The present-day number of tectonic plates

The number of tectonic plates on Earth described in the literature has expanded greatly since the start of the plate tectonic era, when only about a dozen plates were considered in global models of present-day plate motions. With new techniques of more accurate earthquake epicenter locations, modern ways of measuring ocean bathymetry using swath mapping, and the use of space based geodetic techniques, there has been a huge growth in the number of plates thought to exist. The study by Bird (2003) proposed 52 plates, many of which were delineated on the basis of earthquake locations. Because of the pattern of areas of these plates, he suggested that there should be more small plates than he could identify. In this paper, I gather together publications that have proposed a total of 107 new plates, giving 159 plates in all. The largest plate (Pacific) is about 20 % of the Earth's area or 104 Mm (super 2) , and the smallest of which (Plate number 5 from Hammond et al. 2011) is only 273 km (super 2) in area. Sorting the plates by size allows us to investigate how size varies as a function of order. There are several changes of slope in the plots of plate number organized by size against plate size order which are discussed. The sizes of the largest seven plates is constrained by the area of the Earth. A middle set of 73 plates down to an area of 97,563 km (super 2) (the Danakil plate at number 80, is the plate of median size) follows a fairly regular pattern of plate size as a function of plate number. For smaller plates, there is a break in the slope of the plate size/plate number plot and the next 32 plates follow a pattern of plate size proposed by the models of Koehn et al. (2008) down to an area of 11,638 km (super 2) (West Mojave plate # 112). Smaller plates do not follow any regular pattern of area as a function of plate number, probably because we have not sampled enough of these very small plates to reveal any clear pattern. Copyright 2016 The Author(s) and Harrison

Protein and amino acid metabolism in splanchnic organs in metabolic acidosis

Metabolic acidosis causes a cooperative participation of different organs such as the liver, kidney, and muscle in restoring acid-base balance. In splanchnic organs, metabolic acidosis has repercussions on several nitrogen metabolism pathways. The decrease in urea synthesis due to reduced activity of urea cycle enzymes, ammonia uptake and amino acid transport, and changes in glutamine metabolism support renal ammoniagenesis thus offering a response to rid the body of excess protons. While some of the mechanisms are adaptive others may be harmful for the body. Metabolic acidosis may have effects on splanchnic protein turnover. In severe acidosis, synthesis of secreted liver proteins may be reduced. Acidosis may also modulate the response of the liver to growth hormone (GH) for insulin-like growth factor-I synthesis, thus inducing a state of GH resistance. Splanchnic abnormalities in acidosis might contribute to the malnutrition observed in uremi

LEG METABOLISM OF AMINO ACIDS AND AMMONIA IN PATIENTS WITH CHRONIC RENAL FAILURE

1. Leg metabolism of amino acids and ammonia in the postabsorptive state was evaluated in 10 patients with chronic renal failure (CRF) and in 10 patients with normal renal function (controls) by measuring the arterial-femoral venous (A-FV) differences for free amino acids and ammonia. 2. Total amino acid release from the leg and alanine and glutamine release, which accounts for the greatest amount of the total amino acid release, are similar in patients and controls. Total amino acid uptake from the arterial blood and glutamate uptake, which is the amino acid extracted at the highest rate, are comparable in both groups. Taken together these data, in addition to the similarity of A-FV differences for proteolytic markers, namely tyrosine, phenylalanine and histidine, suggest that protein breakdown in peripheral tissues is not increased in patients with CRF. 3. In CRF selective metabolic abnormalities for some amino acids are evident. Whilst only the A-FV differences for valine, leucine and isoleucine are decreased, additional alterations are observed by relating the A-FV difference for each amino acid to that of proteolytic markers. Such a procedure demonstrates that in CRF histidine release relative to that of proteolytic markers is reduced, whereas proline and arginine release is increased. 4. In CRF the reduced release of some amino acids, mainly branched-chain amino acids, by the leg probably affects the pattern of circulating amino acids. 5. Finally, both in patients and in controls a significant uptake of ammonia is observed; the ammonia uptake is related to arterial levels of this metabolite, confirming the role of peripheral tissues in removing ammonia from circulation.</jats:p

Renal metabolism of amino acids in early insulin-dependent diabetes mellitus

Renal metabolism of amino acids (AAs) was evaluated in 5 patients with early IDDM, and in 7 controls (C) in the basal state for 80 minutes after the ingestion of an AA mixture simulating an animal protein meal. Insulin was withdrawn 20 hours before the study. Renal metabolism of AAs was evaluated by the arterial-venous difference technique. In the basal state in IDDM, as in C, the kidney takes up large amounts of a few nonessential AAs (NEAAs): it releases many NEAAs and a few essential AAs (EAAs). After AA ingestion in C, renal extraction of most EAAs, mainly BCAAs, Lys, and Thr, occurs; Pro extraction also increases and a significant uptake of Gly, Glu, Asp, Orn, and Tyr takes place. EAA extraction accounts for 30-40% of total AA uptake. In IDDM, after AA ingestion, a) renal uptake of total AAs is significantly lower, owing mainly to a markedly lower uptake of BCAAs, Lys, and also of Pro, Orn, and Ala; b) renal EAA uptake accounts for less than 20% of total AA extraction. These results indicate that in IDDM postprandial renal N repletion is impaired and unbalanced