Slum Settlements Regeneration in Lagos Mega-city: an Overview of a Waterfront Makoko Community

Urban degradation is caused principally by urbanization process, however, most of the environmental problems in Lagos suburbs result largely from its unplanned landuses, swampy nature of built areas and weak development control. Other critical problems that bother minds also include lack of open space, poor management of flood channels and substandard housing. This paper discuses the possible intervention strategies in the regeneration effort of Makoko - a submerged residential enclave located in Yaba local government area of Lagos. The research method which is both narrative and statistically descriptive in nature enables the author engage in a detailed literature study of the chronological development of Lagos with view to determining how the mega city came about the current level of degenerating infrastructural facilities. The study found that the principle of cooperative leadership by government at all levels is fundamental to making important difference in qualitative development controls of the study area. It however concluded that the duo role of the public and traditional power structure of the community leaders must be involved in the conception and implementation of Makoko’s environmental planning programmes

Distributed Relay Protocol for Probabilistic Information-Theoretic Security in a Randomly-Compromised Network

We introduce a simple, practical approach with probabilistic information-theoretic security to mitigate one of quantum key distribution's major limitations: the short maximum transmission distance (~200 km) possible with present day technology. Our scheme uses classical secret sharing techniques to allow secure transmission over long distances through a network containing randomly-distributed compromised nodes. The protocol provides arbitrarily high confidence in the security of the protocol, with modest scaling of resource costs with improvement of the security parameter. Although some types of failure are undetectable, users can take preemptive measures to make the probability of such failures arbitrarily small.Comment: 12 pages, 2 figures; added proof of verification sub-protocol, minor correction

Autophagy takes it all - autophagy inducers target immune aging

Autophagy, as the key nutrient recycling pathway, enables eukaryotic cells to adapt to surging cellular stress during aging and, thereby, delays age-associated deterioration. Autophagic flux declines with age and, in turn, decreases in autophagy contribute to the aging process itself and promote senescence. Here, we outline how autophagy regulates immune aging and discuss autophagy-inducing interventions that target senescent immune cells, which are major drivers of systemic aging. We examine how cutting-edge technologies, such as single-cell omics methods hold the promise to capture the complexity of molecular and cellular phenotypes associated with aging, driving the development of suitable putative biomarkers and clinical bioassays. Finally, we debate the urgency to initiate large-scale human clinical trials. We give special preference to small molecule probes and to dietary interventions that can extend healthy lifespan and are affordable for most of the world's population

Hallmarks and detection techniques of cellular senescence and cellular ageing in immune cells

The ageing of the global population brings about unprecedented challenges. Chronic age-related diseases in an increasing number of people represent an enormous burden for health and social care. The immune system deteriorates during ageing and contributes to many of these age-associated diseases due to its pivotal role in pathogen clearance, tissue homeostasis and maintenance. Moreover, in order to develop treatments for COVID-19, we urgently need to acquire more knowledge about the aged immune system, as older adults are disproportionally and more severely affected. Changes with age lead to impaired responses to infections, malignancies and vaccination, and are accompanied by chronic, low-degree inflammation, which together is termed immunosenescence. However, the molecular and cellular mechanisms that underlie immunosenescence, termed immune cell senescence, are mostly unknown. Cellular senescence, characterised by an irreversible cell cycle arrest, is thought to be the cause of tissue and organismal ageing. Thus, better understanding of cellular senescence in immune populations at single-cell level may provide us with insight into how immune cell senescence develops over the life time of an individual. In this review, we will briefly introduce the phenotypic characterisation of aged innate and adaptive immune cells, which also contributes to overall immunosenescence, including subsets and function. Next, we will focus on the different hallmarks of cellular senescence and cellular ageing, and the detection techniques most suitable for immune cells. Applying these techniques will deepen our understanding of immune cell senescence and to discover potential druggable pathways, which can be modulated to reverse immune ageing

One Health proof of concept: Bringing a transdisciplinary approach to surveillance for zoonotic viruses at the human-wild animal interface.

As the world continues to react and respond inefficiently to emerging infectious diseases, such as Middle Eastern Respiratory Syndrome and the Ebola and Zika viruses, a growing transdisciplinary community has called for a more proactive and holistic approach to prevention and preparedness - One Health. Such an approach presents important opportunities to reduce the impact of disease emergence events and also to mitigate future emergence through improved cross-sectoral coordination. In an attempt to provide proof of concept of the utility of the One Health approach, the US Agency for International Development's PREDICT project consortium designed and implemented a targeted, risk-based surveillance strategy based not on humans as sentinels of disease but on detecting viruses early, at their source, where intervention strategies can be implemented before there is opportunity for spillover and spread in people or food animals. Here, we share One Health approaches used by consortium members to illustrate the potential for successful One Health outcomes that can be achieved through collaborative, transdisciplinary partnerships. PREDICT's collaboration with partners around the world on strengthening local capacity to detect hundreds of viruses in wild animals, coupled with a series of cutting-edge virological and analytical activities, have significantly improved our baseline knowledge on the zoonotic pool of viruses and the risk of exposure to people. Further testament to the success of the project's One Health approach and the work of its team of dedicated One Health professionals are the resulting 90 peer-reviewed, scientific publications in under 5 years that improve our understanding of zoonoses and the factors influencing their emergence. The findings are assisting in global health improvements, including surveillance science, diagnostic technologies, understanding of viral evolution, and ecological driver identification. Through its One Health leadership and multi-disciplinary partnerships, PREDICT has forged new networks of professionals from the human, animal, and environmental health sectors to promote global health, improving our understanding of viral disease spillover from wildlife and implementing strategies for preventing and controlling emerging disease threats

