Debris discs around M stars: non-existence versus non-detection

Motivated by the reported dearth of debris discs around M stars, we use survival models to study the occurrence of planetesimal discs around them. These survival models describe a planetesimal disc with a small number of parameters, determine if it may survive a series of dynamical processes and compute the associated infrared excess. For the Wide-field Infrared Survey Explorer (WISE) satellite, we demonstrate that the dearth of debris discs around M stars may be attributed to the small semimajor axes generally probed if either: (1) the dust grains behave like blackbodies emitting at a peak wavelength coincident with the observed one; (2) or the grains are hotter than predicted by their blackbody temperatures and emit at peak wavelengths that are shorter than the observed one. At these small distances from the M star, planetesimals are unlikely to survive or persist for time-scales of 300 Myr or longer if the disc is too massive. Conversely, our survival models allow for the existence of a large population of low-mass debris discs that are too faint to be detected with current instruments. We gain further confidence in our interpretation by demonstrating the ability to compute infrared excesses for Sun-like stars that are broadly consistent with reported values in the literature. However, our interpretation becomes less clear and large infrared excesses are allowed if only one of these scenarios holds: (3) the dust grains are hotter than blackbody and predominantly emit at the observed wavelength; (4) or are blackbody in nature and emit at peak wavelengths longer than the observed one. Both scenarios imply that the parent planetesimals reside at larger distances from the star than inferred if the dust grains behaved like blackbodies. In all scenarios, we show that the infrared excesses detected at 22 μm (via WISE) and 70 μm (via Spitzer) from AU Mic are easily reconciled with its young age (12 Myr). Conversely, the existence of the old debris disc (2–8 Gyr) from GJ 581 is due to the large semimajor axes probed by the Herschel PACS instrument. We elucidate the conditions under which stellar wind drag may be neglected when considering dust populations around M stars. The WISE satellite should be capable of detecting debris discs around young M stars with ages ∼10 Myr.

A steerable UV laser system for the calibration of liquid argon time projection chambers

A number of liquid argon time projection chambers (LAr TPCs) are being built or are proposed for neutrino experiments on long- and short baseline beams. For these detectors, a distortion in the drift field due to geometrical or physics reasons can affect the reconstruction of the events. Depending on the TPC geometry and electric drift field intensity, this distortion could be of the same magnitude as the drift field itself. Recently, we presented a method to calibrate the drift field and correct for these possible distortions. While straight cosmic ray muon tracks could be used for calibration, multiple coulomb scattering and momentum uncertainties allow only a limited resolution. A UV laser instead can create straight ionization tracks in liquid argon, and allows one to map the drift field along different paths in the TPC inner volume. Here we present a UV laser feed-through design with a steerable UV mirror immersed in liquid argon that can point the laser beam at many locations through the TPC. The straight ionization paths are sensitive to drift field distortions, a fit of these distortion to the linear optical path allows to extract the drift field, by using these laser tracks along the whole TPC volume one can obtain a 3D drift field map. The UV laser feed-through assembly is a prototype of the system that will be used for the MicroBooNE experiment at the Fermi National Accelerator Laboratory (FNAL).

Ms. hebr. oct. 109 - Rav ṭuv

Vorbesitzer: Eljāqīm Carmoly; Abraham Merzbacher

MYB-FL controls gain and loss of floral UV absorbance, a key trait affecting pollinator preference and reproductive isolation

Adaptations to new pollinators involve multiple floral traits, each requiring coordinated changes in multiple genes. Despite this genetic complexity, shifts in pollination syndromes have happened frequently during angiosperm evolution. Here we study the genetic basis of floral UV absorbance, a key trait for attracting nocturnal pollinators. In Petunia, mutations in a single gene, MYB-FL, explain two transitions in UV absorbance. A gain of UV absorbance in the transition from bee to moth pollination was determined by a cis-regulatory mutation, whereas a frameshift mutation caused subsequent loss of UV absorbance during the transition from moth to hummingbird pollination. The functional differences in MYB-FL provide insight into the process of speciation and clarify phylogenetic relationships between nascent species.

