Rheumatoid arthritis (RA) is caused by aberrant attack of the joints by native inflammatory system. This can lead to joint destruction and pain that can be debilitating. Increased angiogenesis and innervation by nociceptive afferent fibers are characteristic features of RA joints, which in addition to the elevated levels of a wide variety of inflammatory mediators, are thought to play an important role in the pathogenesis of chronic inflammatory pain associated with RA. Interestingly, a recent report indicates that C–type natriuretic peptide (CNP) is increased in the blood serum of RA patients. Natriuretic peptides (NPs) control natriuresis and normalize changes in blood pressure. Many biological effects of NPs are mediated by guanylate cyclase (GC)–coupled NP receptors, NPR–A and NPR–B, whereas the third NP receptor, NPR–C, lacks the GC kinase domain and acts as the NP clearance receptor. In addition, NPR–C can couple to specific Gái–βã–mediated intracellular signaling cascades in numerous cell types. Recent studies suggest that NPs are also involved in the regulation of pain sensitivity, although the underlying mechanisms remain largely unknown. In Aim 1, I show that CNP acutely sensitized the excitation of mouse dorsal root ganglia (DRG) sensory neurons that is dependent on the transient receptor potential vanilloid–1 (TRPV1). CNP potentiated capsaicin– and proton–activated TRPV1 currents in cultured mouse DRG neurons and increased neuronal firing frequency, an effect that was absent in DRG neurons from TRPV1−/−mice. Further, CNP injection into mouse hind paw led to the development of thermal hyperalgesia, which was absent in TRPV1−/−mice. In Aim 2, I dissected the signaling mechanism underlying TRPV1 sensitization by CNP. My results show that all 3 functional NPRs are expressed in mouse DRG neurons; however NPR–A/B–cGMP signaling is not involved in CNP–mediated sensitization of TRPV1. Interestingly, I observed that sensitization of TRPV1 by CNP is dependent on protein kinase C (PKC) activity. Furthermore, I found that NPR–C is co–expressed in TRPV1–expressing mouse DRG neurons and can be co–immunoprecipitated with Gαi, but not with Gαq/11 or Gαs subunits. CNP treatment induced translocation of PKCå to the plasma membrane of these neurons, which was attenuated by pertussis toxin pre–treatment. Accordingly, CNP–induced sensitization of TRPV1 was attenuated by pre–treatment of DRG neurons with the specific inhibitors of Gβã, phospholipase–Cβ (PLCβ) or PKC, but not of protein kinase A (PKA), and by mutations at two PKC phosphorylation sites, S502 and S800, in the TRPV1 protein. Furthermore, the development of thermal hyperalgesia in CNP–injected hindpaw was attenuated by administration of specific inhibitors of Gβã or PKC. Thus, my work identifies the Gβã–PLCâ–PKC–dependent potentiation of TRPV1 as a novel signaling cascade recruited by CNP in mouse DRG neurons that can lead to enhanced nociceptor excitability and thermal hypersensitivity. Such signaling cascade could presumably constitute one of the mechanisms underlying chronic inflammatory joint pain associated with RA.

