Amended Safety Assessment of Hydroquinone As Used in Cosmetics
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Biodegradation of 2-Chloro-4-Nitrophenol Via A
Min et al. AMB Expr (2018) 8:43 https://doi.org/10.1186/s13568-018-0574-7 ORIGINAL ARTICLE Open Access Biodegradation of 2‑chloro‑4‑nitrophenol via a hydroxyquinol pathway by a Gram‑negative bacterium, Cupriavidus sp. strain CNP‑8 Jun Min1, Jinpei Wang2, Weiwei Chen1 and Xiaoke Hu1* Abstract Cupriavidus sp. strain CNP-8 isolated from a pesticide-contaminated soil was able to utilize 2-chloro-4-nitrophenol (2C4NP) as a sole source of carbon, nitrogen and energy, together with the release of nitrite and chloride ions. It could degrade 2C4NP at temperatures from 20 to 40 °C and at pH values from 5 to 10, and degrade 2C4NP as high as 1.6 mM. Kinetics assay showed that biodegradation of 2C4NP followed Haldane substrate inhibition model, with the maximum specifc growth rate (μmax) of 0.148/h, half saturation constant (Ks) of 0.022 mM and substrate inhibi- tion constant (Ki) of 0.72 mM. Strain CNP-8 was proposed to degrade 2C4NP with hydroxyquinol (1,2,4-benzenetriol, BT) as the ring-cleavage substrate. The 2C4NP catabolic pathway in strain CNP-8 is signifcant from those reported in other Gram-negative 2C4NP utilizers. Enzymatic assay indicated that the monooxygenase initiating 2C4NP catabolism had diferent substrates specifcity compared with previously reported 2C4NP monooxygenations. Capillary assays showed that strain CNP-8 exhibited metabolism-dependent chemotactic response toward 2C4NP at the optimum concentration of 0.5 mM with a maximum chemotaxis index of 37.5. Furthermore, microcosm studies demonstrated that strain CNP-8, especially the pre-induced cells, could remove 2C4NP rapidly from the 2C4NP-contaminated soil. -
Comparative Transcriptome Analysis of Embryo Invasion in the Mink Uterus
Placenta 75 (2019) 16–22 Contents lists available at ScienceDirect Placenta journal homepage: www.elsevier.com/locate/placenta Comparative transcriptome analysis of embryo invasion in the mink uterus T ∗ Xinyan Caoa,b, , Chao Xua,b, Yufei Zhanga,b, Haijun Weia,b, Yong Liuc, Junguo Caoa,b, Weigang Zhaoa,b, Kun Baoa,b, Qiong Wua,b a Institute of Special Animal and Plant Sciences, Chinese Academy of Agricultural Sciences, Changchun, China b State Key Laboratory for Molecular Biology of Special Economic Animal and Plant Science, Chinese Academy of Agricultural Sciences, Changchun, China c Key Laboratory of Embryo Development and Reproductive Regulation of Anhui Province, College of Biological and Food Engineering, Fuyang Teachers College, Fuyang, China ABSTRACT Introduction: In mink, as many as 65% of embryos die during gestation. The causes and the mechanisms of embryonic mortality remain unclear. The purpose of our study was to examine global gene expression changes during embryo invasion in mink, and thereby to identify potential signaling pathways involved in implantation failure and early pregnancy loss. Methods: Illumina's next-generation sequencing technology (RNA-Seq) was used to analyze the differentially expressed genes (DEGs) in implantation (IMs) and inter- implantation sites (inter-IMs) of uterine tissue. Results: We identified a total of 606 DEGs, including 420 up- and 186 down-regulated genes in IMs compared to inter-IMs. Gene annotation analysis indicated multiple biological pathways to be significantly enriched for DEGs, including immune response, ECM complex, cytokine activity, chemokine activity andprotein binding. The KEGG pathway including cytokine-cytokine receptor interaction, Jak-STAT, TNF and the chemokine signaling pathway were the most enriched. -
IL-10-Null Mice Inflammation-Induced Fetal Demise in Uterine NK Cells Mediate
