Climate change in the kitchen and on the public health agenda

Direct or indirect consequences of climate change on the vulnerable groups within communities are discussed. The health impacts of climate change will be felt in all facets of life and will be a significant challenge to public health systems and in health promotion fields.<br /

Climate change and social inclusion: opportunities for justice and empowerment

...the greatest untapped resource at our disposal lies in the disadvantaged Australians living in our most excluded communities. (Nicholson 2007 p. 4)The commons are where justice and sustainability converge, where ecology and equity meet. (Shiva 2005 p. 50)Since 1990, the Intergovernmental Panel on Climate Change (IPCC) has recognised human induced climate change to be primarily a result of burning fossil fuels and land clearing (Lee 2007). Changes to the world\u27s climate patterns have been occurring for decades, but only in recent times has climate change arrived in our collective conscious. An onslaught of extreme weather events, destruction and failure of crops, increasing levels of water restrictions, government announcement of desalination plants. proposed increase in prices for utilities such as power and water - have ushered climate change into the Australian lexicon.The challenges for all of us are many and varied and perhaps even unimaginable. as many propose a global reduction in annual C02 emissions of between 60-80% (compared to 1990 levels) by 2050. We are not talking just about the re-construction of our world, but about its re-invention. Ryan (2007)How will climate change affect us? Who is most vulnerable? What will be the features of policies and strategies to combat climate change that ensure an equitable and just response across our entire society? Are our present social-cultural justice paradigms of social exclusion and inclusion adequate in addressing the impending health consequences that are likely to result from climate change, and in supporting an equitable. harmonious and fruitful life for all population groups in the future?This paper, written in the spirit of solution-oriented research. focusing on the causes of positive health rather than the causes of disease and other problems (Robinson &amp; Sirard 2005). explores the possibility of a paradigm shift which imagines the social inclusion of specific population groups, not as an appended extra, but integral to the design of an equitable, sustainable low carbon society of the future.<br /

Topical and Systemic Effects of Retinoids on Horn-Filled Utriculus Size in the Rhino Mouse. A Model to Quantify “Antikeratinizing” Effects of Retinoids

A method was developed to quantify the “antikeratinizing” effects of various retinoids (all-trans-retinoic acid, 13-cis-retinoic acid, motretinide, etretinate) in rhino mouse skin, which contains many keratinized pilosebaceous structures or horn-filled utriculi. Mean utriculus diameters in whole mount epidermis were determined and dose-response relationships were constructed after topical or oral administration of test retinoids. All- trans-retinoic acid was 3.7×, 12.5×, and 50× more potent than 13-cis-retinoic acid, etretinate, and motretinide, respectively, after topical administration. Administered orally, all-trans-retinoic acid was 2.3× more potent than 13-cis-retinoic acid At 5 mg/kg, each retinoid produced a significant reduction in utriculus size. The rhino mouse model represents a novel and useful assay to quantify antikeratinizing activity and potency differences of biologically active retinoids

Effects of Topical Retinoids on Cytoskeletal Proteins: Implications for Retinoid Effects on Epidermal Differentiation

In vivo effects of retinoids on epidermal differentiation were investigated by analyzing cytoskeletal proteins in rhino mice treated topically with all-trans-retinoic acid (RA) and other retinoids (13-cis-retinoic acid, etretinate, TTNPB). Non-disulfide-linked cytoskeletal proteins, including keratins from the epidermal “living layers,” were first selectively extracted using 9.5 M urea; subsequently, keratins of the stratum corneum were isolated using 9.5 M urea plus a reducing agent. Gel electrophoresis and immunoblot analysis showed that urea extracts of epidermis from vehicle-treated skin were composed predominantly of four major keratins (analogous to human epidermal keratins K1, K5, K10, and K14), and the keratin filament-associated protein filaggrin. In contrast, extracts of epidermis from retinoid-treated skin contained additional keratins (K6, K16, and K17) and almost no detectable filaggrin. Furthermore, similar analysis of stratum corneum keratins demonstrated that extracts from RA-treated skin did not contain the partially proteolyzed keratins typically observed in stratum corneum extracts of control animals. Hyperplasia-inducing agents (salicylic acid, croton oil) caused an increase in keratins K6, K16, and K17, but they did not effect filaggrin or alter proteolysis of stratum corneum keratins.The result that RA induced expression of keratins K6, K16, and K17, as commonly expressed in hyperproliferative epidermis, is consistent with the notion that retinoids increase epidermal cell proliferation in the basal and/or lower spinous layers. The findings that topical RA decreased filaggrin expression and reduced proteolysis of stratum corneum keratins, despite increased size and number of granular cells and the presence of an anucleate stratum corneum, suggest that topical RA may also modulate a later stage of epidermal differentiation involved in stratum corneum formation

Suprofen, A New Peripheral Analgesic1

ABSTRACT Capetola, Rober