Worldwide research devotes significant effort to identify new, targetable molecular mechanisms in the field of angiogenesis, since therapeutic modulation of angiogenesis can critically alter the progression of a number of diseases. Stimulation of angiogenesis is desirable in situations characterized by tissue-damaging ischemia where blood supply is severely reduced, such as lower limb diabetic arteriopathy or following myocardial infarct. In contradistinction, stemming excessive or ectopic angiogenesis can be beneficial in situations such as solid tumor growth or in neovascular age-related macular degeneration. It has been previously shown that Hydrogen Sulfide (H2S), a new vasoactive gasotransmitter, can initiate angiogenic responses which depend on the activation of ATP-sensitive potassium channels (KATP). Intriguingly, C-type Natriuretic Peptide (CNP), which is also known to activate KATP, has been reported to promote endothelial cell growth; however, its angiogenic properties have not been explored at any depth. This pattern prompted us to investigate whether direct KATP activation induces angiogenic responses and whether endothelial responses to CNP or Vascular Endothelial Growth Factor (VEGF) indeed require KATP activation. We undertook a dual-pronged approach, based on both in vivo and in vitro experimental approaches. In vivo, chick embryo chorioallantoic membrane (CAM) angiogenesis was similarly enhanced by the direct KATP channel activator SG-209 and by the polypeptides CNP or VEGF. Two KATP inhibitors, Glibenclamide and 5-Hydroxydecanoate (5-HD), abrogated both basal and CNP-induced CAM angiogenesis. In vitro, direct activators of KATP such as Nicorandil and SG- 209 and receptor-acting agonists such as VEGF and CNP, increased proliferation and migration in the mouse brain endothelial cell line bEnd.3. In addition, VEGF and CNP induced comparable capillary tube-like formation by Human Umbilical Vein Endothelial cells (HUVECs) in low growth factor Matrigel. All these in vitro pro-angiogenic endothelial responses were effectively abrogated by Glibenclamide or by 5-HD. Transfection of HUVECs with a siRNA specifically targeting the inwardly rectifying potassium channel (Kir) 6.1 subunit decreased the expression of this subunit at both the mRNA and the protein level. The resulting knock-down of the Kir6.1 KATP subunit impaired HUVEC migration through transwells in vitro and substantially decreased tubular network formation in Matrigel in response to either the direct KATP activator SG-209 or the receptor-operating KATP activator CNP. Furthermore, the bEnd.3 endothelial cell proliferation and migration responses to SG-209 required mobilization of the “classic” endothelial pro-angiogenesis kinases Erk1/2, p38 and Akt, since the responses to SG-209 were all abolished by each of the respective kinase inhibitors. This work allows us to firmly conclude that: a) direct pharmacological modulation of KATP channels affects angiogenic responses in vitro and in vivo, b) CNP is a bona fide angiogenic factor, as potent and efficient to mobilize endothelial cells as VEGF, c) the angiogenic effects of CNP and VEGF depend on the activation of endothelial KATP channels and specifically require the expression of the Kir6.1 pore-forming KATP subunit, and finally d) KATP activation may be a common molecular mechanism that underpins angiogenesis to a wide variety of endogenous vasoactive stimuli that includes