15Due to their fundamentally different biology, archaea are consistently overlooked in conventional 16 microbiome surveys. Using amplicon sequencing, we evaluated methodological set-ups to detect 17 archaea in samples from five different body sites: respiratory tract (nose), digestive tract (mouth, 18 appendix, and stool) and skin. With the optimized protocols, the detection of archaeal ribosomal 19 sequence variants (RSVs) was increased from one (found in currently used, so-called "universal" 20 approach) to 81 RSVs in a representative sample set. In order to assess the archaeome diversity, a 21 specific archaea-targeting methodology is required, for which we propose a standard procedure. This 22 methodology might not only prove useful for analyzing the human archaeome in more detail but 23 could also be used for other holobionts' samples. 24 25 26 27

Four patients with severe hyperglycemia and hyperosmolality were studied to quantitate the major mechanisms responsible for the fall in blood glucose concentration. Insulin was not administered to any of these patients during the first 15 h of therapy. In each case, there was a fall in glucose concentration due to dilution; this was quantitated by chloride space analysis and accounted for 24-34% of the fall in concentration. The size of the glucose pool decreased for two reasons. Glucosuria accounted for the majority of the reduction in the size of the glucose pool in the patients with the smallest decrease in extracellular fluid (ECF) volume [and hence the best preserved glomerular filtration rate (GFR)]. In contrast, glucosuria was a less important factor in causing glucose loss in the patients with very low GFR values. The size of the glucose pool also decreased due to glucose metabolism that did not require exogenous insulin. Thus the fall in glucose concentration in the initial therapy in patients with the hyperglycemic hyperosmolar syndrome is multifactorial and is not absolutely dependent on exogenous insulin. Furthermore, the patients grouped in this diagnostic category represent a heterogeneous population with the common features of severe hyperglycemia, hyperosmolality, and a negative or weakly reactive test for serum ketones.

Insulin resistance is the main factor involved in the occurrence of the metabolic syndrome and later development of type2 diabetes. Despite decades of research on hormone's target tissues and the identification of most diverse candidates, the factors responsible for insulin resistance are still largely undefined. There is also a large discrepancy between in vitro and in vivo insulin sensitivity. Finally it is increasingly demonstrated that insulin resistance is found very early in life, long before metabolic syndrome is established. In search for commonalities, this book deals therefore with a new hypothesis considering microcirculation as one prime, possibly causal effector of insulin resistance. To present this novel hypothesis, the specificities of microvascular physiological mechanisms and the limits of interpretations of data according to the measurement techniques used are first thoroughly described. Several chapters deal with experimental and clinical investigations showing the involvement of microcirculation in insulin resistance. This book provides sound support for microcirculation being linked to insulin resistance at least in a bidirectional way. Supportive evidence suggests that microvascular dysfunction may lie upstream of insulin resistance in many of them. While this is still a hypothesis, the authors believe that there is enough data supporting it and hope that this book will stimulate researchers to provide the necessary final proofs.

Thirteen subjects were investigated to compare the effects of pre-event glucose (G) and placebo (P) ingestion on plasma free fatty acid (FFA) concentration during mental work. Subjects performed two trials of a videogame and received money for each point scored. Thirty minutes before commencing each trial, subjects ingested either a solution containing 50 g of G or an identically sweetened and colored placebo. Order of ingestion was partially counterbalanced. Heart rate, the measure of arousal monitored, increased significantly above baseline during each trial, but there was no difference in this rise between trials. The main finding from this experiment was that after ingesting glucose, subjects had a stable blood FFA concentration during the videogame, while after the ingestion of placebo subjects had a significantly higher blood FFA during videogames than they had at baseline. These data suggest that arousal-induced hyperlipidemia can be prevented by pre-event glucose ingestion.