With the recent advent of 4G LTE networks, there has been increasing interest to better understand the performance and power characteristics, compared with 3G/WiFi networks. In this paper, we take one of the first steps in this direction.Using a publicly deployed tool we designed for Android called 4GTest attracting more than 3000 users within 2 months and extensive local experiments, we study the network performance of LTE networks and compare with other types of mobile networks. We observe LTE generally has significantly higher downlink and uplink throughput than 3G and even WiFi, with a median value of 13Mbps and 6Mbps, respectively. We develop the first empirically derived comprehensive power model of a commercial LTE network with less than 6% error rate and state transitions matching the specifications. Using a comprehensive data set consisting of 5-month traces of 20 smartphone users, we carefully investigate the energy usage in 3G, LTE, and WiFi networks and evaluate the impact of configuring LTE-related parameters. Despite several new power saving improvements, we find that LTE is as much as 23 times less power efficient compared with WiFi, and even less power efficient than 3G, based on the user traces and the long high power tail is found to be a key contributor. In addition, we perform case studies of several popular applications on Android in LTE and identify that the performance bottleneck for web-based applications lies less in the network, compared to our previous study in 3G [24]. Instead, the device's processing power, despite the significant improvement compared to our analysis two years ago, becomes more of a bottleneck.

No abstract

Web caching in mobile networks is critical due to the unprecedented cellular traffic growth that far exceeds the deployment of cellular infrastructures. Caching on handsets is particularly important as it eliminates all network-related overheads. We perform the first network-wide study of the redundant transfers caused by inefficient web caching on handsets, using a dataset collected from 3 million smartphone users of a large commercial cellular carrier, as well as another five-month-long trace contributed by 20 smartphone users. Our findings suggest that redundant transfers contribute 18% and 20% of the total HTTP traffic volume in the two datasets. Also they are responsible for 17% of the bytes, 7% of the radio energy consumption, 6% of the signaling load, and 9% of the radio resource utilization of all cellular data traffic in the second dataset. Most of such redundant transfers are caused by the smartphone web caching implementation that does not fully support or strictly follow the protocol specification, or by developers not fully utilizing the caching support provided by the libraries. This is further confirmed by our caching tests of 10 popular HTTP libraries and mobile browsers. Improving the cache implementation will bring considerable reduction of network traffic volume, cellular resource consumption, handset energy consumption, and user-perceived latency, benefiting both cellular carriers and customers.

No abstract

Parkinson's disease (PD) is a movement disorder resulting from nigrostriatal dopaminergic neurodegeneration. The impairment of mitochondrial function and dopamine synaptic transmission are involved in the pathogenesis of PD. Two mitochondrial inhibitors, 1-methyl-4-phenylpyridine (MPP(+)) and rotenone, have been used to induce dopaminergic neuronal death both in in vitro and in vivo models of PD. Because the uptake of MPP(+) is mediated by the dopamine transporter (DAT), we used a cell-permeable rotenone-induced PD model to investigate the role of DAT and dopamine D2 receptor (D2R) on dopaminergic neuronal loss. Rotenone subcutaneously infused for 14 days induced PD symptoms in rats, as indicated by reduced spontaneous locomotor activity (hypokinesis), loss of tyrosine hydroxylase (TH, a marker enzyme for dopamine neurons) immunoreactivity in the substantia nigra and striatum, obvious alpha-synuclein accumulation, downregulated DAT protein expression, and upregulated D2R expression. Interestingly, rotenone also caused significant noradrenergic neuronal loss in the locus coeruleus. Melatonin, an antioxidant, prevented nigrostriatal neurodegeneration and alpha-synuclein aggregation without affecting the rotenone-induced weight loss and hypokinesis. However, rotenone-induced hypokinesis was markedly reversed by the DAT antagonist nomifensine and body weight loss was attenuated by the D2R antagonist sulpiride. In addition, both antagonists significantly prevented the reduction of striatal TH or DAT immunoreactivity but not the loss of nigral TH- and DAT-immunopositive neurons. These results suggested that oxidative stress and DAT downregulation are involved in the rotenone-induced pathogenesis of nigrostriatal dopaminergic neurodegeneration, whereas D2R upregulation may simply represent a compensatory response.

