White spot lesions (WSLs) are a common complication of orthodontic treatment. However, the cariogenic discrepancy in the supragingival microbiome between demineralized and non-demineralized surfaces and the influence of Candida albicans associated with WSLs remain unexplored. This study investigated the changes in supragingival microbiome of orthodontic adolescents with WSLs, encompassing both demineralized and non-demineralized sites, and explored C. albicans colonization in these patients. Supragingival plaques were collected from 29 orthodontic adolescents with WSLs (categorized into demineralized and non-demineralized groups based on the presence/absence of demineralization at sampling sites) and 23 healthy orthodontic adolescents. Supragingival microbiome composition was evaluated using 16S rRNA sequencing, and C. albicans colonization was identified using fungal culture methods. The supragingival microbiome on non-demineralized surfaces showed intermediate cariogenic potential between demineralized and healthy states, but closer to the demineralized state. C. albicans exhibited a propensity for colonization in WSLs patients without site-specificity. C. albicans influenced bacterial composition, with Streptococcus mutans significantly enriched on the demineralized surfaces of C. albicans-positive patients. In orthodontic adolescents with WSLs, non-demineralized surfaces showed microbiome shifts, necessitating interventions to promote a healthy microbiome. C. albicans can impact microbiome composition and potentially contribute to WSLs pathogenesis.

IntroductionStreptococcus mutans and Candida albicans are common pathogenic organisms from the oral microbial community, and are associated with the pathogenesis of caries. We investigated the repressive effects of arginine on the cross-kingdom interactions and synergistic cariogenicity between S. mutans and C. albicans.MethodsThe effect of arginine on the growth of S. mutans and C. albicans in the planktonic state was reflected by analyzing growth curves and pH measurements. Biofilm biomass was measured using growth curves, crystal violet staining, and colony-forming unit measurements; fluorescence in situ hybridization indicated the physical relationship between S. mutans and C. albicans in biofilms. The cariogenic properties of dual-species biofilms were analyzed through extracellular polysaccharide and lactic acid production assessments.ResultsArginine inhibited the planktonic growth and biofilm formation of S. mutans and C. albicans, with reduced biofilm formation, biomass, and physical adhesion between strains. Moreover, arginine suppressed the production of extracellular polysaccharides and lactic acid. In addition, short-term arginine treatment effectively inhibited the growth of S. mutans and C. albicans.ConclusionL-Arginine inhibited both mono- and dual-species growth of S. mutans and C. albicans. Thus, L-arginine may serve as a novel approach to inhibit the cross-kingdom interactions and synergistic cariogenicity of S. mutans and C. albicans.

Introduction Gingivitis is a prevalent complication in adolescents undergoing fixed orthodontic treatments. However, changes in the supragingival microbiome associated with gingivitis and the impact of Candida albicans remain elusive. Therefore, we investigated supragingival microbiome discrepancy and C. albicans colonization in adolescent orthodontic patients with gingivitis.Methods Dental plaques were collected from 30 gingivitis patients and 24 healthy adolescents, all undergoing fixed orthodontic treatment. The supragingival microbiome composition was analyzed using 16S rRNA sequencing. C. albicans colonization was determined using fungal culture and real-time quantitative polymerase chain reaction.Results Our analysis revealed significantly heightened microbial diversity in the Gingivitis group. Notably, patients with gingivitis exhibited an enrichment of periodontal pathogens, such as Saccharibacteria (TM7) [G-1], Selenomonas, Actinomyces dentalis, and Selenomonas sputigena. Additionally, 33% of the gingivitis patients tested positive for C. albicans, exhibiting significantly elevated levels of absolute abundance, while all healthy patients tested negative. Significant differences in microbial composition were also noted between C. albicans-positive and -negative samples in the Gingivitis group.Conclusion Significant disparities were observed in the supragingival microbiome of adolescent orthodontic patients with and without gingivitis. The presence of C. albicans in the supragingival plaque may alter the microbiome composition and potentially contribute to gingivitis pathogenesis.

