Wearable Devices for Caloric Intake Assessment: State of Art and Future Developments

Background: The self-monitoring of caloric intake is becoming necessary as the number of pathologies related to eating increases. New wearable devices may help people to automatically record energy assumed in their meals. Objective: The present review collects the released articles about wearable devices or method for automatic caloric assessments. Method: A literature research has been performed with PubMed, Google Scholar, Scopus and ClinicalTrials.gov search engines, considering released articles regarding applications of wearable devices in eating environment, from 2005 onwards. Results: Several tools allow caloric assessment and food registration: wearable devices counting the number of bites ingested by the user, instruments detecting swallows and chewings, methods that analyse food with digital photography. All of them still require more validation and improvement. Conclusion: Automatic recording of caloric intake through wearable devices is a promising method to monitor body weight and eating habits in clinical and non-clinical settings, and the research is still going on. \ua9 2017 Magrini et al

Oxidative stress and the altered reaction to it in Fabry disease: A possible target for cardiovascular-renal remodeling?

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Oxidative stress and the altered reaction to it in Fabry disease: A possible target for cardiovascular-renal remodeling?

BACKGROUND:Fabry disease is characterized by deficient expression/activity of α-GalA with consequent lysosomal accumulation in various organs of its substrate Gb3. Despite enzyme replacement therapy, Fabry disease progresses with serious myocardial, cerebral and renal manifestations. Gb3 accumulation may induce oxidative stress (OxSt), production of inflammatory cytokines and reduction of nitric oxide, which may impact on Fabry disease's clinical manifestations. METHODS:OxSt status was characterized in 10 patients compared with 10 healthy subjects via protein expression of p22phox, subunit of NADH/NADPH oxidase, (Western blot), Heme oxygenase (HO)-1 levels (ELISA), antioxidant/anti-inflammatory, lipid peroxidation as malondialdehyde (MDA) production (colorimetric assay), phosphorylation state of Extracellular Signal Regulated Kinase (ERK)1/2 and Myosin Phosphatase Target Protein (MYPT)-1 (Western blot), marker of Rho kinase activation, both involved in OxSt signaling. Cardiac left ventricular (LV) mass was also evaluated (M-mode echocardiography). RESULTS:LV mass was higher in Fabry's males (123.72±2.03SEM g/m2) and females (132.09±6.72g/m2). p22phox expression was also higher in patients (1.04±0.09 d.u. vs 0.54±0.05 d.u. p<0.01) as well as MDA levels (54.51±3.97 vs 30.05±7.11 nmol/mL p = 0.01) while HO-1 was reduced (8.84±0.79 vs 14.03±1.23 ng/mL, p<0.02). MYPT-1's phosphorylation was increased in patients (0.52±0.11 d.u. vs 0.03±0.08 d.u., p<0.01) while phosphorylation of ERK1/2 was reduced (0.91±0.08 d.u. vs 1.53±0.17 d.u., p = 0.004). CONCLUSIONS:This study documents OxSt activation and the altered reaction to it in Fabry patients. Cardiac remodeling, Rho kinase signaling activation and reduction of protective HO-1 might suggest that, in addition to enzyme replacement therapy, OxSt inhibition by either pharmacological or nutritional measures, is likely to prove useful for the prevention/treatment of Fabry patients' cardiovascular-renal remodeling

Modulation of inflammation in IBD: Alpha7nAChR expression and role of nicotine

Objective: The divergent effects of nicotine on natural history of inflammatory bowel diseases (IBD) are wellknown: while it\u2019s beneficial in ulcerative colitis (UC) it increases risk of surgery and relapse in Crohn\u2019s disease (CD). It has been shown that in animal models the modulatory effect of nicotine in intestinal inflammation involves the alpha7 nicotinic acetylcholine receptor (a7nAChR), activating a cholinergic counterinflammatory mechanism. Thus, aims of the study were to evaluate a7nAChmRNA levels on macrophages from patients with MC, UC and controls (HV) and nicotine effects on LPS-induced TNFa and IL10 production. Methods: Macrophages obtained from peripheral blood monocytes of UC and CD patients and HV were supplemented with M-CSF (7 days). a7nAchR-mRNA and protein levels were evaluated by qRT-PCR and FACS analysis using aBgt-FICS specific binding, respectively. Macrophages were pre-incubated with nicotine (1 mg ml-1 30 min) and then stimulated with LPS (1 lg ml-1 24 h). TNFa and IL10 levels were measured on supernatant using ELISA. Results: Macrophages from UC showed greater a7nAchR mRNA levels then cells from CD (0.00092 copies in UC Vs 0.000212 copies in CD, P = 0,006), while no differences were found with HV. FACS analysis confirmed greater a7AChR expression in UC patients (90.75 Gmean in UC Vs 15.62 Gmean in MC, P 0.031). Higher a7nAchR mRNA levels were observed in macrophages from IBD with colonic disease compared with small bowel involvement (P = 0.007). Nicotine significantly decreased LPS-stimulated TNFa release in macrophages from HV (from 13122.7 pg ml-1 to 9790.2 pg ml-1; P = 0.03), CD (14291.7 pg ml-1 to 10613.2 pg ml-1; P = 0.003) and UC (from 13723.9 pg ml-1 to 10238.5 pg ml-1; P = 0.000). This effect was more pronounced in macrophages from UC patients (-22.9%) compared with CD (-6.1%) and in IBD with colonic disease (-17.4%) compared to CD with small bowel involvement (+3.8%), although it did not reach statistical significance. Pretreatment with nicotine inhibited LPS-stimulated IL10 production by macrophages in HV, UC and CD, but not differences were observed among groups. Conclusion: Nicotine has a suppressive effect on TNFa and IL10 production by macrophages: diseaserelated or site-related differences in a7nAChR levels may justify the divergent effects of nicotine in IBD patients

Tip60 is a haplo-insufficient tumour suppressor required for an oncogene-induced DNA damage response

The acetyl-transferase Tip60 might influence tumorigenesis in multiple ways. First, Tip60 is a co-regulator of transcription factors that either promote or suppress tumorigenesis, such as Myc and p53. Second, Tip60 modulates DNA-damage response (DDR) signalling, and a DDR triggered by oncogenes can counteract tumour progression. Using E\u3bc-myc transgenic mice that are heterozygous for a Tip60 gene (Htatip) knockout allele (hereafter denoted as Tip60+/- mice), we show that Tip60 counteracts Myc-induced lymphomagenesis in a haplo-insufficient manner and in a time window that is restricted to a pre- or early-tumoral stage. Tip60 heterozygosity severely impaired the Myc-induced DDR but caused no general DDR defect in B cells. Myc- and p53-dependent transcription were not affected, and neither were Myc-induced proliferation, activation of the ARF-p53 tumour suppressor pathway or the resulting apoptotic response. We found that the human TIP60 gene (HTATIP) is a frequent target for mono-allelic loss in human lymphomas and head-and-neck and mammary carcinomas, with concomitant reduction in mRNA levels. Immunohistochemical analysis also demonstrated loss of nuclear TIP60 staining in mammary carcinomas. These events correlated with disease grade and frequently concurred with mutation of p53. Thus, in both mouse and human, Tip60 has a haplo-insufficient tumour suppressor activity that is independent from - but not contradictory with - its role within the ARF-p53 pathway. We suggest that this is because critical levels of Tip60 are required for mounting an oncogene-induced DDR in incipient tumour cells, the failure of which might synergize with p53 mutation towards tumour progression