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I am looking for a lipid biomarker of BBB leakage. There are recently published blood and brain lipidomics datasets but it is not clear which lipids are exclusive to the blood and if such lipids (in bound or unbound forms) are found in the brain parenchyma, can be construed as an indicator of BBB leakage (or transport across the BBB).
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As I have argued in a recent paper (DOI: 10.3233/ADR-210299), non-esterified or "free" fatty acids (especially those bound to serum albumin) should be largely excluded by a non-disrupted BBB from the brain. That aside, cells of the brain parenchyma would appear to need much the same lipids as cells in the rest of the body, so I'm not convinced that looking for individual lipids as markers of BBB disruption will work. All the evidence I've seen suggests that you would be better looking for changes in the way these lipids are being transported. As a rule, lipoproteins in the brain parenchyma are typically smaller than in the bloodstream, similar in size (and in some cases identical) to HDL (DOI: 10.1111/j.1749-6632.2000.tb06365.x), with an absence of larger lipoproteins such as LDL, IDL and VLDL. So, detecting the presence of lots of these larger lipoprotein in the brain parenchyma would seem to me to be a more reliable marker of BBB disruption.
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Which method do you think is more reliable and effective for the analysis of lipid biomarkers from the Precambrian? is cutting, hydropyrolysis or fluid inclusion assemblages analysis?
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First step, i) pick out rocks of suitable thermal maturity (preferably prior to peak oil window-maturity) as gauged from HAWK pyrolysis or elemental analysis screening, ii) use proven analytical methodology with full procedural blanks on a series of samples (depth series from core or outcrop), iii) use a combination of bitumen and kerogen analyses, iv) make sure the molecular distributions are self-consistent with i), ii) and iii).
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Dear colleagues;
I look for young scientists for authoring a book deals with subjects belongs to medical biochemistry. Are you interested?
A priority is to the English native speakers
Regards;
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Am very much interested. please how do i contact you . And again what are the subjects of interest
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I was wondering about the role of free fatty acids in dinoflagellates, more specifically the symbiodiniaceae? What are the metabolic pathways and where are the different types of lipids usually manufactured?
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Thank you Dr. Mukherjee
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Dear colleagues;
What are the novel and accurate methods for testing the following:
  1. Total cholesterol conc.
  2. Triglycerides conc.
  3. HDL-C conc.
  4. LDL-C & VLDL-C
  5. Lipid peroxidation marker (MDA)
Best regards;
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Hello, see the info below you can find some news there.
Good luck!
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This  is the second time I failed to see red lipid droplets in my adipogenesis culture. Gene expression and lipid quantification already show that the differentiation is successful but no red droplets after staining. Any idea? I meticulously follow the protocol step by step, but still no success! 
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If You already quantified lipid then which method you used?
How long (Days) you stimulated cells with adipogenic hormonal stimuli?
If Lipid Droplets are visible under light microscope the ORO should work.
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Can anyone help in finding out LDL for atomic absorption spectroscopy?
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As a rule of thumb, multiply the standard deviation of several blank absorbance values (minimum 10) by the factor three (based on the three-sigma rule) and use your sensitivity (i.e. the slope of your calibration curve) to convert that absorbance value to concentration.
Another approach is to calculate it from the residual variance of your calibration curve, like in DIN 32645.
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I have been using Anti-fade Prolong Gold but observed diffused bodipy florescence. I came across Mowiol-488 (Calbiobchem) and  Fluoromount-G (southern biotechnology) has been used in papers. Which one I should go for or someone suggest me protocol for bodipy staining.
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Hi!
All of those should work ok, but be vary that lipids may diffuse and lipid structures such as intracellular lipid droplets may fuse after fixation. To avoid such artefacts consider imaging quite soon after mounting (and imaging all samples to be compared within the same imaging session). Alternatively you could mount with PBS and seal with glue or nail polish or not mount at all (ie use dishes with glass bottoms after fixation and staining).
