[Diagnosis and treatment of incomplete Kawasaki disease in children]. / å„¿ç«¥ä¸å®Œå ¨æ€§å·å´Žç— çš„è¯Šæ²».

Kawasaki disease (KD) is a febrile disease mainly observed in children aged <5 years, with medium- and small-vessel vasculitis as the main lesion. Although KD has been reported for more than 50 years and great progress has been made in the etiology and pathology of KD in recent years, there is still a lack of specific indicators for the early diagnosis of KD, especially with more difficulties in the diagnosis of incomplete Kawasaki disease (IKD). At present, there are no clear diagnostic criteria for IKD, which leads to the failure of the timely identification and standardized treatment of IKD in clinical practice and even induce the development of coronary artery lesion. This article reviews the concept, epidemiological features, diagnosis, treatment, and follow-up management of IKD, in order to deepen the understanding of IKD among clinical workers and help to improve the clinical diagnosis and treatment of KD in China.

N-cadherin cleavage: A critical function that induces diabetic retinopathy fibrosis via regulation of ß-catenin translocation.

Retinal fibrosis is a severe pathological change in the late stage of diabetic retinopathy and is also the leading cause of blindness. We have previously revealed that N-cadherin was significantly increased in type 1 and type 2 diabetic mice retinas and the fibrovascular membranes from proliferative diabetic retinopathy (PDR) patients. However, whether N-cadherin directly induces retinal fibrosis in DR and the related mechanism is unknown. Here, we investigated the pathogenic role of N-cadherin in mediating retinal fibrosis and further explored the relevant therapeutic targets. We found that the level of N-cadherin was significantly increased in PDR patients and STZ-induced diabetic mice and positively correlated with the fibrotic molecules Connective Tissue Growth Factor (CTGF) and fibronectin (FN). Moreover, intravitreal injection of N-cadherin adenovirus significantly increased the expression of FN and CTGF in normal mice retinas. Mechanistically, overexpression of N-cadherin promotes N-cadherin cleavage, and N-cadherin cleavage can further induce translocation of non-p-ß-catenin in the nucleus and upregulation of fibrotic molecules. Furthermore, we found a novel N-cadherin cleavage inhibitor, pigment epithelial-derived factor (PEDF), which ameliorated the N-cadherin cleavage and subsequent retinal fibrosis in diabetic mice. Thus, our findings provide novel evidence that elevated N-cadherin level not only acts as a classic EMT maker but also plays a causative role in diabetic retinal fibrosis, and targeting N-cadherin cleavage may provide a strategy to inhibit retinal fibrosis in DR patients.

RadarPDR: Radar-Assisted Indoor Pedestrian Dead Reckoning.

Pedestrian dead reckoning (PDR) is the critical component in indoor pedestrian tracking and navigation services. While most of the recent PDR solutions exploit in-built inertial sensors in smartphones for next step estimation, due to measurement errors and sensing drift, the accuracy of walking direction, step detection, and step length estimation cannot be guaranteed, leading to large accumulative tracking errors. In this paper, we propose a radar-assisted PDR scheme, called RadarPDR, which integrates a frequency-modulation continuous-wave (FMCW) radar to assist the inertial sensors-based PDR. We first establish a segmented wall distance calibration model to deal with the radar ranging noise caused by irregular indoor building layouts and fuse wall distance estimation with acceleration and azimuth signals measured by the inertial sensors of a smartphone. We also propose a hierarchical particle filter(PF) together with an extended Kalman filter for position and trajectory adjustment. Experiments have been conducted in practical indoor scenarios. Results demonstrate that the proposed RadarPDR is efficient and stable and outperforms the widely used inertial sensors-based PDR scheme.

Immunoregulatory effects of Tetrastigma hemsleyanum polysaccharide via TLR4-mediated NF-κB and MAPK signaling pathways in Raw264.7 macrophages.

