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Survival and growth of the anaerobic gut fungi (AGF; Neocallimastigomycota) in the herbivorous gut necessitate the possession of multiple abilities absent in other fungal lineages. We hypothesized that horizontal gene transfer (HGT) was instrumental in forging the evolution of AGF into a phylogenetically distinct gut-dwelling fungal lineage. The patterns of HGT were evaluated in the transcriptomes of 27 AGF strains, 22 of which were isolated and sequenced in this study, and 4 AGF genomes broadly covering the breadth of AGF diversity. We identified 277 distinct incidents of HGT in AGF transcriptomes, with subsequent gene duplication resulting in an HGT frequency of 2 to 3.5% in AGF genomes. The majority of HGT events were AGF specific (91.7%) and wide (70.8%), indicating their occurrence at early stages of AGF evolution. The acquired genes allowed AGF to expand their substrate utilization range, provided new venues for electron disposal, augmented their biosynthetic capabilities, and facilitated their adaptation to anaerobiosis. The majority of donors were anaerobic fermentative bacteria prevalent in the herbivorous gut. This study strongly indicates that HGT indispensably forged the evolution of AGF as a distinct fungal phylum and provides a unique example of the role of HGT in shaping the evolution of a high-rank taxonomic eukaryotic lineage.IMPORTANCE The anaerobic gut fungi (AGF) represent a distinct basal phylum lineage (Neocallimastigomycota) commonly encountered in the rumen and alimentary tracts of herbivores. Survival and growth of anaerobic gut fungi in these anaerobic, eutrophic, and prokaryote-dominated habitats necessitates the acquisition of several traits absent in other fungal lineages. We assess here the role of horizontal gene transfer as a relatively fast mechanism for trait acquisition by the Neocallimastigomycota postsequestration in the herbivorous gut. Analysis of 27 transcriptomes that represent the broad diversity of Neocallimastigomycota identified 277 distinct HGT events, with subsequent gene duplication resulting in an HGT frequency of 2 to 3.5% in AGF genomes. These HGT events have allowed AGF to survive in the herbivorous gut by expanding their substrate utilization range, augmenting their biosynthetic pathway, providing new routes for electron disposal by expanding fermentative capacities, and facilitating their adaptation to anaerobiosis. HGT in the AGF is also shown to be mainly a cross-kingdom affair, with the majority of donors belonging to the bacteria. This study represents a unique example of the role of HGT in shaping the evolution of a high-rank taxonomic eukaryotic lineage.

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The ageing process is noticeable within all organs of the body and manifests itself visibly in the skin. Skin ageing is influenced by several factors including genetics, environmental exposure, hormonal changes and metabolic processes. Together these factors lead to cumulative alterations of skin structure, function and appearance. The functioning of the central nervous, immune, endocrine and cardiovascular systems, as well as the skin is also impaired with age. Chronologically, aged skin is thin, relatively flattened, dry and unblemished, with some loss of elasticity and age-related loss of architectural regularity. General atrophy of the extracellular matrix is reflected by a decrease in the number of fibroblasts. Reduced levels of collagen and elastin, with impaired organization are primarily because of decreased protein synthesis affecting types I and III collagen in the dermis, with an increased breakdown of extracellular matrix proteins. Oxidative stress is considered of primary importance in driving the ageing process. The original free radical theory of ageing purported that the molecular basis of ageing was derived from a lifetime accumulation of oxidative damage to cells resulting from excess reactive oxygen species (ROS) produced as a consequence of aerobic metabolism. Although the skin possesses extremely efficient anti-oxidant activities, during ageing, ROS levels rise and anti-oxidant activities decline. The ROS are necessary in multiple MAP kinase pathways and the induction of AP-1, in turn, up-regulates expression of matrix-metalloproteinases providing a plausible mechanism for the increased collagen degradation in aged human skin.

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With the advancement of skin research, today's consumer has increased access to technological information about ageing skin and hair care products. As a result, there is a rapidly increasing demand for proof of efficacy of these products. Recognizing these demands has led to the development and validation of many clinical methods to measure and quantify ageing skin and the effects of anti-ageing treatments. Many of the current testing methods used to research and evaluate anti-ageing product claim to employ sophisticated instruments alongside more traditional clinical methods. Intelligent use of combined clinical methods has enabled the development of technologically advanced consumer products providing enhanced efficacy and performance. Of non-invasive methods for the assessment and quantification of ageing skin, there is a plethora of tools available to the clinical researcher as defined by key clinically observed ageing parameters: skin roughness and surface texture; fine lines and wrinkles; skin pigmentation; skin colour; firmness and elasticity; hair loss; and proliferative lesions. Furthermore, many clinical procedures for the evaluation of ageing skin treatments are combined with invasive procedures, which enable added-value to claims (such as identification and alteration of biochemical markers), particularly in those cases where perception of product effect needs additional support. As discussed herein, clinical methods used in the assessment of skin ageing are many and require a disciplined approach to their use in such investigations.

