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Interleukin (IL)-1 beta has been reported to be a marker of shorter survival in gastric and colorectal adenocarcinoma. In the present study, we examined the potential role and prognostic value of IL-1 beta in esophageal squamous cell carcinoma (SCC). Human esophageal SCC cell line, CE81T, was selected for cellular and animal experiments, in which biological changes after experimental manipulation of IL-1 beta signaling were explored, including tumor growth, invasion capacity, and the sensitivity to treatment. Moreover, 147 esophageal SCC samples were analyzed using immunohistochemical staining to correlate the expression of IL-1 beta with clinical outcome. Our data revealed that IL-1 beta was significantly overexpressed both at mRNA and protein levels in cancer specimens compared to nonmalignant tissues. When IL-1 beta signaling was blocked, tumor growth, invasion ability, and treatment resistance were attenuated. Activation of NF-kappa B, increase of E2-EPF ubiquitin carrier protein and subsequent epithelial-mesenchymal transition might be the underlying mechanisms of the more aggressive tumor growth in IL-1 beta-positive esophageal cancer. The immunochemistry findings indicate that positivity staining of IL-1 beta correlated significantly with higher clinical stage, lower response rate to concurrent chemoradiotherapy (CCRT), and higher recurrence rate after curative treatment. Moreover, IL-1 beta was a significant predictor of survival in patients undergoing surgical intervention or definite CCRT. In conclusion, IL-1 beta is significantly linked to poor prognosis for patients with esophageal cancer and may be a promising molecular target for therapeutic intervention for esophageal SCC. [ABSTRACT FROM AUTHOR]

Abstract  We consider a C 1 smooth surface with prescribed p (or H)-mean curvature in the 3-dimensional Heisenberg group. Assuming only the prescribed p-mean curvature $${H\in C^{0},}$$ we show that any characteristic curve is C 2 smooth and its (line) curvature equals  − H in the nonsingular domain. By introducing characteristic coordinates and invoking the jump formulas along characteristic curves, we can prove that the Legendrian (or horizontal) normal gains one more derivative. Therefore the seed curves are C 2 smooth. We also obtain the uniqueness of characteristic and seed curves passing through a common point under some mild conditions, respectively. These results can be applied to more general situations. [ABSTRACT FROM AUTHOR]

The ubiquitin proteasome pathway has been implicated in carcinogenesis. However, the role of E2-EPF ubiquitin carrier protein (UCP) in esophageal cancer remains relatively unstudied. In the study, we examined the mRNA level of circulating tumor cells from 60 esophageal cancer patients by membrane arrays consisting of a panel of potential markers including UCP, compared to 40 normal populations. The predictive capacity of UCP was also assessed by immunohistochemical staining of a retrospective series of 84 biopsied esophageal squamous cell carcinomas in relation to clinical outcome. In addition, we studied in vitro biological changes including tumor growth, metastatic capacity, and the sensitivity to irradiation and cisplatin, after experimental manipulation of UCP expression in esophageal cancer cells. By the data of 25-gene membrane array analysis, UCP was the only factor significantly associated with the extent of tumor burden in esophageal cancer patients. Our immunochemistry findings further indicate that UCP positivity was linked to poor response to neoadjuvant therapy and worse survival. In cell culture, inhibited UCP significantly decrease tumor growth and the capacity for metastasis. The epithelial–mesenchymal transition (EMT) induced by VHL/HIF-1α-TGF-β1 pathway might be the underlying mechanism responsible to the more aggressive tumor growth in UCP-positive esophageal cancer. Our results suggest that UCP was significantly associated with poor prognosis of esophageal cancer and may be a new molecular target for therapeutic intervention for esophageal squamous cell carcinoma. [ABSTRACT FROM AUTHOR]

Abstract  Branson’s Q-curvature is now recognized as a fundamental quantity in conformal geometry. We outline its construction and present its basic properties. [ABSTRACT FROM AUTHOR]

Abstract.  In this paper we develop a bubble tree structure for a degenerating class of Riemannian metrics satisfying some global conformal bounds on compact manifolds of dimension 4. Applying the bubble tree structure, we establish a gap theorem, a finiteness theorem for diffeomorphism type for this class, and make a comparison of the solutions of the σk equations on a degenerating family of Bach-flat metrics. [ABSTRACT FROM AUTHOR]

AbstractIn [3] we studiedp-mean curvature and the associatedp-minimal surfaces in the Heisenberg group from the viewpoint of PDE and differential geometry. In this paper, we look into the problem through the variational formulation. We study a generalizedp-area and associated (p-) minimizers in general dimensions. We prove the existence and investigate the uniqueness of minimizers. Since this is reduced to solving a degenerate elliptic equation, we need to consider the effect of the singular set and this requires a careful study. We define the notion of weak solution and prove that in a certain Sobolev space, a weak solution is a minimizer and vice versa. We also give many interesting examples in dimension 2. An intriguing point is that, in dimension 2, aC2-smooth solution from the PDE viewpoint may not be a minimizer. However, this statement is true for higher dimensions due to the relative smallness of the size of the singular set. [ABSTRACT FROM AUTHOR]

Delineating neurons that underlie complex behaviors is of fundamental interest. Using adeno-associated virus 2, we expressed the Drosophila allatostatin receptor in somatostatin (Sst)-expressing neurons in the preBötzinger Complex (preBötC). Rapid silencing of these neurons in awake rats induced a persistent apnea without any respiratory movements to rescue their breathing. We hypothesize that breathing requires preBötC Sst neurons and that their sudden depression can lead to serious, even fatal, respiratory failure. [ABSTRACT FROM AUTHOR]