Dynamics of the Young Binary LMC Cluster NGC 1850

In this paper we have examined the age and internal dynamics of the young binary LMC cluster NGC 1850 using BV CCD images and echelle spectra of 52 supergiants. Isochrone fits to a BV color-magnitude diagram revealed that the primary cluster has an age of $\tau = 90 \pm 30$ Myr while the secondary member has $\tau = 6 \pm 5$ Myr. BV surface brightness profiles were constructed out to R $>$ 40 pc, and single-component King-Michie (KM) models were applied. The total cluster luminosity varied from L$_B$ = 2.60 - 2.65 $\times 10^6$ L$_B$\sol\ and L$_V$ = 1.25 - 1.35 $\times 10^6$ as the anisotropy radius varied from infinity to three times the scale radius with the isotropic models providing the best agreement with the data. Of the 52 stars with echelle spectra, a subset of 36 were used to study the cluster dynamics. The KM radial velocity distributions were fitted to these velocities yielding total cluster masses of 5.4 - 5.9 $\pm 2.4 \times 10^4$ M\sol\ corresponding to M/L$_B$ = 0.02 $\pm 0.01$ M\sol/L$_B$\sol\ or M/L$_V$ = 0.05 $\pm 0.02$ M\sol/L$_V$\sol. A rotational signal in the radial velocities has been detected at the 93\% confidence level implying a rotation axis at a position angle of 100\deg. A variety of rotating models were fit to the velocity data assuming cluster ellipticities of $\epsilon = 0.1 - 0.3$. These models provided slightly better agreement with the radial velocity data than the KM models and had masses that were systematically lower by a few percent. The preferred value for the slope of a power-law IMF is a relatively shallow, x = 0.29 \pmm{+0.3}{-0.8} assuming the B-band M/L or x = 0.71 \pmm{+0.2}{-0.4} for the V-band.Comment: 41 pages (figures available via anonymous FTP as described below

Stably Measurable Cardinals

We define a weak iterability notion that is sufficient for a number of arguments concerning $\Sigma_1$-definability at uncountable regular cardinals. In particular we give its exact consistency strength firstly in terms of the second uniform indiscernible for bounded subsets of $\kappa$: $u_2(\kappa)$, and secondly to give the consistency strength of a property of L\"ucke's. Theorem: The following are equiconsistent: (i) There exists $\kappa$ which is stably measurable; (ii) for some cardinal $\kappa$, $u_2(\kappa)=\sigma(\kappa)$; (iii) The {\boldmath $\Sigma_1$}-club property holds at a cardinal $\kappa$. Here $\sigma(\kappa)$ is the height of the smallest $M \prec_{\Sigma_1} H(\kappa^+)$ containing $\kappa+1$ and all of $H(\kappa)$

Trains, tails and loops of partially adsorbed semi-flexible filaments

Polymer adsorption is a fundamental problem in statistical mechanics that has direct relevance to diverse disciplines ranging from biological lubrication to stability of colloidal suspensions. We combine experiments with computer simulations to investigate depletion induced adsorption of semi-flexible polymers onto a hard-wall. Three dimensional filament configurations of partially adsorbed F-actin polymers are visualized with total internal reflection fluorescence microscopy. This information is used to determine the location of the adsorption/desorption transition and extract the statistics of trains, tails and loops of partially adsorbed filament configurations. In contrast to long flexible filaments which primarily desorb by the formation of loops, the desorption of stiff, finite-sized filaments is largely driven by fluctuating filament tails. Simulations quantitatively reproduce our experimental data and allow us to extract universal laws that explain scaling of the adsorption-desorption transition with relevant microscopic parameters. Our results demonstrate how the adhesion strength, filament stiffness, length, as well as the configurational space accessible to the desorbed filament can be used to design the characteristics of filament adsorption and thus engineer properties of composite biopolymeric materials

Method of remotely characterizing thermal properties of a sample

A sample in a wind tunnel is radiated from a thermal energy source outside of the wind tunnel. A thermal imager system, also located outside of the wind tunnel, reads surface radiations from the sample as a function of time. The produced thermal images are characteristic of the heat transferred from the sample to the flow across the sample. In turn, the measured rates of heat loss of the sample are characteristic of the flow and the sample

A Metabolic Dependency for Host Isoprenoids in the Obligate Intracellular Pathogen Rickettsia parkeri Underlies a Sensitivity to the Statin Class of Host-Targeted Therapeutics.

Gram-negative bacteria in the order Rickettsiales have an obligate intracellular growth requirement, and some species cause human diseases such as typhus and spotted fever. The bacteria have evolved a dependence on essential nutrients and metabolites from the host cell as a consequence of extensive genome reduction. However, it remains largely unknown which nutrients they acquire and whether their metabolic dependency can be exploited therapeutically. Here, we describe a genetic rewiring of bacterial isoprenoid biosynthetic pathways in the Rickettsiales that has resulted from reductive genome evolution. Furthermore, we investigated whether the spotted fever group Rickettsia species Rickettsia parkeri scavenges isoprenoid precursors directly from the host. Using targeted mass spectrometry, we found that infection caused decreases in host isoprenoid products and concomitant increases in bacterial isoprenoid metabolites. Additionally, we report that treatment of infected cells with statins, which inhibit host isoprenoid synthesis, prohibited bacterial growth. We show that growth inhibition correlates with changes in bacterial size and shape that mimic those caused by antibiotics that inhibit peptidoglycan biosynthesis, suggesting that statins lead to an inhibition of cell wall synthesis. Altogether, our results describe a potential Achilles' heel of obligate intracellular pathogens that can potentially be exploited with host-targeted therapeutics that interfere with metabolic pathways required for bacterial growth.IMPORTANCE Obligate intracellular pathogens, which include viruses as well as certain bacteria and eukaryotes, are a subset of infectious microbes that are metabolically dependent on and unable to grow outside an infected host cell because they have lost or lack essential biosynthetic pathways. In this study, we describe a metabolic dependency of the bacterial pathogen Rickettsia parkeri on host isoprenoid molecules that are used in the biosynthesis of downstream products, including cholesterol, steroid hormones, and heme. Bacteria make products from isoprenoids, such as an essential lipid carrier for making the bacterial cell wall. We show that bacterial metabolic dependency can represent a potential Achilles' heel and that inhibiting host isoprenoid biosynthesis with the FDA-approved statin class of drugs inhibits bacterial growth by interfering with the integrity of the cell wall. This work supports the potential to treat infections by obligate intracellular pathogens through inhibition of host biosynthetic pathways that are susceptible to parasitism