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I have extracted DNA from suspended biomass collected on filters. Now I want to divide the OTU counts by the volume of water filtered for each sample, in order to abtain semi-quantitative abundance estimates. Does anyone know a reasonalble way to do it? I'm using the softaware packages "mothur" and "phyloseq". Thus far I only found the option to normalize all samples to one value. In my case, however, I have different values (volumes of filtered water) for each sample.
Thanks for any suggestions,
Yuki.
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Absolute abundances from NGS platforms appear to be not the best way to look at the quantity. It is more a function of the sequencing platform and so sum-constrained data. 
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Any statistical analysis, eg, PCA or other indices, or the concentration of any compounds, eg, sterols and hopanols, may help to address the question.
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I am really sorry for not being able to get back to you sooner (I was out of station). The d13C values for the limestone cluster around -6 permil, much depleted than expected from marine origin. Also I have measured bulk d13C  which cluster around -22 permil, which is again enriched if we consider only C3 vegetation. The TOC content is rather high. These samples are from inter-trappeans layers in a place close to the western margin of peninsular India. The atmospheric CO2 should be more enriched compared to what we have today, and likewise the deposits should also reflect that.
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Fatty Acid analysis using based FAME mixer Standard. but GLA(Gamma Linolinic Acid) is not in FAME mixer Standard.Prime Rose oil Slightly traceable GLA.This GLA in mother feed only. Please if any Standard for GLA in market give details and how to purchase that.
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There are some reports about clozapine that clinical response is dependent on rise in the triglyceride levels. 
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Krishna (How are you going by the way?)
I had a quick look at our database - no evidence that fixing people's TGs changes their apparent response to orexigenic antipsychotics. If anything (remembering we use a multidimensional outcome scale) there are improvements in some dimensions probably relating to the enhancements that follow from exercise regimens. In those with severe triglyceridaemia (>8) where we would be in the statin± fenofibrate± (real) fish-oil and dancing-on-one-leg field of play, we have too few numbers to comment on changes in outcome dimensions but as these patients tend to stick in your mind, I don' t feel there were any indicators that loss of 'effectiveness' followed control of dyslipidaemia.
Tim LAmbert
Collaborative CENTRE FOR CARDIOMETABOLIC HEALTH IN PSYCHOSIS
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 We need to estimate lipid biomarkers contain in soil by GC MC. We have HPLC grade Methanol 99.9 % with water max. 0.05 %. Could we add solid KOH to Methanol without any additional treatment?
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I agree with Mushtaq Ahmad. 99.9%  purity is good enough for transmethylation. However, larger amount of soap will be formed if the reaction is prolonged. Soap is a dead end product (formed by irreversible reaction). Transmethylation is very rapid (in a good mixing solution). So I recommend not to exceed 2 min.(room temperature)  for a 1%KOH in methanol with toluene as a cosolvent.
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We are going to screen the some herbal drugs for its hypolipidemic effect. In this experiment, zebrafish (8 or 9 day post fertilization) must be stained with Oil Red O staining to visualize the lipids. If any one has a working protocol of Oil Red O staining pertaining to zebrafish, please share with us.
Thanking you in advance for sharing your knowledge.
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You can use Oil Red O for detection of lipid droplets. For example, I have used Oil Red O staining in Zebrafish larvae of 7dpf which has already been in the low concentration PTU treated one (so that melanin formation can be inhibited) and observed the liver under the microscope. The fatty liver which occurs sometimes due to a hepatotoxic drug can be visualized with Oil Red O. But I don't think you can measure the lipids in the blood stream. I don't think you can inject it into the circulation as well because Oil Red O is not easily soluble in water and you need to add glycerol. 
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Hi all,
I am looking for a ubiquitous cell membrane marker for murine intestinal tissue. Can anyone recommend one? For human tissue I have been using HLA-ABC, but didn't find an equivalent for mice.
Thanks.
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I am studying the n-alkane from Paleosol and data of GC MS spectra showing 25C to 35C is dominated over the lower chain carbon with odd over even predominance. I am not able to explain the preference of higher length carbon chain in higher plants and lower chain in lower plants. The odd over even predominance is from terrestrial plants. Why is this?
