What are the neural mechanisms underlying beauty based on objective parameters and beauty based on subjective social construction? This study scanned participants with fMRI while they performed aesthetic judgments on concrete pictographs and abstract oracle bone scripts. Behavioral results showed both pictographs and oracle bone scripts were judged to be more beautiful when they referred to beautiful objects and positive social meanings, respectively. Imaging results revealed regions associated with perceptual, cognitive, emotional and reward processing were commonly activated both in beautiful judgments of pictographs and oracle bone scripts. Moreover, stronger activations of orbitofrontal cortex (OFC) and motor-related areas were found in beautiful judgments of pictographs, whereas beautiful judgments of oracle bone scripts were associated with putamen activity, implying stronger aesthetic experience and embodied approaching for beauty were elicited by the pictographs. In contrast, only visual processing areas were activated in the judgments of ugly pictographs and negative oracle bone scripts. Results provide evidence that the sense of beauty is triggered by two processes: one based on the objective parameters of stimuli (embodied natural beauty) and the other based on the subjective social construction (social endowed beauty).

Suppressor of cytokine signaling 3 (SOCS3) is an important intracellular protein that inhibits cytokine signaling in numerous cell types and has been implicated in several inflammatory diseases. However, the expression and function of SOCS3 in osteoblasts are not known. In this study, we demonstrated that SOCS3 expression was transiently induced by LPS in osteoblasts, and apparently contributed to the inhibition of IL-6 induction by LPS treatment. We found that tyrosine 204 of the SOCS box, the SH2 domain, and the N-terminal kinase inhibitory region (KIR) of SOCS3 were all involved in its IL-6 inhibition. Furthermore, we demonstrated that CCAAT/enhancerbinding protein (C/EBP) ␤ was activated by LPS (increased DNA binding activity), and played a key role in LPS-induced IL-6 expression in osteoblasts. We further provided the evidence that SOCS3 functioned as a negative regulator for LPS response in osteoblasts by suppressing C/EBP␤ DNA binding activity. In addition, tyrosine 204 of the SOCS box, the SH2 domain, and the N-terminal kinase inhibitory region (KIR) of SOCS3 were all required for its C/EBP␤ inhibition. These findings suggest that SOCS3 by interfering with C/EBP␤ activation may have an important regulatory role during bone-associated inflammatory responses. SOCS3 belongs to the family of suppressors of cytokine signaling (SOCS)2 proteins, which is induced by a number of mediators, including LPS, TNF-␣, as well as IL-6 and IL-10 (1-3). SOCS3 has been shown to function as a proinflammatory mediator by suppressing IL-6-gp130 signaling, interfering with its ability to inhibit LPS signaling (4, 5). For example, mice lacking SOCS3 in macrophages and neutrophils are resistant to LPS-induced shock (4). In contrast, accumulating data suggest that SOCS3 may suppress inflammatory responses (6). Thus, the function of SOCS3 during inflammation seems to be dependent on the particular disease model used and cell type studied. Moreover, the precise role of SOCS3 in LPS responses remains enigmatic.The stimulation of Toll-like receptor (TLR) 4 by LPS plays a critical role in innate immune responses in mammals. Although most studies on LPS-induced inflammation and the ensuing tissue destruction have been focused on immune systems, recent studies demonstrate that osteoblasts also express functional TLR4, which may play an important role in the pathogenesis of LPS-mediated bone disorders (2,7,8). For example, LPS stimulates osteoblasts to secrete receptor activator of NF-B ligand (RANKL), IL-6, IL-1, TNF-␣, GM-CSF, and PGE 2 , each of which seems to to be involved in LPS-mediated bone resorption (9). Among these proinflammatory mediators, IL-6 regulation in bone is extremely important for tissue homeostasis. Inappropriate expression of IL-6 has been suggested to have an impact on the increase in bone resorption observed in several bone inflammatory diseases (10, 11). Stimulation of IL-6 mRNA synthesis by LPS in human osteoblasts has been suggested to occur through CD14, p38 MAPK, and MEK (12). Several transcription factors s...

