Med Microbiol Immunol 2009, 198:221–238.PubMedCrossRef 10. Kohler S, Foulongne V, Ouahrani-Bettache S, Bourg G, Teyssier J, Ramuz M, Liautard JP: The analysis of the intramacrophagic virulome of Brucella suis deciphers the environment encountered by the pathogen inside the macrophage host cell. Proc Natl Acad Sci USA 2002, 99:15711–15716.PubMedCrossRef 11. Volkert MR, Nguyen DC: Induction of specific Escherichia coli genes by sublethal treatments with alkylating agents. Proc Natl Acad Sci USA 1984, 81:4110–4114.PubMedCrossRef

12. Nakabeppu Y, Kondo H, Sekiguchi M: Cloning and characterization of the alkA gene of Escherichia coli that encodes 3-methyladenine DNA glycosylase II. J Biol Chem 1984, 259:13723–13729.PubMed 13. Yamamoto Y, Katsuki M, Sekiguchi M, Otsuji N: Escherichia coli gene that controls sensitivity to alkylating agents. J Bacteriol 1978, 135:144–152.PubMed 14. Taverna

P, Sedgwick B: Generation Stattic in vitro of an endogenous DNA-methylating agent by nitrosation in Escherichia coli . J Bacteriol 1996, 178:5105–5111.PubMed 15. this website Dricot A, Rual JF, Lamesch P, Bertin N, Dupuy D, Hao T, Lambert C, Hallez R, Delroisse JM, Vandenhaute J, et al.: Generation of the Brucella melitensis BLZ945 concentration ORFeome version 1.1. Genome Res 2004, 14:2201–2206.PubMedCrossRef 16. Mignolet J, Van der Henst C, Nicolas C, Deghelt M, Dotreppe D, Letesson JJ, De Bolle X: PdhS, an old-pole-localized histidine kinase, recruits the fumarase FumC in Brucella abortus . J Bacteriol

2010, 192:3235–3239.PubMedCrossRef 17. Hallez R, Mignolet J, Van Mullem V, Wery M, RANTES Vandenhaute J, Letesson JJ, Jacobs-Wagner C, De Bolle X: The asymmetric distribution of the essential histidine kinase PdhS indicates a differentiation event in Brucella abortus . EMBO J 2007, 26:1444–1455.PubMedCrossRef 18. Bowles T, Metz AH, O’Quin J, Wawrzak Z, Eichman BF: Structure and DNA binding of alkylation response protein AidB. Proc Natl Acad Sci USA 2008, 105:15299–15304.PubMedCrossRef 19. Rippa V, Amoresano A, Esposito C, Landini P, Volkert M, Duilio A: Specific DNA binding and regulation of its own expression by the AidB protein in Escherichia coli . J Bacteriol 2010, 192:6136–6142.PubMedCrossRef 20. Sedgwick B: Repairing DNA-methylation damage. Nat Rev Mol Cell Biol 2004, 5:148–157.PubMedCrossRef 21. Volkert MR: Adaptive response of Escherichia coli to alkylation damage. Environ Mol Mutagen 1988, 11:241–255.PubMedCrossRef 22. Lawley PD, Brookes P: Cytotoxicity of alkylating agents towards sensitive and resistant strains of Escherichia coli in relation to extent and mode of alkylation of cellular macromolecules and repair of alkylation lesions in deoxyribonucleic acids. Biochem J 1968, 109:433–447.PubMed 23. Alvarez G, Campoy S, Spricigo DA, Teixido L, Cortes P, Barbe J: Relevance of DNA alkylation damage repair systems in Salmonella enterica virulence. J Bacteriol 2010, 192:2006–2008.PubMedCrossRef 24.

