Energy-Efficient Optimization for Wireless Information and Power Transfer in Large-Scale MIMO Systems Employing Energy Beamforming

In this letter, we consider a large-scale multiple-input multiple-output (MIMO) system where the receiver should harvest energy from the transmitter by wireless power transfer to support its wireless information transmission. The energy beamforming in the large-scale MIMO system is utilized to address the challenging problem of long-distance wireless power transfer. Furthermore, considering the limitation of the power in such a system, this letter focuses on the maximization of the energy efficiency of information transmission (bit per Joule) while satisfying the quality-of-service (QoS) requirement, i.e. delay constraint, by jointly optimizing transfer duration and transmit power. By solving the optimization problem, we derive an energy-efficient resource allocation scheme. Numerical results validate the effectiveness of the proposed scheme.Comment: 4 pages, 3 figures. IEEE Wireless Communications Letters 201

Buying Products from Whom You Know: Personal Connections and Information Asymmetry in Supply Chain Relationships

This study investigates the role personal connections play in a crucial element of the supply chain—supplier selection. We find that the likelihood that a potential supplier (hereafter, a vendor) is selected to be an actual supplier (hereafter, supplier) increases when personal connections between executives of the vendor and the customer exist. The magnitude of the effect varies predictably across management ranks and positions and is stronger when information asymmetries between a vendor and a customer are high. Conditioning on the existence of a supply-chain partnership, a departure of a personally connected executive prompts the termination of the supply-chain relationship more often than a departure of an unconnected executive. Additional analyses show personal connections are associated with less restrictive procurement contracts and with improved customer performance after the formation of a supply-chain relationship. Overall, our study highlights the role of personal connections in reducing information asymmetry and improving operating efficiency in the supply chain

Deciphering the mechanism of PSORI-CM02 in suppressing keratinocyte proliferation through the mTOR/HK2/glycolysis axis

Hyperplasia of epidermal keratinocytes that depend on glycolysis is a new hallmark of psoriasis pathogenesis. Our previous studies demonstrated that PSORI-CM02 could halt the pathological progression of psoriasis by targeting inflammatory response and angiogenesis, but its effect(s) and mechanism(s) on proliferating keratinocytes remained unclear. In this study, we aim to identify components of PSORI-CM02 that are absorbed into the blood and to determine the effect(s) of PSORI-CM02 on keratinocyte proliferation and its molecular mechanism(s). We used the immortalized human epidermal keratinocyte cell line, HaCaT, as an in vitro model of proliferating keratinocytes and the imiquimod-induced psoriasis mouse (IMQ) as an in vivo model. Metabolite profiles of vehicle pharmaceutic serum (VPS), PSORI-CM02 pharmaceutic serum (PPS), and water extraction (PWE) were compared, and 23 components of PSORI-CM02 were identified that were absorbed into the blood of mice. Both PPS and PWE inhibited the proliferation of HaCaT cells and consequently reduced the expression of the proliferation marker ki67. Additionally, PPS and PWE reduced phosphorylation levels of mTOR pathway kinases. Seahorse experiments demonstrated that PPS significantly inhibited glycolysis, glycolytic capacity, and mitochondrial respiration, thus reducing ATP production in HaCaT cells. Upon treatments of PPS or PWE, hexokinase 2 (HK2) expression was significantly decreased, as observed from the set of glycolytic genes we screened. Finally, in the IMQ model, we observed that treatment with PSORI-CM02 or BPTES, an inhibitor of mTOR signaling, reduced hyperproliferation of epidermal keratinocytes, inhibited the expression of p-S6 and reduced the number of proliferating cell nuclear antigen (PCNA)-positive cells in lesioned skin. Taken together, we demonstrate that PSORI-CM02 has an anti-proliferative effect on psoriatic keratinocytes, at least in part, by inhibiting the mTOR/HK2/glycolysis axis

Grazing weakens N-addition effects on soil greenhouse gas emissions in a semi-arid grassland

Grazing and anthropogenic nitrogen (N) enrichment co-occur in most grassland ecosystems and may have substantial effects on production of soil greenhouse gases (GHGs). Although the individual effects of N addition and grazing on soil GHGs are well understood, their long-term interactive effects on grassland soil GHGs remain unclear. We conducted seven-year in situ measurement of three major GHGs in a long-term experiment comprising grazing (no, light, moderate, and heavy grazing intensity) and N-addition treatments (control, N addition: 10 g N m−2 year−1) in a semi-arid grassland, to determine the effects of N addition and grazing on GHGs. We found that moderate grazing reduced cumulative CO2 emissions by 10%–11% compared with no, light, and heavy grazing. Unusually, CH4 emissions from soils and N2O uptake were found in this semi-arid grassland. Soil CH4 uptake was markedly inhibited by moderate and heavy grazing. Relative to no grazing, grazing significantly reduced 60%–88% N2O uptake over seven years on average. Nitrogen addition alone increased cumulative CO2 emissions by 16% relative to control. An antagonistic effect between grazing and N addition was found on cumulative CO2 emissions, cumulative CH4 uptake, and global warming potential (GWP). Light grazing on this semi-arid grassland could offset 14% of the soil GHG emissions induced by N addition. Soil NO3 − -N was the most important factor controlling soil CO2 emissions and CH4 uptake, and soil pH was a major factor mediating soil N2O uptake or consumption. Our study highlights the importance that adjusting the grazing intensity of grassland is one of efficient strategies to mitigate GHGs emissions in the context of climate change

