Cognitive behavioral treatment for young children with obsessive-compulsive disorder.

Obsessive-compulsive disorder (OCD) is a distressing and functionally impairing disorder that can emerge as early as age 4. Cognitive behavior therapy (CBT) for OCD in youth shows great promise for amelioration of symptoms and associated functional impairment. However, the empirical evidence base for the efficacy of CBT in youth has some significant limitations, particularly as related to treating the very young child with OCD. This report includes a quantitative review of existing child CBT studies to evaluate evidence for the efficacy of CBT for OCD. It identifies gaps in the literature that, when addressed, would enhance the understanding of effective treatment in pediatric OCD. Finally, it presents a proposed research agenda for addressing the unique concerns of the young child with OCD.     

The timing of surgical intervention in craniofacial anomalies

When treating an infant or younger child with severe craniofacial synostosis, the burden is placed on the surgeon in making a decision regarding not only the design of the osteomy but also the timing of the surgical intervention. This article reviews the current treatment protocols for craniofacial anomalies.     

Acute vascular rejection is associated with up-regulation of vitronectin receptor (alphavbeta3), increased expression of tissue factor, and activation of the extracellular matrix metalloproteinase induction system.

BACKGROUND: A cascade of inflammatory reactions characterize acute vascular rejection after heart transplantation. This study was undertaken to test the hypothesis that acute vascular rejection is associated with up-regulation of vitronectin receptor (alphavbeta3), increased expression of tissue factor, and activation of the extracellular matrix metalloproteinase induction system. METHODS: Acute vascular rejection developed in 14 heart transplant recipients within 2 weeks of transplantation, confirmed by immunofluorescence (AVR group). We compared these patients with 10 transplant recipients who had no evidence of acute vascular rejection or peritransplant ischemic injury (control group). We evaluated endomyocardial biopsy specimens for alphavbeta3, tissue factor, and extracellular matrix metalloproteinase inducer (EMMPRIN). RESULTS: Compared with the control group, the AVR group demonstrated evidence of significantly increased expression of alphavbeta3 (1.9-fold, p < 0.001), tissue factor (1.8-fold, p < 0.001), and EMMPRIN (1.5-fold, p < 0.001). All patients in the AVR group received plasmapheresis; 11 of 14 patients had evidence of ischemic necrosis on biopsy specimens, and 3 of 14 patients experienced hemodynamic compromise and graft dysfunction and died within 3 weeks of transplant. Another patient died at 10 months after transplant. CONCLUSIONS: Acute vascular rejection is associated with up-regulation of alphavbeta3, tissue factor, and activation of the matrix metalloproteinase induction system, which may contribute to the lethal morbidity associated with this disease.     

Renin secretion by the spontaneously diabetic rat

Renal function studies and measurements of in vivo plasma renin activity (PRA), kidney renin content, and renin secretion by isolated, perfused kidneys were performed in spontaneously diabetic and nondiabetic BioBreeding/Worcester (BB/W) rats. Diabetic animals evidenced hyperglycemia, glycosuria, and plasma volume expansion. After dietary sodium deprivation, plasma volume fell to levels equivalent to those of sodium-deprived, nondiabetic rats. Dietary sodium deprivation evoked a larger proportional increase in PRA among diabetic than nondiabetic animals, although PRA before sodium restriction was equivalent in the two groups. Basal renin release (RR) was higher from isolated, perfused kidneys from diabetic rats than from nondiabetic kidneys. Diabetic kidneys, moreover, displayed increased kidney renin content (KRC). By contrast, while isoproterenol (10(-5) M) stimulated a nearly fivefold increment in RR from nondiabetic, perfused kidneys, a negligible effect was observed in diabetic kidneys. The dose-response curve of renin secretion (as a proportion of total renal content) in response to isoproterenol was shifted downward. Hence, while KRC and spontaneous RR by isolated, perfused kidneys were increased, the increment in PRA with salt depletion and the renin-secretory response to isoproterenol in vitro were impaired. We propose that specific defects in renin secretion, in particular, the response to beta-adrenergic stimulation, may be operative in diabetes.     

The occurrence of chemically induced hormesis

This paper will provide an overview of the potential general applicability of chemical hormesis. Evidence will be presented on the occurrence of chemical hormesis by chemical classes studied (e.g. heavy metals, polycylic aromatic hydrocarbons, etc.), by affected biological and toxic end points (e.g. growth enzyme activities, DNA-repair capacity, life span, tumor incidence) and by biological/taxonomic systems. Several specific examples of possible hormetic effects with respect to agents of environmental concern, such as chloroform, will be presented along with a discussion of future research directions.     

Radioautographic evidence for slow astrocyte turnover and modest oligodendrocyte production in the corpus callosum of adult mice infused with 3H-thymidine

To find out whether glial cells proliferate in the corpus callosum of adult mice, two series of experiments were carried out. The first one made use of 9-month-old "aged" male mice. Some of them were given 3H-thymidine as a 2-hour pulse to examine which cells became labeled and, therefore, had the ability to divide. Others were sacrificed after a continuous infusion of 3H-thymidine for 30 days to examine whether the label would then appear in different cells. In other aged animals, the 30-day infusion was followed by 60 or 180 days without 3H-thymidine to determine whether cells retained or lost their label with time. A second series of experiments was carried out in 4-month old "young adult" male mice to seek confirmation of the main conclusions. Following the 3H-thymidine pulse given to aged mice, only immature glial cells were labeled. After a 30-day infusion, 12.1% astrocytes and 1.1% oligodendrocytes were labeled, so that the net daily addition rate of astrocytes averaged 0.4% and of oligodendrocytes, 0.04%. In young adult mice, the rate after a 7-day infusion averaged 0.9% for astrocytes and 0.08% for oligodendrocytes. However, when the 30-day infusion into aged mice was followed by 60 and 180 days without 3H-thymidine, the labeled astrocytes decreased to 5.3% and 0%, respectively, whereas the number of labeled oligodendrocytes did not change significantly. The interpretation of the results is that the immature cells present in the corpus callosum of mice continue dividing throughout life and their progeny give rise to astrocytes and oligodendrocytes. In the case of astrocytes, the production of new cells occurs in parallel with a loss, so that the astrocyte population turns over. In the case of oligodendrocytes, there is a small production of new, apparently stable cells.     

Radiographical documentation of direct injury of the intracanalicular segment of the optic nerve in the orbital apex syndrome

In the radiographical evaluation of the orbital apex syndrome, standard radiographs, tomograms, and computed tomographic scans have proved useful in the demonstration of the bony pathology, especially for optic canal fractures. The limitation of these methods, however, remains in their inability to provide accurate delineation of the associated soft tissue pathology, including the presence of optic nerve sheath hematoma. Recent developments in computer technology and graphic imaging are now available to provide an accurate three-dimensional radiographical analysis of the extent of skeletal and soft tissue injury in the orbital apex syndrome. The physician, in essence, can perform a radiographical "living autopsy". The technique was used to evaluate a patient with bilateral apex syndrome. It clearly showed that a severe direct injury to the intracanalicular portion of the optic nerve was responsible for the development of blindness in this patient. The progression of optic nerve injury, from perineural sheath hematoma to the ultimate development of optic nerve atrophy and fibrosis, was radiographically documented.