Maturation of myocardial capillaries in the fetal and neonatal rat: An ultrastructural study with a morphometric analysis of the vesicle populations

The ultrastructural morphology of the cellular and extracellular components of the developing myocardial capillary wall—from the 16-day-gestation fetus of the rat to the 21-day neonate—was examined. A morphometric analysis of plasmalemmal vesicles and of coated vesicles and pits of capillary endothelial cells was performed during the same developmental period. As the lateral extensions of the capillary endothelial cells change from irregular to regular in their thickness during development, there is an increase in the number of plasmalemmal vesicles and a progression from clusters of plasmalemmal vesicles to a uniform distribution in the endothelial cell. The ratio of vesicles which are open to the luminal front, which are “free” in the cytoplasm, or which are open to the abluminal front of the endothelial cell was consistent throughout development. The numerical density of plasmalemmal vesicles demonstrates a gradual and significant increase. In contrast, the numbers of coated vesicles and pits are variable within a very narrow range, and no pattern of increase or decrease is discernible during development. Similarly, there is no change in interendothelial cell junctions, which consist of occluding and primitive adhesive junctional types, during development. The lamina densa of the basal lamina gradually develops from discontinuous, patchy densities along the abluminal surface of the endothelial cells to a continuous and distinct layer by 21 days gestation. The presence of the proteoglycan species in the developing basal lamina was assessed with the cationic dye ruthenium red (RR), and the appearance of RR-marked proteoglycans was found to parallel the appearance of lamina densa material. The RR sites appear discontinuously in patches; and later, the RR sites appear in a continuous and regular planar lattice in the lamina rara interna and externa at 21 days gestation. A complete array of RR-stainable anionic sites outside a continuous lamina densa near birth indicates that the basal laminae of developing capillaries in the heart are morphologically, and in part biochemically, mature by the end of the first neonatal week. Our results show that the endothelial cells and the subtending basal lamina of myocardial capillaries gradually mature morphologically during the final days of gestation and the first neonatal week. The finding of tight junctions and small areas of vesicle concentration in fetal endothelial cells could indicate that sites of permeability are limited early in myocardial capillary development and that these vesicular sites increase as gestation proceeds and as the myocardial capillaries mature.     

Interdisciplinary shared governance: a partnership model for high performance in a managed care environment

Today's managed care environment is forcing hospitals to seek new and innovative ways to deliver a seamless continuum of high-quality care and services to defined populations at lower costs. Many are striving to achieve this goal through the implementation of shared governance models that support point-of-service decision making, interdisciplinary partnerships, and the integration of work across clinical settings and along the service delivery continuum. The authors describe the key processes and strategies used to facilitate the design and successful implementation of an interdisciplinary shared governance model at The University Hospital, Cincinnati, Ohio. Implementation costs and initial benefits obtained over a 2-year period also are identified.     

Student outcomes in a postprofessional online master's-degree program

The outcomes of five cohorts of occupational therapists who completed an online postprofessional master's degree program were evaluated. Data on graduates' satisfaction with professional skills and status, contribution of the program to their satisfaction, and engagement in professional activities since graduation were collected using an online survey. Forty-nine of 65 surveys distributed were returned (75% response rate). Respondents indicated high levels of satisfaction with professional skills and status and high levels of contribution of the program to their satisfaction. Respondents also reported participation in a variety of professional leadership activities. Results suggest that postprofessional graduate-level education is effective in developing advanced critical reasoning, reflection, and leadership skills in occupational therapists and in facilitating a variety of professional contributions. The online mode was effective in delivering the program content. The value of postprofessional education to individuals and the profession is discussed.     

Diagnosing the patient with abdominal pain and altered bowel habits: is it irritable bowel syndrome?

Diagnosing a patient who presents with abdominal pain and altered bowel habits can be challenging. Although serious organic illnesses can cause these symptoms, irritable bowel syndrome is commonly responsible. It can be difficult to properly evaluate these patients without overusing diagnostic tests and consultation. A practical approach for diagnosing irritable bowel syndrome is suggested, using the Rome II criteria and the presence of alarm symptoms such as weight loss, gastrointestinal bleeding, anemia, fever, or frequent nocturnal symptoms as starting points. If there are no alarm symptoms and the Rome II criteria are not met, it is acceptable to reevaluate the patient at a later date. If there are no alarm symptoms and the Rome II criteria are met, the patient should be categorized on the basis of age: patients 50 years or younger can be evaluated on the basis of predominant symptoms--constipation, diarrhea, or abdominal pain. Patients older than 50 years should be fully evaluated and considered for gastroenterology referral. If alarm symptoms are present, a full evaluation should be performed (and gastroenterology referral considered), regardless of the patient's age.     

Effects of Industrial and Domestic Wastewaters on Selected Biological Indicators in Aquatic Organisms

No abstract available.     

Oligodendroglia and neurotrophic factors in neurodegeneration

Myelination by oligodendroglial cells (OLs) enables the propagation of action potentials along neuronal axons, which is essential for rapid information flow in the central nervous system. Besides saltatory conduction, the myelin sheath also protects axons against inflammatory and oxidative insults. Loss of myelin results in axonal damage and ultimately neuronal loss in demyelinating disorders. However, accumulating evidence indicates that OLs also provide support to neurons via mechanisms beyond the insulating function of myelin. More importantly, an increasing volume of reports indicates defects of OLs in numerous neurodegenerative diseases, sometimes even preceding neuronal loss in pre-symptomatic episodes, suggesting that OL pathology may be an important mechanism contributing to the initiation and/or progression of neurodegeneration. This review focuses on the emerging picture of neuronal support by OLs in the pathogenesis of neurodegenerative disorders through diverse molecular and cellular mechanisms, including direct neuron-myelin interaction, metabolic support by OLs, and neurotrophic factors produced by and/or acting on OLs.     

αE-catenin is an autoinhibited molecule that coactivates vinculin

αE-catenin, an essential component of the adherens junction, interacts with the classical cadherin-β-catenin complex and with F-actin, but its precise role is unknown. αE-catenin also binds to the F-actin-binding protein vinculin, which also appears to be important in junction assembly. Vinculin and αE-catenin are homologs that contain a series of helical bundle domains, D1-D5. We mapped the vinculin-binding site to a sequence in D3a comprising the central two helices of a four-helix bundle. The crystal structure of this peptide motif bound to vinculin D1 shows that the two helices adopt a parallel, colinear arrangement suggesting that the αE-catenin D3a bundle must unfold in order to bind vinculin. We show that αE-catenin D3 binds strongly to vinculin, whereas larger fragments and full-length αE-catenin bind approximately 1,000-fold more weakly. Thus, intramolecular interactions within αE-catenin inhibit binding to vinculin. The actin-binding activity of vinculin is inhibited by an intramolecular interaction between the head (D1-D4) and the actin-binding D5 tail. In the absence of F-actin, there is no detectable binding of αE-catenin D3 to full-length vinculin; however, αE-catenin D3 promotes binding of vinculin to F-actin whereas full-length αE-catenin does not. These findings support the combinatorial or "coincidence" model of activation in which binding of high-affinity proteins to the vinculin head and tail is required to shift the conformational equilibrium of vinculin from a closed, autoinhibited state to an open, stable F-actin-binding state. The data also imply that αE-catenin must be activated in order to bind to vinculin.