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1. Cholera R, Brittain NJ, Gillrie MR, Lopera-Mesa TM, Diakité SA, Arie T, Krause MA, Guindo A, Tubman A, Fujioka H, Diallo DA, Doumbo OK, Ho M, Wellems TE, Fairhurst RM: Impaired cytoadherence of Plasmodium falciparum-infected erythrocytes containing sickle hemoglobin. Proc Natl Acad Sci U S A; 2008 Jan 22;105(3):991-6
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  • [Title] Impaired cytoadherence of Plasmodium falciparum-infected erythrocytes containing sickle hemoglobin.
  • Sickle trait, the heterozygous state of normal hemoglobin A (HbA) and sickle hemoglobin S (HbS), confers protection against malaria in Africa.
  • These findings identify a mechanism of protection for HbS that has features in common with that of hemoglobin C (HbC).
  • Coinherited hemoglobin polymorphisms and naturally acquired antibodies to PfEMP-1 may influence the degree of malaria protection in AS children by further weakening cytoadherence interactions.

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  • (PMID = 18192399.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hemoglobin, Sickle; 0 / Protozoan Proteins; 0 / erythrocyte membrane protein 1, Plasmodium falciparum
  • [Other-IDs] NLM/ PMC2242681
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2. Sidani CA, Ballourah W, El Dassouki M, Muwakkit S, Dabbous I, Dahoui H, Al-Kutoubi A, Abboud MR: Venous sinus thrombosis leading to stroke in a patient with sickle cell disease on hydroxyurea and high hemoglobin levels: treatment with thrombolysis. Am J Hematol; 2008 Oct;83(10):818-20
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  • [Title] Venous sinus thrombosis leading to stroke in a patient with sickle cell disease on hydroxyurea and high hemoglobin levels: treatment with thrombolysis.
  • A 21-year-old man with homozygous sickle cell disease maintained on hydroxyurea for 1 year developed thrombosis of the superior sagittal, right transverse, and right sigmoid dural sinuses with a large venous infarct.
  • Investigation did not reveal any inherited or acquired hypercoagulable state.
  • This patient however had consistently elevated hemoglobin levels both at the time of the initial event and on follow up.
  • High hemoglobin levels resulting from hydroxyurea therapy may have contributed to development of complications in this patient.

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  • [Copyright] Copyright 2008 Wiley-Liss, Inc.
  • (PMID = 18756541.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antisickling Agents; 0 / Hemoglobins; X6Q56QN5QC / Hydroxyurea
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3. Mocny JC, Olson JS, Connell TD: Passively released heme from hemoglobin and myoglobin is a potential source of nutrient iron for Bordetella bronchiseptica. Infect Immun; 2007 Oct;75(10):4857-66
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  • [Title] Passively released heme from hemoglobin and myoglobin is a potential source of nutrient iron for Bordetella bronchiseptica.
  • Colonization by Bordetella bronchiseptica results in a variety of inflammatory respiratory infections, including canine kennel cough, porcine atrophic rhinitis, and a whooping cough-like disease in humans.
  • A vast amount of Fe within the host is sequestered within heme, a metalloporphyrin which is coordinately bound in hemoglobin and myoglobin.
  • Utilization of hemoglobin and myoglobin as sources of nutrient Fe by B. bronchiseptica requires expression of BhuR, an outer membrane protein.
  • We hypothesize that hemin is acquired by B. bronchiseptica in a BhuR-dependent manner after spontaneous loss of the metalloporphyrin from hemoglobin and/or myoglobin.
  • Sequestration experiments demonstrated that direct contact with hemoglobin or myoglobin was not required to support growth of B. bronchiseptica in an Fe-limiting environment.
  • Collectively, these experiments provided strong experimental support for the model that BhuR is a hemin receptor and B. bronchiseptica likely acquires heme during infection after passive loss of the metalloporphyrin from hemoglobin and/or myoglobin.
  • These results also suggest that spontaneous hemin loss by hemoglobin and myoglobin may be a common mechanism by which many pathogenic bacteria acquire heme and heme-bound Fe.

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  • (PMID = 17664260.001).
  • [ISSN] 0019-9567
  • [Journal-full-title] Infection and immunity
  • [ISO-abbreviation] Infect. Immun.
  • [Language] ENG
  • [Grant] United States / NIDCR NIH HHS / DE / DE007034; United States / NIDCR NIH HHS / DE / T32 DE007034; United States / NHLBI NIH HHS / HL / HL47020; United States / NIGMS NIH HHS / GM / GM35649; United States / NIGMS NIH HHS / GM / R01 GM035649; United States / NHLBI NIH HHS / HL / R01 HL047020
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bacterial Proteins; 0 / Hemoglobins; 0 / Myoglobin; 0 / Receptors, Cell Surface; 743LRP9S7N / Hemin; E1UOL152H7 / Iron
  • [Other-IDs] NLM/ PMC2044545
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4. Qi JY, Zhang FK, Zhou ZP, Zhao YP, Yang RC, Qian LS, Zheng YZ: [Myelodysplastic syndromes associated with acquired hemoglobin H disease]. Zhonghua Xue Ye Xue Za Zhi; 2007 May;28(5):327-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Myelodysplastic syndromes associated with acquired hemoglobin H disease].
  • OBJECTIVE: To report 7 cases of acquired hemoglobin H in myelodysplastic syndromes.
  • [MeSH-major] Myelodysplastic Syndromes / complications. alpha-Thalassemia / complications


5. Alli NA: Acquired haemoglobin H disease. Hematology; 2005 Oct;10(5):413-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acquired haemoglobin H disease.
  • Acquired haemoglobin H disease has been described in various premalignant haematological conditions and is most commonly associated with myelodysplastic and myeloproliferative syndromes.
  • Affected individuals have no family or past history of alpha thalassaemia and these subjects usually suffer from severe uncompensated haemolysis.
  • Extensive mapping and sequence analysis of the alpha globin gene cluster have demonstrated intact alpha globin genes, leading workers to conclude that an acquired in trans mechanism is responsible for the disorder.
  • ATRX gene mutations on the X chromosome have been shown to be instrumental in the suppression of alpha globin gene expression.
  • Despite recent advances in the understanding of its pathogenesis, the precise mechanism of acquired haemoglobin H disease remains a mystery.
  • [MeSH-major] Chromosomes, Human, X / genetics. DNA Helicases / genetics. Gene Expression Regulation / genetics. Globins / genetics. Mutation. Nuclear Proteins / genetics. alpha-Thalassemia / genetics

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  • (PMID = 16273735.001).
  • [ISSN] 1024-5332
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Nuclear Proteins; 9004-22-2 / Globins; EC 3.6.4.- / DNA Helicases; EC 3.6.4.12 / ATRX protein, human
  • [Number-of-references] 58
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6. Yin XL, He YY, Zhang XH, Zhou TH, Zhang TL: Acquired hemoglobin h disease associated with Down syndrome. J Pediatr Hematol Oncol; 2010 Aug;32(6):e244-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acquired hemoglobin h disease associated with Down syndrome.
  • [MeSH-major] Down Syndrome / complications. alpha-Thalassemia / etiology

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  • (PMID = 20628319.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
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7. Hsieh MM, Linde NS, Wynter A, Metzger M, Wong C, Langsetmo I, Lin A, Smith R, Rodgers GP, Donahue RE, Klaus SJ, Tisdale JF: HIF prolyl hydroxylase inhibition results in endogenous erythropoietin induction, erythrocytosis, and modest fetal hemoglobin expression in rhesus macaques. Blood; 2007 Sep 15;110(6):2140-7
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  • [Title] HIF prolyl hydroxylase inhibition results in endogenous erythropoietin induction, erythrocytosis, and modest fetal hemoglobin expression in rhesus macaques.
  • HIF-alpha is an essential component of the oxygen-sensing mechanisms and under normoxic conditions is targeted for degradation via hydroxylation by HIF-prolyl hydroxylases.
  • Furthermore, several PHIs induced fetal hemoglobin (HbF) expression in primary human erythroid cells in vitro, as determined by flow cytometry.
  • HIF PHIs represent a novel class of molecules with broad potential clinical application for congenital and acquired anemias.

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  • [CommentIn] Blood. 2007 Sep 15;110(6):1709
  • (PMID = 17557894.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 11096-26-7 / Erythropoietin; 9034-63-3 / Fetal Hemoglobin; EC 1.14.11.2 / Procollagen-Proline Dioxygenase; S88TT14065 / Oxygen
  • [Other-IDs] NLM/ PMC1976368
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8. Segawa Y, Hotta K, Umemura S, Fujiwara Y, Shinkai T, Ueoka H, Takigawa N, Tabata M, Kiura K, Tanimoto M: Clinical factors affecting acquired resistance to gefitinib in previously treated Japanese patients with advanced nonsmall cell lung cancer. Cancer; 2006 Oct 15;107(8):1866-72
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  • [Title] Clinical factors affecting acquired resistance to gefitinib in previously treated Japanese patients with advanced nonsmall cell lung cancer.
  • BACKGROUND: The risk factors for the development of acquired resistance in nonsmall cell lung cancer (NSCLC) patients responding to gefitinib are unclear.
  • The current study assessed clinicopathologic factors affecting acquired resistance to gefitinib in previously treated patients with advanced NSCLC.
  • Of these patients, 56 who had continued gefitinib treatment without disease progression for at least 6 months were included in the study.
  • RESULTS: At a median follow-up time of 21.6 months (range, 7.7-59.7 months), the median time to disease progression was 19.5 months, with progression-free survival rates of 68.5% at 1 year, 33.6% at 2 years, and 21.2% at 3 years.
  • In a multivariate analysis using a Cox regression model, baseline brain metastasis was the strongest prognostic factor affecting acquired resistance to gefitinib (hazards ratio, 2.14; 95% confidence interval, 1.10- 4.17 [P = .025]).
  • In addition, a decreased baseline hemoglobin level (P = .074) and the administration of >1 chemotherapy regimen before gefitinib treatment (P = .069) tended to be significant negative prognostic factors.
  • CONCLUSIONS: In patients undergoing treatment with gefitinib, the presence of brain metastasis was strongly associated with the emergence of acquired resistance in the current series of NSCLC patients.
  • [MeSH-minor] Adult. Aged. Brain Neoplasms / secondary. Disease Progression. Disease-Free Survival. Female. Humans. Japan. Male. Middle Aged. Retrospective Studies. Risk Factors

