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  • June 1, 2017
  • 12:59 AM

D10 in the Treatment of Prehospital Hypoglycemia: A 24 Month Observational Cohort Study

by Rogue Medic in Rogue Medic

Why treat hypoglycemia with 10% dextrose (D10), rather than the more expensive, potentially more harmful, and less available traditional treatment of 50% dextrose (D50)? Why not? The only benefit of 50% dextrose appears to be that it is what people are used to using, but aren't we used to starting IVs (IntraVenous lines) and running fluids through the IVs? ... Read more »

  • January 20, 2017
  • 06:19 AM

RCC: Updates on Guidelines for Adjuvant Therapy and new drug combination

by Joana Guedes in BHD Research Blog

The European Association of Urology (EAU) Renal Cell Carcinoma (RCC) guidelines panel has recently updated its recommendation on adjuvant therapy with sunitinib in non-metastatic RCC after surgical tumour removal (Bex et al., 2016). These clinical guidelines provide urologists with evidence-based information and recommendations for the management of RCC and the panel includes urological surgeons, oncologists, pathologists, radiologists and patient advocates. Based on the conflicting results of two available clinical studies (ASSURE and S-TRAC), the panel rated the quality of the evidence of the trials, the harm-to-benefit ratio, the patient preferences and the costs. As a result, the EAU panel, including representatives from a patient advocate group (International Kidney Cancer Coalition) voted and reached a consensus recommendation that adjuvant therapy with sunitinib for patients with high-risk RCC after nephrectomy should not be given.... Read more »

  • July 18, 2016
  • 08:26 AM

The Internet asks me about smelly things

by Rosin Cerate in Rosin Cerate

Whenever I'm working on a new post, I like to take a bit of time to check in on the stats for this blog. I'm particularly interested in what people are typing into their search engines to find their way here. For whatever reason, a post I wrote about what poisons smell like is very popular among users of the Internet. I'm taking this as a sign that people like to read about smells, so I thought I'd look into a couple of odour-related search queries via which people have found this blog.'type of algae has strong garlic like odour'Members of the genus Chara are plant-like green algae found in lakes, rivers, and ponds all over the world. They have fun names like muskgrass or skunkweed on account of their intense unpleasant odour, which has been described as vaguely resembling that of garlic. Many sulfur-containing organic molecules (take for example, diallyl disulfide) tend to smell like garlic. Chara globularis is known to produce at least two organosulfur compounds, 4-methylthio-l,2-dithiolane and 5-methylthio-l,2,3-trithiane. Both can inhibit photosynthesis, so I'm guessing they're produced by the algae to help it compete with other sun-using aquatic organisms.'are there pesticides smell like fish?'Yes, at least one pesticide does indeed smell like fish. 2,4-D is herbicide discovered by the Allies during WII (fruit of their efforts to develop new chemical weapons) and used by the US during the Vietnam War (as an ingredient in Agent Orange). What makes 2,4-D so useful is it's way less toxic to grasses compared to other plants, meaning it can be applied to lawns and cereal crops in order to selectively disrupt the growth of their competitors (AKA weeds). While it's good at what it does, 2,4-D does not dissolve well in water. To fix this, chemists have played around with it a bit over the years. One of the more successful modifications was a salt, 2,4-D dimethylamine. It's very good at dissolving in water, but has an intense fishy odour because it contains a small amine. Amines are derivatives of ammonia found in, among other things, raw fish.'why do some toxic chemicals smell sweet?'Toxic chemicals with a sweet odour include benzene, carbon tetrachloride, chloropicrin, cyclosarin, and diborane. From a structural standpoint, they don't appear to have much in common:Benzene is an electron-rich ring of six carbon atomsCyclosarin consists of a phosphorus atom attached to atoms of carbon, oxygen, and fluorine, as well as a ring of carbon atoms.Carbon tetrachloride and chloropicrin have no rings but contain a bunch of chlorine atoms.Diborane consists only of boron and hydrogen.Smelling is complicated. We sense odours via the activation of receptors inside our nose, which transmit signals to our brain. Sounds pretty straightforward right? Problem is, there are hundreds of receptor types, and the signals they produce interact with one another in specific ways to form the information passed on to the brain. It's not uncommon for molecules with very different chemical structures to have similar odours, and for similarly structured molecules to have very different odours.ReferencesSell CS. 2006. On the unpredictability of odor. Angewandte Chemie International Edition 45(38):6254-6261. [Full text]Stonard RJ, Miller-Wideman MA. 1994. Herbicides and plant growth regulators. In: Agrochemicals from Natural Products, Ed. CRA Godfrey. CRC Press. [Link]Volgas GC, Mack RE, Roberts JR. 2005. Benefits of a 2,4-D acid herbicide formulation. In: Pesticide Formulations and Delivery Systems, Ed. GR Goss. ASTM International. [Link] Read more »

Sell CS. (2006) On the unpredictability of odor. Angewandte Chemie (International ed. in English), 45(38), 6254-6261. PMID: 16983730  

  • July 14, 2016
  • 02:27 PM

Weird stuff found in recreational drugs: Cocaine edition

by Rosin Cerate in Rosin Cerate

This is the fifth and final post in a series on strange substances accidentally or intentionally added to street drugs. When you're done here, check out the posts on alcohol, meth, opioids, and pot/LSD.If a drug is being sold illegally, chances are its sellers have added crap to it in order to make more money. Cocaine is no exception to this deception. Substances added to nose candy because they resemble the drug but otherwise don't mimic or influence its effects include talc powder, flour, cornstarch, inositol and other sugar alcohols, various salts, boric acid, and microcrystalline cellulose. Snorting any of talc, starch, or cellulose into your lungs can result in an inflammation that disrupts your ability to breathe normally.A decidedly artsy photo of talc powder between two brushes (Source)There are also a bunch of drugs known to be mixed in with cocaine to dupe a buyer into believing they're purchasing a higher quality product. Caffeine is used in this capacity because it's cheap and is a stimulant (it perks you up) like cocaine, albeit a way less intense one. Several relatives of cocaine, including procaine, lidocaine, and benzocaine, are used as local anesthetics to do things like numb your mouth at the dentist before the drilling commences. Cocaine also causes mouth numbness, so adding these other drugs to it can trick customers into thinking they're getting a higher quality product.One of the stranger yet very common additions to cocaine is a drug called levamisole. It's good at killing parasitic worms and also appears to be able to influence the immune system in useful ways. Unfortunately, it also has a tendency to ruin bone marrow and cause a serious dip in the number of white blood cells being made there (agranulocytosis), which is a fantastic way to catch a life-threatening infection. Snorting cocaine contaminated with levamisole can also damage blood vessels in the arms and legs via vasculitis. The role of levamisole as a cocaine adulterant is a bit of a mystery. It's apparently transformed into aminorex, an amphetamine-like drug, when given to racehorses, suggesting it can enhance the effects of cocaine. There's also some evidence that levamisole can act on receptors in the brain to enhance how good cocaine makes you feel. Alternatively, it may simply be added because it's cheap, resembles cocaine, and is often easy to acquire since it's sold as a veterinary medication.Our tour of drug additions to cocaine ends with diltiazem. This drug acts to block the movement of calcium through channels in the outer membranes of heart cells, permitting it to be used to help control an erratic heartbeat (arrhythmia) and other heart issues. It's been suggested that some distributors decided to add diltiazem to their cocaine in order to negate the negative effects it can have on the heart, which happen to include arrhythmias. Even so, there isn't any evidence diltiazem can provide a protective effect. If anything, it might actually make things worse.ReferencesBrunt TM, Rigter S, Hoek J, Vogels N, van Dijk P, Niesink RJ. 2009. An analysis of cocaine powder in the Netherlands: Content and health hazards due to adulterants. Addiction 104(5):798-805.Cole C, Jones L, McVeigh J, Kicman A, Syed Q, Bellis M. 2011. Adulterants in illicit drugs: A review of empirical evidence. Drug Testing and Analysis 3(2):89-96.Tallarida CS, Tallarida RJ, Rawls SM. 2015. Levamisole enhances the rewarding and locomotor-activating effects of cocaine in rats. Drug and Alcohol Dependence 149:145-150. [Full text]... Read more »