Uterine NK Cells Mediate Inflammation-Induced Fetal Demise in IL-10-Null Mice This information is current as Shaun P. Murphy, Loren D. Fast, Nazeeh N. Hanna and of September 27, 2021. Surendra Sharma J Immunol 2005; 175:4084-4090; ; doi: 10.4049/jimmunol.175.6.4084 http://www.jimmunol.org/content/175/6/4084 Downloaded from References This article cites 52 articles, 13 of which you can access for free at: http://www.jimmunol.org/content/175/6/4084.full#ref-list-1 http://www.jimmunol.org/ Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication by guest on September 27, 2021 *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2005 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Uterine NK Cells Mediate Inflammation-Induced Fetal Demise in IL-10-Null Mice Shaun P. Murphy,* Loren D. Fast,† Nazeeh N. Hanna,‡ and Surendra Sharma2* Specialized NK cells are recruited in high numbers to the mammalian embryo implantation sites, yet remain pregnancy com- patible. -
(10) Patent No.: US 8119385 B2
US008119385B2 (12) United States Patent (10) Patent No.: US 8,119,385 B2 Mathur et al. (45) Date of Patent: Feb. 21, 2012 (54) NUCLEICACIDS AND PROTEINS AND (52) U.S. Cl. ........................................ 435/212:530/350 METHODS FOR MAKING AND USING THEMI (58) Field of Classification Search ........................ None (75) Inventors: Eric J. Mathur, San Diego, CA (US); See application file for complete search history. Cathy Chang, San Diego, CA (US) (56) References Cited (73) Assignee: BP Corporation North America Inc., Houston, TX (US) OTHER PUBLICATIONS c Mount, Bioinformatics, Cold Spring Harbor Press, Cold Spring Har (*) Notice: Subject to any disclaimer, the term of this bor New York, 2001, pp. 382-393.* patent is extended or adjusted under 35 Spencer et al., “Whole-Genome Sequence Variation among Multiple U.S.C. 154(b) by 689 days. Isolates of Pseudomonas aeruginosa” J. Bacteriol. (2003) 185: 1316 1325. (21) Appl. No.: 11/817,403 Database Sequence GenBank Accession No. BZ569932 Dec. 17. 1-1. 2002. (22) PCT Fled: Mar. 3, 2006 Omiecinski et al., “Epoxide Hydrolase-Polymorphism and role in (86). PCT No.: PCT/US2OO6/OOT642 toxicology” Toxicol. Lett. (2000) 1.12: 365-370. S371 (c)(1), * cited by examiner (2), (4) Date: May 7, 2008 Primary Examiner — James Martinell (87) PCT Pub. No.: WO2006/096527 (74) Attorney, Agent, or Firm — Kalim S. Fuzail PCT Pub. Date: Sep. 14, 2006 (57) ABSTRACT (65) Prior Publication Data The invention provides polypeptides, including enzymes, structural proteins and binding proteins, polynucleotides US 201O/OO11456A1 Jan. 14, 2010 encoding these polypeptides, and methods of making and using these polynucleotides and polypeptides. -
Role of Some Cytokines on Reproduction
Middle East Fertility Society Journal (2011) 16, 220–223 Middle East Fertility Society Middle East Fertility Society Journal www.mefsjournal.com www.sciencedirect.com ORIGINAL ARTICLE Role of some cytokines on reproduction Batool Mutar Mahdi * Department of Microbiology, Al-Kindy College of Medicine, Baghdad University, AL-Nahda Square, Baghdad, Iraq Received 11 December 2010; accepted 13 March 2011 Available online 9 April 2011 KEYWORDS Abstract Background: The etiology of female reproductive failure may be very complex owing to Infertility; a neuro-endocrine-immune association. Dysregulated immunity has been implicated in reproductive Cytokines; failure. Lower TH1 cytokines is supportive for physiological pregnancy. IL-10; Aim of the study: To measure serum levels of pro-inflammatory cytokines (tumor necrosis factor IL-6; (TNF-a), interferon-gamma (IFN-c) and anti-inflammatory cytokines (IL-10 and IL-6) in repro- IFN-c; ductive failure women. TNF-a Patients and methods: A cross- sectional study was carried out in Kammal El-Sammrari Hospital from 2008 to 2010. Forty-five women with reproductive failure participated in the study. Serum lev- els of cytokines (IL-6, IL-10, TNF-alpha and IFN-gamma) were done by Enzyme Linked Immuno Sorbent Assay (ELISA) and compared with age, body mass index and ethnicity matched thirty fer- tile women. Results: There is a significant increase in IL-10 (18.09) (p = 0.002) and IFN-c (49.62) (p = 0.0001) in women with reproductive failure. TNF-a and IL-6 showed no significance different with fertile group. Conclusions: There is increase in IL-10 and IFN-c in women with reproductive failure. -
