acetylation

Product of an acetylation. Hard to believe, but only less than 1% of byproduct causes the black coloration on the white crystals. Just a quick wash with methanol and white crystals will be obtained.

What is acetylation? Making an acetyl ester of an alcohol, in this case with acetic anhydride.

How does this looks? Here is an example with acetylsalicylic acid (Aspirin): 

Ferrocene

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.

7.3.9 Protein amino-terminal modifications and proteomic approaches for N-terminal profiling

7.3.9 Protein amino-terminal modifications and proteomic approaches for N-terminal profiling

7.3.9 Protein amino-terminal modifications and proteomic approaches for N-terminal profiling

Larry H Bernstein, MD, FCAP, Writer and Curator

http://pharmaceuticalintelligence.com/2013/04/07/larryhbern/Protein_amino-terminal_modifications_and_proteomic_approaches_for_N-terminal_profiling

Protein amino-terminal modifications and proteomic approaches for N-terminal profiling

Lai ZW1, Petrera A2, S…

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Regioselective acetylation of carbohydrates and diols catalyzed by tetramethyl-ammonium hydroxide in water

Regioselective acetylation of carbohydrates and diols catalyzed by tetramethyl-ammonium hydroxide in water

Regioselective acetylation of carbohydrates and diols catalyzed by tetramethyl-ammonium hydroxide in water

Green Chem., 2014, Advance Article
DOI: 10.1039/C4GC00770K, Communication Yuchao Lu,a   Peng Wei,a   Yuxin Pei,*a   Hengfu Xu,a  Xiaoting Xina and   Zhichao Pei*ab     *Corresponding authors aState Key Laboratory of Crop Stress Biology for Arid Areas and College of Science, Northwest A&F…

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WHY NO CARBS MEANS MUSCLE LOSS:

Glucose is essential to burn fat. Fat and Glucose both enter into the Krebs Cycle at the same point as acetyl CoA. However, Glucose also contributes to other parts of the cycle. Without Glucose, that big wheel won’t keep turning. 

Without Glucose, fat continues to accumulate in the form of Acetyl CoA but can’t get through the Krebs Cycle. The body responds by letting the liver convert the Acetyl CoA to an acid called a ketone. Ketones slow the metabolic rate , reduce appetite and build up levels of acid in the blood (and your body does not like acid). Left unchecked ketosis can lead a person with diabetes into a coma.
In healthy people , restricting carbs (as you do in a low/no carb diet) also brings on ketosis. However, instead of just messing with their fat metabolism, they also start losing muscle mass. Here’s why: Protein can be used for ATP production within the Krebs Cycle, and the liver can turn protein into glucose! If you deprive your body of glucose, it responds by depriving you of your muscle mass, a situation that slows metabolic rate even more and makes it hard to lose body fat. SO EAT YOUR CARBS!
-Kinesiology For Dummies- Steve Glass, Brian Hatzel & Rick Albrecht

Transcriptional silencing and longevity protein Sir2

Larry H Bernstein, MD, FCAP, Writer and Curator

Aviva Lev-Ari, PhD, RN, Curator

http://pharmaceuticalintelligence.com/4-21-2014/2.27/larryhbern/Transcriptional silencing and longevity protein Sir2 

Transcriptional silencing and longevity protein Sir2 is an NAD-dependent histone deacetylase.

Imai S1, Armstrong CM, Kaeberlein M, Guarente L.
Nature.  Feb 17, 2000; 403(6771): 795-800.  PMID:…

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Medication Update 2015 June 22

Here is my morning lineup:

RX

  • Wellbutrin XL (as Bupropion XL)  1 x 300mg
  • Daytrana patch  1 x 30 mg  [applied to hip]
  • Dymista  50 mcg spray in each nostril

OTC

  • Nexium OTC  1 x 22.3 mg

VITAMINS/SUPPLEMENTS

  • Vitamin D3  1 x 5,000 IU
  • Phytophanere Hair & Nail Supplement  x 2
  • Biotin
  • MethylPro

Here is my afternoon/evening lineup:

RX

  • Ritalin (as Methyphenidate HCL  1 or ½ x 20mg  [only as needed at around 4:30pm, when the Daytrana patch has worn off]
  • Neurontin (as Gabapentin)  1 x 300 mg
  • Trazodone  2 x 100 mg

VITAMINS/SUPPLEMENTS

  • Vitron-C  2 x 65mg  [Iron + C]
  • Omega 3 Fish Oil  1 x 1,000 mg
  • N-Acetyl Cysteine (aka NAC)  2 x 1,000 mg

Stil not taking:

  • Strattera  2 x 18mg  [morning + evening]

Why?  Because I’m trying to take LESS medicine, not MORE.  I’m afraid to add this to my regimen because it brings up another set of side effects.  The downside to NOT taking this is that I am not on any medication for anxiety.  This comes into play when I am pre-menstrual, BIG TIME.  My last cycle, I was a mess.  It does help to know exactly when I’m PMS’ing, but it doesn’t take away the symptoms.  I’m going to try and exercise and continue eating healthy and see how that goes.

