- Imam Hassouna added an answer:1Is it possible to deliver EdU to mice through drinking water and for this to pass from mother to neonatal pups?
I want to label postnatally born neurons and to use EdU through drinking water. The only way I can think of doing this is by delivering it to the mother and for the mother to pass it to the pups through her milk. But I don't know if this has been done before
I think it is better to give EdU to the mother during pregnancy, it is simply pass through placenta and you will be able to detect it in the brain of pups but it does not pass through lactationFollowing
- Paul Dessauer added an answer:10What evidence exists that novel synthetic cannabinoids may act in a clinically signficant fashion at receptor sites beyond CB1?
The synthetic cannabinoids (SC) currently being marketed as alternatives to plant cannabis have a higher risk of adverse outcomes than phyto (plant) cannabinoids.
The SC products on the market are much stronger agonists at the CB1 receptor than THC, and none contain a synthetic equivalent to the phyto-cannabinoid CBD, but is part of the increased risk also due to SC substances acting at other receptor sites?
Thanks Volker. I wish I could upvote your response more than once!Following
- Krishnan Umachandran added an answer:14Is organic mercury a more toxic that metallic and ionic mercury?
Toxicological Sciences - Medical Sciences
Mercury is not essential to living cells and performs no known biological function. The toxicity of mercury is primarily associated with ionic Hg(II). However, absorption, tissue distribution and biotransformation are influenced significantly by the valence state of the metal.Following
- Witold Orlik added an answer:3How can one estimate the health cost of workers due to exposure ?
plz suggest me that what methodology should i use to evaluate the adverse health effect of workers working in toxic waste?
I was able to provide information on more "general" level. Unfortunately I am not an expert within your research domain. So if I want to be honest, my ability to help you with regard to more sophisticated "angles" of your task is somewhat limited.
- Maria Gabriella Verso added an answer:5Why isn’t clinical toxicology a more significant part of medical school education?With abundant evidence in the literature that many health afflictions result from toxicant exposures, and with published NHANES data from CDC that most people have bioaccumulated numerous persistent toxicants within their body, why are medical students not taught about clinical toxicology and approaches to investigate and treat toxicant-related health problems?
In Italy Occupational and environmental Medicine, with clinical toxicology, is a fundamental subject of the degree course in Medicine and Surgery and is subject of study in almost all the Degree Courses of the Medical Schools (to become nurses, midwives, rehabilitation technicians etc) .Following
- Kari Radha Krishna Murthy added an answer:7I´m currently doing a study about scorpionism in Ecuador, Panamá and Uruguay, but there is little information. Does anyone know something?
Due to a poor record of this accidents in Latin America, there´s little information about this public health problem. I´m looking for numbers of incidence and mortality by scorpion sting in Ecuador, Panmá and Uruguay.
I am working on scorpion envenoming syndrome for the last 40 years. We advocate the use of insulin-glucose infusion , continuous infusion of regular crystalline insulin should be given at the rate of 0.3 U/g glucose and glucose at the rate of 0.1 g/kg body weight /hour for 48-72 hours, with supplementation of potassium as needed and maintenance of fluid, electrolytes and acid-base balance. Administration of insulin-glucose infusion to scorpion sting victims appears to the physiological basis for the control of the metabolic response when that has become a determinant to survival. My e-mail id: email@example.com, firstname.lastname@example.org. Kindly give your e-mail id. I will send copies of all my research publications to you.
With best wishes,
(Dr. K. Radha Krishna Murthy)Following
- Priyamvada Sharma added an answer:6Can anybody suggest me information about “Chronic Methanol Poisoning Effects"?
Can anyone suggest me any information about “Chronic Methanol Poisoning or Repeated Exposure to Methyl Alcohol or its Metabolites and its effects in human health” either in published or unpublished works (gray literature).
I searched PubMed many times but, I did not find almost anything.
In case of methanol poisoning Formic acid, ethoxy acetic acid, methoxy acetic acid and glycolic acid are measured in different biological fluids using gas chromatography mass spectrometer . You can get idea from the article
J Pharm Biomed Anal. 2015 Oct 10;114:16-21. doi: 10.1016/j.jpba.2015.04.039. Epub 2015 May 6.
