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Jeffrey A Brinker, M.D.

Jeffrey A Brinker, M.D.

  • Professor of Medicine
  • Joint Appointment in Radiology and Radiological Science


Martin-Martinez (Massachusetts N-Doped Graphene Oxide and Transition Institute of Technology) Metal Doped MnO with Enhanced 2 09:30 501 Efect of Adscititious Water on the Bifunctional Activity for Zinc Air Battery Mechanism of Mg2+ Intercalation in Tungsten Applications – A buy procyclidine visa medications you cant drink alcohol. Halder (Indian Oxides from Non-Aqueous Electrolytes – Institute of Technology Mandi) R purchase procyclidine cheap symptoms renal failure. Augustyn (North Carolina Nanocarbons / Battery / Physical and Analytical Electrochemistry State University) City View 8 buy discount procyclidine online treatment of bronchitis, Dallas Sheraton Hotel 09:40 Break 10:10 502 Origin of Fast Ion Conduction in Li GeP S, Energy Storage 1 – 08:00 – 12:00 10 2 12 a Superionic Conductor – A. Chen (University of Waterloo) Carbonate Electrolyte: Understanding the Role of Sulfur Phase and Solid Electrolyte 08:20 642 Hierarchically Designed 3D-Nanostructures Interphase – R. Struck (Rhine-Waal 10:30 504 the Electrochemistry of Low-Temperature University of Applied Sciences), and S. Saxena Molten Quinones for All-Organic Redox Flow (Indian Institute of Technology Bombay) Batteries – B. Gallaway (Northeastern University) 08:40 643 Polyluminol Modifed Carbon Nanotube Electrodes for Electrochemical Capacitors – 10:40 505 Efects of Particle Sizes of Active J. Lian (University of Toronto) Materials and Conductive Additive on the Electrochemical Performance of a Semi-Solid 09:00 644 (Invited) Fundamental Understanding of Flow Battery – B. Faradaic and Non-Faradaic Processes in Zheng (Zhejiang University) Carbon-Based Supercapacitors – G. Hwang (University of Texas at Austin) 10:50 506 Failure Analysis of the Rechargeable Porous Zinc Electrode in Alkaline Electrolyte – M. Messinger (The City College of New York), and Thomas (NanoScience Technology Center, S. Lu (Argonne National Laboratory) 10:20 647 (Invited) Encapsulating Various Sulfur Allotropes Within Graphene Nanocages for Long-Lasting Lithium Storage – J. Related Materials for Energy-Storage and Jang (Georgia Institute of Technology) Energy-Conversion Applications – S. Dai 11:20 649 (Invited) Holey Graphene Electrode (Oak Ridge National Laboratory) Architectures – Y. Lin (National Institute of 16:40 659 High Performance Supercapacitor Electrode Aerospace) and J. Ferraris (University of Taxas 11:40 650 Biomass Based Porous Carbons As at Dallas), K. Kristianto (University of Taxas at Dallas) (Parahyangan Catholic University), and J. Lee (Korea Institute of Science and Technology) Carbon Nanostructures in Medicine and Biology B02 Nanocarbons / Organic and Biological Electrochemistry / Sensor Energy Technology Division Graduate Student Award Address City View 6, Dallas Sheraton Hotel sponsored by Bio-Logic – 12:00 – 12:20 Chair(s): Jeffrey L. Blackburn Carbon Nanotubes 1 – 08:00 – 09:40 Chair(s): Tatiana DaRos and Januka Budhathoki-Uprety 12:00 651 (Energy Technology Division Graduate Student Award Address sponsored by Bio 08:00 673 Oxygen-Doped Carbon Nanotubes for Near Logic) Biomass-Derived Carbon Materials Infrared Imaging Probes – T. Li 08:20 674 (Invited) Single Luminescent Carbon (University of Virginia) Nanotubes Interrogate the Live Brain Extracellular Space at the Nanoscale – L. Mitlin Functionalized Single-Walled Carbon (Clarkson University) Nanotubes for Optical Sensing – K. Jeon (University of Texas at 15:20 656 Bipolar Electrochemically Exfoliated Arlington), C. Lee (Ulsan National Institute Graphene for Supercapacitor Application of Science and Technology), and K. Rabiei Baboukani (Florida (University of Texas at Arlington) International University), A. Wang (Florida International 10:40 680 (Invited) Step-Wise Molecular Self-Assembly University) on Single-Wall Carbon Nanotube Networks: Towards Development of Delivery