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It is a challenge to measure sexual selection because both stochastic events (chance) and deterministic factors (selection) generate variation in individuals' reproductive success. Most researchers realize that random events ('noise') make it difficult to detect a relationship between a trait and mating success (i.e. the presence of sexual selection). There is, however, less appreciation of the dangers that arise if stochastic events vary systematically. Systematic variation makes variance-based approaches to measuring the role of selection problematic. This is why measuring the opportunity for sexual selection (I(s) and I(mates)) is so vulnerable to misinterpretation. Although I(s) does not measure actual sexual selection (because it includes stochastic variation in mating/fertilization success) it is often implicitly assumed that it will be correlated with the actual strength of sexual selection. The hidden assumption is that random noise is randomly distributed across populations, species or the sexes. Here we present a simple numerical example showing why this practice is worrisome. Specifically, we show that chance variation in mating success is higher when there are fewer potential mates per individual of the focal sex [i.e. when the operational sex ratio (OSR), is more biased]. This will lead to the OSR covarying with I(s) even when the strength of sexual selection is unaffected by the OSR. This can generate false confidence in identifying factors that determine variation in the strength of sexual selection. We emphasize that in nature, even when sexual selection is strong, chance variation in mating success is still inevitable because the number of mates per individual is a discrete number. We hope that our worked example will clarify a recent debate about how best to measure sexual selection.

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Parental care is expected to increase the likelihood of offspring survival at the cost of investment in future reproductive success. However, alternative parental behaviours, such as filial cannibalism, can decrease current reproductive success and consequently individual fitness. We evaluate the role of among-offspring relatedness on the evolution of parental care and filial cannibalism. Building on our previous work, we show how the evolution of care is influenced by the effect of among-offspring relatedness on both the strength of competition and filial cannibalism. When there is a positive relationship between among-offspring competition and relatedness, parental care will be favoured when among-offspring relatedness is relatively low, and the maintenance of both care and no-care strategies is expected. If the relationship between among-offspring competition and relatedness is negative, parental care is most strongly favoured when broods contain highly related offspring. Further, we highlight the range of conditions over which the level of this among-offspring relatedness can affect the co-occurrence of different care/no care and cannibalism/no cannibalism strategies. Coexistence of multiple strategies is independent of the effects of among-offspring relatedness on cannibalism but more likely when among-offspring relatedness and competition are positively associated.

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Parental care is of fundamental importance to understanding reproductive strategies and allocation decisions. Here, we explore how parental care strategies evolve in variable environments. Using a set of life-history trait trade-offs, we explore the relative costs and benefits of parental care in stochastic environments. Specifically, we consider the cases in which environmental variability results in varying adult death rates, egg death rates, reproductive rate and carrying capacity. Using a measure of fitness appropriate for stochastic environments, we find that parental care has the potential to evolve over a wide range of life-history characteristics when the environment is variable. A variable environment that affects adult or egg death rates can either increase or decrease the fitness of care relative to that in a constant environment, depending on the specific costs of care. Variability that affects carrying capacity or adult reproductive rate has negligible effects on the fitness associated with care. Increasing parental care across different life-history stages can increase fitness gains in variable environments. Costly investment in care is expected to affect the overall fitness benefits, the fitness optimum and rate of evolution of parental care. In general, we find that environmental variability, the life-history traits affected by such variability and the specific costs of care interact to determine whether care will be favoured in a variable environment and what levels of care will be selected.

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Sexual selection can explain major micro- and macro-evolutionary patterns. Much of current theory predicts that the strength of sexual selection (i) is driven by the relative abundance of males and females prepared to mate (i.e. the operational sex ratio, OSR) and (ii) can be generally estimated by calculating intra-sexual variation in mating success (e.g. the opportunity for sexual selection, I(s)). Here, we demonstrate the problematic nature of these predictions. The OSR and I(s) only accurately predict sexual selection under a limited set of circumstances, and more specifically, only when mate monopolization is extremely strong. If mate monopolization is not strong, using OSR or I(s) as proxies or measures of sexual selection is expected to produce spurious results that lead to the false conclusion that sexual selection is strong when it is actually weak. These findings call into question the validity of empirical conclusions based on these measures of sexual selection.

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In budding yeast (Saccharomyces cerevisiae), the periodic expression of the G2/M-specific gene CLB2 depends on a DNA binding complex that mediates its repression during G1 and activation from the S phase to the exit of mitosis. The switch from low to high expression levels depends on the transcriptional activator Ndd1. We show that the inactivation of the Sin3 histone deacetylase complex bypasses the essential role of Ndd1 in cell cycle progression. Sin3 and its catalytic subunit Rpd3 associate with the CLB2 promoter during the G1 phase of the cell cycle. Both proteins dissociate from the promoter at the onset of the S phase and reassociate during G2 phase. Sin3 removal coincides with a transient increase in histone H4 acetylation followed by the expulsion of at least one nucleosome from the promoter region. Whereas the first step depends on Cdc28/Cln1 activity, Ndd1 function is required for the second step. Since the removal of Sin3 is independent of Ndd1 recruitment and Cdc28/Clb activity it represents a unique regulatory step which is distinct from transcriptional activation.

