Automorphisms of surfaces of general type with q>=2 acting trivially in cohomology

A compact complex manifold X is said to be rationally cohomologically rigidified if its automorphism group Aut(X) acts faithfully on the cohomology ring H*(X,Q). In this note, we prove that, surfaces of general type with irregularity q>2 are rationally cohomologically rigidified, and so are minimal surfaces S with q=2 unless K^2=8X. This answers a question of Fabrizio Catanese in part. As examples we give a complete classification of surfaces isogenous to a product with q=2 that are not rationally cohomologically rigidified. These surfaces turn out however to be rigidified.Comment: 18 pages; a remark and a closely relevant reference are adde

Cryptopleurine Targets NF-κB Pathway, Leading to Inhibition of Gene Products Associated with Cell Survival, Proliferation, Invasion, and Angiogenesis

Cryptopleurine, a phenanthroquinolizidine alkaloid, was known to exhibit anticancer activity; however, the underlying mechanism is poorly understood. Because the nuclear factor-κB (NF-κB) transcription factors control many physiological processes including inflammation, immunity, and development and progression of cancer, we investigated the effects of cryptopleurine on tumor necrosis factor alpha (TNF-α)-induced NF-κB activation pathway and on the expression of NF-κB-regulated gene products associated with many pathophysiological processes.MDA-MB231, MDA-MB435, MCF-7, HEK293, RAW264.7 and Hep3B cells were used to examine cryptopleurine's effect on the NF-κB activation pathway. Major assays were promoter-reporter gene assay, electrophoretic mobility shift assay (EMSA), in vitro immune complex kinase assay, real-time PCR, Western blot analysis, and Matrigel invasion assay. Experiments documenting cell proliferation and apoptosis were analyzed by MTT method and flow cytometry, respectively. The results indicated that cryptopleurine suppressed the NF-κB activation through the inhibition of IκB kinase (IKK) activation, thereby blocking the phosphorylation and degradation of the inhibitor of NF-κB alpha (IκBα) and the nuclear translocation and DNA-binding activity of p65. The suppression of NF-κB by cryptopleurine led to the down-regulation of gene products involved in inflammation, cell survival, proliferation, invasion, and angiogenesis.Our results show that cryptopleurine inhibited NF-κB activation pathway, which leads to inhibition of inflammation, proliferation, and invasion, as well as potentiation of apoptosis. Our findings provide a new insight into the molecular mechanisms and a potential application of cryptopleurine for inflammatory diseases as well as certain cancers associated with abnormal NF-κB activation

5-(1H-Tetra­zol-5-yl)-1H-indole monohydrate

In the title compound, C9H7N5·H2O, the inter­planar angles between the benzene and tetra­zole rings and between the benzene and imidazole rings are 8.71 (3) and 1.32 (2)°, respectively. In the crystal, strong N—H⋯N hydrogen bonds link the organic 5-(1H-tetra­zol-5-yl)-1H-indole mol­ecules into chains extended along the b axis. The chains are further inter­connected into layers parallel to (100) via strong O—H⋯N and N—H⋯O hydrogen bonds. Furthermore, the layers are inter­connected via strong O—H⋯N hydrogen bonds. Moreover, cohesion between the layers is provided by the π–π inter­actions between the imidazole, tetra­zole and benzene rings with centroid–centroid distances of 3.766 (2), 3.832 (2) and 3.733 (2) Å

On the strong laws for weighted sums of ρ∗-mixing random variables,”

Complete convergence is studied for linear statistics that are weighted sums of identically distributed ρ * -mixing random variables under a suitable moment condition. The results obtained generalize and complement some earlier results. A Marcinkiewicz-Zygmund-type strong law is also obtained

Ulinastatin attenuates oxidation, inflammation and neural apoptosis in the cerebral cortex of adult rats with ventricular fibrillation after cardiopulmonary resuscitation

OBJECTIVE: The role of Ulinastatin in neuronal injury after cardiopulmonary resuscitation has not been elucidated. We aim to evaluate the effects of Ulinastatin on inflammation, oxidation, and neuronal injury in the cerebral cortex after cardiopulmonary resuscitation. METHODS: Ventricular fibrillation was induced in 76 adult male Wistar rats for 6 min, after which cardiopulmonary resuscitation was initiated. After spontaneous circulation returned, the rats were split into two groups: the Ulinastatin 100,000 unit/kg group or the PBS-treated control group. Blood and cerebral cortex samples were obtained and compared at 2, 4, and 8 h after return of spontaneous circulation. The protein levels of tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6) were assayed using an enzyme-linked immunosorbent assay, and mRNA levels were quantified via real-time polymerase chain reaction. Myeloperoxidase and Malondialdehyde were measured by spectrophotometry. The translocation of nuclear factor-κB p65 was assayed by Western blot. The viable and apoptotic neurons were detected by Nissl and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL). RESULTS: Ulinastatin treatment decreased plasma levels of TNF-α and IL-6, expression of mRNA, and Myeloperoxidase and Malondialdehyde in the cerebral cortex. In addition, Ulinastatin attenuated the translocation of nuclear factor-κB p65 at 2, 4, and 8 hours after the return of spontaneous circulation. Ulinastatin increased the number of living neurons and decreased TUNEL-positive neuron numbers in the cortex at 72 h after the return of spontaneous circulation. CONCLUSIONS: Ulinastatin preserved neuronal survival and inhibited neuron apoptosis after the return of spontaneous circulation in Wistar rats via attenuation of the oxidative stress response and translocation of nuclear factor-κB p65 in the cortex. In addition, Ulinastatin decreased the production of TNF-α, IL-6, Myeloperoxidase, and Malondialdehyde

Super Yangian Double DY(gl(1∣1))DY( gl(1|1)) and Its Gauss Decomposition

We extend Yangian double to super (or graded) case and give its Drinfel'd generators realization by Gauss decomposition.Comment: 6 pages, Latex, no figure