Systems 15:40 Break of Highly Potent but Difcult to Administer 16:00 657 Ni Wrapped-Carbon Nanofber Based Anode Drugs – M. Islam (Carnegie Mellon for High Areal Capacity for Li-Ion Battery University) – T. Plateau (Missouri University of Science 11:00 681 (Invited) Targeted Near Infrared Sensing and Technology), S. Budhathoki Nanotube Applications in Biomedicine and Uprety (North Carolina State University) and the Exoneration of Toxicity – D. Jena (Memorial Sloan 11:40 683 Understanding Corona Exchange Dynamics Kettering Cancer Center), G. Landry (Chan (Memorial Sloan Kettering Cancer Center) Zuckerberg Biohub) 12:00 684 Real-Time Near-Infrared Confocal Imaging Nano in Latin America of Bacterial Cell Division in the Presence B04 Nanocarbons / Dielectric Science and Technology / Electronics of Single-Walled Carbon Nanotubes – A. Roxbury (University of 09:20 756 (Invited) Graphitization of Carbon Obtained Rhode Island) from Local Biomass (babassu) and Their 14:20 686 Biomolecular Sensors Based on Electrochemical Properties – A. Terrones (Pennsylvania State System to Quantify Extracellular Nitric University), and B. Corr (Rice Dichalcogenides: Doping, Alloys, Interfaces, University, Baylor College of Medicine), Vacancies and Their Efects in Catalysis & E. Boghossian (École Polytechnique Medical and Electrochemical Applications – Fédérale de Lausanne) E. Chazaro Ruiz (Instituto Potosino de Investigación Cientifca y City View 7, Dallas Sheraton Hotel Tec), J. Rangel Biological Systems – 08:00 – 09:40 Mendez (Instituto Potosino de Investigación Chair(s): Koichiro Ishimori and Muniappan Sankar Científca y Tec), and C. Vik 14:00 764 (Invited) Tuning the Electrocatalytic Activity (Tulane University) of Fe Phthalocyanine Via Axial Ligation 09:00 942 Supramolecular Assemblies Recognized to Multiwalled Carbon Nanotubes and Gastric Cancer Biomarkers in Biological Via Ligand Substitution: Electrochemistry Fluids – R. Zagal 09:20 943 Erythropoietin Accelerates a Cancer Specifc (University of Santiago de Chile) Porphyrins’ Accumulation – H. Porphyrinoid Photo Physics – 10:00 – 12:20 Mendez-Rojas (Fundacion Universidad de las Americas Puebla) Chair(s): Victor V.

Hepatocellular injury with marked increases in transaminases is often accompanied by hypersensitivity features (rash and eosinophilia) order cheap procyclidine treatment lichen sclerosis. Antifungals (see Antifungals) Ketoconazole: this is the most hepatotoxic oral azole antifungal drug order procyclidine 5 mg with mastercard 5 medications, due to buy discount procyclidine online medications routes its extensive metabolism within the liver. Mild asymptomatic and transient elevations (<2 times upper limit of normal) of transaminases have been estimated to occur in up to 20% of patients, with clinically apparent hepatotoxicity incidence in approximately 1 in 2000 and 1 in 15,000 users. The presentation is usually with acute hepatitis any time between 1 and 6 months after starting the drug. Recovery is usual within 3 months of drug discontinuation of the drug, but acute fulminant hepatic failure requiring transplantation has been reported. Biochemically the abnormalities are typically cholestatic but hepatitic or mixed pictures can occur. The severity of liver injury ranges from transient asymptomatic enzyme elevations in the majority to clinically apparent hepatitis and acute fatal liver failure in a very small number of cases. The liver injury is typically hepatocellular, occurs within the frst few weeks of therapy and can be associated with a rash, fever and eosinophilia. With all the azoles, there are little data regarding cross-reactivity and extreme caution should be applied when exposing patients who have had hepatotoxicity to other agents in the same class. In a surveillance study including over 25,000 patients there were only two reports of symptomatic cholestatic liver injury. Mild transient and asymptomatic rises in serum aminotransferase levels are common during the frst 3 months of therapy and resolve