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Questions related to Toxicology
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I have now started working with the antibacterial and toxic effects of piperididinic alkaloids. Problem is, we know very few people in our institution that is experienced with such substances.
Would anyone here know practical methods to quantify piperidines in solution (i.e. spectrophotometrically, dyes)?
Can I dissolve them in aqueous solutions, using e.g. acidic water?
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Experience in Xenobiotic metabolism and cell based bioassays. Willing to collaborate with your team
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Mercury, chromium, nickel, and manganese.
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For quality assurance metal salt is better
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I am conducting an experimental design in view to relate between repeated lead nitrate oral administration to non-lactating ewes with toxicological responses such as oxidative stress and immunotoxicity (Immuglobulins, B and T Lymphocyts). I am surprised to find a value of blood lead lower than that observed after repeated lead chloride. Note that the accuracy of analytical method is good.
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Dear Dr. Smail, I know well the meaning of bioavailability, and now that you've well explained that the used dosages were comparable in the lead content it seems that, from your experimental data, some evidence of different bioavailability arises. Now could be interesting to explain this difference.
In fact, if we consider that lead nitrate is more soluble [525 g/l (20 °C)] than lead chloride [10,7 g/l (20°C)] in acqueous solution is expected a major blood level for the nitrate but this is not in accordance with the experimental results.
One explaination could be in a different absorption of the nitrate and the chloride anions, which inevitably should be absorbed togheter with lead to have an electrochemical balance between negative and positive ions. In this aspect the chloride ions could be favoured to pass membranes instead of nitrate firstly because their small dimensions but also a facilitated transport could be possible.
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In my research I found out that the levels of arsenic were generally below
the maximum contamination levels of 0.05 mg/L set for water by the WHO.
Arsenic toxicity is a global health problem affecting many millions of people. Contamination is caused by arsenic from natural geological sources leaching into aquifers, contaminating drinking water and may also occur from mining and other industrial processes. Arsenic poisoning can also occur over a period of time as small doses are regularly taken by the users of homemade alcoholic brews.
Since arsenic is an element, it doesn't break down, but remains in the victim's hair, fingernails, and urine. Any death occurring after several days will show arsenic in the liver and kidney. Continued exposure to arsenic builds up in the system and there is an accumulated effect. The absorption of trivalent arsenic is limited, although the toxicity is greater because of the high lipid solubility pentavalent arsenic compounds are almost totally absorbed (till 90%) in most species. The more you are exposed to Arsenic the more serious are the consequences. Long term poisoning causes burning pains in the hands and feet, a numbing sensation throughout the body, swelling and skin irritations, hair loss, weight loss, cramps, vomiting, nausea, visual impairment, and eventually heart failure.
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"Despite the predominance of more toxic arsenite and arsenate in wine and beer, the estimated weekly exposure to As (via consumption of beer, wine and rice wine) is low", the issue is what is the effect of long term exposure on the users?
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Homogenetisic acid from strawberry tree honey has been reported for antioxidant activity. Also its an intermediate metabolism in tyrosine degradation. Its accumulation can cause alkaptonuria.
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There are two CAS# listings.  451-13-8 and 102-32-9.  One is the 3,4 and the other is the 2,5 dihydroxy-.  I don't think there has been much toxicity testing on it.  I did find a citation of a simple cytotox in vitro test and an amusing article about an alkaptuonuria patient who had his b&w photo developed in his own urine.  Note similarity of structure to hydroquinone which is in regular developer.
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Kindly provide information regarding systemic study of acute and subacute toxicity studies on animals
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Hello Dr. Pravin,
Plz go throught the following OECD and EPA links and download the guidelines relevant for you. They are the most trusted source of information regarding your query.
Best regards,
Varun
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I was interested in how closely the 3 monkey species can predict human risk assessment.
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This question is better stated by asking how cholinesterase reactivation in monkeys correlates with that in humans for purposes of predicting preclinical drug safety.
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Hormones and vitamins normally fall into this category. How does a substance qualify for this sort of categorization?
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Arvind,
This is a good question. The most notable person promoting the idea of hormesis is Ed Calabese in Amherst, Mass., USA. Here is his email address:
edwardc@schoolph.umass.edu. I am uploading one of his recent publications on mechanisms of hormesis. In my opinion, hormesis consists of a normal signaling that is compensating for a stress to the cell, and it could theoretically be observed with any stress that is not overwhelming.
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Some studies show that copper can be used for controlling mosquito breeding.
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Many techniques are used to demonstrate the critical role of potential targets in cellular assays. But what methods are available to validate that the appropriate (patho)physiology is displayed in a cell system? It is critical, in many cases, that the target of interest is being studied in the proper context.
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Comparison with similar cells from ex-vivo whole tissue or organ exposure (where possible) should provide good validation for in vitro cellular assays.
Sometimes, results of in vivo assays can also be used to validate in vitro cellular assays by properly extrapolating the conditions in both assays.
Using different methods to perform the same assay may validate the results but not necessarilly for appropriate physiology.
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My first memory of poison was a tale of the Brothers Grimm, Snow White or I have heard something on poisonous mushrooms.
J.F. Borzelleca (2001) illustrated the origin of “poison” in Principles and methods of toxicology (ed. W. Hayes):
“Toxin was originally tekw, a word meaning to run or flee, later becoming toxsa in Persian and toxon in Greek, meaning bow and arrow; the toxin meaning may have come from the poison used to tip the arrows, or, as Robert Graves suggested, from the yew tree taxus, from which arrows were best made and whose berries were long known to be poisonous. The word poison came by a devious route, like a long-delayed afterthought. It derives from poi, to drink, becoming potare in Latin, whence „potion” (and also „symposium” from sym, together, plus posis, to drink). “
I think it would be more than interesting to compare how and when researchers in various cultures met with the notion of poison and what can be the original meaning of this word in their mother tongue?
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You may add the Paracelsus quotes:
“Everything is a poison only the dose differentiates a poison from a remedy.”
or
“All things are poisons, for there is nothing without poisonous qualities. It is only the dose which makes a thing poison.”
(which one is correct I do not know - but the meaning is similar)
Today we would echange" dose" with " exposure".
kind regards
Lars
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Silver nanoparticles size 10 and molecular weight 107.87
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Hi,
probably would be useful the NanoCalc web tool. You can find it at the following link
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When I treat MDCK cells (adherent epithelial cells from dog's kidney) with different metal ions, they start to detach from the cell culture flask surface. These kinds of cells are often regarded as dead, but they do not become stained with trypan blue. If I transfer those detached cells to new culture flask with fresh medium, they remain detached and they still don't become stained with tripane blue. If we perform some cytotoxicity assay (such as MTT assay), we regard that kind of cells as dead, as they are washed away during protocol (but I've observed, that they are still metabolically active). Is it possible that those cells have become senescent? Or do you have some other possible explanation?
