Concert recording 2017-11-13c

[Track 1]. Flow, my tears / John Dowland -- [Track 2]. An Chloë, K. 524 / Wolfgang Amadeus Mozart -- [Track 3]. Der Kuss, op. 128 / Ludwig van Beethoven -- [Track 4]. From Sept mélodies, op. 2. III. Les Papillons [Track 5]. VI. Le Colibri / Ernest Chausson -- [Track 6]. Sogno / Francesco Totti -- [Track 7]. From Five Shakespeare songs, op. 23. I. Fear no more the heat o\u27 the sun [Track 8]. IV. Take, o take those lips away [Track 9]. V. Hey, ho, the wind and the rain / Roger Quilter

Correlation between ankle-brachial index, symptoms, and health-related quality of life in patients with peripheral vascular disease

AbstractObjectiveImproving health-related quality of life (HRQL) is the main goal of surgery to treat peripheral vascular disease (PVD); however, HRQL is rarely measured directly. Rather, most surgeons use other measures, such as patient symptoms and ankle-brachial index (ABI) to determine the need for intervention in PVD. The accuracy of these surrogates in representing HRQL has been untested. The purpose of this study was to determine the correlation of these measures with HRQL in patients undergoing evaluation for intervention in symptomatic PVD.MethodsPatients (n = 108) referred to the vascular surgery service with symptoms of PVD were enrolled in a prospective study of HRQL. Patients completed two validated HRQL questionnaires: the short form-36 (SF-36) and the Walking Impairment Questionnaire (WIQ). All patients had symptoms consistent with PVD, including claudication (n = 69; 63.9%), ischemic rest pain (n = 17; 15.7%), or tissue loss (n = 22; 20.4%). ABI was measured at presentation.ResultsThe mean ABI was 0.53 (range, 0.00-0.98). The maximal correlation between SF-36 score and ABI was reflected in the Physical Component Summary score (r = 0.25). WIQ score also exhibited modest correlation with ABI, with maximal correlation noted for stair climbing (r = 0.26). Both SF-36 and WIQ scores exhibited a highly significant association with symptoms. Patients with more severe symptoms, such as lifestyle-limiting claudication or limb-threatening ischemia, had lower HRQL scores compared with patients with non-lifestyle-limiting claudication. Multivariate analysis demonstrated that SF-36 and WIQ physical summary scores are better predicted by symptoms than by ABI (P < .01).ConclusionsHRQL in patients with PVD correlates weakly with ABI, but exhibits a closer association with vascular symptoms. However, neither variable fully expresses patient HRQL. These data suggest that sole reliance on these surrogates may not accurately reflect the effect of PVD on HRQL, or the potential benefit of vascular surgery in improving HRQL

Concert recording 2016-02-19

[Track 01]. My Johann / Edvard Grieg -- [Track 02]. Batti, batti bel Masetto / Wolfgang Amadeus Mozart -- [Track 03]. Ah mio cor / George Frideric Handel -- [Track 04]. Bright is the ring of words / Ralph Vaughan Williams -- [Track 05]. Le colibri / Ernest Chausson -- [Track 06]. Do not go, my love / Richard Hageman -- [Track 07]. Go, lovely rose / Roger Quilter -- [Track 08]. Sonntag / Johannes Brahms -- [Track 09]. O mio babbino caro from Gianni Schicchi / Giacomo Puccini -- [Track 10]. Spiel auf deine Geige from Venus in Seide / Robert Stolz -- [Track 11]. Die Spröde / Hugo Wolf -- [Track 12]. I want magic! from A streetcar named desire / Andre Previn -- [Track 13]. What if... / Lee Hoiby -- [Track 14]. Va! laisse couler mes larmes from Werther / Jules Massenet

The effect of S-substitution at the O6-guanine site on the structure and dynamics of a DNA oligomer containing a G:T mismatch

