Synthesizing, acetylating and separating using column chromatography was actually very interesting. Remaking the point in history when the first “sandwich” compound was discovered in 1951, a very cool structure to a molecule that has proven itself to be very useful through the ages.
Everyone on a steady low carb diet had, sooner or later, to start researching about reasons behind things like dry eyes, bruises, muscle cramps, constipation, energy levels and such. These is what I take daily and why and in most cases (except Alpha Lipoic Acid) I take these supplements in the morning before/during breakfast. Feel free to add up and let me know what you need and use.
Magnesium: 400mg x 4 pills turns out to be the ideal amount for me to keep cramps (especially leg cramps which used to wake me up in the middle of the night) at bay, along with managing bowel movements and general lack of energy/keto flu symptoms, which are usually due to lack of electrolytes. Some take Milk of Magnesia for the latter but I personally can’t stand the taste (it literally makes me puke), so I find magnesium caps to make up perfectly for it.
L-Carnitine: 588mg x 4 pills. the New Atkins book is the first source where Ilearned about Carnitine. It is an amino acid that helps metabolising fat, basically transporting the fat out of the fat cells. Everyone in a state of ketosis could use more of this. It also apparently helps a lot with brain activity and energy, especially the Acetyl l-carnitine version, though the L-Carnitine tartarate seems to be the preferred version for fat loss. In my case I have had Acetyl-l-carnitine in the last 6/8 months and I can tell given equal inputs in terms of food and water I do see a difference when I take 2400mg of carnitine per day.
CoQ10: 200mg x 2. Suggested by the Atkins book as well as a fat transporter just like l-carnitine. CoQ10 can have a balancing effect on blood sugars and insulin, and may be helpful for reducing insulin resistance which ultimately can boost fat-burning. Dr Atkins tells of a study which showed improved fat-burning and weight loss when persons who were previously deficient in CoQ10 were given the supplement. Apparently the best form to consume as supplement is Ubiquinol, which is the synthesised version of the CoQ10 our body actually uses. Although in Ubiquinol form the cost is unsustainable to me, even though it’s told to be so much more concentrated than the simple CoQ10 pills. For economical reasons though I am still personally on the simple CoQ10, 200mg. If you’re under 25 years old, your body is capable of converting CoQ10 to the reduced Ubiquinol form fairly well and the additional expense of purchasing the reduced form is unnecessary. However, if you’re older, your body becomes increasingly challenged to convert the oxidized CoQ10 to ubiquinol.
Choline: 500mg x 1. I’ve just recently come around this as it’s supposed to support the L-Carnitine function and metabolisation of fat, though it’s supposed to be taken around meals and I haven’t quite done that yet.
Omega-3: 1400mg x1 (EPA 647mg + DHA 253mg) evn though I should get to 2. Besides the general appreciation for omega 3 oils they support increased absorption of L-Carnitine as well as helping the ones suffering from hypothyroidsm. What’s important and defines the quality in Omega-3 pills is the actual EPA & DHA content, which for low carbers is suggested to be around EPA 1,500 mg / DHA 750 mg daily. Should be taken with Choline just before meals.
Alpha Lipoic Acid/R-Lipoic Acid: 1200mg ad hoc before sleep or before uncontrollable carb-y meals. ALA reduces blood sugar by pushing glucose into the muscle for use rather than toward conversion for fat deposits. it basically flips a “switch” that causes increase in the amount of energy to go towards building muscle and decrease in the amount of energy used to go towards adding fat, Usually when my carbs intake is worryingly close or maybe even over 20g per day I usually take 1200 to 2400mg and if it doesn’t prevent me from slipping out of ketosis it certainly helps me to go back into it sooner. Be careful though to have it really just when you have had carbs and you actually have glucose to push into muscles, cause if taken when eating super low carb, even just 1200mg can send you into hypoglycaemia and knock you down for an entire day. Believe me, it happened twice to me and once you’re there you just need to wear it off, even eating sugar won’t help. Beside this keto-help effect though it is known to be a quite potent anti radicals.
