Knowledge mapping of neonatal electroencephalogram: A bibliometric analysis (2004-2022).

BACKGROUND: Electroencephalography (EEG), a widely used noninvasive neurophysiological diagnostic tool, has experienced substantial advancements from 2004 to 2022, particularly in neonatal applications. Utilizing a bibliometric methodology, this study delineates the knowledge structure and identifies emergent trends within neonatal EEG research. METHODS: An exhaustive literature search was conducted on the Web of Science Core Collection (WoSCC) database to identify publications related to neonatal EEG from 2004 to 2022. Analytical tools such as VOSviewer, CiteSpace, and the R package "bibliometrix" were employed to facilitate this investigation. RESULTS: The search yielded 2501 articles originating from 79 countries, with the United States and England being the predominant contributors. A yearly upward trend in publications concerning neonatal EEG was observed. Notable research institutions leading this field include the University of Helsinki, University College London, and University College Cork. Clinical Neurophysiology is identified as the foremost journal in this realm, with Pediatrics as the most frequently co-cited journal. The collective body of work from 9977 authors highlights Sampsa Vanhatalo as the most prolific contributor, while Mark Steven Scher is recognized as the most frequently co-cited author. Key terms such as "seizures," "epilepsy," "hypoxic-ischemic encephalopathy," "amplitude-integrated EEG," and "brain injury" represent the focal research themes. CONCLUSION: This bibliometric analysis offers the first comprehensive review, encapsulating research trends and progress in neonatal EEG. It reveals current research frontiers and crucial directions, providing an essential resource for researchers engaged in neonatal neuroscience.

Immune control in Kawasaki disease knowledge mapping: a bibliometric analysis.

BACKGROUND: Kawasaki disease is a systemic vascular disease with an unclear pathophysiology that primarily affects children under the age of five. Research on immune control in Kawasaki disease has been gaining attention. This study aims to apply a bibliometric analysis to examine the present and future directions of immune control in Kawasaki disease. METHODS: By utilizing the themes "Kawasaki disease," "Kawasaki syndrome," and "immune control," the Web of Science Core Collection database was searched for publications on immune control in Kawasaki disease. This bibliometric analysis was carried out using VOSviewers, CiteSpace, and the R package "bibliometrix." RESULTS: In total, 294 studies on immune control in Kawasaki disease were published in Web of Science Core Collection. The three most significant institutions were Chang Gung University, the University of California San Diego, and Kaohsiung Chang Gung Memorial Hospital. China, the United States, and Japan were the three most important countries. In this research field, Clinical and Experimental Immunology was the top-referred journal, while the New England Journal of Medicine was the most co-cited journal. The Web of Science Core Collection document by McCrindle BW et al. published in 2017 was the most cited reference. Additionally, the author keywords concentrated on "COVID-19," "SARS-CoV-2," and "multisystem inflammatory syndrome in children" in recent years. CONCLUSION: The research trends and advancements in immune control in Kawasaki disease are thoroughly summarised in this bibliometric analysis, which is the first to do so. The data indicate recent research frontiers and hot directions, making it easier for researchers to study the immune control of Kawasaki disease.

Andrographolide reduces cisplatin resistance of endometrial cancer Ishikawa/DPP cells by inhibiting the Fas/FasL signaling axis / 中国肿瘤生物治疗杂志

