A Mathematica script for harmonic oscillator nuclear matrix elements arising in semileptonic electroweak interactions

Semi-leptonic electroweak interactions in nuclei - such as \beta decay, \mu capture, charged- and neutral-current neutrino reactions, and electron scattering - are described by a set of multipole operators carrying definite parity and angular momentum, obtained by projection from the underlying nuclear charge and three-current operators. If these nuclear operators are approximated by their one-body forms and expanded in the nucleon velocity through order |\vec{p}|/M, where \vec{p} and M are the nucleon momentum and mass, a set of seven multipole operators is obtained. Nuclear structure calculations are often performed in a basis of Slater determinants formed from harmonic oscillator orbitals, a choice that allows translational invariance to be preserved. Harmonic-oscillator single-particle matrix elements of the multipole operators can be evaluated analytically and expressed in terms of finite polynomials in q^2, where q is the magnitude of the three-momentum transfer. While results for such matrix elements are available in tabular form, with certain restriction on quantum numbers, the task of determining the analytic form of a response function can still be quite tedious, requiring the folding of the tabulated matrix elements with the nuclear density matrix, and subsequent algebra to evaluate products of operators. Here we provide a Mathematica script for generating these matrix elements, which will allow users to carry out all such calculations by symbolic manipulation. This will eliminate the errors that may accompany hand calculations and speed the calculation of electroweak nuclear cross sections and rates. We illustrate the use of the new script by calculating the cross sections for charged- and neutral-current neutrino scattering in ^{12}C.Comment: 15 pages, 2 tables, Mathematica notebook included in the form of figures. Mathematica package and documentation available at http://www.int.washington.edu/users/lunardi/7o.htm. Replaced version has improved graphics; text unchange

Metastatic eccrine porocarcinoma: report of a case and review of the literature

Eccrine porocarcinoma (EPC) is a rare type of skin cancer arising from the intraepidermal portion of eccrine sweat glands or acrosyringium, representing 0.005-0.01% of all cutaneous tumors. About 20% of EPC will recur and about 20% will metastasize to regional lymph nodes. There is a mortality rate of 67% in patients with lymph node metastases. Although rare, the occurrence of distant metastases has been reported

Dichloroacetate reverses the hypoxic adaptation to bevacizumab and enhances its antitumor effects in mouse xenografts.

Inhibition of vascular endothelial growth factor increases response rates to chemotherapy and progression-free survival in glioblastoma. However, resistance invariably occurs, prompting the urgent need for identification of synergizing agents. One possible strategy is to understand tumor adaptation to microenvironmental changes induced by antiangiogenic drugs and test agents that exploit this process. We used an in vivo glioblastoma-derived xenograft model of tumor escape in presence of continuous treatment with bevacizumab. U87-MG or U118-MG cells were subcutaneously implanted into either BALB/c SCID or athymic nude mice. Bevacizumab was given by intraperitoneal injection every 3 days (2.5 mg/kg/dose) and/or dichloroacetate (DCA) was administered by oral gavage twice daily (50 mg/kg/dose) when tumor volumes reached 0.3 cm(3) and continued until tumors reached approximately 1.5-2.0 cm(3). Microarray analysis of resistant U87 tumors revealed coordinated changes at the level of metabolic genes, in particular, a widening gap between glycolysis and mitochondrial respiration. There was a highly significant difference between U87-MG-implanted athymic nude mice 1 week after drug treatment. By 2 weeks of treatment, bevacizumab and DCA together dramatically blocked tumor growth compared to either drug alone. Similar results were seen in athymic nude mice implanted with U118-MG cells. We demonstrate for the first time that reversal of the bevacizumab-induced shift in metabolism using DCA is detrimental to neoplastic growth in vivo. As DCA is viewed as a promising agent targeting tumor metabolism, our data establish the timely proof of concept that combining it with antiangiogenic therapy represents a potent antineoplastic strategy

Periodontal Ehlers-Danlos Syndrome Is Caused by Mutations in C1R and C1S, which Encode Subcomponents C1r and C1s of Complement

Periodontal Ehlers-Danlos syndrome (pEDS) is an autosomal-dominant disorder characterized by early-onset periodontitis leading to premature loss of teeth, joint hypermobility, and mild skin findings. A locus was mapped to an approximately 5.8 Mb region at 12p13.1 but no candidate gene was identified. In an international consortium we recruited 19 independent families comprising 107 individuals with pEDS to identify the locus, characterize the clinical details in those with defined genetic causes, and try to understand the physiological basis of the condition. In 17 of these families, we identified heterozygous missense or in-frame insertion/deletion mutations in C1R (15 families) or C1S (2 families), contiguous genes in the mapped locus that encode subunits C1r and C1s of the first component of the classical complement pathway. These two proteins form a heterotetramer that then combines with six C1q subunits. Pathogenic variants involve the subunit interfaces or inter-domain hinges of C1r and C1s and are associated with intracellular retention and mild endoplasmic reticulum enlargement. Clinical features of affected individuals in these families include rapidly progressing periodontitis with onset in the teens or childhood, a previously unrecognized lack of attached gingiva, pretibial hyperpigmentation, skin and vascular fragility, easy bruising, and variable musculoskeletal symptoms. Our findings open a connection between the inflammatory classical complement pathway and connective tissue homeostasis

Liver dendritic cells present bacterial antigens and produce cytokines upon Salmonella encounter.

