Leveraging Effective Consulting to Advance Diversity, Equity, and Inclusion in Philanthropy

In 2018, the National Network of Consultants to Grantmakers launched an initiative to sharpen the impact of diversity, equity, and inclusion (DEI) work in grantmaking by increasing the capacity of consultants and grantmakers engaged in these efforts. Network researchers used a systematic protocol to interview consultant members about their most effective partnerships with grantmakers. Case studies drawn from those interviews yielded valuable lessons for advancing DEI in philanthropy. In sharing some of these lessons, this article advises consultants to be prepared to help grantmakers define or refine the meaning of DEI and understand where equity fits into their values and mission. It also explores how a good DEI consulting process helps to distinguish technical and complex dimensions of a DEI commitment, and how the scope of work should encompass both development of internal leadership skills and investment in grantee, community, and issue leaders. This article concludes with tips on how smart DEI consultant/grantmaker partnerships can understand and honor emergent strategy and help the funder follow opportunities without overwhelming the size and scale of the funder’s capacity

[5,10,15,20-Tetra­kis(4-tol­yl)porphyrin]zinc(II) dichloro­methane solvate

In the title complex, [Zn(C48H36N4)]·CH2Cl2, the ZnII atom lies on an inversion center and the dichloro­methane solvent mol­ecule is disordered around an inversion center. The tolyl substituents are twisted compared to the central aromatic ring system of the porphyrin, similar to what is seen in previously published structures of this molecule [Dastidar & Goldberg (1996 ▶). Acta Cryst. C52, 1976–1980]. The dihedral angles between the mean planes of the tolyl rings and the central ring are 66.98 (6) and 60.40 (6)°

Source-sink cooperation dynamics constrain institutional evolution in a group-structured society

Societies change through time, entailing changes in behaviors and institutions. We ask how social change occurs when behaviors and institutions are interdependent. We model a group-structured society in which the transmission of individual behavior occurs in parallel with the selection of group-level institutions. We consider a cooperative behavior that generates collective benefits for groups but does not spread between individuals on its own. Groups exhibit institutions that increase the diffusion of the behavior within the group, but also incur a group cost. Groups adopt institutions in proportion to their fitness. Finally, cooperative behavior may also spread globally. As expected, we find that cooperation and institutions are mutually reinforcing. But the model also generates behavioral source-sink dynamics when cooperation generated in institutional groups spreads to non-institutional groups, boosting their fitness. Consequently, the global diffusion of cooperation creates a pattern of institutional free-riding that limits the evolution of group-beneficial institutions. Our model suggests that, in a group-structured society, large-scale change in behavior and institutions (i.e. social change) can be best achieved when the two remain correlated, such as through the spread successful pilot programs

What is the microbiome of the human home?

There is currently little known about the range and diversity of microorganisms in the indoor home, particularly in the context of modern airtight homes. People spend a great deal of time in their homes, especially those at the extremes of age, and it is possible that the indoor microbiome could impact upon human health in ways not yet understood. This project aimed to systematically screen sites in 100 houses in the Lanarkshire community in order to determine the amount and type of cultivable aerobic bacteria and fungi in the home. It was hoped to be able to characterise the microbiome of the ‘normal’ home. Chosen sites were: indoor bathroom handle; telephone; kettle handle; bedside table; top of bedroom door; TV remote; toilet handle; and bedroom window sill (Table 1). These sites were screened using double-sided dipslides coated with nutrient and staphylococcal selective agars (Figure 1). Bacteria and fungi were quantified for each site and staphylococci and Gram- negative bacilli identified if possible. Each of the eight sampled sites revealed its own distinct microbiological character, both in the type and amount of cultivable microbes. Human pathogens, particularly S.aureus, were more likely to be associated with commonly touched sites such as TV remote, kettle handle and telephone. Whole houses also demonstrated unique microbiological characteristics, with morphologically similar and identifiable microbes observed at multiple sites within the same home. Each home thus displayed it own unique microbiome but with identifiable similarities between other homes according to site