@#目的：探讨穿心莲内酯（Andro）调节脂肪酸合成酶（Fas）/脂肪酸合成酶配体（FasL）信号轴对子宫内膜癌Ishikawa细胞顺铂（DDP）耐药性的影响。方法：采用0、5、10、20 μg/mL DDP分别处理Ishikawa细胞和顺铂耐药的Ishikawa/DPP细胞，0、5、10、25、50 μmol/L Andro处理Ishikawa/DDP细胞，MTT法检测细胞增殖情况并为后续实验选择合适的给药剂量。将Ishikawa/DDP细胞随机分为对照组、DDP组（DDP干预）、Andro组（DDP、Andro干预）、pcDNA3.1-NC组（转染pcDNA3.1+DDP、Andro干预）、pcDNA3.1-Fas/FasL组（转染pcDNA3.1-Fas/FasL+DDP、Andro干预），24 h后，采用qPCR法检测Fas、FasL mRNA的表达，平板克隆形成实验、Transwell实验和流式细胞术分别检测细胞克隆能力、细胞迁移与侵袭和细胞凋亡，WB法检测增殖细胞核抗原（PCNA）、BAX、Bcl-2、MMP-2、PD-L1、多药耐药蛋白-1（MDR-1）及Fas、FasL蛋白表达。结果：DDP以剂量依赖的方式抑制Ishikawa和Ishikawa/DPP细胞增殖，并且与Ishikawa细胞比较，Ishikawa/DPP细胞对DDP的敏感性更低（均P<0.05）；Andro以剂量依赖性的方式抑制Ishikawa/DPP细胞的增殖（均P<0.05）。Ishikawa/DPP细胞中Fas、FasL的表达水平均高于Ishikawa细胞（均P<0.05）。选取20 μg/mL DDP和25 μmol/L Andro为干预剂量，干预时间24 h。与对照组比较，DDP组Ishikawa/DPP细胞中PD-L1、MDR-1、Fas、FasL mRNA及蛋白表达水平显著升高（P<0.05），而克隆形成率、迁移与侵袭细胞数、凋亡率差异均无统计学意义（均P>0.05）；与DDP组比较，Andro组Ishikawa/DPP细胞中Fas、FasL mRNA表达水平、细胞克隆形成率、迁移与侵袭细胞数、PCNA、Bcl-2、MMP-2、PD-L1、MDR-1、Fas、FasL蛋白表达水平显著降低，BAX蛋白表达水平及凋亡率显著升高（P<0.05或P<0.01），pcDNA3.1-NC组与Andro组类似；与pcDNA3.1-NC组比较，pcDNA3.1-Fas/FasL组Ishikawa/DPP细胞上述指标变化均被逆转（P<0.05）。结论：Andro可能通过抑制Fas/FasL信号轴来抑制Ishikawa/DPP细胞增殖、迁移与侵袭，促进凋亡，从而降低细胞对DDP的耐药性。

Bacteremia caused by Comamonas kerstersii in a patient with acute perforated appendicitis and localized peritonitis: case report and literature review.

Comamonas kerstersii (C. kerstersii) is a Gram-negative bacterium that was initially thought to be non-pathogenic to humans and is abundant in the environment. In recent years, with the availability of matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS) that enable fast and accurate bacterial identification, there have been increasing number of reports of human infections caused by C. kerstersii, indicating that this organism has emerged as human pathogen. In fact, most clinical isolates of C. kerstersii are recovered from peritoneal liquid, and bacteremia has been infrequently reported. Here, we report a case of bacteremia caused by C. kerstersii in a 28-year-old male patient with acute perforated appendicitis and localized peritonitis and present a comprehensive review of C. kerstersii infections in pathogenic diagnosis and clinical treatment as well as prognosis, thus providing a better understanding of C. kerstersii-related infections.

Genomic characterization of Pantoea anthophila strain UI705 causing urinary tract infections in China.

Introduction: Pantoea anthophila (P. anthophila) is a Gram-negative bacterium initially isolated from Impatiens balsamina in India. P. anthophila has been characterized with low pathogenicity, and no human infections caused by this organism have been reported yet. We report the first case of urinary tract infection caused by P. anthophila in a 73-year-old man after bladder cancer surgery. Methods: The bacterial isolate gained from urine was named UI705 and identified as P. anthophila by MALDI-TOF mass spectrometry. The genome sequencing and analysis were performed to further characterize the pathogenesis of the clinical isolate. Result and discussion: To the best of our knowledge, this is the first report of human infection caused by P. anthophila in China. The draft genome sequence of P. anthophila UI705 provides a fundamental resource for subsequent investigation of its virulence factors, antibiotic resistance, host-pathogen interactions, and comparative genomics of genus Pantoea.

Ratiometric Luminescent Thermometer Based on the Lanthanide Metal-Organic Frameworks by Thermal Curing.

