2006)

Abstract Protein transport plays a critical role in the interaction of the cell with its environment. Recent studies have identified TSC1 and TSC2, two tumor suppressor genes involved in tuberous sclerosis complex, as regulators of the mammalian target of rapamycin (mTOR) pathway. Cells deficient in TSC1 or TSC2 possess high levels of Rheb-GTP resulting in constitutive mTOR activation. We have shown previously that the TSC1/TSC2 complex is involved in post-Golgi transport of VSVG and caveolin-1 in mammalian cells. Here, we show that modulation of mTOR activity affects caveolin-1 localization and that this effect is independent of p70S6K. Tsc1- and Tsc2-null cells exhibit abnormal caveolin-1 localization that is accompanied by disorganized microtubules in the subcortical region. Analyses of green fluorescent protein-EB1 and tubulin in live mutant cells suggest a failure of the plus-ends to sense cortical signals and to halt microtubule growth. Down-regulation of CLIP-170, a putative mTOR substrate with microtubule-binding properties, rescued the abnormal microtubule arrangement and caveolin-1 localization in Tsc2−/− cells. Together, these findings highlight a novel role of the TSC2/mTOR pathway in regulating microtubule-dependent protein transport. (Cancer Res 2006; 66(10): 5258-69)
Chronic granulomatous disease. Expression of the metabolic defect by in vitro culture of bone marrow progenitors.
Authors: P E Newburger, M S Kruskall, J M Rappeport, S H Robinson, M E Chovaniec, H J Cohen
Journal: Journal of Clinical Investigation (1980)

Chronic granulomatous disease (CGD), an often fatal syndrome of recurrent infections results from the inability of patients' peripheral blood phagocytic leukocytes to generate superoxide despite otherwise normal phagocytic functions such as ingestion and degranulation. Circulating granulocytes and monocytes are the progeny of bone marrow progenitor cells, colony-forming units in culture. We compared the function of cells grown in two different in vitro cuture systems from the bone marrow of a CGD patient with those from normal subjects. The cells of normal colony-forming unit in culture colonies grown in semisolid medium reduced nitroblue tetrazolium dye when stimulated by phorbol myristate acetate; none of the cells from colonies derived from CGD marrow did so. Cells grown in liquid suspension culture from normal marrow generated superoxide nearly as well as normal peripheral blood granulocytes; those from CGD marrow produced no superoxide, similarly cultured cells from both normal and CGD marrow ingested opsonized bacteria at rates equal to peripheral blood granulocytes. CGD marrow-derived cells showed increased exocytic degranulation relative to both normal marrow-derived cells and normal peripheral blood granulocytes. These studies demonstrate that the basic functional characteristics of CGD are embedded in the genetic program of granulocyte progenitors.
Transmission of Gonorrhea
Authors: Charles J. Wibbelsman
Journal: JAMA (1978)

To the Editor.—  In the article by Fiumara, The Treatment of Gonococcal Proctitis (239:735, 1978), the author cites that in his sample of 633 patients who were named as contacts of gonorrhea or were  by their  that they had the disease, the infection rate was 18%.  Our experience in the San Francisco Department of Public Health Venereal Disease Clinic for 1977 is quite different. During the calendar year 1977, we examined 3,436 men in the clinic as contacts to gonococcal urethritis; 1,567 of the men had positive rectal cultures for Neisseria gonorrhoeae , yielding an infection rate of 45.6%—almost triple the rate in the reported study. In the same year, 1,444 women examined were named as contacts to gonococcal urethritis; of these, 699 had positive cultures, an infection rate of 48.4%. Although the study by Fiumara includes contacts told by their friends in addition to named contacts, the difference
Shared T cell recognition sites on human histocompatibility leukocyte antigen class II molecules of patients with seropositive rheumatoid arthritis.
Authors: J Goronzy, C M Weyand, C G Fathman
Journal: Journal of Clinical Investigation (1986)

