Biola Hour Highlights, 1974 - 07

If I Were the Devil by Paul Harvey I Pledge Allegiance by Red Skelton Communicating the Gospel by Al Sanders Last Days: Perilous Times by Al Sanders The Revelation of Jesus Christ by Lloyd Anderson Panel Discussions with Richard Chase, Charles Feinberg, and Samuel Sutherlandhttps://digitalcommons.biola.edu/bhhs/1006/thumbnail.jp

Biola Hour Highlights, 1974 - 07

If I Were the Devil by Paul Harvey I Pledge Allegiance by Red Skelton Communicating the Gospel by Al Sanders Last Days: Perilous Times by Al Sanders The Revelation of Jesus Christ by Lloyd Anderson Panel Discussions with Richard Chase, Charles Feinberg, and Samuel Sutherlandhttps://digitalcommons.biola.edu/bhhs/1006/thumbnail.jp

Research on the strategy of multinational enterprises: Key approaches and new avenues

Over decades, research on multinational enterprises’ (MNEs) strategies has been anchored in internalization theory. Strongly grounded in transaction cost economics to explain foreign market entry, it hardly explains how MNEs can build and sustain a competitive advantage. Thus, this paper aims at understanding how the nature of strategic thinking has influenced the research in the field of MNEs’ strategy. A content analysis of 1116 papers was conducted. The intellectual structure and dynamics of research to date are provided, without losing sight of the key foundations of strategy and strategic management. The links between human capital and knowledge are the factors on which to underpin the explanation of the MNEs’ strategies and support the coevolving theory. This theory is a promising avenue of research under the umbrella of RBV and KBV approaches. The context-dependency of strategy implies that different contexts require different approaches. Accordingly, we provide insights for future research by combining main schools of strategy though

Dynamical Color Correlations in a SU(2)cSU(2)_c Quark Exchange Model of Nuclear Matter

The quark exchange model is a simple realization of an adiabatic approximation to the strong-coupling limit of Quantum Chromodynamics (QCD): the quarks always coalesce into the lowest energy set of flux tubes. Nuclear matter is thus modeled in terms of its quarks. We wish to study the correlations imposed by total wavefunction antisymmetry when color degrees of freedom are included. To begin with, we have considered one-dimensional matter with a $SU(2)$ color internal degree of freedom only. We proceed by constructing a totally antisymmetric, color singlet {\it Ansatz} characterized by a variational parameter $\lambda$ (which describes the length scale over which two quarks in the system are clustered into hadrons) and by performing a variational Monte Carlo calculation of the energy to optimize $\lambda$ for a fixed density. We calculate the $q-q$ correlation function as well, and discuss the qualitative differences between the system at low and high density.Comment: 32 pages in REVTeX, IU/NTC 93-28, FSU-SCRI-93-161. The postscript file, including 12 figures, is available via anonymous ftp from ftp.scri.fsu.edu in /pub/jorgep/magic.p

Two-dimensional superstrings and the supersymmetric matrix model

We present evidence that the supersymmetric matrix model of Marinari and Parisi represents the world-line theory of N unstable D-particles in type II superstring theory in two dimensions. This identification suggests that the matrix model gives a holographic description of superstrings in a two-dimensional black hole geometry.Comment: 22 pages, 2 figures; v2: corrected eqn 4.6; v3: corrected appendices and discussion of vacua, added ref

The Impact of the Fusarium Mycotoxin Deoxynivalenol on the Health and Performance of Broiler Chickens

