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Two escape hood designs (Draeger DefendAir and the Fume Free Quick Mask 2000) were tested to assess their capability to protect in a chemical warfare (CW) agent environment. Sarin and mustard vapor tests were performed on both types of hoods, and there were no breakthroughs during the 65-min tests. The hoods were also tested to assess their ability to protect the wearer from an aerosolized threat. Human test subjects donned the hoods and entered a corn oil aerosol chamber. The Draeger DefendAir achieved a 95.8% pass rate at a PF of 2,000, and the Fume Free Quick Mask 2000 achieved a 100% pass rate at a PF of 2,000.

HC Synth

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Organophosphorus nerve agent irreversibly inhibit acetylcholinesterase, causing a toxic buildup of acetylcholine at muscarinic and nicotinic receptors. Current medical countermeasureres to nerve agent intoxication increase survival if administered within a short period of time following exposure but may not fully prevent neurological damage. Therefore, there is a need to discover drug treatments that are effective when administered after the onset of seizures and secondary responses that lead to brain injury.

The former leader of Aum Shinrikyo, the Japanese doomsday cult that carried out a fatal gas attack on the Tokyo subway in March 1995 was executed on July 6. Subscribe on YouTube: https://bit.ly/2JjpnIb - - - - - - - - - - - - - Facebook: https://www.facebook.com/Newsweek Twitter: https://twitter.com/Newsweek Instagram: https://www.instagram.com/Newsweek

On stage at the Coralville Center for the Performing Arts - June 10, 2016.

I really love this song, it is a reminder of who i use to be and who i am now in a way. I hope I didnt fuck it up to bad.. this is my 2nd remix

The probability of cyclo-sarin (GF) vapor-induced miosis (defined as a post-exposure pupil diameter 50% or less of the pre-exposure pupil diameter) was estimated in rats exposed to various combinations of exposure concentration and duration. Groups of male and female Sprague-Dawley rats were exposed to GF vapor for a single duration (10, 60 or 240 minutes) in a whole-body dynamic chamber. Pupil diameter was measured by an infrared camem technique. For the six combinations of gender and exposure duration, the effective concentration for miosis in 50% of the exposed population (EC50) and the common probit slope were determined. Contrary to Haber's rule, ECt50 values increased with exposure duration (i.e., the Ct for 50% of the exposed population to show miosis was not constant over time). Female rats were more sensitive to GF vapor toxicity than male rats. Miosis was the only clinical sign noted following GF vapor exposure. Possible depression of blood esterase (acetylcholinesterase, butyrylcholinesterase and carboxylesterase) activities due to low-level range of GF vapor concentrations was also investigated. GF was regenerated from blood samples of vapor-exposed rats by the addition of fluoride ion at pH 4 and the samples were analyzed by GC-FPD and GC-MS. Levels of regenerated GF in the red blood cell (RBC) fraction of the samples were five to 40 times lower than in plasma. All controls were negative for regenerated GF.

A leading United Nations investigator says she is 'stupefied' by the testimony from victims of the Syrian conflict that rebels have used nerve agent SARIN. Carla del Ponte told Swiss TV there were "strong, concrete suspicions but not yet incontrovertible proof". She said her panel had not yet seen evidence of government forces using chemical weapons. Reported on 6 May 2013 - Follow us on Facebook | http://fb.com/handsoffsyria

A method has been developed for the analysis of a Sarin (GB) nerve agent biomarker in the tissue and biological fluids of minipigs that is very sensitive and selective. The GB biomarker was the fluoride ion regenerated GB and was found in minipig samples such as red blood cells, brain, liver, lung, and adipose tissue after whole body inhalation exposure. Regenerated GB in the samples was analyzed by GC-FPD after homogenization, addition of fluoride, pH adjustment and C18 solid-phase extraction. Samples were concentrated by injecting 2-200 uL of extract on a Tenax -TA sorbent tube along with 100 pg of decadeuterated diethyl ethyl phosphonate as the internal standard followed by thermal desorption on to the GC column. The method detection limit was 10.5 pg of agent on column. Highest levels were seen in the lungs (22.8 ng/g) and blood (18.8 ng/g) as expected after an inhalation exposure. Regenerated GB levels in red blood cells were approximately 10 times greater than in the plasma. Outside of the lungs and blood certain sections of the brain had some of the highest level of regenerated GB such as the caudate nucleus (5.46 ng/g). Other significant depots of regenerated GB included saliva (137 ng/g), nasal discharge (72 ng/g), and lachrymal discharge (186 ng/g). Limited amounts of free GB were also isolated from saliva (6.91 ng/g) and nasal discharge (0.65 ng/g).

