Library

Notes: A discription of a thin film deposition source which is based upon the "Smalley metal cluster source" is presented. Our laser assisted molecular beam deposition source incorporates four major innovations: (1) placing the source so it sits external to the deposition chamber, (2) positioning the ablation target at an angle greater than 90° with respect to the laser entrance window, (3) placing the laser entrance window/lens further from the ablation target, and (4) the addition of a second optical window for laser alignment and in situ spectral analysis of the laser ablation plume. Novel molecules can be generated in this source through use of a reactive carrier gas. For example, employing a Ti target rod and O2 carrier gas; flat, uniform micron thick thin films of TiO2 can be easily generated. © 1998 American Institute of Physics.

Notes: The American College of Prosthodontists has developed a classification system for complete edentulism based on diagnostic findings. These guidelines may help practitioners determine appropriate treatments for their patients. Four categories are defined, ranging from Class I to Class IV, with Class I representing an uncomplicated clinical situation and a Class IV patient representing the most complex and higher-risk situation. Each class is differentiated by specific diagnostic criteria. This system is designed for use by dental professionals who are involved in the diagnosis of patients requiring treatment for complete edentulism. Potential benefits of the system include: 1) better patient care, 2) improved professional communication, 3) more appropriate insurance reimbursement, 4) a better screening tool to assist dental school admission clinics, and 5) standardized criteria for outcomes assessment.

Notes: Abstract: The neuroprotective action of (S)-α-phenyl-2-pyridineethanamine dihydrochloride (FPL 15896AR), a novel noncompetitive N-methyl-d-aspartate (NMDA) receptor antagonist, was examined in primary rat cortical neuronal cultures. Exposure of cortical cultures to NMDA (50 µM) or glutamate (50 µM) for 15 min resulted in the death of 85–95% of the neurons during the next 24 h. This neurotoxicity was completely eliminated by adding FPL 15896AR (50 µM) to the cultures during the time of NMDA or glutamate exposure. Neuroprotective concentrations of FPL 15896AR also inhibited other acute effects of NMDA. FPL 15896AR (50 µM) prevented the loss of membrane-associated protein kinase C activity that developed by 4 h after transient exposure to 50 µM NMDA or 50 µM glutamate. FPL 15896AR also reduced by ∼35% the magnitude of NMDA-triggered increases in intracellular free Ca2+ concentration in the cortical cultures. These data indicate that NMDA-mediated toxicity in cultured cortical neurons can be blocked by the NMDA antagonist FPL 15896AR.

Notes: Abstract: The neuroprotective actions of remacemide and its anticonvulsant metabolite 1,2-diphenyl-2-propylamine monohydrochloride (desglycinylremacemide; DGR), a low-affinity NMDA receptor antagonist, were investigated using primary rat cortical neuronal cultures. Exposure of cortical cultures to NMDA (100 µM) for 15 min killed 85% of the neurons during the next 24 h. This neurotoxicity was blocked in a concentration-dependent manner by adding DGR (5–20 µM), but not its remacemide precursor (10–100 µM), to the cultures during the time of NMDA exposure. This suggests that the neuroprotective, as well as the anticonvulsant, activity of remacemide is mediated by DGR. Neuroprotective concentrations of DGR also inhibited two of the principal acute effects of NMDA. DGR (5–20 µM) prevented the loss of membrane-associated protein kinase C (PKC) activity that developed by 4 h after transient exposure to 100 µM NMDA and reduced the NMDA-triggered increases in intracellular free Ca2+ concentration ([Ca2+]i) by up to 70%. By contrast, remacemide (50 and 100 µM) did not prevent the NMDA-induced loss of PKC activity or reduce the [Ca2+]i responses. These data suggest that DGR protection against NMDA-mediated toxicity in cultured cortical neurons is associated with a reduction of NMDA-triggered [Ca2+]i surges and a prevention of the loss of membrane-associated PKC activity. In addition, the inhibition of NMDA-triggered [Ca2+]i responses by DGR was qualitatively different from the inhibition of these responses by the high-affinity NMDA-receptor antagonists MK-801 and phencyclidine. This may be a consequence of DGR's lower affinity for the NMDA receptor.

