Nonlinear Outcome of Gravitational Instability in Disks with Realistic Cooling

We consider the nonlinear outcome of gravitational instability in optically thick disks with a realistic cooling function. We use a numerical model that is local, razor-thin, and unmagnetized. External illumination is ignored. Cooling is calculated from a one-zone model using analytic fits to low temperature Rosseland mean opacities. The model has two parameters: the initial surface density Sigma_0 and the rotation frequency Omega. We survey the parameter space and find: (1) The disk fragments when t_c,eff Omega = 1, where t_c,eff is an effective cooling time defined as the average internal energy of the model divided by the average cooling rate. This is consistent with earlier results that used a simplified cooling function. (2) The initial cooling time t_c0 or a uniform disk with Q = 1 can differ by orders of magnitude from t_c,eff in the nonlinear outcome. The difference is caused by sharp variations in the opacity with temperature. The condition t_c0 Omega = 1 therefore does not necessarily indicate where fragmentation will occur. (3) The largest difference between t_c,eff and t_c0 is near the opacity gap, where dust is absent and hydrogen is largely molecular. (4) In the limit of strong illumination the disk is isothermal; we find that an isothermal version of our model fragments for Q < 1.4. Finally, we discuss some physical processes not included in our model, and find that most are likely to make disks more susceptible to fragmentation. We conclude that disks with t_c,eff Omega < 1 do not exist.Comment: 30 pages, 12 figure

Analysis of Clumps in Molecular Cloud Models: Mass Spectrum, Shapes, Alignment and Rotation

Observations reveal concentrations of molecular line emission on the sky, called ``clumps,'' in dense, star-forming molecular clouds. These clumps are believed to be the eventual sites of star formation. We study the three-dimensional analogs of clumps using a set of self-consistent, time-dependent numerical models of molecular clouds. The models follow the decay of initially supersonic turbulence in an isothermal, self-gravitating, magnetized fluid. We find the following. (1) Clumps are intrinsically triaxial. This explains the observed deficit of clumps with a projected axis ratio near unity, and the apparent prolateness of clumps. (2) Simulated clump axes are not strongly aligned with the mean magnetic field within clumps, nor with the large-scale mean fields. This is in agreement with observations. (3) The clump mass spectrum has a high-mass slope that is consistent with the Salpeter value. There is a low-mass break in the slope at \sim 0.5 \msun, although this may depend on model parameters including numerical resolution. (4) The typical specific spin angular momentum of clumps is $4 \times 10^{22} {\rm cm^2 s^{-1}}$. This is larger than the median specific angular momentum of binary stars. Scaling arguments suggest that higher resolution simulations may soon be able to resolve the scales at which the angular momentum of binary stars is determined.Comment: 14 pages, 13 figures, to appear in 2003 July 20 Ap

Twist-mediated Epithelial-mesenchymal Transition Promotes Breast Tumor Cell Invasion via Inhibition of Hippo Pathway

Twist is a key transcription factor for Epithelial-mesenchymal transition (EMT), which is a cellular de-differentiation program that promotes invasion and metastasis, confers tumor cells with cancer stem cell (CSC)-like characteristics, and increases therapeutic resistance. However, the mechanisms that facilitate the functions of Twist remain unclear. Here we report that Twist overexpression increased expression of PAR1, an upstream regulator of the Hippo pathway; PAR1 promotes invasion, migration, and CSC-like properties in breast cancer by activating the transcriptional co-activator TAZ. Our study indicates that Hippo pathway inhibition is required for the increased migratory and invasiveness ability of breast cancer cells in Twist-mediated EMT

Three-color femtosecond source for simultaneous excitation of three fluorescent proteins in two-photon fluorescence microscopy

We demonstrate a fiber-based, three-color femtosecond source for simultaneous imaging of three fluorescent proteins (FPs) using two-photon fluorescence microscopy (2PM). The three excitation wavelengths at 775 nm, 864 nm and 950 nm, are obtained through second harmonic generation (SHG) of the 1550-nm pump laser and the 1728-nm and 1900-nm solitons generated through soliton self-frequency shift (SSFS) in a large-mode-area (LMA) fiber. These energetic pulses are well matched to the two-photon excitation peaks of red, cyan and yellow fluorescent proteins (TagRFPs, TagCFPs, and TagYFPs) for efficient excitation. We demonstrate simultaneous 2PM of human melanoma cells expressing a “rainbow” combination of these three fluorescent proteins

Imaging leukocyte trafficking in vivo with two-photon-excited endogenous tryptophan fluorescence

We describe a new method for imaging leukocytes in vivo by exciting the endogenous protein fluorescence in the ultraviolet (UV) spectral region where tryptophan is the major fluorophore. Two-photon excitation near 590 nm allows noninvasive optical sectioning through the epidermal cell layers into the dermis of mouse skin, where leukocytes can be observed by video-rate microscopy to interact dynamically with the dermal vascular endothelium. Inflammation significantly enhances leukocyte rolling, adhesion, and tissue infiltration. After exiting the vasculature, leukocytes continue to move actively in tissue as observed by time-lapse microscopy, and are distinguishable from resident autofluorescent cells that are not motile. Because the new method alleviates the need to introduce exogenous labels, it is potentially applicable for tracking leukocytes and monitoring inflammatory cellular reactions in humans

Interleukin-32β Propagates Vascular Inflammation and Exacerbates Sepsis in a Mouse Model

Inflammation is associated with most diseases, which makes understanding the mechanisms of inflammation vitally important.Here, we demonstrate a critical function of interleukin-32beta (IL-32beta) in vascular inflammation. IL-32beta is present in tissues from humans, but is absent in rodents. We found that the gene is highly expressed in endothelial cells. Three isoforms of IL-32, named IL-32alpha, beta, and epsilon, were cloned from human endothelial cells, with IL-32beta being the major isoform. Pro-inflammatory cytokines (TNFalpha and IL-1beta) induced IL-32beta expression through NF-kappaB. Conversely, IL-32beta propagated vascular inflammation via induction of vascular cell adhesion molecules and inflammatory cytokines. Accordingly, IL-32beta increased adhesion of inflammatory cells to activated endothelial cells, a paramount process in inflammation. These results illustrate a positive feedback regulation that intensifies and prolongs inflammation. Importantly, endothelial/hematopoietic expression of IL-32beta in transgenic mice elevated inflammation and worsened sepsis. This was demonstrated by significant elevation of leukocyte infiltration and serum levels of TNFalpha and IL-1beta, increased vascular permeability and lung damage, and accelerated animal death. Together, our results reveal an important function of IL-32 in vascular inflammation and sepsis development.Our results reveal an important function of IL-32 in vascular inflammation and sepsis development