Autophagy orchestrates the crosstalk between cells and organs

Over the recent years, it has become apparent that a deeper understanding of cell-to-cell and organ-to-organ communication is necessary to fully comprehend both homeostatic and pathological states. Autophagy is indispensable for cellular development, function, and homeostasis. A crucial aspect is that autophagy can also mediate these processes through its secretory role. The autophagy-derived secretome relays its extracellular signals in the form of nutrients, proteins, mitochondria, and extracellular vesicles. These crosstalk mediators functionally shape cell fate decisions, tissue microenvironment and systemic physiology. The diversity of the secreted cargo elicits an equally diverse type of responses, which span over metabolic, inflammatory, and structural adaptations in disease and homeostasis. We review here the emerging role of the autophagy-derived secretome in the communication between different cell types and organs and discuss the mechanisms involved

Blocking glycosphingolipid production alters autophagy in osteoclasts and improves myeloma bone disease

Glycosphingolipids (GSLs) are key constituents of membrane bilayers playing a role in structural integrity, cell signalling in microdomains, endosomes and lysosomes, and cell death pathways. Conversion of ceramide into GSLs is controlled by GCS (glucosylceramide synthase) and inhibitors of this enzyme for the treatment of lipid storage disorders and specific cancers. With a diverse range of functions attributed to GSLs, the ability of the GSC inhibitor, eliglustat, to reduce myeloma bone disease was investigated. In pre-clinical models of multiple myeloma, osteoclast-driven bone loss was reduced by eliglustat in a mechanistically separate manner to zoledronic acid, a bisphosphonate that prevents osteoclast-mediated bone destruction. Autophagic degradation of TNF receptor-associated factor 3 (TRAF3), a key step for osteoclast differentiation, was inhibited by eliglustat as evidenced by TRAF3 lysosomal and cytoplasmic accumulation. By altering GSL composition, eliglustat prevented lysosomal degradation whilst exogenous addition of missing GSLs rescued TRAF3 degradation to restore osteoclast formation in bone marrow cells from myeloma patients. This work highlights the clinical potential of eliglustat as a therapy for myeloma bone disease. Furthermore, using eliglustat as a lysosomal inhibitor in osteoclasts may widen its therapeutic uses to other bone disorders such as bone metastasis, osteoporosis and inflammatory bone loss

Quantifying marine plastic debris in a beach environment using spectral analysis

Marine plastic debris (MPD) is a globally relevant environmental challenge, with an estimated 8 million tons of synthetic debris entering the marine environment each year. Plastic has been found in all parts of the marine environment, including the surface layers of the ocean, within the water column, in coastal waters, on the benthic layer and on beaches. While research on detecting MPD using remote sensing is increasing, most of it focuses on detecting floating debris in open waters, rather than detecting MPD on beaches. However, beaches present challenges that are unique from other parts of the marine environment. In order to better understand the spectral properties of beached MPD, we present the SWIR reflectance of weathered MPD and virgin plastics over a sandy substrate. We conducted spectral feature analysis on the different plastic groups to better understand the impact that polymers have on our ability to detect synthetic debris at sub-pixel surface covers that occur on beaches. Our results show that the minimum surface cover required to detect MPD on a sandy surface varies between 2–8% for different polymer types. Furthermore, plastic composition affects the magnitude of spectral absorption. This suggests that variation in both surface cover and polymer type will inform the efficacy of beach litter detection methods

Constraints on the uncertainties of entangled symmetric qubits

We derive necessary and sufficient inseparability conditions imposed on the variance matrix of symmetric qubits. These constraints are identified by examining a structural parallelism between continuous variable states and two qubit states. Pairwise entangled symmetric multiqubit states are shown here to obey these constraints. We also bring out an elegant local invariant structure exhibited by our constraints.Comment: 5 pages, REVTEX, Improved presentation; Theorem on neccessary and sufficient condition included; To appear in Phys. Lett.

Proteostasis in T cell aging

Aging leads to a decline in immune cell function, which leaves the organism vulnerable to infections and age-related multimorbidities. One major player of the adaptive immune response are T cells, and recent studies argue for a major role of disturbed proteostasis contributing to reduced function of these cells upon aging. Proteostasis refers to the state of a healthy, balanced proteome in the cell and is influenced by synthesis (translation), maintenance and quality control of proteins, as well as degradation of damaged or unwanted proteins by the proteasome, autophagy, lysosome and cytoplasmic enzymes. This review focuses on molecular processes impacting on proteostasis in T cells, and specifically functional or quantitative changes of each of these upon aging. Importantly, we describe the biological consequences of compromised proteostasis in T cells, which range from impaired T cell activation and function to enhancement of inflamm-aging by aged T cells. Finally, approaches to improve proteostasis and thus rejuvenate aged T cells through pharmacological or physical interventions are discussed