Prognostic effect is known to depend on certain biological factors as well as a combination of cytogenetics and other mutations such as those in FLT3 and NPM1[3, 6, 8]. Somatic mutations in IDH1/2 occur in 5–30% patients with AML and are commonly associated with nucleophosmin 1 (NPM1) mutations [9, 10]. Both the genes play a critical role in the citric acid cycle

BI 10773 nmr IDH1 in the cytoplasm and peroxisome and IDH2 in the mitochondria. Both IDH1 and IDH2 promote the Inhibitor Library chemical structure conversion of isocitrate to α-ketoglutarate (α-KG) that is associated with the reduction of nicotinamide adenine dinucleotide phosphate (NADP+) to NADPH [8, 11, 20]. Mutations in IDH1 and IDH2 are heterozygous and occur in highly conserved arginine residues (IDH1 R132 and IDH2 R140/R172). Mutations at IDH2 R140 always result in the conversion of arginine to glutamine, whereas substitutions at IDH1 R132 and IDH2 R172 result in a wide range selleck chemicals llc of amino acid replacements [12]. All point mutations in IDH1/2 lead to a gain of function, enabling the conversion of α-KG to 2-hydroxyglutarate (2-HG) and oxidation of NADPH to NADP+. Furthermore, an increase in 2-HG-levels leads to the functional impairment of α-KG-dependent enzymes through competitive inhibition [13]. In contrast to the impact of DNMT3A mutations, the impact of IDH1/2 mutations on prognosis is not completely understood. It appears that prognosis may depend on specific patient populations

and a combination with NPM1 mutations [21–23]. The increasing evidence of high incidence particularly in cytogenetically normal AML and prognostic pertinence of DNMT3A and IDH1/2 mutations support the need to identify Temsirolimus these mutations in routine diagnostic screening. Importantly, the presence of DNMT3A and IDH1/2 mutations may confer sensitivity to novel therapeutic approaches, including demethylating agents [24, 25]. The current available methods like direct sequencing are informative but time consuming and cost intensive. In this study, we validated the polymerase chain reaction (PCR)-based

high resolution melt (HRM) assay for screening DNMT3A, IDH1 and IDH2 mutations in samples obtained from patients with AML at diagnosis and developed 2 rapid methods for detecting more common mutations, DNMT3A R882H and IDH2 R140Q. We evaluated the utility of endonuclease restriction-based detection method to identify mutations in DNMT3A and designed an amplification-refractory mutation system (ARMS) to detect mutations in IDH2. In addition we compared both the systems with the HRM assay for all the studied mutations. Methods Patient characteristics Bone marrow (BM) samples from 230 patients with newly diagnosed AML were included in the study. All patients were treated at the University Clinic Charité, Campus Benjamin Franklin, from May 2000 to July 2013. Patient’s characteristics are summarised in the Additional file 1: Table S1.

and Methanosarcina spp. [22, 23]. This hampers any cell counting attempt by microscopy as well as flow cytometry. In addition, some of these cell associations can reach a thickness that inhibits the penetration of FISH probes into deeper layers of cell clusters. In consequence, only the surface Selleckchem ON-01910 cells are hybridized with FISH probes and are detectable by Flow-FISH. Hence, samples from this environment have to be pretreated to purify and to isolate all microbial cells of the whole biogas reactor biocenosis. Despite the number of different selleck inhibitor pretreatment approaches developed for a variety of samples of different environmental origins [24–28],

up to now no procedures are published for the purification of samples from biogas reactors leading to preparations suited for the measurement of the microbial community by Flow-FISH. To overcome these technical limitations, the aim of this study was to establish a high-throughput technique for the

detection and the quantification of process relevant, active microorganisms in anaerobic digestion using the process liquor of an upflow anaerobic solid-state (UASS) biogas reactor as test material [29]. Therefore, a purification technique was primarily optimized to fulfill the following requirements: (1) detachment of cells from organic and inorganic particles, (2) disbandment of cell aggregates, (3) no or low cell loss, and (4) a rapid implementation. Furthermore, a modified Flow-FISH

protocol based on different already published see more protocols [12, 20, 30] was developed and tested regarding following influencing parameters: (1) type of fixative used for cell fixation directly after sampling, (2) possible cell losses by centrifugation during FISH procedure, and (3) cell activity. Results and discussion Optimization of the purification technique The application of flow cytometry for the analysis of the microbial community in biogas reactors requires previous sample purification due to its high content of organic and inorganic particles and the presence of huge cell aggregates and biofilms. The capillary within the flow cytometer could clog due to such large particles. Moreover, the microbes bound in aggregates and biofilms are hardly detectable and countable with the Flow-FISH. In this study, six purification procedures with in total 29 modifications (-)-p-Bromotetramisole Oxalate were tested (Table 1). These six purification strategies are based on the use of a detergent to dissolve cell aggregates and to detach cells from different surfaces in soils [24–26, 28] or turbid seawater [27]. A current method to increase the effect of detergent is the ultrasonic treatment [31] and homogenization of the sample with a dispersion unit [26]. The concentration of the used detergent and the settings of ultrasound and homogenization should be adjusted because these treatments can also destroy the cell wall of microbes.