Notes: Abstract: Retinoic acid-treated murine P19 embryonal carcinoma cells differentiate into cells with neuronal morphology that display typical neuronal markers. In this study, the presence of glutamate receptors linked to Ca2+-signaling mechanisms on these neurons was demonstrated by testing the effects of glutamate agonists and antagonists on the intracellular calcium ion concentration ([Ca2+]i). Glutamate (1 mM) induced either sustained or transient increases in [Ca2+]i. The sustained glutamate-induced increase in [Ca2+]i was mimicked by NMDA (40 µM). The NMDA-triggered [Ca2+]i response was abolished by incubating the cells in Ca2+-free medium or by pretreating them with Mg2+ (2 mM) or MK-801 (0.1 µM). These responses were unaffected by the non-NMDA antagonist CNQX (10 µM), but they required glycine (3–30 µM). Kainate (40 µM) and AMPA (40 µM) did not affect [Ca2+]i. Without external Ca2+, glutamate triggered transient, sometimes oscillating, increases in [Ca2+]i. These responses were mimicked by the metabotropic agonist trans-(1S,3R)-1-amino-1,3-cyclopentanedicarboxylic acid (300 µM). These results suggest that neurons derived from P19 embryonal carcinoma cells have NMDA and metabotropic, but not AMPA/kainate receptors, which are linked to Ca2+-signaling mechanisms. These cells could provide a consistent and reproducible model with which to study neuronal differentiation, neurotoxicity, and glutamate receptor-signaling mechanisms.

Notes: Abstract: Activity of the stress protein, heme oxygenase-1 (hsp32; HO-1), produces carbon monoxide (CO), the potential messenger molecule for excitatory N-methyl-d-aspartate receptor-mediated events, in the hippocampus. Long-term stress caused by elevated adrenocorticoids induces pathological changes in CA1–CA3 neurons, of the hippocampus; the adrenal hormones also exacerbate damage from stress. In rats chronically treated with corticosterone, we examined expression of HO-1 and its response to thermal stress in the hippocampus. An unprecedented appearance of scattered immunoreactive astrocytes marked the molecular layer of the hippocampus in corticosterone-treated rats. Steroid treatment showed no discernible effect on whole-brain HO-1 mRNA. When these rats were subjected to hyperthermia, neurons in the CA1–CA3 area, including pyramidal cells, exhibited intense immunoreactivity for the oxygenase and a pronounced increase (∼10-fold) in number. HO-1 is essentially undetectable in this area when rats are exposed to chronic corticosterone alone or thermal stress by itself, or in control rats. In contrast, similar analysis of hilar neurons showed no apparent effect on either the number or relative intensity of HO-1-immunostained cells after treatment. Corticosterone treatment also intensified the stress response of cerebellum, including Purkinje cells and Bergmann glia in the molecular layer. In brain, despite a pronounced reduction in NO synthase activity in corticosterone-treated and/or heat-stressed animals, the level of cyclic GMP was not significantly reduced. These observations are consistent with the hypothesis that responsiveness to environmental stress of CA1–CA3 neurons brought about by chronic elevation in circulating adrenocorticoids results in an increased excitatory neuronal activity and eventual hippocampal degeneration. Moreover, these findings yield further support for a role of CO in the production of cyclic GMP in the brain.