Phase 11 Metabolism of Benzene Have to Be Identified
Phase 11 Metabolism of Benzene have to be identified. Application of single metabolites of benzene such as phenol Dieter Schrenk,1 Achim Orzechowski,1 (PH), catechol (CT), hydroquinone (HQ), and 1,2,4-trihydroxybenzene (THB) to Leslie R. Schwarz,2 Robert Snyder,3 Brian Burchell,4 rodents failed to reproduce the characteristic Magnus lngelman-Sundberg,5 and Karl Walter Bock1 toxic effects of benzene in the bone marrow (4,5). In several studies the possible syner- 1'nstitute of Toxicology, University of Tubingen, Tubingen, Germany; gistic action of certain metabolites of ben- 2GSF-lnstitute of Toxicology, Neuherberg/Munchen, Germany; zene on the bone marrow was investigated. 3Department of Pharmacology and Toxicology, EOHSI, Piscataway, It was shown that PH enhanced the conver- New Jersey; 4Department of Biochemical Medicine, University of sion of HQ into 1,4-benzoquinone cat- Dundee, Ninewells Hospital and Medical School, Dundee, United alyzed in vitro by myeloperoxidase (6,7), an Kingdom; 5Department of Physiological Chemistry, Karolinska Institute, enzyme present in abundance in the bone marrow (8). The electrophilic 1,4-benzo- Stockholm, Sweden quinone thus formed is able to bind to cel- The hepatic metabolism of benzene is thought to be a prerequisite for its bone marrow toxicity. lular proteins and DNA. Binding to critical However, the complete pattern of benzene metabolites formed in the liver and their role in bone proteins such as tubulin (9) or DNA poly- marrow toxicity are not fully understood. Therefore, benzene metabolism was studied in isolated merase-a (10) may play an important role rodent hepatocytes. Rat hepatocytes released benzene-1,2-dihydrodiol, hydroquinone (HQ), in benzene toxicity. -
For Review Only 19 10 Telephone: +44 1223 333729 20 21 Fax: +44 1223 333346
Submitted to Phil. Trans. R. Soc. B - Issue The role of the maternal immune system in the regulation of human birth weight For ReviewJournal: Philosophical Only Transactions B Manuscript ID: RSTB-2014-0071.R1 Article Type: Review Date Submitted by the Author: n/a Complete List of Authors: Moffett, Ashley; University of Cambridge, Pathology Hiby, Susan; University of Cambridge, Pathology Sharkey, Andrew; University of Cambridge, Pathology Issue Code: Click <a href=http://rstb.royalsocietypublishing.org/site/misc/issue- BIRTH codes.xhtml target=_new>here</a> to find the code for your issue.: Developmental biology < BIOLOGY, Evolution Subject: < BIOLOGY, Genetics < BIOLOGY, Immunology < BIOLOGY Birth weight, Natural Killer (NK) cells, Keywords: Immunology, pre-eclampsia, fetal growth restriction, placental development http://mc.manuscriptcentral.com/issue-ptrsb Page 1 of 27 Submitted to Phil. Trans. R. Soc. B - Issue 1 1 2 3 4 5 The role of the maternal immune system in the regulation of 6 7 human birth weight 8 9 10 1,2 1 1 11 5 Ashley Moffett , Susan E . Hiby and Andrew Sharkey 12 1 Department of Pathology and Centre for Trophoblast Research, 13 14 University of Cambridge, Tennis Court Road, Cambridge CB2 1QP, UK 15 16 17 2Corresponding author. E-mail address: [email protected] (A. Moffett). 18 For Review Only 19 10 Telephone: +44 1223 333729 20 21 Fax: +44 1223 333346. 22 23 24 Summary 25 26 Human birth weight is subject to stabilizing selection. Large babies are at 27 15 risk of obstetric complications such as obstructed labour, which endangers 28 29 both mother and child. -
Early Pregnancy Diagnosis and Embryo/Fetus Mortality