H2S, VEGF and CNP. The therapeutic implications of this work are significant: Sulfonylurea-type KATP channel inhibitors, with questionable selectivity for pancreatic β-cells, are widely used drugs to treat type II diabetes, a disease characterized by arterial dysfunction and higher incidence of myocardial and lower limb ischemia. The outcome of cardiac ischemia in diabetic patients is worse if they have been treated with sulfonylureas, indicating some, until now unresolved, deleterious cardiovascular activity of this class of compounds. The present demonstration that endothelial KATP channel activation is a common pro-angiogenic mechanism, may in part explain this unfavorable outcome of sulfonylurea treatment in diabetics. Furthermore, it raises the need to design new molecules which, while inhibiting the pancreatic KATP channels, should spare the endothelial KATP channels and the ensuing angiogenesis, thus exhibiting increased therapeutic benefit. / Σε πολλά εργαστήρια, σε παγκόσμιο επίπεδο, συντελείται σημαντική ερευνητική προσπάθεια για την ταυτοποίηση νέων μοριακών μηχανισμών στο πεδίο της αγγειογένεσης ως στόχων ανάπτυξης φαρμάκων, καθώς η θεραπευτική ρύθμιση της αγγειογένεσης μπορεί να επηρεάσει σημαντικά την εξέλιξη πολλών ασθενειών. Η διέγερση της αγγειογένεσης είναι επιθυμητή σε καταστάσεις ισχαιμίας όπου η παροχή αίματος μειώνεται σοβαρά, με αποτέλεσμα δυσλειτουργία ή νέκρωση ιστών, όπως πχ συμβαίνει κατά την εμφάνιση αρτηριοπάθειας στο διαβητικό κάτω άκρο ή μετά από έμφραγμα του μυοκαρδίου. Σε αντιδιαστολή, η αναστολή υπερβολικής ή έκτοπης αγγειογένεσης μπορεί να είναι επωφελής σε καταστάσεις όπως κατά την ανάπτυξη συμπαγούς όγκου ή σε νεοαγγειακή εκφύλιση της ωχράς κηλίδας σχετιζόμενη με την ηλικία. Έχει δειχθεί ότι το Υδρόθειο (H2S), ένας νέος αγγειοδραστικός αέριος διαβιβαστής (gasotransmitter), μπορεί να εκκινήσει αγγειογόνες αποκρίσεις που εξαρτώνται από την ενεργοποίηση των ευαίσθητων στο ΑΤΡ διαύλων καλίου (ΚΑTP). Μας κίνησε επίσης το ενδιαφέρον η αναφορά οτι το C-νατριουρητικό πεπτίδιο (CNP), που είναι γνωστό ότι ενεργοποιεί τους ίδιους διαύλους καλίου, δύναται να προάγει τον πολλαπλασιασμό των ενδοθηλιακών κυττάρων. Ωστόσο, οι αγγειογενετικές ιδιότητες του CNP δεν έχουν διερευνηθεί σε βάθος. Αυτή η σύγκλιση μας ώθησε στη διερεύνηση του κατά πόσον η άμεση ενεργοποίηση των ΚΑTP διαύλων καλίου προκαλεί αγγειογενετική απόκριση και επίσης εάν η απόκριση των ενδοθηλιακών κυττάρων στο CNP ή στον αγγειακό ενδοθηλιακό αυξητικό παράγοντα (VEGF) απαιτούν πράγματι ενεργοποίηση των διαύλων ΚΑTP. Η πειραματική προσέγγιση σχεδιάστηκε με βάση τόσο in vivo, όσο και in vitro μεθόδους. In vivo, η φυσιολογικά συντελλούμενη αγγειογένεση στην χοριοαλλαντοϊκή μεμβράνη εμβρύου όρνιθας (CAM) ενισχύθηκε απο τον άμεσο ενεργοποιητή των διαύλων ΚΑTP, το μόριο SG-209, καθώς και απο τα πολυπεπτίδια CNP και VEGF. Δύο αναστολείς των διαύλων ΚΑTP, η γλιβενκλαμίδη (glibenclamide) και το 5-υδροξυδεκανοϊκό οξύ (5-HD), ανέστειλαν τόσο την αγγειογένεση υποβάθρου (basal) της χοριοαλλαντοϊκής μεμβράνης, όσο και την επαγόμενη απο το CNP αγγειογένεση το σύστημα αυτό. In vitro, άμεσοι ενεργοποιητές των διαύλων ΚΑTP όπως η νικορανδίλη (nicorandil) και το SG-209, καθώς και έμμεσοι ενεργοποιητές, μέσω αρχικής αγωνιστικής δράσης τους σε ειδικούς υποδοχείς, όπως ο VEGF και το CNP, αύξησαν τον πολλαπλασιασμό και τη μετανάστευση εγκεφαλικών ενδοθηλιακών κυττάρων ποντικού της κυτταρικής σειράς bEnd.3. Επιπλέον, ο VEGF και το