Background: Cardiovascular disease is the leading cause of mortality and morbidity in the world and has something to do with daily diet. The polyphenol is the most abundant compound in daily diet, including grape. The red wine was rich in polyphenol because of composing much grape. Early study has already confirmed the “French Paradox” in cardiovascular protection power, which shed light on the dietary modulation on disease. Objective: The main objective of the study was to evaluate the effect of products containing polyphenol such as red wine extract, grape juice and grape extract tablets or powder on cardiovascular disease risk factors. It mainly examined relationship between polyphenol and serum lipid in addition to blood pressure. Methods: Studies working on effects of grape extract products on cardiovascular disease were searched from electronic resources MEDLINE and EMBASE. Nine clinical controlled trials were identified through PubMed and Ovid. CONSORT guideline and Jadad Score were used to appraise the quality of trials. Weighing two assessment guidelines, a total of three studies were in good quality, one was in bad quality while the rest four were fair to middle. Results: The changes before and after intervention on serum lipid and blood pressure were contradictory. Some studies found polyphenol was statistically significant protective factors, while some did not find it siginificant but still showed a protective effect. One study found polyohenol had no effect on cardiovascular disease risk factors. Conclusion: The prevention of polyphenol was not consistent in nine trials and there is no sufficient and strong evidence supporting its cardiovascular protection effect given that the study design of each trial differed. It was not recommeded to use grape polyphenol as cardiovascular protect products. There were limitations and weakness of current study on the association of polyphenol and cardiovascular disease. Further research on this topic is required, both in vivo and in vitro. / published_or_final_version / Public Health / Master / Master of Public Health

One thousand Holstein-Friesian heifer calves were studied to evaluate the effects of colostrum-derived 24 to 48 h serum Ig concentrations on growth and survival. The rate of growth increased as 24 to 48 h serum Ig concentrations increased. Calves born to first-calf heifers had higher 24 to 48 h serum Ig concentrations and gained weight at a higher rate of gain than heifers born to 3-year-old and older cows. The concentration of serum Ig at 24 to 48 h in the dairy heifer is a significant source of variation affecting average daily gain through the first 180 d of life. Seasonal factors were also significant in influencing rate of gain from birth to 6 months. Age of dam was a significant source of variation in calf weight gains, but only for the first 35 d of life. Approximately 28% of the calves absorbed less than 12 mg/ml of maternally-derived antibody. Heifers in this category suffered a death loss of 6.78% compared to only a 2.59% loss for heifers absorbing greater than 40 mg/ml Ig. Both season and age of dam were significant in affecting the concentration of 24 to 48 h serum Ig acquired. Forty-nine percent of the variation in 35 d serum Ig can be attributed to the variation found at 24 to 48 h. The data presented here indicate that proper management of factors influencing the absorption of colostral immunoglobulins by the neonatal dairy heifer would enhance the replacement rearing program.

No description available.

No description available.

This research study is divided into 4 major sections. Section A deals with the world-wide distribution of the haematoprotozoan parasites of marine fishes. These are tentatively divided into 3 major groups: the Haemogregarines, the Trypanosomes and the Trypanoplasms and one group of ill defined and controversal organisms including Haemohormidium sp. and Dactylosoma sp. The results of extensive surveys of the coastal waters of France, Scotland and Wales with added examples from the Mediterranean Sea substantiate the zoogeographical distribution of these parasites. Two species of haematoprotozoan parasites Haemogregarina simondi and Trypanosoma soleae are re-described, earlier accounts dating from the beginning of the century being considered incomplete. A new species of haemogregarine is described from the farmed turbot (Scophthalmus maximus) as Haemogregarina sachai