AGEs are 31% higher in aHFD (42.8 ± 7.6 ng quinine/mg Selleck ��-Nicotinamide collagen) vs. aLFD (56.1 ± 9.2 ng/mg, p < 0.001) and 6% higher in yHFD vs. yLFD (41.3 ± 5.5 ng/mg vs. 39.1 ± 8.7 ng/mg, respectively, p > 0.05). Mechanical S3I-201 testing: mechanical properties compromised with diabetic obesity

Overall, mechanical properties of cortical bone are compromised by diabetic obesity in both young and adult groups, as summarized in Fig. 4. Compared to the control groups, the yield strength of the bone was unchanged in aHFD (9% less, not significant), but was 17% less in yHFD (p < 0.01); corresponding maximum strengths were 15% less in aHFD (p < 0.05) and 26% less in yHFD (p < 0.01). The bending modulus was 18% less in aHFD and 32% less in yHFD (p < 0.01); fracture toughness, K c , values were 21% less in aHFD (p < 0.05), but unchanged in yHFD (8% higher, not significant). Finally, the maximum loads sustained by the bone were 22% less in aHFD (p < 0.01) and 12.5% less in yHFD (p < 0.05). These results indicate a profound reduction in mechanical quality and performance of the bone with diabetic obesity. Fig. 4 Cortical bone quality: whole-bone and tissue-level mechanical property measurements. a Young and f adult bending modulus; b young and g adult maximum load; c young and h adult yield stress; d young

and i adult max stress; e young and j adult fracture toughness. Measured size-independent mechanical properties were significantly decreased for HFD group vs. LFD Selleck JQ1 groups ROS1 (modulus, yield and maximum stress, and fracture toughness); these parameters are an indication of bone tissue quality. Size-dependent measures which address whole-bone behavior (specifically, load) also declined for HFD at both ages, likely due in part to modest bone size changes, as bone size was not able to compensate for poor

mechanical quality. yLFD n = 15, yHFD n = 15, aLFD n = 13, aHFD n = 14 (* p < 0.05; ** p < 0.01) Structural characterization: poor mineral organization and lamellar alignment of cortical bone in diabetic obese mice SEM was performed on cross-sections of femora near the fracture surface to evaluate lamellar-level structural changes. Changes in structure were most apparent at the posterior site (Fig. 5). In both the young and adult groups, the HFD bone showed marked areas of lamellar disorganization, whereas a similar area in the LFD mice appeared well-ordered. Fig. 5 SEM images of the fracture region showing cortical bone tissue structure changes at the posterior region. a yLFD group; b yHFD; c aLFD; d aHFD. The scale bar indicates 20 μm. The posterior cortex in HFD bone in (b) and (d) shows reduced alignment of osteocyte lacunae and reduction in lamellar alignment at the tissue level. These images are representative of three samples each of aHFD, yHFD, aLFD, and yLFD.

cup of Starbucks regular drip coffee has been found to contain as much as 480 mg of caffeine [212]. The potential side effects of caffeine include: insomnia, nervousness, restlessness,

gastric irritation, nausea, vomiting, tachycardia, tremors, and anxiety; which have been reported at doses as low as 250 to 300 mg [5, 201–204, 209]. Caffeine EX527 availability is ubiquitous and it is one of the most extensively studied substances in the food supply with a long history as generally regarded as safe when consumed in moderation [61]. However, all substances may be toxic under the right conditions, with toxicity being a function of the interaction of many physiologic variables that include the following: acute and chronic dosing, route of administration, genetics, age, sex, environment, and intrinsic health of the individual being