Seropositive rheumatoid arthritis (RA) in adult and juvenile patients is associated with the serologic marker HLA-DR4. This association is incomplete; about one-third of the patients lack the disease-associated HLA-DR4 haplotype. The main biological function of class II molecules is to restrict the recognition of antigen by T lymphocytes. We therefore tested the hypothesis that patients with seropositive RA share T cell recognition sites for an unknown antigen and that such T cell "epitopes" are not identified by conventional serologic typing. We generated alloreactive human T cell clones by stimulating peripheral blood lymphocytes of normal donors against a lymphoblastoid cell line from a juvenile patient with seropositive RA. A panel of clones that recognized only HLA-Dw14 cells on a panel of homozygous typing cells was used to analyze class II molecules of adult patients with seropositive RA. By inhibition studies using monoclonal antibodies, the epitopes recognized by the different clones could be further characterized and assigned either to DR- or to DQ-encoded cell surface products. By using four different clones, it was possible to identify Dw14-associated T cell epitopes on all seropositive rheumatoid patients tested who typed HLA-DR4-positive and also on all eight DR4-negative patients tested. Approximately one-half of nonrheumatoid DR4-positive donors carried one or more determinants recognized by these clones; the expression of these allodeterminants in DR4-negative nonrheumatoid patients was rare (less than 10%). Thus, alloreactive human T cell clones are powerful tools to define T cell recognition sites on class II molecules that are not identified by conventional typing. Using T cell clones with specificities for determinants expressed on Dw14 homozygous typing lines, we were able to demonstrate shared epitopes on cells of all patients tested with seropositive RA irrespective of their HLA-D or HLA-DR type. These data suggest that major histocompatibility complex class II antigens of RA patients might be much more homogeneous than demonstrated by the incomplete HLA-DR4 association.
Hypertransferrinemia Simulating Paraproteinemia.
Authors: Zbigniew A. Zawadzki
Journal: Annals of Internal Medicine (1969)

s1 May 1969Hypertransferrinemia Simulating Paraproteinemia.Zbigniew A. Zawadzki, M.D., George A. Edwards, M.D., F.A.C.P.Zbigniew A. Zawadzki, M.D.Search for more papers by this author, George A. Edwards, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-70-5-1105_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptA 42-year-old white man with a beta-spike deformity of the serum electrophoretic pattern and severe iron deficiency initially was thought to have paraproteinemia, but by immunochemical and radioautographic means the apparent M protein was identified as transferrin. Serial observations of the patient's serum were made as the iron deficiency was being corrected. Also, 10 iron-deficient men and 10 women in the third trimester of pregnancy (conditions characterized by hypertransferrinemia) were studied. In each subject electrophoresis and immunoelectrophoresis of serum proteins were performed, the levels of serum iron and total iron-binding capacity were determined, and the concentration of serum transferrin was... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Pittsburgh, Pa.; and Cincinnati, Ohio PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 May 1969Volume 70, Issue 5Page: 1105-1105KeywordsAttentionImmunoelectrophoresisIron deficiencyPregnancySerum proteinsTotal iron binding capacity ePublished: 1 December 2008 Issue Published: 1 May 1969 PDF downloadLoading ...
Daily Vitamin E Supplements Improve Metabolic Control But Not Insulin Secretion in Elderly Type II Diabetic Patients
Authors: Giuseppe Paolisso, Anna D'Amore, Domenico Galzerano, Vinicio Balbi, Dario Giugliano, Michele Varricchio, Felice D'Onofrio
Journal: Diabetes Care (1993)

To investigate the potential metabolic benefits deriving from daily vitamin E administration in type II diabetic patients.Twenty-five type II diabetic patients were invited to randomly take placebo or vitamin E (d-alpha-tocopherol; 900 mg/day) along a similar 3-mo period in a double-blind, crossover procedure. A wash-out period of 30 days separated the two treatment periods. At the end of each treatment period blood samples were drawn for plasma metabolites determination, and an intravenous glucose tolerance test (25 g of glucose as bolus in 3 min) was performed. During this study oral hypoglycemic agents were not discontinued or changed in their dosage.Chronic vitamin E administration reduced plasma glucose (8.3 +/- 0.3 vs. 7.5 +/- 0.2 mM, P > 0.05), triglycerides (2.27 +/- 0.08 vs. 1.67 +/- 0.09 mM, P < 0.02), free fatty acids (786 +/- 116 vs. 483 +/- 64 mM), total cholesterol (6.74 +/- 0.09 vs. 5.50 +/- 0.10 mM, P < 0.05), low-density lipoprotein cholesterol (4.73 +/- 0.11 vs. 3.67 +/- 0.07 mM, P < 0.04), and apoprotein B (1.7 +/- 0.3 vs. 1.0 +/- 0.1 g/L) levels but did not affect beta-cell response to glucose. HbA1 levels (7.8 +/- 0.3 vs. 7.1 +/- 0.5%, P < 0.05) were also significantly lowered after chronic vitamin E administration.Daily vitamin E supplements seem to produce a minimal but significant improvement in the metabolic control in type II diabetic patients. More studies are necessary before conclusions can be drawn about the safety of vitamin E during long-term administration.
Clinical Trials and the Right to Remain Silent
Authors: Michelle M. Mello, I. Glenn Cohen
Journal: JAMA Internal Medicine (2014)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Internal Medicine HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Internal Medicine journal
1023-93 Anti-inflammatory effects of the V-protectant AGI-1067 in the Canadian antioxidant restenosis trial (CART-1)
Authors: Jean-Claude Tardif, Philippe L L'Allier, Leonard Schwartz, Lawrence Title, Louise Laramee, Francois Reeves, Joel Lavoie, Marie-Claude Guertin, Jean Gregoire
Journal: Journal of the American College of Cardiology (2004)
Changes in levels of soluble T-cell activation markers, sIL-2R, sCD4 and sCD8, in relation to disease exacerbations in patients with systemic lupus erythematosus: a prospective study.
Authors: P E Spronk, E J ter Borg, M G Huitema, P C Limburg, C G Kallenberg
Journal: Annals of the Rheumatic Diseases (1994)

