Results of a fish health survey of North Biscayne Bay, June 1976-June 1977

Fish were collected weekly in Biscayne Bay using a monofilament gill net set from a small skiff during 20-30 minute intervals. Although weekly sampling took place for 2.5 years, only the data from samples collected from June 1976 to June 1977 were used in this document. Abnormal external conditions of fins and body were observed on each fish and recorded. Fish were returned immediately to their habitats. Fish collected in the time period for this study numbered 3,765 and included 32 species. Of these, 16 species, totaling 3,556 fish, were caught in sufficient numbers (20 or more) to warrant data analysis. Only 3 of the 16 species could be considered relatively unafflicted: Aetobatus narinari (spotted eagle ray), Diodon hystrix (porcupinefish), and Selene vomer (lookdown). More than 80% of the examined specimens of these three species were unaffected. Less than 20% of the specimens of Diapterus plumieri (striped mojarra), Micropogonias undulatus (Atlantic croaker), and Pogonias cromis (black drum) displayed normal conditions. The three most afflicted species were Diapterus plumieri, striped mojarra; Micropogonias undulatus, Atlantic croaker; and Pogonias cromis, black drum. Only 7, 3, and 7% respectively showed no external evidence of disease. Data described in this document were originally tabulated in the mid-1970s, remained unpublished, and are no longer available. This document was based on archived unpublished text, a data summary table, and figures. Most of the text and cited references were the ones used in the original manuscript and no attempt was made to update them. (PDF contains 44 pages

Cancer-associated epithelial cell adhesion molecule (EpCAM; CD326) enables epidermal Langerhans cell motility and migration in vivo

After activation, Langerhans cells (LC), a distinct subpopulation of epidermis-resident dendritic cells, migrate from skin to lymph nodes where they regulate the magnitude and quality of immune responses initiated by epicutaneously applied antigens. Modulation of LC-keratinocyte adhesion is likely to be central to regulation of LC migration. LC express high levels of epithelial cell adhesion molecule (EpCAM; CD326), a cell-surface protein that is characteristic of some epithelia and many carcinomas and that has been implicated in intercellular adhesion and metastasis. To gain insight into EpCAM function in a physiologic context in vivo, we generated conditional knockout mice with EpCAM-deficient LC and characterized them. Epidermis from these mice contained increased numbers of LC with normal levels of MHC and costimulatory molecules and T-cell-stimulatory activity in vitro. Migration of EpCAM-deficient LC from skin explants was inhibited, but chemotaxis of dissociated LC was not. Correspondingly, the ability of contact allergen-stimulated, EpCAM-deficient LC to exit epidermis in vivo was delayed, and strikingly fewer hapten-bearing LC subsequently accumulated in lymph nodes. Attenuated migration of EpCAM-deficient LC resulted in enhanced contact hypersensitivity responses as previously described in LC-deficient mice. Intravital microscopy revealed reduced translocation and dendrite motility in EpCAM-deficient LC in vivo in contact allergen-treated mice. These results conclusively link EpCAM expression to LC motility/migration and LC migration to immune regulation. EpCAM appears to promote LC migration from epidermis by decreasing LC-keratinocyte adhesion and may modulate intercellular adhesion and cell movement within in epithelia during development and carcinogenesis in an analogous fashion

A causal model of radiating stellar collapse

We find a simple exact model of radiating stellar collapse, with a shear-free and non-accelerating interior matched to a Vaidya exterior. The heat flux is subject to causal thermodynamics, leading to self-consistent determination of the temperature $T$. We solve for $T$ exactly when the mean collision time $\tau_{c}$ is constant, and perturbatively in a more realistic case of variable $\tau_{c}$. Causal thermodynamics predicts temperature behaviour that can differ significantly from the predictions of non-causal theory. In particular, the causal theory gives a higher central temperature and greater temperature gradient.Comment: Latex [ioplppt style] 9 pages; to appear Class. Quantum Gra

Exact non-equilibrium solutions of the Einstein-Boltzmann equations. II

We find exact solutions of the Einstein-Boltzmann equations with relaxational collision term in FRW and Bianchi I spacetimes. The kinematic and thermodynamic properties of the solutions are investigated. We give an exact expression for the bulk viscous pressure of an FRW distribution that relaxes towards collision-dominated equilibrium. If the relaxation is toward collision-free equilibrium, the bulk viscosity vanishes - but there is still entropy production. The Bianchi I solutions have zero heat flux and bulk viscosity, but nonzero shear viscosity. The solutions are used to construct a realisation of the Weyl Curvature Hypothesis.Comment: 16 pages LaTex, CQG documentstyle (ioplppt

D-Dimensional Radiative Plasma: A Kinetic Approach

The covariant kinetic approach for the radiative plasma, a mixture of a relativistic moving gas plus radiation quanta (photons, neutrinos, or gravitons) is generalized to D spatial dimensions. The operational and physical meaning of Eckart's temperature is reexamined and the D-dimensional expressions for the transport coefficients (heat conduction, bulk and shear viscosity) are explicitly evaluated to first order in the mean free time of the radiation quanta. Weinberg's conclusion that the mixture behaves like a relativistic imperfect simple fluid (in Eckart's formulation) depends neither on the number of spatial dimensions nor on the details of the collisional term. The case of Thomson scaterring is studied in detail, and some consequences for higher dimensional cosmologies are also discussed.Comment: 28 pages, 1 figure, uses REVTE

Cosmological particle production, causal thermodynamics, and inflationary expansion

Combining the equivalence between cosmological particle creation and an effective viscous fluid pressure with the fact that the latter represents a dynamical degree of freedom within the second-order Israel-Stewart theory for imperfect fluids, we reconsider the possibility of accelerated expansion in fluid cosmology. We find an inherent self-limitation for the magnitude of an effective bulk pressure which is due to adiabatic (isentropic) particle production. For a production rate which depends quadratically on the Hubble rate we confirm the existence of solutions which describe a smooth transition from inflationary to noninflationary behavior and discuss their interpretation within the model of a decaying vacuum energy density. An alternative formulation of the effective imperfect fluid dynamics in terms of a minimally coupled scalar field is given. The corresponding potential is discussed and an entropy equivalent for the scalar field is found.Comment: 16 pages, revtex file, submitted to Phys. Rev.