I would like to thank you in advance for all the answers/comments.
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I agree with the answer from Attila. Many of the primary cells need contact/adherence, which provide them signalling for proliferation e.g. lymphocytes from spleen/blood, keratinocytes etc. These cell colonies are usually a bunch of cells. When they are dispersed/single, it means they are either dead or on the verge of death.
I have not worked with cell-lines, but probably the same argument works there also, as in your case.
What is the major constitutents of snake venom?
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Snake venom contain so many enzymes but the concentration are different and which one is mostly available is still a question for most of people.
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Of more than 90% are proteins and polypeptides that may possess either enzyme and non-enzyme activities. Some are polypeptide toxins (small proteins).
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60 kg Human : 2.7 to 5.4 g
50 kg Human : 2.25 to 4.5 g
1 kg Human : 0.045 to 0,09 g...
a. 60 kg to 150 g Rat conversion factor = 7
Kg/Rat = 0.315 to 0.63 g
b. 50 kg to 150 g Rat conversion factor = 6.47
Kg/Rat = 0.282 to 0.567 g.
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A 2nd paper on dose translation.
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The manuscript is about 3800 words, and should be suitable for publication in a medical journal with low impact factor indexed in PubMed/Medline.
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Dear sir
You can send it to Saudi journal of kidney diseases and transplantation
We will review it a and see if it is suitable www.sjkdt.org
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In that study food consumption of all groups was reduced, including control groups, and body weights & water consumption were normal.
What may be the plausible reasons?
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Are you doing the study on rodents? They have a habit known as 'Capophagy' i.e. they eat their own feces. That should be the reason why food consumption of all groups was reduced, including control groups also and body weights & water consumption were normal. To prevent capophagy, keep them in a metabolic cage, if required in your study.
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Generally, the echo analysis is clinically used for diagnosis of steatosis (fatty liver). I would like to know any other tools or biomarkers to detect steatosis in the preclinical or clinical study?
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you may consider cholinesterase. see O.O. Ogunkeye, E.K. Chuhwak, A.A.E. Otokwula, Serum cholinesterase activity in the diagnosis of nonalcoholic fatty liver disease in type 2 diabetic patients, Pathophysiology, 2010, 17, 1, 29
Did you please suggest me the journal for Ayurvedic product Sub-chronic toxicty study????????/
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I' m searching for a good journal for the publication of my toxicity study???
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You can try in Ancient Science of Life, Indian Journal of Traditional Knowledge, Indian Journal of Pharmacology, Indian Journal of Experimental Biology, Indian Journal of Pharmaceutical Sciences, Journal of Ethnopharmacology, Pharmaceutical Biology, Pharmacognosy Magazine. Although I could have suggested lot of big names but that would not serve your cause. These are some of the journals where you will get prompt response for the type of study you are mentioning. All of them have good impact also. NO point in searching for higher impact factors and wasting time, of course it's my personal view :). Gud Luck and regards
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I want to know the methods to induce hepatocellular carcinoma in rat in a fast way
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You can try DEN 'diethylnitrosamine' treatment. We have used this carcinogen to induce HCC in mice and you can see my paper appeared in hepatology for dose and time. If you have any question, let me know..
Best of luck,
Jyoti
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.
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Rather soluble in alcohol
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I would like 3 MCPD validation , but i haven't IS for 3-MCPD , can any specialists help me for this
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d5-3-MCPD IS - 1 mg/ml in ethyl acetate. See EN 14 573:2004.
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Can anyone suggest the method or assay to detect the volatile toxic alcohols such as isopropanol,methanol or ethylene glycol? (for patients)
Automated enzymatic assay for ethanol is available like Gas-Liquid chromatography(GLC). But GLC do not detect those volatile toxic alcohols.
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As dr. Samir said by using hs.gc-fid you can detect a huge number of volatile compounds included acetone methanol ,ethanol, isopropanol etc.
Temp. Started from 40-50 c
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The old overload theory by Morrow (1988) has been given new light by the work of Jurgen Pauluhn. Is anybody aware on recent reviews putting volumetric loading versus surface area as a metric?
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Hi Paul,
which type of risk are you talking about ? I understand some work has been done on interacting particle systems filters applied to credit risk, but is this your intended topic ? or is it health hazard ?
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I’d be glad to link your references.
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How was liver/kidney damage evaluated?
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How do silver nanoparticles interact with protein?
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Due to environmental toxicants, several specific gene expressions increase in nuclear dna and this gene expression also affects the mitochondrial gene expressions.
I want to examine the correlation between nuclear and mitochondrial dna expressions and how they affect both expressions.
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Mitochondrial disorders are complex and heterogeneous diseases that may be caused by molecular defects in either the nuclear or mitochondrial genome.
Mitochondrial Disorders
Methods in Molecular Biology Volume 837, 2012, pp 327-335
Measurement of Mitochondrial DNA Copy Number
Victor Venegas, Michelle C. Halberg
Real-time quantitative polymerase chain reaction (qPCR) analysis of mtDNA content
go with this article buddy
All the very best
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I need only 2 types of bacteria for a toxicology study. Please help me out.
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you can mix 1gram stool sample/15ml PBS. Shake it rigorously for 5 minutes. Make a serial dilution from supernatant in PBS. Then spread from each diluted tube on individual agar plate. You can use selective media if you know what the bacterial strain you are looking for.
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formaldehyde in different concentrations are used to convert many bacterial toxins
in order to prepare vaccines . Eg:- diphtheria toxins
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From what i remember old school..
this comes to mind
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Usually people create BCG vaccines by growing M.bovis on selective medium (by incubating it for long time), so why can't we use chemicals?
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Formaldehyde would probably prevent M. bovis from being pathogenic...by killing it.
"The aqueous solution is a bactericide, tuberculocide, fungicide, virucide and sporicide"
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Formaldehyde is actually used in converting toxins to toxoids in order to prepare vaccines.