  • June 23, 2016
  • 09:55 AM

Weird stuff found in recreational drugs: Pot/LSD edition

by Rosin Cerate in Rosin Cerate

This is the fourth post in a series on strange substances accidentally or intentionally added to street drugs. When you're done here, check out the posts on alcohol, meth, opioids, and cocaine.In the autumn of 2007, hospitals near Leipzig, Germany admitted 29 people after they inadvertently smoked weed contaminated with lead. Yep, some dealer or grower decided it was a good idea to drop a bunch of small lead particles into the marijuana they were selling, presumably to increase its weight (lead is super dense) and thus make mad bank. The average lead content of stashes recovered from the poisoned individuals was 10% by weight, translating into an additional ~$1500 per kg of pot sold.It turns out the center of a lit joint can reach temperatures up to 1200°C, sufficient to ensure a bunch of lead particles will end up in the inhaled smoke and so be absorbed via the lungs (particularly if the inhaled smoke is being held in to maximize absorption of non-lead stuff like THC). Those with lead poisoning showed up to the hospitals with stomach cramps, feeling like they were going to barf, lacking sufficient numbers of red blood cells (anemia), and being unreasonably tired. Most had basophilic stippling and exhibited Burton's line (here's a gross photo), which are classic indicators of lead poisoning. One particularly unfortunate person also had their nervous system seriously damaged by lead. In addition to experiencing hallucinations, this individual exhibited wrist drop because a nerve connecting their spine with their arms stopped working properly.Aluminum and small bits of glass have also been found in marijuana sold on the street. The aluminum was attributed to using unreasonably dirty water to grow the plants, while the glass was thought to be intentionally added to make the pot look better (like it has lots of crystals) and increase its weight. Inhaling hot glass fumes isn't pleasant since they can severely burn your mouth and lungs.Claviceps purpurea fungus growing on grain (Source)Very rarely, dropping acid (LSD) can result in ergot poisoning, which is probably one of the worst possible outcomes for a trip. If the LSD is synthesized from lysergic acid obtained from the ergot fungus (Claviceps purpurea), it may be contaminated with other toxic fungal alkaloids. Ergot poisoning (aka St. Anthony’s fire) has been around since we first began harvesting rye and other grains to eat. The fungus grows on these plants, producing a bunch of compounds that aren't very nice to the human body. They act on the intestines to produce diarrhea and on the nervous system to produce seizures. Ergot alkaloids also cause blood vessels to constrict, reducing blood (and thus oxygen) flow to the arms and legs (aka limb ischemia, usually accompanied by burning pain). In severe cases, the reduced blood flow can lead to gangrene, where the ends of one's fingers and toes to die, turn black, and eventually fall off.ReferencesBusse F, Omidi L, Timper K, Leichtle A, Windgassen M, Kluge E, Stumvoll M. 2008. Lead poisoning due to adulterated marijuana. New England Journal of Medicine 358(15):1641-1642. [Full text]Cole C, Jones L, McVeigh J, Kicman A, Syed Q, Bellis M. 2011. Adulterants in illicit drugs: A review of empirical evidence. Drug Testing and Analysis 3(2):89-96.Raval MV, Gaba RC, Brown K, Sato KT, Eskandari MK. 2008. Percutaneous transluminal angioplasty in the treatment of extensive LSD-induced lower extremity vasospasm refractory to pharmacologic therapy. Journal of Vascular and Interventional Radiology 19(8):1227-1230.... Read more »

Busse F, Omidi L, Timper K, Leichtle A, Windgassen M, Kluge E, & Stumvoll M. (2008) Lead poisoning due to adulterated marijuana. The New England Journal of Medicine, 358(15), 1641-1642. PMID: 18403778  

  • June 21, 2016
  • 09:17 AM

Weird stuff found in recreational drugs: Opioid edition

by Rosin Cerate in Rosin Cerate

This is the third post in a series on strange substances accidentally or intentionally added to street drugs. When you're done here, check out the posts on alcohol and meth.Opioids are drugs that affect the human body by binding to a group of related proteins conveniently known as opioid receptors. By connecting to these receptors in a certain manner, they convince receptor-bearing cells in the brain, spinal cord, and intestine to do useful things like reduce the sensation of pain (while making you feel warm and fuzzy), suppress coughing, and prevent an onslaught of diarrhea. In addition to opiates such as morphine and codeine that are naturally produced by the opium poppy, we've figured out how to put together a whole slew of opioids both by modifying opiates, as is done to make heroin (from morphine) and oxycodone (from thebaine), or synthesizing entirely new drugs such as fentanyl from scratch.Desmethylprodine, also known as 1-methyl-4-phenyl-4-propionoxypiperidine (MPPP), was invented by a pair of drug company scientists in 1947. Structurally, it's very similar to meperidine (pethidine, Demerol), another entirely synthetic opioid. Seeing as it wasn't any more effective than meperidine at killing pain, the drug company decided to nix its production. Nearly thirty years later, a chemistry grad student by the name of Barry Kidston read about MPPP and decided to try making some of it for personal use. While the first couple of batches yielded a successful means of getting high, the situation soon devolved into an imaginary TV show I'm calling Breaking Sad. Kidston got sloppy. He apparently started to rush the reactions used to make MPPP and then didn't isolate the drug properly. As a result, an impurity called 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) ended up in the final product. If you put MPTP in your body, it's converted into a neurotoxic substance with a fine-tuned appetite for destruction. It specifically annihilates dopamine-releasing neurons in a part of the brain responsible for controlling muscle movements, resulting in permanent symptoms resembling those seen in people with Parkinson's disease (parkinsonism). Kidston ended up hospitalized with acute parkinsonism after unwittingly dosing himself with MPTP. Although doctors eventually figured out they could treat his condition with a L-DOPA, which boosts dopamine levels in the brain, Kidston shortly passed away after overdosing on cocaine and codeine. A couple of other folks subsequently ended up in hospital after using poorly made MPPP and having their brains partially wrecked by MPTP. In at least two cases, the drug was tested and found to consist mostly of MPTP with only trace amounts of MPPP!MPTP brings about destruction of neurons in the substantia nigra (Photo source)Heroin, a suped-up version of morphine, is sold on the street mixed with an assortment of materials intended to do some combination of (1) cheaply bulking up the drug so it can be sold for more money, (2) deceiving buyers into thinking the quality of the drug is better than it really is so it can be sold for more money, (3) altering its effects in a desirable way, and (4) making it easier to use. Inexpensive materials used to dilute heroin include sugars, flour, and talc. Black tar heroin, a heroin-containing mixture named for its appearance and consistency, has been known to be bulked up by adding dirt or ground up paper previously soaked in black shoe polish. Quinine, a plant-derived alkaloid used to treat malaria, is used to dilute heroin in part because it also has a bitter taste and apparently produces a sensation in the lungs resembling what you feel after injecting heroin. Another bitter heroin mimic is paracetamol (acetaminophen, Tylenol), which has the added bonuses of also being painkiller, albeit a way weaker one, and having a similar melting point. Fentanyl is an incredibly strong opioid sometimes added to low quality heroin to increase its potency. Caffeine and procaine, when mixed with heroin, cause the latter to vaporize at a lower temperature, making it easier to smoke. Additionally, procaine is a local anesthetic (a numbing agent) and so can reduce any pain caused by injecting heroin.By far the nastiest accidental addition to heroin has to be people-eating bacteria such as Bacillus anthracis (causes anthrax) and Clostridium botulinum (causes botulism). They produce spores capable of surviving being heated up within a spoonful of heroin before it's injected into a vein or under the skin. In fact, the heat can cause the spores to germinate, priming them for action. Injection means instant access to the human buffet. Heroin can become contaminated with harmful bacteria during its production, shipment, sale, or use. Cases of anthrax in heroin users living in Western Europe have been explained as being the result of Bacillus anthracis spores getting into the drug as it's moved from Afghanistan via Turkey, possibly from the animal skins in which the drug is smuggled (livestock in the Middle East are occasionally killed by the bacterium) or because bone meal contaminated with spores is used to bulk up the drug prior to selling it. Spores of Clostridium botulinum, naturally found in soil, are thought to get into heroin via the materials added to bulk it up or from dirty tools used to administer the drug. Although C. botulinum requires an environment lacking in oxygen in order to flourish, and the tissues of the human body are typically well-supplied with oxygen via the blood flowing to and from them, a heroin user can inadvertently create oxygen-poor pockets within their body where the bacterium can grow and pump out toxins. Heroin doesn't dissolve well in water, so people looking to inject it into them typically use a solution of citric acid, heated gently, to facilitate dissolution. Repeatedly introducing citric acid into the body results in tissue damage and scar formation, reducing blood flow and thus the local level of oxygen. That's how you become infected with C. botulinum.ReferencesBrett MM, Hallas G, Mpamugo O. 2004. Wound botulism in the UK and Ireland. Journal of Medical Microbiology 53(Pt 6):555-561. [Full text]Cole C, Jones L, McVeigh J, Kicman A, Syed Q, Bellis M. 2011. Adulterants in illicit drugs: A review of empirical evidence. Drug Testing and Analysis 3(2):89-96.Fahn S, Sulzer D. 2004. Neurodegeneration and neuroprotection in Parkinson disease. NeuroRx 1(1):139-154. [Full text]Price EP et al. 2012. Molecular epidemiologic investigation of an anthrax outbreak among heroin users, Europe. Emerging Infectious Diseases 18(8):1307-1313. [Full text]... Read more »