exposed. Young adults have been found to have subclinical coronary NVP-BGJ398 atherosclerosis [213]. In addition, post-mortem assessment of sudden cardiac death in young persons (<35 years) reveals a variety of anatomic abnormalities of the coronary arteries, myocardium, valves and the conduction system [214]. Such unknown pre-existing risk factors may increase the risk of adverse events, particularly cardiovascular ones, in individuals consuming EDs, due to underlying disease. In fact, even water can be toxic given certain conditions with an LD50 (lethal acute dose for 50 percent in test species) of greater than 90 mL/kg in rats [215]. It is possible to overdose on caffeine and there are a handful of case reports

in the literature [5, 209, 216–218]. A lethal dose of caffeine has been typically in excess Phosphatidylinositol diacylglycerol-lyase of 5 g [217], which equates to about 42 cups of coffee at 120 mg of caffeine per cup. Sepkowitz [201] recently suggested that an intake of 3 grams of caffeine (equivalent to ingesting 12 or so highly caffeinated ED within a few hours) could elicit significant adverse effects. The average caffeine per serving in most ED and ES range between 75 and 200 mg, an amount similar to the caffeine found in a premium cup of coffee [202]. Nawrot and colleagues [219] stated that in a healthy adult population, up to 400 mg of caffeine daily was not associated with any adverse effects. In another selleck review, Higdon et al. [220] presented data in children stating no adverse effects were seen with doses under 3 mg·kgBM-1·day-1. As with most drugs, the exact amount of caffeine where side effects will occur varies from person to person based on genetics, age, liver cytochrome P450-CYP1A2 isozyme function, concurrent medications or substances that may affect hepatic metabolism, body mass, and sensitivity. Additionally, it is unknown whether inclusion of other stimulants in ED and/or ES may increase or decrease the threshold for experiencing side effects.

41 – 0.55%. Test-retest reliability studies performed with this DXA machine have previously yielded mean coefficients of variation for total bone mineral content and total fat free/soft tissue mass of 0.31 – 0.45% with a mean intra-class correlation of 0.985 [31]. Resting energy expenditure Resting energy expenditure (REE) was assessed using a ParvoMedics TrueMax 2400 Metabolic Measurement System (ParvoMedics, Inc., Sandy, UT). This test was a non-exertional test performed in a fasted state with the participants lying supine on an exam table. A

clear, hard plastic hood and soft, clear plastic drape was placed over the participants’ neck and head in order to determine resting AZD6244 price oxygen uptake and energy expenditure. All participants remained motionless without falling Fosbretabulin nmr asleep for approximately 20 minutes. Data were recorded after the first ten minutes of testing during a five minute Selleckchem LGX818 period of time in which criterion variables (e.g., VO2 L/min) changed less than 5%. Test-retest measurements on 14 participants from a study previously reported [20] revealed that test-retest correlations (r) of collected VO2 in l/min ranged

from 0.315 – 0.901 and coefficient of variation ranged from 8.2% – 12.0% with a mean intra-class coefficient of 0.942, p < 0.001. Anthropometrics Active range of motion for right/left knee extension and flexion was measured with a standard 12"" goniometer to determine knee range of motion. The participant was made to lie supine with one leg extended and the other leg bent with the heel resting on table. The extended leg was measured for knee extension. Next, the measurement of the same leg was measured for flexion range of motion by having the participant raise the extended leg slightly off the table and bring the heel toward the gluteus maximus. These procedures were repeated on the opposite leg. Test to test reliability of performing these tests were 0.75-0.98. Knee circumference was measured as a general indicator of knee inflammation/swelling. The participant lied supine with one leg extended and the other leg bent

with the heel resting on table. The circumference of the extended leg was measured Megestrol Acetate and then repeated on the opposite leg. Measurements were performed utilizing a Gulick anthropometric tape (Model J00305, Lafayette Instruments, Lafayette, IN) at the joint line of both knees. Test to test reliability of performing these tests were 0.86-0.92. Exercise capacity Resting heart rate was determined by palpitation of the radial artery using standard procedures [32]. Blood pressure was assessed by auscultation of the brachial artery using a mercurial sphygmomanometer using standard clinical procedures [32]. Resting heart rate and blood pressure measurements were taken on the participant in the supine position after resting for 5-min.