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In this publication different detachment factors were tested for enhancing carrier to carrier transfer for scale-up of macroporous microcarrier based bioprocesses. Two Chinese hamster ovary cell lines, CHO-K1 and a genetically engineered CHO-K1 derived cell line (CHO-MPS), producing recombinant human Arylsulfatase B, were examined. The cells were grown on Cytoline 1microcarriers (Amersham Biosciences, Uppsala, Sweden) in protein-free and chemically defined medium respectively. Fully colonised microcarriers were used at passage ratios of approximately 1:10 for carrier to carrier transfer experiments. To accelerate the colonisation of the non-colonised, freshly added microcarriers the detachment reagents trypsin, papain, Accutasetrade mark (PAA, Linz, Austria), heparin and dextransulphate were used. Both cell lines showed good results with trypsin, Accutase and dextransulphate (Amersham Biosciences, Uppsala, Sweden), while papain failed to enhance carrier to carrier transfer in comparison to the non-treated reference. The maximum growth rate of cells on microcarriers with 2% dextransulphate in the medium was 0.25 +/- 0.02d(-1) and 0.27 +/- 0.03d(-1) for the CHO-MPS and CHO-K1, respectively. TheCHO-K1 grew best after detachment with trypsin (mu = 0.36 +/- 0.03d(-1)). This indicates, that one of the key parameters for carrier to carrier transfer is the uniform distribution of cells on the individual carriers during the initial phase. When this distribution can be improved, growth rate increases, resulting in a faster and more stable process.

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We recently reported a novel autosomal recessive mouse mutation designated nackt (nkt). Homozygous mutant mice have diffuse alopecia and a marked reduction in the proportion of CD4+ T cells in the thymus and peripheral lymphoid tissues. Here we show that the CD4 T-cell deficiency is due to a defect in the thymic microenvironment rather than the hematopoietic compartment. Furthermore, we identified the molecular basis of the mutant phenotype by demonstrating that the nkt mutation represents a 118-bp deletion of the cathepsin L (Ctsl) gene which is required for degradation of the invariant chain, a critical chaperone for major histocompatibility complex class II molecules. This finding explains the similarities in skin and immune defects observed in nkt/nkt and Ctsl -/- mice. The data reported here provide further in vivo evidence that the lysosomal cysteine protease cathepsin L plays a critical role in CD4+ T-cell selection in the thymus.

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Using surviving human skin, percutaneous absorption following topical application of hematoporphyrin derivative was investigated. Hematoporphyrin derivative gave strong red fluorescence, which was dependent from it's actual concentration, from the used kind of vehicle, from preparation time, and from time between preparation and application of hematoporphyrin derivative solution. Ultrastructural investigation verified cytoplasmatic membranes and mitochondria as the principal targets also after topical application followed by irradiation with visible light.

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The ultrastructural feature of keratinocytes was investigated in human superficially spreading melanomas of type B. The tumor cells of these melanomas are characterized by spheroidal melanosomes and containing pheomelanins. Contrary to type A melanomas the keratinocytes show no striking transformation reaction neither in the nucleus nor in the cytoplasm although this part of the cell mostly contains abundant melanin granules surrounding the nucleus. Whether there exists a relation to the clinical course still has to be clarified.

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Testicular biopsies were obtained from Wistar rats that had been infected artificially with Ureaplasma urealyticum, serotype 3. Approximately 50% of the biopsy specimens obtained 3 and 6 months after infection showed degeneration of the germinal epithelium, giant cell formation and Leydig cell hyperplasia. Electron microscopic studies revealed striking alterations of Sertoli cells, germ cells, and Leydig cells as well as ureaplasma organisms inside the seminiferous tubules. The changes noted in the ertoli cells were apparent as early as one week after infection.

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Electron microscopy was used in investigations of interdigitating reticulum cells of axillary lymph nodes sampled from patients with atopic eczema in different clinical stages. The ultrastructure of these cells was found to differ clearly from that of cells under largely normal conditions. For example, the lumina of the so-called tubulovesicular structures (TV) were clearly reduced. Considerable lobulation of peripheral cytoplasm was an additional finding recorded from the acute clinical stage, while in terms of cellular morphology (interdigitation) contact with T-lymphocytes was obviously reduced. Cytoplasmic processus were clearly decreased in the chronic stage.

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Epidermal Langerhans cells (LC) from skin of clinically normal appearance in psoriatics were studied electron microscopically and compared with LC from the skin of healthy volunteers and from those with other dermatoses. Results show that LC from psoriatics display partly distinct cytoplasmic alterations. Moreover, about half of LC investigated were partly or mainly surrounded by clearly widened intercellular spaces, such that an immediate cellular contact with neighbouring keratinocytes was correspondingly decreased. Whether such LC are functionally altered remains to be clarified.

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Male Wistar rats were infected with Ureaplasma urealyticum, serotype 3 or 7, by injecting broth containing organisms into the urinary bladder following laparatomy. Animals were sacrificed 3, 7 and 21 days after infection. Ureaplasmas were detected in the organs of the genital tract by culture in 43% (serotype 3) and in 60% (serotype 7) of the animals. Type-specific ureaplasma antigen was detected in the genital organs in 44% (serotype 3) and 45% (serotype 7) of the animals. Control animals injected with sterile bouillon were negative for organisms and antigen. Male Wistar rats artificially infected with Ureaplasma urealyticum, serotype 3, were mated 3 and 6 months after infection with ureaplasma free female rats. The mating experiment revealed a smaller mean litter size and a lower birth weight in the offspring of infected males compared with the control animals, but no general influence on the fertility of infected animals.

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Electron microscopic investigation of skin biopsies revealed that keratinocytes in clinically uninvolved skin from psoriatic patients show the same mitochondrial ring phenomenon after the application of dithranol as has been observed in the cutaneous lesions proper. In various other skin diseases no mitochondrial reaction was evident after dithranol treatment, nor was it seen in chronic dermatitis when dithranol was not applied. It appears, therefore, that this morphological phenomenon is specific to psoriasis and may provide information concerning functional alterations in the pathogenesis of this disease.

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Morphological changes occurring in the rabbit retina after fast neutron irradiation levels of 250,500 and 1,000 cGy are discussed. The threshold dose that may cause damage to retinal structures is 250 cGy.

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