Optimization Modeling for Airlift Mobility

We describe a multi-period optimization model, implemented in GAMS, to help the U.S. Air Force improve logistical efficiency. It determines the maximum on-time throughput of cargo and passengers that can be transported within a given aircraft fleet over a given network, subject to appropriate physical and policy constraints. The model can be used to help answer questions about selecting airlift assets and about investing or divesting in airfield infrastructure

Phorbol 12-Myristate 13-Acetate Stimulates Lysophosphatidic Acid Secretion from Ovarian and Cervical Cancer Cells but Not From Breast or Leukemia Cells

Lysophosphatidic acid (LPA) is present in ascites from patients with ovarian cancer. It stimulates calcium release and growth of ovarian cancer cells bothin vitroandin vivo.Recently, we found that LPA levels were significantly elevated in plasma from patients with ovarian cancer and other gynecological cancers. In contrast, LPA levels were not elevated in patients with breast cancer and leukemias. In view of this, we investigated whether gynecological cancer cells could produce LPA. LPA was extracted from the supernatant of cells culturedin vitroand purified by thin layer chromatography. After hydrolysis and transmethylation, the fatty acid derivatives were analyzed by gas chromatography. We found that the phorbol ester, phorbol 12-myristate 13-acetate (PMA), significantly stimulated the production of LPA in ovarian and cervical cancer cells. In contrast, a small or negligible amount of LPA was produced in breast cancer and leukemia cells upon PMA stimulation. This cell type specificity correlates with our values of plasma LPA, suggesting that gynecological tumor cells may be an important source of the elevated LPA noted in the plasma of patients with these cancers. The cytosolic PLA2(cPLA2)/Ca2+-independent PLA2(iPLA2) inhibitor, AACOCF3, inhibited 75.6% PMA-stimulated LPA secretion in ovarian cancer cells, suggesting a cPLA2/iPLA2activity was involved in LPA production from ovarian cancer cells

Phorbol 12-Myristate 13-Acetate Stimulates Lysophosphatidic Acid Secretion from Ovarian and Cervical Cancer Cells but Not From Breast or Leukemia Cells

Lysophosphatidic acid (LPA) is present in ascites from patients with ovarian cancer. It stimulates calcium release and growth of ovarian cancer cells bothin vitroandin vivo.Recently, we found that LPA levels were significantly elevated in plasma from patients with ovarian cancer and other gynecological cancers. In contrast, LPA levels were not elevated in patients with breast cancer and leukemias. In view of this, we investigated whether gynecological cancer cells could produce LPA. LPA was extracted from the supernatant of cells culturedin vitroand purified by thin layer chromatography. After hydrolysis and transmethylation, the fatty acid derivatives were analyzed by gas chromatography. We found that the phorbol ester, phorbol 12-myristate 13-acetate (PMA), significantly stimulated the production of LPA in ovarian and cervical cancer cells. In contrast, a small or negligible amount of LPA was produced in breast cancer and leukemia cells upon PMA stimulation. This cell type specificity correlates with our values of plasma LPA, suggesting that gynecological tumor cells may be an important source of the elevated LPA noted in the plasma of patients with these cancers. The cytosolic PLA2(cPLA2)/Ca2+-independent PLA2(iPLA2) inhibitor, AACOCF3, inhibited 75.6% PMA-stimulated LPA secretion in ovarian cancer cells, suggesting a cPLA2/iPLA2activity was involved in LPA production from ovarian cancer cells

Will spin-relaxation times in molecular magnets permit quantum information processing?

Using X-band pulsed electron spin resonance, we report the intrinsic spin-lattice ($T_1$) and phase coherence ($T_2$) relaxation times in molecular nanomagnets for the first time. In Cr$_7M$ heterometallic wheels, with $M$ = Ni and Mn, phase coherence relaxation is dominated by the coupling of the electron spin to protons within the molecule. In deuterated samples $T_2$ reaches 3 $\mu$s at low temperatures, which is several orders of magnitude longer than the duration of spin manipulations, satisfying a prerequisite for the deployment of molecular nanomagnets in quantum information applications.Comment: 4 pages, 3 figures, in press at Physical Review Letter

MyD88-dependent interplay between myeloid and endothelial cells in the initiation and progression of obesity-associated inflammatory diseases.

Low-grade systemic inflammation is often associated with metabolic syndrome, which plays a critical role in the development of the obesity-associated inflammatory diseases, including insulin resistance and atherosclerosis. Here, we investigate how Toll-like receptor-MyD88 signaling in myeloid and endothelial cells coordinately participates in the initiation and progression of high fat diet-induced systemic inflammation and metabolic inflammatory diseases. MyD88 deficiency in myeloid cells inhibits macrophage recruitment to adipose tissue and their switch to an M1-like phenotype. This is accompanied by substantially reduced diet-induced systemic inflammation, insulin resistance, and atherosclerosis. MyD88 deficiency in endothelial cells results in a moderate reduction in diet-induced adipose macrophage infiltration and M1 polarization, selective insulin sensitivity in adipose tissue, and amelioration of spontaneous atherosclerosis. Both in vivo and ex vivo studies suggest that MyD88-dependent GM-CSF production from the endothelial cells might play a critical role in the initiation of obesity-associated inflammation and development of atherosclerosis by priming the monocytes in the adipose and arterial tissues to differentiate into M1-like inflammatory macrophages. Collectively, these results implicate a critical MyD88-dependent interplay between myeloid and endothelial cells in the initiation and progression of obesity-associated inflammatory diseases