Lightweight Self-Detection and Self-Calibration Strategy for MEMS Gas Sensor Arrays.

With the development of Internet of Things (IoT) and edge computing technology, gas sensor arrays based on Micro-Electro-Mechanical System (MEMS) fabrication technique have broad application prospects in intelligent integrated systems, portable devices, and other fields. In such complex scenarios, the normal operation of a gas sensing system depends heavily on the accuracy of the sensor output. Therefore, a lightweight Self-Detection and Self-Calibration strategy for MEMS gas sensor arrays is proposed in this paper to monitor the working status of sensor arrays and correct the abnormal data in real time. Evaluations on real-world datasets indicate that the strategy has high performance of fault detection, isolation, and data recovery. Furthermore, our method has low computation complexity and low storage resource occupation. The board-level verification on CC1350 shows that the average calculation time and running power consumption of the algorithm are 0.28 ms and 9.884 mW. The proposed strategy can be deployed on most resource-limited IoT devices to improve the reliability of gas sensing systems.

Ellagic Acid Protects Dopamine Neurons via Inhibition of NLRP3 Inflammasome Activation in Microglia.

Neuroinflammation plays a crucial role in the pathological process of Parkinson's disease (PD). Nod-like receptor protein 3 (NLRP3) inflammasome was highly located in microglia and involved in the process of neuroinflammation. Activation of the NLRP3 inflammasome has been confirmed to contribute to the progression of PD. Thus, inhibition of NLRP3 inflammasome activation could be an important breakthrough point on PD therapy. Ellagic acid (EA) is a natural polyphenol that has been widely found in soft fruits, nuts, and other plant tissues with anti-inflammatory, antioxidant, and neuroprotective properties. However, the mechanisms underlying EA-mediated anti-inflammation and neuroprotection have not been fully elucidated. In this study, a lipopolysaccharide- (LPS-) induced rat dopamine (DA) neuronal damage model was performed to determine the effects of EA on the protection of DA neurons. In addition, the DA neuronal MN9D cell line and microglial BV-2 cell line were employed to explore whether EA-mediated neuroprotection was through an NLRP3-dependent mechanism. Results indicated that EA ameliorated LPS-induced DA neuronal loss in the rat substantia nigra. Further, inhibition of microglial NLRP3 inflammasome signaling activation was involved in EA-generated neuroprotection, as evidenced by the following observations. First, EA reduced NLRP3 inflammasome signaling activation in microglia and subsequent proinflammatory cytokines' excretion. Second, EA-mediated antineuroinflammation and further DA neuroprotection from LPS-induced neurotoxicity were not shown upon microglial NLRP3 siRNA treatment. In conclusion, this study demonstrated that EA has a profound effect on protecting DA neurons against LPS-induced neurotoxicity via the suppression of microglial NLRP3 inflammasome activation.

Age-Associated Dopaminergic Neuron Loss and Midbrain Glia Cell Phenotypic Polarization.

In response to changes in brain micro-environment caused by aging, microglia could polarize into proinflammatory M1 phenotype and anti-inflammatory M2 phenotype. Besides, astroglia could polarize into A1 phenotype, exhibiting neurotoxicity, or A2 phenotype, showing neuroprotection. This study aimed to investigate the change of glial cells and dopaminergic (DA) neuron in midbrain with age. Two-, 6-, 18- and 28- months old rat brains were collected. The DA neurons were detected using anti-TH and anti-DAT antibodies. The expressions of astroglia markers (glial fibrillary acidic protein, GFAP), microglia markers (ionized calcium binding adaptor molecule 1, Iba-1), M1 markers (tumor necrosis factor-α (TNF-α) and interleukin-1ß (IL-1ß), M2 markers (arginase 1 (Arg1) and IL-10), A1 markers (lipocalin-2 (Lcn2) and complement C3 (C3), A2 markers (brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF) were examined by real time RT-PCR and Western Blotting. DA neuron expressions decreased in 18-, 28- months old rat brains. In addition, microglia and astroglia have different degrees of activation with age. Besides, M1 markers (TNF-α and IL-1ß) increased and M2 markers (Arg1 and IL-10) decreased in aged rats. Furthermore, A2 markers (BDNF and GDNF) decreased and A1 markers (Lcn2 and C3) increased in aged rats. Age induced DA neuron loss and influenced midbrain glial cells phenotypic polarization, which might account for the occurrence and pathogenesis of Parkinson's diseases.