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I agree with comments reported by Dr Hudrisier. Formaldehyde is a very reactive substance and the epsilon-amino groups of lysines are favourite sites for reactions since they're less sterically hindered. But also other amino groups may react. All these reactions brings changes in the toxin structure, these changes are reflected in the loss of toxicity. However, most of the protein structure remains unaltered and this preserves its antigenic determinants, the portions of the protein structure that stimulate the production of antibodies.
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How to infer the results of toxicological study parameters?
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Like body weight and water intake?
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Recently, I watched a documentary on scientists' work on orcas in New Zealand. It was about PCBs (polychorinated biphenyl) and fire retardant ending up in the entire food chain from plankton and fish up to orcas or killer whales. Pollution came from manufacturing cities that was drained through the rivers down to seaports and straight to the bottom of the ocean. I am wondering if anyone noticed or observed PCBs and fire retardant in plants on the ground and in oceans (I mean inside plants).
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Some literature says accumulation of PCB-5 in the root retrials. Phytoextraction contributed insignificantly toward the loss of the soil-borne PCB-5. Also hytoremediation prosses is described to remove the PCBs from soil (Chemosphere. 2011 Aug;84(7):943-9. doi: 10.1016/j.chemosphere.2011.06.007. Epub 2011 Jul 2.). But it is very difficult to explain the absorption mechanism. How ever, remediation of PCB by plants is often slow and incomplete. Also it is not clear this absorption is related to their nutrient absorption process. Testing of faty tissues of plan is very important to take a Idea .
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I'm trying to regulate water temperature for aquatic toxicology laboratory experiments, but the solutions I've found, like water chillers and heaters, are very expensive. Is there an easier and cheaper way to regulate water volumes of 500 liters?
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Cooling can also be provided through a home made cooler such as an extended hose (use a thin but long one) running from the tank to a chilled system, such as a cooler/freezer, or worst case scenario - a bucket/styrofoam box of ice replaced/added to keep temp. Length of hose will determine temp. Fans will evaporate water, which might mess with your parameters, especially substance concentrations in ecotox. Watch the temp though and test it thoroughly for a consistent parameter. Remember that room temp can affect ice melting as well, so keep this constant. Use many small aquarium heaters to heat water, rather than a large one, since this will minimise any effects of over heating from a broken heater. Cheap heaters regularly function about a year without fault. Insulate aquaria to keep temp consistent. If they are bubbled, use lid to prevent evaporation and temp loss.
Good luck!
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Our group is using a toxin that we know produces free radicals via activation of nitric oxide synthase-dependent calcium. When measuring other parameters such as lipid peroxidation, GSH and GSSG concentration, the GSH/GSSG also find rate behavior as we expect and this was previously reported (by us and by other groups). But when we measured ROS by this technique, we found that the fluorescence decreases to below baseline. We have hypothesized that the technique fails to measure reactive nitrogen species. Do you agree or think it could be something else?
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Let me start by giving this reference which is worth a read if you have even a passing interest in DCFDA: "Measuring reactive oxygen and nitrogen species with fluorescent probes: challenges and limitations" by B Kalyanaraman et al in FRBM 2012 vol 52.
DCFDA is really worth a skeptical look as a ROS-indicating dye because it is not a direct measure of H2O2 and it also redox cycles to auto-amplify signaling. However, it does react with several varieties RNS such as NO2 radical and ONOO. I see no reason why an RNS-heavy cellular system would not light up with DCFDA. Although the biggest fear with DCFDA is the false positive, that apparently is not the problem you are having but it may be as good a time as any to look for another marker of ROS.
In addition to the other problems of self-amplification and an utter lack of R(O/N)S specificity associated with DCFDA, B Kalyanaraman et al put it very well with this quote from the paper I cited: "In addition, one cannot always assume that control and experimental samples exhibit the same efficiency in DCF radical generation and the same linear dependence of self-propagating redox-cycling reactions induced by the DCF radical (Fig. 1)." -- Highlighted mar 14, 2013
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Curcumin can cause free radical trapping so may be lower antioxidant enzymes in hepatic tissue.
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Also this one
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I am trying to analyze Cadmium and Selenium in herbal samples using an atomic absorption analyzer. The characteristic value for 5 mg/L Cadmium standard is always far from the reference value. I guess I need appropriate matrix modifier to increase the signal and get the comparative characteristic value close to the reference one.
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Dr. Fekret, Dr. Franchini, thanks for your kind responses. Dr. Franchini, I am running pure Cd standard diluted with D.I.W. which I guess does not require digestion, in addition to using different matrix modifiers including MgNO3. Yet even with this solution, the experiment hasn't been successful so far because of the double peaks problem. This is why I opted to use flame mode instead of furnace, and so far so good. Thanks again
Where can one get innovative, interesting papers (on environmental sciences, life sciences) online free?
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Topics: ecology, aquatic, sciences, environmental, ecological, toxicology, water quality, protection, conservation, biological, sustainability, biosphere, chemico-biotic interactions, pollution control, water, self-purification, detergents, phytoremediation, filter-feeders, suspension feeders, surfactants, environment, pollution, water quality, aquatic organisms...
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This is the link to the useful List of 100 bibliographic references. Papers and books on environmental sciences, ecology, biology, water science, ecotoxicology. Here You will find many links/web pages of full texts online free. https://www.researchgate.net/publication/259639072_100_innovative_articles.Discoveries._Ecology._Environmental_science._Biology._Water_safety?ev=prf_pub
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What chemicals induce neuropathy?
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A classical drug-induced neuropathy is due to Vinca alcaloids (vincristine) or to taxanes; also quite effectives are cis-platin compounds and arsenites. a bit less fashionable is n-hexane neuropathy.
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Trying to figure out if these babies are at risk for esophageal stricture or pulmonary scarring.
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The NPIS study is large and there are no long term sequelae reported (the citation in Stacey's response is not correct - see Williams, H. et al., 2014. Reported toxicity in 1486 liquid detergent capsule exposures to the UK National Poisons Information Service 2009-2012, including their ophthalmic and CNS effects. Clinical toxicology (Philadelphia, Pa.), 52(2), pp.136–40. Available at: http://www.ncbi.nlm.nih.gov/pubmed/24199643 doi: 10.3109/15563650.2013.855315). The most likely serious sequelae are corneal injury (Horgan N , McLoone E , Lannigan B , Flitcroft I . Eye injuries in children: a new household risk . Lancet 2005 ; 366 : 547 – 548 and Mathew, R.G., Kennedy, K. & Corbett, M.C., 2010. Eyes and alkalis. Wave of paediatric eye injuries from liquid detergent capsules. BMJ (Clinical research ed.), 340, p.c1186. Available at: http://www.ncbi.nlm.nih.gov/pubmed/20197325).
