Origin of the different conductive behavior in pentavalent-ion-doped anatase and rutile TiO2_2

The electronic properties of pentavalent-ion (Nb$^{5+}$, Ta$^{5+}$, and I$^{5+}$) doped anatase and rutile TiO$_2$ are studied using spin-polarized GGA+\emph{U} calculations. Our calculated results indicate that these two phases of TiO$_2$ exhibit different conductive behavior upon doping. For doped anatase TiO$_2$, some up-spin-polarized Ti 3\emph{d} states lie near the conduction band bottom and cross the Fermi level, showing an \emph{n}-type half-metallic character. For doped rutile TiO$_2$, the Fermi level is pinned between two up-spin-polarized Ti 3\emph{d} gap states, showing an insulating character. These results can account well for the experimental different electronic transport properties in Nb (Ta)-doped anatase and rutile TiO$_2$.Comment: 4 pages, 5 figure

Type I Interferon Production Enhances Susceptibility to Listeria monocytogenes Infection

Numerous bacterial products such as lipopolysaccharide potently induce type I interferons (IFNs); however, the contribution of this innate response to host defense against bacterial infection remains unclear. Although mice deficient in either IFN regulatory factor (IRF)3 or the type I IFN receptor (IFNAR)1 are highly susceptible to viral infection, we show that these mice exhibit a profound resistance to infection caused by the Gram-positive intracellular bacterium Listeria monocytogenes compared with wild-type controls. Furthermore, this enhanced bacterial clearance is accompanied by a block in L. monocytogenes–induced splenic apoptosis in IRF3- and IFNAR1-deficient mice. Thus, our results highlight the disparate roles of type I IFNs during bacterial versus viral infections and stress the importance of proper IFN modulation in host defense

Three distinct IL-2 signaling pathways mediated by bcl-2, c- myc, and lck cooperate in hematopoietic cell proliferation

Two interleukin-2 receptor-dependent signaling pathways have thus far been identified: the c-fos/c- jun induction pathway mediated by src family protein-tyrosine kinases and the c- myc induction pathway. Here, we provide evidence for the existence of a third, rapamycin-sensitive pathway, which- results in the induction of another proto-oncogene, bcl-2. In the hematopoietic cell line BAF-1303, the expression of any two of lckF505 (an active form of [56 lck ), Bcl-2, or c-Myc is sufficient to promote transit of the cell cycle, regardless of the activation state of the third pathway. We also provide evidence that epidermal growth factor receptor signaling may act through the same pathway that involves [56 lck . These studies demonstrate a novel approach to dissecting signaling pathways regulating cellular proliferation

The Role of Interleukin-converting Enzyme in Fas-mediated Apoptosis in HIV-1 Infection

Apoptosis of CD4 � lymphocytes is partially responsible for the depletion of these cells in HIV-infected individuals. CD4 � lymphocytes from HIV-1–infected patients express higher membrane levels of the Fas receptor, and are particularly susceptible to apoptosis after Fas triggering. IL-1�– converting enzyme (ICE) is a key enzyme of the apoptotic machinery involved in Fas-mediated apoptosis of normal lymphocytes. The role of ICE in mediating the increased susceptibility of CD4 � lymphocytes from HIV-1–infected patients to apoptosis has not been examined. In this study, we found that ICE mRNA was present in T cells from both HIV-1–infected patients and controls. Active ICE proteins, p10 and p20, were demonstrated by immunoblot in lymphocytes from HIV-1–infected patients and in normal lymphocyte

Cell cycle regulation of histone H4 gene transcription requires the oncogenic factor IRF-2

Histone genes display a peak in transcription in early S phase and are ideal models for cell cycle-regulated gene expression. We have previously shown that the transcription factor interferon regulatory factor 2 (IRF-2) can activate histone H4 gene expression. In this report we establish that a mouse histone H4 gene and its human homolog lose stringent cell cycle control in synchronized embryonic fibroblasts in which IRF-2 has been ablated. We also show that there are reduced mRNA levels of this endogenous mouse histone H4 gene in the IRF-2(-/-) cells. Strikingly, the overall mRNA level and cell cycle regulation of histone H4 transcription are restored when IRF-2 is reintroduced to these cells. IRF-2 is a negative regulator of the interferon response and has oncogenic potential, but little is known of the mechanism of these activities. Our results suggest that IRF-2 is an active player in E2F-independent cell cycle-regulated gene expression at the G1/S phase transition. IRF-2 was previously considered a passive antagonist to the tumor suppressor IRF-1 but can now join other oncogenic factors such as c-Myb and E2F1 that are predicted to mediate their transforming capabilities by actively regulating genes necessary for cell cycle progression