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  • [Copyright] 2006 American Cancer Society
  • (PMID = 16967452.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Quinazolines; S65743JHBS / gefitinib
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9. Abbas SQ, Nasiruddin, Al-Gethami MM: Acquired haemoglobin H disease associated with myelodysplastic syndrome. J Coll Physicians Surg Pak; 2008 Dec;18(12):784-6
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  • [Title] Acquired haemoglobin H disease associated with myelodysplastic syndrome.
  • Considering hemolysis low MCV and basophilic stippling on peripheral film, hemoglobin electrophoresis was done that showed Haemoglobin H (15.5%) that in the absence of family history was thought to be acquired.
  • After bone marrow examination, the final diagnosis was Myelodysplastic Syndrome (MDS), Refractory anemia with excess of blast (RAEB) associated with acquired Haemoglobin H (Hb H) disease.
  • [MeSH-major] Myelodysplastic Syndromes / complications. alpha-Thalassemia / etiology

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  • (PMID = 19032897.001).
  • [ISSN] 1022-386X
  • [Journal-full-title] Journal of the College of Physicians and Surgeons--Pakistan : JCPSP
  • [ISO-abbreviation] J Coll Physicians Surg Pak
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Pakistan
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10. Vargas E, Spielvogel H: Chronic mountain sickness, optimal hemoglobin, and heart disease. High Alt Med Biol; 2006;7(2):138-49
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  • [Title] Chronic mountain sickness, optimal hemoglobin, and heart disease.
  • Since CMS was first described by Carlos Monge in the Peruvian Andes in 1925, numerous research papers have been devoted to this topic, but many unanswered questions still exist with respect to the beginning of the disease and its cause(s).
  • The experience with CMS has shown that an excessively high hemoglobin concentration is not favorable for high altitude acclimatization, and the hypothesis of theoretically "optimal" hematocrit and "optimal" hemoglobin has been made.
  • The calculated optimal hemoglobin concentration of 14.7 g/dL for resting men in the Andes is discussed as theoretical and not applicable in real life.
  • The most frequent congenital and acquired heart diseases are discussed, such as patent ductus, atrial septum defect, ventricle septum defect among congenital heart diseases and the still very frequent rheumatic valve cardiopathies and Chagas disease as acquired cardiopathies.
  • Among the typical acquired heart diseases of the high altitude dweller, special attention is given to chronic cor pulmonale as a consequence of severe CMS with pulmonary hypertension.
  • [MeSH-minor] Altitude. Animals. Bolivia. Chronic Disease. Hematocrit. Humans. Indians, South American. Oxygen Consumption / physiology

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  • (PMID = 16764527.001).
  • [ISSN] 1527-0297
  • [Journal-full-title] High altitude medicine & biology
  • [ISO-abbreviation] High Alt. Med. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hemoglobins
  • [Number-of-references] 53
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11. Lau B, Gange SJ, Phair JP, Riddler SA, Detels R, Margolick JB: Use of total lymphocyte count and hemoglobin concentration for monitoring progression of HIV infection. J Acquir Immune Defic Syndr; 2005 Aug 15;39(5):620-5
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  • [Title] Use of total lymphocyte count and hemoglobin concentration for monitoring progression of HIV infection.
  • Prior research has demonstrated rapid declines in total lymphocyte count (TLC) and hemoglobin levels before AIDS, but the prognostic accuracy of these declines has not been examined prospectively.
  • METHODS: Longitudinal TLC and hemoglobin data from men in the Multicenter AIDS Cohort Study (MACS) before the introduction of potent HIV therapy were used to identify the first time when the TLC was <or=1200 cells/mm, TLC declined by >33% per year, and hemoglobin declined by >11.6% per year.
  • RESULTS: Rapid declines in TLC or hemoglobin were associated with progression to AIDS (relative hazard [RH]=4.70, 95% confidence interval [CI]: 3.23-6.86 for TLC; RH=5.55, 95% CI: 3.69-8.36 for hemoglobin).
  • Even among those with a TLC>1200 cells/mm, a rapid decline in TLC or hemoglobin was strongly associated with progression to AIDS (RH=2.53, 95% CI: 1.56-4.10 for TLC; RH=5.28, 95% CI: 3.11-8.97 for hemoglobin).
  • CONCLUSIONS: In the MACS, rapid declines in TLC or hemoglobin concentration indicated an increased likelihood of progression of HIV infection to AIDS.
  • [MeSH-minor] Biomarkers / blood. Disease Progression. Humans. Male. Proportional Hazards Models

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  • (PMID = 16044017.001).
  • [ISSN] 1525-4135
  • [Journal-full-title] Journal of acquired immune deficiency syndromes (1999)
  • [ISO-abbreviation] J. Acquir. Immune Defic. Syndr.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / 5-M01-RR-00052; United States / NIAID NIH HHS / AI / UO1-AI-35039; United States / NIAID NIH HHS / AI / UO1-AI-35040; United States / NIAID NIH HHS / AI / UO1-AI-35041; United States / NIAID NIH HHS / AI / UO1-AI-35042; United States / NIAID NIH HHS / AI / UO1-AI-35043; United States / NIAID NIH HHS / AI / UO1-AI-37613; United States / NIAID NIH HHS / AI / UO1-AI-37984
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Hemoglobins
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12. Woo PC, Lau SK, Tsoi HW, Huang Y, Poon RW, Chu CM, Lee RA, Luk WK, Wong GK, Wong BH, Cheng VC, Tang BS, Wu AK, Yung RW, Chen H, Guan Y, Chan KH, Yuen KY: Clinical and molecular epidemiological features of coronavirus HKU1-associated community-acquired pneumonia. J Infect Dis; 2005 Dec 1;192(11):1898-907
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical and molecular epidemiological features of coronavirus HKU1-associated community-acquired pneumonia.
  • METHODS: Prospectively collected (during a 12-month period) nasopharyngeal aspirates (NPAs) from patients with community-acquired pneumonia from 4 hospitals were subjected to reverse-transcription polymerase chain reaction, for detection of CoV-HKU1.
  • RESULTS: NPAs from 10 (2.4%) of 418 patients with community-acquired pneumonia were found to be positive for CoV-HKU1.
  • The 2 patients who died had significantly lower hemoglobin levels, monocyte counts, albumin levels, and oxygen saturation levels on admission and had more-extensive involvement visible on chest radiographs.
  • CONCLUSIONS: CoV-HKU1 accounts for 2.4% of community-acquired pneumonia, with 2 genotypes in the study population.
  • Without performance of diagnostic tests, the illness was clinically indistinguishable from other community-acquired pneumonia illnesses.
  • [MeSH-major] Community-Acquired Infections. Coronavirus / genetics. Coronavirus Infections. Pneumonia, Viral

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  • (PMID = 16267760.001).
  • [ISSN] 0022-1899
  • [Journal-full-title] The Journal of infectious diseases
  • [ISO-abbreviation] J. Infect. Dis.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Membrane Glycoproteins; 0 / Nucleocapsid Proteins; 0 / Spike Glycoprotein, Coronavirus; 0 / Viral Envelope Proteins
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13. Haas PS, Roy NB, Gibbons RJ, Deville MA, Fisher C, Schwabe M, Bissé E, van Dorsselaer A, Higgs DR, Lübbert M: The role of X-inactivation in the gender bias of patients with acquired alpha-thalassaemia and myelodysplastic syndrome (ATMDS). Br J Haematol; 2009 Feb;144(4):538-45
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The role of X-inactivation in the gender bias of patients with acquired alpha-thalassaemia and myelodysplastic syndrome (ATMDS).
  • Alpha thalassaemia myelodysplastic syndrome (ATMDS) is an unusual complication of chronic myeloid malignancy that is associated with a striking red cell phenotype.
  • It represents an acquired form of alpha-thalassaemia that most commonly arises in the context of myelodysplasia.
  • It has recently been shown that this condition occurs in association with somatic mutations of a known X-encoded trans-acting regulator of alpha globin gene (HBA) expression, ATRX.
  • There is an unexplained, strong male preponderance of individuals with the ATMDS phenotype with a >5:1 male-female ratio and furthermore, all the somatic ATRX mutations described to date have been in males.
  • Here we report the identification, in a single centre, of two females with ATMDS and mutations in the ATRX gene, proving that ATMDS associated with such mutations may occur, albeit rarely, in females.
  • It seemed possible that females might be less likely to develop ATMDS if the inactivated copy of the ATRX gene (ATRX) became progressively re-activated throughout life.

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  • (PMID = 19055664.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] ENG
  • [Grant] United Kingdom / Medical Research Council / / MC/ U137961147; United Kingdom / Medical Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Nuclear Proteins; EC 3.6.4.- / DNA Helicases; EC 3.6.4.12 / ATRX protein, human
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14. Larakeb AS, Evrard S, Louillet F, Kwon T, Djaffar H, Llanas B, Deschênes G, Hurtaud-Roux MF, Baudouin V: Acute renal cortical necrosis due to acquired antiprotein S antibodies. Pediatr Nephrol; 2009 Jan;24(1):207-9
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  • [Title] Acute renal cortical necrosis due to acquired antiprotein S antibodies.
  • Although varicella is a common disease of childhood, renal complications are quite rare.
  • We report here the interesting case of a-22 month-old boy exhibiting renal cortical necrosis related to an acquired protein S deficiency following varicella.
  • Ten days after the vesicle eruption appearance, he presented with ecchymosed heels, oligoanuric kidney failure, anemia [hemoglobin (Hb) 78 g/L], schizocytosis (2.5%), but normal platelet count.
  • All together, these features suggested acquired protein S deficiency secondary to varicella.