rapidly with dose reduction or discontinuation. Baseline and regular assessment of liver function is therefore required throughout treatment. Corticosteroids (see Corticosteroids) Corticosteroids can have major effects on the liver, particularly with long-term or high dose therapy. Corticosteroid therapy can cause steatohepatitis, especially when given in high doses for prolonged periods. Biochemical features include elevated transaminases and liver histology demonstrates steatosis, hepatocyte ballooning and an infammatory infltrate. Dose minimization and alternative drugs should be considered, with monitoring for liver fbrosis in those on long-term treatment. Such patients should be given prophylactic antiviral therapy with lamivudine 100 mg once daily prior to commencing steroids. Dapsone (see Dapsone) Dapsone can cause an acute hepatitis and cholestatic jaundice. The onset is usually sudden and associated with fever and a rash followed by jaundice, and it occurs within a few days or weeks of starting treatment. Methotrexate (see Methotrexate) Short-term low to moderate dose treatment with methotrexate causes mild, self-limiting elevation in the serum transaminases in about 15–50% of patients. About 5% of patients develop more signifcantly elevated liver enzymes that usually normalize rapidly with dose reduction or drug discontinuation. Folic acid supplementation has been shown to be protective against this effect and is routinely prescribed in conjunction with methotrexate. Long-term methotrexate therapy is associated with development of dose dependent hepatic fbrosis and this drug is therefore contraindicated in those with underlying chronic liver disease, apart from in exceptional circumstances. The risk and rate of progression to fbrosis or cirrhosis is increased in patients with a heavy alcohol intake, those with diabetes, obesity, renal failure, age >60 years and concomitant use of other potentially hepatotoxic drugs. These factors are therefore considered to be relative contraindications to methotrexate therapy. Nowadays, a pre-treatment liver biopsy to assess the degree of fbrosis is only recommended in patients who are suspected clinically, biochemically or radiologically to be at risk of, or to have underlying liver disease. If fbrosis is confrmed then methotrexate is best avoided and an alternative therapy considered. A signifcant fbrosis risk is associated with a cumulative dose of methotrexate exceeding 2. Historically, due to the dose dependent development of hepatic fbrosis, guidelines have recommended liver biopsy prior to commencement of therapy and after a cumulative dose of 1, 3 and 8 grams. While liver biopsy remains the gold standard for assessment of fbrosis, it carries a signifcant risk of morbidity and is subject to sampling error. Over the last decade other additional non-invasive methods to assess hepatic fbrosis have become widely available. Transient elastography (FibroScan) is a rapid, immediate, cheap, non-invasive, reproducible and validated test that uses ultrasound to measure liver stiffness gauged in kilopascals (kPa) as a marker of fbrosis. It may help limit the need for biopsies, with the latter being reserved for patients whose score is suggestive of moderate fbrosis. The sensitivity and specifcity of combining these non-invasive markers of fbrosis need to be validated in future studies. However, the majority of the patients were also receiving concomitant corticosteroids (see Corticosteroids). Clinically apparent liver injury due to acitretin is rare, but several cases have been reported. The time of onset is wide, ranging from 1 week to 9 months after commencing therapy. The biochemical profle is typically of raised transaminases but cholestatic hepatitis has been reported and may be accompanied by rash, fever and eosinophilia. Modest increases in serum aminotransferases occur in up to 15% of patients taking isotretinoin, but fewer than 1% of patients have abnormalities greater than three times the upper limit of normal.

