scholarly journals An Ecology of Innovation: Adapt, Reuse and Reimagine

Author(s):  
Peter S. Raab ◽  

This paper questions the role of ecology through the design of three small, but impactful projects from different political and bioclimatic regions in North America. An adobe home in the Sonoran desert ofMexico, a rope pavilion in the Texas hill country, and an ice hut in Manitoba, Canada. Each of these investigations reveal site-specific ecologies to determine interventions rooted in local cultural and biological systems. The three solutions probe dis-global networks using unique environmental foci in the hopes of transferring knowledge of how ecology, architectural design and material construction may deal with the abstract nature of ecology in tangible terms. These diverse, ecologically sensitive and material specific solutions belie the premise of singular solutions for all ecologies, but insist on sharing singular explorations employed to fully nest design ideations within the local environs by balancing culture, site, ecological and programmatic issues.

2021 ◽  
Vol 9 (1.2) ◽  
pp. 7881-7885
Author(s):  
John Sharkey ◽  

Peripheral neuropathies can have a plethora of origins including physical insults resulting from connective tissue compression and entrapment. Observational investigations, using biotensegrity focused dissections, have identified site-specific fascial structures that are hypothesised to afford integrity to neurovascular structures by providing appropriate tension and compression. These myofascial structures act as site-specific fascia tuning pegs. While these ‘tuning pegs’ are capable of having a whole body impact, this paper will look specifically at the local influences on pelvis and lower limb. The analogy of a fascia ‘tuning peg’, similar to the tuning peg of a string instrument, is adopted to help explain this unfamiliar concept. An ‘out of tune’ fascial system would lead to hypertonic and inhibited tissues, dissonant notes, one could say. Hypertonic tissues increase tensional forces acting within local and global networks leading to inappropriate densification of fascial structures, fibrosis and neurovascular fascial adhesions. Inhibited tissues, unable to generate sufficient force to ensure appropriate fascial integrity, lead to excessive compression on neurovascular structures like a dissonant note striking a wrong cord. Site-specific fascia tuning pegs provide appropriate frequency and note specific tension and compression ensuring combined forces operate in an omnidirectional manner resulting in pain free physiology, neurology and motion. The role of muscles in metabolism, physiology, heat production and motion is well described within the scientific literature. Less understood is the local role of myofascial structures providing mechanotransductive forces resulting in fascial expansive responses ensuring appropriate gliding and decompression of neurovascular structures. It is proposed that failure of site-specific fascia tuning pegs results in excessive compression, friction, inflammation, pathology, pain and changes in sensations. KEY WORDS: Biotensegrity, Fascia, Site specific fascia tuning pegs, Tensegrity, Neuropathy, Dynamic ischemia.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Eva Höllmüller ◽  
Simon Geigges ◽  
Marie L. Niedermeier ◽  
Kai-Michael Kammer ◽  
Simon M. Kienle ◽  
...  

AbstractDecoding the role of histone posttranslational modifications (PTMs) is key to understand the fundamental process of epigenetic regulation. This is well studied for PTMs of core histones but not for linker histone H1 in general and its ubiquitylation in particular due to a lack of proper tools. Here, we report on the chemical synthesis of site-specifically mono-ubiquitylated H1.2 and identify its ubiquitin-dependent interactome on a proteome-wide scale. We show that site-specific ubiquitylation of H1 at position K64 modulates interactions with deubiquitylating enzymes and the deacetylase SIRT1. Moreover, it affects H1-dependent chromatosome assembly and phase separation resulting in a more open chromatosome conformation generally associated with a transcriptionally active chromatin state. In summary, we propose that site-specific ubiquitylation plays a general regulatory role for linker histone H1.