Polysaccharide of Tetrastigma hemsleyanum (THP) exert antioxidant, antibacterial, lipid-lowering, and anti-inflammatory properties, especially some evidences have highlighted the efficiency of it as an anti-tumor agent. However, as a biological macromolecule with bidirectional immune regulation, the immunological enhancement effects of THP on macrophages and its underlying mechanisms are still largely unknown. In the present study, THP was prepared and characterized, and then the effect of THP on Raw264.7 cell activation was investigated. Structural characteristics of THP showed that the average molecular weight was 370.26 kDa, and the main monosaccharide composition was galactose, glucuronic acid, mannose, and glucose at a ratio of 31.56: 25.15: 19.44: 12.60, with high viscosity causing by relative high uronic acid. For immunomodulatory activity investigation, THP promoted the production of NO, IL-6 and TNF-α, as well as the expression of IL-1ß, MCP-1, iNOS and COX-2, which were almost completely inhibited by TLR4 antagonist. Further study showed that THP could activate NF-κB and MAPK signaling pathways, and thus enhanced the phagocytic activity of Raw264.7 macrophages. In conclusion, the present study provided evidences that THP could be served as a new immunomodulator in both functional foods and the pharmaceutical field.

Development of an efficient method for separation and purification of cordycepin from liquid fermentation of Cordyceps militaris and analysis of cordycepin antitumor activity.

Cordycepin (3 '-deoxyadenosine) is the main active component of Cordyceps militaris, which is a chemical marker for quality detection of Cordyceps militaris and has important medicinal development value. Existing methods for obtaining cordycepin are complex and costly. In this study, an economical and simple method for separation and purification of cordycepin from Cordyceps militaris fermentation liquid through physical crystallization was explored. First, lyophilized powdered fermentation liquid (LPFL) and pure methanol (1 g/100 mL, w/v) were mixed, and then repeatedly dissolved and crystallized until the precipitation was white. Purified product was obtained by freeze-drying the precipitate. The substance was determined to be cordycepin by high performance liquid chromatography, mass spectrometry and infrared spectroscopy, and the purity was 94.26%. Compared with the existing methods, this method is simple and low cost. In addition, the functional activity of cordycepin was determined by in vitro test. The results exhibited that cordycepin caused death and morphological changes in human colon cancer Caco-2 cells, and significantly inhibited the proliferation of Caco-2 cells, with a half-maximal inhibitory concentration (IC50) of 107.2 µg/mL. Cordycepin could induce early apoptosis of Caco-2 and caused cell cycle arrest in the G2 phase. Caco-2 cell apoptosis and cell cycle arrest showed dose dependence to cordycepin over a certain range. These results improved cordycepin purification method, provided insights into the mechanism of cordycepin in cancer inhibition, and would provide important reference for further development and clinical application of cordycepin.

Graphene Oxide-Mediated Synthesis of Ultrathin Co-MOL for CO2 Photoreduction.

Metal-organic framework (MOF) materials have broad application prospects in catalysis because of their ordered structure and molecular adjustability. However, the large volume of bulky MOF usually leads to insufficient exposure of the active sites and the obstruction of charge/mass transfer, which greatly limits their catalytic performance. Herein, we developed a simple graphene oxide (GO) template method to fabricate ultrathin Co-metal-organic layer (2.0 nm) on reduced GO (Co-MOL@r-GO). The as-synthesized hybrid material Co-MOL@r-GO-2 exhibits highly efficient photocatalytic performance for CO2 reduction, and the CO yield can reach as high as 25,442 µmol/gCo-MOL, which is over 20 times higher than that of the bulky Co-MOF. Systematic investigations demonstrate that GO can act as a template for the synthesis of the ultrathin Co-MOL with more active sites and can be used as the electron transport medium between the photosensitizer and the Co-MOL to enhance the catalytic activity for CO2 photoreduction.

Case Report: Cranial Tuberculosis in a Patient without Tuberculosis Foci Elsewhere in the Body.

Cranial tuberculosis is a relatively infrequent inflammatory reaction caused by tuberculous bacilli invading the skull. Most cases of cranial tuberculosis are secondary to tuberculosis foci in other parts of the body; primary cranial tuberculosis is extremely rare. Herein, we report a case of primary cranial tuberculosis. A 50-year-old man presented to our hospital with a mass in the right frontotemporal region. Chest computed tomography and abdominal ultrasonography findings were normal. Magnetic resonance imaging of the brain revealed a mass in the right frontotemporal skull and scalp with cystic changes, adjacent bone destruction, and meningeal invasion. The patient underwent surgery and was diagnosed with primary cranial tuberculosis; he was treated with antitubercular therapy postoperatively. No recurrent masses or abscesses were observed during the follow-up.