One-Hundred-Fifty-Third Hate exclusive podcast with Sarin Download available. Tracklist: Go Away – Lapse of Reason Fucking Humans (Delectro Remix) - 2XNI Sentinel – Sarin Opioid Slot Machine Will to Destroy – Sarin x Imperial Black Unit Forthcoming Human Performance Lab Forthcoming Konkurs Forthcoming Sarin Scanner – Primary Kontrolle – HKKPTR Zech Groove – Wumpscut Machine Gun – TGT Orgasm – Ursula Hybsch Nautilus – Klinik (Ah Cama Sotz Remix) Kein Schmerz – Marc Ash Terrorvision – Manufacture In Memoriam – Templer Sublimate – Para (Mat Cangiano) Follow Sarin here: @ sarinvx www.instagram.com/sarinvx/ www.facebook.com/sarinberlin/ www.discogs.com/artist/4668022 www.residentadvisor.net/dj/sarin www.x-img.de/ Follow HATE here: www.facebook.com/hatecollective/ www.instagram.com/hate_collective/

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Russia today's propaganda in French

'Hindi Kavya Sangrah by Hemraj Mani and Mira Sarin - Kendriya Hindi Samsthan'

The fluoride reactivation process was evaluated for measuring the level of sarin or soman nerve agents reactivated from substrates in plasma and tissue from in vivo exposed guinea pigs (Cava porcellus), in blood from in vivo exposed rhesus monkeys (Macaca mulatta), and in spiked human plasma and purified human albumin. Guinea pig exposures ranged from 0.05 to 44 LD50, and reactivated nerve agent levels ranged from 1.0 ng/mL in plasma obtained from 0.05 LD50 sarin exposed guinea pigs to an average of 147 ng/g in kidney tissue obtained from two 2.0 LD50 soman-exposed guinea pigs. Positive dose-response relationships were observed in all low-level, 0.05 to 0.4 LD50, exposure studies. An average value of 2.4 ng/mL for reactivated soman was determined in plasma obtained from two rhesus monkeys three days after a 2 LD50 exposure. Of the five types of guinea pig tissue studied, plasma, heart, liver, kidney and lung, the lung and kidney tissue yielded the highest amounts of reactivated agent. In similar tissue and with similar exposure procedures, reactivated soman levels were greater than reactivated sarin levels. Levels of reactivated agents decreased rapidly with time while the guinea pig was alive, but decreased much more slowly after death. This latter chemical stability should facilitate forensic retrospective identification. The high level of reactivated agents in guinea pig samples led to the hypothesis that the principal source of reactivated agent came from the agent-carhoxylesterase adduct. However, there could be contributions from adducts of the cholinesterases, albumin and fibrous tissue, as well. Quantitative analysis was performed with a GC-MS system using selected ion monitoring of the 99 and 125 ions for sarin and the 99 and 126 ions for soman. Detection levels were as low as 0.5 ng/mL. The assay was precise and easy to perform, and has potential for exposure analysis from organophosphate nerve agents and pesticides in other animal species.

Organophosphorous (OP) nerve agents, such as sarin, exert acute effects by inhibiting acetylcholinesterase in the central and peripheral nervous systems, which results in accumulation of acetylcholine and, in turn, an excessive stimulation of nicotinic and muscarinic receptors. Preliminary evidence using diverse OPs indicates that the DARPP-32/PP-1 signaling pathway is activated by nicotinic receptor stimulation. We investigated whether treatment of whole animals with sarin activated the DARPP-32/PP-1 signaling cascade. Both a seizure-inducing dose (1.0 x LD50) and a sub-seizure threshold dose (0.5 x LD50) of sarin were tested. Rats receiving the sub-threshold dose were asymptomatic for seizures. A selective increase in phospho-T75 DARPP-32 levels was observed in striatum from these rats 30 min after exposure. Rats displaying seizure activity following administration of a 1.0 x LD50 dose of sarin displayed changes in several phosphoproteins, including T75 DARPP-32. Transient increases in T75 DARPP-32, T183 ERK, and S133 CREB phosphorylation were followed by reductions in phosphorylation at three DARPP-32 sites (T34, S102, and S137) and reductions in 594 spinophilin and S897 NR1. Another glutamate receptor site, S845 GluR1, was unaffected by sarin treatment. This study represents the first comprehensive analysis of signal transduction pathways activated in response to sarin exposure in whole animals.

