Dashbell: A Low-cost Smart Doorbell System for Home Use

Smart doorbells allow home owners to receive alerts when a visitor is at the door, see who the guest is, and communicate with the visitor from a smart device. They greatly improve people's life quality and contribute to the evolution of smart homes. However, the commercial smart doorbells are quite expensive, usually cost more than 190 US dollars, which is a substantial impediment on the pervasiveness of smart doorbells. To solve this problem, we introduce the Dashbell-a budget smart doorbell system for home use. It connects a WiFi-enabled device, the Amazon Dash Button, to a network and enables the home owner to answer the bell triggered by the dash button using a smartphone. The Dashbell system also enables fast fault detection and diagnosis due to its distributed framework.Comment: Accepted by IEEE PerCom 201

Characterisation of novel therapies to mitigate inflammation in retinal degenerations

Inflammation is established as a key factor in mediating the progression of a number of retinal degenerations, including both wet and dry age-related macular degeneration (AMD) [1-3]. MicroRNAs (miRNAs) are a class of endogenously occurring non-coding RNA (ncRNA) molecules that are gaining momentum as therapeutic targets for treating a number of human conditions [4-6] and have been identified to modulate inflammation [7]. The purpose of this study is to investigate the modulation of miRNAs in a model of retinal degeneration, the light damage model. MiRNA and their potential roles in mitigating retinal inflammation will also be investigated in animals treated with 670nm red light therapy. Albino rats raised in dim cyclic light conditions (5lux; 12hr on, 12hr off; controls) were exposed to bright continuous light (1000lux) for 24 hours and returned to dim light conditions for 0, 3 or 7 days. At each timepoint animals were culled and their eyes removed and processed either for histological analyses or RNA based analyses. For histology eyes were fixed in 4% paraformaldehyde, cryoprotected and sectioned to determine the photoreceptor cell death using TUNEL or perform immunohistochemistry experiments using Vimentin and IBA1 or in situ hybridisation for Ccl2 and miR-124-3p. RNA was extracted from dissected retinas, reverse transcribed and used for low density array and qPCR analysis to determine the expression changes of genes and miRNAs. Immortalised cell lines were also used for performing cell transfections and similar RNA based analyses as above. Intense light exposure for 24 hours led to differential expression of a number of miRNAs, 37 of which were significantly modulated by 2-fold or more. Of those, 19 may potentially regulate the inflammatory immune response observed in the model. MicroRNAs -125-3p, -155, -207, -347, -449a, -351, and -542-3p are all upregulated at 24 hours of exposure along with peak photoreceptor cell death. The miRNAs -542-3p and -351 reached maximum expression at 7 days after exposure, while -125-3p, -155, -207, -347, and -449 reached a peak expression at 3 days. MiR-124-3p expression showed significant downregulation post intense (1000lux) light induced damage to the rat retina. Its expression was localized predominantly to the Müller glia and showed co-localisation with expression of a target gene, Ccl2 (which is a potent chemoattractant molecule responsible for targeted monocyte recruitment in the retina). Luciferase assays in MIO-M1 and HeLa cells confirmed direct binding between miR-124-3p and the CCL2-3’UTR. Additionally, in vitro overexpression of miR-124-3p in Müller cells using miRNA mimics significantly inhibited CCL2 upregulation post stimulation with inflammatory cues. Post mortem human tissue showed a similar expression profile for miR-124-3p in the retina. Changes is miRNA expression were also seen in 670nm light treated retinas with or without bright light induced damage, along with the modulation of chemokine gene expression in the pre-treated retinas. Differential expression of miR-351 and miR-155 was confirmed using qPCR, both of which are predicted to target inflammation related genes. The data indicate that miRNAs are involved in modulating the inflammatory immune response elicited during retinal degeneration. Indeed we found a number of potential candidates, including miR-124-3p, which could prove to be novel therapeutic interventions in mitigating retinal inflammation and the consequent photoreceptor death. 670nm light therapy mitigated retinal inflammation including the modulation of specific miRNAs in the retina