L. japonica was shown to consist of moisture (7.7%), volatile matter (53.1%), fixed carbon (11.0%), and ash (28.3%) on a mass basis, whereas most mass (99.8%) was volatiles with only 0.2% of ash in the case of PP. Elemental analyses showed that L. japonica was composed of C (30.6%), H (4.9%), O (62.4%), N (1.5%), and S (0.5%) on a mass basis, whereas PP was composed only of C (85.4%) and H (14.6%). Synthesis and characterization of the catalyst Mesoporous Al-SBA-15 was synthesized using a method suggested in a previous study [3]. The characterization of the synthesized catalyst was performed using BET, N2 adsorption-desorption analysis,

X-ray diffraction patterns (XRD) and temperature-programmed desorption (TPD) of ammonia. selleckchem Refer to a previously published report for more detailed analysis procedure [1, 3]. Catalytic pyrolysis and co-pyrolysis using a fixed-bed reactor A U-type quartz reactor was used to investigate the change in the yields of gas and bio-oil by co-pyrolysis. To make an oxygen-free condition, 50-mL/min nitrogen gas flow was used to purge the reactor for 30 min prior to each experiment. Experiments were conducted with a 5-g L. japonica sample for 1 h at 500°C using 50-mL/min N2 gas as the carrier gas. In the case of co-pyrolysis of L. japonica

and waste plastics, a mixture of 2.5-g L. japonica and 2.5-g PP was used for the experiments. In the case of catalytic pyrolysis, a catalyst/feedstock ratio of 1/10 was used. The pyrolysis product oil was collected P5091 manufacturer in two consecutive condensers maintained at −20°C. A Teflon bag (DuPont Co., Wilmington, DE, USA) was installed after the condensers to collect the gaseous species that were not condensed in the condensers owing to their too low boiling points. The H2O content in bio-oil was analyzed using a Karl Fischer Titrator. www.selleck.co.jp/products/Nutlin-3.html Refer to previously published papers for more detailed experimental procedures [1, 2, 5]. Catalytic pyrolysis and co-pyrolysis using a pyrolysis gas chromatography/mass

spectrometry For more detailed in situ analysis of pyrolysis product composition, a single-shot pyrolyzer (Py-2020iD, Frontier-Lab Co., Koriyama, Fukushima, Japan) connected directly to GC/MS (called hereafter pyrolysis gas chromatography/mass spectrometry (Py-GC/MS)) was used. The pyrolyzer was maintained at 500°C. When pyrolyzing L. japonica only, 2 mg of L. japonica sample was put in a cup, whereas a mixture of 1 mg of L. japonica sample and 1 mg of PP was put in the cup for co-pyrolysis. When the experiments were performed with catalyst, quartz wool was laid over the cup containing the Pictilisib solubility dmso biomass sample forming an intermediate layer, over which 2 mg of catalyst was placed. The pyrolysis product vapor was upgraded catalytically while passing through the catalyst layer. Each test was conducted three times to check the reproducibility. One can refer to a previous paper [1, 3] for more detailed experimental procedures.

coli O157:H7 and P. aeruginosa by inhibiting polymeric matrix production [42]. Hence, indole and 3-indolylacetonitrile are possible spore maturation inhibitors against spore-forming P. alvei and biofilm inhibitors against pathogenic biofilm formation. Currently, various indole derivatives from plants and numerous synthetic indole derivatives are commercially available and work is in progress to identify universal and stronger sporocides and to understand their genetic mechanism in

action. Conclusions The current study demonstrates that i) indole is an extracellular stationary phase molecule in a Gram-positive bacteria P. alvei, ii) indole clearly inhibits spore maturation and Veliparib nmr survival rates under several stresses in P. alvei without affecting cell growth, iii) plant auxin 3-indolylacetonitrile dramatically decreased the heat resistance of P. alvei, iv) electron microscopy shows that indole and 3-indolylacetonitrile inhibit the development of spore coats and cortex in P. alvei. This study shows that indole, as a signaling molecule in quorum-sensing manner, plays a role in sporulation of P. alvei and that 3-indolylacetonitrile