Chemical warfare nerve agents (CWNAs), such as sarin, soman, and VX, are organophosphorus compounds (OPs). They dismpt normal nervous system transmissions through the irreversible inhibition of acetylcholinesterase (AChE), the enzyme that breaks down the cholinergic neurotransmitter (NT) acetylcholine (ACh). The buildup of ACh in response to a large exposure to nerve agents can lead, unless promptly treated, to muscle weakness, increased secretions (i.e., lacrimation, rhinorrhea, salivation), convulsions and seizures, respiratory depression, coma, and death (Taylor, 2001). The progression of signs, their neuropharmacological basis, and toxic consequence elicited from acute high-dose exposures have been well characterized (McDonough and Shih, 1993, 1997; Shih et al., 2003). However, much less is known about the long-term effects of repeated low-dose CWNA exposure. Comprehensive reviews of the available literature on the long- term health effects of exposure to low level CWNAs have been published (Panel on Anticholinesterase Chemicals, 1982; Coordinating Subcommittee, 1985; Moore, 1998; Romano et al., 2001). In general, exposure to low-level CWNAs is a potential emerging health hazard that requires further investigation (Romano et al., 2001).

The aims of the present study were to (a) establish the parameters associated with oxime concentration in plasma following oral administration of 2-PAMC1 (2-pyridine aldoxime methochloride) to rats, (b) determine the combined effect of prophylaxis with 2-PAMC1 and treatment with atropine on the toxicity of sarin (isopropyl methylphosphonofluoridate, GB) in rats, and (c) establish a correlation between oxime level in plasma and protection afforded against sarin poisoning. It was concluded that: (1) When 2-PAMC1 is administered orally to rats, the plasma oxime level rises rapidly, reaches a maximum after about 1 hr, and then decreases at a first-order rate. The biological half-life of 2-PAMC1 in the rat is estimated to be 1.4 hr. (2) A prophylactic effect of 2-PAMC1, when used in conjunction with atropine, has been demonstrated in rats poisoned with sarin. (3) The protection afforded by 2-PAMC1 against sarin poisoning in rats can be correlated with the oxime level in the plasma at the time of sarin poisoning.

Perma.cc archive of https://home.treasury.gov/news/featured-stories/the-case-for-a-robust-attack-on-the-tax-gap created on 2022-06-02 14:53:18.576475+00:00.

A mid-era release of Seth Haley's pre Com Truise alias Sarin Sunday

Sarin Shoko Favorites

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Sarin Singhal Favorites

Regards, Maya

Document number CIA-RDP82-00457R004400600003-1 declassified and released through the CIA's CREST database. Previously available only on four computers located outside of Washington D.C., the Agency was successfully pressured into putting the files online as a result of a MuckRock lawsuit and the efforts of Emma Best. The metadata was collected by Data.World, and the files are now being archived and made text searchable by the Internet Archive.

Control of seizure activity is critical to survival and neuroprotection following nerve agent exposure. Extensive research has shown that three classes of drugs, muscarinic antagonists, benzodiazepines, and N-methyl-oaspartate antagonists, are capable of moderating these seizures. This study began to map the neural areas in rat brain that respond to these three drug classes resulting in anticonvulsant effects. Drugs of each class (scopolamine, midazolam, MK-801) were evaluated for their ability to prevent sarin-induced seizures when injected into specific brain areas (lateral ventricle, anterior piriform cortex, basolateral amygdala, area tempestas). Animals were pretreated by microinjection with saline or a dose of drug from one of the three classes 30 min prior to receiving 150 g/kg sarin, subcutaneously, followed by 2.0 mg/kg atropine methylnitrate, intramuscularly. Animals were then returned to their cages, where electroencephalographic activity was monitored for seizures. Anticonvulsant effective doses (ED so) were determined using an up-down dosing procedure over successive animals. Scopolamine provided anticonvulsant effects in each area tested, while midazolam was effective in each area except the lateral ventricle. MK- 801 was only effective at preventing seizures when injected into the basolateral amygdala or area tempestas. The results show a unique neuroanatomical and pharmacological specificity for control of nerve agent-induced seizures.