Brett M, Hallas G, & Mpamugo O. (2004) Wound botulism in the UK and Ireland. . Journal of Medical Microbiology, 53(6), 555-561. DOI: 10.1099/jmm.0.05379-0  

  • June 15, 2016
  • 11:18 AM

Weird stuff found in recreational drugs: Meth edition

by Rosin Cerate in Rosin Cerate

As Breaking Bad has taught us, the clandestine manufacture of methamphetamine is a very dangerous undertaking. It involves the use of many harmful substances, which depending on the synthesis method include highly corrosive acids and bases, cancer-causing benzene, brain-damaging mercury and lead, jaw-wrecking phosphorus, and blood-breaking sodium cyanide. Blending these various substances together can produce noxious fumes, making gas masks and chemical suits a necessity if you want to avoid getting seriously hurt.Meth cooks, at least those involved in small scale operations, tend not to be trained chemists. If they don't follow the correct recipe, either because they lack the necessary knowledge or skill, or they just don't care, the aforementioned harmful substances can end up in the final product. Lead is a particularly dangerous meth contaminant. A batch of meth responsible for an outbreak of acute lead poisoning in Oregon in 1988 was found to contain >60 percent lead by weight, which is insane! If meth is synthesized using crushed tablets of pseudoephedrine, granules from the tablets can make their way into the veins of intravenous users, causing skin irritation and the increased likelihood of nasty bacterial infections. Meth can also be contaminated with organic compounds closely related to something called alpha-benzyl-N-methylphenethylamine, which when tested in mice proved to be more potent inducers of seizures compared to meth.In addition to the nasty stuff inadvertently introduced into a batch of meth during its manufacture, an interesting collection of substances are used to dilute meth prior to selling it (got to maximize those profits). These cutting agents are known to include sugars such as lactose and mannitol (cheap way to add bulk), methylsulfonylmethane (physically resembles meth, improving the perceived quality of the drug), mild stimulants such as caffeine and ephedrine (mimic the effects of meth), and sidewalk chalk (used to provide a splash of colour). ReferencesBurton BT. 1991. Heavy metal and organic contaminants associated with illicit methamphetamine production. NIDA Research Monograph 115:47-59. [Full text]Cole C, Jones L, McVeigh J, Kicman A, Syed Q, Bellis M. 2011. Adulterants in illicit drugs: A review of empirical evidence. Drug Testing and Analysis 3(2):89-96. [First page]Poulsen EJ, Mannis MJ, Chang SD. 1996. Keratitis in methamphetamine abusers. Cornea 15(5):477-482.Strathdee SA et al. 2008. The color of meth: Is it related to adverse health outcomes? An exploratory study in Tijuana, Mexico. American Journal on Addictions 17(2):111-115. [Full text]... Read more »

Cole C, Jones L, McVeigh J, Kicman A, Syed Q, & Bellis M. (2011) Adulterants in illicit drugs: A review of empirical evidence. Drug Testing and Analysis, 3(2), 89-96. PMID: 21322119  

