The effect of topical corticosteroids on refractive outcome and corneal haze after photorefractive keratectomy

BACKGROUND: The effect of topical corticosteroids after excimer laser photorefractive keratectomy (PRK) remains a matter of some controversy. Refractive effects may be different according to the amount of myopia and timing of instillation. METHODS: Two groups of patients were studied: Study A consisted of 215 eyes (128 patients) with PRK (mean baseline myopia, -6.53 +/- 2.22 D) that received no corticosteroids (No Corticosteroid Group) unless significant regression or corneal haze appeared (Delayed Corticosteroid Group), and in Study B, we randomly assigned eyes to the Initial Corticosteroid Group (mean baseline myopia, -6.39 +/- 1.84 D) or the No/delayed Corticosteroid Group (mean baseline myopia -5.78 +/- 2.02 D). Clinical results after PRK for low-to-moderate and high myopia were compared. RESULTS: In the first group, 70.9% (73 eyes) of moderately myopic eyes (mean, -4.56 +/- 1.10 D) belonged to the No Corticosteroid Group that had a mean refraction of -5.39 +/- 1.77 D. Delayed Corticosteroid Group eyes were more myopic (mean, -7.52 +/- 2.10 D), and showed more severe haze than those in the No Corticosteroid Group. In study B, only in high myopes with more than -6.00 D (mean, -7.76 +/- 1.15 D) did refraction and corneal haze outcomes show significant difference between the Initial Corticosteroid Group and the No/delayed Corticosteroid Group. CONCLUSIONS: The effects of topical corticosteroids after PRK were less in moderate myopes compared to high myopes. Delayed instillation of corticosteroids did not reverse the regression or haze whereas initial instillation showed a beneficial effect on high myopes but not on moderate myopes.     

Functional role of high-affinity anandamide transport, as revealed by selective inhibition

Anandamide, an endogenous ligand for central cannabinoid receptors, is released from neurons on depolarization and rapidly inactivated. Anandamide inactivation is not completely understood, but it may occur by transport into cells or by enzymatic hydrolysis. The compound N-(4-hydroxyphenyl)arachidonylamide (AM404) was shown to inhibit high-affinity anandamide accumulation in rat neurons and astrocytes in vitro, an indication that this accumulation resulted from carrier-mediated transport. Although AM404 did not activate cannabinoid receptors or inhibit anandamide hydrolysis, it enhanced receptor-mediated anandamide responses in vitro and in vivo. The data indicate that carrier-mediated transport may be essential for termination of the biological effects of anandamide, and may represent a potential drug target.     

Longitudinal weight changes, length of survival, and energy requirements of long-term care residents with dementia

OBJECTIVE: We hypothesized that institutionalized patients with dementia, who frequently have feeding problems and require supervised and assisted feeding, would lose more weight during their residency than nondemented, independently functioning residents and have compromised survival. To test this hypothesis, we examined the survival and longitudinal changes in weight of two cohorts of institutionalized residents with dementia and compared these cohorts with a cohort of nondemented residents. We also measured the resting energy expenditures of a subset of the subjects with dementia as an indicator of their energy needs. DESIGN: A longitudinal cohort study with retrospective baseline chart review and subsequent follow-up of monthly weights and mortality over 4 years. SETTING: A 725-bed long-term care institution with specified levels of care. SUBJECTS: Two cohorts of residents with dementia, one consisting of subjects who required total care throughout their institutional stay (n = 31) and another group who did not initially require total care (n = 48); these were compared with a cohort with normal mentation who were functionally independent in their daily activities (n = 26). The total number of subjects was 105. MEASUREMENTS: Demographics, medical problems, and medications by chart review; functional and mental status evaluations; longitudinal monthly weights and mortality for the 48-month study period; and resting energy expenditures by indirect calorimetry. MAIN RESULTS: Residents with dementia had lower weights on admission and throughout their stay than nondemented, independently functioning residents, and they were more likely to have a weight loss of 10 lbs or more at some point during the 4-year study period. However, their mean weights did not change during the study period. The mean survival from admission of those demented residents who died was more than 3 years. Resting energy expenditures of women residents with advanced dementia were 12% lower than predicted from the Harris Benedict equations. CONCLUSION: Dementia is not necessarily associated with unremitting weight loss during institutionalization despite the frequent occurrence of feeding difficulties and temporary weight loss. This may be caused partly by the lower than expected resting energy expenditures and, hence, energy needs of affected residents as their dementia progresses. Demented residents weighed significantly less than nondemented, independently functioning residents throughout their institutional stay. Nevertheless, nursing staff are able to maintain weight and survival for extended periods even in very impaired residents.     