This report describes the effects of treatment with low levels of the cholinesterase (ChE) inhibitors Sarin (0.5 LDSO s.c. 3 times weekly) and pyridostigmine bromide (PB, 80 mg/L in drinking water) alone or in combination for 3 weeks as compared with untreated controls. At 2, 4 and 16 weeks after exposure, we studied the brain regional levels of glucose utilization (rCGU), as well as electroencephalographic activity, heart rate and locomotor activity with a telemetry system, on an hourly basis throughout the day, during seven-day periods. Statistical parametric maps of cerebral cortex rCGU obtained were compared with similar maps of cortical cerebral blood flow (rCBF) obtained during the previous year. The slope relating rCBF to rCGU in cerebral cortex was enhanced by sarin and depressed by sarin + PB four weeks after treatment. The analysis of cardiovascular regulation indicated significant reduction of heart rate and enhanced heart rate variability during PB treatment that recovered partially one week after treatment. Sarin (4 weeks) and PB (4 and 16 weeks) also showed enhanced HR variability. Sarin induced enhanced heart rate variability at all times after treatment. In conclusion, the changes in rCBF/rCGU coupling observed 4 weeks after sarin are consistent with residual cholinesterase inhibition in vascular compartments. The changes in heart rate variability deserve further exploration.

Results of performance testing of the 3M Model BE10 powered air-purifying respirator (PAPR) are described. Three series of tests were performed: (1) breakthrough time determinations of PAPR Cartridge Model AP3 against Sarin (GB) (2) GB vapor penetration determination of entire PAPR systems using manikin headform and simulated breathing, and (3) corn-oil protection factor determinations of PAPR systems using human subjects. Results indicate that cartridges provide adequate resistance to GB penetration against high-concentration challenges, but that corn oil aerosol and high concentration GB vapor penetration into the breathing zone of the PAPR occurs at high levels, possibly through the hood-type head enclosure and/or the exhalation valve.

Results of performance testing of the 3M Model BE10 powered air-purifying respirator (PAPR) are described. Three series of tests were performed: (1) breakthrough time determinations of PAPR Cartridge Model AP3 against Sarin (GB) (2) GB vapor penetration determination of entire PAPR systems using manikin headform and simulated breathing, and (3) corn-oil protection factor determinations of PAPR systems using human subjects. Results indicate that cartridges provide adequate resistance to GB penetration against high-concentration challenges, but that corn oil aerosol and high concentration GB vapor penetration into the breathing zone of the PAPR occurs at high levels, possibly through the hood-type head enclosure and/or the exhalation valve.

Sarin Earthsea Favorites

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This item represents a case in PACER, the U.S. Government's website for federal case data. This information is uploaded quarterly. To see our most recent version please use the source url parameter, linked below. To see the canonical source for this data, please consult PACER directly.

This item represents a case in PACER, the U.S. Government's website for federal case data. This information is uploaded quarterly. To see our most recent version please use the source url parameter, linked below. To see the canonical source for this data, please consult PACER directly.

This item represents a case in PACER, the U.S. Government's website for federal case data. This information is uploaded quarterly. To see our most recent version please use the source url parameter, linked below. To see the canonical source for this data, please consult PACER directly.

Wieland, Sundali, Kemmelmeier and Sarin (2014) conducted three studies to explore contexts and mechanisms that might account for the gender effect in risk aversion. They found evidence to suggest that gender effects in risk aversion may be affected by elicitation method (willingness to pay, WTP vs. willingness to accept, WTA) and by decision domain (gambling framed vs. non-gambling framed decisions). Women offered significantly less money than men in WTP conditions but the same amounts as men in WTA conditions, suggesting a gender difference in the endowment effect. This gender effect was stronger in gambling framed tasks than in non-gambling framed tasks.

