The Solomon effect in learning disabilities diagnosis: Can we learn from history?

The Individuals with Disabilities Act (Individuals with Disabilities Education Improvement Act; IDEIA, 2004) has been reauthorized, and new parameters for defining learning disabilities (LD) have been established that provide more flexibility for corresponding state and local regulations. The field now has a unique opportunity to shape the practice of LD diagnosis and should consider important conceptual, theoretical, empirical, economic, legal, and practical issues related to LD diagnosis. This article highlights five key recommendations for the diagnostic definition of learning disabilities: (1) the definition needs to be unambiguous; (2) it must be universally accepted across professions, researchers, and governmental entities; (3) it must incorporate clearly defined subtypes of learning disabilities; (4) it must be empirically supported; and (5) it must point to valid, reliable, and cost-effective procedures for the identification of children with and without learning disabilities. Consideration of these points may help the field to avoid repeating past mistakes and returning to the folly of poor LD diagnostic practice. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Timed excitatory conditioning under zero and negative contingencies.

Rats (rattus norvegicus) anticipated the arrival of a food pellet unconditioned stimulus (US) even when the conditioned stimulus (CS) signaled no overall change or a substantial decrease in the overall rate of US occurrence. Pellet USs were scheduled probabilistically in the intertrial interval at either an equivalent rate (Experiment 1) or a four times higher rate (Experiments 2 and 3) than in the CS, which included one fixed-time target US. Conditioning has been said to involve learning "whether" (contingency) the CS signals a change in the US, and if so, "when" (contiguity) the US is scheduled to arrive. Our results suggest that "when" trumps "whether," challenging the received view that a positive CS-US contingency is necessary for successful conditioning. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

The block to apoptosis in bovine two-cell embryos involves inhibition of caspase-9 activation and caspase-mediated DNA damage

The capacity of the preimplantation embryo to undergo apoptosis in response to external stimuli is developmentally regulated. Acquisition of apoptosis does not occur in the cow embryo until between the 8- and 16-cell stages. The purpose of the present experiments was to determine the mechanism by which apoptosis is blocked in the bovine two-cell embryo. Heat shock (41 degrees C for 15 h) did not increase activity of caspase-9 or group II caspases (caspase-2, -3, and -7) in two-cell embryos but did in day 5 embryos. Exposure of embryos to carbonyl cyanide 3-chlorophenylhydrazone (CCCP) to depolarize mitochondria resulted in activation of caspase-9 and group II caspases at both stages of development. For day 5 embryos, CCCP also increased the proportion of blastomeres that underwent DNA fragmentation as determined by the TUNEL assay. In contrast, CCCP did not increase TUNEL labeling when applied at the two-cell stage. In conclusion, failure of heat shock to increase caspase-9 and group II caspase activity in the two-cell embryo indicates that the signaling pathway leading to mitochondrial depolarization and caspase activation is inhibited at this stage of development. The fact that CCCP treatment of two-cell embryos induced caspase-9 and group II-caspase activity indicates that caspase activation is possible following mitochondrial depolarization. However, since CCCP did not increase TUNEL labeling of two-cell embryos, actions of group II-caspases to activate DNases is inhibited.     

Heat shock and tumor necrosis factor-alpha induce apoptosis in bovine preimplantation embryos through a caspase-9-dependent mechanism

Heat shock and tumor necrosis factor-alpha (TNF-alpha) induce apoptosis through different mechanisms, with heat shock acting to cause mitochondrial depolarization and caspase-9 activation, while TNF-alpha acts through a receptor-mediated process to activate caspase-8. In some cells, however, TNF-alpha can also cause mitochondrial depolarization and caspase-9 activation. In the present study, we tested the hypothesis that heat shock at 41 degrees C and TNF-alpha induce apoptosis in bovine preimplantation embryos through a caspase-9-dependent mechanism. Treatment of embryos with either heat shock (41 degrees C) or TNF-alpha increased the proportion of blastomeres that were TUNEL positive and the proportion of embryos exhibiting elevated caspase-9 activity. Furthermore, the caspase-9 inhibitor, z-LEHD-fmk, blocked the increase in TUNEL-positive nuclei caused by both heat shock and TNF-alpha. For embryos at day 6 after insemination, for example, the percent of blastomeres positive for TUNEL was 3.6% for control embryos, 11.1% for embryos cultured at 41 degrees C, and 15.1% for embryos cultured with 10 ng/ml TNF-alpha. In the presence of z-LEHD-fmk, the percent of cells positive for TUNEL was 3.7% for control embryos, 6.1% for embryos cultured at 41 degrees C, and 8% for embryos cultured with 10 ng/ml TNF-alpha. Although TNF-alpha did not cause a measurable increase in caspase-8 activity, there was a tendency (P = 0.07) for treatment of embryos with z-IETD-fmk, an inhibitor of caspase-8, to partly reduce the magnitude of the increase in TUNEL-positive cells caused by TNF-alpha. The percent of cells that were TUNEL positive was increased by TNF-alpha from 9.7 to 19.7% in the absence of inhibitor and from 13.0 to 15.6% in the presence of z-IETD-fmk. Results indicate that induction of apoptosis by both heat shock and TNF-alpha involve activation of caspase-9-dependent pathways. It is likely that TNF-alpha also activates apoptotic pathways involving caspase-8 but that the degree of activation is small and caspase-9-dependent pathways are required for full activation of apoptosis.     

