Anyone? Tim and Bill need your help.
I mean surely a born in the 50s ain't tolerating sexuality or bisexuality, so how the will Junior Jim explain this to his father???
Anyone? Tim and Bill need your help.
I mean, if you guys aren't helping, the situation might turn out like this:
"Hey, dad."
"What is it, Junior?"
"I'm gay."
"Hey look, Iona. A got."
Maybe the first thing Bill should do before freaking out is see if he's able to name ONCE source that has given a single quote on this situation
^ His son just told him he's ing gay!!
0/10, won't recommend to my family & friends. Didn't bookmark.
I mean if no one post after your 3rd bump than the thread is a failure. LOSER.
^ consecutive 4-timers speaking
Having to bump your own thread three times
I made 3 posts in under 5 minutes, and it's considered bumping.
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I you're Duncan you go ahead and Sweep the OP's Lakers![]()
"hey look, Dad. There's goes the mansion I was going to buy you."
prejudice is taught and inherited imho, but the society is becoming more and more open, and in a few decades your children will ask you "what, you guys were around when gay people weren't allowed to get married?"
Sarin
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For other uses, see Sarin (disambiguation).
Not to be confused with Serine, Sarrin, or Saran.
Sarin, or GB, is an organophosphorus compound with the formula [(CH3)2CHO]CH3P(O)F. It is a colorless, odorless liquid,[4] used as a chemical weapon owing to its extreme potency as a nerve agent. It has been classified as a weapon of mass destruction in UN Resolution 687.[not in citation given] Production and stockpiling of sarin was outlawed by the Chemical Weapons Convention of 1993 where it is classified as a Schedule 1 substance.
Sarin[1] (RS)-Propan-2-yl methylphosphonofluoridate
Other names[hide](RS)-O-Isopropyl methylphosphonofluoridate; IMPF;
GB;[2]
2-(Fluoro-methylphosphoryl)oxypropane;
Phosphonofluoridic acid, P-methyl-, 1-methylethyl ester
Identifiers CAS number 107-44-8 PubChem 7871 ChemSpider 7583 UNII B4XG72QGFM ChEMBL CHEMBL509554 Jmol-3D images Image 1 Properties Molecular formula C4H10FO2P Molar mass 140.09 g mol−1 Appearance Clear colorless liquid Odor Odorless in pure form Density 1.0887 g/cm³ (25 °C)
1.102 g/cm³ (20 °C)Melting point -56 °C, 217 K, -69 °F Boiling point 158 °C, 431 K, 316 °F Solubility in water Miscible Hazards MSDS Lethal Nerve Agent Sarin (GB) EU classification Extremely Toxic (T+)[3] Main hazards It is a lethal cholinergic agent. NFPA 704
140LD50 70 mg-min/m3 (verify) (what is:
/
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Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa)Infobox references
Even at very low concentrations, sarin can be fatal within one minute after direct ingestion of a lethal dose, due to suffocation from lung muscle paralysis, unless some antidotes, typically atropine or Biperiden and pralidoxime, are quickly administered to a person.[4] People who absorb a non-lethal dose, but do not receive immediate medical treatment, may suffer permanent neurological damage.
Contents
- 1 Production and structure
- 2 Biological effects
- 3 Degradation and shelf life
- 4 Effects and treatment
- 5 History
- 6 References
- 7 External links
Production and structure
Sarin is a chiral molecule because it has four chemically different subs uents attached to the tetrahedral phosphorus center.[5] The SP form (the (–) optical isomer) is the more active enantiomer due to its greater binding affinity to acetylcholinesterase.[6][7] The P-F bond is easily broken by nucleophilic agents, such as water and hydroxide. At high pH, sarin decomposes rapidly to nontoxic phosphonic acid derivatives. It is usually manufactured and weaponized as a racemic mixture—an equal mixture of both enantiomeric forms—by the alcoholysis reaction of methylphosphonyl difluoride with isopropyl alcohol:
Isopropylamine is also included in the reaction to neutralize the hydrogen fluoride byproduct. As a binary chemical weapon, it can be generated in situ by this same reaction.
Biological effects
Like other nerve agents, sarin attacks the nervous system. It stops nerve endings in muscles from switching off. Death will usually occur as a result of asphyxia due to the inability of the muscles involved in breathing to function.
