Constraints on Stirring and Dissipation of MHD Turbulence in Molecular Clouds

We discuss constraints on the rates of stirring and dissipation of MHD turbulence in molecular clouds. Recent MHD simulations suggest that turbulence in clouds decays rapidly, thus providing a significant source of energy input, particularly if driven at small scales by, for example, bipolar outflows. We quantify the heating rates by combining the linewidth-size relations, which describe global cloud properties, with numerically determined dissipation rates. We argue that, if cloud turbulence is driven on small internal scales, the $^{12}$CO flux (enhanced by emission from weakly supersonic shocks) will be much larger than observed; this, in turn, would imply excitation temperatures significantly above observed values. We reach two conclusions: (1) small-scale driving by bipolar outflows cannot possibly account for cloud support and yield long-lived clouds, unless the published MHD dissipation rates are seriously overestimated; (2) driving on large scales (comparable to the cloud size) is much more viable from an energetic standpoint, and if the actual net dissipation rate is only slightly lower than what current MHD simulations estimate, then the observationally inferred lifetimes and apparent virial equilibrium of molecular clouds can be explained.Comment: 5 pages, 1 figure. To appear in ApJ (2001 April 10

Determining the galactic mass distribution using tidal streams from globular clusters

We discuss how to use tidal streams from globular clusters to measure the mass distribution of the Milky Way. Recent proper motion determinations for globular clusters from plate measurements and Hipparcos astrometry provide several good candidates for Galactic mass determinations in the intermediate halo, far above the Galactic disk, including Pal 5, NGC 4147, NGC 5024 (M53) and NGC 5466; the remaining Hipparcos clusters provide candidates for measurements several kpc above and below the disk. These clusters will help determine the profile and shape of the inner halo. To aid this effort, we present two methods of mass determination: one, a generalization of rotation-curve mass measurements, which gives the mass and potential from complete position-velocity observations for stream stars; and another using a simple chi^2 estimator, which can be used when only projected positions and radial velocities are known for stream stars. We illustrate the use of the latter method using simulated tidal streams from Pal 5 and find that fairly accurate mass determinations are possible even for relatively poor data sets. Follow-up observations of clusters with proper motion determinations may reveal tidal streams; obtaining radial velocity measurements would enable accurate measurements of the mass distribution in the inner Galaxy.Comment: 21 pages, 6 figures, published in A

The Magellanic Stream and the density of coronal gas in the Galactic halo

The properties of the Magellanic Stream constrain the density of coronal gas in the distant Galactic halo. We show that motion through ambient gas can strongly heat Stream clouds, driving mass loss and causing evaporation. If the ambient gas density is too high, then evaporation occurs on unreasonably short timescales. Since heating dominates drag, tidal stripping appears to be responsible for producing the Stream. Requiring the survival of the cloud MS IV for 500 Myr sets an upper limit on the halo gas density n_H< 10^{-5} cm^{-3} at 50 kpc, roughly a factor of 10 lower than that estimated from the drag model of Moore & Davis (1994). Implications for models of the evolution of gas in galaxy halos are discussed.Comment: 4 pages, 1 figure, in press, ApJ

The growth of galaxies in cosmological simulations of structure formation

We use hydrodynamic simulations to examine how the baryonic components of galaxies are assembled, focusing on the relative importance of mergers and smooth accretion in the formation of ~L_* systems. In our primary simulation, which models a (50\hmpc)^3 comoving volume of a Lambda-dominated cold dark matter universe, the space density of objects at our (64-particle) baryon mass resolution threshold, M_c=5.4e10 M_sun, corresponds to that of observed galaxies with L~L_*/4. Galaxies above this threshold gain most of their mass by accretion rather than by mergers. At the redshift of peak mass growth, z~2, accretion dominates over merging by about 4:1. The mean accretion rate per galaxy declines from ~40 M_sun/yr at z=2 to ~10 M_sun/yr at z=0, while the merging rate peaks later (z~1) and declines more slowly, so by z=0 the ratio is about 2:1. We cannot distinguish truly smooth accretion from merging with objects below our mass resolution threshold, but extrapolating our measured mass spectrum of merging objects, dP/dM ~ M^a with a ~ -1, implies that sub-resolution mergers would add relatively little mass. The global star formation history in these simulations tracks the mass accretion rate rather than the merger rate. At low redshift, destruction of galaxies by mergers is approximately balanced by the growth of new systems, so the comoving space density of resolved galaxies stays nearly constant despite significant mass evolution at the galaxy-by-galaxy level. The predicted merger rate at z<~1 agrees with recent estimates from close pairs in the CFRS and CNOC2 redshift surveys.Comment: Submitted to ApJ, 35 pp including 15 fig

Constraints on the mass and abundance of black holes in the Galactic halo: the high mass limit