Previous research has focused primarily on corporal punishment as a cause and adolescents' physical aggression as an outcome. However, there is a large gap in knowledge of the potentially bidirectional association and explanatory mechanism underlying the association between corporal punishment and physical aggression. The current study, using a longitudinal design across three time points (the fall semester of 7th grade, the fall of 8th grade, and the fall of 9th grade), aimed to a) examine the reciprocal processes between corporal punishment and physical aggression, and b) explore whether deviant peer affiliation may explain such reciprocal connections. Only adolescents participating in all the three time points were included in this study, resulting in a final sample of 342 adolescents (175 boys, 167 girls) who completed questionnaires regarding corporal punishment, deviant peer affiliation, and aggression. Gender, age and socioeconomic status were controlled for in the analyses. Autoregressive cross-lagged models showed that the results did not support the direct reciprocal effect between corporal punishment and physical aggression among Chinese adolescents. A direct longitudinal link from corporal punishment to physical aggression was found, however, the inverse association was not significant. Moreover, regarding the longitudinal underlying process, in one direction, corporal punishment at 7th grade predicted higher levels of deviant peer affiliation at 8th grade. In turn, higher deviant peer affiliation at 8th grade predicted increased physical aggression at 9th grade. At the same time, in the other direction, adolescent physical aggression at 7th grade significantly predicted deviant peer affiliation at 8th grade. In turn, higher deviant peer affiliation at 8th grade predicted decreased corporal punishment at 9th grade. Identifying the direct and underlying reciprocal processes between corporal punishment and adolescent physical aggression has important implications for an integrative framework of theory and prevention.

Ultraviolet light causes both acute and chronic changes in extracellular matrix. We sought to examine the effects of different ultraviolet wavelengths on expression of matrix-related genes in fibroblasts. We previously reported that tropoelastin gene expression in vivo decreases with acute ultraviolet B exposure, and interleukin-1 alpha-mediated upregulation of tropoelastin is blocked in vitro after ultraviolet B radiation. In this study, we found that only ultraviolet B, but not ultraviolet A or ultraviolet A1, blocked the ability of interleukin-1 alpha to stimulate tropoelastin expression in vitro. Ultraviolet B and interleukin-1 alpha synergistically increased tumor necrosis factor-alpha secretion by fibroblasts, a finding not seen with ultraviolet B alone nor with ultraviolet A or ultraviolet A1 combined with interleukin-1 alpha. Keratinocytes showed a similar ultraviolet B-specific induction of tumor necrosis factor-alpha production. Addition of tumor necrosis factor-alpha to cultured fibroblasts blocked interleukin-1 alpha-induced stimulation of tropoelastin message, and addition of anti-tumor necrosis factor-alpha antibodies restored the responsiveness of tropoelastin and collagen messages to exogenous interleukin-1 alpha after ultraviolet B exposure. We conclude that interleukin-1 alpha in combination specifically with ultraviolet B induces fibroblasts to secrete tumor necrosis factor-alpha, and that this ultraviolet B-specific induction of tumor necrosis factor-alpha secretion is responsible for effects of ultraviolet B on the expression of matrix-related genes in the skin.

No abstract

The insula is a region that integrates interoception and drug urges, but little is known about its role in behavioral addiction such as internet addiction. We investigated insula-based functional connectivity in participants with internet gaming disorder (IGD) and healthy controls (HC) using resting-state functional MRI. The right and left insula subregions (posterior, ventroanterior, and dorsoanterior) were used as seed regions in a connectivity analysis. Compared with the HC group, the IGD group showed decreased functional connectivity between left posterior insula and bilateral supplementary motor area and middle cingulated cortex, between right posterior insula and right superior frontal gyrus, and decreased functional integration between insular subregions. The finding of reduced functional connectivity between the interoception and the motor/executive control regions is interpreted to reflect reduced ability to inhibit motor responses to internet gaming or diminished executive control over craving for internet gaming in IGD. The results support the hypothesis that IGD is associated with altered insula-based network, similar to substance addiction such as smoking.

