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We compare these effects based on the experience in Iranian veterans exposed to the agent during the Iran‐Iraq conflict (1983–88). The first clinical manifestations of sulfur mustard poisoning occurred in the eyes with a sensation of grittiness, lacrimation, photophobia, blepharospasm, and corneal ulceration. Respiratory effects appeared as rhinorhea, laryngitis, tracheobronchitis, and dyspnoea. Skin lesions varied from erythema to bullous necrotization. Initial leukocytosis and lymphopenia returned to normal within four weeks in recovered patients, but marked cytopenia with bone marrow failure occurred in fatal cases. Late toxic effects of sulfur mustard were most commonly found in lungs, skin and eyes. Main respiratory complications were chronic obstructive pulmonary disease, bronchiectasis, asthma, large airway narrowing, and pulmonary fibrosis. Late skin lesions were hyperpigmentation, dry skin, atrophy, and hypopigmentation. Fifteen of the severely intoxicated patients were diagnosed with delayed keratitis, having corneal vascularization, thinning, and epithelial defect. Respiratory complications exacerbated over time, while cutaneous and ocular lesions decreased or remained constant. Both the severity and frequency of bronchiectatic lesions increased during long‐term follow‐up. The only deteriorating cutaneous complication was dry skin. The maximum incidence of delayed kaeratitis was observed 15 to 20 years after initial exposure. Being suggested as the main cause ofassociated with malignancies and recurrent infections, natural killer cells were significantly lower 16 to 20 years after intoxication.\u003C\u002Fjats:p>",{"EN":134},"Comparison of Early and Late Toxic Effects of Sulfur Mustard in Iranian Veterans",{"VOID":136},"17040211",{"VOID":138},"10.1111\u002Fj.1742-7843.2006.pto_429.x","PUBLICATION","VERIFIED","Auto Verify",[143],"EN","https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1111\u002Fj.1742-7843.2006.pto_429.x",[146,167],{"id":147,"sortIndex":25,"researcher":24,"roles":148,"affiliations":149,"properties":160},"377bebfb-b25e-4226-985e-1a3bec5e24f3",[],[150],{"id":151,"sortIndex":25,"affiliation":152,"properties":24},"c63995e6-c0da-4bdd-a64a-a734e46577d9",{"id":153,"createTime":154,"updateTime":154,"relativeEntities":155,"slug":156,"properties":157,"entityType":60,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"syncStatus":23,"languages":24,"translateLanguages":24,"viewCount":25},"98341a37-9018-4f35-9e4c-11f76542ecc1","2024-09-28T21:35:42.205+00:00",[],"Medical-Toxicology-Center-Imam-Reza-Hospital-Mashhad-University-of-Medical-Sciences-Mashhad-Iran",{"title":158},{"EN":159},"Medical Toxicology Center, Imam Reza Hospital, Mashhad University of Medical Sciences, Mashhad, Iran",{"openalex":161,"orcid":163,"title":165},{"VOID":162},"A5086109376",{"VOID":164},"https:\u002F\u002Forcid.org\u002F0000-0003-2543-7420",{"EN":166},"Mahdi Balali‐Mood",{"id":168,"sortIndex":169,"researcher":24,"roles":170,"affiliations":171,"properties":178},"bf645a61-f8b8-4822-b05c-b4a4a15589a4",1,[],[172],{"id":173,"sortIndex":25,"affiliation":174,"properties":24},"05655c50-354c-4a92-9299-02fb9c6c9887",{"id":153,"createTime":154,"updateTime":154,"relativeEntities":175,"slug":156,"properties":176,"entityType":60,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"syncStatus":23,"languages":24,"translateLanguages":24,"viewCount":25},[],{"title":177},{"EN":159},{"openalex":179,"orcid":181,"title":183},{"VOID":180},"A5067492340",{"VOID":182},"https:\u002F\u002Forcid.org\u002F0000-0001-8860-3380",{"EN":184},"Mehrdad