The high-performance optical thermometer probes are of great significance in diverse areas; lanthanide metal-organic frameworks (Ln-MOFs) are a promising candidate for luminescence temperature sensing owing to their unique luminescence properties. However, Ln-MOFs have poor maneuverability and stability in complex environments due to the crystallization properties, which then hinder their application scope. In this work, the Tb-MOFs@TGIC composite was successfully prepared using simple covalent crosslinking through uncoordinated -NH2 or COOH on Tb-MOFs reacting with the epoxy groups on TGIC {Tb-MOFs = [Tb2(atpt)3(phen)2(H2O)]n; H2atpt = 2-aminoterephthalic acid; phen = 1,10-phenanthroline monohydrate}. After curing, the fluorescence properties, quantum yield, lifetime, and thermal stability of Tb-MOFs@TGIC were remarkably enhanced. Meanwhile, the obtained Tb-MOFs@TGIC composites exhibit excellent temperature sensing properties in the low-temperature (Sr = 6.17% K-1 at 237 K), physiological temperature (Sr = 4.86% K-1 at 323 K), or high-temperature range (Sr = 3.88% K-1 at 393 K) with high sensitivity. In the temperature sensing process, the sensing mode of single emission changed into double emission for ratiometric thermometry owing to the back energy transfer (BenT) from Tb-MOFs to TGIC linkers, and the BenT process enhanced with the increase of temperature, which further improved the accuracy and sensitivity of temperature sensing. Most notably, the temperature-sensing Tb-MOFs@TGIC can be easily coated on the surface of polyimide (PI), glass plate, silicon pellet (SI), and poly(tetrafluoroethylene) plate (PTFE) substrates by a simple spraying method, which also exhibited an excellent sensing property, making it applicable for a wider T range measurement. This is the first example of a postsynthetic Ln-MOF hybrid thermometer operative over a wide temperature range including the physiological and high temperature based on back energy transfer.

Efficacy of levofloxacin on macrolide-unresponsive and corticosteroid-resistant refractory Mycoplasma pneumoniae pneumonia in children.

BACKGROUND: This study aimed to summarize the experience in treatment of Mycoplasma pneumoniae pneumonia (MPP) with worsening lung shadow despite treatment with appropriate antimicrobials and corticosteroid in children. METHODS: All patients satisfied refractory MP pneumonia (RMPP) diagnostic criteria were enrolled. The clinical manifestations, laboratory findings, imaging features, treatments, and outcomes were retrospectively reviewed. RESULTS: Six patients with an average age of 7.83±3.13 years old were included in this study. All the patients were non-responsive to macrolide (ML) and glucocorticoids treatment shown by aggravated clinical symptoms and chest radiographies. The average total duration of fever was 19.5±8.34 days and the average time before levofloxacin (LVX) therapy was 10±2.97 days. After LVX treatment, the time of fever was from 1 to 3 days in five cases and 11 days in one case. The MP-DNA copies in the sputum decreased slowly after ML treatment in six patients, while they decreased quickly after LVX treatment in 5 children. A2063G mutation of domain V of 23SrRNA gene was found in five cases. Five patients recovered completely 16-32 days after treatment. One patient developed acute disseminated encephalomyelitis (ADEM) with abnormal brain magnetic resonance imaging and occurred serious sequelae. CONCLUSIONS: The sputum MP-DNA copies and clinical symptoms have a positive correlation with therapeutic efficacy. LVX may be beneficial in treatment of ML-unresponsive and corticosteroid-resistant RMPP in children. RMPP can be gradually cured by effective treatment of LVX, while which can damage the nervous system and lead to severe complications once MP invades brain tissues.

IL-33 ameliorates experimental colitis involving regulation of autophagy of macrophages in mice.

BACKGROUND: Previously, we have demonstrated that IL-33 administration protecting TNBS-induced experimental colitis is associated with facilitation of Th2/Tregs responses in mice. However, whether IL-33 regulates autophagy to ameliorate experimental colitis is unclear. RESULTS: IL-33 administration (2 µg/day, intraperitoneal injection), while facilitating Th2/Tregs responses, also enhances the autophagy in mice with TNBS-induced colitis as well as macrophages. In the meantime, we observed that inhibition of the autophagy with 3-methyladenine (3-MA) (24 mg/kg, intraperitoneal injection) in mice exacerbates TNBS-induced experimental colitis. On the contrary, administration of rapamycin (2 mg/kg,intragastric administration), an autophagy-enhancer, alleviates the colitis in mice. In vivo, Immunofluorescence analysis revealed that TNBS combined with IL-33 enhanced the autophagy of macrophages in the inflammatory gut tissue. In vitro, treatment with IL-33 promoted the autophagy of macrophages generated from bone marrow cells in dose-dependant manner. Furthermore, the effect of autophagy-enhancement by IL-33 is TLR4 signaling pathway dependant. Our notion was further confirmed by IL-33-deficient bone marrow-derived macrophages cells. CONCLUSIONS: IL-33 regulates the autophagy is a new immunoregulatory property on TNBS-induced experimental colitis in mice.

