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Background-Thailand has a substantial variety of vegetables, including aquicolous, terricolous and edible algae. However, there has been no data available on polyunsaturated fatty acid content in Thai common vegetables. Objective- The aim of the present study was to investigate the content of lipid and fatty acid in Thai common vegetables. Designs- Total lipid content and polyunsaturated fatty acid PUFA ; composition and concentration in 17 Thai common vegetables including six species of aquicolous, two algae and nine terricolous were analyzed. The lipids were extracted by methanol chloroform 2 1, v v ; containing 10mg L of butylatedhydroxytoluene BHT ; and 0.1 mg mL of tricosanoic acid 23: 0 ; as internal standard. Fatty acid was analyzed by using gas chromatographic, and identified by comparison the standard mixtures. Outcomes- The total PUFA was abundant found in the samples, ranged from 38.5% in Wan to 67.7% in Khrached. Kwinin had the highest total PUFA concentration of 612.6mg 100g, and Tao num had the lowest of 8.5mg 100g. Palmitic acid, linoleic acid and linolenic acid 18: 3n-3 ; were the main fatty acids, with the composition ranged from 12.7% in Krached to 29.3% in Koon, 5% in Koon to 52.3% in Krached, 12.6% in Tao num to 45% in Bon, respectively. 20: 5n-3 was present in only three vergetables, Sao Bao 5.0mg 100g ; , Bung Jeen 6.3mg 100g ; , and Pum 31.3mg 100g ; . The ranges of n-6 n-3 ratio in algae, aquicolous and terricolous samples were 0.6-0.8, 0.3-6.3, 0.8-2.0, respectively. Conclusions-The present results showed that Thai common vegetables are potential sources of PUFA, vegetables supplementation may contribute to human health.

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1 Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD. 2 Division of Forensic Toxicology, Office of the Armed Forces Medical Examiner, Rockville, MD. * Address correspondence to this author at: Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, 5500 Nathan Shock Drive, Baltimore, MD 21224. Fax 410-550-2468; e-mail mhuestis intra.nida.nih.gov. Received June 30, 2005; accepted September 23, 2005. Previously published online at DOI: 10.1373 clinchem.2005.056838.

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5. Saada V, Janssen F, Vignon-Pennamen MD, Flageul B, Cottenot F. Association pemphigoide bulleuse-sclerose en plaques. Ann Dermatol Venereol. 1990; 117: 459-461. Machet L, Vaillant L, de Muret A, Clavere A, Lorette G. Pemphigoide bulleuse et sclerose en plaques [letter]. Ann Dermatol Venereol. 1991; 118: 47. Doutre MS, Beylot C, Delage F, Hans P. Pemphigoide bulleuse et sclerose en plaques [letter]. Ann Dermatol Venereol. 1991; 118: 49. Tomasini D, Bonfacini V. Pemphigoide bulleuse et sclerose en plaques [letter]. Ann Dermatol Venereol. 1991; 118: 474. Martin-Ortega E, Puig S, Vicente A, Herrero C, Mascaro JM. Pemphigoide bul leuse et sclerose en plaques [letter]. Ann Dermatol Venereol. 1991; 118: 475. Tohme A, Mattar L, Zebouni A, Koussa S. Pemphigoide bulleuse et sclerose en plaques. Ann Dermatol Venereol. 1994; 121: 139-142. Kirtschig G, Walkden VM, Venning VA, Wojnarowska F. Bullous pemphigoid and multiple sclerosis: a report of three cases and review of the literature. Clin Exp Dermatol. 1995; 20: 449-453. Chou SM, Wang HS, Taniguchi A, Bucala R. Advanced glycation endproducts in neurofilament conglomeration of motoneurons in familial and sporadic amyotrophic lateral sclerosis. Mol Med. 1998; 4: 324-332. Joly P, Gilbert D, Thomine E, et al. Relationship between the in vivo localization and the immunoblotting pattern of antibasement membrane zone antibodies in patients with bullous pemphigoid. Arch Dermatol. 1997; 133: 719-724. Lacomblez L, Bensimon G, Leigh PN, Guillet PH, Meninger V. Dose-ranging study of riluzole in amyotrophic lateral sclerosis. Lancet. 1996; 347: 1425-1431. Stanley JR. Bullous pemphigoid. In: Freedberg IM, Eisen AZ, Wolff K, et al, eds. Dermatology in General Medicine. New York, NY: McGraw-Hill Book Co; 1999: 666-673. 