Hefazi","ARTICLE",{"url":24,"publisher":187,"properties":212},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":188,"slug":10,"properties":189,"entityType":22,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"syncStatus":23,"languages":24,"translateLanguages":24,"viewCount":25,"subjectFields":195,"manageAffiliations":196,"indexDatabases":197,"url":115,"thumbnailPath":24,"statistic":24,"gsStatistic":24,"type":24,"analyzePriority":24},[],{"country":190,"issn":191,"introduce":192,"eissn":193,"title":194},{"VOID":13},{"VOID":15},{"EN":17},{"VOID":19},{"EN":21},[],[],[198,205],{"id":75,"indexDatabase":199,"url":88,"indexYears":89,"academicFieldIds":204,"indexDatabaseRanking":94},{"id":77,"createTime":78,"updateTime":79,"relativeEntities":200,"label":201,"description":202,"key":85,"publicationTags":203,"standard":24},[],{"EN":82,"VI":82},{"EN":82,"VI":84},[87],[91,92,93],{"id":96,"indexDatabase":206,"url":111,"indexYears":24,"academicFieldIds":211,"indexDatabaseRanking":24},{"id":98,"createTime":99,"updateTime":100,"relativeEntities":207,"label":208,"description":209,"key":107,"publicationTags":210,"standard":24},[],{"EN":103,"VI":103},{"VI":105,"EN":106},[109,110],[113,114],{"volume":213,"pages":215,"issue":217},{"VOID":214},"99",{"VOID":216},"273-282",{"VOID":218},"4",324,{"total":219,"publishYear":24,"statisticByYear":221},{"2012":222,"2013":223,"2014":224,"2015":225,"2016":223,"2017":226,"2018":227,"2019":223,"2020":228,"2021":222,"2022":229,"2023":230,"2024":71},20,16,21,34,18,19,25,14,11,"2006-10-01",2006,[234,237,240,243,246,249,252,255,258,261,264,267,270,273,276,279,282,285,288,291,294,298,301,304,307,310,313,316,319,322,325,328,331,334,337,340,343,346,349,352,355,358,361,364,367,370,373,376,379,382,385,388,391,395,398,401,404,407,410,413,416,419,422,425,428,431,434,437,440,444,447,450,453,456,459,462,465],{"id":24,"text":235,"url":24,"identifiers":236},"Afshinniaz F., 1996, Relationship of the chronic respiratory symptoms with spirometric and laboratory parameters",{},{"id":24,"text":238,"url":24,"identifiers":239},"10.1152\u002Fajplung.00169.2003",{"doi":238},{"id":24,"text":241,"url":24,"identifiers":242},"Alexander S. 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Z., 1992, Skin manifestations of mustard gsa. A clinical study of 535 patients eposed to mustard gas, Arch. Dermatol., 128, 575, 10.1001\u002Farchderm.1992.01680160059004",{"doi":394},"10.1001\u002Farchderm.1992.01680160059004",{"id":24,"text":396,"url":24,"identifiers":397},"Moradi A.&S.Aghaei:Erupted cherry angioma secondary to exposure to mustard gas. In: Proceedings of the 7th international congress of dermatology.Iranian Society of Dermatology Tehran Iran 2004 .",{},{"id":24,"text":399,"url":24,"identifiers":400},"10.1136\u002Fbmj.302.6769.129",{"doi":399},{"id":24,"text":402,"url":24,"identifiers":403},"Nishimoto Y., 1987, Epidemiological studies of lung cancer in Japanese mustard gas workers, Princess Takamatsu. Symp., 18, 95",{},{"id":24,"text":405,"url":24,"identifiers":406},"Papirmeister B., 1991, Medical defense against mustard gas: Toxic mechanisms and pharmacological implications",{},{"id":24,"text":408,"url":24,"identifiers":409},"10.1016\u002FS0002-9394(19)90351-5",{"doi":408},{"id":24,"text":411,"url":24,"identifiers":412},"10.1042\u002Fbj0410185",{"doi":411},{"id":24,"text":414,"url":24,"identifiers":415},"10.1016\u002FS0002-9394(99)00178-6",{"doi":414},{"id":24,"text":417,"url":24,"identifiers":418},"Razavi S. M. M.Mahmoudi A.Keyhani M. B.Eslami&B.Eftekhar:Study of some components of complement system in Iranian combatants poisoned with mustard gas. In:Abstracts of the first international medical congress on chemical warfare agents in Iran.Mashhad University of Medical Sciences Mashhad Iran 1988 .",{},{"id":24,"text":420,"url":24,"identifiers":421},"Renshaw B., 1946, Division 9, National Defense Research Committee, Comp. Chemical Warfare Agents, and Related Chemical Problems. 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Therap., 13, 1",{},{"id":24,"text":441,"url":24,"identifiers":442},"Smith W. J., 1991, Medical defense against blistering chemical warfe agents, Arch. Dermatol., 127, 1207, 10.1001\u002Farchderm.1991.01680070107017",{"doi":443},"10.1001\u002Farchderm.1991.01680070107017",{"id":24,"text":445,"url":24,"identifiers":446},"10.1016\u002FS0039-6257(97)00021-0",{"doi":445},{"id":24,"text":448,"url":24,"identifiers":449},"Tabarestani M. M.Farhoudi&M.Balali:Stem cell and erythroid precursors disorders in three patients with sulfur mustard poisoning. In:Abstracts of the first international medical congress on chemical warfare agents in Iran.Mashhad University of Medical Sciences Mashhad Iran 1988 .",{},{"id":24,"text":451,"url":24,"identifiers":452},"United Nations Security Council, 1988, Report of the mission dispatched by the Secretary General to investigate allegations of the use of chemical weapons in the conflict between the Islamic Republic of Iran and Iraq. 