Identification and quantification of acidosis inducing metabolites in cases of alcohols intoxication by GC-MS for emergency toxicology.Following
- Ali A R Aldallal added an answer:1Have you ever witnessed linezolid-induced lactic acidosis?
We've recently had a case. Systemic oxygen consumption and extraction progressive decreased while refractory lactic acidosis progressive developed (likely due to mitochondrial "poisoning"). Anyone willing to share data on other cases to write something interesting together?
Linezolid-Induced Lactic Acidosis
N Engl J Med 2003; 348:86-87January 2, 2003
Linezolid is an oxazolidinone antibiotic used to treat a variety of gram-positive infections, including those due to methicillin-resistant Staphylococcus aureus and vancomycin-resistant enterococci, as well as nocardia species.1,2 Lactic acidosis is an adverse effect that has been associated with other drugs, including metformin and the nucleoside reverse-transcriptase inhibitors,3 but not with linezolid. We report a case in which severe lactic acidosis developed as an adverse effect of linezolid treatment.
A 52-year-old woman presented with fever, chills, and a two-week history of intermittent cough. Computed tomography (CT) of her chest revealed an infiltrate in the right middle lobe, as well as mediastinal adenopathy. Nocardia otitidis-caviarum was isolated from bronchoalveolar-lavage fluid as well as from a mediastinal biopsy specimen. Additional CT scanning revealed disseminated disease with involvement of the brain, kidneys, and adrenals.
The patient was initially treated with trimethoprim–sulfamethoxazole but had serious side effects that necessitated discontinuation. She was subsequently switched to linezolid and clarithromycin. Her treatment was complicated by myelosuppression, nausea, and vomiting, and gatifloxacin was substituted for the clarithromycin in the hope of relieving the nausea. During the subsequent five weeks, she had persistent vomiting and ongoing myelosuppression. Endoscopy revealed duodenal ulcers, and pantoprazole was started. The patient was hospitalized for intractable nausea and vomiting after 11 weeks of treatment with linezolid and 5 weeks of treatment with gatifloxacin. The findings on repeated endoscopy were normal. The patient was euvolemic and received intravenous fluids during hospitalization.
Because she had low bicarbonate levels, the patient's lactate level was checked and found to be more than 9.9 mmol per liter. Both antibiotics were stopped, resulting in a normalization of lactate levels at 1.4 mmol per liter after 10 days. Both antibiotics were then restarted, but the lactate level measured seven days later was 4.8 mmol per liter. Her nausea returned. The gatifloxacin was discontinued, and the lactate level had increased to 6.5 mmol per liter one week later. Discontinuation of linezolid resulted in normalization of the lactate level after two weeks. There were no other changes in medications during that time. The patient was then treated with moxifloxacin. Her lactate levels remained normal, and the disseminated nocardiosis resolved.
Lactic acidosis is a toxic effect of linezolid whose mechanism is unknown. Other drugs, including metformin and nucleoside reverse-transcriptase inhibitors, have been associated with lactic acidosis. In the case of nucleoside reverse-transcriptase inhibitors, lactic acidosis is thought to involve mitochondrial toxicity,4,5 and linezolid may have a similar effect. As we report here, a potentially serious side effect occurred in a patient receiving linezolid. The serum lactate level in patients taking linezolid should be measured if they have nausea or a low serum bicarbonate level.
- Simon C Johnson added an answer:2What is rapamycin dose for live animals?
i want to use rapamycin in my control group of hamsters infected with prion...whats the recommended dose?
We recently characterized the dose response profile of rapamycin in mice, this may be helpful for you:
- Mustafa I Elbashir added an answer:1Anyone aware of any work/research on off-gassing from patients who have ingested cyanide?
Interested in any:
Case reports/research or animal models etc.
sorry Dr Muhaammad I have no idea on the topicFollowing
- Prabhat Kumar Upadhyay added an answer:2Magnesium chloride works more intracellularly than magnesium sulphate. What are the impacts on clinical effects?