Objectives: This study aimed to evaluate the molecular epidemiology and antimicrobial resistance of invasive pneumococcal isolates from children in Shenzhen, China, in the early stage of the pneumococcal 13-valent conjugated vaccine (PCV-13) era from 2018 to 2020. Methods: Invasive pneumococcal strains were isolated from hospitalized children with invasive pneumococcal diseases (IPDs) from January 2018 to December 2020. The serotype identification, multilocus sequence typing (MLST), and antibiotic susceptibility tests were performed on all culture -confirmed strains. Results: Sixty-four invasive strains were isolated mainly from blood (70.3%). Prevalent serotypes were 23F (28.1%), 14 (18.8%), 19F (15.6%), 6A/B (14.1%), and 19A (12.5%), with a serotype coverage rate of 96.9% for PCV13. The most common sequence types (STs) were ST876 (17.1%), ST271 (10.9%), and ST320 (7.8%). Half of the strains were grouped in clonal complexes (CCs): CC271 (21.9%), CC876 (20.3%), and CC90 (14.1%). Meningitis isolates showed a higher resistance rate (90.9% and 45.5%) to penicillin and ceftriaxone than the rate (3.8% and 9.4%) of non -meningitis isolates. The resistance rates for penicillin (oral), cefuroxime, and erythromycin were 53.13%, 73.4%, and 96.9%, respectively. The dual ermB and mefA genotype was found in 81.3% of erythromycin -resistant strains. The elevated minimum inhibitory concentration (MIC) of beta-lactam antibiotics and dual -genotype macrolide resistance were related mainly to three major serotype-CC combinations: 19F-CC271, 19A-CC271, and 14-CC876. Conclusion: Invasive pneumococcus with elevated MICs of beta-lactams and increased dual ermB and mefA genotype macrolide resistance were alarming. Expanded PCV13 vaccination is expected to reduce the burden of paediatric IPD and to combat antibiotic -resistant pneumococcus in Shenzhen. (c) 2024 Published by Elsevier Ltd on behalf of International Society for Antimicrobial Chemotherapy. This is an open access article under the CC BY -NC -ND license ( http://creativecommons.org/licenses/by-nc-nd/4.0/ )

Purpose: This study aimed to investigate the diagnostic and prognostic values of neuropilin-1 (NRP-1) in triple-negative breast cancer (TNBC) and analyze its immune function in the tumor microenvironment. Methods: Based on The Cancer Genome Atlas (TCGA), Gene Expression Omnibus, Genotype Tissue Expression, Immune Cell Abundance Identifier (ImmuCellAI), Reactome, and Genomics of Drug Sensitivity in Cancer databases, the cancer tissues from 50 patients with TNBC and corresponding adjacent noncancerous tissues from 10 patients (tissue microarrays were purchased from Shanghai Xinchao Biotechnology Co., Ltd.) were collected for validation. Bioinformatics combined with immunohistochemistry was used to analyze the relationship among NRP-1 expression, prognosis, tumor immune cell infiltration, immune genes, and drug resistance so as to investigate the role of NRP-1 in the development of TNBC. Results: A significant difference in NRP-1 gene expression was found between the cancerous and noncancerous tissues (p-value < 0.05); NRP-1 expression was high in carcinoma. No significant correlation was found between NRP-1 protein expression levels and each stage in the TCGA database. Prognostic expression survival analysis showed that the survival probability of patients with high NRP-1 expression was significantly lower than that of patients with low NRP-1 expression (p-value < 0.05), suggesting that the gene might be a pro-oncogene. The data from 50 clinical samples also confirmed that the NRP-1 expression was significantly higher in triplenegative breast cancer (TNBC) tissues than in adjacent noncancerous tissues. The NRP-1 expression significantly correlated with the tumor diameter and pathological grade (p-value < 0.05), but not with age, stage, and ki67 (p-value > 0.05). The Kaplan-Meier survival curves suggested that the median overall survival was significantly shorter in patients with high NRP-1 expression than in those with low NRP-1 expression (13.6 months vs 15.2 months, p-value < 0.05). The 300 genes most significantly positively associated with this gene were selected for Gene Ontology (including Biological Process, Molecular Function, and Cellular Component groups) and Kyoto Encyclopedia of Genes and Genomics enrichment analysis. The findings showed that NRP-1 was involved in immune regulation in TNBC. In addition, the NRP-1 expression in TNBC positively correlated with a variety of immune cells and checkpoints. Conclusion: NRP-1 can be used as a potential biomarker and therapeutic target in TNBC.