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Metabolic plasticity maintains proliferation in pyruvate dehydrogenase deficient cells.

PubMed: Metabolic plasticity maintains proliferation in pyruvate dehydrogenase deficient cells.

Cancer Metab. 2015;3:7

Authors: Rajagopalan KN, Egnatchik RA, Calvaruso MA, Wasti AT, Padanad MS, Boroughs LK, Ko B, Hensley CT, Acar M, Hu Z, Jiang L, Pascual JM, Scaglioni PP, DeBerardinis RJ

Abstract
BACKGROUND: Pyruvate dehydrogenase (PDH) occupies a central node of intermediary metabolism, converting pyruvate to acetyl-CoA, thus committing carbon derived from glucose to an aerobic fate rather than an anaerobic one. Rapidly proliferating tissues, including human tumors, use PDH to generate energy and macromolecular precursors. However, evidence supports the benefits of constraining maximal PDH activity under certain contexts, including hypoxia and oncogene-induced cell growth. Although PDH is one of the most widely studied enzyme complexes in mammals, its requirement for cell growth is unknown. In this study, we directly addressed whether PDH is required for mammalian cells to proliferate.
RESULTS: We genetically suppressed expression of the PDHA1 gene encoding an essential subunit of the PDH complex and characterized the effects on intermediary metabolism and cell proliferation using a combination of stable isotope tracing and growth assays. Surprisingly, rapidly dividing cells tolerated loss of PDH activity without major effects on proliferative rates in complete medium. PDH suppression increased reliance on extracellular lipids, and in some cell lines, reducing lipid availability uncovered a modest growth defect that could be completely reversed by providing exogenous-free fatty acids. PDH suppression also shifted the source of lipogenic acetyl-CoA from glucose to glutamine, and this compensatory pathway required a net reductive isocitrate dehydrogenase (IDH) flux to produce a source of glutamine-derived acetyl-CoA for fatty acids. By deleting the cytosolic isoform of IDH (IDH1), the enhanced contribution of glutamine to the lipogenic acetyl-CoA pool during PDHA1 suppression was eliminated, and growth was modestly suppressed.
CONCLUSIONS: Although PDH suppression substantially alters central carbon metabolism, the data indicate that rapid cell proliferation occurs independently of PDH activity. Our findings reveal that this central enzyme is essentially dispensable for growth and proliferation of both primary cells and established cell lines. We also identify the compensatory mechanisms that are activated under PDH deficiency, namely scavenging of extracellular lipids and lipogenic acetyl-CoA production from reductive glutamine metabolism through IDH1.

PMID: 26137220 [PubMed - as supplied by publisher] http://dlvr.it/BPjzQs

Inhibition of bromodomain and extra-terminal proteins (BET) as a potential therapeutic approach in haematological malignancies: emerging preclinical and clinical evidence.

Inhibition of bromodomain and extra-terminal proteins (BET) as a potential therapeutic approach in haematological malignancies: emerging preclinical and clinical evidence.

Ther Adv Hematol. 2015 Jun;6(3):128-141

Authors: Chaidos A, Caputo V, Karadimitris A

Abstract
Post-translational modifications of the nucleosomal histone proteins orchestrate chromatin organization and gene expression in normal and cancer cells. Among them, the acetylation of N-terminal histone tails represents the fundamental epigenetic mark of open structure chromatin and active gene transcription. The bromodomain and extra-terminal (BET) proteins are epigenetic readers which utilize tandem bromodomains (BRD) modules to recognize and dock themselves on the acetylated lysine tails. The BET proteins act as scaffolds for the recruitment of transcription factors and chromatin organizers required in transcription initiation and elongation. The recent discovery of small molecules capable of blocking their lysine-binding pocket is the first paradigm of successful pharmacological inhibition of epigenetic readers. JQ1 is a prototype benzodiazepine molecule and a specific BET inhibitor with antineoplastic activity both in solid tumours and haematological malignancies. The quinolone I-BET151 and the suitable for clinical development I-BET762 benzodiazepine were introduced in parallel with JQ1 and have also shown potent antitumour activity in preclinical studies. I-BET762 is currently being tested in early phase clinical trials, along with a rapidly growing list of other BET inhibitors. Unlike older epigenetic therapies, the study of BET inhibitors has offered substantial, context-specific, mechanistic insights of their antitumour activity, which will facilitate optimal therapeutic targeting in future. Here, we review the development of this novel class of epigenetic drugs, the biology of BET protein inhibition, the emerging evidence from preclinical work and early phase clinical studies and we discuss their potential role in the treatment of haematological malignancies.

PMID: 26137204 [PubMed - as supplied by publisher]



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