Infectious thrombosis of the superior sagittal sinus with subarachnoid hemorrhage: A case report.

RATIONALE: Cerebral venous sinus thrombosis (CVST) represents 0.5% to 1% of all strokes. CVST can cause headaches, epilepsy, and subarachnoid hemorrhage (SAH). CVST is easily misdiagnosed because of the variety and non-specificity of symptoms. Herein, we report a case of infectious thrombosis of the superior sagittal sinus with SAH. PATIENT CONCERNS: A 34-year-old man presented to our hospital with a 4-hour history of sudden and persistent headache and dizziness with tonic convulsions of the limbs. Computed tomography revealed SAH with edema. Enhanced magnetic resonance imaging showed an irregular filling defect in the superior sagittal sinus. DIAGNOSES: The final diagnosis was hemorrhagic superior sagittal sinus thrombosis and secondary epilepsy. INTERVENTIONS: He was treated with antibiotic, antiepileptic, fluids to rehydrate, and intravenous dehydration. OUTCOMES: After treatment, the seizures did not recur and the symptoms were relieved. One month after the antibiotic treatment, the muscle strength of the patient's right extremity was restored to level 5, and there was no recurrence of his neurological symptoms. LESSONS: We describe a case of infectious thrombosis of the superior sagittal sinus manifested as SAH, which is easily misdiagnosed, especially when patients present with an infection. Clinicians must therefore take care during the diagnosis and selection of the treatment strategy.

Luteimonas galliterrae sp. nov., isolated from poultry farm soil.

Strain SX5T was isolated from the soil of a poultry farm in Shanxi Province, PR China. The isolate was a Gram-stain-negative, rod-shaped, non-flagellated, and yellow bacterium. Growth occurred at 20-37 °C (optimum, 28 °C), pH 6.0-10.0 (optimum, pH 8.0) and 0-1 % NaCl (optimum, 0 %). Phylogenetic analysis based on 16S rRNA gene sequences indicated that strain SX5T was related to members of the genus Luteimonas, and close to Luteimonas gilva H23T (97.9 %), Luteimonas cucumeris Y4T (97.9 %), Luteimonas aquatica RIB1-20T (96.8 %), Luteimonas notoginsengisoli SYP-B804T (96.4 %) and Luteimonas panaciterrae Gsoil 068T (96.1 %). The major cellular fatty acids of strain SX5T were iso-C16 : 0, iso-C17 : 1 ω9c, iso-C15 : 0 and iso-C11 : 0 3OH. The sole isoprenoid quinone was ubiquinone Q-8, and the major polar lipid profile contained diphosphatidylglycerol, phosphatidylglycerol and phosphatidylethanolamine. Genome analyses revealed that strain SX5T had a genome size of 3.6 Mbp with a G+C content of 65.7 mol% and contained abundant carbohydrate-active enzyme genes and three putative distinct biosynthetic gene clusters, suggesting that it may have great potential to degrade and utilize complex biological organic matter and produce special secondary metabolites. Comparative genomic analyses clearly separated strain SX5T from the known species of the genus Luteimonas based on average nucleotide identity and digital DNA-DNA hybridization values below the thresholds for species delineation. Based on its phenotypic, genotypic properties and phylogenetic inference, strain SX5T represents a novel species in the genus Luteimonas, for which the name Luteimonas galliterrae sp. nov. is proposed. The type strain is SX5T (=GDMCC 1.2162T=KCTC 82443T=JCM 34401T).

Insight into the Surface Reconstruction-Induced Structure and Electrochemical Performance Evolution for Ni-Rich Cathodes with Postannealing after Washing.

