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The high-pathogenicity island (HPI), carried by Yersinia pestis, is an essential pathogenic component of the virulence distributed in Escherichia coli (E. coli). As an NF-κB pathway activator, Ubiquitin (Ub) is crucial in the inflammatory response. However, the molecular mechanismsof Ub in the TLR4/Myd88/NF-κB signaling pathway induced by HPI in E. coliis still unclear. In our experiment, Ub was overexpressed usingsmall intestinal epithelial cells (in vitro), and BALB/c mouse models (in vivo) infected with E. coli HPI and analysed by using qPCR, ELISA, immunofluorescence, immunohistochemistry, and H&E staining assays. We demonstrated that E. coli HPI can promote the expression of TLR4, NF-κB, and Ub in. IPEC-J2 cells. Immunofluorescence and Immunohistochemistry analysis revealed that TLR4 and NF-κB key factor in the E. coli HPI group were expressed, and the NF-κB p65 protein translocated to the nucleus. Further research showed that the mRNA expression levels of TLR4, MyD88, NF-κB, IL-1β, and TNF-α were significantly increased in the Ub overexpression group and BALB/c mice group. H&E staining assay showed that Ub overexpression with IPEC-J2 cells have thecharacteristics of elongated, rounded, fragmented, duodenal villi diminished, and the surface was covered with many sloughed necrotic cells, indicating that exacerbating cell damage and duodenitis. Taken together, this study suggested that E. coliHPI can activate NF-κB via increasing the expression of Ub, andUb can exacerbate E. coli HPI-induced duodenitis through the TLR4/MyD88/NF-κB signaling pathway.

Objective To determine the diagnostic accuracy of pneumococcal antigen detection in diagnosis of pneumococcal meningitis in children. Methods Purulent meningitis was diagnosed according to European Society for Clinical Microbiology and Infectious Diseases (ESCMID) guideline between July 2014 and June 2016. Along with a cerebrospinal fluid (CSF) culture, pneumococcal antigen detection in cerebrospinal fluid (CSF) was performed, and further identification of pathogens was done with 16S rDNA-PCR and high-throughput sequencing. Results CSF samples collected from 184 children (median age of 1.92 mo). CSF culture was used as the gold standard. 46 (25%) had positive results for culture and 10 (5.4%) were pneumococci; 34 (18.5%) were pneumococcal antigen positive. The sensitivity and specificity of pneumococcal antigen detection were 100% (95% CI: 89.4%-100%) and 86.2% (95% CI: 96.4%-99.9%), respectively. 92.3% (12/13) were confirmed by nucleic acid detection to be pneumococci. Conclusions Pneumococcal antigen detection in CSF has adequate sensitivity and specificity in diagnosing pneumococcal meningitis.

Anxiety is a common emotional disorder in children. To understand its underlying mechanisms, chronic unpredictable stress (CUS) has been established as a stress model in zebrafish. By using the tall tank test, the stress response reliability could be improved in adult fish which has not been confirmed in larvae. In addition, the increasing evidences have shown that cerebellum plays important roles in anxiety. Whether CUS will affect cerebellar neuronal activity remains unknown. We found that CUS exposure to larvae (from 10 to 17 days post fertilization) induced anxiety-like behaviors and social cohesion impairments within 1-2 d after CUS, including a prolonged freezing time, an increased time spent at the bottom of tank, an increased thigmotaxis index, and an increased interindividual distance. Our results showed that the four behavioral tests were homogeneous, especially the tall tank test either anxiety-like behaviors or the basal locomotion. Furthermore, we found that CUS enhanced the excitability of cerebellar neurons, as the amplitude, frequency, time to peak and half-width of spontaneous firing significantly decreased, as well as the amplitude of excitatory post-synaptic current when compared with the control group. CUS also activated hyperpolarization-activated cyclic nucleotide-gated and potassium channels of cerebellar neurons. Multiple linear regression analysis showed that the total distance in bottom (tall tank test) was correlated positively with outward Na