EARLY PREGNANCY DIAGNOSIS AND EMBRYO/FETUS MORTALITY IN CATTLE A Dissertation by JUAN EDUARDO ROMANO Submitted to the Office of Graduate Studies of Texas A&M University in partial fulfillment of the requirements for the degree of DOCTOR OF PHILOSOPHY December 2004 Major Subject: Physiology of Reproduction EARLY PREGNANCY DIAGNOSIS AND EMBRYO/FETUS MORTALITY IN CATTLE A Dissertation by JUAN EDUARDO ROMANO Submitted to Texas A&M University in partial fulfillment of the requirements for the degree of DOCTOR OF PHILOSOPHY Approved as to style and content by: _____________________________ _________________________________ Duane C. Kraemer David W. Forrest (Co-Chair of Committee) (Co-Chair of Committee) _____________________________ _________________________________ Mark E. Westhusin James A. Thompson (Member) (Member) _____________________________ John W. McNeill (Head of Department) December 2004 Major Subject: Physiology of Reproduction iii ABSTRACT Early Pregnancy Diagnosis and Embryo/Fetus Mortality in Cattle. (December 2004) Juan Eduardo Romano, D.V.M., University of Uruguay; M.S., University of Minnesota Co-Chairs of Advisory Committee: Dr. Duane C. Kraemer Dr. David W. Forrest Pregnancy diagnosis by transrectal ultrasonography (using a 5 MHZ linear probe) presented the maximum sensitivity and negative predictive values at day 26 and day 29 after estrus in heifers and cows, respectively. Palpation per rectum using the fetal membrane slip for pregnancy diagnosis did not increase embryo/fetus mortality when compared with a positive control group of non-palpated females. The use of a controlled randomized block design was a useful approach to study this problem. Blocking for category and number of embryos allowed us to remove these confounding factors. Factors that affected pregnancy loss during the first four months of pregnancy were: period of pregnancy, age of the animal, number of previous lactations and number of embryos. -
Antibody-Induced Pregnancy Loss
TNF-α Is a Critical Effector and a Target for Therapy in Antiphospholipid Antibody-Induced Pregnancy Loss This information is current as Jessica Berman, Guillermina Girardi and Jane E. Salmon of September 24, 2021. J Immunol 2005; 174:485-490; ; doi: 10.4049/jimmunol.174.1.485 http://www.jimmunol.org/content/174/1/485 Downloaded from References This article cites 48 articles, 7 of which you can access for free at: http://www.jimmunol.org/content/174/1/485.full#ref-list-1 Why The JI? Submit online. http://www.jimmunol.org/ • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average by guest on September 24, 2021 Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2005 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology TNF-␣ Is a Critical Effector and a Target for Therapy in Antiphospholipid Antibody-Induced Pregnancy Loss1 Jessica Berman, Guillermina Girardi, and Jane E. Salmon2 The antiphospholipid syndrome (APS) is characterized by recurrent fetal loss, intrauterine growth restriction, and vascular thrombosis in the presence of antiphospholipid (aPL) Abs. -
Seminal CD38 Is a Pivotal Regulator for Fetomaternal Tolerance
Seminal CD38 is a pivotal regulator for fetomaternal tolerance Byung-Ju Kima,b, Yun-Min Choia,b, So-Young Raha,b, Dae-Ryoung Parka,b, Seon-Ah Parka, Yun-Jo Chunga, Seung-Moon Parkc, Jong Kwan Parkd, Kyu Yun Jange, and Uh-Hyun Kima,b,f,1 + aNational Creative Research Laboratory for Ca2 Signaling Network and Departments of bBiochemistry, dUrology, and ePathology, Chonbuk National University Medical School, Jeonju, 561-180, Korea; cDivision of Biotechnology, College of Environmental and Bioresource Sciences, Chonbuk National University, Iksan, 570-752, Korea; and fInstitute of Cardiovascular Research, Chonbuk National University, Jeonju, 561-180, Korea Edited by John J. Eppig, The Jackson Laboratory, Bar Harbor, ME, and approved December 22, 2014 (received for review July 16, 2014) A successful pregnancy depends on a complex process that estab- a variety of inflammatory diseases (20–23). For example, recombi- lishes fetomaternal tolerance. Seminal plasma is known to induce nant CD38 inhibits LPS-induced inflammatory signals in mouse maternal immune tolerance to paternal alloantigens, but the seminal macrophages and human DCs through an interaction with CD31 factors that regulate maternal immunity have yet to be characterized. (24, 25). Here, we show that a soluble form of CD38 (sCD38) released from In this study, we found that CD38 is truncated and released seminal vesicles to the seminal plasma plays a crucial role in inducing into the seminal plasma from seminal vesicles (SVs) as a soluble + + + tolerogenic dendritic cells and CD4 forkhead box P3 (Foxp3 )reg- form (sCD38) in humans and mice. This finding prompted us to ulatory T cells (Tregs), thereby enhancing maternal immune tolerance examine whether CD38 plays a role in maternal immune toler- and protecting the semiallogeneic fetus from resorption. -
