Endocrine diseases are disorders of the endocrine system. The branch of medicine associated with endocrine disorders is known as endocrinology. Endocrine disorders can usually be divided into three categories: endocrine gland hyposecretion (leading to hormone deficiency), endocrine gland hypersecretion (leading to hormone excess) and tumours of endocrine glands. Endocrine disorders involve a mixed picture of hyposecretion and hypersecretion. "Endocrine" serves as an essential start to master the science and art of clinical practice and is going to discuss endocrine diseases.
There are totally 7 chapters in this book. Chapter 1 gives an outline of pancreatic cancer and reviews the biological character and clinical utility of prostate stem cell antigen (PSCA) in the context of pancreatic cancer. It is worth noting that pancreatic cancer is a highly fatal neoplasm and recent studies revealed involvement of PSCA in its carcinogenesis.
Chapter 2 proposes a role for zinc transporters in cell signalling and glycaemic control in disease processes, especially insulin resistance and type 2 diabetes. It reveals an exciting role for these transporters as novel targets with utility for therapeutic intervention in the treatment of these diseases. Chapter 3 reviews the role of psychosocial factors including personality traits as well as stresses on the onset and clinical course of Graves' disease. In addition, this chapter also introduces the relationships between stress and other thyroid diseases including Hashimoto's thyroiditis, Plummer' disease and benign thyroid nodule.
Chapter 4 summarizes the current and future clinical applications of ghrelin, the endogenous ligand of the growth hormone secretagogue-receptor type-1a (GHS-R1a), in various disorders. Major clinical applications of the available pharmacological tools modulating ghrelin action, in relation to their pharmacological targets, are also discussed.
Chapter 5 describes the regulatory mechanisms underlying the expression of the testis-specific gene PDHA2. Moreover, its somatic activation to correct pyruvate dehydrogenase complex deficiency caused by mutations in the paralog PDHA1 is discussed.
Chapter 6 has linked prolactin and PAK1 as the JAK2 substrate to the stimulation of cyclin D1 promoter activity. The authors propose two PAK1-dependent mechanisms to activate cyclin D1 promoter activity: via nuclear translocation of tyrosyl-phosphorylated PAK1 and via formation of a Nck-PAK1 complex that sequesters PAK1 in the cytoplasm.
Chapter 7 discusses the method of choice for adrenalectomy, depending on the size of the adrenal tumor.