CNP επάγουν με παρόμοιο τρόπο το σχηματισμό τριχοειδών αγγείων απο ενδοθηλιακά κύτταρα απομονωμένα απο φλέβα ανθρώπινου ομφάλιου λώρου (HUVEC) που δημιουργούνται σε Matrigel με χαμηλή περιεκτικότητα σε αυξητικούς παράγοντες. Όλες αυτές οι in vitro θετικές αγγειογενετικές ενδοθηλιακές αποκρίσεις αναστέλλονται παρουσία της γλιβενκλαμίδης και του 5-HD. Διαμόλυνση κυττάρων HUVECs με siRNA που στοχεύει ειδικά την υπομονάδα του δίαυλου καλίου Kir 6.1 μείωσε αποτελεσματικά την έκφραση αυτής της υπομονάδας τόσο σε επίπεδο mRNA όσο και σε πρωτεϊνικό επίπεδο. Η μείωση στην έκφραση της υπομονάδας Kir6.1 των διαύλων καλίου προκάλεσε καταστολή της μετανάστευσης των κυττάρων HUVECs σε θαλάμους τύπου φρέατος (transwells) καθώς και σημαντική απομείωση στο σχηματισμό δικτύου τριχοειδών αγγείων σε Matrigel, όταν αυτές οι αποκρίσεις επάγονται είτε απο τον άμεσο ενεργοποιητή των διαύλων ΚΑTP, το μόριο SG-209, είτε απο τον έμμεσο ενεργοποιητή των διαύλων ΚΑTP (μέσω δράσης σε ειδικούς υποδοχείες), το πεπτίδιο CNP. Επιπλέον, ο πολλαπλασιασμός και η μετανάστευση των ενδοθηλιακών κυττάρων bEnd.3 που διεγείρονται ως απόκριση στο μόριο SG-209 απαιτούν κινητοποίηση των "κλασσικών" ενδοθηλιακών προ-αγγειογενετικών κινασών Erk1 / 2, p38 και Akt, δεδομένου ότι οι αποκρίσεις αυτές στον SG-209 καταστάλθηκαν απο κάθε ένα από τους αντίστοιχους αναστολείς των κινασών. Η παρούσα μελέτη μας επιτρέπει να συμπεράνουμε ότι: α) άμεση φαρμακολογική τροποποίηση της λειτουργίας των διαύλων ΚATP επηρεάζει σημαντικά τις αγγειογόνες αποκρίσεις τόσο in vitro όσο και in νίνο, β) το CNP είναι όντως ένας αγγειογενετικός παράγοντας, τόσο ισχυρός και αποτελεσματικός για την κινητοποίηση ενδοθηλιακών κυττάρων όσο και ο VEGF, γ) οι αγγειογόνες επιδράσεις του CNP και του VEGF εξαρτώνται από την ενεργοποίηση των ενδοθηλιακών διαύλων ΚΑTP και συγκεκριμένα απαιτούν την έκφραση της υπομονάδας Kir6.1 του διαύλου ΚΑTP, και τέλος δ) η ενεργοποίηση των διαύλων ΚΑTP φαίνεται οτι είναι ένας κοινός μοριακός μηχανισμός που υποστηρίζει την αγγειογένεση που διεγείρεται απο ένα ευρύ φάσμα ενδογενών αγγειοδραστικών χυμικών ερεθισμάτων, που περιλαμβάνουν το H2S, τον VEGF και το CNP. Οι επιπτώσεις της μελέτης αυτής στην θεραπευτική πράξη είναι πιθανώς σημαντικές: Οι τύπου σουλφονυλουρίας αναστολείς διαύλων των διαύλων ΚΑTP, που στοχεύουν μη-επαρκώς επιλεκτικά σε β-παγκρεατικά κύτταρα, χρησιμοποιούνται ευρέως ως φάρμακα για τη θεραπεία του διαβήτη τύπου II, μια ασθένεια που χαρακτηρίζεται από γενικευμένη δυσλειτουργία του αρτηριακού συστήματος, με συνέπεια υψηλή επίπτωση εμφράγματος του μυοκαρδίου και ισχαιμίας των κάτω άκρων. Η εξέλιξη ενός επεισοδίου μυοκαρδιακής ισχαιμίας σε διαβητικούς ασθενείς είναι χειρότερη εάν αυτοί ακολουθούσαν φαρμακολογική θεραπεία με σουλφονυλουρίες, υποδεικνύοντας κάποια, μέχρι τώρα σε σημαντικό βαθμό ανεξήγητη, επιβλαβή καρδιαγγειακή επίδραση αυτής της κατηγορίας ενώσεων. Η παρούσα μελέτη αποδεικνύει ότι η ενεργοποίηση ενδοθηλιακών διαύλων ΚΑTP είναι ένας κοινός προ- αγγειογενετικός μηχανισμός, που μπορεί εν μέρει να εξηγήσει αυτή την αρνητική έκβαση της πρότερης θεραπείας με σουλφονυλουρίες σε διαβητικούς. Επιπλέον, η έρευνα αυτή υποστηρίζει την ανάγκη για το σχεδιασμό νέων μορίων, τα οποία, ενώ θα αναστέλλουν τους διαύλους ΚΑTP στο πάγκρεας, δεν θα επηρεάζουν τους ενδοθηλιακούς διαύλους ΚΑTP και την εξαρτώμενη απο αυτούς αγγειογένεση, και έτσι θα παρουσιάζουν, βάσει των ανωτέρω, βελτιωμένη θεραπευτική δράση.

No description available.