Ni-rich layered LiNixCoyAlzO2 (NCA, x ≥ 0.8) oxides have attracted wide attention as cathode materials for lithium-ion batteries due to their higher energy density and lower cost. However, the increase in the capacity for Ni-rich cathodes can cause faster capacity decay and increase sensitivity to ambient air exposure during the storage process. Especially, the residual lithium on the surface of Ni-rich cathodes will cause severe flatulence during cycling which greatly reduces the safety performance of the battery. Washing is an effective method to reduce residual lithium, but it will seriously damage the surface phase structure of Ni-rich materials. Here, we introduce a designed method involving two steps, washing and high-temperature annealing, which can ingeniously modify the surface phase structure of Ni-rich cathodes. The results show that the residual lithium content can be significantly reduced. The thin NiO-like rock-salt phase formed on the surface of Ni-rich cathode annealed at 600 °C improves the diffusion kinetics of Li+, reduces the polarization, and improves the electrochemical performance of Ni-rich materials, while the thick spinel-like phase formed at 400 °C hinders the diffusion kinetics of Li+, significantly increases the polarization, and eventually leads to the structural degradation of Ni-rich materials. As a result, the discharge capacity of the cathode annealed at 600 °C still retains 174.48 mA h g-1 after 100 cycles, with a capacity retention of 92.04%, much larger than the cathode annealed at 400 °C, for which the discharge capacity drops to 107.77 mA h g-1, with a capacity retention of 65.78%.

Activity-Dependent Differential Regulation of Auts2 Isoforms In Vitro and In Vivo.

Autism spectrum disorder (ASD) is a neurodevelopmental disorder of unknown cause, although one hypothesis suggests a potential imbalance between excitation and inhibition that leads to changes in neuronal activity and a disturbance in the brain network. However, the mechanisms through which neuronal activity contributes to the development of ASD remain largely unexplained. In this study, we described that neuronal activity at the transcriptional and translational levels regulated the expression of Auts2 isoforms. The prolonged stimulation of cultured cortical neurons significantly reduced the auts2 transcripts, accompanied by the decrease of FL-Auts2 protein, as well as one of the short isoforms (S-Auts2 var.1). Blocking neuronal activity increased the number of auts2 transcripts but not protein levels. Furthermore, blocking the NMDA receptors during stimulation could partially restore the FL-Auts2 and S-Auts2 var.1 at protein level, but not at mRNA level. Finally, Auts2 expression in the hippocampus was reduced in mice exposed to an enriched environment, a behavior paradigm designed to increase the brain activity through abundant sensory and social stimulations. Thus, our study revealed a novel regulatory effect of neuronal activity on the transcription and translation of ASD-risk gene auts2.

Autophagy in the pathogenesis and therapeutic potential of post-traumatic osteoarthritis.

Autophagy, as a fundamental mechanism for cellular homeostasis, is generally involved in the occurrence and progression of various diseases. Osteoarthritis (OA) is the most common musculoskeletal disease that often leads to pain, disability and economic loss in patients. Post-traumatic OA (PTOA) is a subtype of OA, accounting for >12% of the overall burden of OA. PTOA is often caused by joint injuries including anterior cruciate ligament rupture, meniscus tear and intra-articular fracture. Although a variety of methods have been developed to treat acute joint injury, the current measures have limited success in effectively reducing the incidence and delaying the progression of PTOA. Therefore, the pathogenesis and intervention strategy of PTOA need further study. In the past decade, the roles and mechanisms of autophagy in PTOA have aroused great interest in the field. It was revealed that autophagy could maintain the homeostasis of chondrocytes, reduce joint inflammatory level, prevent chondrocyte death and matrix degradation, which accordingly improved joint symptoms and delayed the progression of PTOA. Moreover, many strategies that target PTOA have been revealed to promote autophagy. In this review,  we summarize the roles and mechanisms of autophagy in PTOA and the current strategies for PTOA treatment that depend on autophagy regulation, which may be beneficial for PTOA patients in the future.

Correlation between the Signal Intensity Alteration of Infrapatellar Fat Pad and Knee Osteoarthritis: A Retrospective, Cross-Sectional Study.

