Among theunlimited possible questions, the question "What is a dictionary? Dictionaries are didactic books used as consultation instruments for self-teaching. They are composed by an ordered set of linguistic units which reflects a doublestructure, the macrostructure which corresponds to the word list and the microstructurethat refers to the contents of each lemma.
The great value of dictionaries nests in thefact that they establish a standard nomenclature and prevent in that way the appearanceof new useless synonyms. Nevertheless we would all curiously ask how does one goabout standarizing nomenclature. It is one of the greatest mistakes to think that the creation of a dictionary starts bysimply deciding a group of entries and filling in equivalents in a target language.
If alexicographer will do that it would be as if he was trying to cook by firstly mixinganything found around without having decided yet if he would like to make a cake orspaghetti. The presently presented dictionary is designed to represent the medical andbiological portion of the lexis of the English, Greek, Italian and German languages andis currently being further developed with the addition of the French and Spanishequivalent lexis that will enrich its next edition.
The incorporation of all the previouslymentioned linguistic systems in a single title was decided in order to fill the great gapthat existed for so long mainly between Greek, Italian, German, French, and Spanishlanguages in the field of specialized dictionaries of life sciences. Also it was decidedthat it should be a multi-directional active dictionary and for that reason speciallanguage indexes were created in order to facilitate encoding in all available targetlanguages.
The dictionary contains a total of about The basic criteria used to accept a word aspart of the dictionary during the development period in order of importance were usage,up-to-dateness, specificity, simplicity and conceptual relationships. The dictionary meets the standards of higher education and covers all main fieldsof life sciences by setting its primary focus on the vastly developing fields of cellbiology, biochemistry, molecular biology, immunology, developmental biology,microbiology, genetics and also the fields of human anatomy, histology, pathology,physiology, zoology, and botany.
The fields of ecology, paleontology, systematics,evolution, biostatistics, plant physiology, plant anatomy, plant histology, biometry andlab techniques have been sufficiently covered but in a more general manner. The latestLatin international anatomical terminology "Terminologia Anatomica" or "TA" has beenfully incorporated and all anatomical entries have been given their international LatinTA synonym. The dictionary tends to be synchronic by ignoring obsolete and archaic words and incorporating the American spelling.
Grammatical information was decidedas standard for all languages since it is extremely essential when encoding in a targetlanguage but it was also taken into consideration that the reader should in no waywonder if he was looking at a dictionary or at a grammar. Finally it is with great pleasure to acknowledge the exceptional and invaluablecooperation of Ms.
Tsiantoula, Ms. Terstall and Ms. Versteeg and the rest of Elsevier'sstaff for their excellent work while developing and finally publishing this book, whichwe all hope will be a valuable and helpful tool for all scientists, teachers, students andgenerally all those that work within the fields of life sciences. Giannis Konstantinidis Looking out the window you see a child walking along the street Whole body metabolism during sleep Contrasting physiological purposes of sleep and wakefulness are mirrored in substrate utilization and energy expenditure differences.
For example, plasma glucose levels strongly follow the circadian pattern and progressively increase during sleep with the highest levels in the early morning [ 21 - 23 ]. Diurnal variations in glucose metabolism are mediated primarily through direct autonomic innervation of target organs from the SCN [ 21 ] and are independent of circulating insulin or glucagon levels [ 24 , 25 ].
In fact, SCN-driven autonomic output has been shown to regulate hepatic glucose output [ 21 , 26 , 27 ] and is most likely also involved in the reduction of skeletal muscle blood flow and decreased muscle glucose uptake during sleep [ 26 - 28 ]. Additionally, decreased neuron activity during slow-wave sleep contributes to decreased glucose utilization by the brain during sleep [ 30 ].
