Proof-of-Principle Experiment on the Dynamic Shell Formation for Inertial Confinement Fusion.

In the dynamic-shell (DS) concept [V. N. Goncharov et al., Novel Hot-Spot Ignition Designs for Inertial Confinement Fusion with Liquid-Deuterium-Tritium Spheres, Phys. Rev. Lett. 125, 065001 (2020).PRLTAO0031-900710.1103/PhysRevLett.125.065001] for laser-driven inertial confinement fusion the deuterium-tritium fuel is initially in the form of a homogeneous liquid inside a wetted-foam spherical shell. This fuel is ignited using a conventional implosion, which is preceded by a initial compression of the fuel followed by its expansion and dynamic formation of a high-density fuel shell with a low-density interior. This Letter reports on a scaled-down, proof-of-principle experiment on the OMEGA laser demonstrating, for the first time, the feasibility of DS formation. A shell is formed by convergent shocks launched by laser pulses at the edge of a plasma sphere, with the plasma itself formed as a result of laser-driven compression and relaxation of a surrogate plastic-foam ball target. Three x-ray diagnostics, namely, 1D spatially resolved self-emission streaked imaging, 2D self-emission framed imaging, and backlighting radiography, have shown good agreement with the predicted evolution of the DS and its stability to low Legendre mode perturbations introduced by laser irradiation and target asymmetries.

Thermal decoupling of deuterium and tritium during the inertial confinement fusion shock-convergence phase.

A series of thin glass-shell shock-driven DT gas-filled capsule implosions was conducted at the OMEGA laser facility. These experiments generate conditions relevant to the central plasma during the shock-convergence phase of ablatively driven inertial confinement fusion (ICF) implosions. The spectral temperatures inferred from the DTn and DDn spectra are most consistent with a two-ion-temperature plasma, where the initial apparent temperature ratio, T_{T}/T_{D}, is 1.5. This is an experimental confirmation of the long-standing conjecture that plasma shocks couple energy directly proportional to the species mass in multi-ion plasmas. The apparent temperature ratio trend with equilibration time matches expected thermal equilibration described by hydrodynamic theory. This indicates that deuterium and tritium ions have different energy distributions for the time period surrounding shock convergence in ignition-relevant ICF implosions.

Pathology of aortic valve stenosis and pure aortic regurgitation. A clinical morphologic assessment--Part I.

This two-part article examines the histologic and morphologic basis for stenotic and purely regurgitant aortic valves. Part I discusses stenotic aortic valves and Part II will discuss causes of purely regurgitant aortic valves. In over 95% of stenotic aortic valves, the etiology is one of three types: congenital (primarily bicuspid), degenerative, or rheumatic. Other rare causes of stenotic aortic valves include active infective endocarditis, homozygous type II hyperlipoproteinemia, and systemic lupus erythematosis. The causes of pure aortic regurgitation are multiple but can be separated into diseases affecting the valve (normal aorta) (infective endocarditis, congenital bicuspid, rheumatic, floppy), diseases affecting the walls of aorta (normal valve) (syphilis, Marfan's, dissection), disease affecting both aorta and valve (abnormal aorta, abnormal valve) (ankylosing spondylitis), and diseases affecting neither aorta nor valve (normal aorta, normal valve) (ventricular septal defect, systemic hypertension). Diseases affecting the aortic valve alone are the most common subgroup of conditions producing pure aortic valve regurgitation.

General concepts in the morphologic assessment of operatively excised cardiac valves--Part I.

This two-part article discusses the general morphologic assessment of operatively excised cardiac valves and applies these principles to functional classifications. All cardiac valves are categorized into stenotic and purely regurgitant (no element of stenosis) groups based upon structural features: presence or absence of commissural fusion, calcific deposits, and degree and location of fibrosis. Of 2980 operatively excised cardiac valves reviewed between 1962 and 1992, the most common lesion was aortic stenosis, followed by mitral stenosis and the combination of aortic and mitral stenosis.

General concepts in the morphologic assessment of operatively excised cardiac valves--Part II.

This 2-part article discusses general morphologic assessment of operatively excised cardiac valves and applies these principles to functional classifications. All cardiac valves are categorized into stenotic and purely regurgitant (no element of stenosis) groups based upon structural features: presence or absence of commissural fusion, calcific deposits, and degree and location of fibrosis. Of 2,980 operatively excised cardiac valves reviewed between 1962 and 1992, the most common lesion was aortic stenosis, followed by mitral stenosis and the combination of aortic and mitral stenosis.

Pathology of pulmonic valve stenosis and pure regurgitation.

Little morphologic information is available on operatively excised pulmonic valves. The causes of pulmonic stenosis are limited to a few conditions: (1) rheumatic and (2) nonrheumatic (congenital, carcinoid, infective endocarditis). Congenital causes of pulmonic stenosis constitute well over 95% of these conditions. Congenital types of pulmonic stenosis include acommissural dome-shaped, dysplastic, and bicuspid. Rare acquired causes of pulmonic stenosis include carcinoid, rheumatic, and infective endocarditis. Of the acquired causes of pulmonic stenosis, carcinoid is the most common condition. In contrast, causes of pure pulmonic regurgitation are multiple. Two major categories of pure pulmonic regurgitation include (1) conditions associated with anatomically abnormal valve cusps (congenital, rheumatic, carcinoid, trauma, and infective endocarditis) and (2) conditions associated with anatomically normal cusps (elevated pulmonary artery systolic pressures, idiopathic dilated pulmonary trunk, and Marfan's syndrome).