On these I can comment myself, although usually there are some more supplements considered default for low-carb diets/keto people, so for reference here they come:
Vitamin K2 complex: if you have noticed extra-bruising occurring since eating low carb, you might be lacking vitamin K.
Iodine/Selenium/Vitamin D3: help with thyroid functions, especially against hypothyroidism. Vitamin D3 is also suspected to be connected with the “killing” of fat cells rather than just the shrinking, it is suggested in quantities up to 10000 IU per day.
Alpha GPC: This nootropic boostsawareness&cognitivecapacity * The significance of choline for yourcreation of attention and memoryraising acetyl choline is efficientlydocumented. It can beguaranteed by a range ofclinical studiesmilligrams - More Information: ThoroughWearing down (with study) And Wikipedia.org/wiki/Alpha-GPC
Huperzine A: Raisesintellectualfunctionality, and possesses neuroprotective outcomes. A studyobtainedresults that proven 58Per cent of patientsaddressed with Huperzine-A hadalterations in cognition, and conduct functionsMore Info: DetailedBreak down (with reports) And Wikipedia.org/wiki/Huperzine_A
Hericium Erinaceus (Lion’s Mane): Improvememory and awareness, improveneurologicalupkeep, detoxes liver, stop alzheimer’s, normalizebloodstreamsugar and cholesteroldiplomas. In just adual sightless, placebo controlledexamine, revealed that Hericium Erinaceus(Lion’s Mane) is effectiveformodest cognitivemilligrams - Much More Information: CompleteFail to function properly (with scientific research) And
Boostsemphasis, restduring the night, safeguardcomponents And blood pressurelevelsmanagement. L-Theanine is becomingstudiedfor theability toreducestress, improve cognition and boost yourmindset. In a 1999 components ofpaperpublished by Food itemsTechnology and
Science, L-Theanine was provided tofolks in dosenumbers of 50 - 200 mgs. It wasbasicallyobserved that L-Theanine straightimpactedthe production of Alpha Surfinside aexcellentstrategy. Alpha waveswould be thequiethowevertellbrainissueneeded to concentrationmg - Much More Information: In depthFail to function properly (with studies) And Wikipedia.org/wiki/Theanine
Caffeinated drinksintake: Boostemphasis, booststorage, raiseenergy, detoxes liver organ, wards far from alzheimer’s, increaseenergy, alleviate despression signs or symptoms, and so forth. According to a new study in Japan, scientists found out that just as
muscle cells are stimulated by caffeine, brain cells in the hippocampus are
stimulated to increase calcium concentration. This raises thecellular materialindicateactivityconsequentlyimprovingstorage. Caffeine intake intakemg - More Details: ThoroughWearing down (with research studies) & Wikipedia.org/wiki/Caffeine intake
Bacopa: Enhancesbrainmemory and function. Bacopa monnieri is extensivelytested and provenas being amemory and concentrationincreaser. Outcomes ofstudyjust recentlyshown that Bacopa decreasedsome timethought it wasnecessary toresearcha freshmethod by virtuallyone half! Memberstaking Bacopa increased the work outin as little as 6 timesin comparison toten daysfor yourmanage teammilligrams - More Information: ThoroughBreaking down (with scientific tests) &
Pterostilbene: Combatsaway from and reverses mentaltumble, it reducesblood circulation lipids and cholestrerol degrees. According to dog reports it can be shown to demonstrate
anti–cancers, contra–hypercholesterolemia, anti–hypertriglyceridemia
qualities.It can bebelieved the substancealso offersanti-diabeticcharacteristics as wellmg - Additional Information: DetailedBreak down (with reports) And Wikipedia.org/wiki/Pterostilbene
Mucuna Pruriens: Raiseenergy, concentration and focus. Mucuna capabilitiesregular dopamine, among the mostvital neurotranmitters, that has aaspect in peoplecapability tocompletely focusamongstall sorts ofother activities. Furthermore, it is actuallymostlyliable for regulating sexuality and frame of mind as wellmilligrams - More Details: ThoroughMalfunction (with analysis) And
