Characterizing Chemical Terrorism Incidents Collected by the Global Terrorism Database, 1970-2015.

BACKGROUND: The Global Terrorism Database (GTD) is an open-source database on terrorist incidents around the world since 1970, and it is maintained by the National Consortium for the Study of Terrorism and Responses to Terrorism (START; College Park, Maryland USA), a US Department of Homeland Security Center of Excellence. The consortium reviews media reports to determine if an event meets eligibility to be categorized as a terrorism incident for entry into the database. OBJECTIVE: The objective of this study was to characterize chemical terrorism incidents reported to the GTD and understand more about the kinds of chemical agents used, the associated morbidity and mortality, the geography of incidents, and the intended targets. METHODS: Chemical terrorism incidents from 1970 through 2015 were analyzed by chemical agent category, injury and fatality, geographic region, and target. RESULTS: During the study period, 156,772 terrorism incidents were reported to the GTD, of which 292 (0.19%) met the inclusion criteria for analysis as a chemical terrorism incident. The reported chemical agent categories were: unknown chemical (30.5%); corrosives (23.3%); tear gas/mace (12.3%); unspecified gas (11.6%); cyanide (8.2%); pesticides (5.5%); metals (6.5%); and nerve gas (2.1%). On average, chemical terrorism incidents resulted in 51 injuries (mean range across agents: 2.5-1,622.0) and seven deaths (mean range across agents: 0.0-224.3) per incident. Nerve gas incidents (2.1%) had the highest mean number of injuries (n = 1,622) and fatalities (n = 224) per incident. The highest number of chemical terrorism incidents occurred in South Asia (29.5%), Western Europe (16.8%), and Middle East/North Africa (13.0%). The most common targets were private citizens (19.5%), of which groups of women (22.8%) were often the specific target. Incidents targeting educational institutions often specifically targeted female students or teachers (58.1%). CONCLUSIONS: Chemical terrorism incidents rarely occur; however, the use of certain chemical terrorism agents, for example nerve gas, can cause large mass-causality events that can kill or injure thousands with a single use. Certain regions of the world had higher frequency of chemical terrorism events overall, and also varied in their frequencies of the specific chemical terrorism agent used. Data suggest that morbidity and mortality vary by chemical category and by region. Results may be helpful in developing and optimizing regional chemical terrorism preparedness activities.

Chemical Hand Warmer Packet Ingestion: A Case of Elemental Iron Exposure.

For individuals who work outdoors in the winter or play winter sports, chemical hand warmers are becoming increasingly more commonplace because of their convenience and effectiveness. A 32-year-old woman with a history of chronic pain and bipolar disorder presented to the emergency department complaining of a "warm sensation" in her mouth and epigastrium after reportedly ingesting the partial contents of a chemical hand warmer packet containing between 5 and 8 g of elemental iron. She had been complaining of abdominal pain for approximately 1 month and was prescribed unknown antibiotics the previous day. The patient denied ingestion of any other product or medication other than what was prescribed. A serum iron level obtained approximately 6 hours after ingestion measured 235 micrograms/dL (reference range 40-180 micrograms/dL). As the patient demonstrated no new abdominal complaints and no evidence of systemic iron toxicity, she was discharged uneventfully after education. However, the potential for significant iron toxicity exists depending on the extent of exposure to this or similar products. Treatment for severe iron toxicity may include fluid resuscitation, whole bowel irrigation, and iron chelation therapy with deferoxamine. Physicians should become aware of the toxicity associated with ingestion of commercially available hand warmers. Consultation with a medical toxicologist is recommended.

Gender- and sex-specific sports-related injury research in emergency medicine: a consensus on future research direction and focused application.

Title IX, the commercialization of sports, the social change in sports participation, and the response to the obesity epidemic have contributed to the rapid proliferation of participation in both competitive organized sports and nontraditional athletic events. As a consequence, emergency physicians are regularly involved in the acute diagnosis, management, disposition, and counseling of a broad range of sports-related pathology. Three important and highly publicized mechanisms of injury in sports relevant to emergency medicine (EM) include concussion, heat illness, and sudden cardiac death. In conjunction with the 2014 Academic Emergency Medicine consensus conference "Gender-specific Research in Emergency Care: Investigate, Understand, and Translate How Gender Affects Patient Outcomes," a consensus group consisting of experts in EM, emergency neurology, sports medicine, and public health convened to deliberate and develop research questions that could ultimately advance the field of sports medicine and allow for meaningful application in the emergency department (ED) clinical setting. Sex differences in injury risk, diagnosis, ED treatment, and counseling are identified in each of these themes. This article presents the consensus-based priority research agenda.

Prolonged zymosan-induced inflammatory pain hypersensitivity in mice lacking glycine receptor alpha2.