1988 ◽  
Vol 263 (36) ◽  
pp. 19662-19669
Author(s):  
T L Solomon ◽  
L R Solomon ◽  
L S Gay ◽  
P A Rubenstein
Keyword(s):  

Biomolecules ◽  
2020 ◽  
Vol 11 (1) ◽  
pp. 15
Author(s):  
Aishat Motolani ◽  
Matthew Martin ◽  
Mengyao Sun ◽  
Tao Lu

The nuclear factor kappa B (NF-κB) is a ubiquitous transcription factor central to inflammation and various malignant diseases in humans. The regulation of NF-κB can be influenced by a myriad of post-translational modifications (PTMs), including phosphorylation, one of the most popular PTM formats in NF-κB signaling. The regulation by phosphorylation modification is not limited to NF-κB subunits, but it also encompasses the diverse regulators of NF-κB signaling. The differential site-specific phosphorylation of NF-κB itself or some NF-κB regulators can result in dysregulated NF-κB signaling, often culminating in events that induce cancer progression and other hyper NF-κB related diseases, such as inflammation, cardiovascular diseases, diabetes, as well as neurodegenerative diseases, etc. In this review, we discuss the regulatory role of phosphorylation in NF-κB signaling and the mechanisms through which they aid cancer progression. Additionally, we highlight some of the known and novel NF-κB regulators that are frequently subjected to phosphorylation. Finally, we provide some future perspectives in terms of drug development to target kinases that regulate NF-κB signaling for cancer therapeutic purposes.


2010 ◽  
Vol 23 (10) ◽  
pp. 2163-2175 ◽  
Author(s):  
J. PÉREZ-ALQUICIRA ◽  
F. E. MOLINA-FREANER ◽  
D. PIÑERO ◽  
S. G. WELLER ◽  
E. MARTÍNEZ-MEYER ◽  
...  

2006 ◽  
Vol 291 (6) ◽  
pp. F1123-F1132 ◽  
Author(s):  
James J. De Yoreo ◽  
S. Roger Qiu ◽  
John R. Hoyer

Calcium oxalate monohydrate (COM) is the primary constituent of the majority of renal stones. Osteopontin (OPN), an aspartic acid-rich urinary protein, and citrate, a much smaller molecule, are potent inhibitors of COM crystallization at levels present in normal urine. Current concepts of the role of site-specific interactions in crystallization derived from studies of biomineralization are reviewed to provide a context for understanding modulation of COM growth at a molecular level. Results from in situ atomic force microscopy (AFM) analyses of the effects of citrate and OPN on growth verified the critical role of site-specific interactions between these growth modulators and individual steps on COM crystal surfaces. Molecular modeling investigations of interactions of citrate with steps and faces on COM crystal surfaces provided links between the stereochemistry of interaction and the binding energy levels that underlie mechanisms of growth modification and changes in overall crystal morphology. The combination of in situ AFM and molecular modeling provides new knowledge that will aid rationale design of therapeutic agents for inhibition of stone formation.


1993 ◽  
Vol 13 (3) ◽  
pp. 1363-1370 ◽  
Author(s):  
K M Sheehan ◽  
M R Lieber

V(D)J recombination in lymphoid cells is a site-specific process in which the activity of the recombinase enzyme is targeted to signal sequences flanking the coding elements of antigen receptor genes. The order of the steps in this reaction and their mechanistic interdependence are important to the understanding of how the reaction fails and thereby contributes to genomic instability in lymphoid cells. The products of the normal reaction are recombinant joints linking the coding sequences of the receptor genes and, reciprocally, the signal ends. Extrachromosomal substrate molecules were modified to inhibit the physical synapsis of the recombination signals. In this way, it has been possible to assess how inhibiting the formation of one joint affects the resolution efficiency of the other. Our results indicate that signal joint and coding joint formation are resolved independently in that they can be uncoupled from each other. We also find that signal synapsis is critical for the generation of recombinant products, which greatly restricts the degree of potential single-site cutting that might otherwise occur in the genome. Finally, inversion substrates manifest synaptic inhibition at much longer distances than do deletion substrates, suggesting that a parallel rather than an antiparallel alignment of the signals is required during synapsis. These observations are important for understanding the interaction of V(D)J signals with the recombinase. Moreover, the role of signal synapsis in regulating recombinase activity has significant implications for genome stability regarding the frequency of recombinase-mediated chromosomal translocations.


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