Abbreviations used: BDNF, brain-derived neurotrophic growth factor; BSA, bovine serum albumin; DA, dopamine; FGF, fibroblast growth factor; GDNF, glial cell line-derived neurotrophic factor; MAP2, microtubule associated protein 2; MTT, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; PBS, phosphate-buffered saline; PD, Parkinson's disease; TH, tyrosine hydroxylase; TH-ir, TH-immunoreactive. AbstractOxidative stress and down-regulated trophic factors are involved in the pathogenesis of nigrostriatal dopamine(DA)rgic neurodegeneration in Parkinson's disease. Fibroblast growth factor 9 (FGF9) is a survival factor for various cell types; however, the effect of FGF9 on DA neurons has not been studied. The antioxidant melatonin protects DA neurons against neurotoxicity. We used MPP + to induce neuron death in vivo and in vitro and investigated the involvement of FGF9 in MPP + intoxication and melatonin protection. We found that MPP + in a dose-and time-dependent manner inhibited FGF9 mRNA and protein expression, and caused death in primary cortical neurons. Treating neurons in the substantia nigra and mesencephalic cell cultures with FGF9 protein inhibited the MPP + -induced cell death of DA neurons. Melatonin co-treatment attenuated MPP + -induced FGF9 down-regulation and DA neuronal apoptosis in vivo and in vitro. Co-treating DA neurons with melatonin and FGF9-neutralizing antibody prevented the protective effect of melatonin. In the absence of MPP + , the treatment of FGF9-neutralizing antibody-induced DA neuronal apoptosis whereas FGF9 protein reduced it indicating that endogenous FGF9 is a survival factor for DA neurons. We conclude that MPP + down-regulates FGF9 expression to cause DA neuron death and that the prevention of FGF9 down-regulation is involved in melatonin-provided neuroprotection.

Today's cellular systems operate under diverse resource constraints: limited frequency spectrum, network processing capability, and handset battery life. We consider a novel and important factor, handset screen status, i.e., whether the screen is on or off, which was ignored by previous approaches for optimizing cellular resource utilization. Based on analyzing real smartphone traffic collected from 20 users over five months, we find that off-screen traffic accounts for 58.5% of the total radio energy consumption although their traffic volume contribution is much smaller. Such unexpected results are attributed to the unique cellular resource management policy that is not well understood by developers, leading to cellularunfriendly mobile apps. We then make a further step by proposing screen-aware optimization, by leveraging the key observation that screen-off traffic is much more delay-tolerant than its screenon counterpart due to a lack of user interaction. Our proposal can better balance the key tradeoffs in cellular networks. It saves up to 60.92% of the network energy and reduces signaling and delay overhead by 25.33% and 30.59%, respectively.

The group I metabotropic glutamate receptor 5 (mGluR5) has been implicated in the pathology of various neurological disorders including schizophrenia, ADHD, and autism. mGluR5-dependent synaptic plasticity has been described at a variety of neural connections and its signaling has been implicated in several behaviors. These behaviors include locomotor reactivity to novel environment, sensorimotor gating, anxiety, and cognition. mGluR5 is expressed in glutamatergic neurons, inhibitory neurons, and glia in various brain regions. In this study, we show that deleting mGluR5 expression only in principal cortical neurons leads to defective cannabinoid receptor 1 (CB1R) dependent synaptic plasticity in the prefrontal cortex. These cortical glutamatergic mGluR5 knockout mice exhibit increased novelty-induced locomotion, and their locomotion can be further enhanced by treatment with the psychostimulant methylphenidate. Despite a modest reduction in repetitive behaviors, cortical glutamatergic mGluR5 knockout mice are normal in sensorimotor gating, anxiety, motor balance/learning and fear conditioning behaviors. These results show that mGluR5 signaling in cortical glutamatergic neurons is required for precisely modulating locomotor reactivity to a novel environment but not for sensorimotor gating, anxiety, motor coordination, several forms of learning or social interactions.