OBJECTIVES--To assess serial activation of T-cell subsets in relation to auto-antibody production and the occurrence of disease exacerbations in patients with systemic lupus erythematosus (SLE). METHODS--To study the possible role of T-cells in the pathophysiology of the disease, 16 consecutive exacerbations were prospectively studied in a cohort of patients with SLE, and serial plasma levels of sIL-2R, sCD4, and sCD8 preceding and during these exacerbations were determined. Levels of these molecules were related to total IgM and IgG, and anti-dsDNA. RESULTS--During major disease exacerbations (n = 6), levels of sIL-2R increased significantly (p &lt; 0.001). Levels of sCD4 were predominantly in the normal range, whereas levels of sCD8 were frequently increased. No change in levels of both molecules could be detected in the period before the exacerbation. During minor exacerbations (n = 10), levels of sIL-2R remained stable. Levels of sCD4, however, tended to drop, whereas levels of sCD8 tended to rise. No correlations were found between sIL-2R, sCD4 or sCD8 on the one hand, and total IgM, IgG, or anti-dsDNA on the other. CONCLUSIONS--Levels of sIL-2R are increased, and rise before major exacerbations of SLE. Levels of sCD4 and sCD8, however, are not related to levels of sIL-2R, and do not reflect B-cell activation, nor disease activity during exacerbations of SLE. Thus for the clinical follow up of SLE measurement of levels of sCD4 or sCD8 is of limited value.
Analysis of CDKN2A, CDKN2B, CDKN2C, and cyclin Ds gene status in hepatoblastoma
Authors: Achille Iolascon, Lucia Giordani, Arcangela Moretti, Giuseppe Basso, Adriana Borriello, Fulvio Della Ragione
Journal: Hepatology (1998)

The status and the expression of cyclin-dependent kinase inhibitor A (CDKN2A) family genes, named CDKN2A, CDKN2B, and CDKN2C and of cyclin Ds (D1, D2, and D3) genes were investigated in 14 cases of human hepatoblastomas. These genes were selected because: 1) CDKN2A and CDKN2B are very frequently inactivated in human cancers; 2) cyclin Ds are overexpressed in several tumors and 3) CDKN2A is posttranscriptionally silenced in hepatocellular carcinomas. Structural analysis of the CDKN2A, CDKN2B, and CDKN2C genes in hepatoblastoma cases showed the absence of deletions and/or point mutations. Moreover, a detailed investigation of loss of heterozygosity at 9p21 and 1p32 (the chromosomal regions where CDKN2A genes are located) rules out the possible loss of one allele. Messenger RNA (mRNA) analysis showed that CDKN2C is expressed in all hepatoblastoma samples studied, while both CDKN2A and CDKN2B genes are not transcribed in the cancer specimens as well as in the matched normal liver tissues. Interestingly, an alternative mRNA expressed by the CDKN2A gene (β-transcript) is detectable in 100% of the samples investigated. The analysis of cyclin D genes expression revealed that cyclin D1 is highly transcribed in normal hepatic tissue while cyclin D2 or D3 genes were extensively expressed in the matched transformed samples. Investigation at protein level confirmed the data obtained on RNA analysis. Indeed, p16 INK4A and p15 INK4B (products of expression of CDKN2A and CDKN2B respectively) were not observable while p18 INK4C (which is codified by CDKN2C) was clearly detectable in the samples analyzed. Moreover, a noticeable decrease of cyclin D1 content and increase of cyclin D3 level were observable in tumor tissues versus normal counterparts. Our findings demonstrated the following: 1) CDKN2A, CDKN2B, and CDKN2C genes are structurally unmodified in human hepatoblastoma, and 2) CDKN2A (α-transcript) and CDKN2B are transcriptionally silenced in normal liver whereas CDKN2A (β-transcript) and CDKN2C were clearly expressed. Finally, a clear shift in cyclin D type expression was observable during malignant transformation. These results show that CDKN2A gene family alterations are not involved in hepatoblastoma development, whereas changes in cyclin D types might play a role in this type of tumor. Furthermore, a highly regulated expression of CDKN2A seems to occur in normal hepatic tissue.