Rett syndrome (RTT) is a neurodevelopmental disease in children that is mainly caused by mutations in the MeCP2 gene, which codes for a transcriptional regulator. The expression of insulin-like growth factor-1 (IGF-1) is reduced in RTT patients and animal models, and IGF-1 treatment is a promising therapeutic strategy for RTT. However, the mechanism underlying the effects of IGF-1 remains to be further explored. FXYD1 is an auxiliary subunit of Na, K-ATPase. Overexpression of FXYD1 is involved in the pathogenesis of RTT. However, whether IGF-1 exerts its effect through normalizing FXYD1 is completely unknown. To this end, we evaluated the effect of IGF-1 on FXYD1 expression and posttranslational modification in a mouse model of RTT (MeCP2308) using both in vitro and in vivo experiments. The results show that FXYD1 mRNA and phosphorylated protein (p-FXYD1) were significantly elevated in the frontal cortex in RTT mice, compared to wild type. In RTT mice, IGF-1 treatment significantly reduced levels of FXYD1 mRNA and p-FXYD1, in parallel with improvements in behavior, motor coordination, and cognitive function. For mechanistic insight into the effect of IGF-1 on p-FXYD1, we found the decreased phosphorylated forms of PI3K-AKT-mTOR signaling pathway components in the frontal cortex of RTT mice and the normalizing effect of IGF-1 on the phosphorylated forms of these components. Interestingly, blocking the PI3K/AKT pathway by PI3K inhibitor could abolish the effect of IGF-1 on p-FXYD1 level, in addition to the effect of IGF-1 on the phosphorylation of other components in the PI3K/AKT pathway. Thus, our study has provided new insights into the mechanism of IGF-1 treatment for RTT, which appears to involve FXYD1.

Background: Tic disorders (TD) are common neuropsychiatric disorders among children and adolescents. It is controversial that trace elements may participate in the pathogenesis of TD. Our study aimed to investigate the trace elements status of zinc (Zn), copper (Cu), iron (Fe), and magnesium (Mg) in children with TD, in comparison to healthy controls.Methods: The medical records of eligible TD children and normal healthy children from January 1 to December 31, 2018 in the outpatient clinic were retrospectively reviewed. The clinical information of all subjects were collected including age, gender, diagnosis, previous health records, and serum trace elements level (Cu, Zn, Fe, Mg) at the time of diagnosis before initiating treatment.Results: In total, 1204 TD children (7.63 ± 2.45 years) and 1,220 healthy children (7.27 ± 3.15 years) who were divided into two gender and three age groups (2–4years, 5–9years, ≥10 years) were reviewed in our study. Our study showed that TD children generally had lower whole blood levels of Zn, Cu, Fe than the normal controls (P < 0.01). No significant difference was observed in whole blood levels of Mg. After adjusting for gender, the trends still remained. Further analysis was performed according to age, the trends still remained in Zn and Fe in all age groups (P < 0.05). However, we observed an almost significantly (P = 0.055) lower level of Cu in TD of 2–4 years group while significant differences in other two groups (P < 0.01). Further multiple linear regression and point biserial correlation showed that the lower blood levels of Zn, Cu, and Fe were correlated with the incidence of TD.Conclusion: The present results indicated that lower blood levels of zinc, iron, copper were associated with TD. Trace elements may be used as an auxiliary treatment for TD and need to be further explored.

Mass customization (MC) under the context ofthe Internet of Things (IoT) is expected to reform traditionalmass manufacturing. To contribute to MC from information communication and user interaction ...

Due to uneven lighting conditions and differences between camera lenses, in actual engineering applications, there is a difference in brightness of the image collected by the camera, which will cause obvious gaps in video stitching and poor stitching effect of panoramic pictures. This paper designs and implements an algorithm based on the gray statistics of overlapping areas to achieve global correction, and combined with the fade-in and fade-out image fusion algorithm to make the splicing transition natural. The experimental results show that in the Visual Studio 2015 platform environment, real-time stitching of 8-channel cameras has a fast algorithm speed and can achieve a stitching speed of 25 frames per second. The video is smooth and the picture quality is good without obvious color difference.

