Energy Efficiency of Software Transactional Memory in a Heterogeneous Architecture

Hardware vendors make an important effort creating low-power CPUs that keep battery duration and durability above acceptable levels. In order to achieve this goal and provide good performance-energy for a wide variety of applications, ARM designed the big.LITTLE architecture. This heterogeneous multi-core architecture features two different types of cores: big cores oriented to performance and little cores, slower and aimed to save energy consumption. As all the cores have access to the same memory, multi-threaded applications must resort to some mutual exclusion mechanism to coordinate the access to shared data by the concurrent threads. Transactional Memory (TM) represents an optimistic approach for shared-memory synchronization. To take full advantage of the features offered by software TM, but also benefit from the characteristics of the heterogeneous big.LITTLE architectures, our focus is to propose TM solutions that take into account the power/performance requirements of the application and what it is offered by the architecture. In order to understand the current state-of-the-art and obtain useful information for future power-aware software TM solutions, we have performed an analysis of a popular TM library running on top of an ARM big.LITTLE processor. Experiments show, in general, better scalability for the LITTLE cores for most of the applications except for one, which requires the computing performance that the big cores offer.

Implication of GluR2 subunit of AMPA receptor in RGS14(414)-mediated memory enhancement

Ongoing quest for finding treatment against memory loss seen in aging and in many neurological and neurodegenerative diseases, so far has been unsuccessful and memory enhancers are seen as a potential remedy against this brain dysfunction. Recently, we showed that gene corresponding to a protein called regulator of G-protein signaling 14 of 414 amino acids (RGS14414) is a robust memory enhancer (Lopez-Aranda et al. 2009: Science). RGS14414-treatment in area V2 of visual cortex caused memory enhancement to such extent that it converted short-term object recognition memory (ORM) of 45min into long lasting long-term memory that could be traced even after many months. Now, through targeting of multiple receptors and molecules known to be involved in memory processing, we found that GluR2 subunit of AMPA receptor might be key to memory enhancement in RGS-animals. RGS14-animals showed a progressive increase in GluR2 protein expression while processing an object information which reached to highest level after 60min of object exposure, a time period required for conversion of short-term ORM into long-term memory in our laboratory set up. Normal rats could retain an object information in brain for 45min (short-term) and not for 60min. However, RGS-treated rats are able to retain the same information for 24h or longer (long-term). Therefore, highest expression of GluR2 subunit seen at 60min suggests that this protein might be key in memory enhancement and conversion to long-term memory in RGS-animals. In addition, we will also discuss the implication of Hebbian plasticity and interaction of brain circuits in memory enhancement.

Improvements in Hardware Transactional Memory for GPU Architectures

In the multi-core CPU world, transactional memory (TM)has emerged as an alternative to lock-based programming for thread synchronization. Recent research proposes the use of TM in GPU architectures, where a high number of computing threads, organized in SIMT fashion, requires an effective synchronization method. In contrast to CPUs, GPUs offer two memory spaces: global memory and local memory. The local memory space serves as a shared scratch-pad for a subset of the computing threads, and it is used by programmers to speed-up their applications thanks to its low latency. Prior work from the authors proposed a lightweight hardware TM (HTM) support based in the local memory, modifying the SIMT execution model and adding a conflict detection mechanism. An efficient implementation of these features is key in order to provide an effective synchronization mechanism at the local memory level. After a quick description of the main features of our HTM design for GPU local memory, in this work we gather together a number of proposals designed with the aim of improving those mechanisms with high impact on performance. Firstly, the SIMT execution model is modified to increase the parallelism of the application when transactions must be serialized in order to make forward progress. Secondly, the conflict detection mechanism is optimized depending on application characteristics, such us the read/write sets, the probability of conflict between transactions and the existence of read-only transactions. As these features can be present in hardware simultaneously, it is a task of the compiler and runtime to determine which ones are more important for a given application. This work includes a discussion on the analysis to be done in order to choose the best configuration solution.

RGS14 (414)-mediated prevention of an episodic memory loss: a study of molecular mechanism

A large proportion of human populations suffer memory impairments either caused by normal aging or afflicted by diverse neurological and neurodegenerative diseases. Memory enhancers and other drugs tested so far against memory loss have failed to produce therapeutic efficacy in clinical trials and thus, there is a need to find remedy for this mental disorder. In search for cure of memory loss, our laboratory discovered a robust memory enhancer called RGS14(414). A treatment in brain with its gene produces an enduring effect on memory that lasts for lifetime of rats. Therefore, current thesis work was designed to investigate whether RGS14(414) treatment can prevent memory loss and furthermore, explore through biological processes responsible for RGS-mediated memory enhancement. We found that RGS14(414) gene treatment prevented episodic memory loss in rodent models of normal aging and Alzheimer´s disease. A memory loss was observed in normal rats at 18 months of age; however, when they were treated with RGS14(414) gene at 3 months of age, they abrogated this deficit and their memory remained intact till the age of 22 months. In addition to normal aging rats, effect of memory enhancer treatment in mice model of Alzheimer´s disease (AD-mice) produced a similar effect. AD-mice subjected to treatment with RGS14(414) gene at the age of 2 months, a period when memory was intact, showed not only a prevention in memory loss observed at 4 months of age but also they were able to maintain normal memory after 6 months of the treatment. We posit that long-lasting effect on memory enhancement and prevention of memory loss mediated through RGS14(414) might be due to a permanent structural change caused by a surge in neuronal connections and enhanced neuronal remodeling, key processes for long-term memory formation. A neuronal arborization analysis of both pyramidal and non-pyramidal neurons in brain of RGS14(414)-treated rats exhibited robust rise in neurites outgrowth of both kind of cells, and an increment in number of branching from the apical dendrite of pyramidal neurons, reaching to almost three times of the control animals. To further understand of underlying mechanism by which RGS14(414) induces neuronal arborization, we investigated into neurotrophic factors. We observed that RGS14 treatment induces a selective increase in BDNF. Role of BDNF in neuronal arborization, as well as its implication in learning and memory processes is well described. In addition, our results showing a dynamic expression pattern of BDNF during ORM processing that overlapped with memory consolidation further support the idea of the implication of this neurotrophin in formation of long-term memory in RGS-animals. On the other hand, in studies of expression profiling of RGS-treated animals, we have demonstrated that 14-3-3ζ protein displays a coherent relationship to RGS-mediated ORM enhancement. Recent studies have demonstrated that the interaction of receptor for activated protein kinase 1 (RACK1) with 14-3-3ζ is essential for its nuclear translocation, where RACK1-14-3-3ζ complex binds at promotor IV region of BDNF and promotes an increase in BDNF gene transcription. These observations suggest that 14-3-3ζ might regulate the elevated level of BDNF seen in RGS14(414) gene treated animals. Therefore, it seems that RGS-mediated surge in 14-3-3ζ causes elevated BDNF synthesis needed for neuronal arborization and enhanced ORM. The prevention of memory loss might be mediated through a restoration in BDNF and 14-3-3ζ protein levels, which are significantly decreased in aging and Alzheimer’s disease. Additionally, our results demonstrate that RGS14(414) treatment could be a viable strategy against episodic memory loss.