Plasma triglycerides and fatty acids demonstrate strong circadian oscillations with progressively decreasing levels during sleep [ 31 ] when lipoprotein lipase LPL activity and fatty acid synthesis in adipose tissue are at their highest [ 28 , 32 , 33 ]. Some authors have reported a slight increase in plasma free fatty acids FFA and glycerol in the late stages of sleep, which has been attributed to central pacemaker activity as well as to the adipose tissue lipolysis promoting effects of growth hormone [ 28 , 34 , 35 ].
Metabolic abnormalities in sleep disorders Inadequate sleep duration together with misaligned or irregular sleep e. More recently, epidemiological and experimental studies have demonstrated that sleep quality and quantity are important determinants of whole-body metabolism. It has been suggested that impaired sleep might causally contribute to the T2DM and obesity epidemic via mechanisms depicted in Figure 1 and described further below.
Figure 1 Metabolic pathways linking sleep disorders with the development of Type 2 diabetes. Short sleep duration Models The detrimental impact of short sleep duration on human health has been demonstrated in multiple studies including: a cross-sectional studies, b longitudinal epidemiological studies and c experimental studies using variable severity and duration of sleep deprivation in human volunteers.
Evidence Large-scale cross-sectional epidemiological studies conducted in various populations including adolescents, middle-aged and elderly subjects, hypertensive patients and pregnant women have convincingly and repeatedly demonstrated that self-reported sleep duration is associated with approximately doubled prevalence of T2DM or impaired glucose tolerance, particularly in women [ 36 - 47 ].
Importantly, cross-sectional associations between T2DM and short sleep are independent of other traditional risk factors for diabetes. Furthermore, subjectively perceived insufficient, poor or short sleep is associated with several pre-diabetic features such as fasting hyperglycemia, elevated postprandial glucose and insulin levels or indices of whole-body insulin resistance [ 39 , 46 , 48 - 56 ]. Finally, inadequate sleep has also been shown to be detrimental in patients who have already developed diabetes, since it negatively impacts glycemic control [ 45 , 47 ].
Interpretation of cross-sectional studies is inherently limited due to the uncertainty of causality and its eventual direction. In fact, several reports suggest that hyperglycemia, hyperinsulinemia and endocrine changes associated with T2DM can significantly influence sleep quality and quantity [ 57 - 59 ]. To better understand possible impact of sleep duration on metabolic homeostasis, observations based on prospective studies have proven to be very informative.
In these studies, subjects with variable sleep habits and sleep duration, but free of diabetes, were followed for an extended period of time while newly diagnosed cases of T2DM were recorded. Results of these studies, which followed from to 70, adults over 4 to 32 years [ 60 - 71 ] plus meta-analyses [ 2 , 72 ] fully support the relationship suggested in cross-sectional studies.
As a consequence of insulin resistance combined with defects in insulin secretion, fasting and postprandial glucose levels were increased following sleep deprivation [ 75 - 79 ]. Despite the heterogeneity of study designs, partially sleep-deprived subjects also exhibited impairments in numerous parameters of glucose tolerance and insulin sensitivity [ 80 - 87 ].
Mechanisms Endocrine Despite the clear association between short sleep and metabolic impairments, the underlying endocrine and molecular mechanisms remain only partially elucidated. Among the suggested mechanisms, the causal role of the hypothalamo-pituitary-adrenal HPA axis and sympathetic activation are supported by the largest body of literature.
Circulating cortisol, assessed either by 24 h profiles or by single measurements of evening cortisol levels, were elevated together with markers of sympathetic activation [ 81 ] and circulating catecholamines [ 86 ] after total or partial sleep deprivation [ 79 - 81 , 83 , 89 , 90 ] as well as in short sleepers [ 91 ].
In contrast, some studies reported impairments in glucose homeostasis in sleep restricted individuals along with unchanged cortisol and catecholamine levels [ 82 - 84 , 88 ]. The complexity of associated endocrine mechanisms can be further demonstrated by observations of elevated levels of pro-inflammatory cytokines, lower circulating testosterone, decreased thyroid stimulating hormone levels, impaired pulsatility of growth hormone secretion [ 81 , 92 , 93 ] and changes in adipokines secreted from adipose tissue [ 94 - 96 ] in short sleepers [ 97 - ] as well as after sleep deprivation [ - ] also reviewed in [ ].