Infrapatellar fat pad (IPFP) inflammation is a common pathological manifestation in knee osteoarthritis (OA). However, the significance of IPFP signal intensity alteration for clinical diagnosis and treatment of knee OA needs further research. We assessed IPFP signal intensity alteration (0-3), IPFP maximum cross-sectional area (CSA) and IPFP depth, meniscus injury, bone marrow edema, and cartilage injury from magnetic-resonance imaging (MRI) in 41 non-KOA patients (K-L grade 0 and grade I) and 68 KOA patients (K-L grade 2,3 and 4). We found that IPFP signaling was altered in all patients with KOA whose alteration was closely related to the K-L grading. We found that the IPFP signal intensity was increased in most OA patients, especially the ones in the late stage. There were significant differences in IPFP maximum CSA and IPFP depth between groups in KOA and non-KOA patients. Moreover, Spearman correlation analysis showed that IPFP signal intensity was moderately positively correlated with age, meniscal injury, cartilage injury, and bone marrow edema, and negatively correlated with height, while not correlated with visual analogue scale (VAS) scoring and body mass index (BMI). In addition, women have higher IPFP inflammation scores on MRI than men. In conclusion, IPFP signal intensity alteration is associated with joint damage in knee OA, which may have clinical significance for diagnosing and treating KOA.

The relationship between the interictal epileptiform discharge source connectivity and cortical structural couplings in temporal lobe epilepsy.

Objective: The objective of this study was to explore the relation between interictal epileptiform discharge (IED) source connectivity and cortical structural couplings (SCs) in temporal lobe epilepsy (TLE). Methods: High-resolution 3D-MRI and 32-sensor EEG data from 59 patients with TLE were collected. Principal component analysis was performed on the morphological data on MRI to obtain the cortical SCs. IEDs were labeled from EEG data and averaged. The standard low-resolution electromagnetic tomography analysis was performed to locate the source of the average IEDs. Phase-locked value was used to evaluate the IED source connectivity. Finally, correlation analysis was used to compare the IED source connectivity and the cortical SCs. Results: The features of the cortical morphology in left and right TLE were similar across four cortical SCs, which could be mainly described as the default mode network, limbic regions, connections bilateral medial temporal, and connections through the ipsilateral insula. The IED source connectivity at the regions of interest was negatively correlated with the corresponding cortical SCs. Significance: The cortical SCs were confirmed to be negatively related to IED source connectivity in patients with TLE as detected with MRI and EEG coregistered data. These findings suggest the important role of intervening IEDs in treating TLE.

Wireless Sensing and Networking for the Internet of Things.

In recent years, we have witnessed the exponential proliferation of the Internet of Things (IoT)-based networks of physical devices, vehicles, and appliances, as well as other items embedded with electronics, software, sensors, actuators, and connectivity, which enable these objects to connect and exchange data [...].

Inhibition of SMAD3 effectively reduces ADAMTS-5 expression in the early stages of osteoarthritis.

OBJECTIVE: As one of the most important protein-degrading enzymes, ADAMTS-5 plays an important role in the regulation of cartilage homeostasis, while miRNA-140 is specifically expressed in cartilage, which can inhibit the expression of ADAMTS-5 and delay the progression of OA (osteoarthritis). SMAD3 is a key protein in the TGF-ß signaling pathway, inhibiting the expression of miRNA-140 at the transcriptional and post-transcriptional levels, and studies have confirmed the high expression of SMAD3 in knee cartilage degeneration, but whether SMAD3 can mediate the expression of miRNA-140 to regulate ADAMTS-5 remains unknown. METHODS: Sprague-Dawley (SD) rat chondrocytes were extracted in vitro and treated with a SMAD3 inhibitor (SIS3) and miRNA-140 mimics after IL-1 induction. The expression of ADAMTS-5 was detected at the protein and gene levels at 24 h, 48 h, and 72 h after treatment. The OA model of SD rats was created using the traditional Hulth method in vivo, with SIS3 and lentivirus packaged miRNA-140 mimics injected intra-articularly at 2 weeks, 6 weeks and 12 weeks after surgery. The expression of miRNA-140 and ADAMTS-5 in the knee cartilage tissue was observed at the protein and gene levels. Concurrently, knee joint specimens were fixed, decalcified, and embedded in paraffin prior to immunohistochemical, Safranin O/Fast Green staining, and HE staining analyses for ADAMTS-5 and SMAD3. RESULTS: In vitro, the expression of ADAMTS-5 protein and mRNA in the SIS3 group decreased to different degrees at each time point. Meanwhile, the expression of miRNA-140 in the SIS3 group was significantly increased, and the expression of ADAMTS-5 in the miRNA-140 mimics group was also significantly downregulated (P < 0.05). In vivo, it was found that ADAMTS-5 protein and gene were downregulated to varying degrees in the SIS3 and miRNA-140 mimic groups at three time points, with the most significant decrease at the early stage (2 weeks) (P < 0.05), and the expression of miRNA-140 in the SIS3 group was significantly upregulated, similar to the changes detected in vitro. Immunohistochemical results showed that the expression of ADAMTS-5 protein in the SIS3 and miRNA-140 groups was significantly downregulated compared to that in the blank group. The results of hematoxylin and eosin staining showed that in the early stage, there was no obvious change in cartilage structure in the SIS3 and miRNA-140 mock groups. The same was observed in the results of Safranin O/Fast Green staining; the number of chondrocytes was not significantly reduced, and the tide line was complete. CONCLUSION: The results of in vitro and in vivo experiments preliminarily showed that the inhibition of SMAD3 significantly reduced the expression of ADAMTS-5 in early OA cartilage, and this regulation might be accomplished indirectly through miRNA-140.

