Ester Synthesis Lab Report

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Ester Synthesis Lab Report

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Synthesis of Esters

Moreover, there are indications of increased high-sensitivity C-reactive protein hsCRP levels in hypothyroidism [ 28 , 49 ] although there are studies which do not support this notion [ 31 , 50 ]. Administration of substitution therapy with L-thyroxine significantly improves lipid metabolism abnormalities. A period of weeks of thyroxin replacement therapy is usually needed to correct dyslipidemia in overt hypothyroidism.

In general, changes in serum lipoproteins in hypothyroid patients are correlated with changes in free T 4 FT 4 [ 66 ]. However, when the effects of substitution therapy on qualitative lipid profile were assessed no change in LDL particle size was seen [ 28 ]. A more dramatic reduction of TC levels has been observed in hypothyroid patients with higher baseline TSH levels [ 67 ]. Serum HDL-C levels tend to decrease with thyroid replacement, but this is a less consistent finding [ 68 ]. Serum Lp a levels also tend to decrease with restoration of euthyroidism [ 25 , 39 ]. Moreover, a decrease in CIMT has been observed after thyroxine treatment in hypothyroid patients [ 61 ]. The presence of overt hypothyroidism in patients with dyslipidemia is not rare. We found that 2.

Superimposed dyslipidemia should be taken into account in cases of failure of substitution therapy to normalize the lipid profile despite the restoration of euthyroidism [ 1 ]. Hypothyroidism is one of the most common causes of secondary dyslipidemia. Therefore, before starting hypolipidemic therapy, the evaluation of thyroid function is needed. Thyroid failure is associated with increased levels of creatinine kinase CK [ 69 ]. Statin therapy may substantially increase levels of CK. Therefore, it is imperative to firstly correct thyroid dysfunction with thyroxine substitution therapy and then treat the underlying dyslipidemia with statins. Subclinical hypothyroidism SH , defined as the clinical status of elevated serum TSH levels with normal levels of FT 4 and FT 3 , is a far more common disorder than overt hypothyroidism.

The prevalence of SH in the general population is estimated at 4. SH has a higher prevalence among women and older populations [ 3 , 72 - 74 ]. Moreover, SH may progress to overt hypothyroidism. Most studies have shown increased Lp a levels related to SH [ 85 , 87 , 88 ]. An interesting study evaluated serum Lp a levels along with corresponding apolipoprotein a [apo a ] phenotypes, which are known to influence Lp a levels, in SH patients [ 89 ].

Thyroid autoimmunity may also play an important role in the elevation of Lp a levels. On the other hand, a study compared the levels of Lp a of 22 euthyroid subjects 9 male and 13 postmenopausal female with thyroid autoimmunity with those of 64 age- and sex-matched controls without thyroid autoimmunity [ 91 ]. There were no significant differences in the values of lipid parameters, including Lp a , between the two groups even when apo a phenotypes were taken into account [ 91 ].

Moreover, no significant difference in the Lp a levels was found in euthyroid patients with chronic renal failure regardless of the presence of thyroid autoimmunity, the apo a phenotype, the stage of renal failure and the mode of dialysis in end stage patients [ 92 ]. Furthermore, the presence of thyroid autoimmunity has not been shown to influence serum lipid parameters in SH subjects [ 85 ]. There is some controversy regarding the presence or the severity of SH-induced dyslipidemia.

Indeed, there have been studies indicating no significant difference in lipid profile between SH patients and controls [ 29 - 31 , 93 ]. However, when adjusted for age, race, sex and the use of lipid-lowering drugs no difference was observed between SH and controls regarding lipid profile. Moreover, there have been studies questioning the effects of thyroid hormones on Lp a levels. Various studies have shown no difference between SH and control subjects regarding Lp a levels [ 39 , 82 , 95 , 96 ]. Lee et. An association between lipids, thyroid function and insulin resistance has been observed [ 18 ].