  • June 8, 2016
  • 08:22 AM

Weird stuff found in recreational drugs: Alcohol edition

by Rosin Cerate in Rosin Cerate

Today's post is the first in a series I'm going to write about extra ingredients found in illicit recreational drugs. One of the major issues with street drugs is their manufacture and distribution is often poorly regulated. This means they can accidentally become contaminated with all sorts of toxic substances during production. Additionally, a wide range of chemical compounds, some of them harmful, may be intentionally added to dilute a drug (like a bar watering down their drinks to make more money) and/or boost its effects.Moonshine (hooch, white lightning) generally refers to any strong alcoholic drink produced illegally via fermentation and distillation. In the US, the starting ingredient is often corn, although any sugar-rich plant material can be used. You ferment sugar water into ethanol water (via the action of yeasts and bacteria), then set up a still to concentrate the ethanol (drinking alcohol) as a liquor. The fermented solution is heated in a pot attached to a coiled condenser. Since ethanol has a lower boiling point than water, the vapour that is produced will initially contain a higher concentration of ethanol compared to the liquid being boiled. The boozy vapour cools back to a liquid as it passes through the condenser, and is collected in a container at the end.A pot still used to make moonshine - pot on the right, coiled condenser on the leftIf a still is constructed using parts not intended for use in a still, it can introduce harmful substances into the moonshine. For example, hooking up a poorly cleaned automotive radiator as a condenser can result in antifreeze (ethylene glycol) ending up in the booze. Lead, a toxic metal capable of causing neurological damage, can leach into moonshine if lead-containing solder and fittings are used to connect the piping of a still. Drinking contaminated moonshine is an important cause of lead poisoning among adults in many parts of the world including the United States. This form of poisoning has a long history. In the 19th century, rum was produced in Antigua using stills with lead condensation coils, resulting in cases of lead poisoning among British soldiers deployed in the Caribbean.Along with ethanol, fermentation produces small amounts of a bunch of other alcohols. These are collectively known as fusel alcohols, and include methanol (wood alcohol) and forms of propanol and butanol. Methanol is particularly bad news, as it's converted in the body to formic acid, which can disrupt the pH balance of the body's fluids (metabolic acidosis) and cause you to go blind. The fusel alcohols usually aren't present in sufficient amounts to cause serious problems, and are removed during distillation provided it is done correctly (methanol has a lower boiling point than ethanol or water, so it's concentrated in the initial bit of liquid exiting the condenser - this is usually discarded).Unfortunately, methanol and other alcohols may be intentionally added to a liquor to boost its strength. Up until the mid-20th century, incidents in which dozens of people were poisoned by a particular batch of methanol-laced homemade alcohol were fairly commonplace in the US. Illegal alcohol remains a major cause of methanol poisoning around the world, with methanol popping up in such drinks as chang'aa (Kenya) and țuică (Romania). It tends to be more of a problem in (1) developing countries, (2) countries where alcohol is taxed up the wazoo, and/or (3) countries where alcohol is illegal or its sale is heavily restricted. In other words, places where there is an impetus to make booze at home.ReferencesHassanian-Moghaddam H et al. 2015. Methanol mass poisoning in Iran: Role of case finding in outbreak management. Journal of Public Health 37(2):354-359. [Full text]Holstege CP, Ferguson JD, Wolf CE, Baer AB, Poklis A. 2004. Analysis of moonshine for contaminants. Journal of Toxicology: Clinical Toxicology 42(5):597-601.Levy P, Hexdall A, Gordon P, Boeriu C, Heller M, Nelson L. 2003. Methanol contamination of Romanian home-distilled alcohol. Journal of Toxicology: Clinical Toxicology 41(1):23-28.... Read more »

Holstege CP, Ferguson JD, Wolf CE, Baer AB, & Poklis A. (2004) Analysis of moonshine for contaminants. Journal of Toxicology. Clinical Toxicology, 42(5), 597-601. PMID: 15462151  

  • June 6, 2016
  • 11:34 AM

Burning seaweed to make glass and avoid a lumpy neck

by Rosin Cerate in Rosin Cerate

Seaweed is one of those tricky biological groups, as membership isn't just about being a close relative. It typically includes plant-like organisms found among several types of algae - green, brown, and red - and depending on who you're talking to also includes masses of cyanobacteria (which are distant relatives of algae). Functionally, all seaweeds enjoy growing in salty water and use the sun to manufacture sugary meals for themselves. Their need for sun means they are found in sunlit coastal areas as opposed to deep dark waters.Seaweed is eaten in such diverse locales as Wales, Japan, and Belize. Agar, the gel upon which microbes are typically grown in a lab, and carrageenan, used to stabilize and thicken a diverse group of products including shampoo and soy milk, are derived from seaweed.Irish moss is a drink is made from Gracilaria seaweed (Source)Historically, certain seaweeds were collected, dried out, and then burned in large quantities to reduce them to ash. Two useful substances, sodium carbonate and iodine, could then be extracted from the ash.Sodium carbonate has many applications but is perhaps best known for being an ingredient in laundry detergent (it's a builder, meaning it softens water and thus makes surfactants more effective at removing oil and grease) and silica-based glass (it serves as flux, drastically reducing the temperature required to melt the silica, also known as quartz sand). During the 18th century and early 19th century, most flat glass had a slight blue-green colour because it was being made using seaweed ash. The development of a cheaper means of sodium carbonate production (the Leblanc process) led to a decline in the use of seaweed in glass production. It's possible to identify seaweed glass by its relatively high strontium content, which is the result of this metal being present in seawater and absorbed by seaweed as it grows.Iodine, a relative of the elements bromine and chlorine, was first discovered in the early 19th century when a French dude noticed that treating seaweed ash (after washing it with water to extract the sodium carbonate) with sulfuric acid produced a vibrant violet vapour (iode is French for violet-coloured). Here's a video to give you an idea of how this went down. As is the case with strontium, iodine is taken up by seaweed from the surrounding seawater as it grows. Iodine went on to be used as a disinfectant (after being dissolved in alcohol or water) and a means of treating goiter (thyroid enlargement due to iodine deficiency, which results in a swollen neck). It was obtained from seaweeds such as Fucus vesiculosus (bladderwrack), a common inhabitant of the coasts of northern Europe and traditionally used to treat thyroid problems. Iodine deficiency is particularly uncommon in Japan on account of seaweed featuring prominently in Japanese food. However, eating too much seaweed (often due to taking pills of it as a supplement) can cause the thyroid gland to go nuts (hyperthyroidism) on account of the large amount of iodine introduced into the body.ReferencesDi Matola T, Zeppa P, Gasperi M, Vitale M. 2014. Thyroid dysfunction following a kelp-containing marketed diet. BMJ Case Reports. DOI: 10.1136/bcr-2014-206330.Fuge R. 2007. Iodine deficiency: An ancient problem in a modern world. AMBIO 36(1):70-72. [First page]Ulbricht C et al. 2013. Seaweed, kelp, bladderwrack (Fucus vesiculosus): An evidence-based systematic review by the Natural Standard Research Collaboration. Alternative and Complementary Therapies 19(4):217-230. [First page]Zava TT, Zava DT. 2011. Assessment of Japanese iodine intake based on seaweed consumption in Japan: A literature-based analysis. Thyroid Research 4:14. [Full text] Read more »

  • May 18, 2016
  • 08:28 AM

Why antibiotics in ointments differ from those in pills

by Rosin Cerate in Rosin Cerate

There are many ways to get a drug into a person. Two common approaches are to swallow a small soluble solid or inject a liquid into a vein, causing it to be transported throughout the body to wherever it is needed.Topical medications are those applied to a body surface, be it skin, eyeballs, or the insides of your lungs. This is usually done to deliver the drug to the particular place requiring repair (e.g. eye drops for an eye infection) while minimizing the amount of drug ending up in other parts of the body where it can cause unwanted (side) effects. Alternatively, a drug may be administered topically but in such a way to ensure it ends up all over (e.g. fentanyl transdermal patches applied to the skin to alleviate severe pain by slowing releasing the drug into the body).In the case of antibacterial ointments, the gooey greases applied to cuts and scrapes to prevent infection, the drugs they contain differ from those typically given as pills or injections. Ointments such Neosporin or the classic Triple Antibiotic Ointment tend to contain three drugs: neomycin, polymyxin B, and bacitracin. All three were originally isolated from bacteria (bacitracin has a particularly interesting origin story) and act in different ways to harm particular groups of bacteria. Together they form a potent team of bacteria killers.Triple Antibiotic Ointment still life (Source)However, none of three drugs are commonly used to fight internal infections. There are two major reasons for this. First of all, they aren't particularly adept at making their way into your bloodstream if you ingest them. In other words, they are poorly absorbed from the gastrointestinal tract. Neomycin has instead been fed to people in order to selectively target and kill off a bunch of the bacteria growing inside their guts, essentially an external internal body surface (and so still a sort of topical application).The second reason for the restricted use of these drugs is their toxicity. All three are toxic to the kidneys if they end up in the bloodstream. Neomycin also tends to cause ear damage and allergic reactions in form of contact dermatitis. Bacitracin also likes to cause allergic reactions (it's up there with penicillin as far as common drug allergies go). Funnily enough, neomycin is pretty good at killing the Gram-negative bacteria usually responsible for kidney-damaging urinary tract infections. It just happens to be a bit overzealous and can hurt the organ it should be helping to protect.Polymyxin B doesn't like the kidneys or nervous system. However, it looks as though its toxicity might not actually be too severe, so the drug has found some use as a non-topical antibacterial agent in cases where people-infecting bacteria have developed resistance to other drugs.ReferencesLeyden JJ, Bartelt NM. 1987. Comparison of topical antibiotic ointments, a wound protectant, and antiseptics for the treatment of human blister wounds contaminated with Staphylococcus aureus. Journal of Family Practice 24(6):601-604.Powell LW, Hooker JW. 1956. Neomycin nephropathy. Journal of the American Medical Association 160(7):557-560. [First page]Weinberg ED. 1967. Bacitracin. In: Antibiotics (Eds. Gottlieb D, Shaw PD). Pages 90-101. Springer. [First two pages]Zavascki AP, Goldani LZ, Li J, Nation RL. 2007. Polymyxin B for the treatment of multidrug-resistant pathogens: A critical review. Journal of Antimicrobial Chemotherapy 60(6):1206-1215. [Full text]... Read more »