Dual modulation on glial cells by tetrahydroxystilbene glucoside protects against dopamine neuronal loss.

BACKGROUND: Microglia-mediated neuroinflammation is recognized to mainly contribute to the pathogenesis of Parkinson's disease (PD). Tetrahydroxystilbene glucoside (TSG) has been proved to be beneficial for health with a great number of pharmacological properties. We examined the effects of TSG against dopamine (DA) neuronal loss towards development of a PD treatment strategy. METHODS: Substantia nigral stereotaxic single injection of lipopolysaccharide (LPS)-induced rat DA neuronal damage was employed to investigate TSG-produced neuroprotection. In addition, primary rat midbrain neuron-glia co-cultures were performed to explore the underlying mechanisms. RESULTS: Daily intraperitoneal injection of TSG for seven consecutive days significantly attenuated LPS-induced loss of DA neurons in the substantia nigra. In addition, glia-dependent mechanisms were responsible for TSG-mediated neuroprotection. First, TSG ameliorated microglia-mediated neuroinflammation and the subsequent production of various pro-inflammatory and neurotoxic factors. Second, astroglial neurotrophic factor neutralization weakened TSG-mediated neuroprotection, showing that TSG was protective in part via increasing astroglia-derived neurotrophic factor secretion. CONCLUSIONS: TSG protects DA neurons against LPS-induced neurotoxicity through dual modulation on glial cells by attenuating microglia-mediated neuroinflammation and enhancing astroglia-derived neurotrophic effects. These findings might open new alternative avenues for PD treatment.

Nanographenes as electron-deficient cores of donor-acceptor systems.

Conjugation of nanographenes (NGs) with electro-active molecules can establish donor-acceptor π-systems in which the former generally serve as the electron-donating moieties due to their electronic-rich nature. In contrast, here we report a series of reversed donor-acceptor structures are obtained by C-N coupling of electron-deficient perchlorinated NGs with electron-rich anilines. Selective amination at the vertexes of the NGs is unambiguously shown through X-ray crystallography. By varying the donating ability of the anilino groups, the optical and assembly properties of donor-acceptor NGs can be finely modulated. The electron-deficient concave core of the resulting conjugates can host electron-rich guest molecules by intermolecular donor-acceptor interactions and gives rise to charge-transfer supramolecular architectures.

T-cadherin is associated with prognosis in triple-negative breast cancer.

The purpose of the present study was to assess the prognostic impact of T-cadherin expression in patients with triple-negative breast cancer (TNBC). On the basis of the results of immunohistochemical analysis, 106 patients with operable TNBC were divided into two groups, the T-cadherin-positive group and T-cadherin-negative group. Fisher's exact and χ2 tests were employed to analyze clinical data, which included the association between T-cadherin expression and clinicopathological features and prognosis. The log-rank test was used to examine the impact of T-cadherin expression on the 5-year disease-free survival (DFS) and the 5-year overall survival (OS) of these patients. Kaplan-Meier and Cox regression analyses were introduced to analyze DFS and OS. Compared with the T-cadherin-positive group (58.3, 52.8 and 47.2, respectively; P=0.018, P=0.017, and P=0.047), tumor size >2 cm, grade II and III (Elston-Ellis modification of Bloom-Richardson grading system), and positive lymph node status were significantly more common in the T-cadherin-negative group compared with the T-cadherin-positive group (80.0 vs. 58.3%, 75.7 vs. 52.8% and 67.1 vs. 47.2%, respectively) (P=0.018, P=0.017, and P=0.047). Compared with the T-cadherin-positive group, 5-year DFS and OS levels were significantly lower in the T-cadherin-negative group (Z=6.233, P=0.013; Z=5.366, P=0.021). Multivariate analysis revealed that negative T-cadherin expression was an independent prognostic factor for DFS (P=0.009) and OS (P=0.048). The results of the present study indicated that negative T-cadherin expression indicated a worse prognosis for patients with TNBC.

Tetrahydroxystilbene Glucoside Improves Neurotrophic Factors Release in Cultured Astroglia.