The capacity of murine liver dendritic cells (DC) to present bacterial Ags and produce cytokines after encounter with Salmonella was studied. Freshly isolated, nonparenchymal liver CD11c(+) cells had heterogeneous expression of MHC class II and CD11b and a low level of CD40 and CD86 expression. Characterization of liver DC subsets revealed that CD8alpha(-)CD4(-) double negative cells constituted the majority of liver CD11c(+) ( approximately 85%) with few cells expressing CD8alpha or CD4. Flow cytometry analysis of freshly isolated CD11c(+) cells enriched from the liver and cocultured with Salmonella expressing green fluorescent protein (GFP) showed that CD11c(+) MHC class II(high) cells had a greater capacity to internalize Salmonella relative to CD11c(+) MHC class II(low) cells. Moreover, both CD8alpha(-) and CD8alpha(+) liver DC internalized bacteria with similar efficiency after both in vitro and in vivo infection. CD11c(+) cells enriched from the liver could also process Salmonella for peptide presentation on MHC class I and class II to primary, Ag-specific T cells after internalization requiring actin cytoskeletal rearrangements. Flow cytometry analysis of liver CD11c(+) cells infected with Salmonella expressing GFP showed that both CD8alpha(-) and CD8alpha(+) DC produced IL-12p40 and TNF-alpha. The majority of cytokine-positive cells did not contain bacteria (GFP(-)) whereas only a minor fraction of cytokine-positive cells were GFP(+). Furthermore, only approximately 30-50% of liver DC containing bacteria (GFP(+)) produced cytokines. Thus, liver DC can internalize and process Salmonella for peptide presentation to CD4(+) and CD8(+) T cells and elicit proinflammatory cytokine production upon Salmonella encounter, suggesting that DC in the liver may contribute to immunity against hepatotropic bacteria

Elevated neutrophil, macrophage and dendritic cell numbers characterize immune cell populations in mice chronically infected with Salmonella.

The present study characterizes immune cell populations in mice chronically infected with Salmonella. Mice were characterized as chronically infected based on persistently high titers of Salmonella-reactive immunoglobulins in the serum > 6 months after a single oral dose of S. enterica serovar Typhimurium. These mice had a visibly enlarged spleen but not liver, while both organs harbored bacteria and had increased total cellularity up to 11 months post-infection. Flow cytometry analysis revealed significantly elevated numbers of neutrophils, dendritic cells (DC) and macrophages in the spleen of chronically infected mice. In contrast, no significant increase in the absolute number of T and B cells was apparent in the spleen and DX5(+) cells, which includes NK cells, some NK T cells and possibly some activated T cells, appears to correlate with chronic Salmonella infection in the liver but not the spleen. In situ analyses revealed that CD8(alpha)(+) DC and Gr-1(+) cells (neutrophils) increased in the splenic red pulp of chronically infected mice. In addition,,Gr-1(+) cells, CD68(+) cells and CD11c(+) cells (DC), the latter lacking detectable staining for CD8 alpha and CD4, accumulated around hepatic blood vessels and in the hepatic network in the liver of mice chronically harboring bacteria. These data provide insight into changes that occur within immune cell populations, most notably within splenic and hepatic phagocytic cell populations, that accompany chronic infection with the intracellular bacterium Salmonella. (c) 2006 Elsevier Ltd. All rights reserved

High-latitude ocean and sea ice surface fluxes: Challenges for climate research

Polar regions have great sensitivity to climate forcing; however, understanding of the physical processes coupling the atmosphere and ocean in these regions is relatively poor. Improving our knowledge of high-latitude surface fluxes will require close collaboration among meteorologists, oceanographers, ice physicists, and climatologists, and between observationalists and modelers, as well as new combinations of in situ measurements and satellite remote sensing. This article describes the deficiencies in our current state of knowledge about air–sea surface fluxes in high latitudes, the sensitivity of various high-latitude processes to changes in surface fluxes, and the scientific requirements for surface fluxes at high latitudes. We inventory the reasons, both logistical and physical, why existing flux products do not meet these requirements. Capturing an annual cycle in fluxes requires that instruments function through long periods of cold polar darkness, often far from support services, in situations subject to icing and extreme wave conditions. Furthermore, frequent cloud cover at high latitudes restricts the availability of surface and atmospheric data from visible and infrared (IR) wavelength satellite sensors. Recommendations are made for improving high-latitude fluxes, including 1) acquiring more in situ observations, 2) developing improved satellite-flux-observing capabilities, 3) making observations and flux products more accessible, and 4) encouraging flux intercomparisons