Objective:To investigate the clinical characteristics, laboratory characteristics and genetic diagnosis of aromatic L-amino acid decarboxylase deficiency (AADCD), and to improve the understanding of this disease.Methods:Four children diagnosed with AADCD from the Department of Neurology, Beijing Children′s Hospital Affiliated to Capital Medical University from August 2016 to June 2020 were collected, and their clinical manifestations, laboratory and imaging data, and genetic test results were retrospectively analyzed.Results:All the 4 cases were diagnosed in early infancy, with the first symptom of feeding difficulties. They developed paroxysmal dyspraxia accompanied by eye movement crisis, movement regression, hypotonia, growth retardation, sleep disorders and autonomic nervous symptoms such as ptosis, excessive sweating and nasal congestion at the age of 2-4 months, respectively. The 4 children were siblings from 2 families with healthy parents. The dihydroxyphenylalanine decarboxylase ( DDC) gene mutations in cases 1 and 2 were derived from the maternal missense mutation c.1040G>A(P.RG347gln), and from the paternal deletion of exons 11 and 12, respectively. The DDC gene mutation in case 3 was derived from the maternal mutation c.419G>A(p.G140E) and the paternal mutation c.1375C>T(p.H459Y), respectively. Case 4 did not undergo genetic testing. Blood amino acid and acylcarnitine profiles and urine organic acid analyses were performed in 3 cases, and no specific abnormalities were found. In case 3, the results of 3-O-methyldopa (3-OMD) screening by blood dry filter paper increased significantly. Cerebrospinal fluid neurotransmitter detection results showed that the concentrations of 3-methoxy-4-hydroxyphenyldiol, vanillic acid and 5-hydroxyindoleacetic acid were significantly decreased, while the levels of 5-hydroxytryptophan and 3-OMD were increased in case 3. Blood aromatic L-amino acid decarboxylase (AADC) activity decreased significantly in case 3. Cranial magnetic resonance imaging (MRI) and electroencephalogram (EEG) examinations were performed in cases 1, 3, and 4, among which the cranial MRI in case 1 was normal, while the cranial MRI in cases 3 and 4 suggested that myelination was slightly backward. The EEG was normal in all the 3 cases. Cases 1 and 2 died of pneumonia and respiratory failure at the age of 1 year and 10 months. Case 3 was given clonazepam, benxel hydrochloride tablets and vitamin B6 tablets orally after diagnosis at the age of 4 months, and then treated with selegiline hydrochloride tablets and pramexol hydrochloride tablets. At the follow-up of 1 year and 6 months, the frequency of eye movement crisis and movement disorder was reduced, sleep was improved and autonomic nervous symptoms were alleviated, but there was no improvement in developmental delay. Case 4 was diagnosed with cerebral palsy and epilepsy, but failed various antiepileptic drugs and rehabilitation training, and died at the age of 10 due to heart failure and kidney failure. Conclusions:The clinical manifestations of AADCD are complicated and the misdiagnosis rate is high. Infants with early-onset hypotonia, developmental retardation, eye movement crisis, and movement disorders should be screened with dry filter paper as soon as possible for 3-OMD level, and suspicious cases should be diagnosed by cerebrospinal fluid neurotransmitter detection, plasma AADC activity determination, and gene examination. Early diagnosis of AADCD in children and gene mutation carriers can guide treatment and provide genetic counseling to reduce the incidence of the offspring.

