Heat capacity of metallic uranium and thorium from 80 to 1000 k

The heat capacities of metallic uranium and thorium from 80 to 1000 K have been determined by laser-flash calorimetry. The results on uranium agree very well with those in the literature over the temperature range investigated. The results on thorium are several percent lower than the heat-capacity values hitherto reported, while the enthalpy data at high temperatures in the literature are in good agreement with the present results. Shomate's analysis showed that the present results are the most consistent through the temperature range from 80 to 1000 K. On this, a revised table of thermodynamic functions of thorium from 80 to 1000 K is presented. The excess heat capacity on thorium has been found to be not appreciable up to 1000 K, in contrast with the large excess heat capacity above 300 K for uranium.     

Flow profile and void fraction of granular solids in a moving bed

In the system consisting of spheres of uniform size flowing downwards with a constant head through a vertical tube, the flow pattern and the void fraction of the descending particles were measured. The particles showed both a constant-velocity region in the central core of the bed and a shear region in the outer section of the core. On the basis of plasticity theory, the boundary surface between those two regions was approximately predicted with the aid of some assumptions. Concerning the void fraction of flowing solids, some interesting results were obtained and they were discussed by considering the “vibratory effect” that results from the random motion of individual particles in the shear region.     

Complicated ulcer; prevention and therapy of upper gastrointestinal bleeding; indications for antacid therapy

Antacids reduce gastric acidity by neutralization, diminish peptic activity by increasing luminal pH above that optimal for proteolysis and provide thereby the rational for their use in ulcer disease. In clinical trials antacids fastened ulcer healing in patients with duodenal ulcer but not with gastric ulcer when compared to placebo. Furthermore, the prophylactic use of antacid medication can significantly reduce the frequency of acute bleeding when gastric content is titrated to a pH greater 3.5 on an hourly basis. Cimetidine does not adequately protect seriously ill patients from acute upper gastrointestinal tract bleeding. Antacids are better for this purpose. So far the efficacy of an antacid therapy has not been proven in controlled trials in patients with chronic ulcer disease, in patients with recurring ulcers following gastric surgery and in patients bleeding from acute or chronic gastroduodenal lesions.     

Studies on the post-mortem fragmentation of myofibrils

1. There was a close relationship between the fragmentation of myofibrils and the tension developed during post-mortem contraction of muscle. The extent of fragmentation was at its maximum when the sarcomeres attained a length of 2.0 to 2.2 micron. 2. The rate of fragmentation of myofibrils depended upon the calcium ion concentration within a range of 10(-5) to 2 x 10(-2) M, with a minimum at pH 6.5. The fragmentation of myofibrils free from muscle fibers was not affected by 10 mM iodoacetate, an irreversible inhibitor of calcium-activated factor (CAF). 3. Incubation of myofibrils with 10 mM CaCl2 caused the release of about 12% of the total myofibrillar proteins after homogenization. The protein solution contained little alpha-actinin, and considerable amounts of 54,000- and 76,000-dalton components which seem to originate from the Z-line. SDS-polyacrylamide gels of troponin prepared from the incubated myofibrils did not change with time of incubation. These findings are in contrast with the proteolytic degradation of Z-lines by CAF treatment, in which alpha-actinin and 87,000 dalton component are released. 4. These data directly demonstrate that the in vitro fragmentation of post-mortem muscle (i.e. duirng its conversion into myofibrils upon mechanical homogenization) is different from that induced by CAF. The possible role of calcium ions during in vitro fragmentation of myofibrils is discussed.