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Fatty acids resources:

Fatty acids research abs 1 || Fatty acids research abs 2 || Fatty acids research abs 3 || Fatty acids research abs 4 || Fatty acids research abs 5





J Invest Dermatol. 2002 Sep;119(3):617-20.
Associations of tumor necrosis factor alpha and HLA polymorphisms with adult dermatomyositis: implications for a unique pathogenesis.

Werth VP, Callen JP, Ang G, Sullivan KE.

Philadelphia V.A. Medical Center, Department of Dermatology, University of Pennsylvania, USA. wertail.med.upenn.edu

We recently reported that the -308A tumor necrosis factor alpha promoter polymorphism is associated with the photosensitive disorder subacute cutaneous lupus erythematosus and mediates an exaggerated tumor necrosis factor alpha response to ultraviolet B. We now sought to examine the association of this polymorphism with adult dermatomyositis, a photosensitive disease that exhibits some features in common with subacute cutaneous lupus erythematosus. Fifty adult patients with dermatomyositis and 239 healthy, race-matched controls were examined for the -308A tumor necrosis factor alpha polymorphism and the more common -308G allele. The frequency of the -308A allele was 0.27 in the entire dermatomyositis group, versus 0.14 in the controls (p = 0.003, chi2 2 x 2 table). Caucasians were the only racial/ethnic group in our study large enough to allow separate statistical analysis (47 dermatomyositis, 223 controls). The frequency of the -308A allele was 0.26 for dermatomyositis and 0.14 for controls (p = 0.014). Caucasians are known to exhibit a linkage disequilibrium between -308A and HLA-DR3, which we previously found to be significantly enhanced in subacute cutaneous lupus erythematosus patients. In contrast, we now found no increase in the association of -308A and HLA-DR3 in Caucasians with dermatomyositis compared to controls. Consistent with this observation, the association of these two genes in dermatomyositis was significantly less than we previously reported in Caucasians with subacute cutaneous lupus erythematosus (p = 0.016). We conclude that the tumor necrosis factor -308A polymorphism is associated with dermatomyositis, which suggests a pathophysiologic contribution from ultraviolet-induced production of tumor necrosis factor alpha, similar to subacute cutaneous lupus erythematosus. The differences in linkage with HLA-DR3, as well as several divergent clinical features, indicate that there are also fundamental mechanistic differences between dermatomyositis and subacute cutaneous lupus erythematosus.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12230503&dopt=Abstract



J Invest Dermatol. 2002 Sep;119(3):692-8.
Refined mapping of Naegeli-Franceschetti- Jadassohn syndrome to a 6 cM interval on chromosome 17q11.2-q21 and investigation of candidate genes.

Sprecher E, Itin P, Whittock NV, McGrath JA, Meyer R, DiGiovanna JJ, Bale SJ, Uitto J, Richard G.

Department of Dermatology and Cutaneous Biology and Jefferson Institute of Molecular Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.

Naegeli-Franceschetti-Jadassohn syndrome and dermatopathia pigmentosa reticularis are autosomal dominant ectodermal dysplasias characterized by the absence of dermatoglyphics, reticulate hyper pigmentation of the skin, hypohidrosis, and heat intolerance. Palmoplantar keratoderma, nail dystrophy, and enamel defects are common in Naegeli-Franceschetti-Jadassohn syndrome, whereas diffuse alopecia is only seen in dermatopathia pigmentosa reticularis. We studied a large Swiss family with Naegeli-Franceschetti-Jadassohn syndrome originally described by Naegeli in 1927 and assessed linkage to chromosome 17q, which was proposed to harbor the Naegeli-Franceschetti-Jadassohn syndrome gene. Our results considerably narrow the Naegeli-Franceschetti-Jadassohn syndrome gene region from 27 cM to 6 cM flanked by D17S933 and D17S934 with a maximum multipoint LOD score of 2.7 at marker locus D17S800. In addition, we studied a small family with dermatopathia pigmentosa reticularis, and our linkage data suggest that dermatopathia pigmentosa reticularis may map to the same chromosomal region. The Naegeli-Franceschetti-Jadassohn syndrome critical interval spans approximately 5.4 Mb and contains a minimum of 45 distinct genes. We scrutinized 13 new prime candidates in addition to five genes previously examined, established the genomic organization of 10 of these genes, and excluded all of them by mutation analysis. Moreover, we identified a cDNA (KRT24) encoding a new keratin protein that bears high similarity to the type I keratins and displays a unique expression profile. No pathogenic mutations were identified in this novel gene either, however. In summary, our results substantially refine the Naegeli-Franceschetti-Jadassohn syndrome region and will aid in identifying a gene that is critical for ontogenesis of multiple ectodermal tissues.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12230514&dopt=Abstract



Proc Nutr Soc. 2002 Aug;61(3):381-9.
Effects of n-3 fatty acids on cartilage metabolism.

Curtis CL, Rees SG, Cramp J, Flannery CR, Hughes CE, Little CB, Williams R, Wilson C, Dent CM, Harwood JL, Caterson B.