Neuropilin 1 (NRP1) is a transmembrane glycoprotein, nontyrosine kinase receptor that plays an important role in axonal growth and angiogenesis in the nervous system. Although currently more and more studies have shown that NRP1 plays an important role in some cancers, no systematic pan-cancer analysis of NRP-1 has been performed to date. Therefore, we aimed to investigate the associated immune function and prognostic value of NRP1 in 33 tumors of various cancer types. In this study, based on The Cancer Genome Atlas, Cancer Cell Line Encyclopedia, Genotype Tissue Expression, cBioportal for cancer genomics, and Human Protein Atlas (HPA databases), various bioinformatics analysis methods were used to investigate the potential carcinogenic effects of NRP1 activation, pan-cancer analysis of NRP1 expression, and the relationship between NRP1 expression and prognosis indicators including overall survival, disease-specific survival, disease-free interval, and progression-free interval, tumor mutational burden (TMB), and microsatellite instability (MSI). The results showed that NRP1 was highly expressed in most tumors. In addition, NRP1 was found to be positively or negatively correlated with the prognosis of different tumors. Also, the expression of NRP1 was associated with TMB and MSI in in 27 and 21 different types of tumors, respectively, and with DNA methylation in almost all the various types of tumors. The expression of the NRP1 gene was negatively correlated with the infiltration levels of most immune cells. In addition, the correlation between the level of immune cell infiltration and NRP1 expression varied according to immune cell subtype. Our study suggests that NRP1 plays an important role in tumor development and tumor immunity and could potentially be used as a prognostic indicator in a variety of malignancies.

Aim To assess the etiologies and adverse outcomes of infantile acquired hydrocephalus and predict prognosis. Methods A total of 129 infants diagnosed with acquired hydrocephalus were recruited from 2008 to 2021. Adverse outcomes included death and significant neurodevelopmental impairment which was defined as Bayley Scales of Infant and Toddler Development III score < 70, cerebral palsy, visual or hearing impairment, and epilepsy. Chi-squared was used to evaluate the prognostic factors of adverse outcomes. A receiver operating characteristic curve was calculated to determine the cutoff value. Results Of 113 patients with outcome data, 55 patients (48.7%) had adverse outcomes. Late surgical intervention time (13 days) and severe ventricular dilation were associated with adverse outcomes. The combination of surgical intervention time and cranial ultrasonography (cUS) indices was a better predictive marker compared with any of them (surgical intervention time, P = 0.05; cUS indices, P = 0.002). Post-hemorrhage (54/113, 48%), post-meningitis (28/113, 25%), and hydrocephalus arising from both hemorrhage and meningitis (17/113, 15%) accounted for a large proportion of the etiologies in our study. Hydrocephalus occurs secondary to post-hemorrhage and had a favorable outcome compared with other etiologies in both preterm and term groups. A significant difference in adverse outcomes between the inherited error of metabolism as a cause and other etiologies (P = 0.02). Conclusion Late surgical treatment times and severe ventricular dilation can predict adverse outcomes in infants with acquired hydrocephalus. It is crucial to identify the causes of acquired hydrocephalus to predict the adverse outcomes. Research into measures of improving adverse outcomes following infantile acquired hydrocephalus is urgently necessary.