can be useful to control of heat and antimicrobial resistant spores of Gram-positive bacteria. Methods Bacterial strains, materials and growth rate measurements P. alvei (ATCC 6344) and B. subtilis strain (ATCC6633) were obtained from Korean Culture Center of Microorganisms. FRAX597 cell line The strain was originally isolated from European foulbrood [43]. Luria-Bertani (LB) [44] was used as a basic medium for growth Anlotinib clinical trial unless indicated. DSM medium (Difco sporulation medium [45]) was used for spore formation and cell survival tests with antibiotics. DSM medium contains 8 g of Bacto nutrient broth (Difco), 10 ml of 10% KCl, 10 ml of 1.2% MgSO4·7H2O, 1.5 ml of 1 M NaOH, 1 ml of 1 M Ca(NO3)2, 1 ml of 0.01 M MnCl2 and 1 ml of 1 mM FeSO4 per liter. BHI agar medium (Difco brain heart infusion agar) was also used for long-term spore formation.

Indole, tryptophan, 3-indoleacetic acid, indole-3-carboxyaldehyde, 3-indolylacetonitrile, indole-3-acetamide, Ureohydrolase tryptamine, 2-oxindole, tetracycline, erythromycin, chloramphenicol, and streptomycin were purchased from Sigma-Aldrich Co. (Missouri, USA). Ethanol and dimethyl sulfoxide (DMSO) were purchased from Duksan Pure Chemical Co. (Ansan, Korea). Bacterial strains were initially streaked from -80°C glycerol stocks on LB plates, and a fresh single colony was inoculated into LB medium (25 ml) in 250 ml flasks and routinely cultured at 250 rpm at 37°C unless otherwise indicated. Overnight cultures were diluted in a 1:100 ratio using LB medium for cell growth and indole production or DSM medium for the test of spore surviving. For cell growth measurements, the optical density was measured at 600 nm (OD600) with a spectrophotometer (UV-160, Shimadzu, Japan). When the value of OD600 was above 0.

In 2001, the Health Council reviewed several screening test methods. A triple test to be offered in

the second trimester of pregnancy was considered as a suitable risk assessment screening for both Down syndrome and neural tube defects and should be aimed at all pregnant women, regardless of age. According to the Heath Council, when certain conditions were met, such as an adequate procedure for informed consent, risk assessment #buy NVP-BSK805 randurls[1|1|,|CHEM1|]# for Down syndrome would be ‘such a superior alternative to the existing practice of maternal age-based screening that there should be no reason to delay its introduction any longer’. The Council argued that screening FG-4592 in vivo based on the triple test would lead to considerably fewer invasive tests and increased detection of Down syndrome pregnancies, while a far larger group would be allowed to benefit from having individual risk assessment. The introduction of screening for neural tube defects was considered a desirable step (Health Council of the Netherlands 2001, 28–29).

At the end of 2001, the Ministry of Health organised a Consultation round inviting several groups, such as obstetricians and patient representatives, to voice their opinions on serum screening (Toom and van Berkel 2003). In the same year, several obstetricians criticised the Health Council’s report in a medical journal. An important point of contention was that the birth prevalence of Down syndrome was higher in the maternal age group over 36 years of age. According to these obstetricians, by setting an age limit, potential psychological harm from screening younger women could be prevented (Hamerlynck and Knuist 2001). Another argument was that test characteristics

for the group of older women were better than for the group of younger women. The number of false negatives in women under 36 years of age was found unacceptably high: approximately half of the cases of Down syndrome in pregnancies of younger women would not be detected, thereby giving false reassurance. In addition, the false positives in the younger age group would require further www.selleck.co.jp/products/Gefitinib.html testing. Based on figures from the Health Council, the obstetricians calculated that via invasive testing about the same number of cases of Down syndrome would be detected (115) as healthy foetuses would be lost because of test-induced iatrogenic abortions (111). Medicalisation of pregnancy was deemed undesirable (Kleiverda and Vervest 2001). The Health Council Committee had based its arguments on calculations for all age groups together. Representatives of the Committee responded by stating that compared to the current age-related diagnostic testing, the total number of invasive tests would drop.