Reheating and causal thermodynamics

The reheating process in inflationary universe models is considered as an out-of-equilibrium mixture of two interacting and reacting fluids, and studied within the framework of causal, irreversible thermodynamics. The evolution of the temperature and the decay rate as determined by causal thermodynamics are estimated at different stages of the process. A simple model is also used to find the perturbations of the expansion rate, including the possibility of damped oscillations.Comment: 11 pages, Revtex, submitted to Phys.Rev.

Abnormal Placental Development and Early Embryonic Lethality in EpCAM-Null Mice

BACKGROUND: EpCAM (CD326) is encoded by the tacstd1 gene and expressed by a variety of normal and malignant epithelial cells and some leukocytes. Results of previous in vitro experiments suggested that EpCAM is an intercellular adhesion molecule. EpCAM has been extensively studied as a potential tumor marker and immunotherapy target, and more recent studies suggest that EpCAM expression may be characteristic of cancer stem cells. METHODOLOGY/PRINCIPAL FINDINGS: To gain insights into EpCAM function in vivo, we generated EpCAM -/- mice utilizing an embryonic stem cell line with a tacstd1 allele that had been disrupted. Gene trapping resulted in a protein comprised of the N-terminus of EpCAM encoded by 2 exons of the tacstd1 gene fused in frame to betageo. EpCAM +/- mice were viable and fertile and exhibited no obvious abnormalities. Examination of EpCAM +/- embryos revealed that betageo was expressed in several epithelial structures including developing ears (otocysts), eyes, branchial arches, gut, apical ectodermal ridges, lungs, pancreas, hair follicles and others. All EpCAM -/- mice died in utero by E12.5, and were small, developmentally delayed, and displayed prominent placental abnormalities. In developing placentas, EpCAM was expressed throughout the labyrinthine layer and by spongiotrophoblasts as well. Placentas of EpCAM -/- embryos were compact, with thin labyrinthine layers lacking prominent vascularity. Parietal trophoblast giant cells were also dramatically reduced in EpCAM -/- placentas. CONCLUSION: EpCAM was required for differentiation or survival of parietal trophoblast giant cells, normal development of the placental labyrinth and establishment of a competent maternal-fetal circulation. The findings in EpCAM-reporter mice suggest involvement of this molecule in development of vital organs including the gut, kidneys, pancreas, lungs, eyes, and limbs

Migratory Dermal Dendritic Cells Act as Rapid Sensors of Protozoan Parasites

Dendritic cells (DC), including those of the skin, act as sentinels for intruding microorganisms. In the epidermis, DC (termed Langerhans cells, LC) are sessile and screen their microenvironment through occasional movements of their dendrites. The spatio-temporal orchestration of antigen encounter by dermal DC (DDC) is not known. Since these cells are thought to be instrumental in the initiation of immune responses during infection, we investigated their behavior directly within their natural microenvironment using intravital two-photon microscopy. Surprisingly, we found that, under homeostatic conditions, DDC were highly motile, continuously crawling through the interstitial space in a Gαi protein-coupled receptor–dependent manner. However, within minutes after intradermal delivery of the protozoan parasite Leishmania major, DDC became immobile and incorporated multiple parasites into cytosolic vacuoles. Parasite uptake occurred through the extension of long, highly dynamic pseudopods capable of tracking and engulfing parasites. This was then followed by rapid dendrite retraction towards the cell body. DDC were proficient at discriminating between parasites and inert particles, and parasite uptake was independent of the presence of neutrophils. Together, our study has visualized the dynamics and microenvironmental context of parasite encounter by an innate immune cell subset during the initiation of the immune response. Our results uncover a unique migratory tissue surveillance program of DDC that ensures the rapid detection of pathogens

The desmosome and pemphigus

Desmosomes are patch-like intercellular adhering junctions (“maculae adherentes”), which, in concert with the related adherens junctions, provide the mechanical strength to intercellular adhesion. Therefore, it is not surprising that desmosomes are abundant in tissues subjected to significant mechanical stress such as stratified epithelia and myocardium. Desmosomal adhesion is based on the Ca2+-dependent, homo- and heterophilic transinteraction of cadherin-type adhesion molecules. Desmosomal cadherins are anchored to the intermediate filament cytoskeleton by adaptor proteins of the armadillo and plakin families. Desmosomes are dynamic structures subjected to regulation and are therefore targets of signalling pathways, which control their molecular composition and adhesive properties. Moreover, evidence is emerging that desmosomal components themselves take part in outside-in signalling under physiologic and pathologic conditions. Disturbed desmosomal adhesion contributes to the pathogenesis of a number of diseases such as pemphigus, which is caused by autoantibodies against desmosomal cadherins. Beside pemphigus, desmosome-associated diseases are caused by other mechanisms such as genetic defects or bacterial toxins. Because most of these diseases affect the skin, desmosomes are interesting not only for cell biologists who are inspired by their complex structure and molecular composition, but also for clinical physicians who are confronted with patients suffering from severe blistering skin diseases such as pemphigus. To develop disease-specific therapeutic approaches, more insights into the molecular composition and regulation of desmosomes are required