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QUESTIONS: Plant facilitation often dominates over competition in stressful environments. However, to our knowledge few studies have examined plant facilitation within the context of herbivore pressure. Herbivory‐induced is a classic example of indirect facilitation. For example, in the temperate steppe region of Inner Mongolia, China, the intensive grazing by domestic animals has induced widespread grassland degradation. Here, we ask whether such long‐term overgrazing leads to facilitation in plants. LOCATION: Xilingol steppe region, Inner Mongolia, China. METHODS: We examined the spatial structure of three dominant plant species, including two species that are palatable to sheep (Leymus chinensis and Agropyron michnoi) and one that is unpalatable (Stipa grandis). We examined whether the spatial aggregation of these three species provided evidence for facilitation by comparing their spatial patterns along a recovery gradient: high grazing pressure (HG), an eight‐years grazing exclusion (early‐stage recovery from grazing; ER), and a 21‐years grazing exclusion (late‐stage recovery; LR). To accomplish this, we used the bivariate pair‐correlation function, g₁₂(r), to assess the spatial association between unpalatable and palatable species. A positive spatial association indicates that facilitation dominates over competition (or dispersal limitation, habitat heterogeneity). We used a null model to assess the significance of spatial associations. Furthermore, we evaluated intraspecific spatial aggregation with the g₁₁(r) by combining to three null models at fine spatial scales. RESULTS: The spatial association between palatable and unpalatable species suggests a hump‐shaped relationship along the gradient of the grazing exclusion time. Specifically, Leymus chinensis and Stipa grandis showed a neutral, positive and negative association across the three stages of natural recovery from 21 years of grazing exclusion to current grazing. Similarly, Agropyron michnoi and Stipa grandis showed a negative, very positive and positive spatial association along the same gradient. Moreover, intraspecific spatial aggregation was higher in the current grazing treatment than in the grazing exclusion treatment. This was particularly true at the finest spatial scales (i.e.

In the current study, we explored the impact of Tudor-staphylococcal nuclease (SN) on obesity induced by a high-fat diet (HFD) in mice, because the functional involvement of Tudor-SN in lipid metabolism in vivo is unknown. HFD-transgenic (Tg) mice exhibited reductions in hepatic steatosis and systemic insulin resistance. There was no difference in hepatic lipid accumulation between chow-fed wild-type (WT) and chow-fed Tg mice; consistently, no difference in activation of the lipogenic pathway was detected. Overactivation of hepatic nuclear sterol regulatory element-binding protein (nSrebp2)-2, the central regulator of cholesterol metabolic proteins, was observed in HFD-Tg livers along with improved cholesterol homeostasis, but no such changes were observed in HFD-WT livers. Consistent results were observed in vitro in α-mouse liver 12 cells treated with palmitate mimicking the HFD state. In addition, global gene analysis indicated that various downstream targets of nSrebp2, were up-regulated in HFD-Tg livers. Moreover, HFD-WT mice displayed islet hypertrophy and suppression of glucose-induced insulin secretion from islets, whereas HFD-Tg mice had normal pancreatic islets. This finding suggests that the improved pancreatic metabolism of HFD-Tg mice is related to the systemic effect of insulin resistance, not to the autonomous influence of pancreatic cells. Tudor-SN is likely to be a key regulator for ameliorating HFD-induced hepatic steatosis and systemic insulin resistance in vivo.-Wang, X., Xin, L., Duan, Z., Zuo, Z., Wang, Y., Ren, Y., Zhang, W., Sun, X., Liu, X., Ge, L., Yang, X., Yao, Z., Yang, J. Global Tudor-SN transgenic mice are protected from obesity-induced hepatic steatosis and insulin resistance.

IL-4 activates STAT6 and causes the subsequent up-regulation of Ig heavy chain germline Ige via chromatin remodeling involved in B lymphocytes development. STAT6 acts as a molecular switch to regulate the higher-order chromatin remodeling via dynamically orchestrating co-activators (CBP/Tudor-SN) and co-repressors (HDAC1/PSF). Here, we demonstrated that STAT6/Tudor-SN/PSF form a complex, balancing the acetylation and deacetylation states to co-regulate IL-4/STAT6 gene transcription. In addition, we confirmed that IL-4 treatment increased the HATs activity in Ramos cells. As "active" markers, the expression of H3K9ac and H3K27ac increased after treatment with IL-4. However, transcriptional repressors such as H3K9me3 and H3K27me3 decreased in response to IL-4 stimulation. Moreover, IL-4 treatment enhanced H3 acetylation at the Ige promoter regions. Our results revealed that the Ige gene transcription is regulated by histone modifications in the IL-4/STAT6 pathway. The study will provide novel insights into the pathogenesis of allergic diseases.

Tudor-SN is a multifunctional protein that is highly expressed in multiple cancers including breast cancer. Tudor-SN, as a component in RNA-induced splicing complex, was recently reported to regulate gene expression in a microRNA (miRNA)-dependent manner, such as let-7, miR-34a and miR-221. However, how Tudor-SN is associated with cancer development still remains largely elusive. In the present study, we explored the role of Tudor-SN in breast cancer. Stable knockdown of endogenous Tudor-SN, performed on the breast cancer cell line MDA-MB-231 by small hairpin RNA expression vectors, suppressed the in vitro migration and invasion ability of the metastatic breast cancer cell line. Interestingly, we found Tudor-SN as a miRNA regulator according to microarray analysis, and further identified that Tudor-SN negatively regulated the expression of miR-127, and consequently increased the expression of the proto-oncogene BCL6 which was a convincing target of miR-127. Moreover, overexpression of miR-127 reduced the in vitro migration and proliferation ability of breast cancer cell MDA-MB-231. Collectively, our results suggested a novel mechanism that Tudor-SN promoted metastasis and proliferation of breast cancer cells via downregulating the miR-127 expression. Anat Rec, 296:1842–1849, 2013. © 2013 Wiley Periodicals, Inc.

