Looking at Participatory Planning in Cuba… through an Art Deco Window

Last January we sat with about thirty Cubans in a community arts center in Boyeros, on the outskirts of Havana, Cuba. The group included artists, teachers, social workers, government officials, architects, engineers and health professionals, all working in Boyeros. We were leading a three-day participatory planning workshop to help this group identify ways that the 1930s Art Deco arts center, currently under renovation, could be used to spark broader community development. As the first day drew to a close, we felt good about the day’s work. We had turned the Cubans loose in a small group exercise that used art to explore community problems and possible solutions. When the small groups presented their skits, poems and drawings, they yielded laughter along with acute insights on life in Boyeros. Following time-honored popular education principles, we kept the focus on the Boyeros community and left our Boston planning experiences off the table. But when it came to evaluating the day’s work, the recurring comment was, We would like the compañeros from Boston to tell us how they do planning at home. Since shortly after its 1959 revolution, Cuba’s variety of socialism has featured both large-scale planning (physical, economic, social) and massive popular participation through active mass organizations and frequent mobilizations. Participatory planning, however, has remained more elusive. Experiments in participatory planning finally began to emerge and then multiply in the late 1980s and 1990s, spurred by the disappearance of Soviet influence and by the economic crisis that paralyzed standard planning methodologies predicated on plentiful resources. Given the country’s high level of collective consciousness and organization, participatory planning would seem like a natural approach for planning in Cuba. Nonetheless, serious obstacles to participatory planning remain, including the veneration of expertise, which took us by surprise at the end of the first day of our workshop. Our January workshop can serve as a useful window through which to look back at the uneven history of participatory planning in Cuba, and forward to future possibilities

Gold(I)-catalysed synthesis of cyclic sulfamidates : current scope, stereochemistry and competing ene-allene cycloisomerisation

AbstractSix-membered cyclic sulfamidates are prepared in high yields by treatment of allenic sulfamates with readily available Ph3PAuNTf2. The reaction enables formation of N-substituted quaternary centres in high yields. The relative stereochemistry has been unambiguously determined. A π-rearrangement is faster than hydroamination in the case of an allyl-substituted sulfamate and a mechanism is proposed for this process

Canine Genetics and Epidemiology is now Canine Medicine and Genetics

From Springer Nature via Jisc Publications RouterHistory: registration 2020-07-17, online 2020-07-27, pub-electronic 2020-07-27, collection 2020-12Publication status: Publishe

Personalised interventions for subgroups of children with conduct problems. Protocol Intervention

This is a protocol for a Cochrane Review (Intervention). The objectives are as follows: To assess the effects of personalised, psychosocial interventions for subgroups of children with conduct problems

Polymorphisms in the CTLA4 promoter sequence are associated with canine hypoadrenocorticism

Canine hypoadrenocorticism is an immune-mediated endocrinopathy that shares both clinical and pathophysiological similarities with Addison’s disease in humans. Several dog breeds are overrepresented in the disease population, suggesting that a genetic component is involved, although this is likely to be polygenic. Previous research has implicated CTLA4 as a potential susceptibility gene. CTLA4 is an important regulator of T cell function and polymorphisms/mutations in CTLA4 have been associated with a number of autoimmune phenotypes in both humans and rodent models of autoimmunity. The aim of the current study was to undertake a case:control association study of CTLA4 promotor polymorphisms in three dog breeds, cocker spaniels, springer spaniels and West Highland white terriers (WHWT)

The relationship of endotoxaemia to peripheral and central nervous system inflammatory responses in Human African Trypanosomiasis

Endotoxaemia has been described in cases of Human African trypanosomiasis (HAT), but it is unclear if this phenomenon influences inflammatory pathology either in the periphery or central nervous system (CNS). We studied endotoxin concentrations in the plasma and cerebrospinal fluid (CSF) of Trypanosoma brucei rhodesiense patients using the chromogenic Limulus Amoebocyte lysate assay. The relationship of endotoxin concentration to the presentation of gross signs of inflammation and the inflammatory/counter-inflammatory cytokine profile of the relevant compartments were analysed. We demonstrate that HAT patients exhibit parasitaemia-independent plasma endotoxaemia, and that this is associated with splenomegaly and lymphadenopathy. Endotoxin concentrations normalize rapidly after treatment. There was no evidence of endotoxin release in the CNS. A rapid normalization of endotoxin levels after treatment and lack of association with parasitaemia suggest that gut leakage is the main source of endotoxin in the circulation. Low CSF endotoxin concentrations and a lack of any association with neuroinflammatory markers or neurological sequelae suggest that endotoxin does not play a role in the pathogenesis of the disease in the CNS

Stage progression and neurological symptoms in Trypanosoma brucei rhodesiense sleeping sickness: role of the CNS inflammatory response

Background: Human African trypanosomiasis progresses from an early (hemolymphatic) stage, through CNS invasion to the late (meningoencephalitic) stage. In experimental infections disease progression is associated with neuroinflammatory responses and neurological symptoms, but this concept requires evaluation in African trypanosomiasis patients, where correct diagnosis of the disease stage is of critical therapeutic importance. Methodology/Principal Findings: This was a retrospective study on a cohort of 115 T.b.rhodesiense HAT patients recruited in Eastern Uganda. Paired plasma and CSF samples allowed the measurement of peripheral and CNS immunoglobulin and of CSF cytokine synthesis. Cytokine and immunoglobulin expression were evaluated in relation to disease duration, stage progression and neurological symptoms. Neurological symptoms were not related to stage progression (with the exception of moderate coma). Increases in CNS immunoglobulin, IL-10 and TNF-α synthesis were associated with stage progression and were mirrored by a reduction in TGF-β levels in the CSF. There were no significant associations between CNS immunoglobulin and cytokine production and neurological signs of disease with the exception of moderate coma cases. Within the study group we identified diagnostically early stage cases with no CSF pleocytosis but intrathecal immunoglobulin synthesis and diagnostically late stage cases with marginal CSF pleocytosis and no detectable trypanosomes in the CSF. Conclusions: Our results demonstrate that there is not a direct linkage between stage progression, neurological signs of infection and neuroinflammatory responses in rhodesiense HAT. Neurological signs are observed in both early and late stages, and while intrathecal immunoglobulin synthesis is associated with neurological signs, these are also observed in cases lacking a CNS inflammatory response. While there is an increase in inflammatory cytokine production with stage progression, this is paralleled by increases in CSF IL-10. As stage diagnostics, the CSF immunoglobulins and cytokines studied do not have sufficient sensitivity to be of clinical value

Spatially and genetically distinct African trypanosome virulence variants defined by host interferon-g response

We describe 2 spatially distinct foci of human African trypansomiasis in eastern Uganda. The Tororo and Soroti foci of <i>Trypanosoma brucei rhodesiense</i> infection were genetically distinct as characterized by 6 microsatellite and 1 minisatellite polymorphic markers and were characterized by differences in disease progression and host-immune response. In particular, infections with the Tororo genotype exhibited an increased frequency of progression to and severity of the meningoencephalitic stage and higher plasma interferon (IFN)–γ concentration, compared with those with the Soroti genotype. We propose that the magnitude of the systemic IFN-γ response determines the time at which infected individuals develop central nervous system infection and that this is consistent with the recently described role of IFN-γ in facilitating blood-brain barrier transmigration of trypanosomes in an experimental model of infection. The identification of trypanosome isolates with differing disease progression phenotypes provides the first field-based genetic evidence for virulence variants in T. <i>brucei rhodesiense</i>