Um Entre Muitos: instituições de ensino superior em um ecossistema de pedagogias urbanas = One Amongst Many: higher education institutions in an ecosystem of urban pedagogies

RESUMO Este artigo examina como e por que os educadores das universidades podem e precisam trabalhar como ‘um entre muitos’ para propor pedagogias críticas para a igualdade urbana. A discussão está embasada em duas experiências distintas: as escolas em rede da Habitat International Coalition América Latina (HIC-AL) – uma coalizão de organizações da sociedade civil, movimentos sociais e universidades que trabalham pela defesa de direitos humanos relacionados à moradia – e os processos de coaprendizagem com ativistas pelos direitos à moradia facilitados pelo Indian Institute for Human Settlements (IIHS) – uma instituição educacional nacional comprometida com a transformação igualitária, sustentável e eficiente dos assentamentos na Índia. Ambas as experiências enfatizam a criação de pedagogias críticas que procuram fundamentalmente romper, reformular e reposicionar relações institucionais de saberes e práticas de aprendizagem ao propor capacidades para uma transformação urbana transformadora. A análise demonstra como as injustiças epistêmicas – muitas vezes proliferadas em e por instituições de ensino superior – podem ser neutralizadas e porque promover a justiça epistêmica exige o reposicionamento das universidades como uma contra muitas em um ecossistema mais amplo de pedagogias urbanas, em diálogo aberto e produtivo com novas formas institucionais, definidas por Boaventura de Sousa Santos como a ‘pluriversidade’ e a ‘subversidade’. // This paper explores how and why pedagogues within universities can and need to work as ‘one amongst many’ to advance critical pedagogies for urban equality. The discussion draws on two contrasting experiences: the networked schools of the Habitat International Coalition in Latin America (HIC-AL) – a coalition of civil society organizations, social movements and universities working in defense of habitat-related human rights – and the co-learning processes with housing rights activists activated by the Indian Institute for Human Settlements (IIHS) – a national education institution committed to the equitable, sustainable and efficient transformation of Indian settlements. Both experiences place emphasis on crafting critical pedagogies that seek to fundamentally disrupt, re-frame and re-position institutional relations of knowledges and learning practices, while advancing capacities for transformative urban change. The analysis demonstrates how epistemic injustices – often proliferated in and by higher education institutions – can be counteracted, and why fostering epistemic justice requires re-positioning universities as one amongst many in a wider ecosystem of urban pedagogies, in open and productive dialogue with new institutional forms that Boaventura de Sousa Santos defines as the ‘pluriversity’ and the ‘subversity’

How Do We Learn Now? Pluralising Urban Pedagogies in the COVID-19 Pandemic

Since 2020, pedagogues and learners in the field of urban planning and practice have rapidly responded to new demands and realities posed by the COVID-19 pandemic. These have included shifting the modes and sites of learning from classrooms to screens, developing new programmes to build urgently required local capacities, fostering partnerships and platforms that sustain remote ways of learning together, and facilitating multi-sensorial and inclusive learning practices. This plurality of pedagogic adaptation and innovation suggests complex and nuanced relations with urban (in)equality, going beyond the dominant narrative of the digital divide and distributive inequalities in higher education. This article reflects on three experiences of critical pedagogies undertaken by researchers and activists, social movements and organised civil society from India, Brazil and Argentina. As the impacts of the pandemic on the nexus between urban practice and pedagogy unfold, we argue that these reflexions-in-action on decisions made, along with their underlying principles, are important stimuli for pluralising questions of what, where, with whom and how we learn to respond to urban inequalities. Moreover, they open nuanced discussions to strategically reimagine future hybrid learning trajectories to support pathways to urban equality