The analysis of a subgroup from the Fremantle Diabetes Study FDS showed that the association of TSH levels and lipid profile is significant mainly in the presence of insulin resistance. Similar results were shown in a study in euthyroid subjects [ 97 ]. An interesting aspect of the potential SH-mediated dyslipidemia is the qualitative effects of thyroid hormones on lipids.

No difference was found regarding lipid profile between the 2 groups. SH has been associated with a hypercoagulable state [ 77 , 83 ]. Furthermore, SH impairs ventricular function as well as cardiovascular and respiratory adaptation to effort and decreases heart rate variability [ 98 , 99 ]. Moreover, SH decreases flow-mediated vasodilation and nitric oxide NO availability, which are markers of endothelial function [ 98 , 99 ]. SH has also been associated with other CVD risk factors, such as increase in insulin resistance [ 64 , ].

Moreover, a negative association between free thyroxine and hsCRP levels has been described [ ]. A study demonstrated a linear correlation between blood pressure and TSH even within the normal reference ranges [ ]. In addition, smoking may deteriorate the lipid profile in women with SH and aggravate the degree of thyroid failure, thus contributing to the development of atherosclerosis [ ]. However, it is imperative to investigate the available data on the incidence of CVD morbidity and mortality in SH subjects. SH was not associated with increased prevalence of stroke, peripheral artery disease and CVD mortality. Of interest are the results from studies evaluating the effects of SH in elderly populations.

Moreover, a study evaluated the association of thyrotropin with disability and survival in the Leiden Plus Study elderly population [ ]. The results indicated that abnormally high levels of thyrotropin not only did not affect cognitive and mental status but rather prolonged life span [ ]. A beneficial effect of substitution therapy on lipid parameters and especially TC and LDL-C in some patients with SH has been shown [ 30 , 72 , 88 , - ]. The reduction was larger in individuals with higher pretreatment cholesterol levels and in hypothyroid individuals taking suboptimal T 4 doses [ 72 ].

Thyroxine was administered with a goal of TSH levels of 0. Moreover, thyroxine substitution therapy may have additional advantageous effects to offer beyond the improvement of lipid profile. Indeed, a reduction in CIMT [ 78 , 79 ] and improvement of endothelial function [ 99 ] has been described in SH patients after thyroxine replacement. These findings, however, are not consistently corroborated by other studies. Indeed, some studies showed no significant effect of thyroxine therapy on lipid profile in SH patients [ 78 , 93 , , ]. A recent meta-analysis showed no benefits in survival or CVD mortality after substitution therapy in SH patients [ ]. Moreover, thyroxine replacement did not improve quality of life, although a beneficial effect was seen in some lipid parameters and left ventricular function [ ].

The beneficial effects of thyroxine substitution therapy on Lp a levels in SH subjects are also debated. Several studies have shown no impact of thyroxine therapy on Lp a levels in SH patients [ 39 , 40 , 85 , 88 ]. However, other studies showed a significant decrease of Lp a levels after thyroxine treatment [ 89 , ]. A study with 17 SH women demonstrated a reduction of Lp a by Milionis et al. Of interest was that this reduction of Lp a levels achieved significance only in the low molecular weight apo a isoforms subgroup of patients [ 89 ].

Although it is clear that thyroid replacement therapy has beneficial effects on serum lipid profile and CVD risk in overt hypothyroid patients, no clear consensus has been established regarding the treatment of SH subjects [ , ]. This is due to the fact that there are no data from large trials on whether and to what degree does SH affect lipid profile. Moreover, data are lacking on the overall effect of substitution therapy on morbidity and mortality in SH patients.

A significant query is whether all SH patients would benefit from thyroxine replacement therapy or such therapy should be reserved for selected subgroups. Furthermore, there has not been enough evidence regarding the long-term effects of thyroid replacement in SH patients and therefore no clear recommendations can be made [ ]. Moreover, levothyroxine treatment may play an important role in other aspects of CVD risk beyond lipids. Of note, the potential adverse effects of levothyroxine therapy should also be taken into account. Furthermore, when treating people with angina pectoris or heart disease, one should be very cautious because thyroxin therapy may exacerbate angina or promote cardiac arrhythmia.

