Supplier Corporate Social Responsibility Policies from a Strategic Perspective

Corporate Social Responsibility (CSR) is a corporate initiative to assess and take responsibility for the company\u27s effects on the environment and impact on social welfare (www.Investopedia.com). The goal of CSR is to embrace responsibility for the company\u27s actions and encourage a positive impact through its activities on the environment, consumers, employees, communities, stakeholders and all others who may also be considered stakeholders. The term generally applies to company efforts that go beyond what may be required by regulators or environmental protection groups. CSR policies function as a built-in, self-regulating mechanism whereby a business monitors and ensures its active compliance with the spirit of the law, ethical standards, and international norms. Corporate social responsibility may also be referred to as corporate citizenship and can involve incurring short-term costs that do not provide an immediate financial benefit to the company, but instead promote positive social and environmental change

Gaps and forks in DNA replication: Rediscovering old models

Most current models for replication past damaged lesions envisage that translesion synthesis occurs at the replication fork. However older models suggested that gaps were left opposite lesions to allow the replication fork to proceed, and these gaps were subsequently sealed behind the replication fork. Two recent articles lend support to the idea that bypass of the damage occurs behind the fork. In the first paper, electron micrographs of DNA replicated in UV-irradiated yeast cells show regions of single-stranded DNA both at the replication forks and behind the fork, the latter being consistent with the presence of gaps in the daughter-strands opposite lesions. The second paper describes an in vitro DNA replication system reconstituted from purified bacterial proteins. Repriming of synthesis downstream from a blocked fork occurred not only on the lagging strand as expected, but also on the leading strand, demonstrating that contrary to widely accepted beliefs, leading strand synthesis does not need to be continuous

The Photoreceptors and Neural Circuits Driving the Pupillary Light Reflex

The visual system utilizes environmental light information to guide animal behavior. Regulation of the light entering the eye by the pupillary light reflex (PLR) is critical for normal vision, though its precise mechanisms are unclear. The PLR can be driven by two mechanisms: (1) an intrinsic photosensitivity of the iris muscle itself, and (2) a neural circuit originating with light detection in the retina and a multisynaptic neural circuit that activates the iris muscle. Even within the retina, multiple photoreceptive mechanisms—rods, cone, or melanopsin phototransduction—can contribute to the PLR, with uncertain relative importance. In this thesis, I provide evidence that the retina almost exclusively drives the mouse PLR using bilaterally asymmetric brain circuitry, with minimal role for the iris intrinsic photosensitivity. Intrinsically photosensitive retinal ganglion cells (ipRGCs) relay all rod, cone, and melanopsin light detection from the retina to brain for the PLR. I show that ipRGCs predominantly relay synaptic input originating from rod photoreceptors, with minimal input from cones or their endogenous melanopsin phototransduction. Finally, I provide evidence that rod signals reach ipRGCs using a non-conventional retinal circuit, potentially through direct synaptic connections between rod bipolar cells and ipRGCs. The results presented in this thesis identify the initial steps of the PLR and provide insight into the precise mechanisms of visual function

Being Green and Social Responsibility: Basic Concepts and Multiple Case Studies in Business Excellence

Through a qualitative business case approach, three major manufacturing firms in Pittsburgh, PA were reviewed for their eco-friendly sustainability strategic initiatives and products/services. Undoubtedly, use of green best practices are value adding steps for a company may be initially difficult to justify to spend the time and resources developing such a process. This is especially true when other core business needs are present, such as driving revenue, product development and meeting governmental or consumer expectations. However, green and sustainability initiatives may not be currently dictated needs, but many companies feel strongly that charting such a course would be to their stakeholders’ mutual advantage. As resources are being consumed more rapidly, it is logical to enact steps to ensure the sustainability of such scare resources. The added benefit of lower input needs greatly improves the companies’ stance in their market while also adding to the firms’ overall profitability

RdgB2 is required for dim-light input into intrinsically photosensitive retinal ganglion cells.