We establish constraints on the mass and abundance of black holes in the Galactic halo by determining their impact on globular clusters which are conventionally considered to be little evolved. Using detailed Monte Carlo simulations and simple analytic estimates, we conclude that, at Galactocentric radius R~8 kpc, black holes with masses M_bh >~(1-3) x 10^6 M_sun can comprise no more than a fraction f_bh ~ 0.025-0.05 of the total halo density. This constraint significantly improves those based on disk heating and dynamical friction arguments as well as current lensing results. At smaller radius, the constraint on f_bh strengthens, while, at larger radius, an increased fraction of black holes is allowed.Comment: 13 pages, 10 figures, revised version, in press, Monthly Notice

A Synthetic Uric Acid Analog Accelerates Cutaneous Wound Healing in Mice

Wound healing is a complex process involving intrinsic dermal and epidermal cells, and infiltrating macrophages and leukocytes. Excessive oxidative stress and associated inflammatory processes can impair wound healing, and antioxidants have been reported to improve wound healing in animal models and human subjects. Uric acid (UA) is an efficient free radical scavenger, but has a very low solubility and poor tissue penetrability. We recently developed novel UA analogs with increased solubility and excellent free radical-scavenging properties and demonstrated their ability to protect neural cells against oxidative damage. Here we show that the uric acid analog (6, 8 dithio-UA, but not equimolar concentrations of UA or 1, 7 dimethyl-UA) modified the behaviors of cultured vascular endothelial cells, keratinocytes and fibroblasts in ways consistent with enhancement of the wound healing functions of all three cell types. We further show that 6, 8 dithio-UA significantly accelerates the wound healing process when applied topically (once daily) to full-thickness wounds in mice. Levels of Cu/Zn superoxide dismutase were increased in wound tissue from mice treated with 6, 8 dithio-UA compared to vehicle-treated mice, suggesting that the UA analog enhances endogenous cellular antioxidant defenses. These results support an adverse role for oxidative stress in wound healing and tissue repair, and provide a rationale for the development of UA analogs in the treatment of wounds and for modulation of angiogenesis in other pathological conditions

Low-Dosage Inhibition of DII4 Signaling Promotes Wound Healing by Inducing Functional Neo-Angiogenesis

Recent findings regarding Dll4 function in physiological and pathological conditions indicate that this Notch ligand may constitute an important therapeutic target. Dll4 appears to be a major anti-angiogenic agent, occupying a central role in various angiogenic pathways. The first trials of anti-Dll4 therapy in mice demonstrated a paradoxical effect, as it reduced tumor perfusion and growth despite leading to an increase in vascular density. This is seen as the result of insufficient maturation of the newly formed vasculature causing a circulatory defect and increased tumor hypoxia. As Dll4 function is known to be closely dependent on expression levels, we envisioned that the therapeutic anti-Dll4 dosage could be modulated to result in the increase of adequately functional blood vessels. This would be useful in conditions where vascular function is a limiting factor for recovery, like wound healing and tissue hypoxia, especially in diabetic patients. Our experimental results in mice confirmed this possibility, revealing that low dosage inhibition of Dll4/Notch signaling causes improved vascular function and accelerated wound healing

β1 Integrin Maintains Integrity of the Embryonic Neocortical Stem Cell Niche

IInteractions between laminins and integrin receptors hold neural stem cells in place at the ventricular surface of embryonic brain. Transient disruption leads to abnormal stem cell divisions and permanent cortical malformation

Significance of Thymosin β4 and Implication of PINCH-1-ILK-α-Parvin (PIP) Complex in Human Dilated Cardiomyopathy

Myocardial remodeling is a major contributor in the development of heart failure (HF) after myocardial infarction (MI). Integrin-linked kinase (ILK), LIM-only adaptor PINCH-1, and α-parvin are essential components of focal adhesions (FAs), which are highly expressed in the heart. ILK binds tightly to PINCH-1 and α-parvin, which regulates FA assembly and promotes cell survival via the activation of the kinase Akt. Mice lacking ILK, PINCH or α-parvin have been shown to develop severe defects in the heart, suggesting that these proteins play a critical role in heart function. Utilizing failing human heart tissues (dilated cardiomyopathy, DCM), we found a 2.27-fold (p<0.001) enhanced expression of PINCH, 4 fold for α-parvin, and 10.5 fold (p<0.001) for ILK as compared to non-failing (NF) counterparts. No significant enhancements were found for the PINCH isoform PINCH-2 and parvin isoform β-parvin. Using a co-immunoprecipitation method, we also found that the PINCH-1-ILK-α-parvin (PIP) complex and Akt activation were significantly up-regulated. These observations were further corroborated with the mouse myocardial infarction (MI) and transaortic constriction (TAC) model. Thymosin beta4 (Tβ4), an effective cell penetrating peptide for treating MI, was found to further enhance the level of PIP components and Akt activation, while substantially suppressing NF-κB activation and collagen expression—the hallmarks of cardiac fibrosis. In the presence of an Akt inhibitor, wortmannin, we show that Tβ4 had a decreased effect in protecting the heart from MI. These data suggest that the PIP complex and activation of Akt play critical roles in HF development. Tβ4 treatment likely improves cardiac function by enhancing PIP mediated Akt activation and suppressing NF-κB activation and collagen-mediated fibrosis. These data provide significant insight into the role of the PIP-Akt pathway and its regulation by Tβ4 treatment in post-MI