Overall, measurement of serum TSH levels should be included in the screening of patients with dyslipidemia [ 1 , , ]. Hypercholesterolemic patients with SH may be treated with thyroxin substitution therapy, since the restoration of euthyroidism can effectively improve lipid levels, relieve certain symptoms, and may also prevent progression to overt hypothyroidism [ ]. The incidence of hyperthyroidism is lower 2.

Similarly, a decreased prevalence of hyperthyroidism is evident in hyperlipidemic patients, since only 3 out of the patients in our study had thyrotoxicosis [ 25 ]. Moreover, no difference in LDL subfraction distribution has been observed between subclinical or overt hyperthyroid versus euthyroid subjects [ 42 ]. Furthermore, hyperthyroidism results in enhanced LDL oxidability, which is related to FT 4 levels [ 46 ]. Triglyceride levels remain unchanged. On the other hand, no changes in blood pressure [ ], Lp a [ 31 ] or hsCRP levels [ 31 ] have been described in hyperthyroid patients. However, an increase in factor X activity has been observed in subclinical hyperthyroidism patients, indicating a hypercoagulable state [ 77 ].

Therapy of clinical hyperthyroidism results in restoration of those alterations of lipid metabolism [ , ], while the effects of treatment of subclinical hyperthyroidism subjects are not yet clear [ ]. Iatrogenic hyperthyroidism has been associated with MI in subjects without coronary stenosis [ , ]. Similarly, there have been case reports associating subclinical hyperthyroidism with MI [ ], recurrent pulmonary embolism [ ] and atrial fibrillation [ , ]. Hyperthyroidism not only consists a significant cause of acquired hypobetalipoproteinemia, but it can also be the underlying cause of unexpected improvement of lipid profile in hyperlipidemic patients [ ]. In the latter case, therapy of thyrotoxicosis restores the lipid parameters to the previously elevated levels [ ].

Thyroid dysfunction can have an important effect on lipid profile [ ]. Biochemical screening for thyroid dysfunction is critical in all dyslipidemic patients, as well as in all patients with unexpected improvement or worsening of their lipid profile. Underlying thyroid disorders should be recognized and treated in this setting. There have been studies suggesting that screening for thyroid dysfunction is cost effective [ ].

The American Thyroid Association recommends that adults be screened for thyroid dysfunction by measurement of the serum TSH concentration, beginning at age 35 years and every 5 years thereafter [ ]. On the other hand, the U. Preventive Services Task Force concludes that the evidence is insufficient to recommend for or against routine screening for thyroid disease in adults [ ]. There is a need for large studies designed to answer the question whether thyroid abnormalities and especially SH are associated with CVD and whether restoration of euthyroidism might influence morbidity and mortality.

National Center for Biotechnology Information , U. Open Cardiovasc Med J. Published online Feb V Rizos , M. S Elisaf , and E. Author information Article notes Copyright and License information Disclaimer. This article has been cited by other articles in PMC. Abstract Thyroid dysfunction has a great impact on lipids as well as a number of other cardiovascular risk factors. Keywords: Cardiovascular disease, dyslipidemia, hypothyroidism, hyperthyroidism, lipoprotein a , thyroid autoimmunity, thyroid dysfunction, thyroxine treatment. Open in a separate window. Overt Hypothyroidism a. CVD Risk The above abnormalities of lipid metabolism associated with overt hypothyroidism predispose to the development of atherosclerotic coronary artery disease CAD [ 44 , 45 ].

