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The purpose of this study was to examine the effects of staff video self-monitoring (SM) training on the accuracy of delivering Discrete Trial Instruction (DTI) to students enrolled in a classroom for children with autism. Staff were trained to self-monitor a five-step DTI trial: (a) delivery of discriminative stimulus, (b) wait time for student response, (c) response-specific feedback, (d) immediacy of specific feedback, and (e) latency before delivery of next discriminative stimulus. The dependent measure was the accuracy of completing the five-step trial. Prior to intervention, staff were trained to criteria using videotapes of their teaching in scoring their DTI delivery. A multiple baseline design across staff was used to evaluate the effectiveness of SM. Results showed that video self-monitoring and self-evaluation increased the accuracy of DTI and, more specifically, the accuracy of managing the intertrial interval. (Contains 2 figures and 1 table.)

With the continued explosive growth of personalized websites, more and more public school administrators can expect to face situations in which inappropriate materials have been posted by a teacher, staff member or student. While failing to recognize employees' rights of free speech can result in legal liability, administrators also must be prepared to identify unprotected speech and determine when Internet postings are causing material disruptions or resulting in a flow of inappropriate materials into the school. In this article, based on the authors' legal representation of school districts, they suggest some approaches for dealing with such issues when they arise. In determining how to deal with such matters, consider first when websites and blogs can be legally monitored; when to actually monitor; how to notify employees of the intent to monitor; and whether any objectionable postings are legally protected or instead form a basis for discipline or discharge.

Research shows that a controlled pH environment helps to protect rat hepatocyte cells following reperfusion injury. Experiments using hepatocytes from male Sprague-Dawley rats show that intracellular mitochondrial permeability transition (MPT) is blocked by biochemical cyclosporin. Glycine has no such affect on the MPT. Viability of cultured hepatocytes at varying pH levels is reported.

Confocal microscopy was utilized to determine the biological significance of mitochondrial permeability transition (MPT) on the progression of oxidant injury in isolated rodent hepatocytes. The biphasic Oxidation of pyrimidine nucleotides and mitochondrial synthesis of reactive oxygen species (ROS) was induced in isolated hepatocytes by the administration of tert-butylhydroperoxide. However, attenuation of the second phase oxidation of reduced nicotinamide adenine dinucleotide phosphate and ROS synthesis inhibited the onset of MPT and cell death in hepatocytes.

ATP depletion in rat cells regulates hepatocyte cell death after the suppression of cellular ATP development. Glycolytic ATP development mediates the protective function of fructose against cyanide and digomycin toxicity. Mitochondrial depolarization does not influence the protective effect or the cell death in rat hepatocytes.

Reperfusion of ischemic myocardium, resulting in reoxygenation and reattainment of physiological pH levels, is attributed to intracellular pH and cytosolic free calcium (Ca2+), as observed in cardiac myocytes from neonated rats. Cellular injury is enhanced and the onset of tissue necrosis is triggered by reperfusion, prior to a crucial phase of ischemia. Artificially induced ischemia by pretreatment of myocytes with a contribution of 20mM 2-deoxyglucose and 2.5mM sodium cyanide (NaCN) exhibits a decrease in pH value, which attains a constant value below a pH of 6.2 and is accompanied by hypercontraction and little blebbing.

Cell killing, inhibitor-insensitive oxygen consumption and hydroperoxide formation were observed in rat hepatocytes after glycolysis and respiration were inhibited. Observations demonstrated that reactive oxygen species take active roles in cell killing during chemical hypoxia. Past studies indicate that myxothiazol reduces Q-cycle mediated ubisemiquinone formation which can react with molecules of oxygen to form superoxide. Decreased hepatocyte killing with myxothizol suggest that oxygen radical formation by complex III in mitochondria is involved in cell killing during hypoxia.