  • April 28, 2016
  • 10:33 AM

Breathing Bordeaux is entirely different from drinking it!

by Rosin Cerate in Rosin Cerate

It was the summer of 1882, and grape farmers in the Médoc region of southwest France (north of Bordeaux, on the Atlantic coast) had a problem.Schoolchildren (or university students, or just anyone travelling the roads along which the grapevines grew, depending on what source you're reading) were pilfering their grapes. To try and ward them off, some farmers decided to dissolve some slaked lime and copper sulfate in water and spray it on their grapevines closest to the roads. The idea was... Read more »

  • April 14, 2016
  • 08:50 AM

Tales from the pharmaceutical minor leagues

by Rosin Cerate in Rosin Cerate

When a drug company first gets its hands on a potential new drug, it will usually assign it a code name. Later on, as the drug works its way through trials designed to make sure it does something useful (e.g. reduce blood pressure) without causing serious harm (e.g. liver failure), it's given a catchier moniker like fluoxetine or atorvastatin. If the trials are a success, and the government is happy with how they were carried out, the drug can be brought to market. Most drugs don't make it. A good number don't even get to the point of being tested in humans, and thus are stuck with their code names. Here are some of their stories.RO 19-8022This is a classic example of a promising new drug gone horribly wrong. RO 19-8022 was initially heralded as an innovative anti-anxiety drug with less side effects compared to benzos. Unfortunately, it failed the Ames test, a quick way of uncovering a carcinogen without having to expose an animal to it and wait to see what develops. The test is based on detecting the ability of a compound to cause mutations in a particular strain of bacteria. Interestingly, a positive result only occurred when the bacteria (and the drug) were exposed to light. The chemical structure of RO 19-8022 is such that it will absorb visible or UV light and use it to generate reactive oxygen species. These substances, being highly reactive, can damage DNA, leading to mutations and ultimately cancer. Although it failed to make it as a medicine, RO 19-8022 found a second life as a tool for helping scientists study DNA damage and repair.Ames test results, left = negative, right = positive (Source)BRL-37344 and CL-316243These beauties turn on lipolysis (increase the breakdown of fat) in rats and dogs, meaning they likely caused drug companies to practically wet themselves when they first stumbled upon them. Diet drug = printing money. However, upon further investigation, it was determined the two compounds don't work the same way in humans as they do in most other mammals. Turns out our fat cells don't appreciably express the particular receptor (beta 3-adrenoceptor) via which these drugs act.RO 15-4513In 1985, researchers at Hoffmann-La Roche reported the discovery of a drug capable of reversing the behavioural effects of ethanol. In other words, it was able to stop mice from being buzzed. RO 15-4513 accomplishes this outcome by blocking the action of ethanol at GABA receptors in the brain. GABA is a neurotransmitter capable of making the brain less excitable, which you feel as being relaxed and less anxious. Amusingly, RO 15-4513 is really bad at its job. It can't reverse being straight up drunk, only being lightly toasted. It doesn't work for very long, so you have to be constantly giving it to people and then making sure they don't do anything stupid before it wears off. It can't be used to treat acute alcohol poisoning since it doesn't prevent the respiratory depression usually responsible for killing people who drink way too much. If all that wasn't it enough, it also appears to increase the risk of experiencing convulsions and doesn't help prevent alcohol-induced birth defects.Ro 15-4513, the pint-killerRU 486Very rarely, a drug company code ends up sticking around even after it gains a supposedly catchier name and is permitted to be sold. RU 486, also known as mifepristone, was developed in France in the 1980s and is used (along with misoprostol or another drug capable of mimicking the action of prostaglandin) to terminate pregnancies. It accomplishes this by blocking receptors otherwise activated by the sex hormone progesterone, bringing about the breakdown of the endometrium (the lining of the uterus to which an embryo is usually attached). Due to its ability to block the effects of glucocorticoids and androgens in addition to progesterone, RU 486 has been used to treat Cushing syndrome and has been investigated as a treatment for cancers of the prostate and meninges (membranes surrounding the brain and spinal cord).ReferencesBousquet-Mélou A, Galitzky J, Carpéné C, Lafontan M, Berlan M. 1994. beta-Adrenergic control of lipolysis in primate white fat cells: A comparative study with nonprimate mammals. American Journal of Physiology 267(1):R115-R123.Jenck F, Moreau JL, Bonetti EP, Martin JR, Haefely WE. 1992. Ro 19-8022, a nonbenzodiazepine partial agonist at benzodiazepine receptors: Neuropharmacological profile of a potential anxiolytic. Journal of Pharmacology and Experimental Therapeutics 262(3):1121-1127.Linden AM et al. 2011. Ro 15-4513 antagonizes alcohol-induced sedation in mice through αβγ2-type GABAA receptors. Frontiers in Neuroscience 5:3. [Full text]Lister RG, Nutt DJ. 1987. Is Ro 15-4513 a specific alcohol antagonist? Trends in Neurosciences 10(6):223-225. [First page]Taplin ME et al. 2008. A phase II study of mifepristone (RU-486) in castration-resistant prostate cancer, with a correlative assessment of androgen-related hormones. BJU International 101(9):1084-1089. [Full text]Touat M, Lombardi G, Farina P, Kalamarides M, Sanson M. 2014. Successful treatment of multiple intracranial meningiomas with the antiprogesterone receptor agent mifepristone (RU486). Acta Neurochirurgica 156(10):1831-1835. [First two pages]Will O et al. 1999. Oxidative DNA damage and mutations induced by a polar photosensitizer, Ro19-8022. Mutation Research 435(1):89-101.Zimmerman EF, Scott WJ Jr, Collins MD. 1990. Ethanol-induced limb defects in mice: Effect of strain and Ro15-4513. Teratology 41(4):453-462.... Read more »

  • April 8, 2016
  • 10:56 AM

The Antibacterial Resistance Threat: Are We Heading Toward a Post-Antibiotic Era?