Tetrahydroxystilbene glucoside (TSG), one of the main ingredients of Polygonum multiflorum, has a great number of beneficial effects for health including anti-oxidant, free radicalscavenging and anti-inflammatory properties. However, the potential effects of TSG on neurotrophic factors release remain unclear. In this study, rat primary astroglia cultures were applied to investigate TSG-mediated neurotrophic effects. The protein levels and production of glial cell-line derived neurotrophic factor (GDNF), brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in astroglia and the culture medium were determined by western blotting assay and ELISA, respectively. Results indicated that TSG increased the production of neurotrophic factors in a concentration-dependent manner. At different time points of TSG treatment, the BDNF and NGF production in the culture medium was increased 48 h after treatment, while GDNF secretion was initially induced 24 h after TSG treatment. Consistent with the neurotrophic factors release, TSG significantly increased the BDNF, GDNF and NGF protein expressions in astroglia. Furthermore, TSG significantly induced the phosphorylation of extracellular signal-regulated kinase (ERK) 1/2 and a specific ERK inhibitor-U0126 inhibited TSG-mediated secretion of BDNF, GDNF and NGF. Overall, this study demonstrated that TSG induces astroglia-derived neurotrophic factors release, suggesting TSG might hold a therapeutic potential for neurological disorders.

[Analysis of Immunophenotypes in 329 Patients with B-ALL at Different Ages].

OBJECTIVE: To investigate the immunophenotypes of B cell acute lymphoblastic leukemia (B-ALL) in patients at different age and to explore its clinical application in prognosis prediction and individualized treatment. METHOD: The immunophenotyping in 329 patients with B-ALL at different ages was performed by CD45/SSC gate four-color fluorescence flow cytometry. RESULTS: In all patients detected the highest incidence of lymphoid-associated antigens was CD19, HLA-DR, CyCD79a and cTdT, followed by CD10, CD22, CD34, CD38, CD20 and CyIg. B-ALL showed a higher concomitant expression rate of myeloid antigens CD13 and CD33; the CD11b, CD15, CD117 and T antigens (CD4, CD7 and CD56) were rarely expressed. CD10⁻ pro-B acute lymphoblastic leukemia (Pro - B-ALL) was predo-minant in infantile group (60%) with CD117 higher expression (40%). Subtype Pro-B-ALL was rarely expressed in childhood and adolescent group, but the incidence of disease increased as the age increase, the incidence of youth group (22.7%) and middle-aged' group (14.8%) were significantly higher than childhood group (4.4%). The influence of age on immunophenotypic characteristics of the adult B-ALL was not significant, the heterogeneity of antigen expression was less in the adult patients at different ages. The expression of CD10 and CD38 was lower, while expression of CD34, CD13 and CD33 were higher in adult patients than those in children patients. There was no significant difference in incidence of precursor-B-ALL (Pre-B-ALL) among different age groups (P > 0.05), but its incidence increased along with age increasing, and the expression of CD20 was higher in Pre - B-ALL than that in Pro - B-ALL and common B-ALL. CONCLUSION: The immunophenotype characteristics of B-ALL in the patients at different ages is of great value in prediction for disease prognosis and guidence of individualized treatment.

T-cadherin association with clinicopathological features and prognosis in axillary lymph node-positive breast cancer.

The purpose of this study was to investigate the correlation of T-cadherin expression with clinicopathological features and prognosis in patients with axillary lymph node-positive breast cancer. Based on the immunohistochemistry results, all 142 patients with operable axillary lymph node-positive breast cancer were divided into the T-cadherin-negative and T-cadherin-positive groups. Clinical data including the association of T-cadherin expression with clinicopathological features and prognosis were analyzed using the Chi square test and Fisher's exact test using SPSS 13.0 software. The impact of T-cadherin expression on the 5-year disease-free survival (DFS) and the 5-year overall survival (OS) of these patients was measured using the log-rank test. DFS and OS were analyzed using both Kaplan-Meier function and Cox regression analyses. Compared with the T-cadherin-positive group (55.07, 28.99, and 13.4 %, respectively; P = 0.030, P = 0.0132, and P = 0.009), tumor size >2 cm, lymph-vascular invasion, and pathological stage III disease were seen more frequently in the T-cadherin-negative group (72.60, 49.32, and 31.51 %, respectively). Both 5-year DFS and 5-year OS were poorer in the T-cadherin-negative group than in the T-cadherin-positive group (log-rank test = 9.295, P = 0.002; log-rank test = 5.718, P = 0.017). On multivariate analysis, T-cadherin-negative expression remained an independent prognostic factor for DFS (P = 0.002) but not for OS (P = 0.067). Our results suggested that negative T-cadherin expression has a worse prognosis in patients with axillary lymph node-positive breast cancer.