Heat storage in alloy transformations

The feasibility of using metal alloys as thermal energy storage media was determined. The following major elements were studied: (1) identification of congruently transforming alloys and thermochemical property measurements; (2) development of a precise and convenient method for measuring volume change during phase transformation and thermal expansion coefficients; (3) development of a numerical modeling routine for calculating heat flow in cylindrical heat exchangers containing phase change materials; and (4) identification of materials that could be used to contain the metal alloys. Several eutectic alloys and ternary intermetallic phases were determined. A method employing X-ray absorption techniques was developed to determine the coefficients of thermal expansion of both the solid and liquid phases and the volume change during phase transformation from data obtained during one continuous experimental test. The method and apparatus are discussed and the experimental results are presented. The development of the numerical modeling method is presented and results are discussed for both salt and metal alloy phase change media

The distinctive structure and composition of arterial and venous thrombi and pulmonary emboli

© 2020, The Author(s). Although arterial and venous thromboembolic disorders are among the most frequent causes of mortality and morbidity, there has been little description of how the composition of thrombi and emboli depends on their vascular origin and age. We quantified the structure and composition of arterial and venous thrombi and pulmonary emboli using high-resolution scanning electron microscopy. Arterial thrombi contained a surprisingly large amount of fibrin, in addition to platelets. The composition of pulmonary emboli mirrored the most distal part of venous thrombi from which they originated, which differed from the structure of the body and head of the same thrombi. All thrombi and emboli contained few biconcave red blood cells but many polyhedrocytes or related forms of compressed red blood cells, demonstrating that these structures are a signature of clot contraction in vivo. Polyhedrocytes and intermediate forms comprised the major constituents of venous thrombi and pulmonary emboli. The structures within all of the thrombi and emboli were very tightly packed, in contrast to clots formed in vitro. There are distinctive, reproducible differences among arterial and venous thrombi and emboli related to their origin, destination and duration, which may have clinical implications for the understanding and treatment of thrombotic disorders

Psychiatric rehabilitation

Psychiatric rehabilitation is an important component in the management of the mentally ill. This article presents a selective review of the publications in this journal. Questions addressed in this review range from assessment of rehabilitation needs to different rehabilitative approaches. Although the number of publications providing the answers is meager, there are innovative initiatives. There is a need for mental health professionals to publish the models they follow across the country

Neutrophil a-defensins promote thrombosis in vivo by altering fibrin formation, structure, and stability

© 2019 by The American Society of Hematology. Inflammation and thrombosis are integrated, mutually reinforcing processes, but the interregulatory mechanisms are incompletely defined. Here, we examined the contribution of a-defensins (a-defs), antimicrobial proteins released from activated human neutrophils, on clot formation in vitro and in vivo. Activation of the intrinsic pathway of coagulation stimulates release of a-defs from neutrophils. a-Defs accelerate fibrin polymerization, increase fiber density and branching, incorporate into nascent fibrin clots, and impede fibrinolysis in vitro. Transgenic mice (Def 11 ) expressing human a-Def-1 developed larger, occlusive, neutrophil-rich clots after partial inferior vena cava (IVC) ligation than those that formed in wild-type (WT) mice. IVC thrombi extracted from Def 11 mice were composed of a fibrin meshwork that was denser and contained a higher proportion of tightly packed compressed polyhedral erythrocytes than those that developed in WT mice. Def 11 mice were resistant to thromboprophylaxis with heparin. Inhibiting activation of the intrinsic pathway of coagulation, bone marrow transplantation from WT mice or provision of colchicine to Def 11 mice to inhibit neutrophil degranulation decreased plasma levels of a-defs, caused a phenotypic reversion characterized by smaller thrombi comparable to those formed in WT mice, and restored responsiveness to heparin. These data identify a-defs as a potentially important and tractable link between innate immunity and thrombosis

Neutrophil a-defensins promote thrombosis in vivo by altering fibrin formation, structure, and stability

© 2019 by The American Society of Hematology. Inflammation and thrombosis are integrated, mutually reinforcing processes, but the interregulatory mechanisms are incompletely defined. Here, we examined the contribution of a-defensins (a-defs), antimicrobial proteins released from activated human neutrophils, on clot formation in vitro and in vivo. Activation of the intrinsic pathway of coagulation stimulates release of a-defs from neutrophils. a-Defs accelerate fibrin polymerization, increase fiber density and branching, incorporate into nascent fibrin clots, and impede fibrinolysis in vitro. Transgenic mice (Def 11 ) expressing human a-Def-1 developed larger, occlusive, neutrophil-rich clots after partial inferior vena cava (IVC) ligation than those that formed in wild-type (WT) mice. IVC thrombi extracted from Def 11 mice were composed of a fibrin meshwork that was denser and contained a higher proportion of tightly packed compressed polyhedral erythrocytes than those that developed in WT mice. Def 11 mice were resistant to thromboprophylaxis with heparin. Inhibiting activation of the intrinsic pathway of coagulation, bone marrow transplantation from WT mice or provision of colchicine to Def 11 mice to inhibit neutrophil degranulation decreased plasma levels of a-defs, caused a phenotypic reversion characterized by smaller thrombi comparable to those formed in WT mice, and restored responsiveness to heparin. These data identify a-defs as a potentially important and tractable link between innate immunity and thrombosis