Early Detection of External Neurological Symptoms through a Wearable Smart-Glasses Prototype

The Internet of Things (IoT) framework is moving the research community to provide smart systems and solutions aimed at revolutionizing medical sciences and healthcare. Given the extreme diffusion of Alzheimer’s disease (AD) and Parkinson’s disease (PD), the demand for a solution to early detect neurological symptoms of such diseases strongly arose. According to the medical literature, such early detection can be obtained through the correlation between PD and AD and some external symptoms: the Essential Tremor (ET) and the number of Eye Blinks (EBs). In this paper, which can be considered as an extended version of [1], we present a prototype of wearable smart glasses able to detect the presence of ET of the head and to count the number of EBs at the same time, in a transparent way with respect to the final user. Numerical results demonstrate the reliability of the proposed approach: the proposed algorithms are able to i) correctly recognize the ET with an overall accuracy above 97% and ii) count the number of EBs with an overall error around 9%

Differential expression of microRNA501-5p affects the aggressiveness of clear cell renal carcinoma

AbstractRenal cell carcinoma is a common neoplasia of the adult kidney that accounts for about 3% of adult malignancies. Clear cell renal carcinoma is the most frequent subtype of kidney cancer and 20–40% of patients develop metastases. The absence of appropriate biomarkers complicates diagnosis and prognosis of this disease. In this regard, small noncoding RNAs (microRNAs), which are mutated in several neoplastic diseases including kidney carcinoma, may be optimal candidates as biomarkers for diagnosis and prognosis of this kind of cancer. Here we show that patients with clear cell kidney carcinoma that express low levels of miR501-5p exhibited a good prognosis compared with patients with unchanged or high levels of this microRNA. Consistently, in kidney carcinoma cells the downregulation of miR501-5p induced an increased caspase-3 activity, p53 expression as well as decreased mTOR activation, leading to stimulation of the apoptotic pathway. Conversely, miR501-5p upregulation enhanced the activity of mTOR and promoted both cell proliferation and survival. These biological processes occurred through p53 inactivation by proteasome degradation in a mechanism involving MDM2-mediated p53 ubiquitination. Our results support a role for miR501-5p in balancing apoptosis and cell survival in clear cell renal carcinoma. In particular, the downregulation of microRNA501-5p promotes a good prognosis, while its upregulation contributes to a poor prognosis, in particular, if associated with p53 and MDM2 overexpression and mTOR activation. Thus, the expression of miR501-5p is a possible biomarker for the prognosis of clear cell renal carcinoma

A breath monitoring approach based on electrical impedance measurements

An approach for monitoring the respiratory rate based on impedance measurements is presented in this paper. In order to possibly obtain a minimally-invasive wearable device, the electrodes are located on the head, near mastoid bones, and measure the variations induced in the electrical impedance by the physiological changes in the pharynx produced by respiration. The feasibility of the adopted configuration has been assessed by means of electromagnetic simulations involving a simplified model. Moreover, an ad-hoc data processing algorithm has been developed for extracting the breath rate from the measured signals. Preliminary experimental results are provided for investigating the capabilities of the developed setup

Sequencing of an RNA transcript of the human estrogen receptor gene: evidence for a new transcriptional event.

none5---nonePIVA R; BIANCHI N; G. AGUIARI; GAMBARI R; DEL SENNO LPiva, Maria Roberta; Bianchi, Nicoletta; Aguiari, Gianluca; Gambari, Roberto; DEL SENNO, Laur

Enzymatic Spermine Metabolites Induce Apoptosis Associated with Increase of p53, caspase-3 and miR-34a in Both Neuroblastoma Cells, SJNKP and the N-Myc-Amplified Form IMR5

Neuroblastoma (NB) is a common malignant solid tumor in children and accounts for 15% of childhood cancer mortality. Amplification of the N-Myc oncogene is a well-established poor prognostic marker in NB patients and strongly correlates with higher tumor aggression and resistance to treatment. New therapies for patients with N-Myc-amplified NB need to be developed. After treating NB cells with BSAO/SPM, the detection of apoptosis was determined after annexin V-FITC labeling and DNA staining with propidium iodide. The mitochondrial membrane potential activity was checked, labeling cells with the probe JC-1 dye. We analyzed, by real-time RT-PCR, the transcript of genes involved in the apoptotic process, to determine possible down- or upregulation of mRNAs after the treatment on SJNKP and the N-Myc-amplified IMR5 cell lines with BSAO/SPM. The experiments were carried out considering the proapoptotic genes Tp53 and caspase-3. After treatment with BSAO/SPM, both cell lines displayed increased mRNA levels for all these proapoptotic genes. Western blotting analysis with PARP and caspase-3 antibody support that BSAO/SPM treatment induces high levels of apoptosis in cells. The major conclusion is that BSAO/SPM treatment leads to antiproliferative and cytotoxic activity of both NB cell lines, associated with activation of apoptosis

NF-kB activation is required for apoptosis in fibrocystin7polyductin-depleted kidney epithelial cells

Autosomal recessive polycystic kidney disease (ARPKD) is caused by mutations in PKHD1, a gene encoding fibrocystin/polyductin (FC1), a membrane-associated receptor-like protein involved in the regulation of tubular cell adhesion, proliferation and apoptosis. Although it is generally accepted that apoptosis is implicated in ARPKD, the question of whether increased apoptosis is a normal response to abnormal cell proliferation or, instead, it is a primary event, is still subject to debate. In support of the latter hypothesis, we hereby provide evidence that apoptosis occurs in the absence of hyper-proliferation of FC1-depleted kidney cells. In fact, a decrease in cell proliferation, with a concomitant increase in apoptotic index and caspase-3 activity was observed in response to FC1-depletion by PKHD1 siRNA silencing in HEK293 and 4/5 tubular cells. FC1-depletion also induced reduction in ERK1/2 kinase activation, upregulation of the pro-apoptotic protein p53 and activation of NF-kB, a transcription factor which reduces apoptosis in many organs and tissues. Interestingly, selective inactivation of NF-kB using either an NF-kB decoy or parthenolide, a blocker of IKK-dependent NF-kB activation, reduced, rather then increased, apoptosis and p53 levels in FC1-depleted cells. Therefore, the proapoptotic function of NF-kB during cell death by FC1-depletion in kidney cells is evident