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Prostaglandins and Arachidonate Metabolites, Volume 86 (Hardcover): Nathan P. Kaplan, Nathan P. Colowick Prostaglandins and Arachidonate Metabolites, Volume 86 (Hardcover)
Nathan P. Kaplan, Nathan P. Colowick; Volume editing by William E. M. Lands, William K. Smith
R1,732 Discovery Miles 17 320 Ships in 12 - 17 working days

The critically acclaimed laboratory standard, Methods in Enzymology, is one of the most highly respected publications in the field of biochemistry. Since 1955, each volume has been eagerly awaited, frequently consulted, and praised by researchers and reviewers alike. The series contains much material still relevant today - truly an essential publication for researchers in all fields of life sciences.

Biochemistry of Arachidonic Acid Metabolism (Hardcover, 1985 ed.): William E. M. Lands Biochemistry of Arachidonic Acid Metabolism (Hardcover, 1985 ed.)
William E. M. Lands
R5,698 Discovery Miles 56 980 Ships in 10 - 15 working days

Prostaglandins, Leukotrienes, and Cancer is a multi-volume series that will focus on an emerging area of cancer research. In 1968, R.H. Williams first reported that elevated prostaglandin levels are present in human medullary car- cinoma. Since that time, the concept that arachidonic acid metabolites may be in- volved in cancer has expanded to include every aspect of the disease from cell transformation through metastasis. Prostaglandins and leukotrienes are generic terms used to describe a family of bioactive lipids produced from unsaturated fatty acids (principally from arachidonic acid) via the cyclooxygenase and lipoxygenase pathways, respec- tively. Cyclooxygenase products consist of diverse products such as prosta- glandin E, (POE,), prostacyclin (POI2) and thromboxane A2 (TXA2), whereas lipoxygenase products consist of hydroperoxy fatty acids and mono-, di- and tri-hydroxy acids including leukotrienes. The precursor fatty acids for the cyclooxygenase and lip oxygenase pathways are present in cellular phospholipids. This finding established an important control point in their biosynthesis-the release of substrate. This occurs in response to numerous stimuli that act at the cell surface. Dr. Bengt Samuelsson's extensive study of the metabolism of pros- taglandins indicated that they are rapidly inactivated on a single pass through pulmonary circulation. Thus, they cannot act as circulating hormones and appear to be made on demand in or in the vicinity of target tissues leading to the concept that prostaglandins are local hormones or autocoids.

Biochemistry of Arachidonic Acid Metabolism (Paperback, Softcover reprint of the original 1st ed. 1985): William E. M. Lands Biochemistry of Arachidonic Acid Metabolism (Paperback, Softcover reprint of the original 1st ed. 1985)
William E. M. Lands
R5,478 Discovery Miles 54 780 Ships in 10 - 15 working days

Prostaglandins, Leukotrienes, and Cancer is a multi-volume series that will focus on an emerging area of cancer research. In 1968, R.H. Williams first reported that elevated prostaglandin levels are present in human medullary car- cinoma. Since that time, the concept that arachidonic acid metabolites may be in- volved in cancer has expanded to include every aspect of the disease from cell transformation through metastasis. Prostaglandins and leukotrienes are generic terms used to describe a family of bioactive lipids produced from unsaturated fatty acids (principally from arachidonic acid) via the cyclooxygenase and lipoxygenase pathways, respec- tively. Cyclooxygenase products consist of diverse products such as prosta- glandin E, (POE,), prostacyclin (POI2) and thromboxane A2 (TXA2), whereas lipoxygenase products consist of hydroperoxy fatty acids and mono-, di- and tri-hydroxy acids including leukotrienes. The precursor fatty acids for the cyclooxygenase and lip oxygenase pathways are present in cellular phospholipids. This finding established an important control point in their biosynthesis-the release of substrate. This occurs in response to numerous stimuli that act at the cell surface. Dr. Bengt Samuelsson's extensive study of the metabolism of pros- taglandins indicated that they are rapidly inactivated on a single pass through pulmonary circulation. Thus, they cannot act as circulating hormones and appear to be made on demand in or in the vicinity of target tissues leading to the concept that prostaglandins are local hormones or autocoids.

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