The effect of S-substitution on the O6 guanine site of a 13-mer DNA duplex containing a G:T mismatch is studied using molecular dynamics. The structure, dynamic evolution and hydration of the S-substituted duplex are compared with those of a normal duplex, a duplex with Ssubstitution on guanine, but no mismatch and a duplex with just a G:T mismatch. The S-substituted mismatch leads to cell death rather than repair. One suggestion is that the G:T mismatch recognition protein recognises the S-substituted mismatch (GS:T) as G:T. This leads to a cycle of futile repair ending in DNA breakage and cell death. We find that some structural features of the helix are similar for the duplex with the G:T mismatch and that with the S-substituted mismatch, but differ from the normal duplex, notably the helical twist. These differences arise from the change in the hydrogen-bonding pattern of the base pair. However a marked feature of the S-substituted G:T mismatch duplex is a very large opening. This showed considerable variability. It is suggested that this enlarged opening would lend support to an alternative model of cell death in which the mismatch protein attaches to thioguanine and activates downstream damage-response pathways. Attack on the sulphur by reactive oxygen species, also leading to cell death, would also be aided by the large, variable opening

Concert recording 2017-11-07

[Track 1]. Sitzzoso, mio stizzoso / Giovanni Pergolesi -- [Track 2]. Widmung / Robert Schumann -- [Track 3]. The roadside fire / Ralph Vaughan Williams -- [Track 4]. La promessa / Gioachino Rossini -- [Track 5]. Non é ver / Tito Mattei -- [Track 6]. Les Chemins d\u27amour / Francis Poulenc -- [Track 7]. Una donna a quindici anni from Cosi fan tutte / Wolfgang Amadeus Mozart -- [Track 8]. Non più andrai from The marriage of Figaro / Mozart -- [Track 9]. Botschaft / Johannes Brahms -- [Track 10]. Du bist die Ruh / Franz Schubert -- [Track 11]. Gualitier Maldè...Caro nome from Reigoletto / Giuseppe Verdi -- [Track 12]. Mondnacht / Robert Schumann -- [Track 13]. Les Roses d\u27Ispahan / Gabriel Fauré -- [Track 14]. An Chloe / Mozart -- [Track 15]. Sogno / Francesco Tosti -- [Track 16]. Er ist\u27s / Hugo Wolf -- [Track 17]. Ah, je ris de me voir from Faust / Charles Gounod -- [Track 18]. Claire du lune / Claude Debussy -- [Track 19]. Kling! / Richard Strauss -- [Track 20]. Erstarrung / Schubert -- [Track 21]. I\u27m glad I\u27m not a tenor / Ben Moore -- -- [Track 22]. Apparition / Debussy

Expression of tumour-specific antigens underlies cancer immunoediting

Cancer immunoediting is a process by which immune cells, particularly lymphocytes of the adaptive immune system, protect the host from the development of cancer and alter tumour progression by driving the outgrowth of tumour cells with decreased sensitivity to immune attack1, 2. Carcinogen-induced mouse models of cancer have shown that primary tumour susceptibility is thereby enhanced in immune-compromised mice, whereas the capacity for such tumours to grow after transplantation into wild-type mice is reduced2, 3. However, many questions about the process of cancer immunoediting remain unanswered, in part because of the known antigenic complexity and heterogeneity of carcinogen-induced tumours4. Here we adapted a genetically engineered, autochthonous mouse model of sarcomagenesis to investigate the process of cancer immunoediting. This system allows us to monitor the onset and growth of immunogenic and non-immunogenic tumours induced in situ that harbour identical genetic and histopathological characteristics. By comparing the development of such tumours in immune-competent mice with their development in mice with broad immunodeficiency or specific antigenic tolerance, we show that recognition of tumour-specific antigens by lymphocytes is critical for immunoediting against sarcomas. Furthermore, primary sarcomas were edited to become less immunogenic through the selective outgrowth of cells that were able to escape T lymphocyte attack. Loss of tumour antigen expression or presentation on major histocompatibility complex I was necessary and sufficient for this immunoediting process to occur. These results highlight the importance of tumour-specific-antigen expression in immune surveillance, and potentially, immunotherapy.National Institutes of Health (U.S.) (Grant 1 U54 CA126515-01)National Cancer Institute (U.S.) (Cancer Center Support Grant P30-CA14051)Margaret A. Cunningham Immune Mechanisms in Cancer Research Fellowship AwardJohnD. Proctor FoundationDaniel K. Ludwig Schola