Cardiff School of Biosciences, Cardiff University, UK.

Although the clinical benefits of dietary supplementation with n-3 polyunsaturated fatty acids (PUFA) has been recognised for a number of years, the molecular mechanisms by which particular PUFA affect metabolism of cells within the synovial joint tissues are not understood. This study set out to investigate how n-3 PUFA and other classes of fatty acids affect both degradative and inflammatory aspects of metabolism of articular cartilage chondrocytes using an in vitro model of cartilage degradation. Using well-established culture models, cartilage explants from normal bovine and human osteoarthritic cartilage were supplemented with either n-3 or n-6 PUFA, and cultures were subsequently treated with interleukin 1 to initiate catabolic processes that mimic cartilage degradation in arthritis. Results show that supplementation specifically with n-3 PUFA, but not n-6 PUFA, causes a decrease in both degradative and inflammatory aspects of chondrocyte metabolism, whilst having no effect on the normal tissue homeostasis. Collectively, our data provide evidence supporting dietary supplementation of n-3 PUFA, which in turn may have a beneficial effect of slowing and reducing inflammation in the pathogenesis of degenerative joint diseases in man.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12230798&dopt=Abstract



Antioxid Redox Signal. 2002 Aug;4(4):675-80.
The A640G and C242T p22(phox) polymorphisms in patients with coronary artery disease.

Zafari AM, Davidoff MN, Austin H, Valppu L, Cotsonis G, Lassegue B, Griendling KK.

Division of Cardiology, Emory University, Atlanta, GA 30322, USA. azafarmory.edu

Oxidative stress plays a significant role in the pathogenesis of coronary artery disease (CAD). A p22(phox)-based NAD(P)H oxidase acts as a potent superoxide-generating system in the vasculature. We studied the association of the A640G and the C242T polymorphisms with clinical risk factors, endothelial function, and severity of CAD in a cohort of 216 patients referred for coronary angiography. The frequency of p22(phox) genotypes for AA, AG, and GG was 22.5, 52.3, and 25.2%, and for CC, CT, and TT 35.5, 51.3, and 13.2%, respectively. The A640G and the C242T polymorphisms were not associated with severity of CAD and endothelial function. The frequency distribution of the genotypes among patients with or without angiographically significant CAD did not reach statistical significance. Our study does not support a functional role for the A640G or C242T polymorphisms either in the severity of CAD or in determining endothelial function in older men.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12230880&dopt=Abstract



Cell. 2002 Sep 6;110(5):639-48.
Disruption of DAG1 in differentiated skeletal muscle reveals a role for dystroglycan in muscle regeneration.

Cohn RD, Henry MD, Michele DE, Barresi R, Saito F, Moore SA, Flanagan JD, Skwarchuk MW, Robbins ME, Mendell JR, Williamson RA, Campbell KP.

Howard Hughes Medical Institute, Department of Physiology and Biophysics, Department of Neurology, Iowa City, IA 52242, USA.

Striated muscle-specific disruption of the dystroglycan (DAG1) gene results in loss of the dystrophin-glycoprotein complex in differentiated muscle and a remarkably mild muscular dystrophy with hypertrophy and without tissue fibrosis. We find that satellite cells, expressing dystroglycan, support continued efficient regeneration of skeletal muscle along with transient expression of dystroglycan in regenerating muscle fibers. We demonstrate a similar phenomenon of reexpression of functional dystroglycan in regenerating muscle fibers in a mild form of human muscular dystrophy caused by disruption of posttranslational dystroglycan processing. Thus, maintenance of regenerative capacity by satellite cells expressing dystroglycan is likely responsible for mild disease progression in mice and possibly humans. Therefore, inadequate repair of skeletal muscle by satellite cells represents an important mechanism affecting the pathogenesis of muscular dystrophy.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12230980&dopt=Abstract







Natural Herbal Supplement: Hair Million


Hair loss alone does not pose significant health problems. In fact, there are people who opt for baldness as an alternative hair style. However, in general, however, hair loss is not considered desirable.

The most ostensive feature that distinguishes us human from chimps and other primates is the lack of bodily hair. During evolutionary process, we have lost the majority of hair. Hair is no longer a biologically essential part of our body, just like appendix. The hair we still have on our scalp and a few other bodily parts is still regarded as significant for reasons other than biological necessity. Hair loss is naturally accompanied by aging process, although the extent of hair loss and the timing of onset vary widely among individuals. Thus, loss of hair and baldness is considered as a symbol of maturity or old age. Like winkles and other signs of aging, hair loss is not welcome by most people, because we don't welcome aging, and being perceived as an aging person. However, it is alopecia, or premature hair loss that especially concerns certain people.

While the hair loss and resulting baldness in general have not been proven to be related to underlying health problems, there are certain correlations between hair loss and health problems. For instance, premature hair loss could suggest premature aging or nutritional and hormonal imbalance, stressful life, use of drugs that cause hair loss as a side effect, skin disease, or heart disease. The balding appearance could also impart a subdued impression of integrity in bodily health and youthfulness.












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