Pasteurization of Apple Cider with UV Irradiation

In a period of increasing concern about food safety, food poisoning outbreaks where unpasterurized apple cider or apple juice was found contaminated with Escherichia coli 0157:H7 reinforces the need for using the best technologies in apple cider production. Most apple cider is sold as an unpasteurized raw product. Because of their acidity, it was believed that juice products do not usually contain microorganisms such as E. coli 0157:H7, Salmonella, and Crytosporidium. Yet all of these foodborne pathogens are capable of being transmitted in unpasteurized juices. It is known that these pathogens can survive for several weeks in a variety of acidic juices. Although heat pasteurization is probably the best method to eliminate these pathogens, it is not the most desirable method as it changes sensory properties and also is very costly for small to mid-sized apple cider processors. Pasteurization of apple cider with Ultraviolet Irradiation (UV) is a potential alternative to heat pasteurization. Germicidal W irradiation is effective in inactivating microorganisms without producing undesirable by-products and changing sensory properties. Unpasteurized raw apple cider from a small local processor was purchased for this study. The effects of physical parameters, exposure time and dosage on the W treatment efficacy were examined as well as the effects of the UV light on apple cider quality. W light with principal energy at a wavelength of 254.7 nm, was effective in reducing bacteria (E .coli, ATCC 25922) inoculated apple cider. The W dosage absorbed by the apple cider was mathematically calculated. A radiation dose of 8,777 μW-s/cm2 reduced bacteria an average of 2.20 logs and in multiple passes, the FDA mandated 5-log reduction was achieved. Sensory analysis showed there was no significant difference between the W treated and non-treated cider. Experiments with W treated apple cider indicated a significant (p < 0.01) extension of product shelf life through inhibition of yeast and mold growth. The extension of the researched performed is applicable to other fruit juice processing operations.

The role of UV radiation in the development of myeloid malignancy in Rag2 knockout mice

Excessive exposure to the UV radiation present in sunlight can lead to the development of skin cancer in humans. Majority of the UV-induced skin tumors in immune-competent mice are highly antigenic in nature. Additionally, they exhibit a high frequency of mutations in the p53 gene, which arise very early in the course of UV radiation and most of them disappear before the development of skin tumors. ^ Initially, this study was to determine whether UV radiation induces skin tumors much earlier in immune deficient Rag2 knockout mice than in immune-competent mice, and if so, compare their antigenic properties and p53 mutation spectra. However, chronic UV irradiation (10 kJ/m2) induced myeloproliferative disease (MPD) as early as 4 weeks in Rag2 knockout mice instead of skin tumors. Conversely, unirradiated Rag2 knockout mice developed MPD at a low frequency, but the frequency increased with the animal's age. Although the UV-irradiated wild type mice (B6129) developed MPD, its frequency was lower and the occurrence much later than the Rag2 knockout mice. ^ This observation led to our new hypothesis that UV irradiation plays a role in the development of MPD in Rag2 knockout mice. After 4 weeks of UV radiation, both histopathology (myeloid:erythroid ratio, number of blast cells) and flow cytometry (mature myeloid, granulocytes and immature cells) demonstrated an increased number of mice affected with the disease in the UV-irradiated Rag2 knockout group than the other groups. ^ We also investigated the role of cytokines and absence of T and B cells in the development of MPD in the Rag2 knockout mice. Results indicated that IL-3 and IL-3Rα chain expression was upregulated in the spleens of the UV-irradiated Rag2 knockout mice (4 weeks). Reconstitution of the Rag2 knockout mice with T and B cells abrogated the UV-accelerated development of MPD. Both histopathology and flow cytometric analysis (mature myeloid cells, granulocytes) showed a decrease in the number of mice affected with the disease in the UV-irradiated, reconstituted group rather than any other group. In summary, this study provides the first experimental evidence that exposure to UV irradiation can lead to the development of MPD in immune deficient mice. ^

Effects of the microenvironment on Fas/Fas ligand interactions and their implications for UV-induced immune suppression