GABA: Stimulatesrobustcalmness, relaxation and sleep lucid dreaming, And
decreasesnervousness. Gaba is a vital&popular inhibitory neurotransmitter inside themind, GABA really helps toimprovemaking alpha brainsearch, proven toincreaseclarity and focus. That are connected to anxiety and anxietymg - More Details, as well
it lessens beta brain waves:DetailedMalfunction (with reports) And Wikipedia.org/wiki/Gamma-Aminobutyric_acidanswer
Nutritional supplement B6: Higherenergy, regulatesensing And appropriatehuman braindevelopment, Scientistsfound out thatNutritionalhealth supplement B6 functionsan important role in the creation of serotonin and dopamine, which can benecessary forneurologicaldialogueVitamin supplement supplementmg - Additional Information: DetailedDeteriorating (with records) & Wikipedia.org/wiki/Vitamin_B6
B Nutritional-12: Decreasesfatigue, betterelectrical energy, decrease instress. B Vitamin-12 is a crucialmethod to obtainnourishmentrequired forevery person. Latestresearch indicatesadequatemeasure of B-12 can quitintellectualdecline. Industry expertsdiscovered thatfolkssuffering fromstoragechallenges, when resolved with B12, lots ofsigns or symptomsfaded in half a yearlinked tomodifications inintellectualtop quality&completely focus. B VitaminMore Information and facts: In depthBreak down (with scientific tests) And Wikipedia.org/wiki/Nutritious_B12
ACETYL L CARNITINE
Carnitine HCL: Effectivecontra--oxidant, also lowerslowenergy. Acetylcarnitine & carnitine performvitalfunctionswithin your body. These vitamins and minerals shuttle acetyl-businesses And essential fatty acids into mitochondria for strength-manufacturing. It may wellwork as astrengthtank of acetyl groupings and similarlynutritionenhancepotentialproducing.
A new study begins to clarify how brain structure and chemistry give
rise to specific aspects of “fluid intelligence,” the ability to adapt
to new situations and solve problems one has never encountered before.
The study, reported in the journal NeuroImage, links higher
concentrations of a marker of energy production in the brain with an
improved ability to solve verbal and spatial problems. It also finds an
association between brain size and number-related problem-solving.
The analysis involved 211 research subjects, making it the largest
study to date linking brain chemistry and intelligence in living humans,
said University of Illinois postdoctoral researcher Erick Paul, who led the work with research scientist Ryan Larsen and Illinois neuroscience professor Aron Barbey. The work was conducted in the Decision Neuroscience Laboratory at the Beckman Institute for Advanced Science and Technology. More studies will be needed to confirm and extend the findings, the researchers said.
“In our data, we observed two facets of fluid intelligence – one that
involves quantitative or numeric reasoning, and another that involves
verbal or spatial reasoning,” Paul said. “A similar separation of
reasoning abilities has been demonstrated in previous studies.”
The researchers conducted magnetic resonance spectroscopy to analyze
brain concentrations of a compound called NAA (N-acetyl aspartate), a
byproduct of glucose metabolism and a marker of energy production. They
measured brain volume in all subjects using magnetic resonance imaging.
“We found that the quantitative reasoning component of intelligence
correlated with brain volume, but not with the concentration of NAA in
the brain,” Paul said. “And the verbal and spatial components of
intelligence correlated with NAA, but not with brain volume.”
The team observed the same basic relationships when analyzing males and females separately.
The findings add to the evidence that fluid intelligence involves distinct yet interrelated processes in the brain, Paul said.