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E‐cigarettes have rapidly gained in popularity in recent years amongst both existing smokers and previous non‐smokers. However, a growing literature demonstrates that E‐cigarettes are not as safe as generally believed. Here, we discuss the immunological, and other, deleterious effects of E‐cigarettes on a variety of cell types and host defence mechanisms in humans and in murine models. We review not only the effects of complete E‐cigarette liquids, but also each of the main components—nicotine, humectants and flavourings. 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Mizoribine, an immunosuppressive anti‐metabolite, is largely excreted into urine in its unchanged form, and its pharmacokinetics has been considered to be dependent on the glomerular filtration rate. However, the pharmacokinetic disposition of mizoribine has not been fully clarified. The aim of this study was to evaluate the pharmacokinetic disposition of mizoribine based on polymorphism of concentrative nucleoside transporter (CNT) 1 gene in kidney transplant recipients. Thirty‐four Japanese stable recipients receiving an immunosuppressive regimen containing mizoribine for more than four months after transplantation were enrolled. Each recipient had been receiving a fixed dose of mizoribine for at least one month before enrolment. Oral bioavailability of mizoribine was obtained by dividing its amount in 24‐hr urine by the daily dose. The median and interquartile range of the dose‐normalized plasma concentration of mizoribine at 12 hr (\u003Cjats:italic>C\u003C\u002Fjats:italic>\u003Cjats:sub>12\u003C\u002Fjats:sub>) were 6.11 and 3.47–10.9 ng\u002Fml per mg, respectively. The median bioavailability of mizoribine was 44.8%, and interindividual variability was also observed (interquartile range, 37.8–61.5%). The correlation coefficient between creatinine clearance and substitute renal clearance (CL\u003Cjats:sub>MZ\u003C\u002Fjats:sub>) estimated from the mizoribine \u003Cjats:italic>C\u003C\u002Fjats:italic>\u003Cjats:sub>12\u003C\u002Fjats:sub> was 0.65. The \u003Cjats:italic>CNT1 G565A\u003C\u002Fjats:italic> allele frequency was 51.5%. The mizoribine bioavailability was significantly lower in \u003Cjats:italic>565GA\u003C\u002Fjats:italic> and \u003Cjats:italic>AA\u003C\u002Fjats:italic> than that in \u003Cjats:italic>GG\u003C\u002Fjats:italic> (median, 42.0%, 41.4% and 62.4%, respectively). No significant differences were observed in the dose‐normalized \u003Cjats:italic>C\u003C\u002Fjats:italic>\u003Cjats:sub>12\u003C\u002Fjats:sub> of mizoribine and substitute CL\u003Cjats:sub>MZ\u003C\u002Fjats:sub> between the \u003Cjats:italic>G565A\u003C\u002Fjats:italic> genotypes. The mizoribine bioavailability was affected by \u003Cjats:italic>CNT1 G565A\u003C\u002Fjats:italic> in kidney transplant recipients. \u003Cjats:italic>CNT1 G565A\u003C\u002Fjats:italic> would contribute to interindividual differences in plasma disposition of mizoribine.\u003C\u002Fjats:p>",{"EN":935},"Impact of Concentrative Nucleoside Transporter 1 Gene Polymorphism on Oral Bioavailability of Mizoribine in Stable Kidney Transplant 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play a central role in inflammation through their direct interaction with other cell types, such as leucocytes and endothelial cells, and by the release of many factors, that is, lipids [such as thromboxane (\u003Cjats:styled-content style=\"fixed-case\">TX\u003C\u002Fjats:styled-content>)\u003Cjats:styled-content style=\"fixed-case\">A\u003C\u002Fjats:styled-content>\u003Cjats:sub>2\u003C\u002Fjats:sub>] and