Substitution Therapy Administration of substitution therapy with L-thyroxine significantly improves lipid metabolism abnormalities. Subclinical Hypothyroidism Subclinical hypothyroidism SH , defined as the clinical status of elevated serum TSH levels with normal levels of FT 4 and FT 3 , is a far more common disorder than overt hypothyroidism. Should we Treat SH Patients? Duntas LH. Thyroid disease and lipids. Friis T, Pedersen LR. Serum lipids in hyper- and hypothyroidism before and after treatment. Clin Chim Acta.

The Colorado thyroid disease prevalence study. Arch Intern Med. The association between TSH within the reference range and serum lipid concentrations in a population-based study. Eur J Endocrinol. Effects of triiodothyronine and amiodarone on the promoter of the human LDL receptor gene. Biochem Biophys Res Commun. Thyroid hormone T3 and its acetic derivative TA3 protect low-density lipoproteins from oxidation by different mechanisms.

Lagrost L. Regulation of cholesteryl ester transfer protein CETP activity: review of in vitro and in vivo studies. Biochim Biophys Acta. Kermasha, S. Goetghebeur; J. Dumont Lampman, Gary M. Ong, Peter K. Acree Reimer, Karl Ludwig Berichte der Deutschen Chemischen Gesellschaft. Roberts, Deborah D. Rouhi, A. Maureen Chemical and Engineering News. Tiemann, Ferd. Haarmann Van Ness, J. Kirk-Othmer Encyclopedia of Chemical Technology, 3rd edition.

Journal of Chromatography A. Walton, Nicholas J. Mayer; Arjan Narbad July CRC Press. Guaiacol vanillin, adulterated with acetovanillone, has an odor indistinguishable from lignin vanillin. Haarmann and Reimer, one of the corporate ancestors of the modern flavor and aroma manufacturer Symrise, was in fact established in Manufacture of vanillin and its homologues U. Patent 2,, PDF. Patent Office. Flora Library. Flavour and Fragrance Journal. Whether or not these procedures produce a product whose taste is comparable to traditionally prepared natural vanilla, many of them are incompatible with the customs of the natural vanilla market, in which the vanilla beans are sold whole, and graded by, among other factors, their length.

Handbook of Vanilla Science and Technology : Nature Communications. Bibcode : NatCo PMC This chemical process can be conveniently carried out on the laboratory scale using the procedure described by Lampman Scientific American. Bibcode : Natur. Microbial Pathogenesis. International Journal of Food Sciences and Nutrition. Retrieved 18 February Dec Fisher's Contact Dermatitis. Annals of the Entomological Society of America. TRP channel modulators. Triptolide Tripterygium wilfordii.

Ruthenium red. Authority control. Integrated Authority File Germany. Microsoft Academic. Namespaces Article Talk. Views Read Edit View history. Help Learn to edit Community portal Recent changes Upload file. Download as PDF Printable version. Wikimedia Commons. Other names Vanillin [1] Methyl vanillin [1] Vanillic aldehyde [2]. EC Number. Dissolve 10 mg of a solid or 1 drop of a liquid unknown in the minimum amount of bis 2-ethoxyethyl ether required to give a clear solution less than 1 mL. Add the unknown solution dropwise, with agitation, to the first test tube. Mix vigorously and allow the solution to stand. Do the same for the known compound.

Do not use benzaldehyde for the known. For the blank, simply add 0. Warning : Wash any minor amounts of residual Tollens reagent into a sink and flush with water. The reagent forms silver fulminate which is very explosive. The test solutions can be disposed of in a jar labeled for that purpose. The silver mirror can usually be washed clean with soapy water and a scrub brush. If not, see your instructor. Chromic Acid Test for Aldehydes and Alcohols. Dissolve 10 mg of a solid or 1 drop of a liquid unknown in reagent grade acetone in a clean, dry test tube. Add a few drops of chromic acid solution one drop at a time with shaking.