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The odd-over-even predominance or, in case of n-fatty acids and n-alcohols even-over-odd predominance, results from the way plants synthesise long-chain alkyl compounds. Starting with short-chain compounds enzymes (prolongase) attach acetate (acetic acid) to the molecule, which is a 2-carbon molecule. The ultimate chain length of an alkyl compound depends on the tissue or cell type it will be incorporated in, i.e. whether it is part of cuticular waxes, cutin or suberin, for example. I recommend reading some papers on alkyl compound biosynthesis. Samuels et al. (2008) is a good starting point, for example.
Samuels et al. (2008), Annual Review of Plant Biology. 59, 683–707
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On our high throughput hospital clinical chemistry analysers we measure haemolysis, icterus and lipaemia using simple spectrophotometric indices. This is to avoid analysing tests where these interference are know to lead to factitious results. 
We have recently observed that some patients with persistent raised triglycerides have high haemolysis indices and there is a relatively strong correlation!
Has anyone else seen this? I am not sure if this represents increased invitro haemolysis in lipaemic samples or a direct analytical interference. The strong correlation suggests the later to me?
All help gratefully received.
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Although we find no correlation between the lipaemic index and haemolysis index on our Roche analysers (c701), this may be due to the Roche spectral correction mentioned by Wesley above.
Goce Dimeski from Brisbane did publish on a possible effect of lipid on RBC membrane fragility a few years ago;
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Many companies providing single reagent solution for enzymatic reactions, by which we can quantify cholesterol, triglycerides, and HDL-C. Can I use the these human compatible reagents with rat or mouse sample? Is it okay scientifically? Thanking you in advance.
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You can use such reagents to the measurement of TG,but take care with the glycerol content of the rat sample because free glycerol measurement is also growing when that condition is present whenrats are  in an active lipolytic state. LDL and HDL- cholesterol may be  run with the  same reagents used for human molecules. Take care because data interpretation is different between human and rat plasma samples. For example, rats  don't  present cholesterol ester transport protein (CETP) , so rat LDL and HDL  molecules show different percentage of cholesterol esters in comparison with LDL and HDL from human  samples. A control group is always needed. 
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I am working with porcine cells and did live staining with green plasma membrane stain from lifetech. The results came out really bad.
I would be thankful to know if anyone has a suggestion other than green plasma membrane stain.
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For fixed tissues use Anirban Banerje's answer.
For live-cell, you can try CellMask from LifeTechnologies. (See attached link)
I've also attached an example image I acquired of CellMask Deep-Red (far red version) so that you can see if it is good enough for you. (There is also a little nuclear staining with DRAQ5 there, so ignore that)
The CellMask probes are a little expensive, but I've been happy with their live-cell performance.
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Recent studies suggest that there is still a benefit without significantly increasing side effects, but I'm not convinced that long term or in certain subgroups of patients, the metabolic change that we generate with very aggressive treatment is safe.
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The original question was what do we have to monitor with high statin therapy. If we use other therapies may other metabolic Parameters would also have to be considered. In statin therapy I would monitor lipids, glucose and HbA1c, ALAT, may be  CK (at least at the beginning) and eventually hsCRP.
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European recommendations about Lp (a) is to recognize it as FR CVD when its plasma concentration is above 50 mg / dl, whereas this value represents the 80th percentile in the population. Nonetheless studies to provide the 80th percentile value of 50 mg / dl, are from Denmark. In Spain (data from unpublished study DRECE) the 80th percentile corresponds to 30 mg / dl. How should we interpret these differences and their value as FR?
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I guess, with the exception of Denmark we have no clear epidemiological evidence in other European Countries to respond to this question. Less uncertaintes can be ascribed to values above the suggested threshold, in particular if associated to coronary or non coronary ischemic events. We deserve epidemiological studies everywhere in Europe and outside E. Warm regards.
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Dyslipidemia
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I have found another publication in which the effect of HDL has been determined using apoB-depleted serums. This other assay looks simple and may work.
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I'm trying to look at the uncategorized lipids out there, ones that might need to be analyzed for classification purposes.
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I've looked at LipidBlast which only generates masses (not really structures).
I've also just started parsing the lipidbank database, as at least it isn't the LMSD.