IL-13 Augments Compressive Stress–Induced Tissue Factor Expression in Human Airway Epithelial Cells

Tissue factor (TF) is best known as a cellular initiator of coagulation, but it is also a multifunctional protein that has been implicated in multiple pathophysiologic conditions, including asthma. In the lung, airway epithelial cells express TF, but it is unknown how TF expression is regulated by asthma-associated mediators. We investigated the role of IL-13, a type 2 cytokine, alone and in combination with compressive stress, which mimics asthmatic bronchoconstriction, on TF expression and release of TF-positive extracellular vesicles from primary normal human bronchial epithelial cells. Well-differentiated normal human bronchial epithelial cells were treated with IL-13 and compressive stress, alone and in combination. TF mRNA, protein and activity were measured in the cells and conditioned media. TF was also measured in the bronchoalveolar lavage (BAL) fluid of allergen-challenged mice and patients with asthma. IL-13 and compressive stress increased TF expression, but only compressive stress induced TF-positive extracellular vesicle release. Pretreatment with IL-13 augmented compressive stress–induced TF expression and release. TF protein and activity in BAL fluid were increased in allergen-sensitized and -challenged mice. TF was elevated in the BAL fluid of patients with mild asthma after an allergen challenge. Our in vitro and in vivo data indicate close cooperation between mechanical and inflammatory stimuli on TF expression and release of TF-positive extracellular vesicles in the lungs, which may contribute to pathophysiology of asthma

Words are monuments: Patterns in US national park place names perpetuate settler colonial mythologies including white supremacy

1. Ecologists, outdoor professionals and the public work and play in lands with complex histories. Part of decolonizing our professional and recreational practices is to expose settler colonial biases and recognize the histories of colonized lands and the peoples who have stewarded these lands for millennia prior to colonization. 2. To provide a quantitative example of settler colonial biases in a familiar context, we examined the origins of over 2,200 place names in 16 national parks in the United States (US; 26% of the parks). Through iterative thematic analysis of place name origins and meanings, we constructed a decision tree for classifying place names according to emergent categories, which enabled the quantification and spatial analysis of place name meanings. 3. All national parks examined have place names that tacitly endorse racist or, more specifically, anti-Indigenous ideologies, thus perpetuating settler colonialism and white supremacy at the system scale for future generations. 4. Looking east to west across the US, the proportion of place names per national park that appropriated Indigenous names increased in parallel with the westward expansion and evolution of US settler colonialism. 5. This examination of place names, name origins and their consequences is an opportunity to make everyday complicity in systemic oppression more visible and to more actively advance decolonizing practices for land and language

Axonal response of mitochondria to demyelination and complex IV activity within demyelinated axons in experimental models of multiple sclerosis

AIMS: Axonal injury in multiple sclerosis (MS) and experimental models is most frequently detected in acutely demyelinating lesions. We recently reported a compensatory neuronal response, where mitochondria move to the acutely demyelinated axon and increase the mitochondrial content following lysolecithin-induced demyelination. We termed this homeostatic phenomenon, which is also evident in MS, the axonal response of mitochondria to demyelination (ARMD). The aim of this study is to determine whether ARMD is consistently evident in experimental demyelination and how its perturbation relates to axonal injury.METHODS: In the present study, we assessed axonal mitochondrial content as well as axonal mitochondrial respiratory chain complex IV activity (cytochrome c oxidase or COX) of axons and related these to axonal injury in nine different experimental disease models. We used immunofluorescent histochemistry as well as sequential COX histochemistry followed by immunofluorescent labelling of mitochondria and axons.RESULTS: We found ARMD a consistent and robust phenomenon in all experimental disease models. The increase in mitochondrial content within demyelinated axons, however, was not always accompanied by a proportionate increase in complex IV activity, particularly in highly inflammatory models such as experimental autoimmune encephalomyelitis (EAE). Axonal complex IV activity inversely correlated with the extent of axonal injury in experimental disease models.CONCLUSIONS: Our findings indicate that ARMD is a consistent and prominent feature and emphasise the importance of complex IV activity in the context of ARMD, especially in autoimmune inflammatory demyelination, paving the way for the development of novel neuroprotective therapies.</p