Motion-Aware Correlation Filters for Online Visual Tracking.

The discriminative correlation filters-based methods struggle deal with the problem of fast motion and heavy occlusion, the problem can severely degrade the performance of trackers, ultimately leading to tracking failures. In this paper, a novel Motion-Aware Correlation Filters (MACF) framework is proposed for online visual object tracking, where a motion-aware strategy based on joint instantaneous motion estimation Kalman filters is integrated into the Discriminative Correlation Filters (DCFs). The proposed motion-aware strategy is used to predict the possible region and scale of the target in the current frame by utilizing the previous estimated 3D motion information. Obviously, this strategy can prevent model drift caused by fast motion. On the base of the predicted region and scale, the MACF detects the position and scale of the target by using the DCFs-based method in the current frame. Furthermore, an adaptive model updating strategy is proposed to address the problem of corrupted models caused by occlusions, where the learning rate is determined by the confidence of the response map. The extensive experiments on popular Object Tracking Benchmark OTB-100, OTB-50 and unmanned aerial vehicles (UAV) video have demonstrated that the proposed MACF tracker performs better than most of the state-of-the-art trackers and achieves a high real-time performance. In addition, the proposed approach can be integrated easily and flexibly into other visual tracking algorithms.

HSV infection is associated with gestational hypertension: results from the US National inpatient sample.

The purpose of this study was to determine if there is an association between maternal herpes simplex virus (HSV) infection and pre-eclampsia/eclampsia or gestational hypertension. The US Nationwide Inpatient Sample database was searched for women aged 15-44 years who delivered in a hospital between 2005 and 2014. The patients were categorized into those with and without HSV and pre-eclampsia/eclampsia and gestational hypertension were compared between the groups. The analytic sample size (n=8 264 076) was equivalent to a population-based sample size of 40 653 030 patients. After adjusting for significant variables including age, race, income, insurance status, diabetes mellitus (DM), gestational DM, obesity, and multiple gestations, multivariate regression analysis indicated that HSV was associated with a higher OR for gestational hypertension (adjusted OR 1.038; 95% CI 1.004 to 1.072). However, HSV was not associated with pre-eclampsia/eclampsia (OR 1.001; 95% CI 0.968 to 1.035) in univariate regression analysis. The results of the current study suggest that HSV infection is associated with gestational hypertension but not pre-eclampsia. Given the prevalence of HSV infection and its potential association with hypertensive disorders of pregnancy, further study of HSV and hypertension in pregnancy is warranted.

Antitumor activity of paederosidic acid in human non-small cell lung cancer cells via inducing mitochondria-mediated apoptosis.

This study was aimed to investigate antitumor activity of paederosidic acid (PA) in human non-small cell lung cancer cells and explore the related mechanisms. The anti-proliferative effects of PA on A549 cells were evaluated by MTT method and the IC50 values were calculated. Furthermore, the PA-induced apoptosis in A549 cells was determined by fluorescence microscope via staining with DAPI and by flow cytometer via staining with FITC conjugated Annexin V/PI. The expression of apoptosis-related or signaling proteins was investigated by Western blotting. Our results demonstrated that PA showed significant anti-tumor activity on lung cancer in vitro; the mechanisms were involved in inducing mitochondria-mediated apoptosis via up-regulation of caspase-3, caspase-8, caspase-9, Bid, Bax, down-regulation of Bcl-2 and stimulating the release of Cyto-C from mitochondria. In addition, JNK phosphorylation levels significantly increased concomitantly with decrease in Akt phosphorylation after treatment with PA in A549 cells. However, JNK siRNA-transfected cells diminished PA-induced caspase-3, 8 and 9, Bid and Bax activaton while enhanced the Bcl-2 activation. Collectively, these results indicated that PA-induced JNK activation played an important functional role in apoptosis.

HMGB1 exacerbates experimental mouse colitis by enhancing innate lymphoid cells 3 inflammatory responses via promoted IL-23 production.

