On the spatial behaviors of local mass transfer coefficients over idealized two-dimensional urban street canyons

ASI 1: Urban Climate for Human Comfort, 5-6 Dec 2011 ; ASI 2: Urban Climate and Air Pollution, 7-8 Dec 2011 ; ASI 3: Climate Change and Urban Design , 9-10 Dec 201

Protein tyrosine phosphatase non-receptor 21 (PTPN21) contributes to Elk-1 dependent NRG3 transcription in mice cortical neuron model

Oral Presentations: Session 2 - Healthy Aging and Chinese Medicine: 2.1

A 1-V24-GHz 17.5-mW phase-locked loop in a 0.18-mu m CMOS process

A 1-V 24-GHz 17.5-mW fully integrated phase-locked loop employing a transformer-feedback voltage-controlled oscillator and a stacked divide-by-2 frequency divider for low voltage and low power is presented. Implemented in a 0.18-mu m CMOS process and operated at 24 GHz with a IN supply, the PLL measures in-band phase noise of -106.3 dBc at a frequency offset of 100 kHz and out-of-band phase noise of -119.1 dBc/Hz at a frequency offset of 10 MHz. The PLL dissipates 17.5 mW and occupies a core area of 0.55 mm(2)

An Akt/hypoxia-inducible factor-1α/platelet-derived growth factor-BB autocrine loop mediates hypoxia-induced chemoresistance in liver cancer cells and tumorigenic hepatic progenitor cells

Purpose: The goals of the present study were to investigate the mechanism of hypoxia-mediated chemoresistance in liver cancer cells and tumorigenic hepatic progenitor (oval) cells and to determine whether disrupting an Akt/hypoxia-inducible factor-1α (HIF-1α)/platelet-derived growth factor (PDGF)-BB autocrine loop can enhance chemotherapeutic efficacy in hypoxia. Experimental Design: Five hepatocellular carcinoma (HCC) cell lines and two hepatic progenitor cell lines were treated in vitro with cisplatin under both normoxic and hypoxic conditions. To generate ischemic hypoxia for tumor cells in vivo, hepatic artery ligation was applied to an orthotopic HCC model. Cisplatin and YC1, which is a HIF-1α inhibitor, were administered by portal vein and intratumoral injections, respectively. Results: Cell viability was higher under hypoxic than normoxic conditions. HIF-1α and Akt were up-regulated under hypoxic conditions, forming an autocrine signaling loop with PDGF-BB. Akt/HIF-1α/PDGF-BB signaling regulated Akt to confer cisplatin resistance to HCC cell lines in vitro. This autocrine signaling loop also contributed to chemoresistance in the tumorigenic hepatic progenitor cell line PIL2 under hypoxic conditions but not in the nontumorigenic cell line PIL4. In an orthotopic HCC model, combining blockade of HIF-1α activity with ischemic hypoxia significantly enhanced the efficacy of chemotherapy, leading to suppression of tumor growth and prolongation of animal survival. Conclusion: Blockade of Akt/HIF-1α/PDGF-BB autocrine signaling could enhance the chemosensitivity of liver cancer cells and tumorigenic hepatic progenitor cells under hypoxic conditions and thus provide an effective therapeutic strategy for HCC. © 2009 American Association for Cancer Research.link_to_subscribed_fulltex

Regulation of NRG3 neurotrophic factor causes instigation on neuritic elongation and surviral by a novel phosphatase PTPN21

Conference Theme: Phosphosignalin

Amyloid pathology in spinal cord of the transgenic Alzheimer's disease mice is correlated to the corticospinal tract pathway

The transgenic TgCRND8 mouse is widely used as an animal model of Alzheimer's disease (AD) and exhibits an early onset of senile plaque pathogenesis in the brain. Here we report that TgCRND8 mice also have amyloid-beta (Abeta) neuropathology in spinal cord. TgCRND8 mice began to show obvious Abeta deposition in both gray matter of dorsal horn and white matter in the central part of dorsal column of the spinal cord at 10 months of age onward. Further experiments showed that the distribution of Abeta deposition in the spinal cord corresponds to the corticospinal tract pathway and its projection regions in TgCRND8 mice. We hypothesized that neurons in the sensorimotor cortex is the source of the Abeta peptide deposited in the spinal cord of these mice. To test the hypothesis, we ablated the sensorimotor cortex to interrupt connections between the sensorimotor cortex and spinal cord. We found that Abeta burden was significantly reduced in the denervated side compared to the contralateral side. Our results suggest that the sensorimotor cortex might be the primary source of Abeta in spinal cord of TgCRND8 mice. This is consistent with the observation that the sensorimotor cortex is one region particularly vulnerable during the progression of AD. The characteristics of Abeta distribution in TgCRND8 mice suggest that there are other ways related to the formation of Abeta plaques in addition to the terminal and synaptic release of Abeta