Formation of chiral branched nanowires by the Eshelby Twist.

Manipulating the morphology of inorganic nanostructures, such as their chirality and branching structure, has been actively pursued as a means of controlling their electrical, optical and mechanical properties. Notable examples of chiral inorganic nanostructures include carbon nanotubes, gold multishell nanowires, mesoporous nanowires and helical nanowires. Branched nanostructures have also been studied and been shown to have interesting properties for energy harvesting and nanoelectronics. Combining both chiral and branching motifs into nanostructures might provide new materials properties. Here we show a chiral branched PbSe nanowire structure, which is formed by a vapour-liquid-solid branching from a central nanowire with an axial screw dislocation. The chirality is caused by the elastic strain of the axial screw dislocation, which produces a corresponding Eshelby Twist in the nanowires. In addition to opening up new opportunities for tailoring the properties of nanomaterials, these chiral branched nanowires also provide a direct visualization of the Eshelby Twist.

Motion and rotation of small glissile dislocation loops in stress fields.

We derive here for the first time the equations that describe the combined motion and rotation of small prismatic dislocation loops in stress fields. When the applied torque is balanced by the self-torque of the loop, we show how the solution can be obtained for the loop orientation, and how this orientation affects the glide force on the loop.

Rupture of a pulmonary artery mycotic aneurysm associated with candidal endocarditis.

Candidal endocarditis can develop if candidemia occurs during Swan-Ganz catheterization. Candida endocarditis may persist for many months and is fatal unless the infected valve is resected. Herein is reported the first case of rupture of a mycotic pulmonary artery aneurysm caused by chronic candidal endocarditis. The endocarditis followed Swan-Ganz catheterization and aneurysm progressed despite appropriate medical and surgical therapy.

Sudden death in mitral valve prolapse.

Four cases of sudden death in young females with clinical and pathologic features of mitral valve prolapse are discussed. The approach to postmortem examination of the mitral valve is reviewed and various risk factors are stressed. Because of the sudden nature of these deaths, this entity is more commonly seen in medical examiner's populations than hospital autopsies. A practical approach to the investigation of such cases is given.

Dispensing error causing fatal chlorpropamide intoxication in a nondiabetic.

A 38-year-old nondiabetic female developed fatal hypoglycemia when chlorpropamide (Diabinese) was accidentally substituted for acetaminophen (Tylenol) with codeine no. 3 in a pharmacy dispensing error. When found, the patient's serum glucose was less than 20 mg/dL. The serum chlorpropamide level on hospital admission was 124 micrograms/mL. The possibility of dispensing error should be considered whenever unexpected drug effects are encountered. In cases of suspected drug overdose, labels and contents of medicine vials found at the scene should be checked for discrepancy.

Hemoglobin A1c compared with three conventional measures of diabetes control.

Control of diabetes was studied during an 8-wk camp program in 18 insulin-dependent counselors with a mean age of 19.3 yr and a mean duration of diabetes of 11.4 yr. A composite score was obtained for each subject derived from three factors: percent sugar-free urine tests, 24-h glucose excretion as percent of carbohydrate intake, and mean preprandial blood glucose (MPBG). The mean hemoglobin A1c (HbA1c) at the end of the period was 8.3 +/- 1.6% (+/ SD) (normal range, 4-6%). Scores ranging from 24 (fair control) to 45 (excellent control) showed a significant inverse correlation with HbA1c (r = 0.807, P less than 0.001) and MPBG (r = -0.674, P less than 0.01). HbA1c showed a significant correlation with the MPBG (r = 0.693, P less than 0.01). The HbA1c level was predicted better by percent sugar-free urine tests than by the 24-h glucose excretion. Thus it appears that accurate quantification of control may be obtained by using a scoring system. Critical comparison of HbA1c levels to various glycemic indices may provide useful alternatives for estimating diabetes control.

Diabetes mellitus and genetic prediabetes. Decreased replicative capacity of cultured skin fibroblasts.

The idea that the gene(s) that cause diabetes mellitus can be expressed in extrapancreatic cells has been examined by tissue culture techniques. Skin biopsies were obtained from 25 normal subjects (N), 26 overt diabetics (D), 16 of juvenile onset (JOD) and 9 of maturity onset (MOD), and 21 subjects genetically predisposed to diabetes (P) on the basis of maturity-onset diabetes in both parents. Each biopsy was subdivided, multiple skin fragments were explanted in vitro, and several parameters of cellular outgrowth were monitored in primary and secondary cultures until cell division ceased because of senescence. In general, the rank order of growth vigor was N greater than P greater than D although differences were often marginal and statistically significant between N and JOD and(or) MOD. Outgrowth of epithelial cells was more vigorous in N explants in early stages, but later, JOD and MOD cells grew better than those of N. Outgrowth of fibroblast cells from N explants was more vigorous both at early and later stages and required less time to achieve maximum percent outgrowth. In secondary cultures, N cells grew faster than the other three groups so that fewer days elapsed between subcultures but significant differences were only seen between N and one or two of the other groups over some of the first seven subcultures. The onset of cellular senescence occurred earlier in P and JOD cultures both in mean population doublings and calendar time. N cultures had a higher percent surviving clones after picking than MOD, and a shorter recloning time than clones of JOD. The replicative life-spans of cultures (mean population doublings +/- SE) were N = 52.54 +/- 2.24, P = 47.84 +/- 2.43, JOD = 47.12 +/- 2.99, and MOD = 46.40 +/- 4.04, but differences did not reach significance for N vs the other three groups. The data demonstrate that cellular growth is impaired in both JOD and MOD types of cultures and to a generally lesser extent in P cultures. This is consistent with intrinsic genetic defects but the possibility that persistent deleterious effects of in vivo pathophysiology contribute alone or in combination cannot be ruled out. Therefore, the diabetic defect(s) can be expressed in extrapancreatic cells of mesenchymal origin. This system should prove useful in exploring the interplay between genetic and environmental factors in diabetes, the mechanisms(s) of hyperglycemia and other metabolic derangements, and the propensity that affected individuals have to develop degenerative diseases.

Chronologic and physiologic age affect replicative life-span of fibroblasts from diabetic, prediabetic, and normal donors.

Cultured skin fibroblasts from subjects with clinically apparent diabetes mellitus and from subjects genetically predisposed to diabetes have a replicative lifespan that is inversely related to donor age. Fibroblasts from carefully defined normal subjects not predisposed to diabetes fail to show this correlation. The data support the idea that physiologic status of the tissue donor is a more precise determinant of fibroblast replicative lifespan than chronologic age.