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  • (PMID = 18777044.001).
  • [ISSN] 0931-041X
  • [Journal-full-title] Pediatric nephrology (Berlin, Germany)
  • [ISO-abbreviation] Pediatr. Nephrol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anticoagulants; 0 / Autoantibodies; 0 / Enoxaparin; 0 / Glucocorticoids; 0 / Protein S
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15. Salisbury AC, Alexander KP, Reid KJ, Masoudi FA, Rathore SS, Wang TY, Bach RG, Marso SP, Spertus JA, Kosiborod M: Incidence, correlates, and outcomes of acute, hospital-acquired anemia in patients with acute myocardial infarction. Circ Cardiovasc Qual Outcomes; 2010 Jul;3(4):337-46
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Incidence, correlates, and outcomes of acute, hospital-acquired anemia in patients with acute myocardial infarction.
  • Less is known about the incidence, correlates, and prognostic implications of acute, hospital-acquired anemia (HAA).
  • METHODS AND RESULTS: We identified 2909 patients with acute myocardial infarction who had normal hemoglobin (Hgb) on admission in the multicenter TRIUMPH registry and defined HAA by criteria proposed by Beutler and Waalen.
  • Independent correlates of HAA included age, female sex, white race, chronic kidney disease, ST-segment elevation myocardial infarction, acute renal failure, use of glycoprotein IIb/IIIa inhibitors, in-hospital complications (cardiogenic shock, bleeding and bleeding severity), and length of stay.

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  • (PMID = 20488919.001).
  • [ISSN] 1941-7705
  • [Journal-full-title] Circulation. Cardiovascular quality and outcomes
  • [ISO-abbreviation] Circ Cardiovasc Qual Outcomes
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / P50 HL077113; United States / NHLBI NIH HHS / HL / P50 HL 077113
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hemoglobins
  • [Other-IDs] NLM/ NIHMS382335; NLM/ PMC3384714
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16. Nelson ME, Thurmes PJ, Hoyer JD, Steensma DP: A novel 5' ATRX mutation with splicing consequences in acquired alpha thalassemia-myelodysplastic syndrome. Haematologica; 2005 Nov;90(11):1463-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A novel 5' ATRX mutation with splicing consequences in acquired alpha thalassemia-myelodysplastic syndrome.
  • BACKGROUND AND OBJECTIVES: Acquired alpha thalassemia (hemoglobin H (HbH) disease) is a rare complication of neoplastic chronic myeloid disorders, especially myelodysplastic syndrome.
  • Acquired HbH has recently been associated with mutations in an X-linked gene, ATRX, previously linked to inherited ATR-X syndrome (alpha thalassemia-retardation-X linked).
  • DESIGN AND METHODS: A Swiss man with chronic myelomonocytic leukemia complicated by various autoimmune disorders and by strikingly microcytic, hypochromic anemia was analyzed for the presence of acquired HbH.
  • Marrow karyotype and the alpha globin cluster were normal.
  • INTERPRETATION AND CONCLUSIONS: Intronic ATRX mutations with splicing consequences, uncommon in inherited ATR-X syndrome because of their devastating effect on expression of functional protein, should be routinely sought when undertaking molecular analysis of acquired HbH disease.
  • Detection of an acquired ATRX mutation can help support clonality in karyotypically normal ambiguous myeloid disorders with HbH.
  • [MeSH-major] 5' Flanking Region / genetics. DNA Helicases / genetics. Myelodysplastic Syndromes / genetics. Nuclear Proteins / genetics. Point Mutation / genetics. alpha-Thalassemia / genetics

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  • (PMID = 16266892.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Databank-accession-numbers] RefSeq/ NM/ 000489
  • [Grant] United States / NCI NIH HHS / CA / K12 CA 90628
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Nuclear Proteins; 0 / RNA Splice Sites; EC 3.6.4.- / DNA Helicases; EC 3.6.4.12 / ATRX protein, human
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17. Awandare GA, Ouma Y, Ouma C, Were T, Otieno R, Keller CC, Davenport GC, Hittner JB, Vulule J, Ferrell R, Ong'echa JM, Perkins DJ: Role of monocyte-acquired hemozoin in suppression of macrophage migration inhibitory factor in children with severe malarial anemia. Infect Immun; 2007 Jan;75(1):201-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of monocyte-acquired hemozoin in suppression of macrophage migration inhibitory factor in children with severe malarial anemia.
  • Although the molecular determinants of SMA are largely undefined, dysregulation in host-derived inflammatory mediators influences disease severity.
  • In addition, PCM levels were a better predictor of hemoglobin and MIF concentrations than parasite density.

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  • (PMID = 17060471.001).
  • [ISSN] 0019-9567
  • [Journal-full-title] Infection and immunity
  • [ISO-abbreviation] Infect. Immun.
  • [Language] eng
  • [Grant] United States / FIC NIH HHS / TW / D43 TW005884; United States / NIAID NIH HHS / AI / R01 AI051305; United States / NIAID NIH HHS / AI / T32 AI007538
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hemeproteins; 0 / Macrophage Migration-Inhibitory Factors; 39404-00-7 / hemozoin
  • [Other-IDs] NLM/ PMC1828375
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18. Wachtman LM, Tarwater PM, Queen SE, Adams RJ, Mankowski JL: Platelet decline: an early predictive hematologic marker of simian immunodeficiency virus central nervous system disease. J Neurovirol; 2006 Feb;12(1):25-33
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Platelet decline: an early predictive hematologic marker of simian immunodeficiency virus central nervous system disease.
  • As the prevalence of human immunodeficiency virus (HIV)-induced central nervous system (CNS) disease has increased with antiretroviral treatment, there is a critical need for identifying biomarkers that predict HIV CNS disease.
  • To identify novel hematologic markers that precede and predict CNS disease, the authors examined longitudinal hematology data from 47 simian immunodeficiency virus (SIV)-infected macaques.
  • Univariate analysis performed on platelet values obtained day 56 post inoculation demonstrated that SIV-infected macaques with the greatest decline in platelet numbers were 18 times more likely to develop SIV CNS disease than SIV-infected animals with minimal to no decline in circulating platelet counts.
  • Decline in platelet number was a more robust marker than decline in hemoglobin levels, a previously identified marker of HIV CNS disease.
  • The identification of an association between decline in platelets and the development of encephalitis demonstrates that monitoring platelet decline in HIV-infected individuals may serve as a predictive marker for clinical progression to HIV-induced CNS disease.
  • Identifying those HIV-infected individuals at risk for CNS disease during asymptomatic stages of infection would promote early interventive, neuroprotective therapy to prevent neuronal damage and loss.
  • [MeSH-major] Central Nervous System Diseases / virology. Platelet Count. Simian Acquired Immunodeficiency Syndrome / physiopathology. Simian Immunodeficiency Virus
  • [MeSH-minor] Animals. Biomarkers. Disease Models, Animal. Macaca

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  • (PMID = 16595371.001).
  • [ISSN] 1355-0284
  • [Journal-full-title] Journal of neurovirology
  • [ISO-abbreviation] J. Neurovirol.
  • [Language] eng
  • [Grant] United States / NIMH NIH HHS / MH / MH 070056; United States / NIMH NIH HHS / MH / MH069116; United States / NINDS NIH HHS / NS / NS 44815; United States / NCRR NIH HHS / RR / RR07002
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers
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19. Andrikovics H, Meggyesi N, Szilvasi A, Tamaska J, Halm G, Lueff S, Nahajevszky S, Egyed M, Varkonyi J, Mikala G, Sipos A, Kalasz L, Masszi T, Tordai A: HFE C282Y mutation as a genetic modifier influencing disease susceptibility for chronic myeloproliferative disease. Cancer Epidemiol Biomarkers Prev; 2009 Mar;18(3):929-34

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  • [Title] HFE C282Y mutation as a genetic modifier influencing disease susceptibility for chronic myeloproliferative disease.
  • (b) to examine associations of genetic variants of proteins involved in iron metabolism; and acquired JAK2 V617F mutation with clinical characteristics of CMPD.
  • At presentation, elevated hemoglobin levels were found in V617F-positive patients compared with V617F-negative counterparts (P<0.000).
  • Because chronic iron deficiency or latent anemia may trigger disease susceptibility for CMPD, HFE C282Y positivity may be a genetic factor influencing this effect.
  • [MeSH-major] Genetic Predisposition to Disease. Histocompatibility Antigens Class I / genetics. Membrane Proteins / genetics. Mutation. Myeloproliferative Disorders / genetics

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  • (PMID = 19258483.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HFE protein, human; 0 / Histocompatibility Antigens Class I; 0 / Membrane Proteins; EC 2.7.10.2 / Janus Kinase 2
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20. Wood KC, Hsu LL, Gladwin MT: Sickle cell disease vasculopathy: a state of nitric oxide resistance. Free Radic Biol Med; 2008 Apr 15;44(8):1506-28
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  • [Title] Sickle cell disease vasculopathy: a state of nitric oxide resistance.
  • Sickle cell disease (SCD) is a hereditary hemoglobinopathy characterized by microvascular vaso-occlusion with erythrocytes containing polymerized sickle (S) hemoglobin, erythrocyte hemolysis, vasculopathy, and both acute and chronic multiorgan injury.
  • It is associated with steady state increases in plasma cell-free hemoglobin and overproduction of reactive oxygen species (ROS).
  • Hereditary and acquired hemolytic conditions release into plasma hemoglobin and other erythrocyte components that scavenge endothelium-derived NO and metabolize its precursor arginine, impairing NO homeostasis.
  • The synergistic bioinactivation of NO by dioxygenation and oxidation reactions with cell-free plasma hemoglobin and ROS, respectively, is discussed as a mechanism for NO resistance in SCD vasculopathy.

