Large Internet services companies like Google, Yahoo, and Facebook use the MapReduce programming model to process log data MapReduce is designed to work on data stored in a distributed filesystem like Hadoop's HDFS As a result, a number of log collection systems have been built to copy data into HDFS These systems often lack a unified approach to failure handling, with errors being handled separately by each piece of the collection, transport and processing pipeline

We argue for a unified approach, instead We present a system, called Chukwa, that embodies this approach Chukwa uses an end-to-end delivery model that can leverage local on-disk log files for reliability This approach also eases integration with legacy systems This architecture offers a choice of delivery models, making subsets of the collected data available promptly for clients that require it, while reliably storing a copy in HDFS We demonstrate that our system works correctly on a 200-node testbed and can collect in excess of 200 MB/sec of log data We supplement these measurements with a set of case studies describing real-world operational experience at several sites

/pdf/chukwa-a-system-for-reliable-large-scale-log-collection-x4n5spde4c.pdf

Chukwa: a system for reliable large-scale log collection

Alzheimer’s disease (AD) is characterized by deficits in learning and memory. A pathological feature of AD is the alterations in the number and size of synapses, axon length, dendritic complexity, and dendritic spine numbers in the hippocampus and prefrontal cortex. Treadmill exercise can enhance synaptic plasticity in mouse or rat models of stroke, ischemia, and dementia. The aim of this study was to examine the effects of treadmill exercise on learning and memory, and structural synaptic plasticity in 3×Tg-AD mice, a mouse model of AD. Here, we show that 12 weeks treadmill exercise beginning in three-month-old mice improves spatial working memory in six-month-old 3×Tg-AD mice, while non-exercise six-month-old 3×Tg-AD mice exhibited impaired spatial working memory. To investigate potential mechanisms for the treadmill exercise-induced improvement of spatial learning and memory, we examined structural synaptic plasticity in the hippocampus and prefrontal cortex of six-month-old 3×Tg-AD mice that had undergone 12 weeks of treadmill exercise. We found that treadmill exercise led to increases in synapse numbers, synaptic structural parameters, the expression of synaptophysin (Syn, a presynaptic marker), the axon length, dendritic complexity, and the number of dendritic spines in 3×Tg-AD mice and restored these parameters to similar levels of non-Tg control mice without treadmill exercise. In addition, treadmill exercise also improved these parameters in non-Tg control mice. Strengthening structural synaptic plasticity may represent a potential mechanism by which treadmill exercise prevents decline in spatial learning and memory and synapse loss in 3×Tg-AD mice.

/pdf/treadmill-exercise-prevents-decline-in-spatial-learning-and-2iwuq8va.pdf

Treadmill Exercise Prevents Decline in Spatial Learning and Memory in 3×Tg-AD Mice through Enhancement of Structural Synaptic Plasticity of the Hippocampus and Prefrontal Cortex

Deep learning based neuronal soma detection and counting for Alzheimer's disease analysis.

Sn–52In eutectic solder has gradually attracted much attention due to the feature of low melting temperature in recent years. However, Sn–52In solder may occur melting due to the severe Joule heating and causes serious reliability problems. This study mainly investigated the interfacial reaction of ball grid array (BGA) structure Cu/Sn–52In/Cu solder joints during electromigration with current densities of 0.5 × 104 A/cm2, 1.0 × 104 A/cm2 and 1.5 × 104 A/cm2 at 70 °C, 115 °C and 140 °C, respectively. Results show that during the solid-solid (S–S) electromigration and liquid-solid (L-S) electromigration process, respectively, both the In and Cu atoms on the cathode side diffuse to the anode side to participate in the interfacial reaction to form the intermetallic compounds (IMCs), which not only causes the dissolution of the Cu substrate on the cathode side, but also leads to the polarity effect in the growth of interfacial IMCs, i.e., the interfacial IMCs on the anode side is much thicker than that on the cathode side, and the higher the current density and temperature, the more obvious the polarity effect. In addition, with the increase of current density and temperature, the type of interfacial IMCs on the anode side changes from the initial Cu6(Sn,In)5 and Cu2In3Sn to Cu6(Sn,In)5 during S–S electromigration, while that changes from the initial Cu6(Sn,In)5 and Cu2In3Sn to the composition of Cu6(Sn,In)5 and Cu3(In,Sn) for L-S electromigration. 

Polarity effect of interfacial intermetallic compounds of BGA structure Cu/Sn–52In/Cu solder joints during electromigration

Spinal cord injury (SCI) is a progressive neurodegenerative disease in addition to a traumatic event. Cognitive dysfunction following SCI has been widely reported in patients and animal models. However, the neuroanatomical changes affecting cognitive function after SCI, as well as the mechanisms behind these changes, have so far remained elusive. Herein, we found that SCI accelerates oxidative stress damage of hippocampal neuronal mitochondria. Then, for the first time, we presented a three-dimensional morphological atlas of rat hippocampal neurons generated using a fluorescence Micro-Optical Sectioning Tomography system, a method that accurately identifies the spatial localization of neurons and trace neurites. We showed that the number of dendritic branches and dendritic length was decreased in late stage of SCI. Western blot and transmission electron microscopy analyses also showed a decrease in synaptic communication. In addition, a battery of behavioral tests in these animals revealed hippocampal based cognitive dysfunction, which could be attributed to changes in the dendritic complexity of hippocampal neurons. Taken together, these results suggested that mitochondrial abnormalities in hippocampal neurons induced the dendritic complexity reduction and cognitive decline following SCI. Our study highlights the neuroanatomical basis and importance of mitochondria in brain degeneration following SCI, which might contribute to propose new therapeutic strategies.