Pathology of tricuspid valve stenosis and pure tricuspid regurgitation--Part I.

This three-part article examines the histologic and morphologic basis for stenotic and purely regurgitant tricuspid valves. In Part I, conditions producing tricuspid valve stenosis are reviewed. In over 90% of stenotic tricuspid valves, the etiology is rheumatic disease. In isolated tricuspid stenosis, the etiology is either carcinoid or congenital. Rare causes of tricuspid stenosis include active infective endocarditis, metabolic or enzymatic abnormalities (Fabry's, Whipple's disease), and giant blood cysts.

Pathology of mitral valve stenosis and pure mitral regurgitation--Part II.

This two-part article examines the histologic and morphologic basis for stenotic and purely regurgitant mitral valves. In Part I, conditions producing mitral valve stenosis were reviewed. In over 99% of stenotic mitral valves, the etiology is rheumatic disease. Other rare causes of mitral stenosis include congenitally malformed valves, active infective endocarditis, massive annular calcium, and metabolic or enzymatic abnormalities. In Part II, conditions producing pure mitral regurgitation are discussed. In contrast to the few causes of mitral stenosis, the causes of pure (no element of stenosis) mitral regurgitation are multiple. Some of the conditions producing pure regurgitation include floppy mitral valves, infective endocarditis, papillary muscle dysfunction, rheumatic disease, and ruptured chordae tendineae.

Pathology of mitral valve stenosis and pure mitral regurgitation--Part I.

This two-part article examines the histologic and morphologic basis for stenotic and purely regurgitant mitral valves. In Part I, conditions producing mitral valve stenosis are reviewed. In over 99% of stenotic mitral valves, the etiology is rheumatic disease. Other rare causes of mitral stenosis include congenital malformed valves, active infective endocarditis, massive annular calcium, and metabolic or enzymatic abnormalities. In Part II, conditions producing pure mitral regurgitation will be discussed. In contrast to the few causes of mitral stenosis, the causes of pure (no element of stenosis) mitral regurgitation are multiple. Some of the conditions producing pure regurgitation include floppy mitral valves, infective endocarditis, papillary muscle dysfunction, rheumatic disease, and ruptured chordae tendinae.

Pathology of tricuspid valve stenosis and pure tricuspid regurgitation--Part II.

This three-part article examines the histologic and morphologic basis for stenotic and purely regurgitant tricuspid valves. In Part I, conditions producing tricuspid valve stenosis were reviewed. In Part II, conditions producing pure tricuspid regurgitation are discussed. In contrast to the relatively few causes of tricuspid stenosis, the causes of pure (no element of stenosis) tricuspid regurgitation are multiple. Some of the conditions producing pure regurgitation include floppy tricuspid valves, infective endocarditis, papillary muscle dysfunction, rheumatic disease, and Ebstein's anomaly.

Pathology of tricuspid valve stenosis and pure tricuspid regurgitation--Part III.

This three-part article examines the histologic and morphologic basis for stenotic and purely regurgitant tricuspid valves. In Part III, morphometric analysis of tricuspid valve annular circumference, leaflet area, and the product of annular circumference and leaflet area are shown to be useful in establishing etiology for the purely regurgitant tricuspid valves and in assessing the anatomic basis of pure tricuspid regurgitation in the presence of mitral stenosis.

Pathology of aortic valve stenosis and pure aortic regurgitation: a clinical morphologic assessment--Part II.

This two-part article examines the histologic and morphologic basis for stenotic and purely regurgitant aortic valves. Part I discussed stenotic aortic valves and Part II discusses causes of purely regurgitant aortic valves. In over 95% of stenotic aortic valves, the etiology is one of three types: congenital (primarily bicuspid), degenerative, and rheumatic. Other rare causes included active infective endocarditis, homozygous type II hyperlipoproteinemia, and systemic lupus erythematosis. The causes of pure aortic regurgitation are multiple but can be separated into diseases affecting the valve (normal aorta) (infective endocarditis, congenital bicuspid, rheumatic, floppy), diseases affecting the walls of aorta (normal valve) (syphilis, Marfan's dissection), disease affecting both aorta and valve (abnormal aorta, abnormal valve) (ankylosing spondylitis), and disease affecting neither aorta nor valve (normal aorta, normal valve) (ventricular septal defect, systemic hypertension). Diseases affecting the aortic valve alone are the most common subgroup of conditions producing purely regurgitant aortic valves.

Randomized comparison of cefamandole, cefazolin, and cefuroxime prophylaxis in open-heart surgery.

A total of 337 patients undergoing coronary artery bypass grafting or cardiac valve replacement were randomly assigned to receive cefazolin (1 g every 8 h [q8h]), cefamandole (2 g q6h), or cefuroxime (1.5 g q12h) as an intravenous antibiotic prophylaxis. All drugs were administered within 60 min before the initial incision and were continued for 48 h postoperatively. No adverse effects related to the study drugs were observed. The percentage of patients with postoperative infection was 9% for the cefazolin group, 6% for the cefamandole group, and 5% for the cefuroxime group or 6.5% overall. There were more infection sites in patients treated with cefazolin than in those treated with cefuroxime (P = 0.05) or cefamandole (P = 0.06). Fewer wound infections occurred with cefuroxime (P less than 0.01) and cefamandole (P = 0.06) than with cefazolin. Analyses of the prophylactic regimens used in this study showed cefazolin and cefuroxime to be less costly than cefamandole.