Flame 2016 Activation

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Objective: Ultraviolet (UV)-perception-type flame sensors detect gamma rays emitted from iodine 131 ((131)I). Explaining the possibility of flame sensor activation to patients when they receive (131)I to treat Graves disease or other ablative purposes is important. We investigate the current situation of flame sensor activation after radioactive iodine (RAI) therapy.

Methods: A total of 318 patients (65 males and 253 females) with Graves disease who received RAI therapy at our clinic between November 2007 and June 2014 participated in this study. Patients were given both written and oral explanations regarding the possibility of flame sensor activation. Participants were surveyed with a questionnaire. The following question was asked: "Did the fire alarm (flame sensor) go off when you used a restroom in places like shopping centers within a few days after your isotope therapy?" To those who answered "yes," we asked where the fire alarm had gone off.

Results: Of the 318 patients, 19 (6.0%) answered "yes," 2 of whom were male while 17 were female. Of the 299 (94.0%) patients who answered "no," 63 were male and 236 were female. As to the place of restroom sensor activation, shopping centers were reported by 9 patients; supermarkets by 5; airports by 2; and a bookstore, the Kyushu Shinkansen (bullet train), and a hospital by 1 each.

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The Flame was also designed to survive the death of its host, the only way to remove it aside from the deactivation passcode. According to Becca, the AI would protect itself such that "if you drown, it will swim; if you burn, it will crawl out of the flames."

HCAs are formed when amino acids (the building blocks of proteins), sugars, and creatine or creatinine (substances found in muscle) react at high temperatures. PAHs are formed when fat and juices from meat grilled directly over a heated surface or open fire drip onto the surface or fire, causing flames and smoke. The smoke contains PAHs that then adhere to the surface of the meat. PAHs can also be formed during other food preparation processes, such as smoking of meats (1).

Melkonian SC, Daniel CR, Ye Y, et al. Gene-environment interaction of genome-wide association study-identified susceptibility loci and meat-cooking mutagens in the etiology of renal cell carcinoma. Cancer 2016; 122(1):108-115.

Le NT, Michels FA, Song M, et al. A prospective analysis of meat mutagens and colorectal cancer in the Nurses' Health Study and Health Professionals Follow-up Study. Environmental Health Perspectives 2016; 124(10):1529-1536.

The Flame Demon stands at the left side of the circle of light. He is a humanoid wearing Male Uniform 2, despite of customization. His head is a large white flame and he holds two white flames in his outstretched hands. He speaks in a slow, deep voice with red text.

To perform the Flame Demon's Ritual, Ayano must obtain the ritual knife from the Occult Club and heat it up with the blowtorches in the Science Club. Then, she must place the ritual knife back in the skull, until it starts to glow in flames. From this point, any student stabbed with the ritual knife will be set on fire. To finish the ritual, Ayano must kill five students and place them in the summoning circle. The screen will then turn black, with shaking red text reading, "You have proven your worth. Very well. I shall lend you my power".

After that, two flame orbs will appear floating on Ayano's hands, her pupils will turn white and she will begin to levitate in a long grey dress. By tapping the left CTRL button, flames will shoot out of Ayano's hands, setting fire to any NPC in her path, excluding NPCs without AI and Senpai.

In our research, we focused on a priority list of 62 synthetic organic FRs that was established by experts from the Human Biomonitoring for Europe (HBM4EU) program (scoping document is accessible in the following link: -substances/flame-retardants/, see also Table 1). HBM4EU represents a joint effort of 28 countries, the European Environment Agency and the European Commission with the aim of providing evidence of the actual exposure of citizens to chemicals and the possible health effects to support policy making. Although this list does not cover all FRs present on the market, it is especially relevant for the identification of priority compounds for the European Union.

To select the most relevant AOPs that would represent plausible mechanisms of toxicity for the FR, we applied three inclusion criteria (Fig. 1c). First, we kept only those AOPs for which the FR was documented to interact at the level of three or more KEs of the AOP (i.e., given AOP appears at least three times in the table, for a given FR). Second, we selected AOPs for which the experimental evidence indicated that FR was highly or moderately toxic (with high or moderate weight of evidence) for at least one of the KE. Third, we included only AOPs applicable to vertebrates and AOPs of minimum acceptable quality (i.e., where MIE and AO were documented or KE-relationships were described). A total of 12 plausible AOPs were found for all Cat I FRs, several of them being shared by several FRs. AOP number, full name, status and link to snapshots representing the status of the AOP at the time when we collected the data can be found in Table 4, and the comprehensive list of plausible AOPs for each Cat I FR, with their corresponding MIE and AO, is provided in Additional file 1: Table S3. We note here that the wiki nature of the AOP-wiki, which is important to encourage crowdsourcing, has some draw-backs that are important to keep in mind when interpreting the results of the AOP search. First, the quality of AOPs that are not yet approved or endorsed after official OECD evaluation panel is quite variable and some of them may not be fully reliable. Another limitation relates to the incomplete representativeness of records in AOP-wiki, where some biological processes are thoroughly covered and included in many different AOPs (e.g., thyroid hormone levels) but others (e.g., activation of progesterone receptor) are not included at all yet, and remain to be further incorporated.

Another possible way to address the identified gaps is to search for mechanisms of toxicity, in the form of novel AOPs, that would link known information on interaction with molecular targets to documented adverse outcomes affected by FRs. For example, the AOP 18 describes activation of PPARα leading to malformation of the male reproductive tract and reduced male fertility by decreasing levels of TSPO and STAR proteins. This AOP appears to be a plausible toxicity pathway for TDCIPP-, TCEP- or TPhP-induced reproductive toxicity, but available data suggest that the MIE, PPARα activation, is unlikely to be affected by these FRs ([23, 33], and results from ToxCast assays). TSPO (i.e., second KE in the AOP 18) may constitute an alternative MIE since several ToxCast assays suggested that it could be a target of TDCIPP and TPhP (AC50s slightly above 2 µM). In the case of TCEP, we could not find any molecular target in published papers or in ToxCast, whereas this was one of the novel FRs that presented the highest toxicological concern based on available in vivo data. A systematic and blind search for direct targets could be envisaged, using for example an approach similar to the one used for TPhP that led to the identification of carboxylesterases as specific targets [45].

In addition to providing mechanistic supports for health outcomes associated with FR exposures, and identifying gaps for future research, the AOP search also highlighted some potential adverse health effects that may be of concern but have been overlooked or not yet studied. For example, we did not find any study addressing the incidence of breast cancer in relation to novel FRs, although there was experimental evidence on interactions of FRs with several KEs of AOP 200 that links mitochondrial dysfunction and oxidative stress to breast cancer as an AO. We also identified mechanistic evidence pointing towards an effect of TPhP and TBBPA on metabolic disorders but only very few studies addressed these adverse effects in animal models or in humans. For example, several in vitro studies reported adipogenesis and/or lipid accumulation and two studies showed increase in body weight associated with TPhP exposure in humans and rodents, and with TBBPA exposure in fish [6, 35, 52, 55, 56, 65, 66, 70]. In addition, activation of PPARγ (the MIE of AOP 72 that leads to obesity) by TPhP and TBBPA has been reported in many in vitro studies, two ToxCast assays and in zebrafish, with effective doses below 1 µM for TBBPA only (for example: [17, 54, 55]). Another pathway for TPhP may also involve carboxylesterases that are identified targets of TPhP and can cause hypertriglyceridemia in mice [45] but it does not correspond to any existing AOP and establishing this AOP would require more research evidence. 2b1af7f3a8