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I want to know normal value of Superoxide dismutase and glutathione peroxidase and reduced glutathione and malinoaldehyde in tissue of rat.
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As Ramasamy say There is no standard value depends on several factors, including changes from one tissue to another, so you should always have a control group against which to compare.
Best wishes
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I need a recent paper
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...isnt`t it the other way round? If I remember right, regular and heavy alcohol consumption should actually reduce blood glucose levels thus alcohol abstention should normalize them again rather than the other way round. ...but I am not sure.
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I had isolated a bacterium which degrades a toxic pollutant such as nitro group containing pesticide. I want to prepare DNA aptamer.
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I did cation exchange chromatography with buffer A (sodium acetate) and buffer B (sodium acetate+NaCl). Now I have a problem, I can not do MS because I have a high concentration of salt in my fraction. So, I can do ziptip purification to the fraction before the MS analysis.
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An other way would be to load the IEX eluate on a C18 trap column from an LC/MS system, wash for an extended time and elute from the trap column onto the analytical column of the lc/ms system. It wolud be an option, if you have limited access to the sample.
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Book for environmental toxicology.
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I will be teaching Environmental Toxicology next semester as a graduate level course, and all these textbooks have been recommended by others. The professor teaching this course in the past used Casarett and Doull's Toxicology: The Basic Science of Poisons. It is an expensive book but very comprehensive in their latest edition. My background is more ecological and addressing biodiversity. I feel that Environmental toxicology is highly human health oriented so I am more inclined to use an Ecotoxicology book like Newan's 3rd ed. Any more discussion on the topic is deeply appreciated
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Especially in alternative medicine, hair analysis often used to detect deficits and surpluses of minerals and trace elements. Are these tests reliable? What are the minerals and trace elements suitable for element analysis in hair, and what are not suitable?
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Is there a toxicologist who would like together with me to write a small article / letter about hair analysis of trace elements and toxic metals?
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I have seen interesting ultrasound findings in some patients with these kind of lesions.
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Mr Pauwels:
The ultrasonography was performed by a specialist, not me.
The estudies were done in lesions caused by Crotalus and Porthidium snakebites, Thalassophryne maculosa (batrachoididae), echinoderms and others. The most important findings have been tendinitis, capsulitis, edema and celulitis.
i want the mehods for determination of AST and ALT and GGT and LDH in details
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i want the methods for determination of AST ALT GGT LDH in serum in details
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I have in house method(protocol) for LDH and GGT I can forward you but for AST and ALT you may need commercial kit.
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In the rat 4-week oral toxicity study of drug A, such finding was seen in drug-treatment group without dose-dependent manner. I am not sure if the finding is drug-related or not, because the effect is not dose-proportionally, and seen in just a few animals.
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In the general situation, it is not known to occur spontaneously in rats.  However, I couldn't state that specifically for your study since there are no details to examine.
Your statistical comparison would be the control group as well as historical information from prior organization experience.  Not all toxic responses occur in a textbook dose-dependent manner.  Real life can often be messier.
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Pesticides are sprayed in the farm to destroy pests and preserve our food products. Plant biotechnology or genetic engineering is the talk of the day and the public is willing and will be happy to buy pesticide free products. In toxicology we try to be careful on non target organisms when applying environmental agents to destroy pests, inorder to minimize toxicity. if genetic engineering is possible on our farm products why not on mosquitoes . I am interested in this!
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Where are you chidi. Plasmodium has a way of changing its nature over time, that is why it has been hard for scientist to get a vaccine . But a recent job in U.K has a vaccine for it although it is still in the test run stage.
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We currently test compounds for toxicity using cell culture systems and assays such as MTT or other cell viability assays. We would like to predict the effects of compounds on cell viability and wondered if anyone could suggest a database or software package to get started.
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Hello Caroline,
My proper advice: you have not enough data to address some prediction toxicity software. To look only on EC50 values for cell toxicity is wasting of time! If you have more than 15 tested compounds you can try to do QSAR study, although the simple value of EC50 for cell toxicity is not suitable value (better enzyme inhibition parameters etc....
Stan
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Blood sampling from Zebrafish
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From adult zebrafish you can watch the following video article:
This recently accepted manuscript gives another technique:
For larvae, I guess that there are no validated methodologies for blood collection, because of its small size. It is more useful to imaging analysis. But I am not really sure about this, maybe someone could find a way out.
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How do we calculate the IC 50 value in antioxidant assays?
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Hi Aastha,
Its a simple calculation
1. make a scatter graph in excel (where X axis is concentration and Y axis is % activity)
2. get the slop equation (Y=mx+c or Y=mx-c) for the graph. option is available in trend line bar
3. for IC50 value in equation
Y=50
M and C values will be present is the equation itself.
4. Now all you have to do is, solve the equation....and find out the value of "X"
5. value of X will be IC50 value for that graph
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I’m trying to perform the colony formation assay (or clonogenic assay) with a cancer cell line to study the effect of DNA repair inhibitors on the cytotoxicity of chemotherapeutic drugs. In several reports I have seen that cells are plated after treatment with the compounds but some authors also seem to seed cells before treatment. Does anyone know the best way to perform this assay?
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Hi Patricia,
I have been wroking with CFA assay for quite a while and I would suggest that you plate the cells first and treat them 24-48h after plating.
I prefer this method because plating single cell suspension (single cell susoension is very important for assaying anchorage idependent growth) at 38-40degrees celsius and trypsinisation e.g. stresses the cells pretty much and giving them time to recover gives the cells time to get back to normal.
My best results for the testing of chemically modified natural compounds I got after letting the cells get back to normal for 24h.
I used to do the assay with 0.6% Agarose/DMEM bottom layer without cells and 0.3% Agarose/DMEM cell layer (2500cells per well in a 6well plate or 1000 per well in a 12well plate) .
Using the two layer system in 6-12Well plates is important to avoid cells from growing beneath the agarose (which will give high background). Staining with 0.005% (w/v) Crystal violett in 25% (v/v) Methanol resulted in best staining/Background after appr. 3 weeks when used at a 1:1 ratio Agarose/DMEM:Staining solution.
I did the counting with Clonocounter (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1770926/) which worked pretty well for me so far, but you will have to cite the authors if you use thier softare.