White spot lesions (WSLs) are common enamel infectious diseases in fixed orthodontic treatment, which might attribute to the dysbiosis of oral microbiome. However, the correlation of Candida albicans with oral bacteriome in WSLs still remains unrevealed. This study investigated the carriage of C. albicans and how it shaped the bacterial community in disease or healthy supragingival plaque, to explore the potential role of interkingdom interaction in orthodontic WSLs. In this study, 31 patients with WSLs (WSLs) and 23 healthy patients (Health) undergoing fixed orthodontic treatment were enrolled. The supragingival microbiota in both groups were determined using 16S rRNA gene sequencing. Colonization and abundance of C. albicans in the plaque were determined via culture-dependent and -independent methods. Among WSLs patients, the correlation of C. albicans and bacteriome was analyzed under QIIME2-based bioinformatics and Spearman’s correlation coefficient. The raw reads were deposited into the NCBI Sequence Read Archive (SRA) database (Accession Number: SRP404186). Significant differences in microbial diversity as well as composition were observed between WSLs and Health groups. Leptotrichia remarkably enriched in the WSLs group, while Neisseria and Cardiobacterium significantly enriched in the Health group. In addition, 45% of WSLs patients were C. albicans carriers but none in patients without WSLs. Among all WSLs patients, beta diversity and microbial composition were distinguished between C. albicans carriers and non-carriers. In C. albicans carriers, Corynebacterium matruchotii and Streptococcus mutans significantly enriched whereas Saccharibacteria_TM7_G-1 significantly depleted. The abundance of C. albicans was positively associated with bacteria such as Streptococcus mutans, while the negative correlation was detected between C. albicans and several bacteria such as Cardiobacterium hominis and Streptococcus sanguinis. Our study elucidated the distinguished supragingival plaque microbiome between orthodontic patients with and without WSLs. C. albicans frequently existed and enriched in orthodontic derived WSLs. The carriage of C. albicans shape plaque bacterial community in demineralized lesions and might play roles in WSLs pathogenesis.

The objective of this study was to develop a novel nanostructured resin composite containing yttrium aluminum garnet (Y3Al5O12, YAG) nanoparticles specialized for clear aligner attachments with enhanced fluidity and relatively high physical and aging properties. After the silanization of YAG nanoparticles, their Fourier-transform infrared (FT–IR) and thermogravimetric (TG) analyses were performed followed by incorporation into a traditional Si-based resin at different mass fractions. The flexural strength, compressive strength, Vickers microhardness, fluidity, and volumetric shrinkage of the produced resins were determinedp. The obtained FT–IR and TG analysis data revealed that γ-methacryloxypropyltrimethoxysilane silane coupling agent was successfully grafted onto the surface of YAG nanoparticles, which enabled their use as inorganic fillers. A composite comprising 9 wt.% YAG nanoparticles exhibited a flexural strength and Vickers hardness comparable to those of a commercial resin and relatively high fluidity. Compared with the silicone resin containing traditional Bis-GMA/TEGDMA (50:50 w/w) organic monomers, adding 9 wt.% YAG increased its Vickers hardness and fluidity and reduced the polymerization shrinkage, which enabled more accurate shape restoration of the clear aligner attachments, thus accurately control tooth movement and improve orthodontic efficiency. Overall, the 9 wt.% YAG resin composite can potentially restore the shape of clear aligner attachments.

OBJECTIVE:To analyze the clinical phenotype and genetic variants of a child with X-linked mental retardation caused by IQSEC2 gene mutation, and provide reference for the diagnosis of the disease.METHODS:The child was subjected to next generation sequencing (NGS), and the diagnosis was made by taking consideration of her clinical characteristics.RESULTS:The child has presented with global developmental delay, particularly in fine motor skill and language development, in addition with intellectual disability. Genetic testing revealed that she has harbored a heterozygous c.1861dup variant of the IQSEC2 gene, which was not detected in either parent.CONCLUSION:The de novo c.186ldup variant of the IQSEC2 gene probably underlay the X-linked mental retardation in this child. Above finding has, expanded the spectrum of IQSEC2 gene mutations and provide a basis for the diagnosis of similar cases.

