Maxwell quasinormal modes on a global monopole Schwarzschild-anti-de Sitter black hole with Robin boundary conditions

We generalize our previous studies on the Maxwell quasinormal modes around Schwarzschild-anti-de-Sitter black holes with Robin type vanishing energy flux boundary conditions, by adding a global monopole on the background. We first formulate the Maxwell equations both in the Regge-Wheeler-Zerilli and in the Teukolsky formalisms and derive, based on the vanishing energy flux principle, two boundary conditions in each formalism. The Maxwell equations are then solved analytically in pure anti-de Sitter spacetimes with a global monopole, and two different normal modes are obtained due to the existence of the monopole parameter. In the small black hole and low frequency approximations, the Maxwell quasinormal modes are solved perturbatively on top of normal modes by using an asymptotic matching method, while beyond the aforementioned approximation, the Maxwell quasinormal modes are obtained numerically. We analyze the Maxwell quasinormal spectrum by varying the angular momentum quantum number $\ell$, the overtone number $N$, and in particular, the monopole parameter $8\pi\eta^2$. We show explicitly, through calculating quasinormal frequencies with both boundary conditions, that the global monopole produces the repulsive force.Comment: 10 pages, 5 figures, to appear in EPJ

Consistently estimating graph statistics using Aggregated Relational Data

Aggregated Relational Data, known as ARD, capture information about a social network by asking about the number of connections between a person and a group with a particular characteristic, rather than asking about connections between each pair of individuals directly. Breza et al. (Forthcoming) and McCormick and Zheng (2015) relate ARD questions, consisting of survey items of the form "How many people with characteristic X do you know?" to parametric statistical models for complete graphs. In this paper, we propose criteria for consistent estimation of individual and graph level statistics from ARD data

A study on influential factors of occupant window-opening behavior in an office building in China

Occupants often perform many types of behavior in buildings to adjust the indoor thermal environment. In these types, opening/closing the windows, often regarded as window-opening behavior, is more commonly observed because of its convenience. It not only improves indoor air quality to satisfy occupants' requirement for indoor thermal comfort but also influences building energy consumption. To learn more about potential factors having effects on occupants' window-opening behavior, a field study was carried out in an office building within a university in Beijing. Window state (open/closed) for a total of 5 windows in 5 offices on the second floor in 285 days (9.5 months) were recorded daily. Potential factors, categorized as environmental and non-environmental ones, were subsequently identified with their impact on window-opening behavior through logistic regression and Pearson correlation approaches. The analytical results show that occupants' window-opening behavior is more strongly correlated to environmental factors, such as indoor and outdoor air temperatures, wind speed, relative humidity, outdoor PM2.5 concentrations, solar radiation, sunshine hours, in which air temperatures dominate the influence. While the non-environmental factors, i.e. seasonal change, time of day and personal preference, also affects the patterns of window-opening probability. This paper provides solid field data on occupant window opening behavior in China, with high resolutions and demonstrates the way in analyzing and predicting the probability of window-opening behavior. Its discussion into the potential impact factors shall be useful for further investigation of the relationship between building energy consumption and window-opening behavior

Shen-Yuan-Dan Capsule Attenuates Atherosclerosis and Foam Cell Formation by Enhancing Autophagy and Inhibiting the PI3K/Akt/mTORC1 Signaling Pathway

