SURF: Subject-Adaptive Unsupervised ECG Signal Compression for Wearable Fitness Monitors

Recent advances in wearable devices allow non-invasive and inexpensive collection of biomedical signals including electrocardiogram (ECG), blood pressure, respiration, among others. Collection and processing of various biomarkers are expected to facilitate preventive healthcare through personalized medical applications. Since wearables are based on size- and resource-constrained hardware, and are battery operated, they need to run lightweight algorithms to efficiently manage energy and memory. To accomplish this goal, this paper proposes SURF, a subject-adaptive unsupervised signal compressor for wearable fitness monitors. The core idea is to perform a specialized lossy compression algorithm on the ECG signal at the source (wearable device), to decrease the energy consumption required for wireless transmission and thus prolong the battery lifetime. SURF leverages unsupervised learning techniques to build and maintain, at runtime, a subject-adaptive dictionary without requiring any prior information on the signal. Dictionaries are constructed within a suitable feature space, allowing the addition and removal of code words according to the signal's dynamics (for given target fidelity and energy consumption objectives). Extensive performance evaluation results, obtained with reference ECG traces and with our own measurements from a commercial wearable wireless monitor, show the superiority of SURF against state-of-the-art techniques, including: 1) compression ratios up to 90-times; 2) reconstruction errors between 2% and 7% of the signal's range (depending on the amount of compression sought); and 3) reduction in energy consumption of up to two orders of magnitude with respect to sending the signal uncompressed, while preserving its morphology. SURF, with artifact prone ECG signals, allows for typical compression efficiencies (CE) in the range $\text {CE} \in [{40,50}]$ , which means that the data rate of 3 kbit/s that would be required to send the uncompressed ECG trace is lowered to 60 and 75 bit/s for CE = 40 and CE = 50, respectively

P2X7 receptor involvement in the pathogenesis of Hidradenitis Suppurativa

The P2X7 receptor (P2X7R) is an ATP-gated plasma membrane ion channel widely distributed in human tissues, the highest expression being in cells of the immune and inflammatory systems, especially of the myeloid lineage [1]. The P2X7R plays different functions depending on the cell type and agonist concentration. One of the most relevant P2X7R activities consists in the regulation of inflammatory responses mainly through NLRP3 inflammasome activation and IL-1β processing and release [2]. Hidradenitis suppurativa (HS) is a chronic skin disease characterized by recurrent, painful nodules and abscesses of apocrine glands. Follicular occlusion and subsequent rupture are central events in HS. HS pathogenesis is not yet understood and many researches have recently focused on possible involvement of components of the immune system, mainly cytokines. Indeed, dysregulated cytokine expression, e.g. IL-1β, TNF-α, IL-6, was found in skin, plasma and immune cells of HS patients [3-6]. The aim of this study was to investigate a possible role of P2X7R in the pathogenesis of HS, also in view of a possible use of P2X7R antagonists in the treatment of this pathology with few options for effective therapy. For this 30 HS patients compared to 30 matched healthy control subjects, have been studied as regard skin biopsies, plasma and peripheral blood mononuclear cells (PBMC). Results show increased P2X7R expression in skin biopsies of HS patients respect to healthy controls (Fig. 1). Higher P2X7R immunostaining was shown by cheratinocytes as well as by some inflammatory cells in the derma, mainly macrophages and plasma cells. Plasma IL-1β levels were increased in HS patients respect to healthy controls suggesting a role for this cytokine in disease development. In apparent contrast with the last finding, PBMC from HS patients appeared defective in IL-1β release upon P2X7R stimulation. This is in agreement with deregulated and compartmentalized cytokine responses found by other authors [3,6]. Further research is necessary to identify the main source of circulating IL-1β as well as the expression of inflammasome components in HS lesional and possibly perilesional skin. Open image in new window Figure 1. Increased P2X7 immunostaining of skin section from HS patient (A) compared to control subject (B). 1. Bours MJ, Dagnelie PC, Giuliani AL, Wesselius A, Di Virgilio F (2011) P2 receptors and extracellular ATP: a novel homeostatic pathway in inflammation. Front Biosci (Schol Ed) 3:1443-1456. 2. Giuliani AL, Sarti AC, Falzoni S, Di Virgilio F (2017) The P2X7 receptor-interleukin-1 liaison. Front Pharmacol 8:123. 3. Kelly G, Hughes R, Mc Garry T, van den Born M, Adamzik K, Fitzgerald R, Lawlor C, Tobin AM, Sweeney CM, Kirby B (2015) Dysregulated cytokine expression in lesional and nonlesional skin in hidradenitis suppurativa. Br J Dermatol 173:1431-1439. 4. Xu H, Xiao X, He Y, Zhang X, Li C, Mao Q, Wu X, Wang B (2017) Increased serum interleuikin-6 levels in patients with hidradenitis suppurativa. Postepy Dermatol Alergol 34:82-84. 5. Van der Zee HH, de Ruiter L, van der Broecke DG, Dik WA, Laman JD, Pren EP (2011) Elevated levels of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta and IL-10 in hidradenitis suppurativa skin: a rationale for targeting TNF-alpha and IL-1beta. Br J Dermatol 164:1292-1298. 6. Kanni T, Tzanetakou V, Savva A, Kersten B, Pistiki A, van der Veerdonk FL, Netea MG, van der Meer J, Giamarellos-Bourboulis EJ (2015) Compartimentalized cytokine responses in hidradenitis suppurativa. PLoS One 10:e0130522