by EE Giorgi in CHIMERAS

Source: PEW Charitable TrustsThe above graphic, from the Antibiotic Resistance Project by the PEW charitable trusts, summarizes how alarming the emergence of drug resistant bacterial strains has gotten over the past few decades. According to data from the Center for Disease Control (CDC), every year 2 million Americans acquire drug-resistant infections [1], in other words infections that do not respond to treatment with ordinary antibiotics. Not only do drug-resistant infections require much stronger drugs, but, when not deadly, they often leave patients with long-lasting complications.One of the scariest threats is carbapenem-resistant Enterobacteriaceae (CRE), bacteria that are resistant to several kinds of antibiotics. In 2001, only North Carolina, out of all 50 states had reported one CRE infection. Last year, in 2015, 48 states reported CRE infections to the CDC. And while drug-resistant strains emerge rapidly, the discovery of antimicrobial substances has stalled: in the last decade, only 9 new antibiotics were approved, compared to 29 discovered in the 1980s and 23 in the 1990s. We are fighting a new war, and we are running out of weapons.How does drug resistance emerge?Bacteria constitute an irreplaceable building block of our ecosystem: they are found in soil, water, air, and in every living organism. In humans, it's estimated that they outnumber our cells by 3:1, and numerous studies have shown that not only do they help us digest and produce enzymes that our body wouldn't otherwise be able to break down, but they can also influence gene expression and certain phenotypes (see some of my past posts for more information).They live in symbiosis with us, yet some bacteria can be highly pathogenic. The overall mortality rate from infectious diseases in the US fell by 75% over the first 15 years following the discovery of antibiotics [3], and researchers estimate that antibiotics have increased our lifespan by 2 to 10 years [4] by enabling us to fight infections that would otherwise be deadly.However, evolution has taught bacteria to fight back. Bacteria develop drug resistance through the acquisition of genetic mutations that either modify the bacteria's binding sites (and therefore the drug can no longer enter the membrane), or reduce the accumulation of the drug inside the bacterium. The latter happens through proteins called "efflux pumps", so called because their function is to pump drugs and other potentially harmful chemicals out of the cell. Once these advantageous mutations appear in the population, they spread very quickly, not only because they are selected for, but also thanks to bacteria's ability to transfer genes: the drug-resistant genes form a circular DNA unit called plasmid, and the unit is passed on to nearby bacteria so that they, too, can become drug resistant. These mechanisms are not new to bacteria, however, what's new is the increasing overuse of antibiotics and antimicrobial chemicals in our modern lifestyle. The antimicrobial agent called triclosan, for example, can be found in all antibacterial soaps, toothpaste, mouthwash, detergents, and even toys and kitchen utensils. Because of its wide use in household and hygiene products, triclosan has been found in water, both natural streams and treated wastewater, as well as human samples of blood, urine, and breast milk. As though that alone wasn't enough to alert consumers, a study published on the Proceedings of the National Academy of Sciences [5] claims that triclosan, which can be absorbed through the skin, can impair the functioning of both skeletal and cardiac muscle. The researchers confirmed these findings both in vitro and in animal models.Resistance is also spread through the use of antibiotics in industrial farming. In the US alone, the daily consumption of antibiotics amounts to 51 tons, of which around 80% is used in livestock, a little under 20% is for human use, and the rest is split between crops, pets, and aquaculture [3]. A meta-analysis published last year in PNAS [6] found that between 2000 and 2010 the global use of antibiotic drugs increased by 36%, with 76% of the increase coming from developing countries. The researchers projected that worldwide antibiotic consumption would rise by 67% by 2030 due to population growth and the increase in consumer demand.These frightening statistics prompted CDC director Tom Frieden to issue a warning: “If we are not careful, we will soon be in a post-antibiotic era.” An era when common infections are deadly again."We need to be very careful in using antimicrobial agents for everything from hand washing to toothpaste," Harshini Mukundan, microbiologist at Los Alamos National Laboratory, explains. "Increased selection of drug resistant organisms means that future generations will be helpless in fighting even the most common bacterial infections." Mukundan and her colleagues have been working on biosurveillance and tracking the emergence of drug resistant strains in high disease burden populations where emerging antibiotic resistance is a huge concern. In collaboration with the Los Alamos National Laboratory metagenomics group, and Los Alamos scientists Ben McMahon and Norman Doggett, the team is working on developing new assays for faster diagnosis of drug resistant infections. Another approach to fight drug resistance is trying to understand how bacterial efflux pumps work at excreting the drug out of the bacterium. Gnana Gnanakaran, a computational biologist at Los Alamos National Laboratory, and his team have developed mathematical models to describe the structure of these pumps [7] and find a way to deactivate them. While this research is highly promising and exciting, we all need to step up and do our part before it's too late: the CDC published a series of recommendations for patients to follow at the doctor's office, and there are smart choices we can make at home, too. In a recent report, the Food and Drug Administration (FDA) claims that there is no evidence that antibacterial soaps do a better job at preventing infections than ordinary soap, and that in fact:"New data suggest that the risks associated with long-term, daily use of antibacterial soaps may outweigh the benefits."In its 2011 policy paper, the Infectious Diseases Society of America (IDSA) recommended a substantial reduction in the use of antibiotics for growth promotion and feed efficiency in animal agriculture, and encouraged the FDA to complete and publish risk assessments of antibiotics currently approved for non-therapeutic use. Just like any other precious resource, antibiotics (and antimicrobial drugs in general) need to be used with parsimony. Resources:[1] Antibiotic Resistance Threats in the United States, 2013 (CDC)[2] PEW Antibiotic Resistance Poject[3] Armstrong GL, Conn LA, & Pinner RW (1999). Trends in infectious disease mortality in the United States during the 20th century. JAMA, 281 (1), 61-6 PMID: 9892452[4] ... Read more »

Hollis, A., & Ahmed, Z. (2013) Preserving Antibiotics, Rationally. New England Journal of Medicine, 369(26), 2474-2476. DOI: 10.1056/NEJMp1311479  

Cherednichenko, G., Zhang, R., Bannister, R., Timofeyev, V., Li, N., Fritsch, E., Feng, W., Barrientos, G., Schebb, N., Hammock, B.... (2012) Triclosan impairs excitation-contraction coupling and Ca2 dynamics in striated muscle. Proceedings of the National Academy of Sciences, 109(35), 14158-14163. DOI: 10.1073/pnas.1211314109  

Van Boeckel, T., Brower, C., Gilbert, M., Grenfell, B., Levin, S., Robinson, T., Teillant, A., & Laxminarayan, R. (2015) Global trends in antimicrobial use in food animals. Proceedings of the National Academy of Sciences, 112(18), 5649-5654. DOI: 10.1073/pnas.1503141112  

  • March 31, 2016
  • 11:40 AM

Extracting goo from corpses to better understand them

by Rosin Cerate in Rosin Cerate

It's goo week here at Rosin Cerate. So far we've looked at forms of natural springtime goo. For today's post, it's on to a much darker and less life-affirming goo. We're going to take a peek at the viscous fluids you can extract from a corpse to determine where/when/how it became a corpse and other useful forensic information.... Read more »

Deking J, Hargrove VM, & Molina DK. (2014) Synovial fluid: An alternative toxicologic specimen?. The American Journal of Forensic Medicine and Pathology, 35(2), 154-6. PMID: 24781403  

