Modeling Hidden Nodes Collisions in Wireless Sensor Networks: Analysis Approach

This paper studied both types of collisions. In this paper, we show that advocated solutions for coping with hidden node collisions are unsuitable for sensor networks. We model both types of collisions and derive closed-form formula giving the probability of hidden and visible node collisions. To reduce these collisions, we propose two solutions. The first one based on tuning the carrier sense threshold saves a substantial amount of collisions by reducing the number of hidden nodes. The second one based on adjusting the contention window size is complementary to the first one. It reduces the probability of overlapping transmissions, which reduces both collisions due to hidden and visible nodes. We validate and evaluate the performance of these solutions through simulations

Neural Regulation of Innate Immunity in Inflammatory Skin Diseases

As the largest barrier organ of the body, the skin is highly innervated by peripheral sensory neurons. The major function of these sensory neurons is to transmit sensations of temperature, pain, and itch to elicit protective responses. Inflammatory skin diseases are triggered by the aberrant activation of immune responses. Recently, increasing evidence has shown that the skin peripheral nervous system also acts as a regulator of immune responses, particularly innate immunity, in various skin inflammatory processes. Meanwhile, immune cells in the skin can express receptors that respond to neuropeptides/neurotransmitters, leading to crosstalk between the immune system and nervous system. Herein, we highlight recent advances of such bidirectional neuroimmune interactions in certain inflammatory skin conditions

Neural Regulation of Innate Immunity in Inflammatory Skin Diseases

As the largest barrier organ of the body, the skin is highly innervated by peripheral sensory neurons. The major function of these sensory neurons is to transmit sensations of temperature, pain, and itch to elicit protective responses. Inflammatory skin diseases are triggered by the aberrant activation of immune responses. Recently, increasing evidence has shown that the skin peripheral nervous system also acts as a regulator of immune responses, particularly innate immunity, in various skin inflammatory processes. Meanwhile, immune cells in the skin can express receptors that respond to neuropeptides/neurotransmitters, leading to crosstalk between the immune system and nervous system. Herein, we highlight recent advances of such bidirectional neuroimmune interactions in certain inflammatory skin conditions

Revisiting the Practicality of Search on Encrypted Data: From the Security Broker’s Perspective

The primary business challenge for the customers to use outsourced computation and storage is the loss of data control and security. So encryption will become a commodity in the near future. There is big diffusion with the above scenario: take advantage of current application’s full functionalities at the same time ensuring their sensitive data remains protected and under customers’ control. Prior works have achieved effective progress towards satisfying both sides. But there are still some technical challenges, such as supporting file or data-stream based applications and supporting full-text and advanced searches. In this paper, a novel security broker based encrypted data search scheme, called Enc-YUN, is proposed, which transparently builds a reverse index at the security broker when the data flow is transmitted to the cloud. And search firstly takes place on the index, in which the mapping structure corresponds to and retrieves the very encrypted data in the cloud on behalf of the client. With this scheme, updated-to-date full-text search techniques can be easily integrated to carry out the most advanced search functionalities, at the same time, maintaining the strongest levels of data protection from curious providers or third parties. Experimental results show that Enc-YUN is effective with broad categories of cloud applications, and the performance overhead induced is minor and acceptable according to user’s perceptual experience

Higher intraoperative mean arterial blood pressure does not reduce postoperative delirium in elderly patients following gastrointestinal surgery: A prospective randomized controlled trial.