Skin cancer is the most common malignancy in humans. Although highly treatable, non-melanoma skin cancer is commonly followed by other non-cutaneous malignancies. Ultraviolet radiation (UVR) acts as both tumor initiator and promoter, and also results in the suppression of specific immune responses. The systemic suppression of immune responses is initiated by DNA damage, which promotes IL-10 production, an important cytokine as anti-IL-10 can abrogate the suppression, and upregulates the pro-apoptotic proteins Fas and Fas ligand (FasL). FasL is a critical factor for UV-induced immune suppression, and the suppressor cell induced by UV expresses FasL. ^ We hypothesized that the microenvironment affects Fas/FasL interactions, and that these interactions are important to the phenomenon of UV induced immune suppression. To determine the effects of the interaction of FasL and IL-10, splenocytes isolated from C57Bl/6 mice were cultured in the presence or absence of IL-10 post-mitogenic activation. We determined that IL-10 protects from Fas-mediated apoptosis by lowering Fas sensitivity and lowering the levels of either Fas or FasL. This protection is stronger when IL-10 is given immediately after mitogenic activation, and does not increase any of the inhibitors of apoptosis studied. In vivo, splenocytes from UV-irradiated mice are resistant to Fas-mediated apoptosis and present very high levels of IL-10, lowered Fas sensitivity and lowered caspase cleavage despite higher expression of Fas and FasL than non-irradiated mice. ^ UV-induced immune suppression affects female mice preferentially, which led us to look at prolactin as a possible component of this suppression since this hormone has also been associated with increased skin carcinogenesis. The interaction of FasL and prolactin results in suppression of the delayed type hypersensitivity response to Candida albicans. This lack of response depends on FasL as is not seen in gld mice. Similar to UV-induced immune suppression, the suppression is caused by a Th2 deviation, and correlates with a significant increase in Fas expression. In the presence of UV, the effects of prolactin seemed to be protective, and UV actually restores the DTH response.^ Taken together, these observations suggest that the microenvironment dictates the outcome of the interaction of FasL with Fas going from promoting apoptosis to preventing apoptosis or mediating a Th2 deviation and suppression of a Th1 response. ^

DNA damage-induced Fas ligand expression by epidermal dendritic cells mediates UV-induced immune suppression of contact hypersensitivity

Exposure to UVB radiation induces local and systemic immune suppression, evidenced by inhibition of the contact hypersensitivity response (CHS). Epidermal dendritic cells, the primary antigen presenting cells responsible for the induction of CHS, are profoundly altered in phenotype and function by UVB exposure and possess UV-specific DNA damage upon migrating to skin-draining lymph nodes. Expression of the proapoptotic protein FasL has been demonstrated in both skin and lymph node cells following UVB exposure. Additionally, functional FasL expression has recently been demonstrated to be required in the phenomenon of UV-induced immune suppression. To test the hypothesis that FasL expression by DNA-damaged Langerhans cells migrating to the skin-draining lymph nodes is a crucial event in the generation of this phenomenon, mice were given a single 5KJ/m2 UV-B exposure and sensitized to 0.5% FITC through the exposed area. Dendritic cells (DC) harvested from skin-draining lymph nodes (DLN) 18 hours following sensitization by magnetic CD11c-conjugated microbeads expressed high levels of Iab, CD80 and CD86, DEC-205 and bore the FITC hapten, suggesting epidermal origin. Radioimmunoassay of UV-specific DNA damage showed that DC contained the vast majority of cyclobutane pyrimidine dimers (CPDs) found in the DLN after UVB and exhibited increased FasL mRNA expression, a result which correlated with greatly increased FasL-mediated cytotoxicity. The ability of DCs to transfer sensitization to naïve hosts was lost following UVB exposure, a phenomenon which required DC FasL expression, and was completely reversed by cutaneous DNA repair. Collectively, these results demonstrate the central importance of DNA damage-induced FasL expression on migrating dendritic cells in mediating UV-induced suppression of contact hypersensitivity. ^

Investigation of the mechanism of increased melanoma incidence in UV -irradiated mouse skin