Japan has executed the remaining six members of the doomsday cult group Aum Shinrikyo on July 26, which carried out the deadly nerve gas attack on the Tokyo subway system in 1995. Subscribe on YouTube: https://bit.ly/2JjpnIb - - - - - - - - - - - - - Facebook: https://www.facebook.com/Newsweek Twitter: https://twitter.com/Newsweek Instagram: https://www.instagram.com/Newsweek

Case name: Sarin v. United States Opinion filed: 1994-03-07 Docket No.: 93-1233 Citations: • 510 U.S. 1178

Tokyo, March 20, 1995. Subway commuters begin to choke and collapse. They've been poisoned with sarin gas. Disciples of an obscure New Religion have decided they need to kill all of humanity to save mankind. How did this happen and why? One Day That Changed Asia playlist: https://www.youtube.com/playlist?list=PLkMf14VQEvTZNcYlHbMrhgLgUff3HX33d ========== About One Day That Changed Asia: In just one day, whole worlds can change. Lives can be lost or saved, futures ruined or restored. This series features stories of mortal danger, terror and loss, redemption and hope, that happened over One Day that Changed Asia. ========== #CNAInsider #CNAInsiderDocumentaries #TokyoSarinAttack For more, SUBSCRIBE to CNA INSIDER! https://www.youtube.com/cnainsider Follow CNA INSIDER on: Instagram: https://www.instagram.com/cnainsider/ Facebook: https://www.facebook.com/cnainsider/ Website: https://cna.asia/cnainsider

This project aimed to investigate the molecular mechanism(s) of organ injury following exposure to sublethal doses of the organophosphorus agent, sarin. The lethal toxic effect of sarin exposure is caused by irreversible inhibition of acetylcholinesterase (AChE) and subsequently excessive stimulation of postsynaptic cholinergic receptors. However, much less is known about the effects of low-dose sarin exposure on functions of critical brain regions. Neurotoxicity caused by sarin exposure can be mediated by pathways independent of the cholinergic system. Since the hippocampus plays an important role in cognitive functions (including learning and memory), and is one of the most sensitive brain regions to sarin-induced injury, the focus of this study is to investigate differential gene expression and pathway perturbation in this brain region, using microarray technology combined with advanced bioinformatics. Sarin treatment resulted in differential expression of a large number of genes. Most of these genes showed increased expression, especially at the 6-hour and 25-day time points. However, significant gene repression was observed at the 10-day time point. Pathway analysis revealed that one of the direct effects of sarin cellular toxicity could be related to DNA damage and inhibition of the glutathione antioxidant system, which triggered the up-regulation of the apoptotic pathways at early time points.

This study is assessing the effects in guinea pigs of repeated low-dose exposure to the nerve agent sarin. Preliminary results suggest no effects of either repeated 0.2 or 0.4 X LD50 sarin exposure (compared with saline) on body weight or temperature, general physical signs, flinch threshold or activity level, or on EEG activity. In contrast, RBC cholinesterase levels dropped to 20% of baseline following the tenth exposure in the 0.4 group. Since this study is ongoing, data from receptor binding and brain cholinesterase assays and histopathology are still being collected and analyzed, and may be influenced by the dramatic changes in cholinesterase activity.

Results of performance testing of six NIOSH approved commercial self-contained breathing apparatus (SCBA) face piece designs are described. A series of tests was performed to determine Sarin (GB) and distilled sulfur mustard vapor breakthrough of SCBA face pieces using manikin head form and simulated breathing.

This project assessed the effects of repeated low-dose exposure of guinea pigs to the organophosphorus nerve agent sarin. Animals were injected once a day, 5 days per week (Monday-Friday), for 2 weeks with fractions (0.3 x, 0.4 x, 0.5 x or 0.6 x) of the established LD50 dose of sarin (42 micrograms/kg, s.c.). Animals were assessed for changes in body weight, red blood cell (RBC) acetylcholinesterase (AChE) levels, neurobehavioral reactions to a functional observational battery (FOB), cortical electroencephalographic (EEG) power spectrum, and intrinsic acetylcholine (ACh) neurotransmitter (NT) regulation over the 2 weeks of sarin exposure and for up to 12 days post-injection.