Multiplexed, waveguide approach to magnetically assisted transport evanescent field fluoroassays

This paper, expanding upon the recently developed magnetically assisted transport evanescent field fluoroassays (MATEFFs), takes advantage of several innovations in order to successfully integrate a microfluidic platform and planar waveguide technology for exploitation of multiplexing advantages. In the current adaptation of MATEFFs, a multiple internal reflection element (waveguide) is created using a simple microscope slide and PDMS microfluidic architecture, allowing simultaneous detection of multiple samples. Furthermore, the magnetic beads are manipulated using a passive pumping technique and a simple external permanent magnet, thereby circumventing the need for electromagnetic fabrication or complicated architectures and equipment. Initial testing, optimization, and calibration were performed using a model sandwich immunoassay system for the detection of rabbit IgG, with which we demonstrate a linear dynamic range of 3 orders of magnitude and physiologically relevant detection limits of nanograms per milliliter. Further work employed a sandwich immunoassay for the detection of interleukin-4, a cytokine that promotes proliferation and differentiation of B cells, to demonstrate technique reproducibility with RSD values of 5% and reported LOD of 10 ng/mL. The use of harvesting magnetic beads resulted in assays with mass-sensing behavior. Using IgG as a model cross-reactant with the interleukin-4 system, we additionally illustrate technique selectivity and multiplexing capability. A DNA hybridization assay is carried out using magnetic bead-immobilized single-stranded DNA with hybridization detected via ethidium bromide intercalation, further establishing technique versatility.     

Barriers to the uptake of combined heat and power technology in the UK higher education sector

To achieve the carbon reduction targets set by the UK Higher Education Funding Council, universities in the UK are investigating a number of energy-efficient technologies including combined heat and power (CHP). However, the growth of the CHP technology in the higher education (HE) sector is slow and this may be because of barriers to implementation. Towards the end of 2011–2012, 59 of the 161 UK universities had installed CHP. The main objective of this study is to identify barriers which may be preventing the growth of CHP technology in the UK's HE sector. An online questionnaire was sent to the Energy Managers at all UK universities. The results reveal a range of barriers, with the most important being the following: lack of funds; site constraints; lack of incentives and lack of support from higher management.     

Copresence of High-Risk Human Papillomaviruses and Epstein–Barr Virus in Colorectal Cancer: A Tissue Microarray and Molecular Study from Lebanon

Colorectal cancer (CRC) is the third most common cause of cancer-related deaths worldwide. Human papillomaviruses (HPVs) and Epstein–Barr virus (EBV) have been reported to be present in different types of human cancers, including CRCs, where they can play a key role in the onset and/or progression of these cancers. Thus, we herein explored the prevalence of high-risk HPVs and EBV in a cohort of 94 CRC tissue samples and 13 colorectal normal tissues from the Lebanese population using polymerase chain reaction, immunohistochemistry, and tissue microarray methodologies. We found that high-risk HPVs are present in 64%, while EBV is present in 29% of our CRC samples. Additionally, our data showed that high-risk HPV types (16, 18, 35, 58, 51, 45, 52, 31, and 33) are the most frequent in CRC in the Lebanese cohort, respectively. Our data point out that HPVs and EBV are copresent in 28% of the samples. Thus, this study clearly suggests that high-risk HPVs and EBV are present/copresent in CRCs, where they could play an important role in colorectal carcinogenesis. Nevertheless, further investigations using a larger cohort are needed to elucidate the possible cooperation between these oncoviruses in the development of CRC.