  • March 22, 2016
  • 04:40 PM

Parsley, prohibition, and machine gun oil: A sorrowful history of tricresyl phosphate poisoning

by Rosin Cerate in Rosin Cerate

Some poisons are better known than others.Arsenic, for example, is famous for its participation in many a murder and suicide from the Middle Ages through to the mid-19th century (after which it became easier to detect and more difficult to acquire). Even to this day, the malicious metalloid remains in the public eye as a contaminant of groundwater in parts of South Asia and of soil in old orchards.A decidedly more obscure poison is a gooey industrial derivative of coal tar (leftovers from converting coal to coal gas) by the name of tricresyl phosphate (TCP). Over the course of the 20th century, up to 60,000 people across the globe ended up with nerve damage after ingesting foods, drinks, or medicines laced with this toxic substance. It's historically been added to plastics such as PVC to ensure their plasticity, to lubricants and hydraulic fluids to boost their effectiveness at high temperatures and pressures, and to gasoline to help ensure any engines it fuels will run smoothly.Other things you can make with coal tar (Source)While its name specifically refers to three similar compounds (isomers), which contain the same number of atoms but are arranged slightly differently, industrial preparations of TCP tend to be mixtures of many different aryl organophosphates. Some of these are toxic to our nervous system. Back in the day, the isomer tri-ortho-cresyl phosphate was thought to be the principal neurotoxic constituent, but it's now known other parts of the mixture are just as good at making people ill.If it gets inside your body, TCP sets about inhibiting ester-breaking enzymes associated with your nerves, causing them to malfunction. Insecticide and nerve gas organophosphates (e.g. parathion and sarin) harm people by turning off the enzyme acetylcholinesterase, flooding nerve endings with overwhelming amounts of the neurotransmitter acetylcholine and thus disrupting our ability to control when our muscles contract and relax. Although constituents of TCP are known to inhibit acetylcholinesterase, their toxicity is primarily due to them inhibiting another esterase known as neuropathy or neurotoxic target esterase. By inactivating this enzyme, a bunch of biochemical changes take place over a week or two via which damage is inflicted on the brain, spinal cord, and peripheral nerves. This is known as organophosphorus-induced delayed neuropathy.Ingesting a liquid contaminated with TCP initially results in an upset stomach (nausea, vomiting, diarrhea, and abdominal cramping). I'm guessing this is due to the inhibition of acetylcholinesterase and subsequent stimulation of acetylcholine receptors in the smooth muscle of the small intestine, causing it to ramp up peristalsis. After a delay of a week or two, a poisoned person's arms and legs start to ache and feel numb and weak (this usually starts in the feet, then moving up to the lower legs and forearms/hands). Within another week or so, this can progress to paralysis. Complete recovery is possible for mild cases, but usually takes several years. Some people end up with permanent nerve damage.Our poisoning journey begins at the very end of the 19th century. French doctors, seeking an effective treatment for pulmonary tuberculosis (still one of the major causes of death in Europe at the time), decided to try giving their patients a substance called phospho-creosote. Instead of helping to fight the bacterial infection in their lungs, the liquid caused some of the patients to develop peripheral nerve inflammation (polyneuritis). It turns out phospho-creosote contains many of the same neurotoxic compounds found in TCP.Moving forward a couple of decades, the largest ever outbreak of TCP poisoning bloomed across the Midwestern and Southwestern United States in the spring of 1930. This was well into the time of Prohibition (it ended in 1933), so black market alcoholic beverages were all the rage. One of the popular spirits was Jamaica ginger extract (also known as fluid extract of ginger or jake), a medicine that conveniently happened to be a >50% solution of ethanol. Tragically, a portion of the 1930 batches somehow became adulterated with TCP. Up until that time, jake had been prepared using, among other things, castor oil. It's thought a manufacturer out of Boston decided to swap the castor oil with TCP (specifically a preparation known as Lyndol), perhaps to save money. As the year drew to a close, some 15-20 thousand people had been affected by the bad booze (the vast majority survived), their illness having acquired the name 'Jamaica ginger paralysis'.Only a year later, several dozen cases of paralysis were reported in the Netherlands among women who took a substance called apiol in an attempt to terminate their pregnancies. Apiol is an extract (essential oil) of parsley with a long history of use as an abortifacient and a treatment for menstrual cramps. Testing revealed the apiol taken by the women contained a substantial amount (28-50%) TCP. It's not known why it was there, but perhaps it was used to water down the apiol. Similar poisoning cases were also reported at the time (1931-32) in Germany, France, Switzerland, and Yugoslavia.A pot of parsley (Source)In 1937, TCP was responsible for an outbreak (68 people affected) of nerve damage in Durban, a port city in South Africa. This was traced back to a soybean cooking oil (Bestol superfine cooking oil, to be precise), which had been shipped from England in large drums previously used to store an industrial liquid containing TCP. The contaminated cooking oil also made its way on board a cargo ship, the Jean LD, which stopped in at Durban for a week. It caused three-quarters of the ship's crew to become ill. A second smaller outbreak affecting 11 people occurred in 1955. In this instance, poisoning resulted from the storage of drinking water in drums formerly filled with TCP. The drums had been obtained from a paint factory by some of the people employed there.During WWII, a shortage of animal- or plant-derived edible fats and oils in Germany caused some of its citizens to make the unfortunate decision to cook their food using industrial oils derived from fossil fuels. These included torpedo oil and machine gun oil, both of which contained substantial amounts of TCP. As an example, factory workers in Münster became ill after bringing home oil from work and using it to fry up potato pancakes. It's not known just how many people were affected in Germany, but the Nazis did appear to be concerned about the problem, instructing factory medical officers to educate workers about the dangers of cooking with industrial oils. Similar poisonings also occurred in Switzerland and England during the war. The illness only went away once edible oils and fats again became widely available.Fifty years after it transpired, a mysterious outbreak of paralysis in WWII-era Italy was attributed to TCP. In 1942, several dozen people living or working at a farm in Saval (on the outskirts of Verona) became ill. At the time, this illness was suspected to be the work of an infectious virus. Then, in 1994, a paper was published in which the authors reported they had examined still-paralyzed survivors of the outbreak and concluded it was likely the result of TCP poisoning. After talking to survivors and sifting through the literature, they proposed that exposure occurred via the consumption of vegetables grown in contaminated soil on the farm. At the time of the outbreak, farm workers collected old drums and tins for recycling. Some of these likely came from a nearby military truck depot, and so included residual amounts of TCP-containing engine oil. As part of the recycling process, the containers were emptied out onto the ground before being pressed into blocks, which contaminated the soil.Olive oil adulterated with TCP struck down 10,000 people over three weeks in Morocco in the autumn of 1959. Most of those who were poisoned were in the city of Meknes. They inadvertently consumed the world's worst cooking oil: A mixture of olive oil and a jet engine lubricant co... Read more »

  • March 17, 2016
  • 04:40 PM

Green fungi for a certain March-based holiday

by Rosin Cerate in Rosin Cerate

In honour of St. Patrick's Day, here are a couple of neat green fungi. I was going to do plants, but there are just so many to choose from. Ha ha.... Read more »

Santi L, Maggioli C, Mastroroberto M, Tufoni M, Napoli L, & Caraceni P. (2012) Acute liver failure caused by Amanita phalloides poisoning. International Journal of Hepatology. DOI: 10.1155/2012/487480  

Schuster A, & Schmoll M. (2010) Biology and biotechnology of Trichoderma. Applied Microbiology and Biotechnology, 87(3), 787-799. DOI: 10.1007/s00253-010-2632-1  

  • March 14, 2016
  • 02:59 PM

How machines used to resurface ice rinks can also resurface your lungs

by Rosin Cerate in Rosin Cerate

In a previous post, I discussed how the introduction of the automobile also introduced a bunch of new ways for people to hurt themselves. Similarly, an injury known as ice hockey lung didn't exist until a key advance was made in the world of ice sports: motorized ice resurfacing machines. Otherwise known as Zambonis (the same way Kleenex is a catch-all term for different brands of tissue paper), they were developed in the 1940s as a means of quickly and efficiently restoring ice sheets carved up by skate blades.... Read more »

