October 1st 2018 prelude:
Basically I felt I was running low on gas. For days I felt exhausted at work, energy supply none.. Also I had huge lymph nodes in my neck and sweated extremely during my sleep. After I told the doctor these symptons he made me do a blood test and redirected me tot the hospital for examination on the lymph nodes out of precaution for lymphe node cancer.
October 2nd 2018: first blood test
ALT: 523 AST: 240 GGT: 566
The scan showed my lymph nodes were only swollen and there was no indication for lymph node cancer. The blood test results were still bad. the doctor told me depending on the causes I was heading for liver failure. He made me do another blood test to see if I had EBV ( Epstein Bar Virus) and/or Cytomegalo virus , also known as CMV. I tested positive on both viruses. EBV and CMV were also a legitimate argument for all symptons and the elevated liver enzymes.
October 10th 2018:
ALT: 156 AST: 57 GGT: 389
only a week after the first test the results were looking already pretty positive. As assumed, the enzymes were progressing towards normal levels. The doctor told me to have no worries seeing the elevated enzyme levels had substantially decreased in such a short amount of time.
I thought i would be back to healthy levels quickly.. this was until I called the doctor a couple of months later in June 2019 to ask for another blood test.
June 27th 2019
ALT: 164 AST: 57 GGT: 140
Main story: after many months it turned out my enzyme levels still werent heading to healthy levels. after seeing these results I was literaly in battle mode. I started to do my own research about the causes of elevated liver enzymes and in particular GGT (main indicator of early mortality). High GGT can be an indicator of depleted glutathione which is basicaly the most important antioxidant in your body. My search for a supplement that raised glutathione levels in my body finally ended after finding n-acetylcysteine (NAC). Since july 20th I have been taking NAC 1x 600mg on a daily basis. 10 days ago i finally took another blood test.
August 29th 2019
ALT: 67 AST: 30 GGT: 95
Roughly 2 months and 10 days after taking NAC on daily basis 1x 600mg capsule my elevated enzyme levels are finally going into the right direction.
Another thing that has happened is that NAC has worked wonders for my blood pressure. I was always in the ranges of 150ish/78. Now my blood pressure has been steady for a couple of weeks in the ranges of 120ish-82.
... keep reading on reddit ➡Biological alkylation is highly selective, yet it depends on complex leaving groups. Now, promiscuous and engineered enzymes achieve selective enzymatic alkylation using simple haloalkanes.
Abstract
Selective alkylation of pyrazoles could solve a challenge in chemistry and streamline synthesis of important molecules. Here we report catalyst‐controlled pyrazole alkylation by a cyclic two‐enzyme cascade. In this enzymatic system, a promiscuous enzyme uses haloalkanes as precursors to generate non‐natural analogs of the common cosubstrate S‐adenosyl‐l‐methionine. A second engineered enzyme transfers the alkyl group in highly selective C−N bond formations to the pyrazole substrate. The cosubstrate is recycled and only used in catalytic amounts. Key is a computational enzyme‐library design tool that converted a promiscuous methyltransferase into a small enzyme family of pyrazole‐alkylating enzymes in one round of mutagenesis and screening. With this enzymatic system, pyrazole alkylation (methylation, ethylation, propylation) was achieved with unprecedented regioselectivity (>99 %), regiodivergence, and in a first example on preparative scale.
https://ift.tt/39Zt3iM
There are numerous substrates for CYP3A4 which could be a hazard if their metabolism is impaired too much: https://en.wikipedia.org/wiki/CYP3A4#Function
It's odd that we don't hear about too many people having problems arising from this. Has the inhibitory ability of CBD been overstated?
Potent inhibition of human cytochrome P450 3A isoforms by cannabidiol
An Update on Safety and Side Effects of Cannabidiol: A Review of Clinical Data and Relevant Animal Studies - see table 1 for some numbers and extrapolations as regard CYP P450 isoforms.
I've recently started working with enzymes and my next assay will be to dose histamine in cider using a DAO-HRP-DAB reaction where absorbance will be measured using spectrophotometry (based on an article by Landete, Ferrer and Pardo). However, I'm stuck trying to understand how I can prepare a dilution of 0,7 UI/mL for DAO (which is what the article recommends) based on the fact that I only have a mg/mL concentration when preparing the enzyme dilution from powder. Can someone explain to me how U works and how to proceed with the conversion? Thanks!
EDIT : I have contacted the company about the unit of DAO, but they had no data on the unit equivalent for histamine, only putrescine (even though they sell the enzyme as degrading both substrates). They have directed me towards some litterature, but I can't seem to access any of it online (some 'Nature' journal article and Methods in Enzymology which I do not have a copy to go through). However, I have found some kind of range on BRENDA to help prepare an assay to determine the specific activity for it. The HRP is a little more vague since it's main substrate is usually ABTS, not H2O2. This means I don't really have any data to base myself on for a workable range.
I found that digestive enzymes helped me manage my IBS/IBD.
Could be there an enzyme production down regulation on the long run?
Thank you.
I've been looking into what enzyme's are need to aid in the breakdown of meat and I found that it is Pepsin. I started searching around and found the digestive supplement Nu-Zymes Plus. From what I read it aids in Pepsin production and overall enzyme production. Has anyone heard if this would aid the Carnivore diet or would I just be throwing money away?