16. Descamps V, Flageul B, Vignon-Pennamen MD, et al. Dyshidrosiform pemphigoid: a report of 3 cases. J Acad Dermatol. 1992; 26: 651-652. Bernard P, Vaillant L, Labeille B, et al. Incidence and distribution of subepidermal autoimmune bullous skin diseases in three French regions. Arch Dermatol. 1995; 131: 48-52. Long CC, Lever LR, Marks R. Unilateral bullous pemphigoid in a hemiplegic patient. Br J Dermatol. 1992; 126: 614-616. Bunker CB, Brown E. Unilateral bullous pemphigoid in a hemiplegic patient [letter]. Br J Dermatol. 1993; 129: 502. Okazaki A, Iida T, Muramatsu T, Shirai T, Murata K, Takayanagi T. Bullous pemphigoid associated with Shy-Drager syndrome. J Dermatol. 1998; 25: 465468. Bastuji-Garin S, Joly P, Picard-Dahan C, et al. Drugs associated with bullous pemphigoid. A case-control study. Arch Dermatol. 1996; 132: 272-276. Kolde G, Bachus R, Ludolph AC. Skin involvement in amyotrophic lateral sclerosis. Lancet. 1996; 347: 1226-1227. Ono S, Imai T, Takahashi K, et al. Decreased type IV collagen of skin and serum in patients with amyotrophic lateral sclerosis. Neurology. 1998; 51: 114-120. Guo L, Degenstein L, Dowling J, et al. Gene targeting of BPAG1: abnormalities in mechanical strength and cell migration in stratified epithelia and neurologic degeneration. Cell. 1995; 81: 233-243. Cleveland DW, Bruijn LI, Wong PC, et al. Mechanisms of selective motor neuron death in transgenic mouse models of motor neuron disease. Neurology. 1996; 47 suppl 2 ; : S54-62. 26. Eyer J, Cleveland DW, Wong PC, Peterson AC. Pathogenesis of two axonopathies does not require axonal neurofilaments. Nature. 1998; 391: 584-587. Figlewicz DA, Krizus A, Martinoli MG, et al. Variants of the heavy neurofilament subunit are associated with the development of amyotrophic lateral sclerosis. Hum Mol Genet. 1994; 3: 1757-1761. Our department was established in April, 2001 to support the translational researches of our hospital. Ongoing projects which we are participating in are immunogene therapy of neuroblastoma and immune therapy for thyroid cancer utilizing dendritic cells immunized with tumor antigens. We are also conducting researches to find responsible SNPs in genes related to drug sensitivity, disease progression, and prognosis in various hematological disorders. In December, 2002 we opened a clinic of genetic counseling in collaboration with the divisions of pediatrics, genetic diagnosis, nursing and so on and ofloxacin and myambutol, because drug information.
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The NFA-DNA system at 272 nm decreases strongly. As the inference of DNA is eliminated by the reference solution, the decrease of the peak is not simple addition. Effect of pH The effect of pH on the NFA-DNA system in aqueous solution was investigated figure 4 ; . As shown in Figure 1, the structure of the NFA molecule contains carbonyl, amino and carboxyl groups. The protonation of the nitrogen atom and oxygen atom in different pH solutions will influence the electronic cloud distribution of system directly, which will then affect the chelate formation ability of NFA. When the pH is in the range of 2-4, the form of quinline occupies a maximal proportion 19 ; , so there is the most strong intensity of fluorescence. When the pH is below 3, some of the double-strand DNA turns to singlestrand DNA. As a result, the optimum pH for the NFADNA system is 4. From controlling the concentration of NFA and DNA, it can be concluded that 1 mL Tris-HCl is the most suitable amount. Effect of ionic strength The effect of controlling the ionic strength using 0.1 molL-1 NaCl solutions is shown in Figure 5. With increasing concentration of NaCl, the fluorescence intensity of the NFA-DNA system increases first and then decreases. There is the same rule for NFA. As the NFA can chelate metal, the ionic strength has a great effect on the system.
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