Effects of antiplatelet therapy on stroke risk by brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases: subgroup analyses of the RESTART randomised, open-label trial

Background Findings from the RESTART trial suggest that starting antiplatelet therapy might reduce the risk of recurrent symptomatic intracerebral haemorrhage compared with avoiding antiplatelet therapy. Brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases (such as cerebral microbleeds) are associated with greater risks of recurrent intracerebral haemorrhage. We did subgroup analyses of the RESTART trial to explore whether these brain imaging features modify the effects of antiplatelet therapy

Enhanced axonal response of mitochondria to demyelination offers neuroprotection:implications for multiple sclerosis

Axonal loss is the key pathological substrate of neurological disability in demyelinating disorders, including multiple sclerosis (MS). However, the consequences of demyelination on neuronal and axonal biology are poorly understood. The abundance of mitochondria in demyelinated axons in MS raises the possibility that increased mitochondrial content serves as a compensatory response to demyelination. Here, we show that upon demyelination mitochondria move from the neuronal cell body to the demyelinated axon, increasing axonal mitochondrial content, which we term the axonal response of mitochondria to demyelination (ARMD). However, following demyelination axons degenerate before the homeostatic ARMD reaches its peak. Enhancement of ARMD, by targeting mitochondrial biogenesis and mitochondrial transport from the cell body to axon, protects acutely demyelinated axons from degeneration. To determine the relevance of ARMD to disease state, we examined MS autopsy tissue and found a positive correlation between mitochondrial content in demyelinated dorsal column axons and cytochrome c oxidase (complex IV) deficiency in dorsal root ganglia (DRG) neuronal cell bodies. We experimentally demyelinated DRG neuron-specific complex IV deficient mice, as established disease models do not recapitulate complex IV deficiency in neurons, and found that these mice are able to demonstrate ARMD, despite the mitochondrial perturbation. Enhancement of mitochondrial dynamics in complex IV deficient neurons protects the axon upon demyelination. Consequently, increased mobilisation of mitochondria from the neuronal cell body to the axon is a novel neuroprotective strategy for the vulnerable, acutely demyelinated axon. We propose that promoting ARMD is likely to be a crucial preceding step for implementing potential regenerative strategies for demyelinating disorders.</p

Enhanced axonal response of mitochondria to demyelination offers neuroprotection:implications for multiple sclerosis

Axonal loss is the key pathological substrate of neurological disability in demyelinating disorders, including multiple sclerosis (MS). However, the consequences of demyelination on neuronal and axonal biology are poorly understood. The abundance of mitochondria in demyelinated axons in MS raises the possibility that increased mitochondrial content serves as a compensatory response to demyelination. Here, we show that upon demyelination mitochondria move from the neuronal cell body to the demyelinated axon, increasing axonal mitochondrial content, which we term the axonal response of mitochondria to demyelination (ARMD). However, following demyelination axons degenerate before the homeostatic ARMD reaches its peak. Enhancement of ARMD, by targeting mitochondrial biogenesis and mitochondrial transport from the cell body to axon, protects acutely demyelinated axons from degeneration. To determine the relevance of ARMD to disease state, we examined MS autopsy tissue and found a positive correlation between mitochondrial content in demyelinated dorsal column axons and cytochromecoxidase (complex IV) deficiency in dorsal root ganglia (DRG) neuronal cell bodies. We experimentally demyelinated DRG neuron-specific complex IV deficient mice, as established disease models do not recapitulate complex IV deficiency in neurons,and found that these mice are able to demonstrate ARMD, despite the mitochondrial perturbation.Enhancement of mitochondrial dynamics in complex IV deficient neurons protects the axon upon demyelination. Consequently, increased mobilisation of mitochondria from the neuronal cell body to the axon is a novel neuroprotective strategy for the vulnerable, acutely demyelinated axon. We propose that promoting ARMD is likely to be a crucial preceding step for implementing potential regenerative strategies for demyelinating disorders.</p