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Participants were randomly allocated a test liquid depending on the day of sampling quality 5mg procyclidine medications bipolar. Participants were excluded if they had consumed food or drink cheap 5 mg procyclidine with visa treatment zollinger ellison syndrome, or performed oral hygiene in the previous 2 hours or consumed alcohol in the previous 24 hours purchase procyclidine paypal symptoms 8dpo. Participants were then instructed to rinse 20ml of the selected test liquid vigorously for 30 seconds and expectorate immediately. Salivary samples were collected after 1 and 5 minutes after the expectoration of test liquid. The cotton rolls were centrifuged for 2 minutes at 3000 g in Salivette saliva collection tubes (Sarstedt, Australia Pty Ltd). A 450 µL sample of the clear saliva supernatant was then transferred to a 10 mL headspace vial containing 50 µL of perchloric acid (20% w/w) (Eriksson et al, 1982). The results shown in Table 1 indicate that the analyte concentration detected from the saliva standards is in good correspondence to that with standards made up in deionized water. There are of course limitations to this preliminary study in particular the small sample size with only nine subjects for each test liquid. The negative control group was treated with phosphate buffered saline solution and the positive control group was treated with 650µM H2O2. Recovery time points of 5, 10 and 20 minutes were allowed before trypsinisation and layering onto slides with low-melting point agarose for electrophoresis. Previous research shows that risk associated with alcohol consumption is not necessarily constant over the multistage pathway to oral cancer (Franceschi S 2000) (Franceschi et al. Traditionally, alcohol has been thought to play a role in the later stages of oral cancer progression (Day & Brown, 1980), a view supported by our results. However newer studies are finding that drinking may exert earlier effects, as cessation does not lower oral cancer risk for up to 9 years (Franceschi S 2000) Temporal mechanisms of alcohol carcinogenicity may be more complex and multifactorial than previously thought. Thus, it would appear that the effect of alcohol consumption on oral epithelial cells is likely to be local, topical and temporally important in oral carcinogenesis. Further, a questionnaire about sexual behaviour, oral hygiene and smoking was collected. The self-collected flocked throat and mouth swab was positive in 33 of the 74 (44. Oral rinse method of sample collection was nearly twice as sensitive as self-collected swab. Significant risk factors included smoking, age greater than 40 and lifetime oral sex partners greater that 100. It could be postulated that there is synergism of these risk factors, particularly if alcohol consumption was also included. There is therefore a need for the development and clinical validation of a simple salivary method for the assessment of risk of developing oral cancer that is not associated with smoking as this is likely to enhance the effectiveness of oral cancer screening services and improving oral cancer outcomes. Novel biomarkers Currently the gold standard in diagnosis of malignant and potentially malignant oral mucosal lesions is incisional biopsy and histo-pathological assessment. However, histopathological examination has concerns related to sampling errors and errors in interpretation, and lacks sensitivity to determine lesion progression. Hence, there is a need for a more accurate system to predict the progression to cancer and currently there is significant work being undertaken in identifying markers in patients with oral cancer and pre-cancer that may serve as a valuable resource in finding markers for the early diagnosis of these conditions. Interestingly, the results of these studies have been varied with some reporting guarded success at predicting outcome of malignant transformation (Torres Rendon and et al. These nuclei were extracted, processed to form a monolayer on glass slides and, after Feulgen staining, individual nuclei selected for integrated optical density analysis. These researchers also reported that the specimens showed cells from two populations, superficial and intermediate cells with only six (4%) of specimens containing parabasal or basal cells (Kujan and et al. This latter finding has significant impact as these superficial cells represent keratinocytes that are terminally differentiating and thus nuclei have become non-functional with condensed and fragmented chromatin. This study found that there was more variabilitiy observed in patients with normal mucosa than in oral mucosal dysplasia and neoplasia. An attempt to circumvent this tissue-sampling problem has been reported by obtained representative tissue specimens by scraping with a dermatological curette (Navone R 2008), thus producing “micro-biopsies” rather than cytological samples from brushing mucosa. Such a technique, which included liquid cytology for tissue