proteins (a wide number of angiogenic and growth factors) stored in α‐granules, and adenosine diphosphate (\u003Cjats:styled-content style=\"fixed-case\">ADP\u003C\u002Fjats:styled-content>), stored in dense granules. These platelet actions trigger autocrine and paracrine activation processes that lead to leucocyte recruitment into different tissues and phenotypic changes in stromal cells which contribute to the development of different disease states, such as atherosclerosis and atherothrombosis, intestinal inflammation and cancer. The signals induced by platelets may cause pro‐inflammatory and malignant phenotypes in other cells through the persistent induction of aberrant expression of cyclooxygenase (\u003Cjats:styled-content style=\"fixed-case\">COX\u003C\u002Fjats:styled-content>)‐2 and increased generation of prostanoids, mainly prostaglandin (\u003Cjats:styled-content style=\"fixed-case\">PG\u003C\u002Fjats:styled-content>)\u003Cjats:styled-content style=\"fixed-case\">E\u003C\u002Fjats:styled-content>\u003Cjats:sub>2\u003C\u002Fjats:sub>. In addition to cardiovascular disease, enhanced platelet activation has been detected in inflammatory disease and intestinal tumourigenesis. Moreover, the results of clinical studies have shown that the antiplatelet drug aspirin reduces the incidence of vascular events and colorectal cancer. All these pieces of evidence support the notion that colorectal cancer and atherothrombosis may share a common mechanism of disease, that is, platelet activation in response to epithelial (in tumourigenesis) and endothelial (in tumourigenesis and atherothrombosis) injury. Extensive translational medicine research is necessary to obtain a definitive mechanistic demonstration of the platelet‐mediated hypothesis of colon tumourigenesis. The results of these studies will be fundamental to support the clinical decision to recommend the use of low‐dose aspirin, and possibly other antiplatelet agents, in primary prevention, that is, even for individuals at low cardiovascular risk.\u003C\u002Fjats:p>",{"EN":1225},"Role of Platelets in Inflammation and Cancer: Novel Therapeutic 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Substantial development in the pharmacological treatment for attention‐deficit hyperactivity disorder (ADHD) has been made recently including approval of new non‐stimulant agents targeting noradrenergic, histaminergic and dopaminergic systems. Among such, atomoxetine has been widely used, although its mechanism of action is poorly understood. It is known that central nervous system histamine is closely associated with cognition and it was recently shown that both atomoxetine and methylphenidate enhance cortical histamine release in rats. To that end, the aim of our study was to investigate the effect of atomoxetine (2 mg\u002Fkg, intraperitoneally) on histamine release using the microdialysis technique in the spontaneously hypertensive rat (SHR), a suitable genetic model for ADHD. Our data confirmed that atomoxetine increases extracellular levels of histamine in the prefrontal cortex, a brain region that is implicated in the pathophysiology of ADHD. Given the tie between histamine neurotransmission and treatment of cognitive dysfunction, we also assessed the effects of atomoxetine on learning and memory as measured by the Morris water maze in SHR. The results indicated that atomoxetine significantly ameliorated performance in the Morris water maze, consistent with its histamine‐enhancing profile. In conclusion, the current study provides further support for the notion that the therapeutic effect of atomoxetine could involve activation of histamine neurotransmission within the prefrontal cortex.