Objective To analyze the phenotypes and to identify SCN1A gene mutation in families with generalized epilepsy accompanied by febrile seizures (GEFS+). Methods The clinical data were collected, and genomic DNA was extracted from peripheral blood lymphocytes of the proband and available members in the GEFS+ families. The phenotypes of the related members were analyzed. The coding regions and flanking intronic regions of the SCN1A gene were screened for mutations using PCR and direct DNA sequencing. Results Thirty-three related members from 10 GEFS+ families, ranged from 2 to 7 members in each family received the examination. Their phenotypes included febrile seizures (FS) in 11 persons (33.3%), febrile seizures plus (Fs+) in 11 (33.3%), FS with partial seizures in 1 (3.0%), afebrile generalized tonic-clonic seizures (AGTCS) in 3 (9.1%), Dravet syndrome in 1 (3.0%), childhood absence epilepsy in 1 (3.0%), and unclassified seizures in 5 members (15.2%). SCN1A mutations were found in 3 families, including one family with missense mutation (glu1444-lys), and silent mutation: synonymous mutation existed in exon 15 (c.2592G>A), with synonymous mutation in exon 9 (c.1212 G>A) and exon 26 (c.5385 G>A) in two families. Conclusions A new missense mutation and three synonymous mutation have been found in the coding regions of SCN1A gene in three families. One of the families has synonymous mutation in two exons. Genetic mechanism is complicated in GEFS+ families. DOI: 10.11855/j.issn.0577-7402.2014.10.09

To determine whether photoreceptor degeneration can stimulate Müller glia to transdifferentiate into neurons in adult mammalian retina, N-methyl-N-nitrosourea (MNU) was injected to induce complete loss of photoreceptors. Following MNU administration, Müller glia underwent reactive gliosis characterized by up-regulation of glial fibrillar acidic protein and nestin, and initiated proliferation through the cyclin D1 and D3 related pathways. Some Müller glia-derived cells were induced to express rhodopsin exclusively. These rhodopsin-positive cells exhibited synaptophysin around them, suggesting possible formation of synapses. After transplanted in to damaged retina, Müller glia migrated, grafted in host retina and produced rhodopsin. These results suggest that degeneration may promote preferential differentiation of Müller glia to photoreceptors and provide a potential therapeutic strategy for retinal degenerative diseases.

This paper presents a phase noise improvement method for fine tuning of type-I ADPLL by exploiting its nonlinear quantization effects. When quantization step approaches the same orders of magnitude of standard deviation of input noise, quantization effects become nonlinear, and additive noise modeling of quantization effects is no longer applicable. By proper offsetting the input signals in this case, the feedback loop of ADPLL can be very sensitive to frequency phase deviation. It results in a larger loop bandwidth, and in turn smaller in-band phase noise than in linear quantization case. A theoretic s-domain noise model is proposed to quantify the phase noise in nonlinear case. Results are verified in Modelsim simulations. Proposed method offers possibility of achieving lower phase noise by lower quantization resolution and less circuit design efforts. QC 20150601

The title compound, [Ni(C3H4N2)5(H2O)](C4H2Br2O4), consists of NiII complex cations and dibromo­succinate anions. The Ni atom, water O atom and one imidazole N atom of the complex cation lie on a twofold axis. The anion lies on an inversion centre. The crystal packing is reinforced by O—H⋯O and N—H⋯O hydrogen bonds, but there are no π–π stacking inter­actions even though the complex contains five aromatic imidazole rings. The compound is isostructural with its cobalt analogue.