Role of General Dental Practitioners in Smoking Cessation Programme

Tobacco use is a dental as well as a medical problem. Its use is the root cause of many oral health problems including periodontal disease and tooth loss. In the past few years, there has been an increasing awareness of the role of tobacco use in the prevalence and severity of periodontal disease. Like other health professions, dentistry has taken a stand against cigarette smoking. Dentists can use a variety of smoking cessation techniques to prevent the oral health problems associated with tobacco use. To carry out a minimal programme of antismoking measures, dentists in general practice can serve as a non-smoking role model for their patients, provide information about the health hazards of smoking, give advice and guidance, refer patients to cessation programmes, recommend cessation measures and monitor patients’ effort to quit smoking. Dental practice in 21st century has to increasingly move from a restorative orientation to one of a broader promotion of health and wellbeing

Identification of allosteric hotspots regulating the ribosomal RNA binding by antibiotic resistance-conferring Erm methyltransferases

Antibiotic resistance via epigenetic methylation of ribosomal RNA is one of the most prevalent strategies adopted by multidrug resistant pathogens. The erythromycin-resistance methyltransferase (Erm) methylates rRNA at the conserved A2058 position and imparts resistance to macrolides such as erythromycin. However, the precise mechanism adopted by Erm methyltransferases for locating the target base within a complicated rRNA scaffold remains unclear. Here, we show that a conserved RNA architecture, including specific bulge sites, present more than 15 Å from the reaction center, is key to methylation at the pathogenic site. Using a set of RNA sequences site-specifically labeled by fluorescent nucleotide surrogates, we show that base flipping is a prerequisite for effective methylation and that distal bases assist in the recognition and flipping at the reaction center. The Erm–RNA complex model revealed that intrinsically flipped-out bases in the RNA serve as a putative anchor point for the Erm. Molecular dynamic simulation studies demonstrated the RNA undergoes a substantial change in conformation to facilitate an effective protein–rRNA handshake. This study highlights the importance of unique architectural features exploited by RNA to impart fidelity to RNA methyltransferases via enabling allosteric crosstalk. Moreover, the distal trigger sites identified here serve as attractive hotspots for the development of combination drug therapy aimed at reversing resistance

The mycotoxin phomoxanthone A disturbs the form and function of the inner mitochondrial membrane.

Mitochondria are cellular organelles with crucial functions in the generation and distribution of ATP, the buffering of cytosolic Ca2+ and the initiation of apoptosis. Compounds that interfere with these functions are termed mitochondrial toxins, many of which are derived from microbes, such as antimycin A, oligomycin A, and ionomycin. Here, we identify the mycotoxin phomoxanthone A (PXA), derived from the endophytic fungus Phomopsis longicolla, as a mitochondrial toxin. We show that PXA elicits a strong release of Ca2+ from the mitochondria but not from the ER. In addition, PXA depolarises the mitochondria similarly to protonophoric uncouplers such as CCCP, yet unlike these, it does not increase but rather inhibits cellular respiration and electron transport chain activity. The respiration-dependent mitochondrial network structure rapidly collapses into fragments upon PXA treatment. Surprisingly, this fragmentation is independent from the canonical mitochondrial fission and fusion mediators DRP1 and OPA1, and exclusively affects the inner mitochondrial membrane, leading to cristae disruption, release of pro-apoptotic proteins, and apoptosis. Taken together, our results suggest that PXA is a mitochondrial toxin with a novel mode of action that might prove a useful tool for the study of mitochondrial ion homoeostasis and membrane dynamics

Protective effects of fecal microbiota transplantation against ischemic stroke and other neurological disorders: an update

The bidirectional communication between the gut and brain or gut-brain axis is regulated by several gut microbes and microbial derived metabolites, such as short-chain fatty acids, trimethylamine N-oxide, and lipopolysaccharides. The Gut microbiota (GM) produce neuroactives, specifically neurotransmitters that modulates local and central neuronal brain functions. An imbalance between intestinal commensals and pathobionts leads to a disruption in the gut microbiota or dysbiosis, which affects intestinal barrier integrity and gut-immune and neuroimmune systems. Currently, fecal microbiota transplantation (FMT) is recommended for the treatment of recurrent Clostridioides difficile infection. FMT elicits its action by ameliorating inflammatory responses through the restoration of microbial composition and functionality. Thus, FMT may be a potential therapeutic option in suppressing neuroinflammation in post-stroke conditions and other neurological disorders involving the neuroimmune axis. Specifically, FMT protects against ischemic injury by decreasing IL-17, IFN-γ, Bax, and increasing Bcl-2 expression. Interestingly, FMT improves cognitive function by lowering amyloid-β accumulation and upregulating synaptic marker (PSD-95, synapsin-1) expression in Alzheimer’s disease. In Parkinson’s disease, FMT was shown to inhibit the expression of TLR4 and NF-κB. In this review article, we have summarized the potential sources and methods of administration of FMT and its impact on neuroimmune and cognitive functions. We also provide a comprehensive update on the beneficial effects of FMT in various neurological disorders by undertaking a detailed interrogation of the preclinical and clinical published literature