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  • (PMID = 18261470.001).
  • [ISSN] 0891-5849
  • [Journal-full-title] Free radical biology & medicine
  • [ISO-abbreviation] Free Radic. Biol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Reactive Oxygen Species; 31C4KY9ESH / Nitric Oxide; EC 1.14.13.39 / Nitric Oxide Synthase Type III
  • [Number-of-references] 289
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21. Wernig G, Mercher T, Okabe R, Levine RL, Lee BH, Gilliland DG: Expression of Jak2V617F causes a polycythemia vera-like disease with associated myelofibrosis in a murine bone marrow transplant model. Blood; 2006 Jun 1;107(11):4274-81
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  • [Title] Expression of Jak2V617F causes a polycythemia vera-like disease with associated myelofibrosis in a murine bone marrow transplant model.
  • An acquired somatic mutation, Jak2V617F, was recently discovered in most patients with polycythemia vera (PV), chronic idiopathic myelofibrosis (CIMF), and essential thrombocythemia (ET).
  • These included striking elevation in hemoglobin level/hematocrit, leukocytosis, megakaryocyte hyperplasia, extramedullary hematopoiesis resulting in splenomegaly, and reticulin fibrosis in the bone marrow.
  • In vitro analysis of primary cells showed constitutive activation of Stat5 and cytokine-independent growth of erythroid colony-forming unit (CFU-E) and erythropoietin hypersensitivity, and Southern blot analysis for retroviral integration indicated that the disease was oligoclonal.
  • We conclude that Jak2V617F expression in bone marrow progenitors results in a PV-like syndrome with myelofibrosis and that there are strain-specific modifiers that may in part explain phenotypic pleiotropy of Jak2V617F-associated myeloproliferative disease in humans.

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  • (PMID = 16478879.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA04002; United States / NCI NIH HHS / CA / CA66996; United States / NIDDK NIH HHS / DK / DK50654
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Jak2 protein, mouse; EC 2.7.10.2 / Janus Kinase 2
  • [Other-IDs] NLM/ PMC1895786
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22. Yamamoto K, Yamamoto H, Yoshida K, Kisanuki A, Hirano Y, Ohte N, Akasaka T, Takeuchi M, Nakatani S, Ohtani T, Sozu T, Masuyama T: Prognostic factors for progression of early- and late-stage calcific aortic valve disease in Japanese: the Japanese Aortic Stenosis Study (JASS) Retrospective Analysis. Hypertens Res; 2010 Mar;33(3):269-74
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  • [Title] Prognostic factors for progression of early- and late-stage calcific aortic valve disease in Japanese: the Japanese Aortic Stenosis Study (JASS) Retrospective Analysis.
  • Calcific aortic valve disease (CAVD) is the most common etiology of acquired valvular heart disease, and hypertension is a principal underlying disease.
  • In late-stage subjects with calcification in two or three leaflets and/or aortic stenosis on the preceding echocardiographic study (n=399), progression was observed in females and in subjects with low hemoglobin and a concentric left ventricle.
  • [MeSH-major] Aortic Valve Stenosis / diagnosis. Calcinosis / diagnosis. Disease Progression

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  • (PMID = 20057483.001).
  • [ISSN] 1348-4214
  • [Journal-full-title] Hypertension research : official journal of the Japanese Society of Hypertension
  • [ISO-abbreviation] Hypertens. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiotensin II Type 1 Receptor Blockers; 0 / Anticoagulants; 5Q7ZVV76EI / Warfarin
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23. Zhou Z, Han H, Cruz MA, López JA, Dong JF, Guchhait P: Haemoglobin blocks von Willebrand factor proteolysis by ADAMTS-13: a mechanism associated with sickle cell disease. Thromb Haemost; 2009 Jun;101(6):1070-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Haemoglobin blocks von Willebrand factor proteolysis by ADAMTS-13: a mechanism associated with sickle cell disease.
  • Vascular occlusion, thromboembolism and strokes are hallmark events in sickle cell disease (SCD).
  • In SCD, a high level of extracellular haemoglobin (Hb) in plasma has been shown parallely associated with the disease pathogenesis.
  • Thus, the observations suggest that the patients with SCD suffer from an acquired ADAMTS-13 deficiency primarily because Hb competitively bound and blocked the proteolysis of VWF, leading to the accumulation of ultra-large VWF multimers in circulation and on endothelium.
  • [MeSH-major] ADAM Proteins / metabolism. Anemia, Sickle Cell / metabolism. Hemoglobin A / metabolism. von Willebrand Factor / metabolism

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  • (PMID = 19492149.001).
  • [ISSN] 0340-6245
  • [Journal-full-title] Thrombosis and haemostasis
  • [ISO-abbreviation] Thromb. Haemost.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL71895
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Blocking; 0 / von Willebrand Factor; 9034-51-9 / Hemoglobin A; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.- / ADAMTS13 protein, human
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24. Lau B, Sharrett AR, Kingsley LA, Post W, Palella FJ, Visscher B, Gange SJ: C-reactive protein is a marker for human immunodeficiency virus disease progression. Arch Intern Med; 2006 Jan 9;166(1):64-70
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  • [Title] C-reactive protein is a marker for human immunodeficiency virus disease progression.
  • Levels of CRP of more than 2.3 mg/L were associated with a decreased time to the development of AIDS (relative time to AIDS, 0.36; P<.001) compared with individuals with CRP levels of 1.2 mg/L or less, which remained significant after adjustment for CD4 lymphocyte counts and HIV RNA and hemoglobin concentrations.
  • CONCLUSIONS: Levels of CRP were associated with HIV disease progression independent of CD4 lymphocyte counts and HIV RNA levels.
  • This may have implications for cardiovascular disease among HIV-infected individuals.
  • [MeSH-major] Acquired Immunodeficiency Syndrome / blood. C-Reactive Protein / analysis
  • [MeSH-minor] Adult. Biomarkers / blood. CD4 Lymphocyte Count. Cohort Studies. Confidence Intervals. Disease Progression. Humans. Male. Multivariate Analysis. Predictive Value of Tests. Proportional Hazards Models. RNA, Viral / blood. Time Factors. Viral Load

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  • (PMID = 16401812.001).
  • [ISSN] 0003-9926
  • [Journal-full-title] Archives of internal medicine
  • [ISO-abbreviation] Arch. Intern. Med.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / 5-M01-RR-00052; United States / NIAID NIH HHS / AI / UO1-AI-35039; United States / NIAID NIH HHS / AI / UO1-AI-35040; United States / NIAID NIH HHS / AI / UO1-AI-35041; United States / NIAID NIH HHS / AI / UO1-AI-35042; United States / NIAID NIH HHS / AI / UO1-AI-35043; United States / NIAID NIH HHS / AI / UO1-AI-37613; United States / NIAID NIH HHS / AI / UO1-AI-37984
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / RNA, Viral; 9007-41-4 / C-Reactive Protein
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25. Hampl H, Riedel E: Cardiac disease in the dialysis patient: good, better, best clinical practice. Blood Purif; 2009;27(1):99-113
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  • [Title] Cardiac disease in the dialysis patient: good, better, best clinical practice.
  • This is an overview of our clinical know-how acquired during the last 30 years.
  • The inability to adequately address iron status in hemoglobin normalization studies and the underprescription of effective cardiac/antihypertensive medication might explain the adverse outcome.
  • Effective cardiac/antihypertensive medication, intensive iron therapy during normalization of hemoglobin, optimized correction of metabolic acidosis and supplementation of vitamins which are involved in the energy metabolism should be considered to significantly improve the outcome of hemodialysis patients.

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  • (PMID = 19169026.001).
  • [ISSN] 1421-9735
  • [Journal-full-title] Blood purification
  • [ISO-abbreviation] Blood Purif.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Number-of-references] 85
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26. Zakrzewski D, Janas J, Heretyk H, Stepińska J: Inflammatory response and postoperative kidney failure in patients with diabetes type 2 or impaired glucose tolerance undergoing heart valve surgery. Kardiol Pol; 2010 May;68(5):530-6
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  • METHODS: Thirty patients with DM or IGT, without fibrate or statin treatment, with a mean LDL-cholesterol below 129 mg/dL, ejection fraction > 45%, in NYHA class II and III, referred for surgery due to acquired heart valve disease entered the study.
  • Patients with acute or chronic inflammatory conditions, coronary artery disease or creatinine clearance below 50 mL/min were excluded.
  • Serum creatinine, glycosylated hemoglobin, LDL-cholesterol and interleukin-10 as well as TNF-alpha were assessed before surgery.
  • Interleukin-10 and TNF-alpha were also measured 4 hours after weaning from cardiopulmonary bypass.
  • Moreover, serum creatinine and hemoglobin were measured 18 +/- 2 hours after surgery.
  • These parameters included: age, weight and body mass index, pre- and postoperative serum level of TNF-alpha and interleukin-10, preoperative concentration of LDL-cholesterol and glycosylated hemoglobin, duration of cardiopulmonary bypass and postoperative hemoglobin.
  • The level of TNF-alpha and interleukin-10 increased significantly postoperatively.
  • A non-significant trend towards correlation between preoperative TNF-alpha and postoperative decrease of creatinine clearance was observed (R = -0.36, p = 0.05).
  • CONCLUSIONS: Postoperative kidney failure with the incidence of 27% is a frequent finding in patients with DM or IGT operated due to acquired heart valve disease.
  • [MeSH-minor] Aged. Causality. Cholesterol, LDL / blood. Comorbidity. Creatinine / blood. Female. Glucose Intolerance / complications. Glucose Intolerance / epidemiology. Hemoglobin A, Glycosylated / analysis. Humans. Interleukin-10 / blood. Male. Middle Aged. Poland / epidemiology. Tumor Necrosis Factor-alpha / metabolism


