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The effect of dolichol C(95) on the structure and thermotropic phase behaviour of dipalmitoylphosphatidylcholine, dipalmitoylphosphatidylethanolamine and stearoyloleoylphosphatidylethanolamine has been examined by synchrotron X-ray diffraction and differential scanning calorimetry. The presence of dolichol C(95) had no detectable effects on the temperature of either the gel to ripple or the ripple to liquid-crystal phase transition of dipalmitoylphosphatidylcholine. A proportionate increase of a few degrees in the temperature of the gel to lamellar liquid-crystal phase transition is observed in dispersions of dipalmitoylphosphatidylethanolamine and significantly there is a decrease in the temperature of the lamellar to non-lamellar phase transition of stearoyloleoylphosphatidylethanolamine. There was no significant change in the bilayer repeat spacing of all three mixed dispersions in gel phase in the presence of up to 20 mol% dolichol C(95). Electron density calculations showed that there was no change of bilayer thickness of dipalmitoylphosphatidylcholine with incorporation of up to 7.5 mol% dolichol C(95). These data suggest that effect of dolichol on the phospholipid model membranes depend on both the head group and the hydrocarbon chains of the phospholipid molecules. The presence of dolichol in phosphatidylcholine bilayers conforms to a model in which the polyisoprene compound is phase separated into a central domain sandwiched between the two monolayers in gel phase. In bilayers of phosphatidylethanolamines dolichol tends to stabilize the bilayers in gel phase at low temperatures and destabilize the bilayers in lamellar disordered structure at high temperatures. Non-lamellar structures coexist with lamellar disordered phase over a wide temperature range suggesting that dolichol is enriched in domains of non-lamellar structure and depleted from lamellar phase. These findings are useful to understand the function of dolichol in cell membranes.

Thyroid produce two important hormone of thyroxine or tetraidothyronine (T4) and triidothyronine (T3), which are involved in whole aspect of metabolism. T4 and T3 play vital role in all biochemical function, growth and development in human body. The basic metabolic pathways in kidney and every organ in human controlled by these hormones. T4 and T3 are involved in kidney function in health and diseases condition therefore the pathophysiology of kidney can be directly influenced and regulated by thyroid hormones. Kidney growth, haemodynamic, blood circulation, tubular, electrolyte balance and glomerular filtration rate (GFR) are among such crucial process. Hypothyroidism which accompanied with reduced thyroid hormone production adversely affect the renal functions, development and eventually leading to reduced weight, kidney vascular disorders, electrolyte, tubular transport imbalances, lower filtration rate and other adverse consequences of hypothyroidism. On other hand kidney diseases can also disrupt the thyroid function metabolism resulting in the subsequent hypothyroidism. It is an interesting subject in how thyroid and kidney in health and diseases closely interacted. For the ideal clinical follow up of either of thyroid and renal diseases the two organs should be simultaneously examined for a proper patient management. Close correlation of thyroid and kidney clinical teams are essential to check the cross reactions and adverse interactions which might be produced between these two vital organs to avoid misdiagnosis either of thyroid or kidney abnormalities.

Iodine is in the crucial parts of two hormones of T4 and T3 produced by the thyroid glands which are essential for all the aspects of human metabolisms. It is demonstrated that iodine deficiency can be considered as sole cause of many thyroid abnormalities including mental disorders. Iodine deficiency of sufficient degree to cause hypothyroidism during fetus life and early infancy will be accompanied with brain abnormality possibly to the stage of mental retardation. The iodine deficiency among subjects in their early stage of childhood is not as severe as those in their fetus or infancy. In adult subjects the sever iodine deficiency can be also associated with mental disorders due to the direct side effects of hypothyroidism occurred by lack of iodine. The clinical manifestation of iodine deficiency show itself with psychological disorders in adult subjects. The status of iodine within blood can be evaluated through measurement of urinary iodine level and the low urinary concentration is an indicative of hypothyroidism. Mental retardation and brain damage due to iodine deficiency can be prevented if iodine supplementation prescribed duly on time.