Identification of miRNAs in a model of retinal degenerations

PURPOSE. We investigated the expression profile of and identify all microRNAs (miRNAs) that potentially regulate inflammation in a light-induced model of focal retinal degeneration. METHODS. Sprague Dawley (SD) rats aged 90 to 140 postnatal days were exposed to 1000 lux white fluorescent light for 24 hours. At 24 hours, and 3 and 7 days after exposure, the animals were euthanized and retinas processed for RNA. Expression of 750 miRNAs at 24 hours of exposure was assessed using low density array analysis. Significantly modulated miRNAs and their target mRNAs were used to assess the potential biological effects. Expression of seven miRNAs, potentially modulating inflammation, was investigated across a protracted time course after light exposure using quantitative PCR. Photoreceptor cell death was analyzed using TUNEL. RESULTS. Intense light exposure for 24 hours led to differential expression of a number of miRNAs, 37 of which were significantly modulated by 2-fold or more. Of those, 19 may potentially regulate the inflammatory immune response observed in the model. MicroRNAs -125-3p, -155, -207, -347, -449a, -351, and -542-3p are all upregulated at 24 hours of exposure along with peak photoreceptor cell death. The MiRNAs -542-3p and -351 reached maximum expression at 7 days after exposure, while -125-3p, -155, -207, -347, and -449 reached a peak expression at 3 days. CONCLUSIONS. The results of the study show that miRNAs are modulated in response to light damage (LD). These miRNAs potentially regulate the inflammatory immune response, triggered as a result of the acute retinal damage, which is a key mediator of retinal degeneration in this model and age-related macular degeneration

Hot deformation studies on 2.7% Si steel using gleeble thermo-mechanical simulator

Uni-axial hot compression tests were conducted at different temperatures(1173-1423 K) and at strain rates of 0.1, 1, 10 and 100/s using Thermo-mechanical Simulator (Gleeble-3500C System) on a 2.7% Si electrical steel to understand the hot workability issues associated with this steel during hot rolling. The flow curves obtained revealed dynamic recovery as the predominant softening mechanism at majority of hot deformation conditions except at lower temperature and high strain rate where work hardening was observed. However, the work hardening was not very prominent due to ferrite structure throughout the hot deformation temperature range established by Thermo-Calc software. Small amount of cementite (pearlite) transformed from austenite along prior ferrite grain was observed due to presence of carbon in excess of 0.02. Strain rate sensitivity varied within a narrow range of 0.18 - 0.21 with rising tendency with an increase in temperature

A surgical system for automatic registration, stiffness mapping and dynamic image overlay

In this paper we develop a surgical system using the da Vinci research kit (dVRK) that is capable of autonomously searching for tumors and dynamically displaying the tumor location using augmented reality. Such a system has the potential to quickly reveal the location and shape of tumors and visually overlay that information to reduce the cognitive overload of the surgeon. We believe that our approach is one of the first to incorporate state-of-the-art methods in registration, force sensing and tumor localization into a unified surgical system. First, the preoperative model is registered to the intra-operative scene using a Bingham distribution-based filtering approach. An active level set estimation is then used to find the location and the shape of the tumors. We use a recently developed miniature force sensor to perform the palpation. The estimated stiffness map is then dynamically overlaid onto the registered preoperative model of the organ. We demonstrate the efficacy of our system by performing experiments on phantom prostate models with embedded stiff inclusions.Comment: International Symposium on Medical Robotics (ISMR 2018

Laparoscopic evaluation of female infertility in low socioeconomic status

Background: Infertility is a multidimensional health issue which is rising dramatically. The common causes include ovarian, uterine, tubal disorders, hormonal imbalance, age-related factors and lifestyle factors. The low economic strata poses a subset of problems like difficulty in seeking healthcare, treatment costs and poor compliance. Authors sought to evaluate the factors for primary and secondary infertility in women of reproductive age group who belong to low socio-economic strata using laparoscopy.Methods: A prospective observational study was conducted in the obstetrics and gynaecology department at Sanjay Gandhi memorial hospital, Delhi comprising 50 infertile women of reproductive age group belonging to low socioeconomic class for a period of 2 years from June 2015 onwards.Results: Among primary infertility, tuberculosis (27.02%), ovarian cyst (16.22%), adhesions (10.81%), polycystic ovaries (10.81%) and Pelvic inflammatory disease (10.81%) were the major findings whereas in secondary infertility Pelvic inflammatory disease (23.07%), tuberculosis (15.38%), adhesions (15.38%) and endometriosis (7.69%) were the major factors seen in the study.Conclusions: Tuberculosis and pelvic inflammatory disease were the major factors seen in infertile women of low socioeconomic status thus, they should be kept high on the list of differential diagnosis even if the investigative work up is negative

