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Toxic histories : poison and pollution in modern India
\"Toxic Histories combines social, scientific, medical and environmental history to demonstrate the critical importance of poison and pollution to colonial governance, scientific authority and public anxiety in India between the 1830s and 1950s. Against the background of India's 'poison culture' and periodic 'poison panics', David Arnold considers why many familiar substances came to be regarded under colonialism as dangerous poisons. As well as the criminal uses of poison, Toxic Histories shows how European and Indian scientists were instrumental in creating a distinctive system of forensic toxicology and medical jurisprudence designed for Indian needs and conditions, and how local as well as universal poison knowledge could serve constructive scientific and medical purposes. Arnold reflects on how the 'fear of a poisoned world' spilt over into concerns about contamination and pollution, giving ideas of toxicity a wider social and political significance that has continued into India's postcolonial era\"-- Provided by publisher.
Book
Trial of Botulinum Toxin for Isolated or Essential Head Tremor
Injection of botulinum toxin into each splenius capitis muscle at baseline and week 12 was more effective than placebo in reducing the severity of essential head tremor over 18 weeks. Effects waned at 24 weeks.
Journal Article
Multiple Chemical Sensitivities
Use of the term \"multiple chemical sensitivity\" (MCS) as a diagnostic label has generated increasing controversy during the past few decades as a phenomenon related to exposure to chemical agents sustained both in indoor and outdoor environments.This volume, prepared in conjunction with Biologic Markers in Immunotoxicology, contains the authored papers of a workshop held to develop an agenda to study the phenomenon of multiple chemical sensitivity. Authored by clinicians, immunologists, toxicologists, epidemiologists, psychiatrists, psychologists, and others involved in research or clinical activities relevant to the problem, the papers contain case evaluations and criteria for diagnosis, mechanisms potentially underlying MCS, and epidemiologic approaches to investigation.
eBook
An interbacterial toxin inhibits target cell growth by synthesizing (p)ppApp
Bacteria have evolved sophisticated mechanisms to inhibit the growth of competitors
1
. One such mechanism involves type VI secretion systems, which bacteria can use to inject antibacterial toxins directly into neighbouring cells. Many of these toxins target the integrity of the cell envelope, but the full range of growth inhibitory mechanisms remains unknown
2
. Here we identify a type VI secretion effector, Tas1, in the opportunistic pathogen
Pseudomonas aeruginosa
. The crystal structure of Tas1 shows that it is similar to enzymes that synthesize (p)ppGpp, a broadly conserved signalling molecule in bacteria that modulates cell growth rate, particularly in response to nutritional stress
3
. However, Tas1 does not synthesize (p)ppGpp; instead, it pyrophosphorylates adenosine nucleotides to produce (p)ppApp at rates of nearly 180,000 molecules per minute. Consequently, the delivery of Tas1 into competitor cells drives rapid accumulation of (p)ppApp, depletion of ATP, and widespread dysregulation of essential metabolic pathways, thereby resulting in target cell death. Our findings reveal a previously undescribed mechanism for interbacterial antagonism and demonstrate a physiological role for the metabolite (p)ppApp in bacteria.
The bacterium
Pseudomonas aeruginosa
attacks competing bacteria using the toxin Tas1, which pyrophosphorylates adenosine nucleotides to generate (p)ppApp, thereby depleting ATP and disrupting multiple cellular functions.
Journal Article
Alpha-1 antitrypsin inhibits Clostridium botulinum C2 toxin, Corynebacterium diphtheriae diphtheria toxin and B. anthracis fusion toxin
The bacterium
Clostridium botulinum
, well-known for producing botulinum neurotoxins, which cause the severe paralytic illness known as botulism, produces C2 toxin, a binary AB-toxin with ADP-ribosyltranferase activity. C2 toxin possesses two separate protein components, an enzymatically active A-component C2I and the binding and translocation B-component C2II. After proteolytic activation of C2II to C2IIa, the heptameric structure binds C2I and is taken up via receptor-mediated endocytosis into the target cells. Due to acidification of endosomes, the C2IIa/C2I complex undergoes conformational changes and consequently C2IIa forms a pore into the endosomal membrane and C2I can translocate into the cytoplasm, where it ADP-ribosylates G-actin, a key component of the cytoskeleton. This modification disrupts the actin cytoskeleton, resulting in the collapse of cytoskeleton and ultimately cell death. Here, we show that the serine-protease inhibitor α
1
-antitrypsin (α
1
AT) which we identified previously from a hemofiltrate library screen for PT from
Bordetella pertussis
is a multitoxin inhibitor. α
1
AT inhibits intoxication of cells with C2 toxin via inhibition of binding to cells and inhibition of enzyme activity of C2I. Moreover, diphtheria toxin and an anthrax fusion toxin are inhibited by α
1
AT. Since α
1
AT is commercially available as a drug for treatment of the α
1
AT deficiency, it could be repurposed for treatment of toxin-mediated diseases.
Journal Article
The toxin solution : how hidden poisons in the air, water, food, and products we use are destroying our health--and what we can do to fix it
\"Eliminate avoidable toxins, mitigate the effects of those you can't avoid, and enjoy a longer life with this ... health guide from a pioneer in integrative medicine, Dr. Joe Pizzorno--the author, teacher, practitioner, and founder of Bastyr University, the country's first and largest fully accredited university of natural medicine\"-- Provided by publisher.
Book
Toxin profile of Gymnodinium catenatum (Dinophyceae) from the Portuguese coast, as determined by liquid chromatography tandem mass spectrometry
The marine dinoflagellate Gymnodinium catenatum has been associated with paralytic shellfish poisoning (PSP) outbreaks in Portuguese waters for many years. PSP syndrome is caused by consumption of seafood contaminated with paralytic shellfish toxins (PSTs), a suite of potent neurotoxins. Gymnodinium catenatum was frequently reported along the Portuguese coast throughout the late 1980s and early 1990s, but was absent between 1995 and 2005. Since this time, G. catenatum blooms have been recurrent, causing contamination of fishery resources along the Atlantic coast of Portugal. The aim of this study was to evaluate the toxin profile of G. catenatum isolated from the Portuguese coast before and after the 10-year hiatus to determine changes and potential impacts for the region. Hydrophilic interaction liquid chromatography tandem mass spectrometry (HILIC-MS/MS) was utilized to determine the presence of any known and emerging PSTs in sample extracts. Several PST derivatives were identified, including the N-sulfocarbamoyl analogues (C1-4), gonyautoxin 5 (GTX5), gonyautoxin 6 (GTX6), and decarbamoyl derivatives, decarbamoyl saxitoxin (dcSTX), decarbamoyl neosaxitoxin (dcNeo) and decarbamoyl gonyautoxin 3 (dcGTX3). In addition, three known hydroxy benzoate derivatives, G. catenatum toxin 1 (GC1), GC2 and GC3, were confirmed in cultured and wild strains of G. catenatum. Moreover, two presumed N-hydroxylated analogues of GC2 and GC3, designated GC5 and GC6, are reported. This work contributes to our understanding of the toxigenicity of G. catenatum in the coastal waters of Portugal and provides valuable information on emerging PST classes that may be relevant for routine monitoring programs tasked with the prevention and control of marine toxins in fish and shellfish.
Journal Article