n. sp. and an unidentified species of Haemohormidium found occasionally in turbot and Dover sole (Solea soles) is also described. In addition Haemogregarina sp. were encountered in certain wild marine fish from the Atlantic coast of France e. g. Zeus faber, Sebastes sp., Trisopterus luscus, Pagellus bogaraveo and Raja sp. and from the coastal waters of Malta e. g. Peristedion cataphractum and Oblade melanura. However, they were not found in sufficient numbers to allow a definite description. The value of surveys of wild fish populations is discussed in the light of zoogeographical distribution, the apparent periodicity of these parasites and a seasonal variation of parasitism. Section B attempts to summarize the knowledge of the mode of transmission of marine haematoprotozoan parasites by piscicolid leeches as intermediate hosts and vectors. The developmental stages of a trypanosome, probably Trypanosoma murmanensis from the Atlantic cod Gadus morhua are described in the marine leech Calliobdella nodulifera. Stages of a haemogregaririe were observed in the same leech. The development of the turbot haemogregarine Haemogregarina sachai n. sp. in artificially infected leeches is also described up to the 20th day post infection. Transmission of this haemogregarine to apparently uninfected turbot via this leech was not successful. Various stages of development of Haemogregarina simondi are described in its apparently natural vector, the marine leech Hemibdella soleae, and transmission with infected leeches to apparently healthy hatchery reared soles was achieved. Thus it was shown for the first time that marine leeches can serve also as vectors for haemogregarines. Stages of this haemogregarine are also described in the blood-sucking ectoparasitic copepod Lernaeocera sp. parasitizing the haemogregarine infected soles. These results are discussed in relation to the feeding behaviour and migration patterns of the fish hosts, the periodicity of the parasites and possible other vectors or other ways of acquiring an infection with these haematoprotozoan parasites. In Section C the pathogenicity of the haematoprotozoan parasites of marine fishes is summarized from previous accounts among wild fish populations and compared with the situation in aquaculture. The pathogenicity of the two haemogregarines, Haemogregarina simondi and Haemogregarina sachai n. sp., accidentally introduced into several fish farming establishments connected with the effluent cooling waters of a nuclear power station is described with special reference to the possible source of the infection. The results of therapy trials and control programs are discussed in the light of the periodic reappearance of the parasites, the possibility of carrier fish existing, the immune status of the host and the possible role of an intermediate host or vector in maintaining the infection. Possible means of controlling the pathogenicity of marine haemogregarines and perhaps other haematoprotozoan parasites when they occur in farmed marine fishes are also discussed. In Section D are described for the first time, the ultrastructural characteristics of various stages of the haematoprotozoan parasites of marine fishes in fish hosts and vectors. The electronmicroscopical studies are limited to Haemogregarina sachai n. sp. and Haemogregarina simondi, for which the ultrastructure of schizonts from the spleen and blood, intracellular merozoites and free gametocytes were contrasted. In addition stages of H. simondi were demonstrated in Hemibdella soleae and Lernaeocera sp. The fine structure of the various organelles encountered was compared with that of related organisms from other cold-and warm-blooded vertebrates. In conclusion attention is drawn to the need for more investigations in this field of host-parasite relationship of marine haematoprotozoan parasites and their vectors and their pathogenic-action as seen in a confined and artificial environment such as the marine aquaculture.