“Surely there are many things about the brain that determine a
person’s intelligence, and the goal is to try to tease apart that
puzzle,” he said. “These two brain biomarkers, brain volume and NAA, are
each giving us independent information about fluid intelligence. There
are different properties of the brain that we can measure, and these
different properties go with these different facets of fluid
“Our findings contribute to a growing body of evidence to suggest
that intelligence reflects multiple levels of organization in the brain –
spanning neuroanatomy, for example brain size, and neurophysiology,
such as brain metabolism – and that specific properties of the brain
provide a powerful lens to investigate and understand the nature of
specific intellectual abilities,” Barbey said.
The citric acid cycle (sometimes called the Krebs cycle) occurs in the mitochondrial matrix and is the third stage in the aerobic breakdown of glucose. The first, of course, is glycolysis, which creates pyruvate, NADH, and ATP. The second—which isn’t long enough to get its own post—is the linking reaction in which pyruvate is converted to Acetyl CoA. This is a coenzyme that the citric acid cycle breaks down to use later in energy production. Basically, the purpose of the linking reaction is to make pyruvate into something the cycle can use.
The main goal of the citric acid cycle is to convert bond energy (in the form of Acetyl CoA) into its reducing equivalents: i.e., to make some more NADH and FADH2, which are electron carriers. These then go through the electron transport chain and use their electron energy to create ATP. Remember, to reduce a compound is to add electrons to it—think of the mnemonic OILRIG.
So, how does the citric acid cycle do this?
Some diagrams get pretty complicated, especially when you include the enzymes responsible and the carbon compounds formed at every stage, but I’m going to break it into relatively simple steps.
An enzyme joins acetyl-CoA to oxaloacetate in order to form citric acid, which is where the cycle gets its name. Then, a water molecule “attacks” the acetyl, and CoA is ejected from the cycle.
Next, water is ejected and then put back in to help facilitate the reduction of NAD+ into NADH. For every turn of the cycle, 3 NADH molecules are created, and 2 molecules of CO2 are released.
ADP plus a free phosphate group (denoted as “Pi”) is put into the cycle, and these are smushed together to form an ATP.
Finally, FAD+ is reduced to FADH2. (FAD and NAD are both very similar coenzymes, performing the same oxidative and reductive roles in a reaction, but they’re different because they work on different classes of molecules: FAD oxidises carbon-carbon bonds, and NAD oxidises carbon-oxygen bonds)
A diagram might make it a little clearer:
So, let’s do a quick round-up of what’s happened:
Acetyl-CoA has been released as two CO2 molecules
3 NAD+ were reduced to 3 NADH
1 FAD+ was reduced to 1 FADH2
1 ADP+Pi formed 1 ATP molecule
This isn’t the end—the main goal of citric acid cycle is to prepare the electron carriers NADH and FADH2 for the electron transport chain, where much more ATP will be made.
ASA / Aspirin : inhibits the synthesis of thromboxane A2 ( thromboxane A2 is an arachidonate product that causes platelets to change shape, release their granules, and aggregate) by irreversible acetylation of the enzyme cyclooxygenase
Clopidogrel & Ticlopidine : reduce platelet aggregation by inhibiting the ADP pathway of platelets. These drugs are thienopyridine derivatives that achieve their antiplatelet effects by irreversibly blocking the ADP receptor on platelets.
Abciximab, Eptifibatide & Tirofiban : target the platelet IIb/IIIa receptor complex. The IIb/IIIa complex functions as a receptor mainly for fibrinogen and vitronectin but also for fibronectin and von Willebrand factor. Activation of this receptor complex is the “final common pathway” for platelet aggregation.
Dipyridamole : vasodilator that inhibits platelet function by inhibiting adenosine uptake and cyclic GMP phosphodiesterase activity.