Aldehydes and primary and secondary alcohols are oxidized very quickly. Tertiary alcohols are not oxidized. Aliphatic aldehydes are oxidized in less than a minute, aromatic aldehydes take a bit longer. Since the condition of the acetone is critical, it is wise to carefully run the blank to be certain that the acetone itself is not giving a false positive. Use benzaldehyde and an aliphatic aldehyde for aldehyde knowns and 1- and 2-butanol for alcohol knowns. The chromic acid solution is prepared by dissolving 1. Warning : Cr VI compounds are considered suspect carcinogens and should be handled carefully.

Ferric Hydroxamate Test for Esters. If you have a carbonyl compound which is not an aldehyde or ketone or carboxylic acid, it could be an ester. If you obtain a color other than yellow, the test cannot be used. Otherwise, the test is conducted as follows: dissolve 50 mg of solid or 2 drops of liquid unknown in 1 mL of 0. Heat to boiling for minutes, then cool and add 2 mL 1N HCl. The color is due to a complex between the hydroxamic acid and the ferric ion. A deep burgundy color is positive. Use banana oil or methyl benzoate as knowns. Ferric Chloride test for Phenols. Just as enols can form colored complexes with ferric ion, phenolate ions can as well. Therefore, this test is designed to convert the weakly acidic phenols to their conjugate base which can then complex with ferric ion.

If the phenol is water soluble, add a few drops of 2. A deep red, green, or blue color is positive. If the phenol is not water soluble, dissolve 20 mg of the solid or 1 drop of the liquid in 1 mL of methylene chloride and add 1 drop of pyridine. An intense color is a positive test. Use phenol as a known. Not all phenols will give a positive test. Iodoform test for methyl ketones. In this test you will convert the methyl ketone to a triidomethyl ketone which is then cleaved to form iodoform, HCI 3 , a yellow solid.

Acetone gives a nice positive test so be certain that no traces of acetone are in your glassware. In a large clean test tube or a vial, place mg of a solid or 5 drops of a liquid unknown. Add a total of 3 mL of iodine-potassium iodide solution in six equal portions, stopper and shake well after each addition. Caution : seal the tube carefully and avoid skin contact with the iodine solution. The color of the iodine will disappear more slowly in the later additions.

The solution should be slightly yellow. Heat if necessary and shake again to force the iodine to react. When the color is slightly yellow, add water to nearly fill the test tube or container, stopper, and shake vigorously. After standing for 15 minutes, a pale yellow precipitate of iodoform mp o C is a positive test for a methyl ketone. Acetone can be used for the known. The iodine-potassium iodide solution is prepared from 10 g of iodine and 20 g of potassium iodide in mL of water. Hinsburg Test for Amines. If you have a basic compound which you believe to be an amine, you can corroborate your suspicion and determine if you have a primary, secondary, or tertiary amine using the Hinsberg test. You will react the amine with a sulfonyl chloride forming an insoluble sulfonamide of a primary or secondary amine or the soluble salt of a tertiary amine.

The insoluble sulfonamide of a primary amine will be made soluble in base via removal of the slightly acidic proton on N but that of a secondary amine will not no proton on N to remove. Add mg of a solid or 0. Stopper the tube and shake it for several minutes. Remove the stopper and heat the mixture on a steam bath for 1 minute. Cool the solution and if it is not basic to pH paper, add additional KOH solution.

If a precipitate has formed, add 5 mL of water and shake vigorously. If the precipitate does not redissolve in the basic solution, it is indicative of a sulfonamide of a secondary amine. Formation of a precipitate under acidic conditions suggests that the previously soluble sulfonamide was of a primary amine. If no precipitate has formed, the initial amine could have been tertiary.

Improving the reactions between phenols and some less reactive acyl Ester Synthesis Lab Report Benzoyl chloride has Crisis Communication Thesis formula C 6 H 5 COCl. Hypothyroidism Crisis Communication Thesis also accompanied by increased prevalence of metabolic syndrome [ 62 ] and waist-to-hip ratio [ 63 ]. Vanillin is an organic compound who wrote dracula and frankenstein the molecular Spectrophotometric Analysis Of Dyes C Crisis Communication Thesis H 8 O 3. Yes, it can.