BackgroundThis study aimed to describe the relationship between the different levels of intraoperative mean arterial blood pressure (MAP) and postoperative delirium in elderly patients undergoing gastrointestinal laparoscopic surgery.Materials and methodsThis prospective controlled clinical trial enrolled 116 patients aged 65 to 85 years who underwent gastrointestinal laparoscopic surgery. These patients were randomized 1:1 to a MAP goal of 65 to 85 mmHg (L group) or an 86 to 100 mmHg (H group). The primary endpoint was the incidence of postoperative delirium, assessed twice daily with the Confusion Assessment Method (CAM) and Richmond Agitation-Sedation Scale (RASS) during the first five postoperative days. Delirium severity was evaluated with the Delirium-O-Meter (D-O-M).Results108 patients (L group n = 55, H group n = 53) were eventually included in intention-to-treat analyses. Postoperative delirium occurred in 18 (32.7%) of 55 cases of L group and in 15 (28.3%) of 53 cases of H group. The incidence of delirium subtypes between the two groups: hypoactive delirium 14.5% (8/55) vs 11.3% (6/53); hyperactive delirium 7.3% (4/55) vs 3.8% (2/53); mixed delirium 10.9% (6/55) vs 13.2% (7/53). However, the L group showed higher D-O-M scores of the first episode of delirium: 14.5 (Q1 = 12, Q3 = 18.5) vs 12 (Q1 = 10, Q3 = 14), which means the delirium is more severe.ConclusionsCompared with 65 to 85 mmHg, maintaining intraoperative MAP at 86-100 mmHg did not reduce the incidence of postoperative delirium in elderly patients undergoing gastrointestinal laparoscopic surgery. However, the severity of delirium could be reduced and blood loss is a risk factor for postoperative delirium

Shc3 facilitates breast cancer drug resistance by interacting with ErbB2 to initiate ErbB2/COX2/MDR1 axis

Abstract Multidrug resistance (MDR) is a primary limitation of breast cancer chemotherapy. The common mechanism of MDR is various anticancer drugs can be effluxed by the cell membrane protein P‐glycoprotein (P‐gp). Here, we found that ectopic overexpression of Shc3 was detected specifically in drug‐resistant breast cancer cells, consequently reducing sensitivity to chemotherapy and promoting cell migration by mediating P‐gp expression. However, the molecular mechanism underlying the interplay between P‐gp and Shc3 in breast cancer is unknown. We reported an additional resistance mechanism involving an increase in the active form of P‐gp after Shc3 upregulation. MCF‐7/ADR and SK‐BR‐3 cells can be sensitive to doxorubicin after knockdown of Shc3. Our results indicated that the interaction between ErbB2 and EphA2 is indirect and regulated by Shc3, and also, this complex is essential for activation of the MAPK and AKT pathways. Meanwhile, Shc3 promotes ErbB2 nuclear translocation, followed by a subsequent increase of the COX2 expression through ErbB2 binding to the COX2 promoter. We further demonstrated that COX2 expression was positively correlated with P‐gp expression and the Shc3/ErbB2/COX2 axis upregulates P‐gp activity in vivo. Our results show the crucial roles of Shc3 and ErbB2 in modulating P‐gp efficacy in breast cancer cells and suggest that Shc3 inhibition may enhance the sensitivity to chemotherapeutic drugs that target oncogene addiction pathways

Triggering Receptor Expressed on Myeloid Cells 2 Overexpression Inhibits Proinflammatory Cytokines in Lipopolysaccharide-Stimulated Microglia

Microglia play an important role in mediating inflammatory processes in the central nervous system (CNS). Triggering receptor expressed on myeloid cells 2 (TREM2) is a microglia-specific receptor and could decrease neuropathology in Alzheimer’s disease (AD). However, the detailed mechanism remains unclear. This study was designed to elucidate the effect of TREM2 on microglia. We showed that lipopolysaccharide (LPS) stimulation significantly increases proinflammatory cytokines and suppressed TREM2 in microglia. In addition, TREM2 overexpression inhibited LPS-induced microglia activation and elevated M2 phenotype of microglia. Together, our results demonstrate that TREM2 overexpression reduced LPS-induced proinflammatory cytokine release in microglia and increased M2 phenotype of microglia. These findings provide novel insights that the regulation of microglia polarization may be an approach for ameliorating microglia inflammation in neurodegenerative diseases