27. Costa DB, Fisher CA, Miller KB, Pihan GA, Steensma DP, Gibbons RJ, Higgs DR: A novel mutation in the last exon of ATRX in a patient with alpha-thalassemia myelodysplastic syndrome. Eur J Haematol; 2006 May;76(5):432-5, 453
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  • [Title] A novel mutation in the last exon of ATRX in a patient with alpha-thalassemia myelodysplastic syndrome.
  • We describe a patient with acquired alpha-thalassemia myelodysplastic syndrome (ATMDS).
  • A previously healthy 66-year-old man presented with hemoglobin of 9.3 g/dL, mean corpuscular volume 59 fL, and a bone marrow aspirate with increased erythroid precursors and hypolobulated megakaryocytes.
  • Hemoglobin H inclusions were seen in most red cells after 1% brilliant cresyl blue supravital stain of the peripheral blood.
  • This case provides further evidence for a link between ATRX mutations and ATMDS, and suggests a possible role for the conserved Q-box element in ATRX function.
  • [MeSH-major] DNA Helicases / genetics. Myelodysplastic Syndromes / genetics. Nuclear Proteins / genetics. Point Mutation. alpha-Thalassemia / genetics

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  • (PMID = 16480427.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Databank-accession-numbers] RefSeq/ NM/ 000489/ NP/ 000480
  • [Grant] United Kingdom / Medical Research Council / / MC/ U137961147
  • [Publication-type] Case Reports; Comparative Study; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Nuclear Proteins; EC 3.6.4.- / DNA Helicases; EC 3.6.4.12 / ATRX protein, human
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28. Erikstrup C, Kallestrup P, Zinyama R, Gomo E, Mudenge B, Gerstoft J, Ullum H: Predictors of mortality in a cohort of HIV-1-infected adults in rural Africa. J Acquir Immune Defic Syndr; 2007 Apr 1;44(4):478-83
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  • CD4 cell count, HIV RNA level, hemoglobin (HB), total lymphocyte count (TLC), body mass index, clinical staging (Centers for Disease Control and Prevention [CDC] classification), and self-reported level of function (Karnofsky Performance Scale score) were assessed at baseline; participants were followed until death or last follow-up (3-4.3 years).

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  • (PMID = 17259906.001).
  • [ISSN] 1525-4135
  • [Journal-full-title] Journal of acquired immune deficiency syndromes (1999)
  • [ISO-abbreviation] J. Acquir. Immune Defic. Syndr.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hemoglobins; 0 / RNA, Viral
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29. Perrin J, Perrot A, Chenot V, Lesesve JF, Guerci A, Marchand-Arvier M, Vigneron C, Lecompte T: [Acquired alpha-thalassemia as early sign for myelodysplastic syndrome (refractory anaemia) with secondary haemochromatosis]. Ann Biol Clin (Paris); 2007 Jul-Aug;65(4):405-9
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  • [Title] [Acquired alpha-thalassemia as early sign for myelodysplastic syndrome (refractory anaemia) with secondary haemochromatosis].
  • [Transliterated title] Alpha-thalassémie acquise révélatrice d'un syndrome myélodysplasique de type anémie réfractaire avec hémochromatose secondaire.
  • The investigations revealed the presence of haemoglobin H, suggesting abnormalities in the alpha-globin chains synthesis.
  • Alpha-thalassemia was thus suspected.
  • The association with aniso-poïkilocytosis and a marked iron overload (ferritinemia > 1,500 microg/L) suggested a myelodysplastic syndrome, which was confirmed with a bone marrow aspiration.
  • The pattern was consistent with the Acquired alpha-Thalassemia-Myelodysplastic Syndrome (ATMDS).
  • The causes of ATMDS are ignored, but recent reports indicate that the ATRX gene may be implicated in the pathogenesis.
  • The alpha globin genes could be one of the targets of the ATRX protein.
  • [MeSH-major] Anemia, Refractory / diagnosis. Hemochromatosis / diagnosis. Myelodysplastic Syndromes / diagnosis. alpha-Thalassemia / etiology


30. Steensma DP, Gibbons RJ, Mesa RA, Tefferi A, Higgs DR: Somatic point mutations in RUNX1/CBFA2/AML1 are common in high-risk myelodysplastic syndrome, but not in myelofibrosis with myeloid metaplasia. Eur J Haematol; 2005 Jan;74(1):47-53
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  • [Title] Somatic point mutations in RUNX1/CBFA2/AML1 are common in high-risk myelodysplastic syndrome, but not in myelofibrosis with myeloid metaplasia.
  • OBJECTIVE: Acquired somatic point mutations in RUNX1/CBFA2/AML1 have recently been described in a subset of patients with myelodysplastic syndrome (MDS) and acute myeloid leukaemia (AML).
  • In addition, it is unclear whether patients with MDS-associated acquired alpha thalassaemia (ATMDS), a special subgroup with a very high incidence of point mutations in the ATRX gene, have an especially high incidence of RUNX1 mutations.
  • METHODS: We analysed samples from 78 patients for RUNX1 point mutations by denaturing high-performance liquid chromatography (DHPLC): 26 with MMM and 52 with MDS, including 18 with ATMDS.
  • ATMDS patients did not have an increased risk of RUNX1 point mutations (2/18, 11.1%) when compared with MDS without thalassaemia (3/34, 8.8%; P = 0.58).
  • [MeSH-minor] Base Sequence. Core Binding Factor Alpha 2 Subunit. DNA / genetics. DNA Mutational Analysis. Humans. Risk Factors


31. Dooley KA, Fraenkel PG, Langer NB, Schmid B, Davidson AJ, Weber G, Chiang K, Foott H, Dwyer C, Wingert RA, Zhou Y, Paw BH, Zon LI, Tübingen 2000 Screen Consortium: montalcino, A zebrafish model for variegate porphyria. Exp Hematol; 2008 Sep;36(9):1132-42
ZFIN. ZFIN .

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  • OBJECTIVE: Inherited or acquired mutations in the heme biosynthetic pathway leads to a debilitating class of diseases collectively known as porphyrias, with symptoms that can include anemia, cutaneous photosensitivity, and neurovisceral dysfunction.
  • Homozygous mutant embryos are deficient in hemoglobin, and by 36 hours post-fertilization are visibly anemic and porphyric.

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  • (PMID = 18550261.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK053298-10; United States / NIDDK NIH HHS / DK / DK053298-02; United States / NIDDK NIH HHS / DK / R01 DK053298-03S1; United States / NIDDK NIH HHS / DK / R01 DK053298-03; United States / NIDDK NIH HHS / DK / DK061685-03; United States / NIDDK NIH HHS / DK / R01 DK053298-09; United States / NIDDK NIH HHS / DK / R01 DK053298-06; United States / NIDDK NIH HHS / DK / K08 DK061685-04S1; United States / NIDDK NIH HHS / DK / K08 DK061685-05; United States / NIDDK NIH HHS / DK / K08 DK061685-04; United States / NIDDK NIH HHS / DK / DK053298-03S1; United States / NIDDK NIH HHS / DK / DK053298-11; United States / NIDDK NIH HHS / DK / DK053298-03; United States / NIDDK NIH HHS / DK / K08 DK061685; United States / NIDDK NIH HHS / DK / DK053298-08; United States / NIDDK NIH HHS / DK / DK061685-01; United States / NIDDK NIH HHS / DK / R01 DK053298-02; United States / NIDDK NIH HHS / DK / DK061685-02; United States / NIDDK NIH HHS / DK / DK053298-04; United States / NIDDK NIH HHS / DK / K08 DK061685-01; United States / NIDDK NIH HHS / DK / DK061685-05; United States / NIDDK NIH HHS / DK / DK053298-07; United States / NIDDK NIH HHS / DK / R01 DK053298-10; United States / Howard Hughes Medical Institute / / ; United States / NIDDK NIH HHS / DK / R01 DK053298-07; United States / NIDDK NIH HHS / DK / R01 DK053298-05; United States / NIDDK NIH HHS / DK / DK053298-06; United States / NIDDK NIH HHS / DK / K08 DK061685-03; United States / NIDDK NIH HHS / DK / DK053298-09; United States / NIDDK NIH HHS / DK / DK061685-04S1; United States / NIDDK NIH HHS / DK / DK053298-05; United States / NIDDK NIH HHS / DK / R01 DK053298; United States / NIDDK NIH HHS / DK / R01 DK053298-04; United States / NIDDK NIH HHS / DK / K08 DK061685-02; United States / NIDDK NIH HHS / DK / DK061685-04; United States / NIDDK NIH HHS / DK / R01 DK053298-08; United States / NIDDK NIH HHS / DK / R01 DK053298-11
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Codon, Nonsense; 0 / DNA, Complementary; 0 / Hemoglobins; 0 / Recombinant Fusion Proteins; 0 / Zebrafish Proteins; EC 1.3.3.4 / Protoporphyrinogen Oxidase
  • [Other-IDs] NLM/ NIHMS68002; NLM/ PMC2630115
  • [Investigator] Bebber van F; Busch-Nentwich E; Dahm R; Frohnhofer HG; Geiger H; Gilmour D; Holley S; Hooge J; Julich D; Knaut H; Maderspacher F; Neumann C; Nicolson T; Nusslein-Volhard C; Roehl H; Schonberger U; Seiler C; Sollner C; Sonawane M; Wehner A; Weiler C; Schmid B; Hagner U; Hennen E; Kaps C; Kirchner A; Koblizek TI; Langheinrich U; Metzger C; Nordin R; Pezzuti M; Schlombs K; deSantana-Stamm J; Trowe T; Vacun G; Walker A; Weiler C
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32. Gibbons RJ, Wada T, Fisher CA, Malik N, Mitson MJ, Steensma DP, Fryer A, Goudie DR, Krantz ID, Traeger-Synodinos J: Mutations in the chromatin-associated protein ATRX. Hum Mutat; 2008 Jun;29(6):796-802
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  • Constitution mutations in the X-encoded gene give rise to alpha thalassemia mental retardation (ATR-X) syndrome and a variety of related conditions that are often associated with profound developmental delay, facial dysmorphism, genital abnormalities, and alpha thalassemia.
  • Acquired mutations in ATRX are observed in the preleukemic condition alpha thalassemia myelodysplastic syndrome (ATMDS).
  • [MeSH-major] Chromatin Assembly and Disassembly. DNA Helicases / genetics. Mental Retardation, X-Linked / genetics. Mutation. Nuclear Proteins / genetics. alpha-Thalassemia / genetics