The aim of the present experiment was to investigate the effects of feeding grains naturally contaminated with Fusarium mycotoxins on morphometric indices of jejunum and to follow the passage of deoxynivalenol (DON) through subsequent segments of the digestive tract of broilers. A total of 45 1-d-old broiler chickens (Ross 308 males) were randomly allotted to three dietary treatments (15 birds/treatment): (1) control diet; (2) diet contaminated with 1 mg DON/kg feed; (3) diet contaminated with 5 mg DON/kg feed for five weeks. None of the zootechnical traits (body weight, body weight gain, feed intake, and feed conversion) responded to increased DON levels in the diet. However, DON at both dietary levels (1 mg and 5 mg DON/kg feed) significantly altered the small intestinal morphology. In the jejunum, the villi were significantly (P < 0.01) shorter in both DON treated groups compared with the controls. Furthermore, the dietary inclusion of DON decreased (P < 0.05) the villus surface area in both DON treated groups. The absolute or relative organ weights (liver, heart, proventriculus, gizzard, small intestine, spleen, pancreas, colon, cecum, bursa of Fabricius and thymus) were not altered (P > 0.05) in broilers fed the diet containing DON compared with controls. DON and de-epoxy-DON (DOM-1) were analyzed in serum, bile, liver, feces and digesta from consecutive segments of the digestive tract (gizzard, cecum, and rectum). Concentrations of DON and its metabolite DOM-1 in serum, bile, and liver were lower than the detection limits of the applied liquid chromatography coupled with mass spectrometry (LC-MS/MS) method. Only about 10 to 12% and 6% of the ingested DON was recovered in gizzard and feces, irrespective of the dietary DON-concentration. However, the DON recovery in the cecum as percentage of DON-intake varied between 18 to 22% and was not influenced by dietary DON-concentration. Interestingly, in the present trial, DOM-1 did not appear in the large intestine and in feces. The results indicate that deepoxydation in the present study hardly occurred in the distal segments of the digestive tract, assuming that the complete de-epoxydation occurs in the proximal small intestine where the majority of the parent toxin is absorbed. In conclusion, diets with DON contamination below levels that induce a negative impact on performance could alter small intestinal morphology in broilers. Additionally, the results confirm that the majority of the ingested DON quickly disappears through the gastrointestinal tract

Sleep architecture as correlate and predictor of symptoms and impairment in inter-episode bipolar disorder: taking on the challenge of medication effects

This study was designed to clarify the association between inter-episode bipolar disorder (BD) and sleep architecture. Participants completed a baseline symptom and sleep assessment and, 3 months later, an assessment of symptoms and impairment. The effects of psychiatric medications on sleep architecture were also considered. Participants included 22 adults with BD I or II (inter-episode) and 22 non-psychiatric controls. The sleep assessment was conducted at the Sleep and Psychological Disorders Laboratory at the University of California, Berkeley. Follow-up assessments 3 months later were conducted over the phone. Results indicate that, at the sleep assessment, BD participants exhibited greater rapid eye movement sleep (REM) density than control participants with no other group differences in sleep architecture. Sleep architecture was not correlated with concurrent mood symptoms in either group. In the BD group, duration of the first REM period and slow-wave sleep (SWS) amount were positively correlated with manic symptoms and impairment at 3 months, while REM density was positively correlated with depressive symptoms and impairment at 3 months. The amount of Stage 2 sleep was negatively correlated with manic symptoms and impairment at 3 months. In contrast, for the control group, REM density was negatively correlated with impairment at 3 months. SWS and Stage 2 sleep were not correlated with symptoms or impairment. Study findings suggest that inter-episode REM sleep, SWS and Stage 2 sleep are correlated with future manic and depressive symptoms and impairment in BD. This is consistent with the proposition that sleep architecture may be a mechanism of illness maintenance in BD.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/79304/1/j.1365-2869.2010.00826.x.pd