Prenatal exposure of diabetes and progestin-mediated autistic biomarker in peripheral blood mononuclear cells.

Despite the importance of early diagnosis and intervention, the diagnosis of autism spectrum disorders (ASDs) remains delayed as it is mostly based on clinical symptoms and abnormal behaviours appearing after 2 years of age. Identification of autistic markers remains a top priority in achieving an early and effective ASD diagnosis. We have previously reported that prenatal exposure of hormones or diabetes triggers epigenetic changes and oxidative stress, resulting in gene suppression with autism-like behaviours in offspring. Here, a potential biomarker for ASD diagnosis was established through gene analysis in peripheral blood mononuclear cells (PBMCs). The study from in vivo mouse showed that prenatal hormone exposure or maternal diabetes suppresses mRNA expression of estrogen-related receptor α (ERRα), superoxide dismutase 2 (SOD2), G protein-coupled estrogen receptor (GPER) and retinoic acid-related orphan receptor α (RORA) in the brain as well as oxidative stress and mitochondrial dysfunction, subsequently triggering autism-like behaviour in mouse offspring. Also, similar gene suppression was found in hematopoietic stem cells (HSCs) and PBMC, with inherited epigenetic changes being identified on the related promoters. The human case-control study found that mRNA levels of ERRα, SOD2, GPER and RORA were significantly reduced in PBMC from ASD subjects (n = 132) compared with typically developing (n = 135) group. The receiver operating characteristic curve showed a .869 ± .021 of area under the curve for ASD subjects with 95% confidence interval of .829-.909, together with 1.000 of sensitivity and .856 of specificity. In conclusion, the combined mRNA expression in PBMC based on prenatal factor exposure-mediated gene suppression could be a potential biomarker for ASD diagnosis.

Applications of chitosan-based biomaterials: From preparation to spinal cord injury neuroprosthetic treatment.

Spinal cord injury (SCI)-related disabilities are a serious problem in the modern society. Further, the treatment of SCI is highly challenging and is urgently required in clinical practice. Research on nerve tissue engineering is an emerging approach for improving the treatment outcomes of SCI. Chitosan (CS) is a cationic polysaccharide derived from natural biomaterials. Chitosan has been found to exhibit excellent biological properties, such as nontoxicity, biocompatibility, biodegradation, and antibacterial activity. Recently, chitosan-based biomaterials have attracted significant attention for SCI repair in nerve tissue engineering applications. These studies revealed that chitosan-based biomaterials have various functions and mechanisms to promote SCI repair, such as promoting neural cell growth, guiding nerve tissue regeneration, delivering nerve growth factors, and as a vector for gene therapy. Chitosan-based biomaterials have proven to have excellent potential for the treatment of SCI. This review aims to introduce the recent advances in chitosan-based biomaterials for SCI treatment and to highlight the prospects for further application.