handling, has been reported to the Changing Aetiology of Oral Cancer and the Role of Novel Biomarkers to Aid in Early Diagnosis 137 be a non-invasive, rapid method that has little patient discomfort and is able to sample a broader area than a single biopsy (Navone R 2008). Ideally, the analyses of the cells collected would include multiple markers, not only assessing the presence of basal cells in the sample, but also the extent of a number of genetic changes known to be linked to the development of oral neoplasia. Such markers may well include the recently reported centrosomal abnormalities reportedly to occur universally in oral dysplasia. Thus, there still remains the need for a robust method to assess molecular changes known to be associated with the early changes in neogenesis to aid in the early detection of oral mucosal lesions with increased malignant potential. Lip lesions exhibited G:C to A:T transitions while intra-oral lesions exhibited an equal frequency of transitions and transversions (G:C to T:A) (Ostwald C, Gogacz P et al. It has been proposed that these transversions are preferentially induced by breakdown products of benz[a]pyrenes, suggesting a strong correlation with tobacco usage (Ostwald C, Gogacz P et al. This polymorphism results in an amino acid substitution from Isoleucine to Valine. Normal Cell Oncogenic miRs Tumour Suppressor miRs Tumour Suppressor Oncogenic Protein Proteins Cancer Cell Fig. There is thus a potential rich source of retrospective information available for comparative genomics and investigation of potential biomarkers that is likely to provide biological insights far more expeditiously than the prospective collection of frozen samples. Over the last 5 years or so, a considerable effort has been undertaken analysing the salivary proteome. There has been a very large number of non-redundant proteins recognised in saliva with one study (Scarano E 2010) reporting over 1400, while a further (Xiao H 2011) almost 2,000, reflecting the potency of salivary biomarker profiles in the identification and management of a range of diseases (Bandhakavi S 2009). Salivary biomarkers have the potential to serve as non-invasive, widely available screening tools that do not rely on the localization of a lesion for diagnosis. This advantage over other detection methods gives salivary biomarker screening the potential to identify patients with premalignant lesions.

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Proleukin should be used during pregnancy only if the potential benefit justifies the potential risk to buy cheapest procyclidine and procyclidine treatment 0 rapid linear progression the fetus order procyclidine with a mastercard medications given during labor. Because many drugs are excreted in human milk and because of the potential for serious adverse reactions in nursing infants from Proleukin buy discount procyclidine online symptoms 7 days post iui, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the importance of the drug to the mother. Pediatric Use Safety and effectiveness in children under 18 years of age have not been established. Geriatric Use There were a small number of patients aged 65 and over in clinical trials of Proleukin; experience is limited to 27 patients, eight with metastatic melanoma and nineteen with metastatic renal cell carcinoma. The response rates were similar in patients 65 years and over as compared to those less than 65 years of age. The median number of courses and the median number of doses per course were similar between older and younger patients. Proleukin is known to be substantially excreted by the kidney, and the risk of toxic reactions to this drug may be greater in patients with impaired renal function. The pattern of organ system toxicity and the proportion of patients with severe toxicities by organ system were generally similar in patients 65 and older and younger patients. There was a trend, however, towards an increased incidence of severe urogenital toxicities and dyspnea in the older patients. In an additional population of greater than 1,800 patients treated with Proleukin-based regimens using a variety of doses and schedules. In the same clinical population, the following fatal events each occurred with a frequency of <1%: malignant hyperthermia; cardiac arrest; myocardial infarction; pulmonary emboli; stroke; intestinal perforation; liver or renal failure; severe depression leading to suicide; pulmonary edema; respiratory arrest; respiratory failure. Most adverse reactions are self-limiting and, usually, but not invariably, reverse or improve within 2 or 3 days of discontinuation of therapy. Examples of adverse reactions with permanent sequelae include: myocardial infarction, bowel perforation/infarction, and gangrene. In a separate study, the effect of immunogenicity on the pharmacokinetics of aldesleukin was evaluated in 13 patients. Immunogenicity assay results are highly dependent on several factors including assay sensitivity and specificity, assay methodology, sample