Gao, Ni. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2009. / Includes bibliographical references (leaves 133-153). / Abstracts also in Chinese. / ACKNOWLEDGEMENTS / TABLE OF CONTENT --- p.1 / LIST OF FIGURES AND TABLES --- p.4 / List of Figures --- p.4 / List of Tables --- p.5 / ABSTRACT --- p.6 / 中文摘要 --- p.9 / ABBREVIATIONS --- p.11 / Chapter CHAPTER 1 - --- BACKGROUND REVIEW AND HYPOTHESIS --- p.13 / Chapter 1.1 --- Overview of Peritoneal dialysis --- p.13 / Chapter 1.2 --- Peritoneal dialysis in Hong Kong --- p.16 / Chapter 1.3 --- Cardiovasular Disease in PD patients --- p.18 / Chapter 1.3.1 --- Arterial disease --- p.21 / Chapter 1.3.2 --- Left ventricular hypertrophy --- p.23 / Chapter 1.4 --- Malnutrition in PD patients --- p.26 / Chapter 1.5 --- Fluid overload in PD patients: a cause and a result of CVD --- p.28 / Chapter 1.5.1 --- Overview --- p.28 / Chapter 1.5.2 --- Fluid overload and residual renal function --- p.29 / Chapter 1.5.3 --- Fluid overload and hypertension --- p.30 / Chapter 1.5.4 --- Fluid overload and malnutrition --- p.32 / Chapter 1.5.5 --- Assessment of fluid status in PD patient --- p.33 / Chapter 1.6 --- Peritoneal transport as the cause of fluid overload --- p.36 / Chapter 1.6.1 --- Structure of peritoneum --- p.36 / Chapter 1.6.2 --- Structural alteration of peritoneal membrane in PD --- p.37 / Chapter 1.6.3 --- Ultrafiltration dysfunction --- p.38 / Chapter 1.6.4 --- Peritoneal transport and outcome of PD patients --- p.40 / Chapter 1.6.5 --- Fluid overload and peritoneal transport --- p.41 / Chapter 1.6.6 --- Peritoneal transport and malnutrition --- p.42 / Chapter 1.6.7 --- Assessment of peritoneal transport --- p.44 / Chapter 1.7 --- Closing the circle: Arterial stiffness as a cause of high peritoneal transport? --- p.47 / Chapter 1.7.1 --- Vascular function and anatomy --- p.47 / Chapter 1.7.2 --- Atherosclerosis --- p.49 / Chapter 1.7.3 --- Atherosclerosis and Endothelial Dysfunction --- p.50 / Chapter 1.7.4 --- Atherosclerosis and Extracellular Matrix --- p.53 / Chapter 1.7.5 --- Arterial stiffness and renal function --- p.54 / Chapter 1.7.6 --- Arterial stiffness in PD --- p.55 / Chapter 1.7.7 --- Arterial stiffness and clinical outcome --- p.55 / Chapter 1.7.8 --- Assessment of arterial stiffness --- p.57 / Chapter 1.8 --- An overall construct --- p.61 / Chapter 1.9 --- Hypothesis --- p.63 / Chapter CHAPTER 2 - --- GENERAL METHODOLOGY --- p.65 / Chapter 2.1 --- Radiographic Parameters of Intravascular Volume Status --- p.65 / Chapter 2.2 --- Pulse Wave Velocity Study --- p.69 / Chapter 2.3 --- Dialysis adequacy study --- p.72 / Chapter 2.4 --- Peritoneal equilibration test (PET) --- p.73 / Chapter 2.5 --- Assessment of nutritional status --- p.75 / Chapter CHAPTER 3 - --- Radiographic Parameters of Intravascular Volume Status as a Prognostic Marker in Chinese Peritoneal Dialysis Patients --- p.77 / Chapter 3.1 --- Introduction --- p.77 / Chapter 3.2 --- Patients and Methods --- p.78 / Chapter 3.3 --- Results --- p.81 / Chapter 3.4 --- Conclusion --- p.90 / Chapter CHAPTER 4 - --- Longitudinal Changes of Radiographic Parameters as the Prognostic Marker of Chinese Peritoneal Dialysis Patients --- p.91 / Chapter 4.1 --- Introduction --- p.91 / Chapter 4.3 --- Results --- p.95 / Chapter 4.4 --- Conclusions --- p.104 / Chapter CHAPTER 5 - --- "The Relation between Arterial Pulse Wave Velocity, Peritoneal Transport Characteristics, and Radiological Parameters of Intravascular Volume Status in Chinese peritoneal dialysis patients" --- p.105 / Chapter 5.1 --- Introduction --- p.105 / Chapter 5.2 --- Patients and Methods --- p.106 / Chapter 5.3 --- Results --- p.110 / Chapter 5.4 --- Conclusions --- p.119 / Chapter CHAPTER 6 - --- DISCUSSION --- p.120 / Chapter 6.1 --- Methodology --- p.120 / Chapter 6.2 --- Results --- p.123 / Chapter 6.3 --- Further Directions of Research --- p.131 / Chapter 6.4 --- Conclusions --- p.132 / REFERENCE --- p.133 / PUBLICATIONS RELATED TO THIS WORK --- p.154 / Index Publication --- p.154 / Abstract --- p.154

Wong, Ying Suet. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2009. / Includes bibliographical references (leaves 120-131). / In English with some Chinese and Japanese; abstract also in Chinese. / Chapter Chapter One: --- Introduction --- p.3 / Literature Review --- p.7 / Structure --- p.10 / Notes on Sources --- p.13 / Chapter Chapter Two: --- Venereal Disease Policies in the Metropole and Their Colonies --- p.15 / The Case of Britain --- p.16 / VD Policy in the Metropole: The case of Britain --- p.16 / VD Policy in the Colonies: The Case of Colonies under Britain --- p.23 / The Case of Japan with Reference of Britain as the Pioneer Policy Maker --- p.28 / Chapter Chapter Three: --- Venereal Disease control in the Metropole --- p.31 / Legislation --- p.32 / Institutions --- p.44 / Education and Social Discussion --- p.49 / Resistance --- p.55 / VD