Background and Aim: The phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin complex 1 (mTORC1) signaling pathway plays a crucial role in autophagy and inflammation. Our previous studies demonstrated that Shen-Yuan-Dan Capsule (SYDC), a Chinese medicine used for treating angina pectoris, has anti-atherosclerotic and anti-inflammatory effects in mice. However, its effects on autophagy and the PI3K/Akt/mTORC1 signaling pathway remain unclear. This study aimed to explore the effects of SYDC on autophagy and PI3K/Akt/mTORC1 signaling in the apolipoprotein E knockout (ApoE−/−) mouse model and in macrophage-derived foam cells to delineate the underlying mechanism.Methods: After 6 weeks of high-fat diet, ApoE–/– mice were randomly grouped into control, Lipitor, low-SYDC (SYDC-L), middle-SYDC (SYDC-M), and high-SYDC (SYDC-H) groups (n = 10). The mice were intragastrically administered the respective treatment for 6 weeks. Murine RAW264.7 cells were stimulated with oxidized low-density lipoprotein (ox-LDL) (80 µg/ml) for 24 h and then pretreated with SYDC freeze-dried powder for another 24 h. Cells treated with SYDC were co-cultured for 24 h with LY294002, tricirbine, and rapamycin to investigate the effects on the PI3K/Akt/mTORC1 signaling pathway.Results: SYDC ameliorated blood lipid levels, reduced the atherosclerotic index and plaque areas in the aortic root in mice, and inhibited total cholesterol (TC) levels and cholinesterase (ChE)/TC ratios in ox-LDL stimulated macrophages. Moreover, SYDC up-regulated Beclin1 and LC3II/I proteins in mice and in the ox-LDL–stimulated macrophages. Moreover, SYDC inhibited AKT phosphorylation at Ser473 and mTOR phosphorylation at Ser2448 in mice and in ox-LDL–stimulated macrophages. Furthermore, SYDC’s inhibitory of ChE/TC ratios in ox-LDL–stimulated macrophages was not changed by selective inhibition of the PI3K/Akt/mTORC1 pathway.Conclusions: Our results highlight that SYDC treatment attenuates foam cell formation by promoting autophagy via inhibiting activation of the PI3K/Akt/mTORC1 signaling pathway. This study provides new insights into the molecular mechanism underlying SYDC’s therapeutic potential for treating atherosclerosis

Cortical morphological heterogeneity of schizophrenia and its relationship with glutamatergic receptor variations

Abstract Background Recent genetic evidence implicates glutamatergic-receptor variations in schizophrenia. Glutamatergic excess during early life in people with schizophrenia may cause excitotoxicity and produce structural deficits in the brain. Cortical thickness and gyrification are reduced in schizophrenia, but only a subgroup of patients exhibits such structural deficits. We delineate the structural variations among unaffected siblings and patients with schizophrenia and study the role of key glutamate-receptor polymorphisms on these variations. Methods Gaussian Mixture Model clustering was applied to the cortical thickness and gyrification data of 114 patients, 112 healthy controls, and 42 unaffected siblings to identify subgroups. The distribution of glutamate-receptor (GRM3, GRIN2A, and GRIA1) and voltage-gated calcium channel (CACNA1C) variations across the MRI-based subgroups was studied. The comparisons in clinical symptoms and cognition between patient subgroups were conducted. Results We observed a “hypogyric,” “impoverished-thickness,” and “supra-normal” subgroups of patients, with higher negative symptom burden and poorer verbal fluency in the hypogyric subgroup and notable functional deterioration in the impoverished-thickness subgroup. Compared to healthy subjects, the hypogyric subgroup had significant GRIN2A and GRM3 variations, the impoverished-thickness subgroup had CACNA1C variations while the supra-normal group had no differences. Conclusions Disrupted gyrification and thickness can be traced to the glutamatergic receptor and voltage-gated calcium channel dysfunction respectively in schizophrenia. This raises the question of whether MRI-based multimetric subtyping may be relevant for clinical trials of agents affecting the glutamatergic system

Inhibition of RhoA-Subfamily GTPases Suppresses Schwann Cell Proliferation Through Regulating AKT Pathway Rather Than ROCK Pathway

Inhibiting RhoA-subfamily GTPases by C3 transferase is widely recognized as a prospective strategy to enhance axonal regeneration. When C3 transferase is administered for treating the injured peripheral nerves, Schwann cells (SCs, important glial cells in peripheral nerve) are inevitably impacted and therefore SC bioeffects on nerve regeneration might be influenced. However, the potential role of C3 transferase on SCs remains elusive. Assessed by cell counting, EdU and water-soluble tetrazolium salt-1 (WST-1) assays as well as western blotting with PCNA antibody, herein we first found that CT04 (a cell permeable C3 transferase) treatment could significantly suppress SC proliferation. Unexpectedly, using Y27632 to inhibit ROCK (the well-accepted downstream signal molecule of RhoA subfamily) did not impact SC proliferation. Further studies indicated that CT04 could inactivate AKT pathway by altering the expression levels of phosphorylated AKT (p-AKT), PI3K and PTEN, while activating AKT pathway by IGF-1 or SC79 could reverse the inhibitory effect of CT04 on SC proliferation. Based on present data, we concluded that inhibition of RhoA-subfamily GTPases could suppress SC proliferation, and this effect is independent of conventional ROCK pathway but involves inactivation of AKT pathway