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18409179.001).
  • [ISSN] 1098-1004
  • [Journal-full-title] Human mutation
  • [ISO-abbreviation] Hum. Mutat.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U137961147
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Codon, Nonsense; 0 / Nuclear Proteins; EC 3.6.4.- / DNA Helicases; EC 3.6.4.12 / ATRX protein, human
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33. Chi BH, Giganti M, Mulenga PL, Limbada M, Reid SE, Mutale W, Stringer JS: CD4+ response and subsequent risk of death among patients on antiretroviral therapy in Lusaka, Zambia. J Acquir Immune Defic Syndr; 2009 Sep 1;52(1):125-31
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  • We used Cox proportional hazards models that accounted for different strata of baseline CD4 counts and adjusted for age, sex, clinical stage, tuberculosis coinfection, baseline hemoglobin, initial ART regimen, and adherence behavior.

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  • (PMID = 19546812.001).
  • [ISSN] 1525-4135
  • [Journal-full-title] Journal of acquired immune deficiency syndromes (1999)
  • [ISO-abbreviation] J. Acquir. Immune Defic. Syndr.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / P30 AI027767; United States / NIAID NIH HHS / AI / K23 AI052481-05; United States / PHS HHS / / U62/CCU12354; United States / FIC NIH HHS / TW / D43 TW001035-10; United States / FIC NIH HHS / TW / TW001035-10; United States / FIC NIH HHS / TW / TW006670-01A1; United States / NIAID NIH HHS / AI / AI027767-18; United States / NIAID NIH HHS / AI / P30 AI027767-18; United States / FIC NIH HHS / TW / K01 TW006670-01A1; United States / NIAID NIH HHS / AI / AI052481-05; United States / NIAID NIH HHS / AI / K23-AI01411; United States / FIC NIH HHS / TW / K01 TW006670; United States / FIC NIH HHS / TW / D43 TW001035; United States / NIAID NIH HHS / AI / P30-AI027767; United States / FIC NIH HHS / TW / K01-TW06670
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-HIV Agents
  • [Other-IDs] NLM/ NIHMS139780; NLM/ PMC2734950
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34. Thompson CB, Barrett LS: Intra-rater/inter-rater reliability of the air transport minimum data set. Air Med J; 2007 May-Jun;26(3):147-53
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  • The purpose of this research was to conduct a pilot study to investigate the intra-rater and inter-rater reliability of the ATMDS.

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  • (PMID = 17467569.001).
  • [ISSN] 1067-991X
  • [Journal-full-title] Air medical journal
  • [ISO-abbreviation] Air Med. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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35. Gupta A, Gupte N, Bhosale R, Kakrani A, Kulkarni V, Nayak U, Thakar M, Sastry J, Bollinger RC, Byramji Jeejeebhoy Medical College-Johns Hopkins University Study Group: Low sensitivity of total lymphocyte count as a surrogate marker to identify antepartum and postpartum Indian women who require antiretroviral therapy. J Acquir Immune Defic Syndr; 2007 Nov 1;46(3):338-42
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  • METHODS: CD4, TLC, and hemoglobin were measured at third trimester, delivery, and 6, 9, and 12 months postpartum (PP) in a cohort of 779 HIV-infected women.
  • Addition of hemoglobin <12 g/dL or <11 g/dL increased the sensitivity of TLC to 74% to 92% for predicting CD4 <200 cells/mm3 but decreased the specificity to 33% to 69% compared to TLC alone.
  • A combination of TLC, hemoglobin, and WHO clinical staging had the highest sensitivity but lowest specificity compared to other possible combinations or use of TLC alone.
  • [MeSH-major] Anti-HIV Agents / therapeutic use. HIV Infections / drug therapy. Infectious Disease Transmission, Vertical / prevention & control. Lymphocyte Count. Pregnancy Complications, Infectious / drug therapy

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  • (PMID = 17846559.001).
  • [ISSN] 1525-4135
  • [Journal-full-title] Journal of acquired immune deficiency syndromes (1999)
  • [ISO-abbreviation] J. Acquir. Immune Defic. Syndr.
  • [Language] eng
  • [Grant] United States / FIC NIH HHS / TW / 2D43TW00010-20-AITRP; United States / NIAID NIH HHS / AI / R01 AI45462
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-HIV Agents; 0 / Biomarkers
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36. Jabs DA, Holbrook JT, Van Natta ML, Clark R, Jacobson MA, Kempen JH, Murphy RL, Studies of Ocular Complications of AIDS Research Group: Risk factors for mortality in patients with AIDS in the era of highly active antiretroviral therapy. Ophthalmology; 2005 May;112(5):771-9
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  • In a multivariate analysis, the following baseline risk factors were associated with an increased mortality: higher human immunodeficiency virus (HIV) viral load (relative risk [RR] = 4.6 for HIV viral load >100,000 copies/ml vs. <400 copies/ml; P<0.0001), lower CD4+ T-cell count at enrollment (RR = 3.8 for CD4+ T cell count 0-49 cells/microl vs. > or = 200 cells/microl; P<0.0001), CMV viral load > or = 400 copies/ml (RR = 1.9; P = 0.002), lower hemoglobin (RR = 1.7 for hemoglobin <10 g/dl; P = 0.009), a history of cryptococcal meningitis (RR = 1.7; P = 0.02), CMV retinitis (RR = 1.6; P = 0.0002), and Karnofsky score < or = 80 (RR = 1.4; P = 0.008).
  • CONCLUSIONS: In the era of HAART, CMV disease as manifested by CMV retinitis and a detectable CMV viral load were associated with an increased risk for mortality, even after adjusting for demographic, treatment, immunologic, and HIV virologic factors.

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  • (PMID = 15878056.001).
  • [ISSN] 1549-4713
  • [Journal-full-title] Ophthalmology
  • [ISO-abbreviation] Ophthalmology
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / 5M01 RR05096; United States / NCRR NIH HHS / RR / 5M01 RR00188; United States / NCRR NIH HHS / RR / 5M01 RR00043; United States / NCRR NIH HHS / RR / 5M01 RR05280; United States / NCRR NIH HHS / RR / 5M01 RR00865; United States / NEI NIH HHS / EY / U10 EY008057; United States / NEI NIH HHS / EY / U10 EY08067; United States / NCRR NIH HHS / RR / 5M01 RR00047; United States / NEI NIH HHS / EY / U10 EY08057; United States / NCRR NIH HHS / RR / M01 RR00052; United States / NCRR NIH HHS / RR / 5M01 RR00046; United States / NEI NIH HHS / EY / U10 EY08052
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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37. Kim HK, DeDent A, Cheng AG, McAdow M, Bagnoli F, Missiakas DM, Schneewind O: IsdA and IsdB antibodies protect mice against Staphylococcus aureus abscess formation and lethal challenge. Vaccine; 2010 Aug 31;28(38):6382-92
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  • Staphylococcus aureus is the most frequent cause of bacteremia and hospital-acquired infection, however a vaccine that prevents staphylococcal disease is currently not available.
  • Antibodies directed against IsdA interfered with heme-binding and IsdB antibodies perturbed the ability of this surface protein to bind hemoglobin.

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  • [Copyright] (c) 2010 Elsevier Ltd. All rights reserved.
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  • (PMID = 20226248.001).
  • [ISSN] 1873-2518
  • [Journal-full-title] Vaccine
  • [ISO-abbreviation] Vaccine
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / AI057153-06; United States / NIGMS NIH HHS / GM / GM07281; United States / NIAID NIH HHS / AI / AI052474-05; United States / NIAID NIH HHS / AI / 1-U54-AI-057153; United States / NIAID NIH HHS / AI / AI52474; United States / NIGMS NIH HHS / GM / T32 GM007281; United States / NIAID NIH HHS / AI / R01 AI052474; United States / NICHD NIH HHS / HD / HD009007; United States / NIAID NIH HHS / AI / R01 AI052474-05; United States / NIAID NIH HHS / AI / U54 AI057153; United States / NIAID NIH HHS / AI / U54 AI057153-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibodies, Bacterial; 0 / Antigens, Bacterial; 0 / Cation Transport Proteins; 0 / Hemoglobins; 0 / IsdA protein, Staphylococcus aureus; 0 / IsdB protein, Staphylococcus aureus; 42VZT0U6YR / Heme
  • [Other-IDs] NLM/ NIHMS284563; NLM/ PMC3095377
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38. Micol R, Buchy P, Guerrier G, Duong V, Ferradini L, Dousset JP, Guerin PJ, Balkan S, Galimand J, Chanroeun H, Lortholary O, Rouzioux C, Fontanet A, Leruez-Ville M: Prevalence, risk factors, and impact on outcome of cytomegalovirus replication in serum of Cambodian HIV-infected patients (2004-2007). J Acquir Immune Defic Syndr; 2009 Aug 1;51(4):486-91
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  • Quantitative CMV polymerase chain reaction (PCR) is the gold standard diagnostic tool for analyzing serum CMV replication and for predicting CMV disease.
  • In multivariate analysis, hemoglobin <9 g/dL, CD4 count <100/mm, and Karnofsky index <50 were independently associated with positive serum CMV DNA at baseline.