妊娠合并子宫肌瘤孕妇的剖宫产率高达50%。为避免严重产后出血、弥漫性血管内凝血和子宫切除术等，传统上并不主张在剖宫产术时行子宫肌瘤剔除术。但近些年不断有研究表明，剖宫产术同时行子宫肌瘤剔除术并不增加产后出血和其他术后并发症的风险，对于有指征的子宫肌瘤孕妇，由经验丰富的医师行剖宫产+子宫肌瘤剔除术是安全可行的。目前，对于不同特征的子宫肌瘤，剖宫产术时是否剔除尚无统一标准。.

BackgroundAromatic amino acid decarboxylase (AADC) deficiency is a rare, autosomal recessive neurometabolic disorder with heterogeneous phenotype, including hypotonia, movement disorders, autonomic dysfunction, and developmental delay. Here, we reported a Chinese patient with AADCD who was initially misdiagnosed with epilepsy.Case presentationThe proband was a 4-month-old Chinese girl, representing hypotonia, episodes of oculogyric crises with dystonia, and delayed developmental milestones. The patient was first misdiagnosed with epilepsy because of the similarity between episodes of oculogyric crisis and epileptic seizure. The accurate diagnosis of AADCD was established through analysis of neurotransmitters in cerebrospinal fluid (CSF). The genetic test confirmed the patient carried novel compound heterozygous mutations in the DDC gene:c.419G>A and c.1375C>T.ConclusionThis study reported a patient with AADCD who was initially misdiagnosed as epilepsy. Two novel missense mutations in the DDC gene were identified from the patient and her family. Little infants with epileptic-like attacks should consider AADCD. An accurate diagnosis of AADCD is essential for drug choice and patient management.

e16090 Background: First-line chemotherapy for advanced human epidermal growth factor receptor 2 (HER2)-negative gastric/gastroesophageal junction (G/GEJ) adenocarcinoma results in median overall survival (mOS) < 1 year. The programmed death (PD)-1 inhibitor provided superior OS in advanced G/GEJ adenocarcinoma combind with chemotherapy. However, the continuous explore about PD-1 inhibitors of first-line treatment with G/GEJ adenocarcinoma patients is promising. Camrelizumab, an anti-PD-1 monoclonal antibody, has been shown to have synergistic antitumor effects in the treatment of G/GEJ adenocarcinoma patients. We aimed to evaluate the safety and efficacy of camrelizumab combined with SOX in the first-line treatment of advanced G/GEJ adenocarcinoma. Methods: In this study (ChiCTR2000029691), eligible patients were diagnosed as unresectable advanced, postoperative recurrent ormetastatic, HER2-negative G/GEJ adenocarcinoma, and treatment-naive with chemotherapy, VEGFR2 inhibitors or PD-1/PD-L1 inhibitors. Patients received camrelizumab (200 mg, I.V., d1) and SOX regimen (oxaliplatin, 130 mg/m2, d1; S-1, 20mg/m2, bid, d1-14) every 3 weeks, until disease progression, intolerable toxicities, or physician/patient withdrawal. The safety and efficacy were assessed by investigators per CTCAE v5.0 and RECIST v1.1, respectively. The primary endpoint was progress free survival (PFS), and the secondary endpoints were overall survival (OS), objective response rate (ORR), and disease control rate (DCR). Results: From March 30, 2020 to March 18, 2021, 27 patients had been enrolled to receive therpy with camrelizumab and SOX regimen. The patients were characterized with a median age of 60 years (range 26-79), 88.9% males and 11.1% females, 40.7% GEJ adenocarcinoma, 88.9% lymph node metastasis, 25.9% liver metastases, and 18.5% of patients had a history of tumor-related surgery. As of Nov 2, 2021, with a median follow-up of 8.8 months (range, 0.9-16.8), safety and efficacy were assessed in 20 evaluable patients, with overall response of 8 partial response (PR) and 9 stable disease (SD). Confirmed ORR and DCR were 40.0% (95% CI, 20.0%-63.6%) and 85.0% (95% CI, 61.1%-96.0%), respectively. The median PFS and OS were 12.7 months (95% CI, 4.9-20.5) and 16.8 months (95% CI, 3.5-30.0), respectively. Grade 3-4 treatment-related adverse events occurred in 18.5% of patients, with anemia and neutropenia ranking the most frequent. No new safety signals was identified. Conclusions: Camrelizumab combined with SOX was well tolerated and demonstrated encouraging efficacy for previously untreated with chemotherapy, VEGFR2 inhibitors or PD-1/PD-L1 inhibitors, unresectable advanced or metastatic, HER2-negative G/GEJ adenocarcinoma. Clinical trial information: ChiCTR2000029691.

