A Spiking Neural Network Based Cortex-Like Mechanism and Application to Facial Expression Recognition

In this paper, we present a quantitative, highly structured cortex-simulated model, which can be simply described as feedforward, hierarchical simulation of ventral stream of visual cortex using biologically plausible, computationally convenient spiking neural network system. The motivation comes directly from recent pioneering works on detailed functional decomposition analysis of the feedforward pathway of the ventral stream of visual cortex and developments on artificial spiking neural networks (SNNs). By combining the logical structure of the cortical hierarchy and computing power of the spiking neuron model, a practical framework has been presented. As a proof of principle, we demonstrate our system on several facial expression recognition tasks. The proposed cortical-like feedforward hierarchy framework has the merit of capability of dealing with complicated pattern recognition problems, suggesting that, by combining the cognitive models with modern neurocomputational approaches, the neurosystematic approach to the study of cortex-like mechanism has the potential to extend our knowledge of brain mechanisms underlying the cognitive analysis and to advance theoretical models of how we recognize face or, more specifically, perceive other people’s facial expression in a rich, dynamic, and complex environment, providing a new starting point for improved models of visual cortex-like mechanism

Necrotizing enterocolitis: clinical characteristics and outcome of a cohort of 106 cases at a children’s hospital in North China

Introduction: Necrotizing enterocolitis (NEC) in neonates, especially in the preterm, is a life-threatening condition. This study aims to analyze the clinical profile of NEC to get an insight for better understanding and management.  Method: This was a retrospective analysis of neonatal NEC during the six-year period from 2014 to 2019. The prevalence and time for the development of NEC, clinical profile (term and preterm, low birth weight, gender, breast and formula feeding, abdominal distension, vomiting, hematochezia, apnea, fever, altered mental status, blood transfusion, breast or formula-fed, intestinal perforation, Bell’s stage and time for the development of NEC) and maternal factors (gestational hypertension, diabetes, premature rupture of membranes PROM, intrauterine fetal distress, placenta previa) were analyzed. Features in preterm and term neonates were compared. Ethical approval was obtained.  Result: There were 106 NEC (0.87% of 12,184 neonatal admissions), 62 (58.49%) male, 90 (84.91%) preterm, and 85 (80.19%) LBW. Overall, 88 (83.02%) were Bell’s stage II, and severe stage III was seen in eight (19.04%) out of 42 babies with formula feeding as compared to one (1.56%) out of 64 in breastfeeding. The median time for the development of NEC was 6 days of life. The yearly prevalence of NEC per thousand neonates admitted during 6-years increased from 2.90 in 2014 to 12.06 in 2019. Overall mortality was 14 (13.20%).  Conclusion: The yearly incidence of NEC increased with a higher incidence in preterm, in low birth weight and formula-fed neonates

Electrophysiological Characteristics in Depressive Personality Disorder: An Event-Related Potential Study

This study aimed to investigate the neurophysiological characteristics of young people with depressive personality disorder using event-related potentials (ERP). To explore the effects of visual-emotional words on ERP, mainly N350, we recruited 19 individuals with a depressive personality disorder and 10 healthy controls. ERP were recorded while the subjects took decisions on target words that were classified into three categories: emotionally positive, negative, and neutral. The ERP signals were then separately averaged according to the subjects’ classifications. Data analysis showed that the amplitude of N350 was larger in response to positive and negative words than to neutral words. The latency of N350 was longer in negative words, in contrast with positive and neutral words. However, no difference was found between the two groups. These results suggest that neurophysiological characteristics of young people with a depressive personality disorder in visual-emotional word processing have not yet been influenced by their personality traits. To some extent, N350 reflected semantic processes and was not sensitive to participants’ mood state

Theory for superconductivity in (Tl,K)Fex_xSe2_2 as a doped Mott insulator

Possible superconductivity in recently discovered (Tl,K)Fe$_x$Se$_2$ compounds is studied from the viewpoint of doped Mott insulator. The Mott insulating phase is examined to be preferred in the parent compound at $x=1.5$ due to the presence of Fe vacancies. Partial filling of vacancies at the Fe-sites introduces electron carriers and leads to electron doped superconductivity. By using a two-orbital Hubbard model in the strong coupling limit, we find that the s-wave pairing is more favorable at small Hund's coupling, and d$_{x^2-y^2}$ wave pairing is more favorable at large Hund's coupling.Comment: 4+ pages, 3 figures, to appear in EP