In this paper, an inkjet-printed electrochromic(EC) paper display integrated with passive UHF-RFID tag is introduced as a solution for passive electronic shelf labels (ESL). To address the system challenges of the limited power budget of passive UHF-RFID tags and the material aging of EC display, a feedback comparator integrated digital displaydriver is proposed based on the study of electrochromic, bi-stable and aging features of the EC display. Modularized baseband with different enableconditions and clock domains is implemented in the system design level. Moreover, to maintain the system functions when the input power is lower than the display refresh power, a duty-cycled power management unit (PMU) is activated to reduce the load current during energy scavenging and drive the display in short intervals, enabling the fast charging of the voltage rectifier and the correct output of the regulated supply for the core circuit. The design is fabricated in a 0.18-um CMOS process with an area of 2.25 mm2. Fed with EPC C1G2 protocol write command, experiments demonstrate correct refresh of EC display with 4 cm2 effective area. System sensitivity at the antenna reference point is basically immune to the display load. Further improvements can be achieved after careful chip-to-antenna impedance matching and PMU efficiency optimization. Qc 20130718

In this paper we study the radio frequency performance of interconnect using anisotropic conductive film (ACF). A series of experiments are conducted in order to measure and model the electrical characteristics of inkjet-printed circuits on paper substrate as well as the impedance parameters of ACF interconnect at high frequency. Four-point measurement structure, time domain reflectometry (TDR), vector network analyzer (VNA) and de-embedded technology are used to ensure the accuracy of experiments. Equivalent circuit models are built based on the experimental results. Finally, these models are considered as parts of the matching network and circuit design for the RFID receiver, which can be co-designed for developing paper-based electronic systems. It is found that since the difference between RFID tags with and without ACF interconnects is negligible, the influence of ACF interconnects can be ignored for paper-based UHF RFID tag. ACF is a feasible interconnect material for paper-based RFID tags. QC 20111129

Purpose: Postconditioning, a series of brief ischemia-reperfusion sequences given before an ischemic heart undergoes sustained reperfusion, has been shown to lessen ischemia/reperfusion injury. The current study establishes a rabbit model of myocardial ischemia-reperfusion and studied the effects of pulmonary remote postconditioning in this model. Methods: Serum levels of creatine kinase (CK), superoxide dismutase (SOD), and malondialdehyde (MDA), protein expression of endothelial nitric oxide synthase (eNOS), Rho kinase (ROCK- 2), and protein kinase B (Akt) in myocardial cells and the apoptosis index of myocardial cells were examined. Results: Pulmonary remote postconditioning decreased CK, significantly decreased MDA, and increased SOD. Postconditioning significantly increased eNOS protein expression. Administration of eNOS inhibitor, L-NAME, dramatically suppressed the postconditioning-induced eNOS protein expression and serum SOD level, but significantly increased MDA level. The two longer sessions of postconditioning increased Akt, although this increase was not accompanied by changes in levels of the Akt inhibitor, ROCK-2. Blocking eNOS activity with L-NAME had no visible effect on either Akt or ROCK-2. Conclusion: Our results suggest a role for Akt in remote postconditioning-induced myocardial protection, but do not support an involvement of eNOS in Akt-mediated action.

Background Clinically mild encephalitis/encephalopathy with a reversible splenial lesion (MERS) is a clinico-radiological syndrome characterized by transient mild symptoms of encephalopathy and a reversible lesion in the splenium of the corpus callosum on magnetic resonance imaging (MRI). It is often triggered by infection. The common pathogens of MERS are viruses, especially influenza virus. However, Mycoplasma pneumoniae (M.pneumoniae) are relatively rare pathogens for MERS. Case presentation Here we report two paediatric cases of M.pneumoniae infection-induced MERS. The diagnosis of M.pneumoniae infection was established based on polymerase chain reaction (PCR) and specific serum antibodies (IgM). Both of the two patients presented with mild encephalopathy manifestations and recovered completely within a few days. The initial MRI showed a lesion in the central portion of the splenium of the corpus callosum, which completely resolved on the seventh and eighth day after admission for case 1 and case 2. Lumbar puncture was performed in both patients, which revealed no pleocytosis. In case 1, the patient had hyponatremia, peripheral facial nerve paralysis, and rash. To the best of our knowledge, it is the first MERS case associated with peripheral nerve damage. In case 2, interleukin-6(IL-6) was moderately increased in the cerebrospinal fluid (CSF). It suggested that IL-6 may play a role in the pathogenesis of M.pneumoniae-induced MERS. Conclusion Our study enriches the available information on the pathogens of MERS and provides valuable data for better understanding of this syndrome.