Specifically, sarin is a potent inhibitor of acetylcholinesterase,[8] a protein that degrades the neurotransmitter acetylcholine after it is released into the synaptic cleft. In vertebrates, acetylcholine is the neurotransmitter used at the neuromuscular junction, where signals are transmitted between neurons from the central nervous systems to muscle fibres. Normally, acetylcholine is released from the neuron to stimulate the muscle, after which it is degraded by acetylcholinesterase, allowing the muscle to relax. A build-up of acetylcholine in the synaptic cleft, due to the inhibition of cholinesterase, means the neurotransmitter continues to act on the muscle fibre, so that any nerve impulses are effectively continually transmitted.
Sarin acts on cholinesterase by forming a covalent bond with the particular serine residue at the active site. Fluoride is the leaving group, and the resulting phosphoester is robust and biologically inactive.[9][10]
Its mechanism of action resembles that of some commonly used insecticides, such as malathion. In terms of biological activity, it resembles carbamate insecticides, such as Sevin, and the medicines pyridostigmine, neostigmine, and physostigmine.
Degradation and shelf life
![]()
Rabbit used to check for leaks at sarin production plant, Rocky Mountain Arsenal (1970)
The most important chemical reactions of phosphoryl halides is the hydrolysis of the bond between phosphorus and the fluoride. This P-F bond is easily broken by nucleophilic agents, such as water and hydroxide. At high pH, sarin decomposes rapidly to nontoxic phosphonic acid derivatives.[11][12]
Sarin degrades after a period of several weeks to several months. The shelf life can be shortened by impurities in precursor materials. According to the CIA, some Iraqi sarin had a shelf life of only a few weeks, owing mostly to impure precursors.[13]
Its otherwise short shelf life can be extended by increasing the purity of the precursor and intermediates and incorporating stabilizers such as tributylamine. In some formulations, tributylamine is replaced by diisopropylcarbodiimide (DIC), allowing sarin to be stored in aluminium casings. In binary chemical weapons, the two precursors are stored separately in the same s and mixed to form the agent immediately before or when the s is in flight. This approach has the dual benefit of solving the stability issue and increasing the safety of sarin munitions.
Effects and treatment
Sarin has a high volatility (ease with which a liquid can turn into a gas) relative to similar nerve agents, therefore inhalation can be very dangerous and even vapor concentrations may immediately penetrate the skin. A person’s clothing can release sarin for about 30 minutes after it has come in contact with sarin gas, which can lead to exposure of other people.[14] People who absorb a non-lethal dose but do not receive immediate appropriate medical treatment may suffer permanent neurological damage.
Even at very low concentrations, sarin can be fatal. Death may follow in one minute after direct ingestion of a lethal dose unless antidotes, typically atropine and pralidoxime, are quickly administered.[4] Atropine, an antagonist to muscarinic acetylcholine receptors, is given to treat the physiological symptoms of poisoning. Since muscular response to acetylcholine is mediated through nicotinic acetylcholine receptors, atropine does not counteract the muscular symptoms. Pralidoxime can regenerate cholinesterases if administered within approximately five hours. Biperiden, a synthetic acetylcholine antagonist, has been suggested as an alternative to atropine due to its better blood–brain barrier penetration and higher efficacy.[15]
Sarin is estimated to be over 500 times more toxic than cyanide.[16] The LD50 of subcutaneously injected sarin in mice is 172 μg/kg.[17] Treatment measures have been described.[18]
Initial symptoms following exposure to sarin are a runny nose, tightness in the chest and constriction of the pupils. Soon after, the victim has difficulty breathing and experiences nausea and drooling. As the victim continues to lose control of bodily functions, the victim vomits, defecates and urinates. This phase is followed by twitching and jerking. Ultimately, the victim becomes comatose and suffocates in a series of convulsive spasms. Moreover, common mnemonics for the symptomatology of organophosphate poisoning, including sarin gas, are the "killer B's" of bronchorrhea and bronchospasm because they are the leading cause of death,[19] and SLUDGE - Salivation, Lacrimation, Urination, Defecation, Gastrointestinal distress, and Emesis.
The DMC school begins about the same time as the graduate school im attending... difference is I have to pay (dad has to pay, to be exact) big $ for that while the DMC's school is totally free.
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