Kupffer cells (KCs) have been demonstrated to play a role in the regulation of intra-hepatic lipid metabolism through the synthesis and secretion of biologically active products. The involvement of KCs in the disturbance of lipid metabolism that induced by perfluorononanoic acid (PFNA), a known agonist of the peroxisome proliferator-activated receptor alpha (PPARα), was investigated in this study. Rats were exposed to PFNA or PFNA combined with gadolinium chloride, an inhibitor of KCs, for 14 days. PFNA exposure dose-dependently increased absolute and relative liver weights, induced triglyceride accumulation, up-regulated the expression of both SERBP-1c and PPARα, and stimulated the release of TNFα and IL-1β. Inactivation of KCs markedly lowered TNFα and IL-1β level, enhanced PFNA-induced expression of PPARα and its target genes, and reduced liver triglyceride levels. In vitro, PFNA-induced expression of PPARα in primary cultured hepatocytes was suppressed by recombinant rat TNFα and IL-1β. However, inhibition of the NF-κB pathway prevented this. Transient transfection and promoter analysis further revealed that these two cytokines and NF-κB were coordinately involved in the suppression of PPARα promoter activity. Our data demonstrate that TNFα and IL-1β released from KCs following PFNA exposure can suppress the expression of PPARα via NF-κB pathway, which partially contribute to the evident accumulation of triglycerides in rat liver.

In recent years, several studies have shown that Rhodiola rosea can enhance cellular immunity and humoral immune function in mice, and thus, it has become a research hotspot. However, its underlying mechanism of action has remained elusive. The present study investigated whether Rhodiola rosea was able to downregulate the expression of tumor necrosis factor-α-inducible protein 8-like 2 (TIPE2), thereby inhibiting the expression of apoptotic genes, attenuating T-lymphocyte apoptosis and improving immunity in septic mice. A mouse model of caecal ligation and puncture (CLP)-induced sepsis was established, and animals in the treatment group were pre-treated with an intraperitoneal injection of Rhodiola rosea extract, while animals in the control group and sham-operated group were injected with an equivalent amount of normal saline. TIPE2, B-cell lymphoma 2 (Bcl-2), Fas and Fas ligand (FasL) mRNA and protein levels in thymic T cells were determined using reverse transcription quantitative polymerase chain reaction and western blot analysis, respectively. Furthermore, the thymus T-lymphocyte apoptosis rate, thymus T-lymphocyte count and thymus T-lymphocyte sub-sets were assessed using flow cytometry. Levels of T-helper cell type 1 (Th1) cytokines [Interleukin (IL)-2, IL-12 and interferon (IFN)-γ] and Th2 cytokines (IL-4 and IL-10) were determined using ELISA. The results showed that, compared to that in the CLP group, the expression of TIPE2, Fas and FasL in the treatment group was significantly decreased, while the expression of Bcl-2 was increased (P<0.05). The thymus lymphocyte count in the CLP group was significantly higher compared with that in the treatment group (P<0.05). Furthermore, the apoptotic rate of thymus T-lymphocytes in the treatment group was significantly lower than that in the CLP group (P<0.05). In addition, treatment with Rhodiola rosea rescued decreased in the counts of the CD3+ T and CD4+ T sub-sets of thymus T lymphocytes in the CLP group (P<0.05), while not affecting the increased levels of Th2 cytokines (IL-4 and IL-10) in the CLP group compared with those in the control groups. In addition, the Th1 cytokines (IL-12, IL-2 and IFN-γ) were significantly increased (P<0.05) in the CLP group, and treatment with Rhodiola rosea led to further increases. The thymus index of septic mice treated with Rhodiola rosea as well as their survival rate were improved as compared with those in the CLP group. These findings suggested that Rhodiola rosea has protective effects against sepsis by decreasing apoptosis, increasing Th1 cytokines and enhancing the host’s immunity via the regulation of TIPE2 expression.