N6-methyladenine: A Newly Discovered Epigenetic Modification
The majority of cellular functions are carried out by proteins encoded by specific genes present in cellular DNA. Genes are first transcribed to RNA which is then translated to proteins. The regulation of this process is important for maintaining correct cellular function. One of the ways that cells regulate gene expression is by epigenetic modifications to chromatin. The term “epigenetics” refers to reversible chemical modifications of DNA and histone proteins (DNA in the nucleus of eukaryotes is wrapped around histones) that affect the transcriptional status of genes. A number of histone modifications such as methylation and acetylation of lysine residues have already been discovered and characterized. Until recently; however, methylation of the 5 position of cytosine was the only known epigenetic DNA modification (A). Methylation of cytosine by DNA methyltransferases is associated with transcriptional silencing, while the removal of these methyl groups by TET enzymes is associated with transcriptional re-activation (B and C). In addition to controlling gene silencing, cytosine methylation also silences retrotransposons, a class of mobile genetic elements. If left unregulated, transposons can insert themselves into important regions of the genome and lead to mutagenesis.
Recently, N6-methyladenine, a new epigenetic modification, was discovered in mammalian cells. N6-mA had previously been discovered in prokaryotes and simple eukaryotes and was shown to function as a transcriptional activator. By contrast, a recent report published in Nature, has shown that N6-mA functions as a transcriptional silencer in mammalian cells, specifically in mouse embryonic stem cells. N6-mA primarily acts to silence the LINE-1 family of retrotransposons during early embryogenesis, which prevents genomic instability. The authors identified N6-mA by using a modified single molecule DNA sequencing technique. DNA bound to a specific modified histone protein was immunoprecipitated using an antibody against a specific histone modification (H2A.X), sequenced, and analyzed by mass spectrometry (D). This identified and determined the position of N6-mA. The authors then generated knockouts of the enzyme Alkbh1, which they believed may function as a demethylase for N6-mA. When Alkbh1 was absent from cells, they found an increase in the levels of N6-mA, showing that Alkbh1 functions as an N6-mA demethylase in vivo. This is important because epigenetic modifications are reversible. Genes can be turned off by methylation and then turned back on by removing the methyl group, so determining the enzyme responsible for the removal of N6-mA supports its role as an epigenetic modification.
“Immunostaining of planktonic Cnidaria. Acetylated tubulin (green), myosin (red), nuclei (blue). Image taken with ZEISS Lightsheet Z.1 during the EMBO course on Marine Animal Models in Evolution & Development, Sweden 2013. www.zeiss.com/lightsheet Sample courtesy of Helena Parra, Institut de Biologia Evolutiva (CSIC-Universitat Pompeu Fabra), Barcelona.”
The association of autism spectrum disorders with oxidative stress, redox imbalance, and mitochondrial dysfunction has become increasingly recognized. In this study, extracellular flux analysis was used to compare mitochondrial respiration in lymphoblastoid cell lines (LCLs) from individuals with autism and unaffected controls exposed to ethylmercury, an environmental toxin known to deplete glutathione and induce oxidative stress and mitochondrial dysfunction. We also tested whether pretreating the autism LCLs with N-acetyl cysteine (NAC) to increase glutathione concentrations conferred protection from ethylmercury. Examination of 16 autism/control LCL pairs revealed that a subgroup (31%) of autism LCLs exhibited a greater reduction in ATP-linked respiration, maximal respiratory capacity, and reserve capacity when exposed to ethylmercury, compared to control LCLs. These respiratory parameters were significantly elevated at baseline in the ethylmercury-sensitive autism subgroup as compared to control LCLs. NAC pretreatment of the sensitive subgroup reduced (normalized) baseline respiratory parameters and blunted the exaggerated ethylmercury-induced reserve capacity depletion. These findings suggest that the epidemiological link between environmental mercury exposure and an increased risk of developing autism may be mediated through mitochondrial dysfunction and support the notion that a subset of individuals with autism may be vulnerable to environmental influences with detrimental effects on development through mitochondrial dysfunction.
To celebrate my finally finishing the semester, I thought I would dish out another OB Science Time, this time in my own fascinating field of epigenetics, and how this relates to the clones of Orphan Black! YAY!!
