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The smartwatch, which is considered as the most complex gadget among the wearables, is becoming ubiquitous with increasing market penetration. High-tech smartwatches are revolutionising the health ...

Additional file 1: Fig. S1. The top 12 proteins that had a greater binding affinity for CHMP2BIntron5 than for CHMP2BWT, as shown by mass spectrometry analysis.

Additional file 2: Fig. S2. Immunocytochemical analysis of the interaction between CHMP2B and EGFP-Spastin in HeLa cells. Flag-CHMP2BIntron5 bound more EGFP-Spastin than Flag-CHMP2BWT. Scale bar, 10 μm.

Additional file 4: Table S1. Nucleotide sequences of SPAST RNAi.

Additional file 3: Fig. S3. Effect of CHMP2BIntron5 on the SPAST mRNA level in HEK293 cells in three independent experiments. ***p

Internet of Things (IoT) is rapidly growing and exploited in almost all the fields such as industrial automation, building automation, smart metering, smart homes etc. IoT is formed mostly from heavily resource constrained and low-cost tiny sensor devices. These devices are battery powered and have memory constraints. 6LoWPAN (IPv6 over Low-Power Wireless Personal Area Networks) is one of the most exciting protocols developed for IoT. 6LoWPAN allows these tiny sensor devices of low-power applications to connect to IPv6 networks. Because of 6LoWPAN, IPv6 packets can be sent over low-power and lossy (IEEE 802.15.4) networks. The IPv6 address space can address trillions of these tiny devices in IoT. Thus, the exhausting IPv4 addresses pool and almost infinite number of unique addresses provided by IPv6 space proves 6LoWPAN to be indispensable. Every node in the network becomes IP addressable and the wireless sensor network is connected to the real IP world. The network formed by the resource constrained devices specified above are low-power and lossy networks (LLN). Thus, LLN have limited power resources and are characterized by lossy links. The routing protocol designed for such IPv6 LLN is called RPL- ‘IPv6 Routing over Low-power and Lossy Networks’. RPL builds the network based on its defined ‘objective function’. In this dissertation, a 6LoWPAN based wireless sensor network application is implemented. The application is to capture CO2 levels in air along with other relevant parameters to know the indoor air quality (IAQ). The setup allows the data to be sensed and displayed in real time. It is developed from Instant Contiki OS. As these sensor devices used in 6LoWPAN networks are highly power constrained, the second objective of the project is to investigate and implement a more energy efficient routing by RPL. A new objective function is implemented based on fuzzy logic. This aims to reduce the energy consumption of the network. Cooja simulator from Contiki OS is used for this RPL implementation. Master of Science (Communications Engineering)

In the retina, Müller glia is a dominant player of immune response. The HIV-1 transactivator viral protein (Tat) induces production of several neurotoxic cytokines in retinal cells. We show that HIV-1 clades Tat B and C act differentially on Müller glia, which is reflected in apoptosis, activation of cell death pathway components and pro-inflammatory cytokines. The harsher immune-mediated pathology of Tat B, as opposed to milder effects of Tat C, manifests at several signal transduction pathways, notably, MAPK, STAT, SOCS, the NFκB signalosome, and TTP. In activated cells, anandamide (AEA), acting as an immune-modulator, suppresses Tat B effect through MKP-1 but Tat C action via MEK-1. AEA lowers nuclear NF-κB and TAB2 for both variants while elevating IRAK1BP1 in activated Müller glia. Müller glia exposed to Tat shows enhanced PBMC attachment. Tat-induced increase in leukocyte adhesion to Müller cells can be mitigated by AEA, involving both CB receptors. This study identifies multiple signalling components that drive immune-mediated pathology and contribute to disease severity in HIV clades. We show that the protective effects of AEA occur at various stages in cytokine generation and are clade-dependant.

A hexanucleotide repeat expansion (HRE) in C9orf72 is the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). However, patients with the HRE exhibit a wide disparity in clinical presentation and age of symptom onset suggesting an interplay between genetic background and environmental stressors. Neurotrauma as a result of traumatic brain or spinal cord injury has been shown to increase the risk of ALS/FTD in epidemiological studies. Here, we combine patient-specific induced pluripotent stem cells (iPSCs) with a custom-built device to deliver biofidelic stretch trauma to C9orf72 patient and isogenic control motor neurons (MNs) in vitro . We find that mutant but not control MNs exhibit selective degeneration after a single incident of severe trauma, which can be partially rescued by pretreatment with a C9orf72 antisense oligonucleotide. A single incident of mild trauma does not cause degeneration but leads to cytoplasmic accumulation of TDP-43 in C9orf72 MNs. This mislocalization, which only occurs briefly in isogenic controls, is eventually restored in C9orf72 MNs after 6 days. Lastly, repeated mild trauma ablates the ability of patient MNs to recover. These findings highlight alterations in TDP-43 dynamics in C9orf72 ALS/FTD patient MNs following traumatic injury and demonstrate that neurotrauma compounds neuropathology in C9orf72 ALS/FTD. More broadly, our work establishes an in vitro platform that can be used to interrogate the mechanistic interactions between ALS/FTD and neurotrauma., Competing Interests: DECLARATION OF INTERESTS E.K is a cofounder of NeuronGrow, SAB member of Axion Biosystems, ResQ Biotech and Synapticure and a consultant for Confluence Therapeutics; named companies were not involved in this project. The authors declare no other competing interests.