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  • (PMID = 19421071.001).
  • [ISSN] 1525-4135
  • [Journal-full-title] Journal of acquired immune deficiency syndromes (1999)
  • [ISO-abbreviation] J. Acquir. Immune Defic. Syndr.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Viral
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39. Cantrell RA, Sinkala M, Megazinni K, Lawson-Marriott S, Washington S, Chi BH, Tambatamba-Chapula B, Levy J, Stringer EM, Mulenga L, Stringer JS: A pilot study of food supplementation to improve adherence to antiretroviral therapy among food-insecure adults in Lusaka, Zambia. J Acquir Immune Defic Syndr; 2008 Oct 1;49(2):190-5
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  • This finding was unchanged after adjustment for sex, age, baseline CD4 count, baseline World Health Organization stage, and baseline hemoglobin.

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  • (PMID = 18769349.001).
  • [ISSN] 1525-4135
  • [Journal-full-title] Journal of acquired immune deficiency syndromes (1999)
  • [ISO-abbreviation] J. Acquir. Immune Defic. Syndr.
  • [Language] ENG
  • [Grant] United States / FIC NIH HHS / TW / K01 TW 06670; United States / FIC NIH HHS / TW / D43 TW 001035; United States / FIC NIH HHS / TW / K01 TW 05708; United States / FIC NIH HHS / TW / K01 TW005708; United States / FIC NIH HHS / TW / K01 TW006670; United States / FIC NIH HHS / TW / D43 TW001035
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS528808; NLM/ PMC3847664
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40. Sinha G, Choi TJ, Nayak U, Gupta A, Nair S, Gupte N, Bulakh PM, Sastry J, Deshmukh SD, Khandekar MM, Kulkarni V, Bhosale RA, Bharucha KE, Phadke MA, Kshirsagar AS, Bollinger RC, Maternal Infant Transmission Study in Pune, India: Clinically significant anemia in HIV-infected pregnant women in India is not a major barrier to zidovudine use for prevention of maternal-to-child transmission. J Acquir Immune Defic Syndr; 2007 Jun 1;45(2):210-7
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  • OBJECTIVES: To determine the prevalence of anemia (serum hemoglobin <10 g/dL) and assess zidovudine use and toxicity in HIV-positive pregnant women in India.
  • [MeSH-major] Anemia. HIV Infections / complications. HIV Infections / transmission. Infectious Disease Transmission, Vertical / prevention & control. Zidovudine / administration & dosage. Zidovudine / pharmacology

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  • (PMID = 17414927.001).
  • [ISSN] 1525-4135
  • [Journal-full-title] Journal of acquired immune deficiency syndromes (1999)
  • [ISO-abbreviation] J. Acquir. Immune Defic. Syndr.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI45 462
  • [Publication-type] Clinical Trial; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 4B9XT59T7S / Zidovudine; 935E97BOY8 / Folic Acid; E1UOL152H7 / Iron
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41. McQuillen PS, Barkovich AJ, Hamrick SE, Perez M, Ward P, Glidden DV, Azakie A, Karl T, Miller SP: Temporal and anatomic risk profile of brain injury with neonatal repair of congenital heart defects. Stroke; 2007 Feb;38(2 Suppl):736-41
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  • BACKGROUND AND PURPOSE: Brain injury is common in newborns with congenital heart disease (CHD) requiring neonatal surgery.
  • Clinical and therapeutic characteristics were compared in newborns with and without newly acquired brain injuries.
  • Risk factors associated with acquired postoperative brain injury included cardiopulmonary bypass (CPB) with regional cerebral perfusion (P=0.01) and lower intraoperative cerebral hemoglobin oxygen saturation during the myocardial ischemic period of CPB (P=0.008).


42. Ostrowski SR, Piironen T, Høyer-Hansen G, Gerstoft J, Pedersen BK, Ullum H: High plasma levels of intact and cleaved soluble urokinase receptor reflect immune activation and are independent predictors of mortality in HIV-1-infected patients. J Acquir Immune Defic Syndr; 2005 May 1;39(1):23-31
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  • RESULTS: Plasma suPAR(I-III), suPAR(II-III), and suPAR(I) were increased in HIV patients and increased with HIV disease progression (P < 0.001 for all).
  • In multivariate linear regression analysis, soluble immune activation markers and hemoglobin were independent predictors of plasma suPAR in HIV patients, whereas the neutrophil concentration was the only independent predictor of plasma suPAR in controls.
  • In multivariate Cox analysis adjusting for CD4+ count, HIV RNA, beta2-microglobulin, hemoglobin and clinical stage, higher levels of suPAR(I-III) and suPAR(II-III) were independent predictors of increased mortality risk (P < 0.05 for both), whereas suPAR(I) was not.
  • [MeSH-minor] Adult. Analysis of Variance. Antigens, CD / blood. Biomarkers / blood. Disease Progression. Enzyme-Linked Immunosorbent Assay. Female. Humans. Leukocyte Count. Lymphocyte Activation. Male. Middle Aged. Multivariate Analysis. RNA, Viral / blood. Receptors, Urokinase Plasminogen Activator. Reference Values. Regression Analysis. Survival Analysis. Viral Load

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  • (PMID = 15851910.001).
  • [ISSN] 1525-4135
  • [Journal-full-title] Journal of acquired immune deficiency syndromes (1999)
  • [ISO-abbreviation] J. Acquir. Immune Defic. Syndr.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers; 0 / PLAUR protein, human; 0 / RNA, Viral; 0 / Receptors, Cell Surface; 0 / Receptors, Urokinase Plasminogen Activator
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43. Drain PK, Kupka R, Msamanga GI, Urassa W, Mugusi F, Fawzi WW: C-reactive protein independently predicts HIV-related outcomes among women and children in a resource-poor setting. AIDS; 2007 Oct 1;21(15):2067-75
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  • DESIGN: We measured serum CRP concentration among 606 HIV-infected women, all of whom were not taking highly-active antiretroviral therapy, 3 to 11 months after they gave birth, and assessed relationships of CRP to HIV-related endpoints, including maternal disease progression, mother-to-child transmission of HIV, and maternal and child mortality.
  • METHODS: We used Cox proportional hazards and regression models adjusted for age, sociodemographic characteristics, anthropometric measurements, hemoglobin, CD4 cell count, HIV viral load, and, for child outcomes, breastfeeding status.
  • Among children, 174 acquired HIV and 116 died by age 2 years, and a high maternal CRP concentration was associated with a 3.03-fold (95% CI, 1.85-4.96) greater risk of child mortality.
  • CONCLUSIONS: A high maternal CRP concentration independently predicts HIV disease progression, maternal mortality, and child mortality in a resource-poor setting.


44. Zhang HF, Maslov K, Stoica G, Wang LV: Imaging acute thermal burns by photoacoustic microscopy. J Biomed Opt; 2006 Sep-Oct;11(5):054033
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  • To this end, photoacoustic microscopy is used to determine the depth of acute thermal burns by imaging the total hemoglobin concentration in the blood that accumulates along the boundaries of injuries as a result of thermal damage to the vasculature.
  • Photoacoustic images of the burns are acquired after skin excision.
  • [MeSH-minor] Acute Disease. Animals. Swine

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  • (PMID = 17092182.001).
  • [ISSN] 1083-3668
  • [Journal-full-title] Journal of biomedical optics
  • [ISO-abbreviation] J Biomed Opt
  • [Language] eng
  • [Grant] United States / NIBIB NIH HHS / EB / R01 EB000712; United States / NINDS NIH HHS / NS / R01 NS46214
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
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45. Minneci PC, Deans KJ, Zhi H, Yuen PS, Star RA, Banks SM, Schechter AN, Natanson C, Gladwin MT, Solomon SB: Hemolysis-associated endothelial dysfunction mediated by accelerated NO inactivation by decompartmentalized oxyhemoglobin. J Clin Invest; 2005 Dec;115(12):3409-17
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  • During intravascular hemolysis in human disease, vasomotor tone and organ perfusion may be impaired by the increased reactivity of cell-free plasma hemoglobin (Hb) with NO.
  • These biochemical and physiological studies demonstrate a major role for the intact erythrocyte in NO homeostasis and provide mechanistic support for the existence of a human syndrome of hemolysis-associated NO dysregulation, which may contribute to the vasculopathy of hereditary, acquired, and iatrogenic hemolytic states.

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  • (PMID = 16294219.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hemoglobins; 0 / Oxyhemoglobins; 059QF0KO0R / Water; 169D1260KM / Nitroprusside; 31C4KY9ESH / Nitric Oxide
  • [Other-IDs] NLM/ PMC1283939
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46. Lee J, El-Abaddi N, Duke A, Cerussi AE, Brenner M, Tromberg BJ: Noninvasive in vivo monitoring of methemoglobin formation and reduction with broadband diffuse optical spectroscopy. J Appl Physiol (1985); 2006 Feb;100(2):615-22
eScholarship, California Digital Library, University of California. Full text from University of California eScholarship .