目的 探讨阿帕替尼联合培美曲塞在铂耐药复发性卵巢癌患者中的疗效.方法 收集2018年4月-2021年5月在本院就诊的30例铂耐药复发性卵巢癌患者的临床资料,分析阿帕替尼联合培美曲塞对晚期铂耐药复发性卵巢癌患者的疗效和不良反应等相关指标.结果 本研究最终入组30例患者,末次随访时间为2021年11月30日,客观缓解率为36.7％(11/30),疾病控制率为86.7％(26/30),中位无进展生存时间为9.2月(95％CI为6.3～12.1月).发生率较高的不良反应集中在1～2级,包括口腔黏膜炎为14例(46.7％)、高血压为14例(46.7％)、乏力为11例(36.7％)、手足综合征为5例(16.7％)、恶心呕吐5例(16.7％)、腹泻4例(13.3％)等;高级别不良反应发生2例,包括3级口腔黏膜炎1例、3级手足综合征1例.所有患者的不良反应经药物治疗后控制良好或无须特别处理.结论 阿帕替尼联合培美曲塞对铂耐药复发性卵巢癌患者疗效满意,且安全性可控.

目的 观察白蛋白结合型紫杉醇联合铂类化疗药物对比吉西他滨联合铂类化疗药物一线治疗中晚期肺鳞癌患者的安全性和有效性.方法 选择2016年6月至2021年3月徐州医科大学附属医院收治的68例存在手术禁忌证的中晚期肺鳞癌患者作为研究对象,根据化疗方案不同,分为白蛋白结合型紫杉醇联合铂类组(NAB-P组)和吉西他滨联合铂类组(GEM组),分析两组患者的临床疗效及不良反应.结果 NAB-P组的客观缓解率为30.56％,GEM组的客观缓解率为28.13％,两组比较差异无统计学意义(P>0.05);NAB-P组的疾病控制率为86.11％,GEM组的疾病控制率为65.63％,两组比较差异有统计学意义(P<0.05);不良反应方面,NAB-P组的周围神经毒性、脱发、黏膜炎发生率高于GEM组(P<0.05);GEM组血小板降低的发生率高于NAB-P组(P<0.05);NAB-P组的无进展生存时间较GEM组长(P<0.05),但1年生存率两组差异无统计学意义(P>0.05).结论 白蛋白结合型紫杉醇联合铂类药物一线治疗中晚期肺鳞癌比吉西他滨联合铂类药物在疗效上更有优势,且NAB-P组的不良反应轻,值得临床进一步推广.