Brat K, Merta Z, Plutinsky M, Skrickova J, & Stanek M. (2013) Ice hockey lung - a case of mass nitrogen dioxide poisoning in the Czech Republic. Canadian Respiratory Journal, 20(6), 100-103. PMID: 24032121  

  • March 7, 2016
  • 11:05 AM

Making booze feel bad

by Rosin Cerate in Rosin Cerate

Alcohol-sensitizing drugs are used to ruin the experience of consuming alcohol. This can be helpful for people seeking treatment for alcohol dependence, but otherwise sounds absolutely terrible. After consuming an adult beverage, alcohol is absorbed into your bloodstream and carried to your liver. There, it is set upon by two enzymes. The first, alcohol dehydrogenase, converts alcohol into acetaldehyde. The second enzyme, aldehyde dehydrogenase, converts the acetaldehyde into acetic acid (the stuff in vinegar) and attaches it to coenzyme A. This two-step process not only detoxifies alcohol, it enables us to use it as an energy source.Alcohol sensitizers work by inhibiting aldehyde dehydrogenase, causing acetaldehyde to accumulate. This leads to bad times, since acetaldehyde is responsible for many of the negative effects brought about by drinking alcohol.... Read more »

  • March 1, 2016
  • 01:26 PM

How bacteria and fungi can poison the air

by Rosin Cerate in Rosin Cerate

One of the main reasons we study how bacteria and fungi work is to minimize their negative effects on our health. These effects usually stem from being munched on (in other words, an infection) and/or being damaged by a toxic substance (being poisoned). While poisonings due to bacteria and fungi predominantly occur either in association with infections (e.g. diphtheria and tetanus) or via eating contaminated food (e.g. botulinum toxin and aflatoxins) or a misidentified mushroom (e.g. amatoxins), it's also possible to become sick after breathing in harmful gases or aerosols produced by these groups of organisms.Our cells can acquire energy by taking electrons from certain bits of organic carbon and transferring them via a series of steps to oxygen, producing water as a byproduct. Sulfur-reducing bacteria do something similar, but instead of oxygen they dump their electrons on sulfate and other electron-deficient forms of sulfur, producing hydrogen sulfide. It's a poisonous (to human cells), corrosive, flammable, AND explosive gas. Hydrogen sulfide lacks colour but is nevertheless detectable at very, very low concentrations because of its potent rotten egg odour. However, our noses quickly adjust to the smell, rendering it odourless.There's an old saying in toxicology, which is the dose makes the poison. Hydrogen sulfide is no exception. It's present in our bodies in very small amounts, where it helps ensure our nerves and blood vessels work properly. Being exposed to low concentrations of the gas isn't too much of a problem, since we're equipped with enzymes able to detoxify limited amounts of it. However, at high concentrations, the gas is a lethal fast-acting poison. It acts much like hydrogen cyanide to prevent our cells from extracting energy from organic carbon using oxygen. Due to its effects on the central nervous system, it quickly knocks people unconscious. Thereafter, death typically occurs as a result of the gas suppressing the region of the brain where breathing is controlled (central respiratory arrest).Hydrogen sulfide is heavier than air, so it can accumulate in low-lying places with poor airflow. The gas tends to show up wherever you have sulfur-reducing bacteria, lots of organic carbon and sulfur (for the bacteria to live off of), no oxygen (otherwise other bacteria would take over), and warm conditions (>20 °C) (to ensure appreciable bacterial growth). These conditions can be found in outhouses, sewers, septic tanks, and manure pits, particularly in the summertime. People can be fatally poisoned by hydrogen sulfide if they enter these confined and poorly ventilated spaces without their own separate air supply.The harmful nature of hydrogen sulfide was reported as early as 1700 by the Italian physician Bernardo Ramazzini, who noted cases of poisoning among those employed to clean bacteria-filled cesspits and latrines. During the 18th and 19th centuries, a number of people working in the sewers of Paris died when they were exposed to hydrogen sulfide. Victor Hugo described how dangerous the situation was in Les Misérables (1862), even mentioning sulphuretted hydrogen (an old way of saying hydrogen sulfide) by name.A section of the sewers beneath Paris (Source)Another airborne poison worth mentioning is clouds of fungal spores. Many of the fungi hiding out as networks of threads inside plants and soils reproduce by creating mushrooms, which serve to spread their spores (seeds) around. In the case of puffballs and earthstars, pushing on them causes a large number of spores (we're talking billions to trillions) to be shot into the air through a central hole. It looks a bit like smoke. The push can happen via falling raindrops or a trampling foot. Puffballs and earthstars often grow in dense groups, so a lot of spores can end up in the air all at once.Animals who breathe in a bunch of fungal spores can end up with a nasty lung-based illness known as hypersensitivity pneumonitis. Essentially, the spores trick the immune system into overreacting, causing a damaging inflammation deep within the lungs. Lycoperdonosis is a form of hypersensitivity pneumonitis specifically caused by inhaling spores from puffballs of the genus Lycoperdon.White blood cells (indicating inflammation) and a fungal spore (arrow) from the lung of a dog (Source)In one particularly unfortunate case, a group of eight apparently sober teenagers decided it would be a good idea to inhale the spores squeezed from some puffballs they had acquired. After a couple of days, they started to cough, had trouble breathing, ran a fever, and felt generally crappy. Things got so bad that five of the teens were hospitalized, two of them needing to be intubated to help them breathe. Their inflamed lungs were treated with corticosteroids and they all eventually recovered from their illness.Lycoperdonosis has also been seen in people who snorted puffball spores as a folk remedy for a nosebleed. Both puffballs and earthstars have killed or seriously injured dogs who disturbed them and inhaled their spores as they ran about or dug holes.ReferencesAlenghat T et al. 2010. Lycoperdonosis in two dogs. Journal of Veterinary Diagnostic Investigation 22(6):1002-1005. [Full text]Nogué S, Pou R, Fernández J, Sanz-Gallén P. 2011. Fatal hydrogen sulphide poisoning in unconfined spaces. Occupational Medicine 61(3):212-214. [Full text]Policastro MA, Otten EJ. 2007. Case files of the University of Cincinnati fellowship in medical toxicology: Two patients with acute lethal occupational exposure to hydrogen sulfide. Journal of Medical Toxicology 3(2):73-81. [Full text]Whitney J, Beijerink N, Martin P, Talbot J, Barrs V. 2013. Hypersensitivity pneumonitis in a dog associated with Geastrum triplex spores. Medical Mycology Case Reports 2:122-124. [Full text] Read more »

Nogué S, Pou R, Fernández J, & Sanz-Gallén P. (2011) Fatal hydrogen sulphide poisoning in unconfined spaces. Occupational Medicine, 61(3), 212-214. PMID: 21467246  

  • February 25, 2016
  • 02:53 PM

How coconuts bring harm and healing

by Rosin Cerate in Rosin Cerate

Curries, macaroons, piña coladas...where would we be without the captivating culinary contributions of the coconut?... Read more »

Campbell-Falck D, Thomas T, Falck TM, Tutuo N, & Clem K. (2000) The intravenous use of coconut water. The American Journal of Emergency Medicine, 18(1), 108-111. PMID: 10674546  

Mulford JS, Oberli H, & Tovosia S. (2001) Coconut palm-related injuries in the Pacific Islands. ANZ Journal of Surgery, 71(1), 32-34. PMID: 11167595  

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