Notes: Abstract Background and Aim of Study: The prevalence of end-stage congestive heart failure and limitation of clinical alternative treatments present the need for creative new solutions. Formation of a ventricle from skeletal muscle (SMV) has shown promise in the animal laboratory. Two modes of the SMV for cardiac assistance, the counterpulsation (CP-SMV) and the ventricular assist (VA-SMV), using the latissimus dorsi muscle were applied in a canine model. Ability to augment arterial pressure was assessed. The effect of stimulation delay on the degree of augmentation was also evaluated. Methods and Results: Thirty-five SMVs were connected in continuity with the bloodstream in the two modes: (1) CP-SMV (aorta-to-aorta) (n =12); and (2) VA-SMV (left ventricular [LV] apex-to-aorta) (n=23). In the CP-SMV mode, designed to simulate the intra-aortic balloon pump, the SMV was simply interposed into the path of the descending aorta (DAo) without prosthetic valves in either the inflow or the outflow conduit. In order to obligate blood flow through the SMV, the DAo was ligated between the two grafts. In the VA-SMV mode, the connection was made with valved conduits from the LV apex (inflow) to the ascending aorta (outflow) (n = 11) or to the DAo (n = 12). The ascending aorta (AAo) was also ligated proximal to the outflow conduit for the same reason of obligating blood flow through the SMV. The SMV was timed to contract in diastole in both the CP-SMV mode and the VA-SMV mode. In the VA-SMV mode, the average systolic pressure without stimulation was 101.6 ± 2.2 mmHg and with stimulation 118.21±4.78 mmHg (mean augmentation, 14.5±2.6 mmHg) (p 〈 0.01). In the CP-SMV mode, the average systolic pressure without stimulation was 97±32 mmHg and with stimulation, 122±26 mmHg (mean augmentation, 25±8.6 mmHg) (p 〈 0.001). We also extended earlier work on timing of stimulation of isolated SMV by evaluating the effect of stimulation delay on the degree of augmentation in continuity with the bloodstream with the SMV in the VA-SMV configuration. Delays of 50 msec to 225 msec were evaluated. SMV stimulation was via the thoracodorsal nerve at an amplitude of 1.5 V and a frequency of 25 Hz. The greatest augmentation occurred at a stimulation delay of 150 msec (p 〈 0.001). Conclusion: Both counterpulsation and assist configurations produced effective diastolic augmentation. Although diastolic augmentation occurred with all timing delays, the optimal delay was 150 msec. Complications in the survival animals include AAo problems, SMV rupture, respiratory insufficiency, intraoperative instability, and thrombosis (which occurred in 51% [18/35] of the animals). This high frequency of thrombosis in the canine model suggests the use of a less thrombogenic SMV lining, more aggressive or prolonged anticoagulation, or an alternative animal model.

Notes: . Programmed DNA rearrangements, including DNA degradation, characterize the development of the soma from the germline in a number of developmental systems. Pddl p (programmed DNA degradation 1 protein), a development-specific polypeptide in Tetrahymena, is enriched in developing macronuclei (anlagen) and has been implicated in DNA elimination and nucleolar biogenesis. Here, immunocytochemistry and fluorescent in situ hybridization (FISH) were employed to follow Pddl p and two nucleolar markers (Nopp52 and rDNA) during macronuclear development. Both Pdd 1p and Nopp52 localize to subnuclear structures, each of which resemble nucleoli. However, while true nucleoli form and persist during development, Pdd 1p-positive structures are only present for a brief period of macronuclear differentiation. Accordingly, two distinct organelles can be recognized in anlagen: (1) Pdd 1p-positive structures, which lack Nopp52 and rDNA, and (2) developing nucleoli which contain rDNA and Nopp52 but lack Pdd 1p. Taken together with recent data corroborating Pdd 1p's role in DNA elimination, we favor the hypothesis that Pdd 1p structures are unique, short-lived organelles, likely to function in programmed DNA degradation and not in nucleolar biogenesis.

Notes: The phonon-limited mobility of strained Si metal–oxide–semiconductor field-effect transistors (MOSFETs) fabricated on a SiGe substrate is investigated through theoretical calculations including two-dimensional quantization, and compared with the mobility of conventional (unstrained) Si MOSFETs. In order to match both the mobility of unstrained Si MOSFETs and the mobility enhancement in strained Si MOSFETs, it is necessary to increase the coupling of electrons in the two-dimensional gas with intervalley phonons, compared to the values used in conventional models. The mobility enhancement associated with strain in Si is attributed to the following two factors: the suppression of intervalley phonon scattering due to the strain-induced band splitting, and the decrease in the occupancy of the fourfold valleys which exhibit a lower mobility due to the stronger interaction with intervalley phonons. While the decrease in the averaged conductivity mass, caused by the decrease in the occupancy of the fourfold valleys, contributes to the mobility enhancement in bulk strained Si, it is not necessarily adequate to explain the mobility enhancement for two-dimensional electrons in strained Si. This is suggested by the fact that the mobility limited by intravalley acoustic phonon scattering, which is the dominant scattering mechanism, has almost the same value in the two- and the fourfold valleys, because the difference in the conductivity mass is compensated by differences in the inversion-layer thickness and the valley degeneracy. © 1996 American Institute of Physics.