The choice Temsirolimus research buy of buffer also had some effect on the amount of specific IgG binding (see Fig. 3c, d). Table 3 Demographic, clinical and functional characteristics of the see more symptomatic patients with MDI exposure history and presumed isocyanate asthma Patient no. # Demographic data MDI exposure. (lag time) year Art of exposure

to MDI (job description) Immunological status Duration of resp. sympt (year) Lung function SPT MDI-HSA MDI-SIC MDI-HSA-specific antibodies Final clinical diagnosis Sex Age Smoking status SPT comm. allerg. Total IgE kU/L FVC  % pred FEV1  % pred NS-BHR MDI-sIgE kU/L MDI-sIgG mg/L Group A: MDI-exposed patients referred to our clinic with presumed isocyanate asthma diagnosis  1 M 29 Yes 5.5 (1) MDI-PUR glue heated; harder, binder Pos. 279 4 86 76 Pos. Pos. Pos. 13.3 <3 OAI    2 M 63 Yes 14 (0.8) MDI-PUR synthesis Pos. 1669 12 97 69 Pos. Pos. Pos. 50.4 7.3 OAI    3 M 36 Ex 3 (1) MDI-PUR manufacture; MDI-lack bystander Neg. 427 1 90 60 Pos. Pos. Pos. 4.8 9.6 OAI    4 M 34 Ex 14 (0.7) MDI-PUR glue heated, MDI cont. coatings Pos. 226 8 97 94 Pos. Pos. Pos. 3.3 <3 OAI    5 M 57 Ex 4 (0) MDI-PUR foam manufacture Pos. 61 3.4 74 78 Pos. Pos. Pos. <0.02 <3 OAI CI  6 M 54 Ex 5 (0) MDI cont. production

of elastomers Neg. 102 4 85 58 Neg. Neg. Pos. <0.02 74.0   PI  7 M 35 Ex 0.4 (0) MDI-PUR cont. check details plastic manufacture Pos. triclocarban 51 0.4 81 69 Pos. Neg. Pos.

<0.02 4.9 OAI    8 M 47 No 11.5 (0) MDI-PUR electrical potting, Neg. 15 10.5 79 68 Pos. Neg. Pos. <0.02 20.2   PI  9 M 49 Yes 11 (0) MDI-PUR manufacture of. hard plastic parts Neg. 8 2.5 85 62 Neg. Neg. Pos. <0.02 3.3 OAI    10 F 43 Yes 0.3 (0) MDI-PUR-durable elastomeric wheels,-foam Neg. 108 0.1 100 57 Pos. Neg. Pos. <0.02 14.8 A1 PI  11 M 49 Ex 13 (0.8) MDI glue, heated, plastic, wood panels Neg. 12 6 79 72 Neg. Neg. Neg. <0.02 3.6   P1  12 M 43 Ex 2 (0.2) MDI-PUR powder, acryl lack parts Neg. 2 1.5 81 73 Pos. Neg. Neg. <0.02 3.7 A1   M, Male; F, Female; comm. allerg., common allergens; MDI exp. duration of work-related exposure to MDI; lag time, lag time since last exposure; resp. sympt, duration of reported respiratory symptoms; FVC, forced vital capacity; FEV1, forced expiratory volume in 1 s; NSBHR, non-specific bronchial hyper-responsiveness; MDI-SIC, MDI-specific inhalation challenge; sIgE, MDI-specific IgE; sIgG, MDI-specific IgG. OAI, occupational MDI asthma; PI, MDI-induced hypersensitivity pneumonitis; DI, dermatitis, due to MDI; CI, conjunctivitis due to MDI; RCI, rhino-conjunctivities, due to MDI; A1, work-aggravated isocyanate asthma (aggravated by MDI exposure) at the time of blood sampling; P1, early stage of hypersensitivity pneumonitis due to MDI (isocyanate alveolitis, that is, mild clinical symptoms and non-significant changes in lung function occurred in the challenge test); n.d.