Membrane filtration is growing in popularity as a viable technology for drinking water treatment to meet high demand and regulatory requirements. While many improvements have been made to the technology in the past decade, fouling continues to be one of the major operational challenges associated with membranes as it increases operating costs and reduces membrane life. Fouling control typically requires some form of pre-treatment. Biofiltration is a ???green??? technique that can minimize chemical usage and waste during water treatment and is a relatively new application as a pre-treatment for membranes. Proteins and polysaccharides (biopolymers) have been found to contribute most to fouling of low pressure polymeric membranes. Biofiltration has recently been demonstrated as an effective pre-treatment method for reducing biopolymer-associated fouling of this type of membrane (Hall?? et al., 2009). Given that the concentration and composition of organic matter in water is variable, there is an opportunity to explore the applicability of this robust technology for different water types. The primary goals of this research were to assess the effectiveness of direct biofiltration in minimizing ultrafiltration polymeric (PVDF) membrane fouling and at the same time evaluate the biofilter development, biofilter performance based on organics removal potential, and the effect of phosphorus addition (as a nutrient) to the biofilter influent. A pilot-scale treatment train was constructed at the Technology Demonstration Facility at the Walkerton Clean Water Centre. It included two parallel dual media (sand/anthracite) biological filters (preceded by roughing filters), followed by an ultrafiltration membrane unit. Experiments were conducted using water from the Saugeen River (Ontario, Canada) whose primary form of carbon is humic material. The biofilters were allowed to acclimate and biofilter performance and organics removal were tested over a fourteen month period, the last four months of which were dedicated to phosphorus enhancement experiments. The membrane fouling experiments started seven months following the start-up of the biofilters, after confirmation of steady-state operation. Biofilter water samples were analyzed for natural organic matter constituents along with other water quality parameters, and biomass quantity and activity in the media were measured. Biomass activity in the biofilter media and biopolymer removal through the biofilter indicated a rapid acclimation period, and also demonstrated similar performance of the parallel biofilters during start-up and steady-state operation. The biofilters achieved 21% removal of the biopolymers on average following acclimation, while reduction of the humic fractions was not observed. A linear relationship between biopolymer removal and its concentration in the river water was observed (first-order process). Membrane fouling experiments were conducted using both untreated and biofiltered river water. The fouling rates were computed by monitoring changes in transmembrane pressure over time. Analysis of the samples with liquid chromatography-organic carbon detection confirmed the significant contribution of biopolymers to irreversible and reversible membrane fouling rates even when only present at low concentrations. During the phosphorus enhancement phase, two different phosphorus doses were fed into the influent of one of the parallel biofilters in order to achieve a target C:N:P ratio of roughly 100:10:1. Although initially (first month of the dosing period) an increase in the removal of dissolved organic carbon and ultraviolet-absorbance was observed in the phosphorus-enhanced biofilter, this was not sustained. Phosphorus addition did not affect biopolymer removal or biomass quantity and activity in the biofilter, and the membrane fouling experiments during this period did not show any significant effect of phosphorus addition.

Mémoire numérisé par la Direction des bibliothèques de l'Université de Montréal.

Submitted by Elesbão Santiago Neto (neto10uepb@cche.uepb.edu.br) on 2018-04-05T19:02:03Z No. of bitstreams: 1 PDF - Valter Angelo da Silva Junior.pdf: 36791695 bytes, checksum: 273ed695189827b6fb638d73013560f2 (MD5) / Made available in DSpace on 2018-04-05T19:02:03Z (GMT). No. of bitstreams: 1 PDF - Valter Angelo da Silva Junior.pdf: 36791695 bytes, checksum: 273ed695189827b6fb638d73013560f2 (MD5) Previous issue date: 2017-06-05 / CAPES / This thesis addresses the topic of geopolitical power calculations from the Chinese perspective. A unique aspect of China's assessment of this subject is the use of an analytical tool called "Comprehensive National Power" (CNP) which aims to measure the power of countries and to rank them according to the results found. This Chinese method evaluation, in most of its variations, emphasizes political power as the basis of state power, as well as considering that these units are responsible for the configuration and definition of the International System, not the opposite the other way around. By doing so, it visualizes international relations from a different parameter of Western mainstream approaches, which are mostly based on material power and the power of structure constraint. This dissertation deals with this matter by contextualizing the reader from the initial theoretical foundations on state power and power in the Chinese context, in the presentation of the various CNP versions in China, and, finally, using the analysis method of Yan Xuetong (2008;2011) to evaluate the evolution of China's CNP in the Hu Jintao period (2003-2013). In this way, the thesis presents the relations between China's action - in the established time interval - and the CNP, aiming to identify how the country uses this in the assessment of the International System. / Esta dissertação aborda o tema de cálculos de poder geopolítico a partir da perspectiva chinesa. Um aspecto singular da avaliação da China a respeito deste tema é a utilização de uma ferramenta analítica chamada “Comprehensive National Power” (CNP) que objetiva mensurar o poder dos países e hierarquizá-los a partir dos resultados encontrados. Este método de avaliação chinês, na maioria de suas variações, enfatiza o poder político como a base do poder de um Estado, além de considerar os que estas unidades são responsáveis pela configuração e definição do Sistema Internacional, não o movimento contrário. Desta maneira visualiza as relações internacionais a partir de um parâmetro diferente das abordagens ocidentais de mainstream, baseadas no poder material e no poder do constrangimento da estrutura. A presente dissertação aborda esta matéria contextualizando o leitor desde os fundamentos teóricos iniciais sobre poder e poder estatal no contexto chinês, na apresentação das diferentes versões do CNP da China, e, por fim, utilizando o método de análise de Yan Xuetong (2008; 2011) para avaliar a evolução do CNP da China no período Hu Jintao (2003-2013). Desse modo, o trabalho apresenta as relações entre a ação da China no interregno temporal estabelecido e o CNP, objetivando identificar de que maneira o país utiliza desta ferramenta em sua avaliação do Sistema Internacional.