Magnesiumchloride has more intra cellular effects while magnesiumsulphate has more extra cellular effects. This explains that magnesium sulphate is clinical less effective but why is it then also more toxic as the toxicity effects are primarily intracellular?
intravenous given magnesium reduces the opioid requirements per operative by reducing the sympathetic outflow.
Simple reasons of acidosis because different abilities of chloride and sulphate ions upon interations with cellular parts and phsiological pH changes drastcally....
Follow this.......Roche, Block, sonie and wilson.....Inoganic med chem bookFollowing
- MOHAMMAD Nabavi added an answer:10What makes titanium implants toxic and cause allergic and autoimmune reactions?Dental implants are made of titanium because of biocompatibililty. Dental implants give titanium toxicity allergic and autoimune reactions.
this is a good article Nikola:
- Amulya Nidhi Shrivastava added an answer:4How we usually determine the neurotoxicity of certain Antibody?
I am working to determine the proper therapeutic dose for certain antibody so I need to know how we can evaluate the toxicity using a validated method ?
Please, could anybody also provide me with a published article about this?
- Venkata Harsha Vardhan Boddeda added an answer:5What are simple assays done for toxicological studies of a compound on zebrafish embryos?
I'm testing a compound (plant extract) on zebrafish embryos. Please suggest a few simple yet effective assays to test toxicity at cellular level.
You can follow the Fish embryotoxicity tests which have been given by OECD guidlines. 6hpf embryos should be taken and should be treated with test drug.
You can also perform cardiotoxicity and hepatotoxicity on 72hpf larvae.
You can do teratogenicity and also you can give scoring system in zebrafish based on structural malformations.
Check these links.Following
- Arik Eisenkraft added an answer:5Which laboratorial methods can be used to search botulinum toxin in food and patients blood or feces to replace the mouse bioassay?
In Brazil we follow the recommendation of the CDC. However, the result of bioassay take much time, can not be used for a fast diagnosis, and causes animal cruelty.
Of course! I'll be happy to help.
- Michele Barone added an answer:9For febrile patients with acute hepatitis there is no safe antipyretic. Is there an acceptable dose of paracetamol ? is measuring drug level useful ?
There is a clear reduced dose for paracetamol for stable cirrhotic, but for acute compromisation of liver function such severe acute hepatitis or post agressive liver resection no clear data about a safe adjusted antipyretic drug use according to liver function. Can monitoring paracetamol level prevent its hepatotoxicity in such citation?
Febrile patients with acute hepatitis can take different types of antipyretic without problems. However, you should avoid cortisone in case of acute viral hepatitis, and paracetamol in case of signs of hepatic insufficiency. Finally, in presence of alterations of coagulation cascade I would avoid NSAIDs.Following
- Federico Emiliano Ghio added an answer:2Is anyone willing to share data on SvO2 (or ScvO2) and cardiac output in patients with lactic acidosis and documented metformin intoxication?
I'm interested in confirming that metformin intoxication is associated with diminished oxygen extraction and consumption (secondary to mitochondrial "poisoning"?). This can be the primary explanation for concomitant lactic acidosis.
Dear Alessandro, i think your hypotesis is right. In fact Metformin reduces pyruvate dehydrogenase activity and mitochondrial transport of reducing agents, and thus enhances anaerobic metabolism. This shift to anaerobic metabolism, in the presence of reduced insulin, increases production of precursors for the Krebs cycle. Consequently, there is a decreased ability to channel those precursors into aerobic metabolism, which, in turn, results in increased metabolism of pyruvate to lactate and increases net lactic acid production. Greetings, FedericoFollowing
- Manikanta Murahari added an answer:7Can anyone suggest a protocol for MTT or SRB assay of nanoformulation?
We have prepared a nanoformulation of anticancer drug and performed MTT and SRB assay of API, nanoformulation and placebo (nanoformulation without drug) at concentrations of 5-100 ug/ml.
OD readings were observed at a range of 2-3 for all the concentrations for MTT assay. We thought that MTT is interfering with the formulation components and tried with SRB assay.
