Self-Renormalization of the Classical Quasilocal Energy

Pointlike objects cause many of the divergences that afflict physical theories. For instance, the gravitational binding energy of a point particle in Newtonian mechanics is infinite. In general relativity, the analog of a point particle is a black hole and the notion of binding energy must be replaced by quasilocal energy. The quasilocal energy (QLE) derived by York, and elaborated by Brown and York, is finite outside the horizon but it was not considered how to evaluate it inside the horizon. We present a prescription for finding the QLE inside a horizon, and show that it is finite at the singularity for a variety of types of black hole. The energy is typically concentrated just inside the horizon, not at the central singularity.Comment: 7 pages, 4 figure

Brown-York Energy and Radial Geodesics

We compare the Brown-York (BY) and the standard Misner-Sharp (MS) quasilocal energies for round spheres in spherically symmetric space-times from the point of view of radial geodesics. In particular, we show that the relation between the BY and MS energies is precisely analogous to that between the (relativistic) energy E of a geodesic and the effective (Newtonian) energy E_{eff} appearing in the geodesic equation, thus shedding some light on the relation between the two. Moreover, for Schwarzschild-like metrics we establish a general relationship between the BY energy and the geodesic effective potential which explains and generalises the recently observed connection between negative BY energy and the repulsive behaviour of geodesics in the Reissner-Nordstrom metric. We also comment on the extension of this connection between geodesics and the quasilocal BY energy to regions inside a horizon.Comment: v3: 7 pages, shortened and revised version to appear in CQ

A Novel Mouse Synaptonemal Complex Protein Is Essential for Loading of Central Element Proteins, Recombination, and Fertility

The synaptonemal complex (SC) is a proteinaceous, meiosis-specific structure that is highly conserved in evolution. During meiosis, the SC mediates synapsis of homologous chromosomes. It is essential for proper recombination and segregation of homologous chromosomes, and therefore for genome haploidization. Mutations in human SC genes can cause infertility. In order to gain a better understanding of the process of SC assembly in a model system that would be relevant for humans, we are investigating meiosis in mice. Here, we report on a newly identified component of the murine SC, which we named SYCE3. SYCE3 is strongly conserved among mammals and localizes to the central element (CE) of the SC. By generating a Syce3 knockout mouse, we found that SYCE3 is required for fertility in both sexes. Loss of SYCE3 blocks synapsis initiation and results in meiotic arrest. In the absence of SYCE3, initiation of meiotic recombination appears to be normal, but its progression is severely impaired resulting in complete absence of MLH1 foci, which are presumed markers of crossovers in wild-type meiocytes. In the process of SC assembly, SYCE3 is required downstream of transverse filament protein SYCP1, but upstream of the other previously described CE–specific proteins. We conclude that SYCE3 enables chromosome loading of the other CE–specific proteins, which in turn would promote synapsis between homologous chromosomes

Smoking reduces surfactant protein D and phospholipids in patients with and without chronic obstructive pulmonary disease

<p>Abstract</p> <p>Background</p> <p>Pulmonary surfactant D (SP-D) has important regulatory functions for innate immunity and has been implicated as a biomarker for chronic obstructive pulmonary disease (COPD). We hypothesized that COPD patients would have reduced bronchoalveolar lavage (BAL) fluid SP-D levels compared to healthy smoking and non-smoking controls.</p> <p>Methods</p> <p>BAL SP-D and phospholipids were quantified and corrected for dilution in 110 subjects (65 healthy never smokers, 23 smokers with normal spirometry, and 22 smokers with COPD).</p> <p>Results</p> <p>BAL SP-D was highest in never smokers (mean 51.9 μg/mL ± 7.1 μg/mL standard error) compared to both smokers with normal spirometry (16.0 μg/mL ± 11.8 μg/mL) and subjects with COPD (19.1 μg/mL ± 12.9 μg/mL; P < 0.0001). Among smokers with COPD, BAL SP-D correlated significantly with FEV₁% predicted (R = 0.43; P < 0.05); however, the strongest predictor of BAL SP-D was smoking status. BAL SP-D levels were lowest in current smokers (12.8 μg/mL ± 11.0 μg/mL), intermediate in former smokers (25.2 μg/mL ± 14.2 μg/mL; P < 0.008), and highest in never smokers. BAL phospholipids were also lowest in current smokers (6.5 nmol ± 1.5 nmol), intermediate in former smokers (13.1 nmol ± 2.1 nmol), and highest in never smokers (14.8 nmol ± 1.1 nmol; P < 0.0001).</p> <p>Conclusions</p> <p>These data suggest that smokers, and especially current smokers, exhibit significantly reduced BAL SP-D and phospholipids compared to nonsmokers. Our findings may help better explain the mechanism that leads to the rapid progression of disease and increased incidence of infection in smokers.</p