Context. Resource allocation is an important issue in order to complete a task in the field of agent system. Several protocols are available for task distribution and for efficient resource allocation among agents. Efficient task distribution and resource allocation among agents are often play important roles to obtain high performance. However, the situation becomes more complicated when the resources are dependent on each other where multiple buyers and providers of resources negotiate in parallel. Objectives. In this paper, we proposed an agent based protocol for synchronizing and allocating dependent resources that involves parallel negotiation between multiple buyers and providers of resources. Methods. Literature survey has been conducted in the studied areas in order to position the work and gain more knowledge. Moreover, to validate the proposed protocol, a simulation study was performed. Results. The suggested protocol can handle dependent resources negotiation parallel and the result illustrates that. Moreover, the approach can avoid broadcasting of call for proposals to reduce the communication overhead, which usually occur in many other protocols. Conclusion. In the suggested protocol, we have presented a new idea of re-planning with other techniques like Information board and leveled commitment. In a simulation study, it was identified that this approach is able to deal with the dependent resources according to the simulation results.

No description available.

Methyl-CpG-binding protein 2 (MeCP2 is) is an epigenetic regulator that binds to methylated DNA. Initially identified as transcriptional repressor, MeCP2 also binds to different proteins functioning as gene activator. Importantly, MecCP2 gene mutations and changes in MeCP2 levels are associated to several forms of mental retardation and autism-related disorders; including Rett, a neurodevelopmental disorder affecting primarily girls. While brain MeCP2 was considered to be exclusively neuronal, this regulator is also present in glia. We found that oligodendrocytes, the myelinating cells of the central nervous system (CNS), express particularly high MeCP2 levels at a developmental stage that precedes their final maturation. Moreover, downregulation of MeCP2 levels by treatment of immature oligodendrocytes with small interference RNA (siRNA), reduced the expression of 14 kDa myelin basic protein (MBP) and MOG, two markers of mature oligodendrocytes. These observations raise the possibility that oligodendrocytes have a direct participation in Rett syndrome and other autism-related disorders.

Our research paper looks at the sustainability challenge as an example of complexity in interrelated nested systems (or meta-problem) and we further explore the consequences of disruptive events induced by climate change (ie. Extreme Climate Events). Due to their potential effects on adaptive capacities of systems at all levels (macro, meso and micro) and the need for Strategic Sustainable Development (SSD) to develop meta-solutions (non-isolated, non-reinforcing) we focus on community-based interventions and participatory facilitation processes. Therefore, we enquire what might a process look like that supports a community’s psychological resilience and strategic sustainable development following a disruptive event. A way to reinforce a community’s adaptive capacities is through making meaning collaboratively and such a process can be supported by the use of stories and narrative. To this intent, we focus on the use of Collective Narrative Practices (CNP) within the implementation process (ABCD process) of the Framework for Strategic Sustainable Development (FSSD). CNP promote desired narratives and strengthen communities’ psychological resilience while the FSSD ensures the development of meta-solutions and their practical application (through the ABCD). Throughout a five-step exploration, we test their theoretical compatibility, interview FSSD and CNP practitioners, design an initial Process Prototype, test its validity by interviewing practitioners with expertise in both fields, and develop a final Process Prototype which embeds recommendations, guidelines and tools. Finally, our paper initiates the academic study of the linkage between FSSD and CNP and is aimed to guide practitioners of both fields to discern an effective way to facilitate the emergence of appropriate responses in a community, while maintaining or rebuilding its resilience and complying with SSD core principles.