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AbstractObjectiveSkin contamination is one of the most likely risks after accidental or occupational radiological accidents. Using scintigraphy, we assessed a topical lotion for its decontamination efficacy (DE) after exposure with short-lived medical radioisotopes technetium Tc 99m (99mTc) and thallium 201Tl (201Tl).MethodsUsing 99mTc (300 ± 5 µCi/100 µl) and 201Tl (100 ± 5 µCi/100 µl), the thoracoabdominal region (shaved skin) of Sprague Dawley rats and human tissue equivalent were contaminated and then decontaminated using cotton swabs soaked in formulated lotion at different time intervals. Static counts were recorded and calculated for DE. Histologic examination was performed on the animal model.ResultsThe DE of the formulation for 99mTc and 201Tl was 85% ± 5 and 88% ± 2, respectively. The prepared formulation effectively removed the radionuclides from the tissue surface.ConclusionsThe formulated lotion assisted in the effective removal of radiocontaminants by decontaminating the radionuclides. Moreover, minimal and easily manageable radioactive waste was generated by this process. Further investigation regarding the infusion of formulated lotion into ready-to-use skin wipes for self-decontamination may be useful for mass casualty scenarios. (Disaster Med Public Health Preparedness. 2014;0:-)

The purpose of this study was to determine whether functional purinergic P2 receptors are present in trabecular meshwork cells. The human trabecular cell line HTM-3 and cultured bovine trabecular cells were used to assess the effects of P2 agonists on intracellular Ca(2+) levels, extracellular signal-regulated kinase (ERK1/2) activation, and P2Y receptor expression. ATP, UTP, ADP, and 2-methyl-thio-adenosine triphosphate (2-MeS-ATP) each produced a concentration-dependent increase in intracellular Ca(2+) in bovine trabecular cells and the HTM-3 cell line. The addition of UDP did not produce any detectable rise in intracellular Ca(2+). Pretreatment with the P2Y(1) receptor antagonist 2'-deoxy-N(6)-methyladenosine-3',5'-diphosphate (MRS-2179) blocked the ADP- and 2-MeS-ATP-induced rise in intracellular Ca(2+). However, the ATP- or UTP-induced rise in intracellular Ca(2+) was not inhibited by MRS-2179 pretreatment. The addition of ADP, 2-MeS-ATP, ATP, or UTP were also found to activate the ERK1/2 signaling pathway. This activation of ERK1/2 was blocked by pretreatment with the mitogen-activated protein kinase kinase inhibitor 1,4-diamino-2,3-dicyano-1,4-bis(o-aminophenylmercapto)butadiene (U-0126) or the protein kinase C inhibitor chelerythrine chloride, but not by MRS-2179. Analysis of mRNA from HTM-3 cells by reverse transcription-polymerase chain reaction revealed the expression of P2Y(1), P2Y(4), and P2Y(11) receptor subtypes. These data demonstrate that multiple P2Y receptors are present in trabecular cells. Our results are consistent with the idea that the mobilization of intracellular Ca(2+)results from the activation of P2Y(1) and P2Y(4) receptors, whereas the activation of the ERK1/2 pathway results from the activation of P2Y(4) receptors alone. However, a role for the P2Y(11) receptors in mobilization of Ca(2+), or activation of the ERK1/2 pathway, cannot be discounted.