Lepton Flavor Non-Conservation

In the present work we review the most prominent lepton flavor violating processes (\mu \ra e\gamma, \mu \ra 3e, $(\mu , e)$ conversion, $M-\bar M$ oscillations etc), in the context of unified gauge theories. Many currently fashionable extensions of the standard model are considered, such as: {\it i)} extensions of the fermion sector (right-handed neutrino); {\it ii)} minimal extensions involving additional Higgs scalars (more than one isodoublets, singly and doubly charged isosinglets, isotriplets with doubly charged members etc.); {\it iii)} supersymmetric or superstring inspired unified models emphasizing the implications of the renormalization group equations in the leptonic sector. Special attention is given to the experimentaly most interesting $(\mu - e)$ conversion in the presence of nuclei. The relevant nuclear aspects of the amplitudes are discussed in a number of fashionable nuclear models. The main features of the relevant experiments are also discussed, and detailed predictions of the above models are compared to the present experimental limits.Comment: (IOA-300/93, review article, 83p, 6 epsf figures , available upon request from [email protected])

RFXB and its splice variant RFXBSV mediate the antagonism between IFNγ and TGFβ on COL1A2 transcription in vascular smooth muscle cells

Cytokines secreted by infiltrating immune cells during atherogenesis modulate vascular remodeling. One exemplary event is the antagonism between transformed growth factor (TGF-β) and interferon gamma (IFN-γ) on the transcriptional control of type I collagen gene (COL1A2). Previously we have reported that IFN-γ up-regulates regulatory factor for X-box B (RFXB) to repress collagen transcription while down-regulates the expression of RFXBSV, a splice variant of RFXB that blocks collagen repression in fibroblasts. Here we demonstrate that TGF-β abrogated COL1A2 repression by IFN-γ through altering the relative expression of RFXB and RFXBSV. Unlike RFXB, RFXBSV did not bind to the collagen promoter and competed with RFXB for the co-repressor histone deacetylase 2 (HDAC2), limiting HDAC2 recruitment to the collagen transcription start site as evidenced by chromatin immunoprecipitation assays. Over-expression of RFXB by lentiviral infection in HASMCs enhanced HDAC2 enlistment, promoted histone deacetylation surrounding the collagen site by IFN-γ, and blocked the TGF-β antagonism, a pattern reversed by RFXBSV infection. On the contrary, silencing of RFXB, but not both RFXB and RFXBSV, expression promoted the TGF-β antagonism. Thus, we have identified a novel mechanism whereby TGF-β antagonizes the IFN-γ repression of collagen transcription in HASMCs and as such provided new insights into antiatherogenic strategies

VILIP-1 Downregulation in Non-Small Cell Lung Carcinomas: Mechanisms and Prediction of Survival

VILIP-1, a member of the neuronal Ca++ sensor protein family, acts as a tumor suppressor gene in an experimental animal model by inhibiting cell proliferation, adhesion and invasiveness of squamous cell carcinoma cells. Western Blot analysis of human tumor cells showed that VILIP-1 expression was undetectable in several types of human tumor cells, including 11 out of 12 non-small cell lung carcinoma (NSCLC) cell lines. The down-regulation of VILIP-1 was due to loss of VILIP-1 mRNA transcripts. Rearrangements, large gene deletions or mutations were not found. Hypermethylation of the VILIP-1 promoter played an important role in gene silencing. In most VILIP-1-silent cells the VILIP-1 promoter was methylated. In vitro methylation of the VILIP-1 promoter reduced its activity in a promoter-reporter assay. Transcriptional activity of endogenous VILIP-1 promoter was recovered by treatment with 5′-aza-2′-deoxycytidine (5′-Aza-dC). Trichostatin A (TSA), a histone deacetylase inhibitor, potently induced VILIP-1 expression, indicating that histone deacetylation is an additional mechanism of VILIP-1 silencing. TSA increased histone H3 and H4 acetylation in the region of the VILIP-1 promoter. Furthermore, statistical analysis of expression and promoter methylation (n = 150 primary NSCLC samples) showed a significant relationship between promoter methylation and protein expression downregulation as well as between survival and decreased or absent VILIP-1 expression in lung cancer tissues (p<0.0001). VILIP-1 expression is silenced by promoter hypermethylation and histone deacetylation in aggressive NSCLC cell lines and primary tumors and its clinical evaluation could have a role as a predictor of short-term survival in lung cancer patients