A subset of retinal ganglion cells is intrinsically photosensitive (ipRGCs) and contributes directly to the pupillary light reflex and circadian photoentrainment under bright-light conditions. ipRGCs are also indirectly activated by light through cellular circuits initiated in rods and cones. A mammalian homologue (RdgB2) of a phosphoinositide transfer/exchange protein that functions in Drosophila phototransduction is expressed in the retinal ganglion cell layer. This raised the possibility that RdgB2 might function in the intrinsic light response in ipRGCs, which depends on a cascade reminiscent of Drosophila phototransduction. Here we found that under high light intensities, RdgB2(-/-) mutant mice showed normal pupillary light responses and circadian photoentrainment. Consistent with this behavioral phenotype, the intrinsic light responses of ipRGCs in RdgB2(-/-) were indistinguishable from wild-type. In contrast, under low-light conditions, RdgB2(-/-) mutants displayed defects in both circadian photoentrainment and the pupillary light response. The RdgB2 protein was not expressed in ipRGCs but was in GABAergic amacrine cells, which provided inhibitory feedback onto bipolar cells. We propose that RdgB2 is required in a cellular circuit that transduces light input from rods to bipolar cells that are coupled to GABAergic amacrine cells and ultimately to ipRGCs, thereby enabling ipRGCs to respond to dim light

Loss of Gq/11 Genes Does Not Abolish Melanopsin Phototransduction

In mammals, a subset of retinal ganglion cells (RGCs) expresses the photopigment melanopsin, which renders them intrinsically photosensitive (ipRGCs). These ipRGCs mediate various non-image-forming visual functions such as circadian photoentrainment and the pupillary light reflex (PLR). Melanopsin phototransduction begins with activation of a heterotrimeric G protein of unknown identity. Several studies of melanopsin phototransduction have implicated a G-protein of the Gq/11 family, which consists of Gna11, Gna14, Gnaq and Gna15, in melanopsin-evoked depolarization. However, the exact identity of the Gq/11 gene involved in this process has remained elusive. Additionally, whether Gq/11 G-proteins are necessary for melanopsin phototransduction in vivo has not yet been examined. We show here that the majority of ipRGCs express both Gna11 and Gna14, but neither Gnaq nor Gna15. Animals lacking the melanopsin protein have well-characterized deficits in the PLR and circadian behaviors, and we therefore examined these non-imaging forming visual functions in a variety of single and double mutants for Gq/11 family members. All Gq/11 mutant animals exhibited PLR and circadian behaviors indistinguishable from WT. In addition, we show persistence of ipRGC light-evoked responses in Gna11−/−; Gna14−/− retinas using multielectrode array recordings. These results demonstrate that Gq, G11, G14, or G15 alone or in combination are not necessary for melanopsin-based phototransduction, and suggest that ipRGCs may be able to utilize a Gq/11-independent phototransduction cascade in vivo

DNA repair, DNA replication and human disorders: A personal journey

I was born in 1946 and grew up in the industrial north-west of England close to the city of Manchester. My parents were German- Jewish refugees, who left Germany fairly early, in 1933. My father helped to establish and was one of the directors of a tannery, which made leather for shoes and handbags. This was part of a group of tanneries established first in Strasbourg by my great-grandfather Ferdinand Oppenheimer. I would describe my childhood and adolescent years as comfortable by general post-war standards. I went to a state primary school and obtained a scholarship to Manchester Grammar School (MGS), a fairly prestigious secondary school. As a child I was always interested in chemistry but had little interest in or knowledge of biology. The educational system in the UK at that time was such that one had to specialise very early and as a consequence I have had no formal biology education since the age of 12, something I have managed to hide reasonably successfully for the rest of my life! In my final two years at MGS I studied just physics, chemistry and mathematics and obtained a scholarship to Pembroke College, Cambridge (England) to study Natural Sciences, with the intention of becoming a chemist. In the second year at Cambridge, one of the options was a course on biochemistry. Having no real idea what this was, I read a book about it in the summer of 1965, and was truly astonished and excited to discover that the basis of life was just a bunch of rather complicated organic chemistry reactions. So I took the biochemistry course in my second year. By the end of that year, I was fed up with chemistry and for my final year I chose to do biochemistry rather than chemistry, a decision I have not regretted. The biochemistry lectures must have been pretty up-to-date, as we were told briefly about the discovery of DNA repair by Dick Setlow [1], a topic that seemed rather esoteric at the time