control in the Japanese Military Force --- p.60 / Summary --- p.67 / Chapter Chapter Four: --- Venereal Disease Control in Colonial Taiwan --- p.70 / Legislation --- p.72 / Licensed prostitution system --- p.72 / The VD Prevention Law --- p.79 / Education and Social Discussion --- p.84 / Before the VD Prevention Law in Japan in 1927 --- p.84 / Education and Public Discussion of VD after the promulgation of the VD Prevention Law in 1927 --- p.90 / The Changing Discourse of VD --- p.95 / Summary --- p.100 / Chapter Chapter Five: --- "Sex, Gender, Class, Race and Colonialism" --- p.101 / Taiwanese Women´ةs image: Scapegoating --- p.101 / Medical Development: State Medicine and Local Elites --- p.106 / VD Control in the Military in Taiwan --- p.109 / Summary --- p.111 / Chapter Chapter Six: --- Conclusion --- p.114 / Bibliography --- p.120

Thesis (MSc)--Stellenbosch University, 2001. / ENGLISH ABSTRACT: Introduction: It is well documented that insulin offers cardioprotection under ischaemic stress. In the past it was believed that the protective effects of insulin, such as the (a) recruitment of glucose transporters to enhance glucose entry into the cell, (b) stimulation of glycolysis, (c) enhancement of glycogen synthesis, (d) improved protein synthesis, and (e) positive inotropic and chronotropic properties, were metabolic of origin, but lately the emphasis has shifted towards the diverse signal transduction pathways elicited by insulin. Although these beneficial effects of insulin on ischaemia/reperfusion induced injury have been studied for many years, the exact protective mechanism is still not resolved. Aim: To investigate the influence of insulin on the signaling pathways as a possible protective mechanism against ischaemia/reperfusion and therefore to investigate the possible roles and cross signaling of cyclic adenosine monophosphate (cAMP), protein kinase B (PKB) and p38 mitogen activated protein kinase (p38 MAPK) in the cardioprotection offered by insulin to the reperfused, ischaemic myocardium. Materials and methods: Isolated rat hearts were perfused retrogradely in accordance with the Langendorff technique (95%02, 5% C02). After 30 min of stabilization, hearts were subjected to 30 min global low flow ischaemia (0,2 ml/min), followed by 30 min of reperfusion. Hearts perfused with standard Krebs Henseleit solution containing 5 mM glucose were compared to hearts perfused with a perfusion solution containing 5 mM glucose and 0,3 IlIU/ml insulin. Wortmannin was added during either ischaemia or reperfusion. Left ventricular developed pressure (LVDP), rate pressure product (RPP), tissue cAMP and PKB and p38 MAPK activation were measured. Results: Insulin treated hearts showed improved functional recovery (P<0.05) during reperfusion after ischaemia vs. non-insulin treated hearts (85.5±4.6% vs. 44.8±4.9%). However, the addition of wortmannin (a Pl3-kinase inhibitor) to the perfusion solution during either ischaemia or reperfusion abolished the improved recovery. At the end of ischaemia, cAMP levels of the insulin treated hearts were elevated significantly, while the cAMP content in the non-insulin treated hearts returned to control levels. Addition of wortmannin during ischaemia abolished this rise in cAMP. Wortmannin added during reperfusion only did not alter the levels of cAMP at the end of reperfusion. Activation of p38 MAPK was transient during ischaemia for both insulin and non-insulin treated hearts. Addition of wortmannin during ischaemia did not alter p38 MAPK levels at the end of ischaemia. P38 MAPK was activated significantly (P<0.001) in the non-insulin treated hearts vs. insulin treated hearts during reperfusion. Wortmannin, added at the onset of reperfusion, could partially abolish the effects of insulin to suppress p38 MAPK activation after 30 min of reperfusion. Activation of PKB in insulin treated hearts was significantly higher than non-insulin treated hearts during stabilization and early ischaemia. This activity was depressed by 30 min of ischaemia in both presence and absence of insulin. Wortmannin, when added before induction of ischaemia did not further lower this. The presence of insulin resulted in occurrence of strong PKB activation during reperfusion, peaking at 15 minutes and diminishing at 30 minutes. Wortmannin, added at the onset of reperfusion, abolished PKB activity measured at the end of reperfusion. Conclusion: Insulin exerted a positive