If any reviewer denies to accept your data and requests nude mice experiments I would confront them with the following article from PNAS (http://www.sciencedirect.com/science/article/pii/0092867474900506#)
Best regards,
Kai
P.S.: Get back to me if you encounter any technical problems concearning this assay (it is'nt easy) ;-)
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Are new cholinesterase activators still being synthesized?
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Cholinesterase activators or Reactivators?
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Mancopper is a dithiocarbamte.
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In my view, Mancopper is an old and obsolete molecule, thus difficult to get from trade. However, can be synthesized by any synthetic chemist in small quantity for R&D work. 
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During measurement of cadmium, lead and other heavy metal toxicities, we used serial concentrations of metal salt geometrically. In the highest doses, we always observe a whitish precipitation and by continuing our experiment, we did not find any mortality after 24 hours. Water quality parameters were checked and listed as follow: pH:7.8/ EC: 0.43 ms.m-2/ DO: 5.6-6.3 ppm/ Hardness: 220 mgCaCo3 and etc.
How could I prepare a toxicological test without facing the precipitation of metal?
And what is the reason(s) for using geometric series in toxicity tests?
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pH is a key element, I am not sure if you can reduce it or not. You can check the precipitation using geochemical model such as Minteq software.
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Is the reuse of PET bottle to fill water harmful to the health? What is the reactivity of this type of polymer with the drinking water? if the number 1 in a triangle is impressed on the bottom of a plastic bottles "see photo" can I use this bottle to fill tap or spring water without heath consequences.
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Hallo Ammar,
may be you think about using glass bottles for the storage of drinking water. PET releases production residues (own experience/measurements) and progesterone/estrogen...
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The key point is how N-succinimide is metabolized in our body. Will it cause major malfunction in the body? Does anyone know the metabolize pathway?
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The main metabolite of N-succinimide is obtained through the nucleophilic opening of the imide ring. Normaly it forms succinamic acid, which is a precursor of the amino acid asparagine (with a amine on carbon 2 - (S)-2-amino-3-carbamoylpropanoic acid.
As is soluble, is excreted by kidneys .
Our, the amide group can be oxidated to carboxilic acid, forming succinic acid (a). Hidroxylation and oxidation at C2 forms oxaloacetic (b) acid which is also a precursor of arginine or aspartic acid.
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Ficus cordata ssp. salicifolia is a toxic plant for cattles, Myburgh, J.G et al. have published a paper in Onderstepoort Journal of Veterinary Research reporting an outbreaks of neurotoxicoses with some clinical signs including hyperaesthesia, ataxia, muscle tremors and padding motions while in lateral recumbency. Could these symptoms be a sign of interaction with serotonin/dopamine receptors?
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I cannot retrieve the original publication to check on the symptomsin detail. However, several Ficus species have been reported to contain AChE inhibitory constituents. Were typical cholinergic symtpms observed?
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Theoretical basis and suitable software if available (the free ones are warmly welcome!)
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Strictly speaking, you don't need any software or theorie for determining a NOAEL or LOAEL since these are the no or lowest OBSERVED adverse effect levels. That is, they are determined by the experimental design and always correspond to a dose level in the study. The only point of discussion could be (in some cases) what adverse is...
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Is there a big difference between sexes?
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The influence of sex on toxicokinetics may involve female–
male differences in physical constitution (body water
space, muscle mass, body fat, and blood flow), physiology
(menopause and menstruation cycle), and metabolizing enzymes.
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UP in India has a high rate of MMR. Obviously there must be some contributory toxicological causes.
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Without details of exposure one cannot be sure, a potential, candidate is aflatoxin. exposure increases non-irondeficient anemia, and adverse pregnancy outcomes. See
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In laboratory work the acute and subacute toxicity study of capreomycin can be performed, if possible what parameters to be included and what are animal models for the same?
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Dear Pushpendra gross electrolyte disturbances including hypokalaemia, hypomagnesaemia, hypocalcaemia, and alkalosis have developed in tuberculous patients who were being treated with capreomycin which produced renal magnesium wasting and possible tubular damage. The major limiting factor for the use of capreomycin in the treatment of MDR-TB is its severe systemic side effects. These include anorexia, thirst, anemia, hearing loss and notably nephrotoxicity (proteinuria, hematuria, nitrogen metabolism and electrolyte disturbances) . There is a model using C57BL/6 female mice
With best regards
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Please specify the treatment modalities for systemic hair dye poisoning containing <4% PPD, Resorcinol and cetosteryl alcohol in a quantity of 100 ml.
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Hepg2 cell line
MTT test
Good positive control is?
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I guess the real question should be on validity of MTT assay for cytotoxicity measurement. MTT reduction simply measures extent of dehydrogenase mediated reduction of MTT into formazan, whih could be modulated at sublethal levels. Best example is the case of rotenone or any other mito respiration inhibitors.
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Literature regarding vitamin E as an antioxidant. My special field is hormonal level and histology of pitutary, kidney and gonads.
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My email id is yogimania1987@gmail.com, kindly post the literature plzzzzzzzz
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Metal ion blood serum levels, cobalt chromium titanium
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You should see a medical toxicologist (MD) for evaluation and to have your blood ion levels rechecked. You can go to the American College of Medical Toxicology (ACMT) website to find doctors in your area who are board certified in the specialty.
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Hi,
could anyone recommend a good starting reference (e.g. textbook or review article(s)) for general toxicology?
Thanks!
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Hello Maria
The standard general text is Casarett & Doull's Toxicology: The Basic Science of Poisons which is now in it's Seventh Edition. It covers all aspects of toxicology in an excellent way with the exception of epidemiology and toxicology testing in animals, which are best treated as seperate subjects.
All the best, Ray
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Toluene Diisocyanate colocalzes with tubulin on cilia of differentiated human airway epithelial cells?
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Toluene Di-isocyanate is severely irritating to tissues, especially to mucous membranes. Inhalation of toluene diisocyanate produces euphoria, ataxia, mental aberrations, vomiting, abdominal pain, respiratory sensitization, bronchitis, emphysema, and asthma.The critical effect of exposure to Toluene Di-isocyanate is developpement of asthma. The mechanism by which toluene diisocyanate produces toxic symptoms is not known, but the compound is highly reactive and may inactivate tissue biomolecules by covalent binding.
I am pleased to share two links with about toluene diisocyanate. I wish that can help you with your search.
