Lipids Lipid-Treatment Assessment

Pearson TA, Laurora I, Chu H, Kafonek S. The Lipid Treatment Assessment Project (L-TAP). Arch Intern Med 2000 160 459 67. 

Since the use of tobacco is a chronic process, the effects of an aqueous extract of STE in rats following low-dose exposure were examined. Female Sprague-Dawley rats were treated orally with 25mg STE/kg every other day for 105 days. The effects of subchronic treatment of STE on hepatic microsomal and mitochondrial lipid peroxidation were assessed. Urinary excretion of the four lipid metabolites malondialdehyde, formaldehyde, acetaldehyde, and acetone was monitored by HPLC, with maximum increases being observed between 60 and 75 days of treatment. The assessment of lipid peroxidation was based on the formation of thiobarbituric acid-reactive substances (TEARS) over the 105 days of the study. 

Sodium dodecyl sulfate has been used to induce a dry, scaly skin condition in human subjects by daily treatment with a 4% aqueous solution on one leg over a period of 2 weeks. Measurements were made of stratum comeum hydration, scaliness, and lipid composition which were used to assess in vivo surfactant perturbations on desquamation [381]. 

The effect of prolonged antioxidant therapy in relation to normal physiological processes (for example, redox cycling, cell-cell signalling, transcription factor activation) must be assessed. It is conceivable that the overload of one antioxidant by dietary supplementation (for example, a-tocopherol) may shift the levels of other antioxidants (for example, by decreasing ascorbate and /3-carotene concentrations), with unknown consequences. To assess the potential for lipid-soluble antioxidant treatment in inflammatory diseases such as RA, further investigations into these questions will be needed. 

The development of CHD is a lifelong process. Except in rare cases of severely elevated serum cholesterol levels, years of poor dietary habits, sedentary lifestyle, and life-habit risk factors (e.g., smoking and obesity) contribute to the development of atherosclerosis.3 Unfortunately, many individuals at risk for CHD do not receive lipid-lowering therapy or are not optimally treated. This chapter will help identify individuals at risk, assess treatment goals based on the level of CHD risk, and implement optimal treatment strategies and monitoring plans. 

Obtain a thorough history of prescription, nonprescription, and natural drug product use. Determine what treatments for cholesterol the patient has used in the past (if any). Assess if the patient is taking any medications that may contribute to his or her abnormal lipid levels. 

The aim of the present study was to evaluate the effect of LLLT on oxidative markers in serum and tissue biopsies of healing ulcers before and after the 8th session of an LLLT course of chronic leg ulcer treatment. Oxidative damage was assessed in terms of lipid peroxidation reflected by serum malondialdehyde (MDA) level, protein oxidation was measured in terms of tissue protein carbonyls (PCb), and DNA damage was measured in terms of DNA fragmentation. Antioxidative activity was estimated by measuring activity of SOD, GPX and CAT enzymes. 

The uses and adverse effects of raloxifene have been reviewed (8-12). Current work seems to show an altogether positive effect of raloxifene (for example 60 mg/ day) on bone metabolism and serum lipids in post-meno-pausal women on chronic hemodialysis, without significant adverse effects in the short term. However, even the authors of very promising work in this connection point to the difficulty in assessing the long-term safety of the treatment in such women (13). Longer-term work elsewhere has pointed particularly to the occurrence of thromboembolic disease, but also of hot flushes, influenza-like symptoms, peripheral edema, and leg cramps. With the exception of thromboembolism these are unpleasant rather than serious, but they still need to be recorded and studied in this very susceptible group of users. 

The brief discussion above shows the difficulty of a straightforward paleoenvironmental assessment based on OSC. Their occurrence seems not to be related to any special type of environment on the contrary, they are widespread. However, several of the encountered compounds cannot be related chemotaxonomically to specific biological contributions yet, because information on the lipid composition of appropriate organisms is still scant. Nevertheless, it is clear that much information is contained in the extractable OSC, information which is not evident when only the aliphatic hydrocarbon fraction is investigated. Furthermore, high-molecular-weight sulfur species not directly amenable to GC-MS analysis is another source of information, but chemical treatment (desulfurization) is required for its disclosure. 

Superior to DSA, MRI can depict arterial flow or lumen as well as the vessel walls. Analysis of plaque morphology was improved in recent years by the development of specific MRI techniques. Plaques can now be characterized in vivo with regard to fibroid or lipid content or hemorrhagic lesions (Fig. 5.8). It can be expected that, in the future, plaque examination will influence stroke treatment protocols if the risk of plaque rupture can be reliably estimated (Cappendijk et al. 2005 Hayes et al. 1996 Trivedi et al. 2004 Yuan et al. 2001). Plaque examinations, however, are not yet clinical routine. Source images of TOF-MRA allow only limited assessment of vascular walls. 

It is well known that lipid peroxidation, DNA singlestrand breaks, and other forms of DNA damage occur in response to oxidative stress (Ames et al, 1982). Depletion of reduced glutathione also commonly precedes or accompanies lipid peroxidation and oxidative stress (Muldoon and Stohs, 1991 Omar et al, 1990). In an in vivo study, the effects of ricin administered orally on hepatic lipid peroxidation, nonprotein sulfhydryl content, and DNA singlestrand breaks were assessed in mice (Muldoon et al, 1992). The incidence of hepatic DNA damage increased 2.9-, 2.8-, and 2.4-fold relative to control values at 24, 36, and 48 h post-treatment with ricin, respectively. Hepatic nonprotein sulfhydryl concentration decreased significantly from 51 to 65% to control values at 24, 36, and 48 h post-treatment (Figures 25.2 and 25.3). 

Therefore, the ability of TNF-a antibody to modulate ricin-induced urinary carbonyl excretion as well as hepatic lipid peroxidation, glutathione depletion, and DNA singlestrand breaks was assessed (Muldoon et al, 1994). Ricin-induced urinary MDA and FA were reduced significantly in mice receiving antibody (15,000 U/kg) 2 h before treatment with ricin (5 pg/kg). At 48 h following ricin treatment, MDA and FA concentrations in the urine of TNF antibody-treated... 

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