In SRB assay, we found OD of placebo was more than control
For nanoformulation OD readings were also more than control but less than placebo
Can anyone suggest the interpretation of results or share any protocol for the same
We also tried to wash with PBS, because of incubation for 24-48 hrs the particles are settling on the plate and we couldnt wash the wells efficiently.Following
- Hossein Rahmani added an answer:1Can anyone suggest me the effect of catalytic domain of diptheria toxin on CHO cells ?
we are planning to express the catalytic domain of diphtheria toxin with signal sequence (without translocation and binding domain) in CHO cells. will cells die due the effect of toxin. Since the toxin will not be processed by furin or lysosomal enzymes.Following
- Adejuwon Adeneye added an answer:5What are the limitations and (dis)advantages of the up and down method for the determination of the median lethal dose (LD50)?
Are there any limitations of the up and down method? (mabye the broad of the LD50 and not an exact value)
in which cases should this test be performed?
And are there already better alternatives available or in development?
thank you in advance
Hi Laurence, Up and Down Procedure (consisting of limit dose test and main test) as stipulated in OECD Guidelines on Acute Oral Toxicity Testing (425) remains the standard in vivo acute oral toxicity measures for determining approximate median LD50 of a chemical substance/chemical/drug with an unknown or closely related drugs of unknown LD50 value. It has the advantage of using few experimental animals which are dosed sequentially depending on its short-term and long-term outcome. This acute oral toxicity test also cuts cost since it involves the use of few experimental animals. However, it has its limitations which include:
1. The test is restricted to female, nulliparous mice and rats only;
2. The test requires close and long term close and strict monitoring for up to two weeks for each experimental animal for you to determine the short- and long-term outcomes;
3. Finally, the test requires an algorithm of strict steps which although simple but could be cumbersome;
4. It provides an estimated LD50 value and not the exact value
Overall, it remains the gold standard for determining the LD50 values of an orally administered substance/chemical/drug with an an unknown toxicity profile. You can check my published article using this procedure: Adeneye AA et al. Journal of Ethnopharmacology 105: 374-379 (see attached).
- Stephen Treimer added an answer:2How can I determine amount of paraquat in water by UV spectroscopy?
please provide method and materials.
Other than METHOD 549.2 DETERMINATION OF DIQUAT AND PARAQUAT IN DRINKING WATER BY LIQUID-SOLID EXTRACTION AND HIGH PERFORMANCE LIQUID CHROMATOGRAPHY WITH ULTRAVIOLET DETECTIONFollowing
- Melissa Chernick added an answer:7How to convert a toxic dose for a zebrafish to be equivalent to the one for rats?I want to use the toxic dose for a rat. I want to ask if I can use the dose without changing anything or do I need to make a certain conversion of the dose for zebrafish to be equivalent to the one for rats?
I agree with the comments above and also suggest reading: http://dx.doi.org/10.1016/j.cbpc.2008.07.013 which handles this topic nicely comparing rats and medaka (similar aquarium model).Following
- Vinuchakkaravarthy Thangaraj added an answer:3Can phenytoin, carbamazepine and nevirapine form covalent bond with cellular proteins in native form or metabolite form?
Can anyone help me in clearing my doubt whether the anticonvulsant drugs like phenytoin, carbamazepine and anti-retroviral drug nevirapine can act as haptens or can they form any covalent bond with any of the extracellular or intracellular proteins either in native form or in metaboilte/hapten form before/during exerting its mechanism of action or they can form any hapten-like molecule during conjugation process in kidney for elimination which can induce immune reaction? Any literature describing the phenomena has been published on this? Please share it here to me...
Thank you Dr. Reza and Dr. AliFollowing
- Milan Fedurco added an answer:7Synthetic cannabinoids- what evidence exists regarding potential for inducing acute or chronic problems with physical or mental health?
A wide variety of synthetic cannabinoids (SC) are now being marketed as "safer" or "quasi legal" alternatives to plant cannabis.
Anecdotally, it appears that these research chemicals are typically associated with a significantly higher risk of acute adverse responses (such as tachycardia, anxiety attacks and transient psychosis) than smoking "real" plant cannabis.