Hi Reddit,
My name is Nicholas Heintz and I am a Professor of Pathology at the University of Vermont Cancer Center. My research has focused on dysregulation of redox signaling in cancer cells, and how the enhanced production of reactive oxygen species (ROS) in tumor cell mitochondria can be exploited for therapeutic purposes in aggressive human malignancies like mesothelioma. My coauthors Brian Cunniff (a former graduate student in my lab), and Kim Nelson (a postdoctoral fellow at Wake Forest) are joining me for this AMA.
My name is Brian Cunniff and I am a Postdoctoral Research Fellow at Harvard Medical School. My research focuses on intracellular trafficking, specifically clathrin mediated endocytosis, during cell migration and tissue organization. Using cutting-edge lattice light sheet microscopy we are able to visualize cellular processes with unprecedented spatial and temporal resolution.
My name is Kim Nelson and I am junior faculty in the Chemistry Department at Wake Forest University. I have been part of a highly collaborative, interdisciplinary team of researchers at Wake Forest who are focused on elucidating how reactive oxygen species are produced in a regulated manner as part of cell signaling events involved in growth, cell division, and cell death. My research has focused on 1) the kinetic, biophysical, and structural analysis of features in the peroxiredoxin family of proteins that modulate their rapid reaction with peroxide and 2) the identification, visualization, and biochemical analysis of proteins that are functionally modified by cysteine oxidation in response to regulated, intracellular hydrogen peroxide production. Along with Todd Lowther, my contribution to this study was in utilizing structural, kinetics and mass spectrometry analyses to characterize the mechanism by which thiostrepton directly associated with and inhibited the activity of purified human Peroxiredoxin 3.
We recently published a research study titled “Disabling mitochondrial peroxide metabolism via combinatorial targeting of peroxiredoxin 3 as an effective therapeutic approach for malignant mesothelioma” in PLOS ONE. In this paper we show that the thiazole antibiotic thiostrepton covalently crosslinks the antioxidant protein peroxired
... keep reading on reddit ➡So, I'm writing a paper on the application of enzymes in the food industry or biotechnology. I wanted to ask for some help. What enzymes do you know are used for improving the taste of food? Examples are tannase for reducing the bitterness of tea.
Title pretty much. I figured CYP3A4 Inhib might work but Wikipedia lists an entirely different Enzyme thats responsible.
I'd be glad with both, more active metab's and longer half life due to inhibited metabolization
Problem: very green swampy pool.
Pool Stats:
Chlorine: 25+ (it read 12 at leslies, then I added 3 bags of cal-hypo)
Ph: 7.2
Alkalinity: 100
Phosphates: 2500 <--- (25 times the recommended level of 100)
Plan-A:
In an attempt to kill a cloudy green pool, I added 3 bags of cal-hypo and generous amounts of blue flocculant, hoping to drop the algae to the floor and vaccum.
While there has been a slight improvement in cloudyness and pool color, I am not seeing large algae deposits on the floor as expected. Chlorine levels remain 25+.
Plan-A has failed!
Plan-B:
I plan to use an enzyme based clarifier next (natural clear - SmartZyme) + phosphate remover.
Will the 25ppm chlorine make my enzyme clarifier ineffective?
Last night i tried (approximately, could be slightly more or slightly less) 90mg of DXM to get an idea of if i may have a CYP2D6 enzyme deficiency, which I’ve heard halves the tolerance of DXM’s effects, and this was my first time on DXM. I read that if you feel significant effects from a dose around that much you could have a deficiency in the enzyme.
About an hour and a bit after taking it I felt a little weird, felt quite tired (then again this was after midnight) and had some occasional very slight nausea that made me feel more uncomfortable than in danger of throwing up. I’m an 80-85kg male which according to dexcalc should put a 1st plateau dose around 120-130mg, but I can’t tell if the effects I experienced are representative of a 1st plateau dose or simply a lower threshold dose (seeing as this is my first time using DXM). I didn’t really get any other noticeable effects, possibly some slight cognitive euphoria but that’s about it.
It’s worth noting I fell asleep about 2 and a half hours after taking it so I didn’t have a chance to see how the dose panned out, but it didn’t seem it was getting much stronger. I woke about 4 hours later still feeling a little strange and with a slightly upset stomach, but it’s also possible i was just hungry (i was starving when i woke up again a few hours later).
Point is, I can’t myself tell what these effects from such a dose indicate, if they indicate anything at all. Would you think i would be safe to go to a 300-400mg dose next time or should i play it safer with 200-250mg first?
Took dxm polistirex cough DM syrup 480mg. Is it normal for poli and weed to raise heart rate to 154bpm? Also my legs were shaking, had a headache, and diarrhea. Is a dxm high actually serotonin Syndrome?? Most of the side effects of high doses of dxm are very similar to serotonin syndrome symptoms. Tachycardia, confusion, hallucinations, restlessness, and nausea. Also what dose of hbr and poli, separately, would get me visuals? And how am I supposed to know if I have serotonin syndrome or not? I took a dose of polistirex ,480mg yesterday, 3:30pm. Smoked weed 7 hours later. Stopped ssri zoloft 17 days ago. Took 2.5mg zyprexa for sleep 2 nights ago.
im confused about kinase and phosphatase. they have similar functions? they both put a phosphoryl group in a catalytic reaction??