So what exactly is epigenetics? Epigenetics refers to the heritable alterations in phenotype without changes to genotype, as well as the modifications of gene activity that are not based on alterations of DNA sequence. In other words, there is a heritable and a non-heritable side to the study of epigenetics.
I’ll make this a tad simpler. Almost every cell in your body contains a nucleus that contains all the DNA in your genome. Brain cells, heart cells, skin cells, kidney cells - they all have the exact same DNA. But then why are some genes only expressed in certain cells, causing every cell type to have different functions? Chromosomal modifications. Certain additions to the chromosome (methyl groups, acetyl groups, ubiquitin, etc.) will cause changes in expression of the genes on that part of the chromosome.
Now some of this is inherited from the parents. When mitosis occurs and the DNA is duplicated, the chromosomal modifications are duplicated to ensure that the expression patterns of the genes is maintained. The same happens in the gametes when meiosis occurs, so the epigenetics of the parents is passed down to the child.
But you can also acquire new epigenetic modifications. Cellular interactions, foreign materials, the microenvironment of the cell, the activities of the person, and many other things can cause alterations in the epigenome of a person. The womb is considered to be an important influence on the epigenome, right down to the minute microenvironments, which is why even identical twins can have epigenetic differences because they are experiencing different microenvironments.
So this is an extremely fascinating field, but what does it mean for twins, or even, say, a whole bunch of clones in some great experimental conspiracy on a certain Canadian sci-fi show? Well, it basically means that, even though all the Leda clones have the exact same genome, they can have many differences in their epigenomes, causing all the differences we see between them.
But epigenetics is specifically interesting when it comes to the clone disease! We know that Sarah and Helena are both fertile, meaning they do not express the synthetic infertility sequence that Ethan created. Now this could be due to a mutation in their sequence, or a complete absence of the sequence from their genome. But then why couldn’t Cosima just use Sarah’s bone marrow for the transplant, because she wouldn’t have the same sequence.
Now, if Sarah and Helena both had the exact same sequence, but had epigenetic modifications that were silencing the synthetic sequence, that would explain why their own cells are not an option. Giving Cosima a transplant from Sarah could maybe have a chance of working, but most likely, the environment of Cosima’s body would maintain the epigenetic patterns that were already present, and would remove the modifications silencing Sarah’s gene, making the whole transplant moot (hehe). And Sarah’s genetics would be no assistance in gene therapy, because gene therapy involves the injection of a single naked gene, without any modifications, so the epigenetic modifications would be removed before the injection.
So, basically, not only is epigenetics a completely fascinating field in reality, it can help explain some of what we have seen in Orphan Black!!
As always, if you have any questions, comments, concerns, don’t be afraid to hit me up so we can discuss all the science!!! And for more OB Science Time click here :D
Decomposing unwanted products after a nitration. In a previous post I mentioned that a compound was nitrated with acetyl nitrate (acetic anhydride + nitric acid). During this step, the product is stirred at 70 °C with 55% nitric acid to decompose side products.
As seen from the brown nitrous fumes, something happened in the flask, hope that white foam in the flask is something what I am looking for…
Immunostaining of planktonic Cnidaria. Acetylated tubulin (green), myosin (red), nuclei (blue). Image taken with ZEISS Lightsheet Z.1 during the EMBO course on Marine Animal Models in Evolution & Development, Sweden 2013. www.zeiss.com/lightsheet Sample courtesy of Helena Parra, Institut de Biologia Evolutiva (CSIC-Universitat Pompeu Fabra), Barcelona.