Inhibitory synapse deficits caused by familial α1 GABAA receptor mutations in epilepsy

Epilepsy is a spectrum of neurological disorders with many causal factors. The GABA type-A receptor (GABA(A)R) is a major genetic target for heritable human epilepsies. Here we examine the functional effects of three epilepsy causing mutations to the alpha 1 subunit (alpha 1(T10T), alpha 1(D192N) and alpha 1(A295D)) on inhibitory postsynaptic currents (IPSCs) mediated by the major synaptic GABA(A)R isoform, alpha 1 eta 2 gamma 2L. We employed a neuron - HEK293 cell heterosynapse preparation to record IPSCs mediated by mutant-containing GABA(A)Rs in isolation from other GABA(A)R isoforms. IPSCs were recorded in the presence of the anticonvulsant drugs, carbamazepine and midazolam, and at elevated temperatures (22, 37 and 40 degrees C) to gain insight into mechanisms of febrile seizures. The mutant subunits were also transfected into cultured cortical neurons to investigate changes in synapse formation and neuronal morphology using fluorescence microscopy. We found that IPSCs mediated by alpha 1(T10T)beta 2 gamma 2L, alpha 1(D192N)beta 2 gamma 2L GABA(A)Rs decayed faster than those mediated by alpha 1 beta 2 gamma 2L receptors. IPSCs mediated by alpha 1(D192N)beta 2 gamma 2L and alpha 1(A295D) beta 2 gamma 2L receptors also exhibited a heightened temperature sensitivity. In addition, the alpha 1(T10T)beta 2 gamma 2L GABA(A)Rs were refractory to modulation by carbamazepine or midazolam. In agreement with previous studies, we found that alpha 1(A295D)beta 2 gamma 2L GABA(A)Rs were retained intracellularly in HEK293 cells and neurons. However, pre-incubation with 100 nM suberanilohydroxamic acid (SAHA) induced alpha 1(A295D)beta 2 gamma 2L GABA(A)Rs to mediate IPSCs that were indistinguishable in magnitude and waveform from those mediated by alpha 1 beta 2 gamma 2L receptors. Finally, mutation specific changes to synaptic bouton size, synapse number and neurite branching were also observed. These results provide new insights into the mechanisms of epileptogenesis of alpha 1 epilepsy mutations and suggest possible leads for improving treatments for patients harbouring these mutations

CDC20 facilitates the proliferation of esophageal carcinoma cell by stabilizing NLRP3 expression

Background and purpose: Esophageal carcinoma (ESCA) is one of the malignant tumors with high mortality rate, and the underlying mechanism of its development is largely unknown. CDC20 plays an important role in tumorigenesis, and its dysregulated expression is closely related to tumor occurrence and development. The expression of CDC20 is increased in a variety of tumors, and knocking down CDC20 can inhibit tumor cell proliferation. NLRP3 is the main component of the inflammasome, and inflammasome is also closely related to tumor occurrence and development. Here, our study aimed to investigate whether CDC20 promotes the proliferation of ESCA cells through NLRP3 and its regulatory mechanism. Methods: The expression levels of CDC20 and NLRP3 genes in ESCA patients were analyzed using The Cancer Genome Atlas (TCGA) detabase and GTEx public database. We collected clinical and pathological data and tissues from 80 ESCA patients at the First Affiliated Hospital of Xinxiang Medical College, and detected the protein expression of NLRP3 in ESCA patients through immunohistochemistry staining. This study was approved by the Ethics Committee of the First Affiliated Hospital of Xinxiang Medical College (Number: EC-021-137). We studied the effects of knocking down CDC20 and NLRP3 gene on the proliferation ability of esophageal squamous cell carcinoma cells EC9706 and KYSE150 using short hairpin RNA (shRNA) technology. Co-immunoprecipitation (Co-IP), proteasome inhibitors and ubiquitination experiments were used to detect whether CDC20 interacts with NLRP3, and to elucidate whether CDC20 regulates NLRP3 expression through the ubiquitination pathway. This study was approved by the Ethics Committee of the First Affiliated Hospital of Xinxiang Medical College (Number: EC-021-137). Results: The TCGA database analysis showed that the expression levels of CDC20 and NLRP3 mRNA were significantly higher in the cancer tissues of ESCA patients than in the adjacent tissues. The immunohistochemistry results further showed that compared with adjacent tissues, the protein expression levels of CDC20 and NLRP3 were increased in ESCA tissues. Knocking down CDC20 and NLRP3 genes inhibited the proliferation of ESCA cells. Co-IP, proteasome inhibitors and ubiquitination experiments confirmed that CDC20 interacted with NLRP3 through its leucine-rich repeat (LRR), and CDC20 stabilized its expression by promoting NLRP3 ubiquitination. Conclusion: CDC20 and NLRP3 are upregulated in ESCA tissues, and CDC20 stabilizes their expression through ubiquitination of NLRP3, promoting ESCA cell proliferation. This suggests that CDC20 and NLRP3 may be potential diagnostic targets for ESCA