The availability of transplantable, syngeneic murine melanomas made it possible to study the potential effects of UV radiation on the growth and progression of melanomas in an animal model. The purpose of my study was to determine how UV-irradiation increases the incidence of melanoma out-growth, when syngeneic melanoma cells are transplanted into a UV-irradiated site. Short term intermittent UVB exposure produces a transitory change in the mice which allows the increased outgrowth of melanoma cells injected into the UV-irradiated site. One possible mechanism is an immunomodulatory effect of UVR on the host. An alternative mechanism to account for the increased tumor incidence in the UV-irradiated site, is the release of inflammatory mediators from UV-irradiated epidermal cells. A third possibility is that UVR could induce the production and/or release of melanoma-specific growth factors resulting in increased melanoma outgrowth.^ My first step in distinguishing among these different possible mechanisms was to characterize further the conditions leading to increased development of melanoma cells in UV-irradiated mouse skin. Next, I attempted to determine which of the 3 proposed mechanisms was most likely. To do this, I defined the specificity of the effect by examining the growth of additional C3H tumorigenic cell lines in UV-irradiated skin. Second, I determined the immunogenicity of these tumor cell lines. The tumor cell lines exhibiting increased tumor incidence are restricted to those tumor cell lines which are immunogenic in normal C3H mice. Third, I determined the effect of UVR on melanoma development did not occur in immunosuppressed mice.^ Because of results from these three lines of investigation suggested that the effect was immunologically mediated, I then investigated whether specific immune reactions were affected by local UV irradiation. To accomplish this, I investigated the effect of UVR on cutaneous immune cells and on induction of contact hypersensitivity (CHS), and I also determined the effect of UVR on the development and the expression of systemic immunity against the melanoma cells. There is no clear cut relationship between the number of Langerhans or Thy1+ cells and the UV effect on tumor incidence. Furthermore, there was no suppression of CHS in the UV-irradiated mice. While the development of systemic immunity is significantly reduced, it appears to be sufficient to provide in vivo immunity to tumor challenge. However the elicitation of tumor immunity in immunized mice can be abrogated if tumor challenge occurs in the site of UV irradiation. This investigation provides new information on an effect of UVR on the elicitation of tumor immunity. Furthermore, it indicates that UV radiation can play a role in the development of melanoma other than just in the transformation of melanocytes. ^

The role of p53 in skin cancer induction by UV radiation and as a potential tumor antigen in UV-induced murine skin tumors

Carcinoma of the skin is the most common type of human cancer in the United States. Ultraviolet radiation (UVR) present in the sunlight is thought to be the major carcinogen responsible for induction of skin cancer. In UV-associated skin carcinogenesis, mutations in p53 are not only present with very high frequency, but occur early in the course of tumor development. In addition, UV-induced skin tumors in mice exhibit unique immunological characteristics. They are highly antigenic and express both individually-specific tumor transplantation antigens recognized by effector T cells and the UV-associated common antigen recognized by UV-induced suppressor T cells. ^ To examine the hypothesis that p53 plays a critical role in preventing skin cancer induction by UVR, mice constitutively lacking one or two functional p53 alleles were compared to wild-type mice for their susceptibility to UV carcinogenesis. Both p53 +/– and –/– mice showed greater susceptibility to skin cancer induction than wild-type mice, and –/– mice were the most susceptible, Accelerated tumor development in the p53 +/– mice was not associated with loss of the remaining wild-type allele of p53 , but in many cases was associated with UV-induced mutations in p53. Our studies clearly demonstrate the essential role of p53 in protection against UV carcinogenesis, particularly in the eye and epidermis. ^ The role of p53 in the antigenicity of UV-induced murine skin tumors was also addressed. Primary UV-induced tumors from p53 –/–, +/– and +/+ mice were transplanted into both normal and immunosuppressed mice, and rates of tumor rejection were compared. Tumors from mice with only one or no functional p53 alleles were less antigenic than those from mice with two functional p53 alleles. Moreover, tumors with no functional p53 also failed to grow well in chronically UV-irradiated mice. These results indicate that p53 contributes to the strong antigenicity of UV-induced murine skin tumors, and suggest that it may play a critical role in expression of the UV-associated common antigen recognized by suppressor T cells. ^ In this study we also monitored the effect of UVR on the development of lymphoid malignancies in p53 deficient mice. The incidence of lymphoid malignancies in UV-irradiated p53 +/– mice was drastically enhanced compared to that in unirradiated counterparts. The immune responses of the mice were identical and were suppressed to the same extent by UV irradiation regardless of the p53 genotype. These data provide the first experimental evidence that exposure to UVR can contribute to the development of lymphoid neoplasms in genetically susceptible hosts. ^