\u003C\u002Fjats:p>",{"EN":1632},"Atomoxetine Increases Histamine Release and Improves Learning Deficits in an Animal Model of Attention‐Deficit Hyperactivity Disorder: The Spontaneously Hypertensive 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The purpose of this study was to evaluate the role of sequence variants in the CYP2C8, ABCB1 and CYP3A4 genes and the CYP3A4 phenotype for the pharmacokinetics and toxicity of paclitaxel in ovarian cancer patients. Thirty‐eight patients were treated with paclitaxel and carboplatin. The genotypes of CYP2C8*1B, *1C, *2, *3, *4, *5, *6, *7, *8 and P404A, ABCB1 G2677T\u002FA and C3435T, as well as CYP3A4*1B, were determined by pyrosequencing. Phenotyping of CYP3A4 was performed \u003Cjats:italic>in vivo\u003C\u002Fjats:italic> with quinine as a probe. The patients were monitored for toxicity and 23 patients underwent a more extensive neurotoxicity evaluation. Patients heterozygous for G\u002FA in position 2677 in ABCB1 had a significantly higher clearance of paclitaxel than most other ABCB1 variants. A lower clearance of paclitaxel was found for patients heterozygous for CYP2C8*3 when stratified according to the ABCB1 G2677T\u002FA genotype. In addition, the CYP3A4 enzyme activity \u003Cjats:italic>in vivo\u003C\u002Fjats:italic> affected which metabolic pathway was dominant in each patient, but not the total clearance of paclitaxel. The exposure to paclitaxel correlated to the degree of neurotoxicity. Our findings suggest that interindividual variability in paclitaxel pharmacokinetics might be predicted by ABCB1 and CYP2C8 genotypes and provide useful information for individualized chemotherapy.\u003C\u002Fjats:p>",{"EN":1940},"Pharmacogenetic Studies of Paclitaxel in the Treatment of Ovarian 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Maximizing the likelihood of success in Phase III is the ultimate goal of the use of modelling and simulation in the drug development process. The success in Phase III depends primarily on two questions: 1) Is the drug regimen actually efficacious and safe in the targeted patient population?, and 2) Will the planned Phase III clinical trial(s) be successful in demonstrating this? Traditionally, the first question is addressed in a qualitative, overall interpretation of available study results. Integrating this information into a formal statistical model of the action of the drug, allows running simulations to investigate the impact of uncertainties and imprecision in this knowledge. The second question is related to having an adequately designed clinical trial. Clinical trial simulation, using a drug action model, supplemented with appropriate models for disease progression and trial execution, allows assessing the impact of typical design features such as doses, sample size, in‐\u002Fexclusion criteria, drop‐out and trial duration on the trial outcome and thus optimising trial design. In this contribution, the use of modelling and simulation in the Phase II to Phase III transition is illustrated using real data of a drug for symptom relief in a chronic condition. A dose‐response model of the clinical response was developed using data from Phase II. Simulations were performed to 1) generate the range of possible outcomes of ongoing Phase III trials and compare these to the blinded data being generated from these trials; 2) assess the robustness of the ongoing Phase III trials with respect to uncertainty of the true dose‐response, patient variability in baseline severity and drug‐response, and 3) assess the likelihood of achieving a clinically relevant response with a dose lower than those included in the trials.\u003C\u002Fjats:p>",{"EN":2291},"Predicting the Outcome of Phase III Trials using Phase II Data: A Case Study of Clinical Trial Simulation in Late Stage Drug Development",{"VOID":2293},"15733220",{"VOID":2295},"10.1111\u002Fj.1742-7843.2005.pto960314.x",[143],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1111\u002Fj.1742-7843.2005.pto960314.x",[2299],{"id":2300,"sortIndex":25,"researcher":24,"roles":2301,"affiliations":2302,"properties":2313},"e8a4ae3c-3d18-400a-9d99-a2a95f43ae45",[],[2303],{"id":2304,"sortIndex":25,"affiliation":2305,"properties":24},"e90c243d-78bd-4042-b131-8fdac7b54afa",{"id":2306,"createTime":2307,"updateTime":2307,"relativeEntities":2308,"slug":2309,"properties":2310,"entityType":60,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"syncStatus":23,"languages":24,"translateLanguages":24,"viewCount":25},"9149df90-5e04-4404-87ad-ab415f6fa10b","2024-09-29T20:01:28.301+00:00",[],"Biometrics-Clinical-Informatics-Johnson-Johnson-Pharmaceutical-Research-and-Development-a-division-of-Janssen-Pharmaceutica-n-v-B-2340-Beerse-Belgium",{"title":2311},{"EN":2312},"Biometrics & Clinical Informatics, Johnson & Johnson Pharmaceutical Research and Development (a division of Janssen Pharmaceutica n.v.), B-2340 Beerse, Belgium",{"openalex":2314,"title":2316},{"VOID":2315},"A5038389080",{"EN":2317},"Filip De Ridder",{"url":24,"publisher":2319,"properties":2344},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":2320,"slug":10,"properties":2321,"entityType":22,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"syncStatus":23,"languages":24,"translateLanguages":24,"viewCount":25,"subjectFields":2327,"manageAffiliations":2328,"indexDatabases":2329,"url":115,"thumbnailPath":24,"statistic":24,"gsStatistic":24,"type":24,"analyzePriority":24},[],{"country":2322,"issn":2323,"introduce":2324,"eissn":2325,"title":2326},{"VOID":13},{"VOID":15},{"EN":17},{"VOID":19},{"EN":21},[],[],[2330,2337],{"id":75,"indexDatabase":2331,"url":88,"indexYears":89,"academicFieldIds":2336,"indexDatabaseRanking":94},{"id":77,"createTime":78,"updateTime":79,"relativeEntities":2332,"label":2333,"description":2334,"key":85,"publicationTags":2335,"standard":24},[],{"EN":82,"VI":82},{"EN":82,"VI":84},[87],[91,92,93],{"id":96,"indexDatabase":2338,"url":111,"indexYears":24,"academicFieldIds":2343,"indexDatabaseRanking":24},{"id":98,"createTime":99,"updateTime":100,"relativeEntities":2339,"label":2340,"description":2341,"key":107,"publicationTags":2342,"standard":24},[],{"EN":103,"VI":103},{"VI":105,"EN":106},[109,110],[113,114],{"volume":2345,"pages":2347,"issue":2349},{"VOID":2346},"96",{"VOID":2348},"235-241",{"VOID":580},37,{"total":2350,"publishYear":24,"statisticByYear":2352},{"2012":169,"2013":493,"2015":493,"2016":169,"2017":169,"2018":493,"2019":169,"2020":583,"2021":493,"2023":493},"2005-03-01",2005,[2356,2359,2362,2365,2368,2371,2374,2377,2380,2383,2386],{"id":24,"text":2357,"url":24,"identifiers":2358},"10.1023\u002FA:1020953107162",{"doi":2357},{"id":24,"text":2360,"url":24,"identifiers":2361},"Goggin T., 2003, Simulation for designing clinical trials, 227",{},{"id":24,"text":2363,"url":24,"identifiers":2364},"Holford N. 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Here, we focus on mechanisms that trigger \u003Cjats:styled-content style=\"fixed-case\">CPM\u003C\u002Fjats:styled-content>‐induced pro‐inflammatory responses. Inflammation has both genotoxic and non‐genotoxic implications and is considered to play a central role in development of various health outcome associated with \u003Cjats:styled-content style=\"fixed-case\">CPM\u003C\u002Fjats:styled-content> exposure, including cancer. Chronic, low‐grade inflammation may cause \u003Cjats:styled-content style=\"fixed-case\">DNA\u003C\u002Fjats:styled-content> damage through a persistent increased level of reactive oxygen species (\u003Cjats:styled-content style=\"fixed-case\">ROS\u003C\u002Fjats:styled-content>) produced and released by activated immune cells. Moreover, a number of pro‐inflammatory cytokines and chemokines display mitogenic, motogenic, morphogenic and\u002For angiogenic properties and may therefore contribute to tumour growth and metastasis. The key triggering events involved in activation of pro‐inflammatory responses by \u003Cjats:styled-content style=\"fixed-case\">CPM\u003C\u002Fjats:styled-content> and soluble \u003Cjats:styled-content style=\"fixed-case\">CPM\u003C\u002Fjats:styled-content> components can be categorized into (i) formation of \u003Cjats:styled-content style=\"fixed-case\">ROS\u003C\u002Fjats:styled-content> and oxidative stress, (ii) interaction with the lipid layer of cellular membranes, (iii) activation of receptors, ion channels and transporters on the cell surface and (iv) interactions with intracellular molecular targets including receptors such as the aryl hydrocarbon receptor (AhR). In particular, we will elucidate the effects of diesel exhaust particles (\u003Cjats:styled-content style=\"fixed-case\">DEP\u003C\u002Fjats:styled-content>) using human lung epithelial cells as a model system.