In inflammatory bowel diseases (IBD), high mobility group box 1 (HMGB1), as an endogenous inflammatory molecule, can promote inflammatory cytokines secretion by acting on TLR2/4 resulting in tissue damage. The underlying mechanisms remain unclear. Here we report a novel role of HMGB1 in controlling the maintenance and function of intestine-resident group-3 innate lymphoid cells (ILC3s) that are important innate effector cells implicated in mucosal homeostasis and IBD pathogenesis. We showed that mice treated with anti-HMGB1 Ab, or genetically deficient for TLR2-/- or TLR4-/- mice, displayed reduced intestinal inflammation. In these mice, the numbers of colonic ILC3s were significantly reduced, and the levels of IL-17 and IL-22 that can be secreted by ILC3s were also decreased in the colon tissues. Furthermore, HMGB1 promoted DCs via TLR2/4 signaling to produce IL-23, activating ILC3s to produce IL-17 and IL-22. Our data thus indicated that the HMGB1-TLR2/4-DCs-IL-23 cascade pathway enhances the functions of ILC3s to produce IL-17 and IL-22, and this signal way might play a vital role in the development of IBD.

Hormone therapy and risk of ovarian cancer in postmenopausal women: a systematic review and meta-analysis.

OBJECTIVE: Our objective was to perform a meta-analysis examining the risk of ovarian cancer with different types and regimens (continuous or sequential) of hormone therapy (HT). METHODS: PubMed, Cochrane, and Embase databases were searched until December 2014 using the terms: HT, estrogen therapy (ET), ovarian cancer, postmenopausal, and menopausal. HT was considered unopposed ET, estrogen-progestin therapy (EPT), or ET+EPT (ET followed by EPT). RESULTS: Of 180 studies identified, 12 were included in the meta-analysis. Of the 12 studies, 9 were cohort studies including 2,350,546 women and 7,549 cases of ovarian cancer, and 3 were case-control studies including a total of 1,347 cases and 2,052 controls. ET, EPT, and ET+EPT were associated with an increased risk of ovarian cancer: pooled hazard ratio (HR)/relative risk (RR) =1.37, 95% CI: 1.19 to 1.58, P<0.001; pooled HR/RR=1.27, 95% CI: 1.18 to 1.36, P<0.001; pooled HR/RR=1.55, 95% CI: 1.05 to 2.30, P=0.027, respectively. Continuous and sequential regimens were associated with an increased risk: pooled HR/RR=1.27, 95% CI: 1.04 to 1.54, P=0.018; pooled HR/RR=1.31, 95% CI: 1.08 to 1.58, P=0.006, respectively. HT was associated with an increased risk of serous ovarian cancer (pooled HR/RR=1.46, 95% CI=1.28-1.67, P<0.001), but not clear cell, endometrioid, or mucinous ovarian cancer. CONCLUSIONS: Hormone therapy, regardless of type or regimen, is associated with an increased ovarian cancer risk.

High-mobility group box 1 accelerates early acute allograft rejection via enhancing IL-17+ γδ T-cell response.

Th17 and γδ T cells are the dominant IL-17-producing cell. We previously reported that high-mobility group box 1 (HMGB1) is critical in inducing IL-17-producing alloreactive T cells during early stage of acute allograft rejection. However, the role of γδ T cells during this process and its implication in HMGB1-mediated allograft rejection are not fully understood. Here, we use a murine model of cardiac allograft transplantation to further study the role of HMGB1 and IL-17-producing γδ T cells in acute allograft rejection. It was found that the expression of HMGB1 was increased in allograft, while blockade of HMGB1 suppressed IL-17(+) γδ T-cell response and inhibited the gene transcription of IL-23 and IL-1ß. Furthermore, in vitro HMGB1 indirectly promoted the development of IL-17(+) γδ T cells by stimulating dendritic cells to produce IL-23 and IL-1ß, meanwhile depletion of γδ T cells in vivo prolonged allograft survival and reduced the level of IL-17 in serum. In conclusion, our findings inferred that increased HMGB1 expression could enhance IL-17(+) γδ T-cell response by promoting the secretion of IL-23 and IL-1ß, while IL-17(+) γδ T cells contribute to the early stage of acute allograft rejection.