handling, timing of sample collection, concomitant medications, and underlying disease. Post Marketing Experience the following adverse reactions have been identified during post-approval use of Proleukin. Persistent but nonprogressive vitiligo has been observed in malignant melanoma patients treated with interleukin-2. Synergistic, additive and novel toxicities have been reported with Proleukin used in combination with other drugs. Generally these medications were discontinued 12 hours after the last dose of Proleukin. Patients with indwelling central lines have a higher risk of infection with gram positive 9-11 organisms. A reduced incidence of staphylococcal infections in Proleukin studies has been associated with the use of antibiotic prophylaxis which includes the use of oxacillin, nafcillin, ciprofloxacin, or vancomycin. Hydroxyzine or diphenhydramine has been used to control symptoms from pruritic rashes and continued until resolution of pruritus. Exceeding the recommended dose has been associated with a more rapid onset of expected dose-limiting toxicities. Symptoms which persist after cessation of Proleukin should be monitored and treated supportively. Life-threatening toxicities may be ameliorated by the intravenous administration of dexamethasone, which may also result in loss of the 12 therapeutic effects of Proleukin. Each course of treatment consists of two 5-day treatment cycles separated by a rest period. Following 9 days of rest, the schedule is repeated for another 14 doses, for a maximum of 28 doses per course, as tolerated. Metastatic melanoma patients received a median of 18 doses during the first course of therapy. Retreatment Patients should be evaluated for response approximately 4 weeks after completion of a course of therapy and again immediately prior to the scheduled start of the next treatment course. Each treatment course should be separated by a rest period of at least 7 weeks from the date of hospital discharge. Dose Modifications Dose modification for toxicity should be accomplished by withholding or interrupting a dose rather than reducing the dose to be given. Decisions to stop, hold, or restart Proleukin therapy must be made after a global assessment of the patient. A new course of treatment, if warranted, should be initiated no sooner than 7 weeks after cessation of adverse event and hospital discharge. Reconstitution and Dilution Directions: Reconstitution and dilution procedures other than those recommended may alter the delivery and/or pharmacology of Proleukin and thus should be avoided. Dilution and delivery of Proleukin outside of this concentration range should be avoided. Glass bottles and plastic (polyvinyl chloride) bags have been used in clinical trials with comparable results. It is recommended that plastic bags be used as the dilution container since experimental studies suggest that use of plastic containers results in more consistent drug delivery. Before and after reconstitution and dilution, store in a refrigerator at 2° to 8°C (36° to 46°F). The solution should be brought to room temperature prior to infusion in the patient. Parenteral drug products should be inspected visually for particulate matter and discoloration prior to administration, whenever solution and container permit. Reconstituted or diluted Proleukin is stable for up to 48 hours at refrigerated and room temperatures, 2° to 25°C (36° to 77°F).

However order procyclidine 5 mg overnight delivery medicinebg, neutrophils are usually not in close proximity to order procyclidine pills in toronto medicine for nausea where sensitization may occur cheap 5 mg procyclidine fast delivery treatment integrity checklist. The list of chemicals dealt with is not comprehensive, nor are the individual examples all exhaus tively described. The rationale behind selection of the examples is to show the range of agents that are potentially associated with auto immunity, debates that have been going on for certain agents. Although the emphasis is on environmental chemicals, some drugs are exemplified to further address and in fact illustrate the potential autoimmune effects of environmental agents. In less than two years, at least 20 096 people were afflicted by and 356 people died from toxic oil syndrome (Philen et al. Women, especially those less than 40 years of age, were affected more severely than men; 61% of the victims and 66% of the deaths were women (Sanchez-Porro Valades et al. Toxic oil syndrome has strik ing similarities to autoimmune diseases, particularly scleroderma. In addition, it resembles eosinophilia myalgia syndrome and diffuse fasciitis with eosinophilia. Toxic oil syndrome-associated manifes tations evolved from initiating vasculitis to eosinophilia in the acute phase and then sicca syndrome, neuropathy, scleroderma, Raynaud phenomenon, and musculoskeletal inflammation in the chronic phase (Kaufman & Krupp, 1995). More than 70% of toxic oil syndrome patients presented with eosinophilia, regardless of age or sex. Chemical analysis