Leukadherin-1-Mediated Activation of CD11b Inhibits LPS-Induced Pro-inflammatory Response in Macrophages and Protects Mice Against Endotoxic Shock by Blocking LPS-TLR4 Interaction

Dysregulation of macrophage has been demonstrated to contribute to aberrant immune responses and inflammatory diseases. CD11b, expressed on macrophages, plays a critical role in regulating pathogen recognition, phagocytosis, and cell survival. In the present study, we explored the effect of leukadherin-1 (LA1), an agonist of CD11b, on regulating LPS-induced pro-inflammatory response in macrophages and endotoxic shock. Intriguingly, we found that LA1 could significantly reduce mortalities of mice and alleviated pathological injury of liver and lung in endotoxic shock. In vivo studies showed that LA1-induced activation of CD11b significantly inhibited the LPS-induced pro-inflammatory response in macrophages of mice. Moreover, LA1-induced activation of CD11b significantly inhibited LPS/IFN-γ-induced pro-inflammatory response in macrophages by inhibiting MAPKs and NF-κB signaling pathways in vitro. Furthermore, the mice injected with LA1-treated BMDMs showed fewer pathological lesions than those injected with vehicle-treated BMDMs in endotoxic shock. In addition, we found that activation of TLR4 by LPS could endocytose CD11b and activation of CD11b by LA1 could endocytose TLR4 in vitro and in vivo, subsequently blocking the binding of LPS with TLR4. Based on these findings, we concluded that LA1-induced activation of CD11b negatively regulates LPS-induced pro-inflammatory response in macrophages and subsequently protects mice from endotoxin shock by partially blocking LPS-TLR4 interaction. Our study provides a new insight into the role of CD11b in the pathogenesis of inflammatory diseases

Antrodia camphorata Mycelia Exert Anti-liver Cancer Effects and Inhibit STAT3 Signaling in vitro and in vivo

Hepatocellular carcinoma (HCC), the major form of primary liver cancer, is a common cause of cancer-related death worldwide. Signal transducer and activator of transcription 3 (STAT3) signaling is constantly activated in HCC and has been proposed as a chemotherapeutic target for HCC. Antrodia camphorata (AC), a medicinal mushroom unique to Taiwan, is traditionally used for treating HCC. Whereas natural AC is scarce, cultured AC mycelia are becoming alternatives. In this study, we investigated the anti-HCC effects of the ethyl acetate fraction of an ethanolic extract of AC mycelia (EEAC), particularly exploring the involvement of STAT3 signaling in these effects. We found that EEAC reduced cell viability, induced apoptosis, and retarded migration and invasion in cultured HepG2 and SMMC-7721 cells. Immunoblotting results showed that EEAC downregulated protein levels of phosphorylated and total STAT3 and JAK2 (an upstream kinase of STAT3) in HCC cells. Real-time PCR analyses showed that STAT3, but not JAK2, mRNA levels were decreased by EEAC. EEAC also lowered the protein level of nuclear STAT3, decreased the transcriptional activity of STAT3, and downregulated protein levels of STAT3-targeted molecules, including anti-apoptotic proteins Bcl-xL and Bcl-2, and invasion-related proteins MMP-2 and MMP-9. Over-activation of STAT3 in HCC cells diminished the cytotoxic effects of EEAC. In SMMC-7721 cell-bearing mice, EEAC (100 mg/kg, i.g. for 18 days) significantly inhibited tumor growth. Consistent with our in vitro data, EEAC induced apoptosis and suppressed JAK2/STAT3 activation/phosphorylation in the tumors. Taken together, EEAC exerts anti-HCC effects both in vitro and in vivo; and inhibition of STAT3 signaling is, at least in part, responsible for these effects. We did not observe significant toxicity of EEAC in normal human liver-derived cells, nude mice and rats. Our results provide a pharmacological basis for developing EEAC as a safe and effective agent for HCC management