“Immunostaining of planktonic Cnidaria. Acetylated tubulin (green), myosin (red), nuclei (blue). Image taken with ZEISS Lightsheet Z.1 during the EMBO course on Marine Animal Models in Evolution & Development, Sweden 2013. www.zeiss.com/lightsheet Sample courtesy of Helena Parra, Institut de Biologia Evolutiva (CSIC-Universitat Pompeu Fabra), Barcelona. Part of the Life:Magnified exhibit at Washington Dulles Airport, 2014″
A relationship between Cellular
respiration, ketone bodies and Diabetes Mellitus
Our cells take up glucose from the blood and oxidize
it through cellular respiration, producing energy which is stored in an
intermediate molecule called adenosine triphosphate (ATP.
Fatty acids are typically used as systemic energy storage because 1g of fat
actually stores more energy than 1g of glucose.
Fatty acids are carried through the bloodstream
towards liver where they are converted into ketones under conditions of continuous starvation. However,
liver can’t use ketones because hepatocytes lack certain enzymes. Instead,
liver returns them into the bloodstream and these ketone bodies in turn are
taken up by our body cells.
In cells, ketone bodies (molecules) are broken down
into acetyl-coA, a key molecule for TCA cycle to run and ultimately drive the
formation of ATP via oxidative phosphorylation in cellular respiration. This is
one way, fat provides us with energy. Then, why didn’t evolution favor human
use fats instead of glucose as primary energy source?
Ketone bodies (3 type of molecules)
have a carboxyl group, -COOH group. They tend to dissociate in the blood (pH of
7.4), thereby acting as an acid.
High school biology has taught us that enzymes are highly sensitive to pH and
have a very narrow range of optimal pH values. Dissociate protons from ketone
bodies will lower the blood pH, which is not great from your body’s proteins.
Mellitus comes in…
The good news is that short-term increase of ketone
bodies in the blood during activities like exercising doesn’t affect our body. However,
chronic conditions like type 2 diabetes mellitus (DM) leads to consistently
high blood ketone bodies and high blood glucose. Normally, insulin helps to
stimulate the absorption of excess glucose into blood cells. However in DM
patient, insulin isn’t loses efficacy and excess blood glucose cannot enter the
cells. Cells take “low cytosolic glucose level” as a sign of high energy demand
and start producing ketones.
What happens with Diabetes Mellitus?
High blood glucose osmotically pulls intracellular
fluid into the blood in an attempt to equalize its tonicity with the cells, bringing
the concentration of blood glucose levels close to normal while dehydrating the
cells. Meanwhile in the kidneys, the normal glucose reabsorption capacity is
reached and large amounts of glucose are excreted in the urine in a condition
called osmotic diuresis.
Overall it causes diffusion of fluid from cells into
the bloodstream and out of the body. The result is excessive thirst
(polydipsia) and excessive urine production (polyuria). The cells are deprived of glucose and will signal
their ‘hunger’ by releasing hormones to the brain (excessive hunger-
polyphagia). Other symptoms include sudden weight loss as the body is breaking
down the fat store to supply energy to compensate for the insufficient supply
of energy by glucose oxidation. The poor glucose supply (due to insulin
malfunction) causes energy supply reduction, the person may become fatigued and
may resort to high carbohydrate food which further aggravate the situation.
Nocturnal (night) polyuria may also affect patient’s sleep and make the
The circulatory system carries out many important
functions. Any alteration in blood content may lead to many complications
including diabetic nephropathy, diabetic retinopathy, and slow wound healing.
Diabetes Mellitus is a long term condition, it not
only causes health complication, it also has a negative impact on their quality of life. However, with a
healthy lifestyle and careful diet control together with medication, well
controlled diabetes mellitus isn’t life threatening.
Yesterday I purified a larger amount on slightly decomposed 1,1′-diacetylferrocene by sublimation/distillation at reduced pressure. After the purification, these crystals were left in the still pot.
1,1′-diacetylferrocene is an orange to red crystalline solid, with a melting point
122-128 °C. It is an organoiron compound with the formula Fe(C5H4COMe)2, it consists of ferrocene substituted by two acetyl group on each of the cyclopentadienyl rings. It is an air-stable solid that is soluble in organic solvents and as seen it forms beautiful crystals.