Photobiomodulation with 670 nm light ameliorates Müller cell-mediated activation of microglia and macrophages in retinal degeneration

Müller cells, the supporting cells of the retina, play a key role in responding to retinal stress by releasing chemokines, including CCL2, to recruit microglia and macrophages (MG/MΦ) into the damaged retina. Photobiomodulation (PBM) with 670 nm light has been shown to reduce inflammation in models of retinal degeneration. In this study, we aimed to investigate whether 670 nm light had an effect on Müller cell-initiated inflammation under retinal photo-oxidative damage (PD) in vivo and in vitro. Sprague-Dawley rats were pre-treated with 670 nm light (9J/cm2) once daily over 5 days prior to PD. The expression of inflammatory genes including CCL2 and IL-1β was analysed in retinas. In vitro, primary Müller cells dissociated from neonatal rat retinas were co-cultured with 661W photoreceptor cells. Co-cultures were exposed to PD, followed by 670 nm light treatment to the Müller cells only, and Müller cell stress and inflammation were assessed. Primary MG/MΦ were incubated with supernatant from the co-cultures, and collected for analysis of inflammatory activation. To further understand the mechanism of 670 nm light, the expression of COX5a and mitochondrial membrane potential (ΔΨm) were measured in Müller cells. Following PD, 670 nm light-treated Müller cells had a reduced inflammatory activation, with lower levels of CCL2, IL-1β and IL-6. Supernatant from 670 nm light-treated co-cultures reduced activation of primary MG/MΦ, and lowered the expression of pro-inflammatory cytokines, compared to untreated PD controls. Additionally, 670 nm light-treated Müller cells had an increased expression of COX5a and an elevated ΔΨm following PD, suggesting that retrograde signaling plays a role in the effects of 670 nm light on Müller cell gene expression. Our data indicates that 670 nm light reduces Müller cell-mediated retinal inflammation, and offers a potential cellular mechanism for 670 nm light therapy in regulating inflammation associated with retinal degenerations.This work was supported by the Australian Government National Health and Medical Research Council Grant (APP1049990), Taiwan-ANU scholarship, the Australian Government Research Training Program and the Gretel and Gordon Bootes Foundation

MicroRNA-124 Dysregulation is Associated With Retinal Inflammation and Photoreceptor Death in the Degenerating Retina

PURPOSE. We sought to determine the role and retinal cellular location of microRNA-124 (miR-124) in a neuroinflammatory model of retinal degeneration. Further, we explored the anti-inflammatory relationship of miR-124 with a predicted messenger RNA (mRNA) binding partner, chemokine (C-C motif) ligand 2 (Ccl2), which is crucially involved in inflammatory cell recruitment in the damaged retina. METHODS. Human AMD donor eyes and photo-oxidative damaged (PD) mice were labeled for miR-124 expression using in situ hybridization. PDGFRa-cre RFP mice were used for Müller cell isolation from whole retinas. MIO-M1 immortalized cells and rat primary Müller cells were used for in vitro analysis of miR-124 expression and its relationship with Ccl2. Therapeutic efficacy was tested with intravitreal administration of miR-124 mimic in mice, with electroretinography used to determine retinal function. IBA1 immunohistochemistry and photoreceptor row counts were used for assessment of inflammation and cell death. RESULTS. MiR-124 expression was correlated with progressive retinal damage, inflammation, and cell death in human AMD and PD mice. In addition, miR-124 expression was inversely correlated to Ccl2 expression in mice following PD. MiR-124 was localized to both neuronal-like photoreceptors and glial (Müller) cells in the retina, with a redistribution from neurons to glia occurring as a consequence of PD. Finally, intravitreal administration of miR-124 mimics decreased retinal inflammation and photoreceptor cell death, and improved retinal function. CONCLUSIONS. This study has provided an understanding of the mechanism behind miR-124 in the degenerating retina and demonstrates the usefulness of miR-124 mimics for the modulation of retinal degenerations.Supported by the National Health and Medical Research Council in Australia (APP1127705, 2017-2019), the Australian Government Research Training Program, the Gretel and Gordon Bootes Foundation (2013), and the Ophthalmic Research Institute of Australia/Eye Surgeons’ Foundation (2015)