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Anatomy
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I would like tp suggest that after you have done the acute toxicity test as suggested by Gabriel you can also determine the EC50 or ED50 as the case may be. Then try doing a pilot experiment using one fifth of the EC50 or ED50 as your high dose, half of it as your middle dose and one quarter of it as your low dose. You should be able to decide on what doses to actually use in your study, guided by the results of the pilot experiment. It does seem like a lot of extra work, but then, you would be able to make an informed decision on the appropriate doses, and that will be the prize or gain of it.
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We are doing toxicology tests on animals, like that any posiblity to do these toxicology test on humans?
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No. You conduct Safety and Tolerability studies in Humans.
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Lorke's method has been used since 1983.
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@ Segun, .... Yes... OECD guideline is confusing at few points. for statistical analysis, you have to use the AOT425 software. This software was free (i am not sure if it free now or not). It is a simple software, where 1st u have to adjust your starting dose and factor value. I am sending you a useful link I hope it will work for you.
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I need references on those differences.
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The two assays measure two different things: MTT assays for metabolic activity of cytoplasmic enzymes while SRB measures total protein amounts. Both assay can be correct yet give different results.
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I am following a set of postgraduate courses in Toxicology in the Netherlands to become a registered toxicologist (ERT). My second last course will be in January 2014 but my last compulsory course will be 'Epidemiology' in September 2014 in Utrecht. I'm wondering if there is any equivalent course in Epidemiology offered somewhere else before Sep 2014 that is also eligible to be counted for ERT registration? The duration of the course in Utrecht is 1 full week (5 days) and the description is attached. Thanks in advance for the help.
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I am studying the effects of mustard gas in my system and would like to parse out if my observations are due to the direct DNA damaging effects of mustard gas versus its ability to generate ROS or both.
In an ideal world, I would hope to be able to inhibit its direct DNA damaging capability but allow it to still generate ROS in one experiment, but in another inhibit its ability to generate ROS, but allow it to damage DNA. Is this even possible? I've looked at the possibility of using glutathione and Trolox, as glutathione seems to reduce both oxidative stress and direct DNA damage, but only Trolox reduces oxidative stress (Inturi et al, 2007).
I'm kind of hoping there might be something that inhibits one or the other, but not both.
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I'm curious about your reaction conditions and method of exposure. You indicate you are using 'mustard gas' so it's not clear to me if you are actually gasing a solution, gasing a dried DNA preparation, or as is most typical, introducing a nitrogen mustard compound (presumably, HN2, (bis(2-chloroethyl)methylamine) to a DNA solution at some specific concentration by delivery from a stock solution in an organic solvent. Obviously, the experimental conditions will determine the set -up. However, assuming you are exposing aqueous solutions of DNA to the nitrogen mustard compound, you can use a combination of incorporating various types and concentrations of known radical ion scavenging agents with known scavenging capacities to your reaction buffer prior to HN2 exposure (i.e. DMSO, EtOH, etc.), and/or using oligos of known sequcence as your DNA damage targets. Use of the radical scavengers should allow you to differentiate between indirect damage due to ROS production and direct damage due to direct interactions between the HN2 and the DNA target. Avoid the use of radical scavenging agents that possess nucelophilic groups such as amines, since these agents may react with the HN2 directly and reduce its effective concentration during the reaction (ie. Tris-Hcl, glutathione, etc.), thus causing artifacual and inconsistent results. Use of oligos of known sequence as your DNA damage target offer the obvious approach of measuring the HN2-specific damage of interstrand cross links formed at appropriately designed sequnces within the target duplex. Such lesions could be detected by, for example, disruption of an appropriate restriction enzyme cleavage site and visulaized by autoradiography of the 32P labeled oligo. This approach also offers the advantage of precise quatification of damage yields through a combination of scintialtion counting and extablishing the proportional yields of the different forms of product (undamaged vs. damaged) via digital densitometry.
I hope this was helpful, and good luck!
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New journal looking for contributions from experts in the field.
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To use a language as a scientific lingua franca can give advantages and disadvantages for the members of the scientific community on the basis of their culture and mother tongue. The status of a scientific or international language developed historically and not according to logical ideas and decisions on equal opportunity. I have tried to classify former scientific languages and some present candidates. I - as a European with my own experiences and preconceptions - have found Italian and German languages as the best fits. I am waiting for your opinion and reasons.
Characteristics of the ideal international scientific language
Grammar: easy
Vocabulary: well known
Script: easy
Pronunciation: easy
Giving equal opportunity: perfect = dead language
Strong cultural background: yes
Strong scientific background: yes
Strong economic/political background: none (= economy and politics do not influence the choice)
Characteristics of historical international scientific languages and candidates
Greek
Grammar: not easy
Vocabulary: well known
Script: not easy
Pronunciation: not easy
Giving equal opportunity? yes, one mother country
Strong cultural background: yes
Strong scientific background: historically yes
Strong economic/political background: none
Latin
Grammar: difficult
Vocabulary: well known
Script: easy
Pronunciation: relatively easy
Giving equal opportunity? perfect
Strong cultural background: yes
Strong scientific background: historically yes
Strong economic/political background: none
Arabic
Grammar: very difficult
Vocabulary: very difficult
Script: very difficult
Pronunciation: very difficult
Giving equal opportunity? too many native speakers
Strong cultural background: yes
Strong scientific background: historically yes
Strong economic/political background: too many countries
Chinese
Grammar: I do not know
Vocabulary: very difficult (for Europeans at least)
Script: very difficult
Pronunciation: very difficult
Giving equal opportunity? too many native speakers
Strong cultural background: yes
Strong scientific background: yes
Strong economic/political background: world power
English
Grammar: at the beginning easy, then difficult
Vocabulary: well known
Script: OK
Pronunciation: difficult
Giving equal opportunity? too many native speakers
Strong cultural background: yes
Strong scientific background: yes
Strong economic/political background: world power
French
Grammar: difficult
Vocabulary: well known
Script: OK
Pronunciation: difficult
Giving equal opportunity? one mother country
Strong cultural background: yes
Strong scientific background: yes
Strong economic/political background: none
German
Grammar: relatively easy
Vocabulary: well known
Script: easy
Pronunciation: easy
Giving equal opportunity? two mother countries (Switzerland has four official languages)
Strong cultural background: yes
Strong scientific background: yes
Strong economic/political background: none
Russian
Grammar: difficult
Vocabulary: not so easy
Script: easy
Pronunciation: easy
Giving equal opportunity? too many native speakers
Strong cultural background: yes
Strong scientific background: yes
Strong economic/political background: world power
Italian
Grammar: easy
Vocabulary: well known
Script: easy
Pronunciation: easy
Giving equal opportunity? one country
Strong cultural background: yes
Strong scientific background: yes
Strong economic/political background: none
Spanish
Grammar: not so easy
Vocabulary: well known
Script: easy
Pronunciation: not so easy
Giving equal opportunity? too many native speakers
Strong cultural background: yes
Strong scientific background: yes
Strong economic/political background: too many countries
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Language creates scientific isolation. I would involve even more competent science translaters, e.g. not only to translate books (which is frequently done), but also well appreciated review papers that were published in top journals (which is rarely or not done).