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Ultraviolet radiation in sunlight produces a range of acute and chronic adverse effects on the skin including sunburn, photosensitivity rashes, immunosuppression, photoageing and carcinogenesis. Sunscreens aim to provide protection, but standard testing procedures primarily involve assessment of ability to protect against acute erythema, as evidenced by the sun protection factor (SPF). The SPF may correlate poorly with other aspects of protection, particularly since ultraviolet A is weakly erythemogenic compared with ultraviolet B, yet may make a greater contribution to certain other skin effects of sunlight. Nevertheless, there is an increasing tendency for the sunscreen industry to make claims for their products beyond the SPF data. There is a need to develop systems for clinical testing of sunscreens against other endpoints caused by ultraviolet exposure of skin, including immunosuppression and photosensitivity rashes. In particular, there is a largely unrecognized need for testing of sunscreens against the condition known as polymorphic light eruption, a photosensitivity disorder estimated to affect a staggering 10-20% of the population in the northern hemisphere. Ultimately, protection of the skin by sunscreens can only be as effective as their adequacy of application to the skin surface in the everyday setting permits. Optimal sunscreen formulation, and public and patient education in appropriate application technique, both make vital contributions to efficacy of sunscreen protection. This article focuses on the need for extended clinical testing of sunscreens, with particular reference to the photosensitivity disorders, and for improvements in sunscreen formulation and in the adequacy of sunscreen application to the skin surface.

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Men over the age of 45 present with thicker, more advanced melanomas than younger people. A randomised trial was conducted in this group to evaluate whether an educational brochure would increase knowledge about melanoma and the ability to recognise and discriminate between pigmented skin lesions. Men in an industrial complex were allocated to an intervention group (n = 110) and two control groups (n = 96 and n = 108). The intervention group was given two educational brochures about melanoma. Their effect on knowledge and ability to detect pigmented lesions was assessed by a questionnaire and a self-examination body chart given before the brochure, and at four weeks and three months after return of the brochure. The control groups did not receive any educational material, but control group 2 received the questionnaire and chart. At the end of the study all participants were examined for pigmented lesions by doctors, whose counts were compared with those of the participants. There was a significant (19.8 per cent) increase in knowledge about melanoma in the intervention group (but not in the control groups), except for discrimination of photos of benign and malignant lesions. The educational material did not improve the ability of those in the intervention group to recognise and count their pigmented lesions nor to discriminate between benign and malignant pigmented lesions. The increased knowledge about melanoma was retained for at least three months.

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We have evaluated the film quality and overall clinical utility of a unique high-resolution portal film system which utilizes high contrast graphics art film. A total of 127 unselected patients had their conventional portal films and high-resolution films of the same site, compared and graded subjectively for a variety of parameters by an independent panel of radiotherapists and radiographers. Although consistent improvements in most aspects of image quality were noted, improved overall clinical usefulness of the high-resolution portal film system in comparison to the conventional films, when subjected to multiple regression analysis, was confined to lateral neck views only. High-resolution portal film utility was also found to depend significantly on field size with areas less than 110 cm2 having a markedly worse clinical utility score.

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Alteration of guinea pig keratinocyte membrane microviscosities (eta) by liposomes of varying composition was determined by fluorescence polarization of 1,6-diphenyl-1,3,5-hexatriene. Measurements performed either with whole cell suspensions or Percoll-separated cell subpopulations, indicate a similar membrane microviscosity (eta = 3.37 poise +/- 10%) compared to those microviscosities reported for other cell types. Our findings show that treatment of guinea pig keratinocytes with liposomes composed of phospholipids results in a decreased membrane microviscosity (1.95 poise), whereas treatment of the cells with an emulsion of cholesterol hemisuccinate, or liposomes composed of cerebrosides, causes an increase in membrane microviscosity (3.85 poise and 5.55 poise +/- 10%, respectively). Changes in membrane fluidity had no significant effect on cell viability. A reduced membrane microviscosity resulted in a decrease in the binding of Concanavalin A to keratinocytes, whereas an increased microviscosity resulted in an increased binding of Concanavalin A. Furthermore, endocytosis of Concanavalin A bound to keratinocytes plasma membranes was not significantly affected by a reduced membrane microviscosity, whereas an increased membrane microviscosity completely blocked the endocytosis of Concanavalin A. Another novel observation was that membranes "fluidified" by phospholipid liposomes could be "rigidified" by treatment with cholesterol hemisuccinate and vice versa. Moreover, these alternate changes in membrane microviscosity resulted in simultaneous alternate changes in the binding of Concanavalin A to the keratinocyte surface.

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