inotropic effect and delayed the onset to ischaemic contracture. Inhibition of Pl3-kinase by wortmannin abolished the protective effects of insulin, arguing for an insulin stimulated PKB involvement in cardiac protection. Insulin also increased cAMP production and attenuated activation of p38 MAPK, both associated with improved recovery. This evidence suggested possible cross signaling between different signaling pathways. / AFRIKAANSE OPSOMMING: Agtergrond: Insulin beskerm harte wat aan isgemiese stres blootgestel word. Alhoewel hierdie voordelige effekte van insulien reeds vir verskeie jare bestudeer is, is die presiese meganisme waarmee insulien die hart beskerm steeds nie duidelik nie. Navorsers het die beskermende effekte van insulien aan metaboliese gevolge soos: (a) verhoogde glukose transport d.m.v. inspanning van meer glukose transporters (b), stimulering van glikolise, (c) vebeterde glikogeensintese, (d) verhoogde proteiensintese, en (e) die positiewe inotropiese en chronotropiese eienskappe van insulien toegeskryf. Onlangs het die fokus verskuif na ander diverse seintransduksiepaaie. Doel: Die doel van hierdie studie was dus om die moontlike betrokkenheid van hierdie sientransduksiepaaie asook die interaksie tussen sikliese adenomonofosfaat (cAMP), proteïn kinase B (PKB) en p38 MAPK in die beskerming wat insulien aan die isgemiese, gereperfuseerde miokardium bied, te bestudeer. Materiale en Metodes: Geïsoleerde rotharte is geperfuseer in ooreenstemming met die Langendorff metode. Na 30 min van stabilisasie is harte blootgestel aan 30 min. globale lae vloei isgemie (0,2 ml/min), en daarna is harte vir 30 min. geherperfuseer. Harte wat geperfuseer is met 'n perfusaat wat 5mM glukose bevat is vergelyk met harte wat geperfuseer is met 'n perfusaat wat 5mM glukose en 0,3 ~IU/ml insulien bevat. Sommige harte is geperfuseer met 'n perfusie oplossing waar wortmannin bygevoeg is tydens óf isgemie óf tydens herperfusie. Linker ventrikulêre ontwikkelde druk (LVDP), tempo-druk produk (RPP), weefsel cAMP-vlakke asook PKB en p38 MAPK aktiwiteit is gemeet. Resultate: Insulien-behandelde harte het funksioneel beduidend beter herstel tydens herperfusie na isgemie as harte wat nie met insulien behandel is nie (85.5±4.6% vs. 44.8±4.9%). Byvoeging van wortmannin by die perfusie oplossing tydens óf isgemie óf reperfusie, het die toename in herstel wat gesien is in die insulien-behandelde harte, opgehef. Die cAMP vlakke in die insulienbehandelde harte het aan die einde van isgemie beduidend gestyg (P<0.001), terwyl vlakke in harte wat nie met insulien behandel is nie, na kontrole vlakke teruggekeer het. Die teenwoordigheid van wortmannin in die perfusie oplossing tydens isgemie, het die styging in cAMP voorkom , terwyl die byvoeging van wortmannin tydens herperfusie. nie die cAMP vlakke beïnvloed het nie. Die aktivering van p38 MAPK tydens isgemie was van verbygaande aard in beide die insulien-behandelde harte en harte wat nie met insulien behandel is nie. Die byvoeging van wortmannin tydens isgemie het nie die p38 MAPK aktivering beïnvloed nie. P38 MAPK is beduidend geaktiveer tydens herperfusie in harte wat nie met insulien behandel is nie vergeleke met die insulien-behandelde harte. Die byvoeging van wortmannin tydens reperfusie kon die effek van insulien om p38 MAPK aktivering te onderdruk, gedeeltelik ophef. PKB aktivering tydens die stabilisasie fase en vroeë isgemie was beduidend hoër in die insulien-behandelde harte vs. die harte wat nie met isulien behandel is nie. Die aktiwiteit is onderdruk deur 30 min isgemie ongeag die teenwoordigheid van insulien. Die byvoeging van wortmannin tydens isgemie het PKB aktivering nie verder verlaag nie. Die teenwoordigheid van insulien het 'n sterk aktivering van PKB tydens herperfusie veroorsaak met 'n piek na 15 min en 'n verlaging na 30 min. Wortmannin bygevoeg aan die begin van herperfusie, het PKB aktiwiteit opgehef aan die einde van reperfusie. Opsomming: Insulien het 'n positiewe inotropiese invloed gehad, en het die begin van isgemiese kontraksie vertraag. Die inhibisie van Pl3-kinase deur wortmannin het die beskermende effekte van insulin opgehef, wat 'n insulin gestimuleerde PKB betrokkenheid aandui. Insulien het ook verhoogte cAMP produksie en verlaagde p38 MAPK aktivering tot gevolg gehad, en beide is geassosieer met verbeterde herstel. Hierdie resultate dui dus op moontlike interaksie tussen die verskillende seintransduksiepaaie.