Growth of highly orientated strontium barium niobate thin films on Si substrates through the sol–gel process using a K: SBN template layer

We report the growth of highly C-axis orientation of Sr _x Ba_1−x Nb₂O₆ (SBN) thin films on p-type (100) Si substrates by using a potassium-substituted SBN template layer with the sol–gel method. The crystallization of SBN thin films was found closely related to the potassium ion doping concentration and the postannealing temperature of the K-SBN template layer. Secondary ion mass spectrometry analysis showed that potassium elements were accumulated at the interface of the template layer and silicon substrate. SBN films postannealed at 750 °C with K-SBN template layer has a smaller full width at half maximum of X-ray rocking curve of 2.45° than that of 5.40° for the pure SBN films. By introducing a template layer, the surface morphologies of SBN films fabricated on silicon substrate were greatly improved.     

Efficacy of surgical treatment in traumatic central cord syndrome

BACKGROUND: Controversy surrounds the treatment of traumatic central cord syndrome (TCCS), as there are strong advocates for nonsurgical treatment for most patients. However, conservative treatment has been shown to yield a longer period of discomfort from pain and weakness in certain cases. METHODS: In a retrospective review of 114 patients presenting with acute or chronic TCCS from 1988-94, four different age groups were separately observed under different treatments. Motor and sensory recovery were assessed. RESULTS: Better results were achieved in younger patients, with or without radiographic abnormalities, and in patients with clinically correlated encroaching cord lesions who received early surgical decompression. CONCLUSIONS: Surgical intervention for TCCS must be addressed with careful clinical and radiographic survey. Removal of offending lesions in the subacute period results in significant motor and sensory improvement in short-term and long-term follow-up.     

Essential contribution of caspase 3/CPP32 to apoptosis and its associated nuclear changes

Caspases are fundamental components of the mammalian apoptotic machinery, but the precise contribution of individual caspases is controversial. CPP32 (caspase 3) is a prototypical caspase that becomes activated during apoptosis. In this study, we took a comprehensive approach to examining the role of CPP32 in apoptosis using mice, embryonic stem (ES) cells, and mouse embryonic fibroblasts (MEFs) deficient for CPP32. CPP32(ex3-/-) mice have reduced viability and, consistent with an earlier report, display defective neuronal apoptosis and neurological defects. Inactivation of CPP32 dramatically reduces apoptosis in diverse settings, including activation-induced cell death (AICD) of peripheral T cells, as well as chemotherapy-induced apoptosis of oncogenically transformed CPP32(-/-) MEFs. As well, the requirement for CPP32 can be remarkably stimulus-dependent: In ES cells, CPP32 is necessary for efficient apoptosis following UV- but not gamma-irradiation. Conversely, the same stimulus can show a tissue-specific dependence on CPP32: Hence, TNFalpha treatment induces normal levels of apoptosis in CPP32 deficient thymocytes, but defective apoptosis in oncogenically transformed MEFs. Finally, in some settings, CPP32 is required for certain apoptotic events but not others: Select CPP32(ex3-/-) cell types undergoing cell death are incapable of chromatin condensation and DNA degradation, but display other hallmarks of apoptosis. Together, these results indicate that CPP32 is an essential component in apoptotic events that is remarkably system- and stimulus-dependent. Consequently, drugs that inhibit CPP32 may preferentially disrupt specific forms of cell death.