Protective effects of fecal microbiota transplantation against ischemic stroke and other neurological disorders: an update

The bidirectional communication between the gut and brain or gut-brain axis is regulated by several gut microbes and microbial derived metabolites, such as short-chain fatty acids, trimethylamine N-oxide, and lipopolysaccharides. The Gut microbiota (GM) produce neuroactives, specifically neurotransmitters that modulates local and central neuronal brain functions. An imbalance between intestinal commensals and pathobionts leads to a disruption in the gut microbiota or dysbiosis, which affects intestinal barrier integrity and gut-immune and neuroimmune systems. Currently, fecal microbiota transplantation (FMT) is recommended for the treatment of recurrent Clostridioides difficile infection. FMT elicits its action by ameliorating inflammatory responses through the restoration of microbial composition and functionality. Thus, FMT may be a potential therapeutic option in suppressing neuroinflammation in post-stroke conditions and other neurological disorders involving the neuroimmune axis. Specifically, FMT protects against ischemic injury by decreasing IL-17, IFN-γ, Bax, and increasing Bcl-2 expression. Interestingly, FMT improves cognitive function by lowering amyloid-β accumulation and upregulating synaptic marker (PSD-95, synapsin-1) expression in Alzheimer’s disease. In Parkinson’s disease, FMT was shown to inhibit the expression of TLR4 and NF-κB. In this review article, we have summarized the potential sources and methods of administration of FMT and its impact on neuroimmune and cognitive functions. We also provide a comprehensive update on the beneficial effects of FMT in various neurological disorders by undertaking a detailed interrogation of the preclinical and clinical published literature

Brief pain inventory scale: An emerging assessment modality for orofacial pain

Pain is an emotional experience almost experienced by almost every one of us. Since the pain can neither be seen nor measured, it poses a challenge to the patient as well as the clinician in understanding its complicated nature and the best way of managing it. There is no simple method of pain evaluation due to its subjective nature. However, comprehensive approaches for its evaluation exists, of which most common pain scale used are visual analog scale, Mc-Gills questionnaire, brief pain inventory (BPI) to name a few. We have tried to highlight the various advantages of the BPI scale over the other pain scales and to emphasize an improved instrument, which can be used as a promising modality for the assessment of orofacial pain

Protease OMA1 modulates mitochondrial bioenergetics and ultrastructure through dynamic association with MICOS complex

Remodeling of mitochondrial ultrastructure is a process that is critical for organelle physiology and apoptosis. Although the key players in this process—mitochondrial contact site and cristae junction organizing system (MICOS) and Optic Atrophy 1 (OPA1)—have been characterized, the mechanisms behind its regulation remain incompletely defined. Here, we found that in addition to its role in mitochondrial division, metallopeptidase OMA1 is required for the maintenance of intermembrane connectivity through dynamic association with MICOS. This association is independent of OPA1, mediated via the MICOS subunit MIC60, and is important for stability of MICOS and the intermembrane contacts. The OMA1-MICOS relay is required for optimal bioenergetic output and apoptosis. Loss of OMA1 affects these activities; remarkably it can be alleviated by MICOSemulating intermembrane bridge. Thus, OMA1-dependent ultrastructure support is required for mitochondrial architecture and bioenergetics under basal and stress conditions, suggesting a previously unrecognized role for OMA1 in mitochondrial physiology