Pugh and Raper
The Journal of Biochemistry , Vol. 35, No. 2. STUDIES ON TYROSINASE . VII. The action of the potatoe tyrosinase on trihydric phenols. BY HISASI SAITO. (Front the Biochemical Institute, Nagasaki Medical College . Director: Prof. Dr. T. Uchino.) (Received for publication, November 4, 1941) INTRODUCTION. Pugh and Raper (1927) pointed out that tyrosinase , being allowed to act on phenol, catechol, p-cresol and m-cresol in the presence of aniline, produces anilino compounds of o-quinones as oxidation products. They thus postulated the formation of ortho quinones from these phenols by the action of tyrosinase. The amount of oxygen, consumed in the enzymic oxidation of phenols, was, however, found by many investigators (Robinson and McCance, 1925; Pugh and Raper, 1927; Kawasaki, 1938; Sasaki, 1940, a) to be one atom more per molecule of substrates than that of corresponding to the formation of o-quinones. This probably indicates that o-quinones are not the final products of enzymic oxidation of phenolic substances. Wagreich and Nelson (1936) found that the amount of oxygen required for the oxidation of catechol by tyrosinase is two atoms and that the subsequent addition of aniline is accompanied by the absorption of another atom of oxygen with the formation of anilino-quinone. On the basis of this finding, they suggested that, in the case of catechol oxidation by tyrosinase, 4-hydroxy-l,2 - quinone is produced rather than o-benzoquinone as an iinternnediate product, and that hydroxyquinone thus formed then reacts withh aniline to produce dianilino quinone. On the other hand, Jackson (1939) examined the action of tyrosinase on cateehol as well as 1,2,4-tribydroxybenzene and came to the conclusion that 4-hydroxy 243 244 H. -
Preterm Birth and Preeclampsia Fetal
The Journal of Immunology TLR9 Provokes Inflammation in Response to Fetal DNA: Mechanism for Fetal Loss in Preterm Birth and Preeclampsia Andrea Scharfe-Nugent,*,1 Sine´ad C. Corr,†,1 Susan B. Carpenter,‡ Louise Keogh,x Brendan Doyle,{ Cara Martin,{ Katherine A. Fitzgerald,‡ Sean Daly,* John J. O’Leary,{,2 and Luke A. J. O’Neill†,2 Preterm birth, the major cause of neonatal mortality in developed countries, is associated with intrauterine infections and inflam- mation, although the exact mechanisms underlying this event are unclear. In this study, we show that circulating fetal DNA, which is elevated in pregnancies complicated by preterm labor or preeclampsia, triggers an inflammatory reaction that results in sponta- neous preterm birth. Fetal DNA activates NF-kB, shown by IkBa degradation in human PBMCs resulting in production of proinflammatory IL-6. We show that fetal resorption and preterm birth are rapidly induced in mice after i.p. injection of CpG or fetal DNA (300 mg/dam) on gestational day 10–14. In contrast, TLR92/2 mice were protected from these effects. Furthermore, this effect was blocked by oral administration of the TLR9 inhibitor chloroquine. Our data therefore provide a novel mechanism for preterm birth and preeclampsia, highlighting TLR9 as a potential therapeutic target for these common disorders of preg- nancy. The Journal of Immunology, 2012, 188: 5706–5712. retermbirth(PTB),definedasdeliverybefore37wk disorders of pregnancy. TLRs are an important class of pathogen gestation, has become an epidemic in developed countries. recognition receptors, which signal during infection to bring about P Indeed, PTB and preeclampsia (PEC) are leading causes of immune reactions that have been implicated in PTB (3).