Stint/CD: A stand-alone explicit time integration package for structural dynamics analysis

This paper is a user's guide for the stand-alone explicit direct time integration package STINT/CD for structural dynamics analysis. STINT/CD uses an automatic variable time increment central difference method. The purpose, function, limitations and usage of the package are described. A FORTRAN listing of STINT/CD is given along with a sample problem which illustrates its usage and performance.     

Perennial Antarctic lake ice: an oasis for life in a polar desert

The permanent ice covers of Antarctic lakes in the McMurdo Dry Valleys develop liquid water inclusions in response to solar heating of internal aeolian-derived sediments. The ice sediment particles serve as nutrient (inorganic and organic)-enriched microzones for the establishment of a physiologically and ecologically complex microbial consortium capable of contemporaneous photosynthesis, nitrogen fixation, and decomposition. The consortium is capable of physically and chemically establishing and modifying a relatively nutrient- and organic matter-enriched microbial "oasis" embedded in the lake ice cover.     

Management of the incidentally discovered adrenal mass or "incidentaloma"

The prevalence of an incidentally discovered adrenal mass or "incidentaloma" by abdominal computerized tomography (CT) scan is 1% to 2%. The majority of patients with incidentalomas do not have clinical manifestations nor require further treatments of their incidentalomas. Thus the goal for their management is two-fold: 1) To identify and treat the hormonally hyperactive adrenal adenoma and the rare adrenal carcinoma, and 2) To avoid creating an iatrogenic disease of medical progress. An adrenal mass > or = 6 cm, excluding metastatic malignant disease, needs to be surgically resected due to the risk for carcinoma. The risk of primary adrenal cancer for a hormonally inactive lesion < or = 3 cm is extremely low and can be safely observed. Treatment for the hormonally inactive lesion between 3 and 6 cm must be individualized, based on age, specific scan characteristics (irregular border, local invasion, metastasis), and clinical status of the patient. All hormonally active adrenal adenomas should be surgically resected. In this article, we review the data to support the above recommendations.     

Edge loading in metal-on-metal hips: low clearance is a new risk factor

The revision rate of large head metal-on-metal and resurfacing hips are significantly higher than conventional total hip replacements. The revision of these components has been linked to high wear caused by edge loading; which occurs when the head-cup contact patch extends over the cup rim. There are two current explanations for this; first, there is loss of entrainment of synovial fluid resulting in breakdown of the lubricating film and second, edge loading results in a large local increase in contact pressure and consequent film thickness reduction at the cup rim, which causes an increase in wear. This paper develops a method to calculate the distance between the joint reaction force vector and the cup rim--the contact patch centre to rim (CPCR) distance. However, the critical distance for the risk of edge loading is the distance from the contact patch edge to rim (CPER) distance. An analysis of explanted hip components, divided into edge worn and non-edge-worn components showed that there was no statistical difference in CPCR values, but the CPER value was significantly lower for edge worn hips. Low clearance hips, which have a more conformal contact, have a larger diameter contact patch and thus are more at risk of edge loading for similarly positioned hips.     

Induction of spreading depression in the ischemic hemisphere following experimental middle cerebral artery occlusion: effect on infarct morphology

This study was undertaken to test whether transient depolarizations occurring in periinfarct regions are important in contributing to infarct spread and maturation. Following middle cerebral artery (MCA) occlusion we stimulated the ischemic penumbra with recurrent waves of spreading depression (SD) and correlated the histopathological changes with the electrophysiological recordings. Halothane-anesthetized, artificially ventilated Sprague-Dawley rats underwent repetitive stimulation of SD in intact brain (Group 1; n = 8) or photothrombotic MCA occlusion coupled with ipsilateral common carotid artery occlusion (Groups 2 and 3, n = 9 each). The electroencephalogram and direct current (DC) potential were recorded for 3 h in the parietal cortex, which represented the periinffarct border zone in ischemic rats. In Group 2, only spontaneously occurring negative DC shifts occurred; in Group 3, the (nonischemic) frontal pole of the ischemic hemisphere was electrically stimulated to increase the frequency of periinfarct DC shifts. Animals underwent perfusion-fixation 24 h later, and volumes of complete infarction and scattered neuronal injury ("incomplete infarction") were assessed on stained coronal sections by quantitative planimetry. Electrical induction of SD in Group 1 did not cause morphological injury. During the initial 3 h following MCA occlusion, the number of spontaneous periinfarct depolarization in Group 2 (7.0 +/- 1.5 DC shifts) was doubled in Group 3 by frontal current application (13.4 +/- 2.7 DC shifts; p < 0.001). The duration as well as the integrated negative amplitude of DC shifts over time were significantly greater in Group 3 than in Group 2 rats (duration, 5.7 +/- 3.8 vs. 4.1 +/- 2.5 min; p < 0.05). Histopathological examination disclosed well-defined areas of pannecrosis surrounded by a cortical rim exhibiting selectively damaged acidophilic neurons and astrocytic swelling in otherwise normal-appearing brain. Induction of SD in the ischemic hemisphere led to a significant increase in the volume of incomplete infarction (19.0 +/- 6.1 mm3 in Group 3 vs. 10.3 +/- 5.1 mm3 in Group 2; p < 0.01) and of total ischemic injury (100.7 +/- 41.0 mm3 in Group 3 vs. 66.5 +/- 24.7 mm3 in Group 2; p < 0.05). The integrated magnitude of DC negativity per experiment correlated significantly with the volume of total ischemic injury (r = 0.780, p < 0.0001). Thus, induction of SD in the ischemic hemisphere accentuated the development of scattered neuronal injury and increased the volume of total ischemic injury. This observation may be explained by the fact that with limited perfusion reserve, periinfarct depolarization are associated with episodic energy failure in the acute ischemic penumbra.