Graduate Choral Recital

Antonio Vivaldi (1678-1741) paved an unconventional path to become a composer. Born in Venice where his father, Giovanni Battista was a violinist at St. Mark’s Basilica, Vivaldi was not trained to be a musician, though it is clear that he studied violin at a young age. Instead, he studied to be a priest, and was ordained in March 1703. In September 1703, Vivaldi was appointed maestro di violino at the Ospedale de Pietá, a Venetian orphanage for girls devoted to musical training and performance. Over the years, he was promoted to successively higher ranks, culminating in his appointment to the position of maestro di capella in 1735. His time at the Ospedale de Pietá was tumultuous. At one point, the institution could not afford to retain him, and at other times Vivaldi took long absences to travel Europe to compose and attend performances of his operas. In 1737, Vivaldi left the priesthood after the Church censured him for inappropriate conduct. In 1738, Vivaldi was terminated from the Ospedale de Pietá. He returned to Vienna, where he died in 1741

Wind storm damage to houses : planning and design consideration

Abstract: Over the last decades, South Africa has experienced a number of devastating wind events occurring almost every year. A large number of housing developments, particularly in the low-income segment, are not engineered adequately and are thus susceptible to high wind speeds, resulting in substantial damage to houses and socio-economic losses. Preventing such wind events from becoming disastrous, as witnessed in recent years, requires improved technical standards and construction practices. In this paper, an investigation is made into housing developments that were exposed to harsh climatic environments with high wind speeds. Two case studies are investigated in Cape Town and in Gauteng. In Cape Town, the housing development is in a coastal area. The houses experienced structural damage of foundations caused by wind-induced erosion of loose unsaturated soils. The study comprised of site visits and assessment of structural damage to houses, analysis of climatic information pertinent to the area and limited wind tunnel tests. The output of the study provided an insight on spatial planning of houses in close proximity to each other, and the need to perform either a wind tunnel test or Computation Fluid Dynamics (CFD) analysis of a development as part of the planning process. The other study was that of a wind disaster in the inland province of Gauteng which occurred in December, 2017. The disaster resulted in damages to houses, substations and a roof of a mall in Protea Glen, South West of Johannesburg. Engineering modelling of the houses subject to these winds indicate a need to review the technical standards and construction practices, and these are highlighted in the paper

Development of an updated fundamental basic wind speed map for SANS 10160-3

This paper evaluates the need for updating the strong wind climate stipulations of South Africa for the design of structures in accordance with SANS 10160-3:2010, as based on the latest information presented by Kruger et al (2013a; 2013b). The primary objective is to provide the geographic distribution of the characteristic gust wind speed by means of the fundamental value of the basic wind speed, stipulated as vb,0 in SANS 10160-3. A reassessment of previously published information is made to incorporate additional wind speed modelling results and to investigate identified anomalies. The format of presentation, based on local municipal districts, is subsequently motivated, assessed and implemented. In order to provide for situations requiring the consideration of the dynamic effects of wind loading, similar information on characteristic hourly mean wind speed is provided. It is concluded that the presentation of wind speed on a district basis provides an effective balance between the spatial resolution of the available information and its use in operational standardised design.http://www.journals.co.za/ej/ejour_civileng.htmlam2018Geography, Geoinformatics and Meteorolog

The potency of the fs260 connexin43 mutant to impair keratinocyte differentiation is distinct from other disease-linked connexin43 mutants

Although there are currently 62 mutants of Cx43 (connexin43) that can cause ODDD (oculodentodigital dysplasia), only two mutants have also been reported to cause palmar plantar hyperkeratosis. To determine how mutants of Cx43 can lead to this skin disease, REKs (rat epidermal keratinocytes) were engineered to express an ODDD-associated Cx43 mutant always linked to skin disease (fs260), an ODDD-linked Cx43 mutant which has been reported to sometimes cause skin disease (fs230), Cx43 mutants which cause ODDD only (G21R, G138R), a mouse Cx43 mutant linked to ODDD (G60S), a non-disease-linked truncated Cx43 mutant that is trapped in the endoplasmic reticulum (Δ244*) or full-length Cx43. When grown in organotypic cultures, of all the mutants investigated, only the fs260-expressing REKs consistently developed a thinner stratum corneum and expressed lower levels of Cx43, Cx26 and loricrin in comparison with REKs overexpressing wild-type Cx43. REKs expressing the fs260 mutant also developed a larger organotypic vital layer after acetone-induced injury and exhibited characteristics of parakeratosis. Collectively, our results suggest that the increased skin disease burden exhibited in ODDD patients harbouring the fs260 mutant is probably due to multiple additive effects cause by the mutant during epidermal differentiation

Connexin 43 mimetic peptide Gap27 reveals potential differences in the role of Cx43 in wound repair between diabetic and non-diabetic cells

During early wound healing (WH) events Connexin 43 (Cx43) is down-regulated at wound margins. In chronic wound margins, including diabetic wounds, Cx43 expression is enhanced suggesting that down-regulation is important for WH. We previously reported that the Cx43 mimetic peptide Gap27 blocks Cx43 mediated intercellular communication and promotes skin cell migration of infant cells in vitro. In the present work we further investigated the molecular mechanism of Gap27 action and its therapeutic potential to improve WH in skin tissue and diabetic and non-diabetic cells. Ex vivo skin, organotypic models and human keratinocytes/fibroblasts of young and old donors and of diabetic and non-diabetic origin were used to assess the impact of Gap27 on cell migration, proliferation, Cx43 expression, localization, phosphorylation and hemichannel function. Exposure of ex vivo WH models to Gap27 decreased dye spread, accelerated WH and elevated cell proliferation. In non-diabetic cell cultures Gap27 decreased dye uptake through Cx hemichannels and after scratch wounding cells showed enhanced migration and proliferation. Cells of diabetic origin were less susceptible to Gap27 during early passages. In late passages these cells showed responses comparable to non-diabetic cells. The cause of the discrepancy between diabetic and non-diabetic cells correlated with decreased Cx hemichannel activity in diabetic cells but excluded differences in Cx43 expression, localization and Ser368-phosphorylation. These data emphasize the importance of Cx43 in WH and support the concept that Gap27 could be a beneficial therapeutic to accelerate normal WH. However, its use in diabetic WH may be restricted and our results highlight differences in the role of Cx43 in skin cells of different origin

Targeting Cx43 and N-Cadherin, Which Are Abnormally Upregulated in Venous Leg Ulcers, Influences Migration, Adhesion and Activation of Rho GTPases

Venous leg ulcers can be very hard to heal and represent a significant medical need with no effective therapeutic treatment currently available

Targeting connexin43 expression accelerates the rate of wound repair.

The repair of tissue damage is a key survival process in all organisms and involves the coordinated activation of several cell types. Cell-cell communication is clearly fundamental to this process, and a great deal is known about extracellular communication within the wound site via cytokines. Here we show that direct cell-cell communication through connexin 43 (Cx43) gap junction channels also plays a major role in the wound healing process. In two different wound healing models, incisional and excisional skin lesions, we show that a single topical application of Cx43 antisense gel brings about a transient downregulation of Cx43 protein levels, and this results in a dramatic increase in the rate of wound closure. Cx43 knockdown reduces inflammation, seen both macroscopically, as a reduction in swelling, redness, and wound gape, and microscopically, as a significant decrease in neutrophil numbers in the tissue around the wound. One long-term consequence of the improved rate of healing is a significant reduction in the extent of granulation tissue deposition and the subsequent formation of a smaller, less distorted, scar. This approach is likely to have widespread therapeutic applications in other injured tissues and opens up new avenues of research into improving the wound healing process