Appetite regulation Prospective and cross-sectional studies have also identified short sleep duration as an independent risk factor for weight gain and abdominal fat accumulation as reviewed in [ , ]. It is therefore reasonable to suggest that insufficient sleep stimulates food intake [ ] and contributes to the development of obesity and metabolic syndrome. Furthermore, short sleep duration decreased the amount of fat overweight subjects lost during caloric restriction [ ].
Within the complex network of factors regulating food intake [ ], increased drive to eat in subjects exposed to sleep deprivation [ 81 , , , - ] or in patients with short sleep duration [ 39 , ] has been linked to decreased leptin limits food intake, secreted from adipose tissue and elevated ghrelin increases food intake, secreted mainly from the stomach plasma levels.
However, opposite or conflicting results have also been published [ 79 , 85 , 90 , , , , , ] pointing to the role of other factors, e. In summary, it is safe to conclude that development of obesity, due to neuroendocrine changes, induced by inadequate sleep represents an additional independent risk factor for the development of metabolic abnormalities. Circadian misalignment and shift working Peripheral tissue pacemakers Non-traditional work schedules including shift and night work together with travel across time zones represent typical examples of circadian disruption.
Furthermore, cells of peripheral organs involved in metabolic control including the liver, adipose tissue and muscle express a functional network of pacemaker genes and exhibit circadian cycling in expression of these genes, similar to the autonomous circadian rhythmicity observed in the SCN. As a result, expression of hundreds of tissue-specific genes undergo circadian variation in peripheral tissues [ - ]. At the transcriptional level, entrainment of metabolic function in peripheral tissues could be mediated by glucocorticoids.
Plasma levels of cortisol or corticosterone in mice exhibit a rigid circadian variability persisting even under conditions of experimental forced desynchronization [ 22 ]. Glucocorticoid synthesis and release is controlled by a peripheral clock-oscillator [ ] entrained to the SCN via direct sympathetic innervation of the adrenals [ - ].
The resulting circadian oscillations in plasma glucocorticoid levels induce oscillations in gene expression in target tissues e. The unique feature of peripheral oscillators is that they can be entrained by external cues.
For example, nutrition has been identified as a potent zeitgeber for peripheral pacemakers even when clock genes were deleted or the SCN damaged [ , ]. Similarly, physical activity and exercise have been shown to entrain peripheral oscillators especially in skeletal muscle [ ]. Together with the transcriptional regulation of genes participating in peripheral pacemaker activity, metabolism in peripheral tissues can be synchronized with SCN via endocrine mechanisms.
For example, metabolic responses to oscillations in plasma levels of melatonin a hormone released from the pineal gland under direct SCN control were documented in fat [ ], muscle [ - ], the liver [ , ] and the pancreas [ ]. Studies revealed that melatonin or melatonin receptor agonist administration improved glucose homeostasis through various mechanisms including enhanced glucose uptake, increased glucose-induced insulin secretion, improved insulin sensitivity or decreased liver gluconeogenesis in various animal models [ , , , , - ].
Melatonin or melatonin receptor agonists also increased glycogen synthesis in hepatocytes [ ], limited fat accumulation in adipocytes [ ] and even decreased adiposity in humans [ ] and rats [ ]. Additionally, growth hormone [ ], thyroid stimulating hormone [ ] and direct sympathetic innervation of peripheral tissues [ ] also exhibits strong circadian rhythmicity and contributes to entrainment of peripheral pacemakers to the SCN and the metabolic needs of the whole organism.
Complete re-setting of the central biological pacemaker to a night shift work is extremely rare in humans, especially under rotating shift schedules [ - ].
FOREX DOJI CANDLESTICK
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