/pdf/hippocampal-mitochondrial-abnormalities-induced-the-1w1sn6b0.pdf

Hippocampal Mitochondrial Abnormalities Induced the Dendritic Complexity Reduction and Cognitive Decline in a Rat Model of Spinal Cord Injury

Alzheimer's disease (AD) is an irreversible, neurodegenerative disease that is characterized by memory impairment and executive dysfunction. However, the change of fine structure of neuronal morphology remains unclear in the AD model mouse. In this study, high-resolution mouse brain sectional images were scanned by Micro-Optical Sectioning Tomography (MOST) technology and reconstructed three-dimensionally to obtain the pyramidal neurons. The method of Sholl analysis was performed to analyze the neurons in the brains of 6- and 12-month-old AD mice. The results showed that dendritic complexity was not affected in the entorhinal cortex between 6-month-old mice and 12-month-old mice. The dendritic complexity had increased in the primary motor cortex and CA1 region of hippocampus of 12- month-old mice compared with 6-month-old mice. On the contrary, dendritic complexity in the prefrontal cortex was decreased significantly between 6-month-old and 12-month-old mice. To our knowledge, this is the first study to provide high-resolution brain images of triple transgenic AD mice for statistically analyzing neuronal dendrite complexity by MOST technology to reveal the morphological changes of neurons during AD progression.

Dendritic complexity change in the triple transgenic mouse model of Alzheimer's disease.

Growth mechanisms of intermetallic compounds and Bi-rich layer in ball grid array structure Cu/Sn-58Bi/Cu solder joints during solid–solid and liquid–solid electromigration

PCB-winding-based planar have been widely adopted for high-frequency, high-power-density, and high-efficiency power conversion. Due to the planarized structure of the magnetics, the position of the air gaps in a planar inductor dominates the flux distribution in the magnetic core, thus the core loss is closely related to the position of the air gaps. This paper thoroughly analyzes the flux in the magnetic core of a four-pole structure coupled inductor for a critical-mode (CRM) Buck converter and studies an optimized four-pole structure with improved air gap configuration to reduce the core loss, as well as the height of the inductor, and to improve its efficiency and power density. The influence mechanism of the air gap position on core loss is revealed, and a detailed optimal design of the studied structure is presented. To verify the effectiveness of the studied coupled inductor, a prototype with a height of 7mm, a power density of 800W/in3, and a peak efficiency of 99% is developed.

Magnetic Integration of Coupled-Inductor with Optimized Air-Gaps for A CRM Buck Converter

A Novel Optimization Method of Flow Channel Structure in Proton Exchange Membrane Fuel Cell Based on the Finite Data Mapping and Multi-Field Synergy Theory

Graphical Abstract Background: Liver disease (LD) is an important cause of morbidity and mortality for people with HIV (PWH). The molecular factors linked with LD in PWH are varied and incompletely characterized. We performed an epigenome-wide association study (EWAS) to identify associations between DNA methylation (DNAm) and biomarkers of liver function—aspartate transaminase, alanine transaminase, albumin, total bilirubin, platelet count, FIB-4 score, and APRI score—in male United States veterans with HIV. Methods: Blood samples and clinical data were obtained from 960 HIV-infected male PWH from the Veterans Aging Cohort Study. DNAm was assessed using the Illumina 450K or the EPIC 850K array in two mutually exclusive subsets. We performed a meta-analysis for each DNAm site measured by either platform. We also examined the associations between four measures of DNAm age acceleration (AA) and liver biomarkers. Results: Nine DNAm sites were positively associated with serum albumin in the meta-analysis of the EPIC and 450K EWAS after correcting for multiple testing. Four DNAm sites (cg16936953, cg18942579, cg01409343, and cg12054453), annotated within the TMEM49 and four of the remaining five sites (cg18181703, cg03546163, cg20995564, and cg23966214) annotated to SOCS3, FKBP5, ZEB2, and SAMD14 genes, respectively. The DNAm site, cg12992827, was not annotated to any known coding sequence. No significant associations were detected for the other six liver biomarkers. Higher PhenoAA was significantly associated with lower level of serum albumin (β = -0.007, p-value = 8.6 × 10–4, CI: -0.011116, -0.002884). Conclusion: We identified epigenetic associations of both individual DNAm sites and DNAm AA with liver function through serum albumin in men with HIV. Further replication analyses in independent cohorts are warranted to confirm the epigenetic mechanisms underlying liver function and LD in PWH.

Epigenome-wide association study of biomarkers of liver function identifies albumin-associated DNA methylation sites among male veterans with HIV

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