The Heavy Vehicle Study: a case-control study investigating risk factors for crash in long distance heavy vehicle drivers in Australia

Background Heavy vehicle transportation continues to grow internationally; yet crash rates are high, and the risk of injury and death extends to all road users. The work environment for the heavy vehicle driver poses many challenges; conditions such as scheduling and payment are proposed risk factors for crash, yet the precise measure of these needs quantifying. Other risk factors such as sleep disorders including obstructive sleep apnoea have been shown to increase crash risk in motor vehicle drivers however the risk of heavy vehicle crash from this and related health conditions needs detailed investigation. Methods and Design The proposed case control study will recruit 1034 long distance heavy vehicle drivers: 517 who have crashed and 517 who have not. All participants will be interviewed at length, regarding their driving and crash history, typical workloads, scheduling and payment, trip history over several days, sleep patterns, health, and substance use. All participants will have administered a nasal flow monitor for the detection of obstructive sleep apnoea. Discussion Significant attention has been paid to the enforcement of legislation aiming to deter problems such as excess loading, speeding and substance use; however, there is inconclusive evidence as to the direction and strength of associations of many other postulated risk factors for heavy vehicle crashes. The influence of factors such as remuneration and scheduling on crash risk is unclear; so too the association between sleep apnoea and the risk of heavy vehicle driver crash. Contributory factors such as sleep quality and quantity, body mass and health status will be investigated. Quantifying the measure of effect of these factors on the heavy vehicle driver will inform policy development that aims toward safer driving practices and reduction in heavy vehicle crash; protecting the lives of many on the road network

Remarkable fly (Diptera) diversity in a patch of Costa Rican cloud forest : Why inventory is a vital science

Study of all flies (Diptera) collected for one year from a four-hectare (150 x 266 meter) patch of cloud forest at 1,600 meters above sea level at Zurqui de Moravia, San Jose Province, Costa Rica (hereafter referred to as Zurqui), revealed an astounding 4,332 species. This amounts to more than half the number of named species of flies for all of Central America. Specimens were collected with two Malaise traps running continuously and with a wide array of supplementary collecting methods for three days of each month. All morphospecies from all 73 families recorded were fully curated by technicians before submission to an international team of 59 taxonomic experts for identification. Overall, a Malaise trap on the forest edge captured 1,988 species or 51% of all collected dipteran taxa (other than of Phoridae, subsampled only from this and one other Malaise trap). A Malaise trap in the forest sampled 906 species. Of other sampling methods, the combination of four other Malaise traps and an intercept trap, aerial/hand collecting, 10 emergence traps, and four CDC light traps added the greatest number of species to our inventory. This complement of sampling methods was an effective combination for retrieving substantial numbers of species of Diptera. Comparison of select sampling methods (considering 3,487 species of non-phorid Diptera) provided further details regarding how many species were sampled by various methods. Comparison of species numbers from each of two permanent Malaise traps from Zurqui with those of single Malaise traps at each of Tapanti and Las Alturas, 40 and 180 km distant from Zurqui respectively, suggested significant species turnover. Comparison of the greater number of species collected in all traps from Zurqui did not markedly change the degree of similarity between the three sites, although the actual number of species shared did increase. Comparisons of the total number of named and unnamed species of Diptera from four hectares at Zurqui is equivalent to 51% of all flies named from Central America, greater than all the named fly fauna of Colombia, equivalent to 14% of named Neotropical species and equal to about 2.7% of all named Diptera worldwide. Clearly the number of species of Diptera in tropical regions has been severely underestimated and the actual number may surpass the number of species of Coleoptera. Various published extrapolations from limited data to estimate total numbers of species of larger taxonomic categories (e.g., Hexapoda, Arthropoda, Eukaryota, etc.) are highly questionable, and certainly will remain uncertain until we have more exhaustive surveys of all and diverse taxa (like Diptera) from multiple tropical sites. Morphological characterization of species in inventories provides identifications placed in the context of taxonomy, phylogeny, form, and ecology. DNA barcoding species is a valuable tool to estimate species numbers but used alone fails to provide a broader context for the species identified.Peer reviewe

Comprehensive inventory of true flies (Diptera) at a tropical site

Peer reviewe