This thesis sought to investigate novel methods for protecting the liver from ischaemia reperfusion injury in the context of liver transplantation. Research in the heart, brain and kidneys has suggested that hypoxia inducible factor (HIF) may play a key role in the delayed phase of ischaemic preconditioning and can protect organs for up to 3 days. However, although there is good evidence for the potential of HIF to protect organs from ischaemia, the HIF pathway still presents some what of a paradox because it targets both pro-death (e.g. BNIP3,NIX) as well as pro-survival genes (e.g. HO-I, EPO). HIF is primarily controlled by 3 oxygen dependent prolyl hydroxylases (PHD 1 , PHD2, PHD3), and inhibition of these prolyl hydroxylases leads to HIF activation. It was hypothesised that differential inhibition of PHD 1,2 or 3 may result in selective gene regulation and may confer greater or less protection against ischaemia reperfusion injury. To investigate this hypothesis mouse embryonic fibroblasts (MEFs) were isolated from PHDl, 2, and 3 knock-out (KO) embryos and compared to MEFs derived from WT littermate controls. In these MEFs, cell growth and proliferation, as well as cell survival following exposure to anoxia and inducers of apoptosis was studied. The principal findings were that PHD2 is the dominant regulator of HIF in normoxia. PHD2 knock-out MEFs exhibited glycolytic metabolism and had a lower oxygen consumption compared to wild-type MEFs. Gene array studies confirmed the dominant role of PHD2 but also demonstrated that PHD 1 upregulates a number of HIF target genes, albeit to a lesser extent than PHD2. There were no differences, however, in susceptibility to hypoxic injury in the PHDl, 2, and 3 knock-out MEFs compared to wild-type controls. A further aim of the study was to investigate whether prolyl hydroxylase inhibition using dimethyloxalyglycerine (DMOG) may protect the liver in a rodent model of ischaemia reperfusion injury. DMOG effectively upregulated HIF and IllF target genes. Serum transaminases (AST and AL T) were significantly lower in the DMOG treated animals compared to the normal saline treated controls 24 hours following ischaemia. This protection was similar to the protection conferred by surgically induced ischaemic preconditioning. This thesis provides important insights into the individual function of the prolyl hydroxylases and provides preliminary evidence that prolyl hydroxylase inhibitors may be useful in the treatment of ischaemia reperfusion injury in liver transplantation.

A research report submitted to the Faculty of Health Sciences, School of Public Health, University of the Witwatersrand, Johannesburg, in partial fulfillment of the requirements for the degree of Master of Public Health: Occupational Hygiene, Johannesburg, 2012 / The aim of the study was to determine if the gold mine under study achieved the 2008 elimination of silicosis occupational hygiene milestones as set out by the South African mining industry in 2003. To identify high risk quartz exposed occupations within the conventional stope and TM³ stope employees of an underground gold mine between July 2008 and June 2010; to describe the personal quartz exposure of conventional stope and TM³ stope employees in an underground gold mine between July 2008 and June 2010; and to compare the time weighted average (TWA) quartz exposures between the conventional stope and TM³ stope to the Department of Mineral Resources-Occupational Exposure Limit (DMR-OEL) of 0.1 mg/m3, the National Institute of Occupational Safety and Health-Recommended Exposure Limit (NIOSH-REL) of 0.05 mg/m3 and the American Conference of Government Industrial Hygienists-Threshold Limit Value (ACGIHTLV) of 0.025 mg/m3.