\u003C\u002Fjats:p>",{"EN":2403},"Triggering Mechanisms and Inflammatory Effects of Combustion Exhaust Particles with Implication for Carcinogenesis",{"VOID":2405},"28001342",{"VOID":2407},"10.1111\u002Fbcpt.12746",[143],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1111\u002Fbcpt.12746",[2411,2430,2445,2462,2479,2496],{"id":2412,"sortIndex":493,"researcher":24,"roles":2413,"affiliations":2414,"properties":2425},"b9c37818-04d0-4a0e-ab53-6ccb00fdf6e1",[],[2415],{"id":2416,"sortIndex":25,"affiliation":2417,"properties":24},"86a54edd-6aa7-4e2f-949c-572c65d88883",{"id":2418,"createTime":2419,"updateTime":2419,"relativeEntities":2420,"slug":2421,"properties":2422,"entityType":60,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"syncStatus":23,"languages":24,"translateLanguages":24,"viewCount":25},"9a23a611-b036-4d50-af77-4dae6a553208","2024-11-25T17:22:19.108+00:00",[],"Department-of-Air-Pollution-and-Noise-Domain-for-Infection-Control-and-Environmental-Health-Norwegian-Institute-of-Public-Health-Oslo-Norway",{"title":2423},{"EN":2424},"Department of Air Pollution and Noise Domain for Infection Control and Environmental Health Norwegian Institute of Public Health Oslo Norway",{"openalex":2426,"title":2428},{"VOID":2427},"A5006674415",{"EN":2429},"Marit Låg",{"id":2431,"sortIndex":169,"researcher":24,"roles":2432,"affiliations":2433,"properties":2440},"fc9743ef-9203-4e04-8a0d-ab42a91fb41f",[],[2434],{"id":2435,"sortIndex":25,"affiliation":2436,"properties":24},"f3e35f3b-afe4-4459-8a7c-99cfee9cd1bf",{"id":2418,"createTime":2419,"updateTime":2419,"relativeEntities":2437,"slug":2421,"properties":2438,"entityType":60,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"syncStatus":23,"languages":24,"translateLanguages":24,"viewCount":25},[],{"title":2439},{"EN":2424},{"openalex":2441,"title":2443},{"VOID":2442},"A5032352078",{"EN":2444},"Magne Refsnes",{"id":2446,"sortIndex":25,"researcher":24,"roles":2447,"affiliations":2448,"properties":2455},"bf1c356c-9e8f-46a0-a765-dcac2d6942d0",[],[2449],{"id":2450,"sortIndex":25,"affiliation":2451,"properties":24},"335a3842-2e7d-4af8-9c4d-374d61b72849",{"id":2418,"createTime":2419,"updateTime":2419,"relativeEntities":2452,"slug":2421,"properties":2453,"entityType":60,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"syncStatus":23,"languages":24,"translateLanguages":24,"viewCount":25},[],{"title":2454},{"EN":2424},{"openalex":2456,"orcid":2458,"title":2460},{"VOID":2457},"A5010012417",{"VOID":2459},"https:\u002F\u002Forcid.org\u002F0000-0003-4324-1536",{"EN":2461},"Johan Øvrevik",{"id":2463,"sortIndex":945,"researcher":24,"roles":2464,"affiliations":2465,"properties":2472},"022aceba-67ae-4fc7-b803-ccca0fc98e46",[],[2466],{"id":2467,"sortIndex":25,"affiliation":2468,"properties":24},"71f926ba-8fec-4f7d-9cb1-6029422ec044",{"id":2418,"createTime":2419,"updateTime":2419,"relativeEntities":2469,"slug":2421,"properties":2470,"entityType":60,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"syncStatus":23,"languages":24,"translateLanguages":24,"viewCount":25},[],{"title":2471},{"EN":2424},{"openalex":2473,"orcid":2475,"title":2477},{"VOID":2474},"A5014466291",{"VOID":2476},"https:\u002F\u002Forcid.org\u002F0000-0001-6085-5471",{"EN":2478},"Jørn A. 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order to explore the possibility of \u003Cjats:sc>l\u003C\u002Fjats:sc>‐carnitine (\u003Cjats:styled-content style=\"fixed-case\">LC\u003C\u002Fjats:styled-content>) as a protector of male fertility in chemotherapy, we observed the damage of cyclophosphamide (\u003Cjats:styled-content style=\"fixed-case\">CTX\u003C\u002Fjats:styled-content>) to Sertoli cells and the protective effect of \u003Cjats:styled-content style=\"fixed-case\">LC\u003C\u002Fjats:styled-content> on the testis Sertoli cells from such damage in this study. Healthy adult male mice were divided into