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And if there is effect of corona (nanoparticles-protein interaction) play role in that?
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From what I've read so far, that's not clear yet. When it comes down to AgNPs, there are much more publications about their ecotoxicity than its possible effects in humans
Difference between rats
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What is the difference between sprague dewely and albino rat and wistar rat and why they called by these names
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https://www.researchgate.net/post/Rats_and_mice_for_in_vivo_studies-strains_specific_usage_and_selectivity Please have a look at this link. I also asked this question. Only the text of question was different but the basic query was the same. I would also like to know the differentiating features.
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In dose response analyses, why are the lethal dose and the effective dose computed at 50%? Is it conventional for comparison purpose or is there a biological or mathematical reason?
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LD50 or LC50 or ED50 are the most reliable values depending on which characteristics you assess. At the LD50 value is the smallest the standard deviation of the data. Generally, when characerising the efficiency of a poison we calculate the LD (LC)50 and the LD (LC)90 values with their fiducial limits. You can find more information in any toxicological textbook.
Can activated charcoal be linked to a specific antibody to increase its anti-toxicity properties?
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In toxicology, activated charcoal is one of the therapeutic choices, but it still remains non-specific. What about linking activated charcoal with a monoclonal antibody to improve its properties?
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Dr Ahad. Activated charcoal is a non specific substance used to trap toxic substances in the gut due to its property and ability to adsorb to other molecules except very large molecules or large molecular weight substances as metals. Activated charcoal may well trap amino acids but not large molecular weight protein like antibody. In addition, any protein ingested is likely to be digested by gut enzymes loosing its efficacy. Activated charcoal could not be a messenger to transport the antidote to the toxic substance still present in the gut. Third, once the activated charcoal is adsorbed to a substance (antibody) it will not release it and will be less able to adsorb the toxic substance owing to reduced adsorbing surface. AC cannot differentiate between toxin and antidote of the toxin Activated charcoal is not water soluble and will not dissolve in plasma. Its injection means development of showers of pulmonary emboli that could be fatal. It was never used and should not be used intravenously. The application and use of activated charcoal is only restricted to the gut except in certain conditions when it might be harmful as during deep coma, lost bowel activity (by effect of some poisons), corrosive ingestion (useless and might be harmful), hydrocarbons, metallic poisons (iron, lithium).
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I use an insect to evaluate the toxicity of endocrine disruptors, and I need to know how to validate a biological model in the laboratory
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Sorry, I fist thought your location was Spain, as I understand now, its Colombia.
Than you should have a try here:
best wishes
Andreas
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Henderson - Hasselbalch equation.
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Sodium bicarbonate is usually used to force alkaline diuresis.
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I would like to hear your point of view.
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Prof. Dr Tomislav Stojanovic
There are no synonymous. Hypercalcemia is a status, and Calcium Toxicity is a process.
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Does anyone know of an assay that can be used to detect protein damage from mustard gas, or 2-CEES, directly? I envision something like a carbonylation assay as with ROS protein damage, but specific for protein damage by MG directly. I'm new to this field so any help is appreciated.
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As far as I know mustard reaches almost every compartment even at the cellular level and it's therefore extremely difficult to control all possible mechanisms. Hoping that I get what your problem is I'd say your task is to prevent SM from accessing not only DNA but also the entire DNA repairing network. (This problem was investigated in depth as PARP was the most promising cellular target for antidotes.) I'm not sure if this is possible. In sum, I think your assumption could be absolutely right as mustard induced ROS activity is a key factor in inducing DNA damage and acute cytotoxic effects. In fact, direct DNA damage may perhaps play a primarily role in chronic consequences such as the development of malignancies.
May you help me to find how establish an experimental protocol for my work please?
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I am working on the relation between water hardness and cardiovascular disease in my country. I need to establish an experimental protocol (animal models particularly rats) to study combined effect of two ions (calcium and magnesium) . May I have your point of you or your help please?
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Yes, your paper states "The most abundant (or predominant) are Ca2 + and Mg2 +. In recent years, the hardness of the water has become an important public health issue. Indeed, it is reported in the literature that there is a relationship between cardiovascular disease mortality and hardness of water for human consumption". Yet, areas with soft water have a higher incident of cardiovascular disease. The first thing that is missing in your water analysis is a total reporting of ALL minerals. Since it is limestone, many limestone deposits have heavy metals that could explain the cardiovascular morbidity Please read my attached PowerPoint to see if you can get some ideas what could be the contributing factors in Haiti Thirdly, what amount of calcium is in the local food in these Haitian areas? Unfortunately, filtration of Ca out of the water will also remove Mg - The secret here is the ratio between Ca and Phosphorus I predict that your water Phosphorus ppm is low - an this is the problem
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Non monotonic-dose response is observed for physiological processes. It is due to different adaptive mechanisms such as receptor desensitization, existence of different receptors, feedback mechanisms, etc. In toxicology, such a non-monotonic dose-response (U-shaped or bell-shaped) is regarded more accurately.
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yes - it is documented in guinea pig experiments using environmental contact sensitizers - see following abstract
Acta Derm Venereol. 1985;65(6):472-8.
Induction of formaldehyde contact sensitivity: dose response relationship in the guinea pig maximization test.
Andersen KE, Boman A, Vølund A, Wahlberg JE.
Abstract
The sensitizing potential of aqueous formaldehyde was evaluated with the guinea pig maximization test (GPMT) in two laboratories (Copenhagen and Stockholm) using different guinea pig strains. Six intradermal (0.01%-3%), and 6 topical (0.5%-20%) concentrations were used for induction, and formaldehyde 1% and 0.1% was used for challenge. The incidence of contact sensitivity depended on the intradermal, but not on the topical induction dose. Statistical analyses showed a non-monotonous (non-linear) dose response relationship. The estimated maximal sensitization rate in Copenhagen was 80% after intradermal induction with 0.65% formaldehyde; in Stockholm it was 84% after induction with 0.34%. The data from the two laboratories could be described by parallel displaced dose response curves suggesting that the guinea pig strain used in Stockholm was significantly more susceptible to formaldehyde than the strain used in Copenhagen. The EC50 (formaldehyde concentration at which 50% of the guinea pigs were sensitized) at the 72 h scoring and a 1% challenge concentration, was 0.061% in Copenhagen and 0.024% in Stockholm.