OBJECTIVE:To evaluate the changes of uterine leiomyoma size during pregnancy and determine the factors influencing it. METHODS:A prospective study was conducted from June 2016 to June 2018. Women with pregnancies complicated by leiomyoma were recruited. Ultrasound examinations were conducted to measure the size of leiomyoma during 6-7, 11-14, 22-24, 28-34 weeks of pregnancy and before delivery. The clinical characteristics and delivery details of the pregnant women were collected. Changes in leiomyoma size during different gestation periods and the influencing factors were analyzed. RESULTS:Leiomyoma size commonly increased before 22-24 weeks of pregnancy and the fastest growth occurred before 11-14 weeks. From 22-24 weeks to the date of delivery, the size of leiomyoma remained unchanged. The initial size of the leiomyoma showed negative correlation with the changes in leiomyoma diameters during pregnancy. Pre-pregnancy body mass index, fetus number, leiomyoma location, and parity were positively correlated with the size changes in leiomyoma from 22-24 to 28-34 weeks of pregnancy. CONCLUSION:Before 22-24 weeks of pregnancy, the size of the leiomyoma was gestation-dependent, which increases with gestational weeks. The fastest growth rate was before 11-14 weeks. The growth of leiomyoma is affected by multiple factors, and different factors can play different roles during different periods of the pregnancy.

Objective: To investigate the etiology of epilepsy onset before 6 months old and improve clinical understanding. Methods: The medical history, electroencephalogram, brain imaging, genetic examination and other clinical data of 340 patients who were diagnosed with epilepsy with onset under 6 months of age and were hospitalized in the Department of Neurology, Beijing Children's Hospital, Capital Medical University between January 2017 and December 2018 were retrospectively analyzed. Rank sum test was used to compare the ages of onset of different etiologic groups. Results: Of the 340 patients, 196 were males and 144 were females. The age of onset was 90.5 (48.0, 135.5) days. In the 250 (73.5%) underwent genetic test, 103 (41.2%) had pathogenic or likely pathogenic variants, involving 43 single gene variants and 2 chromosomal abnormalities. Seventy-nine patients (23.2%) had genetic etiology, 66 (19.4%) had structural etiology, 19 (5.6%) had metabolic etiology, 13 (3.8%) had multiple etiologies, and 163 (47.9%) had unknown etiology. In the 79 cases with genetic etiology, 30 single gene variants were detected, including 19 cases of PRRT2, 10 cases of KCNQ2, 7 cases of SCN1A, 6 cases of SCN2A, 6 cases of STXBP1, 5 cases of CDKL5, 2 cases of ARX, and 1 case of each of 23 gene variants. Two cases had chromosomal abnormalities which were 21-trisomy and 16p11.2 microdeletion syndrome respectively. Among the 66 cases with structural etiologies, 37 cases had acquired factors such as perinatal brain injury, 28 cases had congenital factors such as cortical malformation and 1 case was perinatal brain injury combined megalencephaly. The onset age of genetic etiology was 95 (26, 128) days, that of structural etiology was 90 (58, 30) days, and that of metabolic etiology was 57 (30, 90) days. The onset age of metabolic etiology was earlier than that of structural etiology (U=436.500, P=0.044). Conclusions: Genetic etiology is the most common defined etiology of infants with early-onset epilepsy aged 0-6 months, and there are certain differences in the age of onset between different etiologies. Proper application of genetic test is helpful to identify the etiology and guide treatment.

目的 研究在模拟口腔环境下,热处理、水和热等物理、化学因素对常用的正畸热塑性材料的成分、结构和力学性能的影响,从而认识材料的老化变化,为临床上正确选择和使用隐形矫治器,更精确的预测和控制牙齿移动提供一定的指导作用.方法 将Erkodur材料用压膜机进行热软化处理(160℃),浸泡在人工唾液中,置于37℃恒温箱中老化,分别于浸泡12 h、3天、2周和4周后,测试观察其力学性能、分子结构(红外光谱,FTIR)、表面形貌和内部结构以及化学成分的变化.结果 热处理后,材料的化学组成和一级结构没有发生明显的变化,但力学性能下降.37℃人工唾液浸泡后(最长4周),材料的一级结构仍没有明显的改变,但力学性能提升.结论 模拟口腔环境并不改变Erkodur材料的一级结构,但其高级结构可能由于吸水膨胀而存在一定程度上的破损.因此,热塑性材料力学性能的变化主要来源于高分子聚合物的这些高级结构的改变.