of the case-associated oil identified brassicasterol, a marker for rapeseed oil, trace amounts of aniline, oleyl anilide, and other fatty acid anilides and contaminants (Aldridge, 1992; Posada de la Paz et al. The toxin or toxins appear to be stable in oil, since consumption of toxic oil one year after the main epidemic led to development of the disease. Subjective estimates suggest that the degree of illness varied proportionately with the amount and frequency of intake; however, this has not been validated. The initial event is believed to be a form of vasculitis, a non-necrotizing endo thelial damage in vessels of multiple organs. In the acute phase (0–2 months), patients exhibited endothelial lesions (endovasculitis), eosinophilia, pulmonary infiltrates and oedema, pneumopathy, myal gias, fever, rash, and high IgE levels (Hard, 2000; Gelpi et al. Aniline was detected in pleural effusion in approximately 50% of the victims (Tabuenca, 1981). Approx imately 60% of the patients progressed to the intermediate phase (2– 4 months), characterized by myalgias, eosinophilia, cachexia, liver disease, dermal infiltration/oedema, pulmonary hypertension, sicca syndrome, and hypertriglyceridaemia. The primary causes of toxic oil syndrome-related death in this phase were thromboembolism and pulmonary hypertension. Finally, 10–15% of the original toxic oil syndrome cohort have been estimated to progress to the chronic phase (Weatherill et al. In the early stage of the chronic phase (4 months to 2 years), patients developed sicca syndrome, neuropathy, liver disease, scleroderma, and pulmonary hypertension, and then (>2 years) musculoskeletal pain, lung disease, carpal tunnel syndrome, Raynaud phenomenon, and hyperlipidaemia were com mon. The primary causes of toxic oil syndrome-related death in the 108 Chemical/Physical Agents and Autoimmunity chronic phase were respiratory failure, central nervous system infection, and pulmonary hypertension. While a number of treat ments were tested, none successfully controlled the disease, although corticosteroids and diphenylhydantoin did ameliorate some of the symptoms (Gomez de la Camara et al. The initial chemical analyses identified oleyl anilide as the primary contaminant and marker for case-associated oils, but the number of anilides and unidentified contaminants suggested that other compounds may also be involved (Posada de la Paz et al. No common refinery products, additives, or contaminants were known to induce symptoms and pathological findings consistent with toxic oil syndrome (Hard, 2002). The oleyl anilide and propanediols were formed by the reaction of aniline with the oleyl side-chain of fatty acids that are abundant in rapeseed oil. Inconsistencies may reflect differences in the stage of the disease at the time of testing. Poly morphism of this enzyme determines whether acetylation proceeds at a fast or slow rate. Toxic oil syndrome was suggested to be lethal in the acute phase via Th1 mechanisms involving slow acetylation; in the chronic phase, Th2 mechanisms associated with fast acetylation led to autoimmune disease (Cardaba et al. There was an increase in variant alleles of arylamine N-acetyltransferase-2 in 73 toxic oil syndrome patients (Ladona et al. Different expression of haptoglobin Į (Hp) isoforms was observed in toxic oil syndrome patients compared with controls; the most frequent phenotype in controls was Hp2-2, and the most frequent phenotypes in toxic oil syndrome patients were Hp2-1s and Hp1-1s. The haptoglobin protein binds free haemoglobin during hepatic recyling of iron, acts as an antioxidant, has antibacterial activity, and is involved in the acute-phase immune response. The Hp2 allele has been reported to have greater immune reactivity than the Hp1 allele (Quero et al. Possible explanations for the generally negative results in animal models are that toxic oil syndrome may be a uniquely human disease, animals may have a lower sensitivity to toxic oils, the dose used may not have been adequate, and multiple agents, genetic factors, and biochemical alterations may be involved in disease development. Since many autoimmune diseases require both genetic suscep tibility and an environmental trigger, mice genetically prone to developing autoimmune disease have been employed in toxic oil syndrome research. Serum IgE levels were reduced and serum autoantibodies increased by all three experimental oils compared with levels in naive mice. However, due to many positive responses in mice treated with the canola oil control, this model is generally con sidered to be unsuitable for the study of toxic oil syndrome (Koller et al. Body and organ weights, autoantibody titres, and IgG1, IgG2, and IgE serum levels were unaffected by treatment with case-associated and reconstituted oils (Weatherill et al. Oleyl and linoleyl anilides were found to be toxic to the rat lung (Tena, 1982), and anilides induced elevated IgE levels and T cells in mice (Lahoz et al.


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