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1. Is silver nanoparticle in doses of 100 and 200 micromole intraperitoneal suffient to induce toxicity without killing the rats?
2. Can curcumin be used as hepatoprotective for liver injury induced by silver nanoparticles. Does curcumin degrade in presence of silver nanoparticles?
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1. You should discuss these questions with the author :)
2. Some data: 100 micro mole silver are 10.8 mg nano-silver particles. According to (Silver Nanotechnology Working Group. Re: Silver Nanoparticles (AgNPs); Information and Common Request. CDC-2012-0014; NIOSH-260. Comments of the Silver Nanotechnology Working Group for review by the National Institute for Occupational Safety and Health (NIOSH). February 2013), ORAL NOAEL in rats is 30 mg nano-silver/kg/day. Considering 250 g per adult rat, this is 7.5 mg nano-silver /kg/day, which caused no observational effects after oral intake. However, I do not know the relevance for intraperitoneal application.
Is there anybody working on Poly Implant Prothese implants !?!??
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I am working on the toxicological issues realted to this faulty kind of implants. In particular on the silicone filler and on the late periphrostetic fluid/sterile puss they develope.
Establishing a journal of trace elements. Is anybody interested to join us as a member of editorial board?
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Contact me directly using this e-mail address; moshtaghie@pharm.mui.ac.ir Please attach your recent CV and letter of request.
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There are several unanswered questions, such as: Who is the publisher? What experience do you have from previous work with scientific publications? Which model do you choose? I.e. printed journal or open access on the Internet? Who will be the readers? Why is there a need for the journal? What guidelines do you have for peer-review? What other people than you are involved in this project? How often will the journal be published? How extensive will the individual issue be? As well as marketing and economical questions.
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I have been extracting organic compounds of my water samples using solid phase extraction (SPE) and evaluating them through various bioassays. I have many different tests to do and I have to keep the extracted samples for sometime. I am currently storing them at 4 degree Celsius and the solvent I used for elution was methanol. Does anyone know how long they can be stored and at what temperature condition?
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I also would recommend storage at -20C, where Methanol will remain liquid, or if possibly at -80C, if available and if the storage vial is small enough. The rate of degradation should drop. Note however, that some molecules, such as proteins, will lose their 3-D conformation upon freezing at very low temps. This is probably less of an issue for small molecules. As other respondents have said, it really does depend on the compounds and the tests you are doing. Consider control spikes with a known amount of your analytes in your solvent, or if you have a control matrix, matrix spikes, these can provide holding time info that can allow you to estimate storage effects.
Parameter can be influency determination concentration of ion fluoride in drinking water
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does anyone can tell me after turbidity ,Calcuim ion ,chlorine, what other parameter can be influency determination fluoride ion in drinking water
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Thanks for reply
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In developing countries I've seen that people use expired drugs particularly ceftriaxone for infection. I’ve seen they haven't presented any symptoms and their infection have been treated.
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Medications will work properly when stored in an environment away from light, heat, and moisture. Medications improperly stored can expire before the expiration date. Using expired medication is very risky. Expired medications are not only less potent, but some medications become toxic when used beyond the expiration date. Taking expired drugs can cause an unwanted visit to the emergency department as well having an unnecessary medical bill.
Can anybody suggest list of toxicology journals with charge ?
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Toxicology journals
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Other journal:Journal of Toxicology is a peer-reviewed that publishes original research articles, review articles, and clinical studies in all areas of toxicology. http://www.hindawi.com/journals/jt/
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What is the concentration of nitrates eligible in drinking water? What are the problems that can be recorded with an excessive concentration?
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Nitrate and nitrite are naturally occurring ions that are part of the nitrogen cycle. The nitrate ion (NO3−) is the stable form of combined nitrogen for oxygenated systems. Although chemically unreactive, it can be reduced by microbial action.
The U.S. EPA has set an enforceable standard called a maximum contaminant level (MCL) for nitrates at 10 ppm in drinking water. Excessive concentration of nitrate can cause many effects on human health such as infant methemoglobinemia and gastric cancer… The maternal transfer of these compounds and the potential effect on fetal death and malformation are also described.
Please receive this link that can give you more information about your question.
Please Suggest me some good free ADME/Tox Prediction Servers?
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Adme/tox
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3 dpf larvae of zebrafish will be used to evaluate the body burden concentration of a compound at different period of time.
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My personal interest in this follows an increase in publicity and advocation of "sustainable urban gardening", i.e. using discarded materials such as old tires to create subsistence container gardens in traditionally impoverished high-population density areas or those recovering from natural disasters. While the ability to grow enough nourishing food to sustain life is certainly superior to malnourishment and starvation, I worry about the potential for chronic health risks resulting from increased oral exposure to whatever the decomposition products of tires may be (i.e. PAHs, butadiene, phthalates, metals?). And where food is more easy to obtain, I'm concerned that the potential health risks may begin to outweigh the marginal health benefits. Thoughts? Exposure is not my field of expertise, but I'm curious: has anyone looked for the presence of tire decomposition products in vegetables grown in/near tires? Thank you for your time!
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Not sure about effects of sunlight, but toxicants leach out in fresh water from the tire surface. Zinc is added to tires in the manufacturing process, but there are a host of organic compounds that leach out as well, only some of which have been identified.
Hartwell, S.I., D.M. Jordahl and C.O. Dawson. 2000. The Effect of Salinity on Tire Leachate Toxicity. Water, Air and Soil Pollution. 121:119-131.
Hartwell, S.I., D.M. Jordahl, C.O. Dawson and A.S. Ives. 1998. Toxicity of Scrap Tire Artificial Reef Leachates in Estuarine Salinities: Are Tires Acceptable for Artificial Reefs? Trans. Am. Fish. Soc. 127:796-806.
Anthony, D.H.J., A. Latawiec, S. I. Hartwell and D. M. Jordahl. 1996. A Spectrometric and Chromatographic Chemical Comparison of Solvent Extracts of Whole Tire Leachate and of Shredded Tire Leachates Obtained at Varying Salinity. Environ. Canada, National Water Research Inst., Burlington, Ont., Canada, 95-112. 41pp.