Glycinergic synapses play a major role in shaping the activity of spinal cord neurons under normal conditions and during persistent pain. However, the role of different glycine receptor (GlyR) subtypes in pain processing has only begun to be unraveled. Here, we analysed whether the GlyR alpha2 subunit might be involved in the processing of acute or persistent pain. Real-time RT-PCR and in situ hybridization analyses revealed that GlyR alpha2 mRNA is enriched in the dorsal horn of the mouse spinal cord. Mice lacking GlyR alpha2 (Glra2(-/-) mice) demonstrated a normal nociceptive behavior in models of acute pain and after peripheral nerve injury. However, mechanical hyperalgesia induced by peripheral injection of zymosan was significantly prolonged in Glra2(-/-) mice as compared to wild-type littermates. We conclude that spinal GlyRs containing the alpha2 subunit exert a previously unrecognized role in the resolution of inflammatory pain.

CNGA3: a target of spinal nitric oxide/cGMP signaling and modulator of inflammatory pain hypersensitivity.

A large body of evidence indicates that nitric oxide (NO) and cGMP contribute to central sensitization of pain pathways during inflammatory pain. Here, we investigated the distribution of cyclic nucleotide-gated (CNG) channels in the spinal cord, and identified the CNG channel subunit CNGA3 as a putative cGMP target in nociceptive processing. In situ hybridization revealed that CNGA3 is localized to inhibitory neurons of the dorsal horn of the spinal cord, whereas its distribution in dorsal root ganglia is restricted to non-neuronal cells. CNGA3 expression is upregulated in the superficial dorsal horn of the mouse spinal cord and in dorsal root ganglia following hindpaw inflammation evoked by zymosan. Mice lacking CNGA3 (CNGA3(-/-) mice) exhibited an increased nociceptive behavior in models of inflammatory pain, whereas their behavior in models of acute or neuropathic pain was normal. Moreover, CNGA3(-/-) mice developed an exaggerated pain hypersensitivity induced by intrathecal administration of cGMP analogs or NO donors. Our results provide evidence that CNGA3 contributes in an inhibitory manner to the central sensitization of pain pathways during inflammatory pain as a target of NO/cGMP signaling.

Thyroid hormone controls cone opsin expression in the retina of adult rodents.

Mammalian retinas display an astonishing diversity in the spatial arrangement of their spectral cone photoreceptors, probably in adaptation to different visual environments. Opsin expression patterns like the dorsoventral gradients of short-wave-sensitive (S) and middle- to long-wave-sensitive (M) cone opsin found in many species are established early in development and thought to be stable thereafter throughout life. In mouse early development, thyroid hormone (TH), through its receptor TRß2, is an important regulator of cone spectral identity. However, the role of TH in the maintenance of the mature cone photoreceptor pattern is unclear. We here show that TH also controls adult cone opsin expression. Methimazole-induced suppression of serum TH in adult mice and rats yielded no changes in cone numbers but reversibly altered cone patterns by activating the expression of S-cone opsin and repressing the expression of M-cone opsin. Furthermore, treatment of athyroid Pax8(-/-) mice with TH restored a wild-type pattern of cone opsin expression that reverted back to the mutant S-opsin-dominated pattern after termination of treatment. No evidence for cone death or the generation of new cones from retinal progenitors was found in retinas that shifted opsin expression patterns. Together, this suggests that opsin expression in terminally differentiated mammalian cones remains subject to control by TH, a finding that is in contradiction to previous work and challenges the current view that opsin identity in mature mammalian cones is fixed by permanent gene silencing.

OAT2 catalyses efflux of glutamate and uptake of orotic acid.

OAT (organic anion transporter) 2 [human gene symbol SLC22A7 (SLC is solute carrier)] is a member of the SLC22 family of transport proteins. In the rat, the principal site of expression of OAT2 is the sinusoidal membrane domain of hepatocytes. The particular physiological function of OAT2 in liver has been unresolved so far. In the present paper, we have used the strategy of LC (liquid chromatography)-MS difference shading to search for specific and cross-species substrates of OAT2. Heterologous expression of human and rat OAT2 in HEK (human embryonic kidney)-293 cells stimulated accumulation of the zwitterion trigonelline; subsequently, orotic acid was identified as an excellent and specific substrate of OAT2 from the rat (clearance=106 µl·min⁻¹·mg of protein⁻¹) and human (46 µl·min⁻¹·mg of protein⁻¹). The force driving uptake of orotic acid was identified as glutamate antiport. Efficient transport of glutamate by OAT2 was directly demonstrated by uptake of [³H]glutamate. However, because of high intracellular glutamate, OAT2 operates as glutamate efflux transporter. Thus expression of OAT2 markedly increased the release of glutamate (measured by LC-MS) from cells, even without extracellular exchange substrate. Orotic acid strongly trans-stimulated efflux of glutamate. We thus propose that OAT2 physiologically functions as glutamate efflux transporter. OAT2 mRNA was detected, after laser capture microdissection of rat liver slices, equally in periportal and pericentral regions; previous reports of hepatic release of glutamate into blood can now be explained by OAT2 activity. A specific OAT2 inhibitor could, by lowering plasma glutamate and thus promoting brain-to-blood efflux of glutamate, alleviate glutamate exotoxicity in acute brain conditions.