Basal ganglia volume is strongly related to P3 event-related potential in premanifest Huntington’s disease

Background: The P3 event-related potential (ERP) is presumably partly generated by the basal ganglia. Because degeneration of these brain structures starts many years before clinical disease onset in Huntington's disease (HD), studying the interplay between P3 characteristics and basal ganglia volumes in 'premanifest' carriers might lead to new insights into the disease process. Methods: Fourteen premanifest HD mutation carriers and twelve non-mutation carriers underwent clinical, MRI and P3-ERP investigations. The P3 was measured during the Sustained Attention to Response Task. Results: P3 amplitude and latency did not differ between groups. In carriers, longer P3 latency during Go-trials was strongly associated with smaller caudate, putamen and globus pallidus volumes (r values up to -0.827, P <= 0.001). Conclusion: The exceptionally strong relations of P3 latency with basal ganglia volumes in carriers suggest that the P3 may provide a marker for disease progression in HD.Neurological Motor Disorder

A Novel and Cross-Species Active Mammalian INDY (NaCT) Inhibitor Ameliorates Hepatic Steatosis in Mice with Diet-Induced Obesity

Mammalian INDY (mINDY, NaCT, gene symbol SLC13A5) is a potential target for the treatment of metabolically associated fatty liver disease (MAFLD). This study evaluated the effects of a selective, cross-species active, non-competitive, non-substrate-like inhibitor of NaCT. First, the small molecule inhibitor ETG-5773 was evaluated for citrate and succinate uptake and fatty acid synthesis in cell lines expressing both human NaCT and mouse Nact. Once its suitability was established, the inhibitor was evaluated in a diet-induced obesity (DIO) mouse model. DIO mice treated with 15 mg/kg compound ETG-5773 twice daily for 28 days had reduced body weight, fasting blood glucose, and insulin, and improved glucose tolerance. Liver triglycerides were significantly reduced, and body composition was improved by reducing fat mass, supported by a significant reduction in the expression of genes for lipogenesis such as SREBF1 and SCD1. Most of these effects were also evident after a seven-day treatment with the same dose. Further mechanistic investigation in the seven-day study showed increased plasma β-hydroxybutyrate and activated hepatic adenosine monophosphate-activated protein kinase (AMPK), reflecting findings from Indy (-/-) knockout mice. These results suggest that the inhibitor ETG-5773 blocked citrate uptake mediated by mouse and human NaCT to reduce liver steatosis and body fat and improve glucose regulation, proving the concept of NaCT inhibition as a future liver treatment for MAFLD