As the majority of SC products being marketed contain chemicals that are much stronger cannabinoid receptor ligands than THC, (and some contain mixtures of more than one SC), and as these mixtures do not contain any equivalent to CBD, this is perhaps not surprising.
Does anyone know of animal studies or case histories relevant to the potential of these chemicals to induce such acute problems?
I am also keen to find any research that may indicate the potential for dependence, and likely withdrawal profiles upon abrupt abstinence from regular use, of these chemicals.
<<< The intravenous administration of THC may be associated with a range of schizophrenia-like positive and negative symptoms in psychosis-free individuals (D’Souza et al., 2004).
Conversely, the phytocannabinoid CBD presents with anxiolytic and antipsychotic properties (Zuardi et al., 2006), possibly because CBD may displace the binding of THC from CB-rs.
In contrast, spice products contain no CBD, and the SC chemicals are full agonists at CB-rs and are characterized by both a receptors’ higher affinity and higher potency in comparison with THC (Fattore and Fratta, 2011; EMCDDA, 2011).
Forrester et al. (2012) showed that a “cannabis”-associated psychopathological syndrome occurrence was less likely with marijuana than with SC, with 2% in the marijuana and 11.2% in the SC misusers’ group, having been identified as experiencing hallucinations and delusions.
Those experiencing psychotic episodes related to Spice use are also reported to present with higher/more frequent levels of agitation and behavioral dyscontrol in comparison with those psychotic episodes described in marijuana misusers (Brakoulias, 2012). >>>
“Spiceophrenia”: a systematic overview of “Spice”-related psychopathological issues and a case report
- David Ogbonnaya Onu added an answer:3Methadone poisoning in an addict?How to determine lethal methadone concentration in an addict when one doesn't know the amount of pills taken each day?
I agree with the 2 responders about combining the severity of symptoms and hair analysis. The latter test quantifies the duration of Methadone use. Urine toxicological testing is only qualitative.Following
- Vincent Bloks added an answer:12Can I give DMSO to a rat as a solvent?
Hi all, please give me a hand. I am going to use glibenclamide (from Sigma) to treat diabetic rats as a positive control for my extract. I would like to know which solvent is suitable for dissolving glibenclamide before oral administration. I searched some papers and they use DMSO, however I don't know the concentration of DMSO. May I use the absolute one for rat feed? Or can I use another solvent (which, ?%). Thank you so much!
perhaps dissolve in DMSO and then in oil ( cremaphore 10%) , perhaps that will workFollowing
- Yvonne Hopf added an answer:4Does anybody know a different solvent than DMSO for Everolimus?
Background: it needs to be solved for IV administration to pavians and the current information we have is that it is soluble in DMSO (dimethylsulfoxid). If you don't know a different solvent maybe someone knows a little more about 'safe' concentrations for administration. Many thanks for your help!
- Ludwig Gruber added an answer:1Does anyone know which plastic products contain the most phthalates?With phthalates being measured at higher levels in human biomarkers and being used increasingly in food containers and other products, has anyone examined the products that expose humans the most/least? Presumably those with the least amount of polyvinyl chloride, but is it so? Is there any relationship to the plastic recycle numbers?Plasticised PVc is without doubt the most likely plastic material with high phthalate content. The exposure especially to DEHP from food consumption alone can be in the range of the TDI. And there are a number of other sources which contribute to the overall human exposure. Therefore there is indeed a problem, but we do not observe phthalates increasingly in food containers and other products as You suggest.
Direct contact between PVC and food is not really the predominant scenario for phthalates contamination. It seems that the ubiquitous presence of the phthalates and their lipophilic character are more important.
There is no direct relationship to the overall plastic recycle numbers, things are more complex. A contamination with phthalates is only likely for some kinds of plastics, and these are normally not used as food contact materials. Again, the high production numbers and the resulting ubiquitous presence of the phthalates are more important.Following
- Rahman Maman added an answer:22What are the current methods for determining the median lethal dose (LD50)? What are the advantages of these methods to "Lorke's Method"?Lorke's method has been used since 1983.i wonder if the method (UDP) can be applied for the fishes since we know this oral administration for the rat/mice.. anyone can suggest me?Following