Massive star formation in 100,000 years from turbulent and pressurized molecular clouds

Massive stars (with mass m_* > 8 solar masses) are fundamental to the evolution of galaxies, because they produce heavy elements, inject energy into the interstellar medium, and possibly regulate the star formation rate. The individual star formation time, t_*f, determines the accretion rate of the star; the value of the former quantity is currently uncertain by many orders of magnitude, leading to other astrophysical questions. For example, the variation of t_*f with stellar mass dictates whether massive stars can form simultaneously with low-mass stars in clusters. Here we show that t_*f is determined by conditions in the star's natal cloud, and is typically ~10^5 yr. The corresponding mass accretion rate depends on the pressure within the cloud - which we relate to the gas surface density - and on both the instantaneous and final stellar masses. Characteristic accretion rates are sufficient to overcome radiation pressure from ~100 solar mass protostars, while simultaneously driving intense bipolar gas outflows. The weak dependence of t_*f on the final mass of the star allows high- and low-mass star formation to occur nearly simultaneously in clusters.Comment: 9 pages plus 2 figures, Nature, 416, 59 (7th March 2002

Measurement of Exclusive rho+rho- Production in Mid-Virtuality Two-Photon Interactions and Study of the gamma gamma* -> rho rho Process at LEP

Exclusive rho+rho- production in two-photon collisions between a quasi-real photon, gamma, and a mid-virtuality photon, gamma*, is studied with data collected at LEP at centre-of-mass energies root(s)=183-209GeV with a total integrated luminosity of 684.8pb^-1. The cross section of the gamma gamma* -> rho+ rho- process is determined as a function of the photon virtuality, Q^2, and the two-photon centre-of-mass energy, W_gg, in the kinematic region: 0.2GeV^2 < Q^2 <0.85GeV^2 and 1.1GeV < W_gg < 3GeV. These results, together with previous L3 measurements of rho0 rho0 and rho+ rho- production, allow a study of the gamma gamma* -> rho rho process over the Q^2-region 0.2GeV^2 < Q^2 < 30 GeV^2

Novel derivative of aminobenzenesulfonamide (3c) induces apoptosis in colorectal cancer cells through ROS generation and inhibits cell migration

Background: Colorectal cancer (CRC) is the 3rd most common type of cancer worldwide. New anti-cancer agents are needed for treating late stage colorectal cancer as most of the deaths occur due to cancer metastasis. A recently developed compound, 3c has shown to have potent antitumor effect; however the mechanism underlying the antitumor effect remains unknown. Methods: 3c-induced inhibition of proliferation was measured in the absence and presence NAC using MTT in HT-29 and SW620 cells and xCELLigence RTCA DP instrument. 3c-induced apoptotic studies were performed using flow cytometry. 3c-induced redox alterations were measured by ROS production using fluorescence plate reader and flow cytometry and mitochondrial membrane potential by flow cytometry; NADPH and GSH levels were determined by colorimetric assays. Bcl2 family protein expression and cytochrome c release and PARP activation was done by western blotting. Caspase activation was measured by ELISA. Cell migration assay was done using the real time xCELLigence RTCA DP system in SW620 cells and wound healing assay in HT-29. Results: Many anticancer therapeutics exert their effects by inducing reactive oxygen species (ROS). In this study, we demonstrate that 3c-induced inhibition of cell proliferation is reversed by the antioxidant, N-acetylcysteine, suggesting that 3c acts via increased production of ROS in HT-29 cells. This was confirmed by the direct measurement of ROS in 3c-treated colorectal cancer cells. Additionally, treatment with 3c resulted in decreased NADPH and glutathione levels in HT-29 cells. Further, investigation of the apoptotic pathway showed increased release of cytochrome c resulting in the activation of caspase-9, which in turn activated caspase-3 and −6. 3c also (i) increased p53 and Bax expression, (ii) decreased Bcl2 and BclxL expression and (iii) induced PARP cleavage in human colorectal cancer cells. Confirming our observations, NAC significantly inhibited induction of apoptosis, ROS production, cytochrome c release and PARP cleavage. The results further demonstrate that 3c inhibits cell migration by modulating EMT markers and inhibiting TGFβ-induced phosphorylation of Smad2 and Samd3. Conclusions: Our findings thus demonstrate that 3c disrupts redox balance in colorectal cancer cells and support the notion that this agent may be effective for the treatment of colorectal cancer