Guinea pigs were exposed 5 days/week/two weeks to saline or one of two sarin doses (0.2 or 0.4 x LD50). Animals were assessed for signs of toxicity, changes in body weight and temperature, EEG activity, behavioral and biochemical parameters during exposure (E1-10) and up to 100 days post-exposure (P100). Red blood cell AChE was depressed 60% and 80% respectively in the 0.2 and 0.4 x LD50 groups following E10, returning to baseline by P100. Brain AChE was significantly reduced in the 0.4 x LD50 animals only following E10, returning to baseline by P100. The 0.4 x LD50 animals exhibited a significant increase in beta2 EEG activity across exposure days, but returned to control levels by P3. No differences were noted among groups on toxicity signs, weight or temperature. A significant increase in flinch threshold in both sarin groups was found only on P3, P10 and P30. There were significant increases in vertical movement and activity-chamber center time in the 0.4 xLD50 animals at P100; due to high variability, a supplementary cohort was exposed and tested; no significant changes were found. These results suggest that the initial depression of AChE does not result in persistent changes that influence physiology or behavior.

Chemical warfare nerve agents and certain pesticides are organophosphorus compounds (OPs) that potently inhibit cholinesterases (ChEs), in particular acetylcholinesterase (AChE), an enzyme that hydrolyzes the cholinergic neurotransmitter acetylcholine (ACh) in the peripheral and central nervous system (CNS) (Taylor 2001).

The central nervous system (CNS) is an immuneprivileged site where the role of immune cells and mediators in brain injury caused by organophosphates (OP) is poorly understood. Many mediators have been identified in nervous system tissue. For instance, interleukin-6 (IL-6), a cytokine that acts on a wide range of tissue influencing cell growth and differentiation, is an agonist for vascular endothelial growth factor (VEGF). CNS cells producing IL-6 include astrocytes, macrophages, microglia, neurons, and brain endothelial cells. Here we describe the response of five different mediators, human interleukin-1beta (hIL-1b), hIL-6, hIL-8, tumor necrosis factor alpha (hTNF-a), and human granulocyte macrophage-colony stimulating factor (hGM-CSF) associated with human astrocytes incubated with an OP, sarin (GB). Human astrocytes ( 106 cell density) were stimulated with a high concentration of GB (0.8 mM) for 48 hours at 37 degrees C. The expressed mediators in human astrocytes were detected by using the Luminex100 trademark protein multiplex immunoassay. Constitutive non-stimulated human astrocytes secreted hGM-CSF (0.59 0.03 ng/mL), hIL- 1b (0.33 0.05 ng/mL), hIL-6 (1.43 0.02 ng/mL) and hIL-8 (0.39 0.02 ng/mL). hTNF-a secretion was not detected or observed. GB decreased the endogenous secretion of these mediators as follows: hGM-CSF (0.51 0.02 ng/mL), hIL-1b (0.28 0.03 ng/mL), hIL-6 (1.00 0.02 ng/mL). Meanwhile, the induction chemokine hIL-8 was increased 0.42 0.03 ng/mL by GB as measured by Luminex100 trademark. Up and down-regulation of these mediators in human astrocytes promises a nonintrusive mechanism for assessment of the role of individual mediators in brain cell development, function and response to insult, such as that caused by the OP. Many neurodegenerative disorders are associated with inflammatory processes in the central nervous system (CNS).

This study tested and optimized various methodologies to generate, sample and characterize GB test atmospheres in an inhalation chamber. A syringe drive spray atomization system was used for GB vapor generation. Stable GB test atmospheres (0.5 -50 mg/cu cm) were generated over different duration's (60, 240, 360 min) and sampled with solvent bubblers as well as an automated solid sorbent sampling system. Concentrations derived from each sampling method were compared against each other and statistically evaluated. A paired t-test showed no statistical difference between the two methods at the 95% confidence interval. Future applications include the ability to generate and monitor GB levels approaching the TLV-TWA of 0.0001 mg/cu cm.

This study tested and optimized various methodologies to generate, sample, and characterize sarin (GB) test atmospheres in an inhalation chamber, particularly at low-vapor levels. A syringe drive/spray atomization system produced GB vapor at lethal concentrations of 1-44 mg/m3. A saturator cell was used to generate GB vapor at sub-lethal concentrations from 1 mg/m down to very low GB levels approaching the TLV-TWA of 0.0001 mg/m3. Both generation techniques demonstrated the ability to produce stable vapor concentrations over extended exposure periods. This capability was important to determine sub-lethal nerve agent effects for inhalation toxicology studies. In addition, the techniques employed for producing and maintaining low-level GB vapor would lay the foundation for testing other chemical warfare agents, such as GF or VX.