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  • Tissue concentrations (denoted by brackets) of methemoglobin ([MetHb]), deoxyhemoglobin ([Hb-R]), and oxyhemoglobin ([HbO2]) were determined from absorption spectra acquired in "real time" during nitrite infusions in nine pathogen-free New Zealand White rabbits.
  • As little as 30 nM [MetHb] changes were detected for levels of [MetHb] that ranged from 0.80 to 5.72 microM, representing 2.2 to 14.9% of the total hemoglobin content (%MetHb).
  • [MeSH-minor] Animals. Disease Models, Animal. Hemoglobins / metabolism. Kinetics. Methemoglobinemia / chemically induced. Methemoglobinemia / drug therapy. Methemoglobinemia / metabolism. Methylene Blue / administration & dosage. Methylene Blue / pharmacokinetics. Oxidation-Reduction. Oxyhemoglobins / metabolism. Photons. Rabbits. Scattering, Radiation. Sodium Nitrite

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  • (PMID = 16223982.001).
  • [ISSN] 8750-7587
  • [Journal-full-title] Journal of applied physiology (Bethesda, Md. : 1985)
  • [ISO-abbreviation] J. Appl. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hemoglobins; 0 / Oxyhemoglobins; 9008-02-0 / deoxyhemoglobin; 9008-37-1 / Methemoglobin; M0KG633D4F / Sodium Nitrite; T42P99266K / Methylene Blue
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47. Schneider A, Neas L, Herbst MC, Case M, Williams RW, Cascio W, Hinderliter A, Holguin F, Buse JB, Dungan K, Styner M, Peters A, Devlin RB: Endothelial dysfunction: associations with exposure to ambient fine particles in diabetic individuals. Environ Health Perspect; 2008 Dec;116(12):1666-74
The Lens. Cited by Patents in .

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  • BACKGROUND: Exposure to fine airborne particulate matter [< or =2.5 microm in aerodynamic diameter (PM(2.5))] has been associated with cardiovascular and hematologic effects, especially in older people with cardiovascular disease.
  • We acquired daily measurements of PM(2.5) and meteorologic data at central monitoring sites.
  • These PM(2.5)-associated decrements in endothelial function were greater among participants with a high body mass index, high glycosylated hemoglobin A1c, low adiponectin, or the null polymorphism of glutathione S-transferase M1.

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  • (PMID = 19079718.001).
  • [ISSN] 0091-6765
  • [Journal-full-title] Environmental health perspectives
  • [ISO-abbreviation] Environ. Health Perspect.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / M01 RR000046; United States / NCATS NIH HHS / TR / UL1 TR000454; United States / NCRR NIH HHS / RR / RR 00046
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Air Pollutants
  • [Other-IDs] NLM/ PMC2599761
  • [Keywords] NOTNLM ; air pollution / diabetes / endothelial dysfunction / environmental epidemiology / particulate matter
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48. Brodsky RA: Advances in the diagnosis and therapy of paroxysmal nocturnal hemoglobinuria. Blood Rev; 2008 Mar;22(2):65-74
SciCrunch. KEGG: Data: Disease Annotation .

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  • PNH is an uncommon acquired hemolytic anemia that often manifests with hemoglobinuria, abdominal pain, smooth muscle dystonias, fatigue, and thrombosis.
  • The disease results from the expansion of hematopoietic stem cells harboring a mutation in a gene, PIG-A, that is required for the biosynthesis of a lipid moiety, glycosylphosphatidylinositol (GPI), that attaches dozens of different proteins to the cell surface.
  • Free hemoglobin released from intravascular hemolysis leads to circulating nitric oxide depletion and is responsible for many of the clinical manifestations of PNH, including fatigue, erectile dysfunction, esophageal spasm, and thrombosis.

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  • (PMID = 18063459.001).
  • [ISSN] 0268-960X
  • [Journal-full-title] Blood reviews
  • [ISO-abbreviation] Blood Rev.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA070970-10A16431; United States / NCI NIH HHS / CA / P01 CA070970; United States / NCI NIH HHS / CA / CA70970; United States / NCI NIH HHS / CA / P01 CA070970-10A16431
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Complement C5; 0 / Membrane Proteins; 0 / phosphatidylinositol glycan-class A protein; A3ULP0F556 / eculizumab
  • [Number-of-references] 54
  • [Other-IDs] NLM/ NIHMS42901; NLM/ PMC2290854
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49. Shalev H, Kapelushnik J, Moser A, Knobler H, Tamary H: Hypocholesterolemia in chronic anemias with increased erythropoietic activity. Am J Hematol; 2007 Mar;82(3):199-202
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  • We studied 59 patients with chronic anemias associated with high-erythropoietic activity (thalassemia intermedia, congenital dyserythropoietic anemia type I, congenital spherocytosis), 8 patients with low-erythropoietic activity anemias (acquired aplastic anemia, Fanconi anemia, and Diamond Blackfan anemia), and 20 healthy controls.
  • Mean serum cholesterol, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, triglycerides, hemoglobin, serum ferritin, soluble transferrin receptor (STR), and serum erythropoietin levels were determined in each patient.
  • [MeSH-minor] Child. Chronic Disease. Ferritins / blood. Humans. Lipids / blood. Receptors, Transferrin / blood

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  • [Copyright] Copyright (c) 2006 Wiley-Liss, Inc.
  • (PMID = 17039515.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Lipids; 0 / Receptors, Transferrin; 11096-26-7 / Erythropoietin; 9007-73-2 / Ferritins; 97C5T2UQ7J / Cholesterol
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50. Ganzevoort W, Rep A, de Vries JI, Bonsel GJ, Wolf H, PETRA-investigators: Prediction of maternal complications and adverse infant outcome at admission for temporizing management of early-onset severe hypertensive disorders of pregnancy. Am J Obstet Gynecol; 2006 Aug;195(2):495-503
MedlinePlus Health Information. consumer health - High Blood Pressure in Pregnancy.

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  • STUDY DESIGN: We drew data from a randomized trial of temporizing management in 216 patients with hemolysis, elevated liver enzymes, and low platelets syndrome; severe preeclampsia; eclampsia; or hypertension-related fetal growth restriction and gestational ages between 24 and 34 completed weeks.
  • End points were adverse infant outcome (perinatal death, severe morbidity) and major maternal complications (major morbidity; recurrent and newly acquired hemolysis, elevated liver enzymes, and low platelets; eclampsia) after admission.
  • The association with age, parity, ethnicity, body mass index, gestational age, estimated fetal weight, blood pressure, antihypertensive medication, pulse rate, hemoglobin concentration, admitting center, diagnosis at inclusion, chronic hypertension, and thrombophilia was explored by logistic regression analysis.
  • CONCLUSION: Prediction at admission of the clinical course of the disease and the development of additional maternal complications was not feasible.
  • [MeSH-minor] Birth Weight. Eclampsia / therapy. Female. Gestational Age. HELLP Syndrome / therapy. Humans. Infant, Newborn. Maternal Age. Morbidity. Multivariate Analysis. Parity. Pre-Eclampsia / therapy. Pregnancy. Prognosis. ROC Curve. Risk Factors

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  • (PMID = 16643825.001).
  • [ISSN] 1097-6868
  • [Journal-full-title] American journal of obstetrics and gynecology
  • [ISO-abbreviation] Am. J. Obstet. Gynecol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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51. Behler C, Shade S, Gregory K, Abrams D, Volberding P: Anemia and HIV in the antiretroviral era: potential significance of testosterone. AIDS Res Hum Retroviruses; 2005 Mar;21(3):200-6
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  • Anemia, the most common hematological disorder in human immunodeficiency virus (HIV) infection and acquired immunodeficiency syndrome (AIDS), is associated with decreased quality of life and survival.
  • Hypogonadism is prevalent in advanced HIV disease, however, low testosterone levels have not been customarily implicated in HIV-associated anemia.
  • Anemia was defined as hemoglobin <13.5 g/dl in men and <11.6 g/dl in women.
  • Low testosterone levels may have a positive association and supplemental androgens a negative association with anemia in HIV disease.

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  • (PMID = 15795525.001).
  • [ISSN] 0889-2229
  • [Journal-full-title] AIDS research and human retroviruses
  • [ISO-abbreviation] AIDS Res. Hum. Retroviruses
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / P30 AI 27763-11
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 3XMK78S47O / Testosterone
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52. Chavers BM, Solid CA, Daniels FX, Chen SC, Collins AJ, Frankenfield DL, Herzog CA: Hypertension in pediatric long-term hemodialysis patients in the United States. Clin J Am Soc Nephrol; 2009 Aug;4(8):1363-9
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  • DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: This cross-sectional study of all U.S. pediatric (aged 0-< 18 yr, n = 624) long-term hemodialysis patients was performed as part of the Centers for Medicare & Medicaid Services End-Stage Renal Disease (ESRD) Clinical Performance Measures Project.
  • Characteristics associated with hypertension included acquired kidney disease, shorter duration of ESRD, and lower mean hemoglobin and calcium values.

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  • (PMID = 19556378.001).
  • [ISSN] 1555-905X
  • [Journal-full-title] Clinical journal of the American Society of Nephrology : CJASN
  • [ISO-abbreviation] Clin J Am Soc Nephrol
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / HHSN267200715003C; United States / PHS HHS / / HHSN267200715003C
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antihypertensive Agents
  • [Other-IDs] NLM/ PMC2723970
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53. Rinaldi CR, Rinaldi P, Pane F, Camera A, Rinaldi C: Acquired Hb H disease associated with elevated Hb F level in patient affected by primary myelofibrosis. Ann Hematol; 2010 Aug;89(8):827-8
Genetic Alliance. consumer health - Myelofibrosis.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acquired Hb H disease associated with elevated Hb F level in patient affected by primary myelofibrosis.
  • [MeSH-major] Fetal Hemoglobin / metabolism. Primary Myelofibrosis. alpha-Thalassemia
  • [MeSH-minor] Adult. Female. Hemoglobin H / metabolism. Humans

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  • (PMID = 20024550.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Germany
  • [Chemical-registry-number] 9034-63-3 / Fetal Hemoglobin; 9034-79-1 / Hemoglobin H
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