Measurement of Exclusive rho^0 rho^0 Production in Mid-Virtuality Two-Photon Interactions at LEP

Exclusive rho^0 rho^0 production in two-photon collisions between a quasi-real and a mid-virtuality photon is studied with data collected at LEP at centre-of-mass energies 183GeV < sqrt{s} < 209GeV with a total integrated luminosity of 684.8/pb. The cross section of the process gamma gamma* -> rho^0 rho^0 is determined as a function of the photon virtuality, q^2, and the two-photon centre-of-mass energy, Wgg, in the kinematic region: 0.2GeV^2 < q^2 < 0.85GeV^2 and 1.1GeV < Wgg < 3GeV

Transient Alteration of Cellular Redox Buffering before Irradiation Triggers Apoptosis in Head and Neck Carcinoma Stem and Non-Stem Cells

Background: Head and neck squamous cell carcinoma (HNSCC) is an aggressive and recurrent malignancy owing to intrinsic radioresistance and lack of induction of apoptosis. The major focus of this work was to design a transient glutathione depleting strategy during the course of irradiation of HNSCC in order to overcome their radioresistance associated with redox adaptation. Methodology/Principal Findings: Treatment of SQ20B cells with dimethylfumarate (DMF), a GSH-depleting agent, and L-Buthionine sulfoximine (BSO), an inhibitor of GSH biosynthesis 4 h before a 10 Gy irradiation led to the lowering of the endogenous GSH content to less than 10 % of that in control cells and to the triggering of radiation-induced apoptotic cell death. The sequence of biochemical events after GSH depletion and irradiation included ASK-1 followed by JNK activation which resulted in the triggering of the intrinsic apoptotic pathway through Bax translocation to mitochondria. Conclusions: This transient GSH depletion also triggered radiation-induced cell death in SQ20B stem cells, a key event to overcome locoregional recurrence of HNSCC. Finally, our in vivo data highlight the relevance for further clinical trials o

Measurement of Exclusive \rho^+\rho^- Production in High-Q^2 Two-Photon Collisions at LEP

Exclusive rho^+ rho^- production in two-photon collisions involving a single highly-virtual photon is studied with data collected at LEP at centre-of-mass energies 89 GeV < \sqrt{s} < 209 GeV with a total integrated luminosity of 854.7 pb^-1. The cross section of the process gamma gamma^* -> rho^+ rho^- is determined as a function of the photon virtuality, Q^2, and the two-photon centre-of-mass energy, W_gg, in the kinematic region: 1.2 GeV^2 < Q^2 < 30 GeV^2 and 1.1 GeV < W_gg < 3 GeV. The \rho^+\rho^- production cross section is found to be of the same magnitude as the cross section of the process gamma gamma^* -> rho^0 rho^0, measured in the same kinematic region by L3, and to have similar W_gg and Q^2 dependences

Hankel Tournaments and Special Oriented Graphs

[Chapter Abstract] A Hankel tournament T of order n (an n × n Hankel tournament matrix T = [tij]) is a tournament such that i → j an edge implies (n + 1 − j) → (n + 1 − i) is also an edge (tij = tn+1−j,n+1−i) for all i and j. Hankel tournament matrices are (0, 1)-matrices which are combinatorially antisymmetric about the main diagonal and symmetric about the Hankel diagonal (the antidiagonal). Locally transitive tournaments are tournaments such that the in-neighborhood and the out-neighborhood of each vertex are transitive. Tournaments form a special class of oriented graphs. The score vectors of Hankel tournaments and of locally transitive tournaments have been characterized where each score vector of a locally transitive tournament is also a score vector of a Hankel tournament. In this paper we continue investigations into Hankel tournaments and locally transitive tournaments. We investigate Hankel cycles in Hankel tournaments and show in particular that a strongly connected Hankel tournament contains a Hankel Hamilton cycle and, in fact, is Hankel “even-pancyclic” or Hankel “odd-pancyclic.” We show that a Hankel score vector can be achieved by a Hankel “half-transitive” tournament, extending the corresponding result for score vectors of tournaments. We also consider some results on oriented graphs and the question of attainability of prescribed degrees by oriented graphs. Finally, we extend some results on 2-tournaments to Hankel 2-tournaments. In some instances we rely on the reader to extend arguments already in the literature. We illustrate our investigations with many examples.https://nsuworks.nova.edu/cnso_math_facbooks/1026/thumbnail.jp