Recent studies have shown that mast cells are involved in pathophysiologic processes of chronic inflammation. However, little is known about the distribution of mast cells in nasal polyps, which is a chronic inflammatory disease of the upper airways. Biopsy specimens from patients with nasal polyps (n = 20) and control patients without nasal polyps (n = 8) were included in this study. The distribution of mast cells in nasal polyps was determined by immunohistochemistry. Meanwhile, we detected the expression of chemokines (CCL5, CCL11, CX3CL1, IL-8, IL-6) in the epithelial cells of normal nasal mucosa and nasal polyps. In addition, the expression of these chemokines was investigated by western bolting in airway epithelial cells line (A549 cells) under inflammatory condition. Mast cells migrated toward intraepithelium in nasal polyps and the expression of chemokines (CCL5, CCL11, CX3CL1, IL-8) was up-regulated in the epithelial cells of nasal polyps compared with normal nasal mucosa. The expression of chemokines was also up-regulated in A549 cells after Lipopolysaccharide (LPS)-treatment for 3 hr and 6 hr. Our findings showed that mast cells migrate toward intraepithelium in nasal polyps and the overexpression of chemokines (CCL5, CCL11, CX3CL1, IL-8) suggested that they might be responsible for mast cells migration. It implies that mast cell play potential roles in the development of nasal polyps.

Nasal polyposis is a chronic inflammatory disease of the nasal mucosa. The etiology and the mechanisms of formation of nasal polyps are still not clear. Interleukin (IL)-18 is a novel proinflammatory cytokine that plays important roles in regulating immune inflammatory responses. However, the presence of IL-18 in human nasal mucosa and its roles in the inflammatory process of nasal polyps has not been studied yet. In this study, it was the first time to investigate the expression of IL-18 in human nasal mucosa and nasal polyps, and its potential function in the formation of nasal polyps. Surgical samples were analyzed by Western blot and immunohistochemistry to evaluate the expression and location of IL-18, and its correlated cytokines, IL-4, and IFN-γ. Furthermore, the airway epithelial cell line, A549, was used to investigate the mutual regulation of IFN-γ, IL-4, and IL-18. IFN-γ, IL-4, and IL-18 were all highly expressed in the epithelial cells, submucosal glands, and infiltrating inflammatory cells in the nasal polyp tissues, comparing with the control samples. Especially, the expression of IL-18 was upregulated significantly in nasal polyp tissues compared with control tissues. In addition, IL-18 was expressed in A549 cells in response to lipopolysaccharide and IL-4. Our data suggest that nasal epithelial cells are involved in the pathogenesis of nasal polyps formation and potentially via the secretion of IL-18, which is likely to play important roles in the formation of nasal polyps.

The family of STAT proteins consists of seven members that mediate highly specific functions in cytokine signaling. STAT6 is a critical regulator of transcription for interleukin-4 (IL-4)-induced genes. Activation of gene expression involves recruitment of coactivator proteins that function as bridging factors connecting sequence-specific transcription factors to the basal transcription machinery, and as chromatin-modifying enzymes. In this report, we show that the coacitivator p100 protein can interact with STAT6 through its SN domain both in vivo and in vitro, resulting in enhancement of STAT6-mediated gene transcriptional acitivation. Consistent with our previous reports, we identified intracellular localization of p100 and STAT-6 by confocal microscopy examined in response to IL-4. Moreover, in consideration of STAT molecules sharing significant homology in structure and function, we detected whether p100 can associate with STAT-1. In conclusion, this study found no evidence that p100 functions as a transcriptional coactivator for STAT1-dependent gene regulation. Anat Rec, 2010. © 2010 Wiley-Liss, Inc.

There is a burgeoning demand for polyolefin based fibrous membranes with antibacterial properties due to the increasing awareness about recyclable materials for air and water purification. This paper presents a systematic study on the development of dual component, polypropylene (PP), and high density polyethylene (HDPE) fibrous membranes based on a continuous coextrusion and multiplication manufacturing technique. Chlorhexidine dihydrochloride (CHDH), an organic low molecular weight antibacterial additive, is melt-compounded to impart antibacterial characteristics to the fibrous membranes. The PP/HDPE membranes are hydrophobic and possess 77% porosity, whereas inclusion of CHDH increases the porosity to 91% and the surface area increases almost twofold. In addition, the membranes possess a mean flow pore size of 7 μm. ATR-FTIR study on the PP/CHDH/HDPE membranes indicate the presence of CHDH on the fiber surface, which imparts antibacterial character to the membrane. Investigations carried out on the CHDH containing PP/HDPE fibrous membranes using E. Coli indicate that the presence of CHDH on the fiber surface results in a bacterial growth inhibition zone on solid growth media. In addition, quantitative studies result in the complete reduction of colony forming units after 4 h of contact time.