A diallel analysis of cellular membrane thermostability in common bean (Phaseolus vulgaris L.)

Call number: LD2668 .T4 1986 X8Master of ScienceHorticulture, Forestry, and Recreation Resource

A peculiar young eruptive star in the dark cloud Lynds 1340

We conducted a long-term optical photometric and spectroscopic monitoring of the strongly variable, accreting young sun-like star [KOS94] HA11, associated with the dark cloud Lynds 1340, that exhibited large amplitude (5-6 magnitudes in the I_C band) brightness variations on 2-3 years timescales, flat spectral energy distribution (SED), and extremely strong (300 < EW/Angstrom < 900) H alpha emission. In this Letter we describe the basic properties of the star, derived from our observations between 1999 and 2011, and put into context the observed phenomena. The observed variations in the emission spectra, near-infrared colors, and SED suggest that [KOS94] HA11 (spectral type: K7--M0) is an eruptive young star, possibly similar in nature to V1647 Ori: its large-scale photometric variations are governed by variable accretion rate, associated with variations in the inner disk structure. The star recently has undergone strong and rapid brightness variations, thus its further observations may offer a rare opportunity for studying structural and chemical rearrangements of the inner disk, induced by variable central luminosity.Comment: 15 pages, 4 figures, 1 table; accepted by ApJ

Loss of ATF3 exacerbates liver damage through the activation of mTOR/p70S6K/ HIF-1α signaling pathway in liver inflammatory injury.

Activating transcription factor 3 (ATF3) is a stress-induced transcription factor that plays important roles in regulating immune and metabolic homeostasis. Activation of the mechanistic target of rapamycin (mTOR) and hypoxia-inducible factor (HIF) transcription factors are crucial for the regulation of immune cell function. Here, we investigated the mechanism by which the ATF3/mTOR/HIF-1 axis regulates immune responses in a liver ischemia/reperfusion injury (IRI) model. Deletion of ATF3 exacerbated liver damage, as evidenced by increased levels of serum ALT, intrahepatic macrophage/neutrophil trafficking, hepatocellular apoptosis, and the upregulation of pro-inflammatory mediators. ATF3 deficiency promoted mTOR and p70S6K phosphorylation, activated high mobility group box 1 (HMGB1) and TLR4, inhibited prolyl-hydroxylase 1 (PHD1), and increased HIF-1α activity, leading to Foxp3 downregulation and RORγt and IL-17A upregulation in IRI livers. Blocking mTOR or p70S6K in ATF3 knockout (KO) mice or bone marrow-derived macrophages (BMMs) downregulated HMGB1, TLR4, and HIF-1α and upregulated PHD1, increasing Foxp3 and decreasing IL-17A levels in vitro. Silencing of HIF-1α in ATF3 KO mice ameliorated IRI-induced liver damage in parallel with the downregulation of IL-17A in ATF3-deficient mice. These findings demonstrated that ATF3 deficiency activated mTOR/p70S6K/HIF-1α signaling, which was crucial for the modulation of TLR4-driven inflammatory responses and T cell development. The present study provides potential therapeutic targets for the treatment of liver IRI followed by liver transplantation