three groups: chemotherapy group were injected intraperitoneally with the \u003Cjats:styled-content style=\"fixed-case\">CTX\u003C\u002Fjats:styled-content>; protective agent group were injected both \u003Cjats:styled-content style=\"fixed-case\">LC\u003C\u002Fjats:styled-content> and \u003Cjats:styled-content style=\"fixed-case\">CTX\u003C\u002Fjats:styled-content>; control group mice were injected only with isochoric physiological saline; all once a day for 5 days. After 5 days, the mice were, respectively, killed at 24 hr after the last injection. The testis and epididymis were removed. Epididymis was for sperm analysis immediately, and immunohistochemistry, \u003Cjats:styled-content style=\"fixed-case\">RT\u003C\u002Fjats:styled-content>‐\u003Cjats:styled-content style=\"fixed-case\">PCR\u003C\u002Fjats:styled-content> and Western blot for the assessments of occludin, glial cell‐derived neurotrophic factor (\u003Cjats:styled-content style=\"fixed-case\">GDNF\u003C\u002Fjats:styled-content>) and \u003Cjats:styled-content style=\"fixed-case\">TGF\u003C\u002Fjats:styled-content>‐β3 \u003Cjats:styled-content style=\"fixed-case\">mRNA\u003C\u002Fjats:styled-content> and protein expression. The sperm analysis of epididymis showed that \u003Cjats:styled-content style=\"fixed-case\">CTX\u003C\u002Fjats:styled-content> can significantly decrease sperm count and motility; and administration of \u003Cjats:styled-content style=\"fixed-case\">LC\u003C\u002Fjats:styled-content> resulted in significant recovery of the sperm count and sperm motility. Compared with control group, the expressions of occludin and \u003Cjats:styled-content style=\"fixed-case\">GDNF\u003C\u002Fjats:styled-content> decreased and the expression of \u003Cjats:styled-content style=\"fixed-case\">TGF\u003C\u002Fjats:styled-content>‐β3 increased significantly (\u003Cjats:italic>p\u003C\u002Fjats:italic> < 0.05) in the \u003Cjats:styled-content style=\"fixed-case\">CTX\u003C\u002Fjats:styled-content> group. In the \u003Cjats:styled-content style=\"fixed-case\">LC\u003C\u002Fjats:styled-content> + \u003Cjats:styled-content style=\"fixed-case\">CTX\u003C\u002Fjats:styled-content> group, the expressions of occludin and \u003Cjats:styled-content style=\"fixed-case\">GDNF\u003C\u002Fjats:styled-content> were higher than those of the \u003Cjats:styled-content style=\"fixed-case\">CTX\u003C\u002Fjats:styled-content> group and similar to those of the control group; the \u003Cjats:styled-content style=\"fixed-case\">TGF\u003C\u002Fjats:styled-content>‐β3 expression was lower (\u003Cjats:italic>p\u003C\u002Fjats:italic> < 0.05) than that of the \u003Cjats:styled-content style=\"fixed-case\">CTX\u003C\u002Fjats:styled-content> group and similar to that of the control group. The results of this study showed that \u003Cjats:styled-content style=\"fixed-case\">CTX\u003C\u002Fjats:styled-content> could damage the spermatogenesis and reduce the expression of occludin and \u003Cjats:styled-content style=\"fixed-case\">GDNF\u003C\u002Fjats:styled-content>, and increase the expression of \u003Cjats:styled-content style=\"fixed-case\">TGF\u003C\u002Fjats:styled-content>‐β3 in testis of mouse, which indicates \u003Cjats:styled-content style=\"fixed-case\">CTX\u003C\u002Fjats:styled-content>'s damage or efficacy to testis Sertoli cells. \u003Cjats:styled-content style=\"fixed-case\">LC\u003C\u002Fjats:styled-content> could protect the Sertoli cells of testis from these damages caused by \u003Cjats:styled-content style=\"fixed-case\">CTX\u003C\u002Fjats:styled-content>, and promote or protect the spermatogenesis. In conclusion, this study provides meaningful information about the possible damage to male fertility by chemotherapeutics and potential of \u003Cjats:styled-content style=\"fixed-case\">LC\u003C\u002Fjats:styled-content> in the protection of male fertility during chemotherapy.\u003C\u002Fjats:p>",{"EN":2707},"The Effects of \u003Cscp>l\u003C\u002Fscp>‐Carnitine Against Cyclophosphamide‐Induced Injuries in Mouse 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