Volume 133 · Issue 16 · 2020

Surgical left atrial appendage occlusion (SLAAO) may be associated with a lower risk of thromboembolism in patients with atrial fibrillation undergoing cardiac surgery. However, evidence regarding the effectiveness of SLAAO in patients undergoing mechanical heart valve replacement (MHVR) is lacking. Therefore, we aimed to evaluate the association between SLAAO and the cardiovascular outcomes in patients with atrial fibrillation undergoing MHVR.

We retrospectively analyzed data for 497 patients with atrial fibrillation; 27.6% of the patients underwent SLAAO, and the remainder of the patients did not (No-SLAAO group). The primary outcome was a composite of ischemic stroke, systemic embolism, and all-cause mortality. Cumulative event-free survival rates were estimated using Kaplan-Meier curves, and we performed multivariate Cox analyses to evaluate the association between SLAAO and outcomes. We used one-to-one propensity score matching to balance patients’ baseline characteristics, and analyzed 120 matching pairs.

Five patients died within 30 days postoperatively, and there were no significant differences between the two groups regarding in-hospital complications (all P > 0.05). After a median follow-up of 14 months, 14 primary events occurred. Kaplan-Meier curves showed no difference in the cumulative incidence of freedom from the primary outcome (log-rank P = 0.830), hemorrhagic events (log-rank P = 0.870), and the secondary outcome (log-rank P = 0.730), between the two groups. Multivariable Cox proportional hazards regression analysis showed no association between SLAAO and any outcome (all P > 0.05). After propensity score matching, cardiopulmonary bypass time and aortic cross-clamp time, and the postoperative length of stay were significantly longer in the SLAAO group (all P < 0.05); results were similar to the unadjusted analyses.

Concomitant SLAAO and MHVR was associated with longer length of stay, and cardiopulmonary bypass time and aortic cross-clamp time, but was not associated with additional protective effects against thromboembolic events and mortality during the 14-month follow-up.

Total and differential white blood cell counts are important for the diagnostic evaluation of suspected diseases. To facilitate the interpretation of total and differential white blood cell counts in pediatric patients, the present study investigated age-dependent changes in total and differential white blood cell counts in healthy reference children.

Data were obtained from the Pediatric Reference Intervals in China study (PRINCE), which aims to establish and verify pediatric reference intervals for Chinese children based on a nationwide multicenter cross-sectional study from January 2017 to December 2018. Quantile curves were calculated using the generalized additive models for location, shape, and scale method. The 2.5th, 50th, and 97.5th quantile curves were calculated for both total and differential white blood counts. Percents of stacked area charts were used to demonstrate the proportions of differential white blood cells. All statistical analyses were performed using R software.

Both 50th and 97.5th quantiles of total white blood cell count and monocyte count were highest at birth, then rapidly decreased in the first 6 months of life; relatively slow reduction continued until 2 years of age. The lymphocyte count was low during infancy and increased to its highest level at 6 months of age; it then exhibited moderate and continuous reduction until approximately 9 years of age. The pattern of neutrophil count changed with age in a manner opposite to that of lymphocyte count. Besides, there were two inter-sections of lymphocyte count and neutrophil count during infancy and at approximately 5 years of age, based on locally weighted regression (LOESS) analysis. There were no apparent age-related changes in eosinophil or basophil counts.

These data regarding age-related changes in total and differential white blood cell counts can be used to assess the health of pediatric patients and guide clinical decisions.

There is limited evidence of the effects of local anesthesia (LA) on outcomes of non-surgical periodontal treatment (NSPT), in particular among the Chinese. This retrospective cohort study aimed to evaluate the effects of LA on short-term treatment outcomes of NSPT and to determine under what circumstances LA should be prescribed to improve these outcomes.

Data from periodontal examinations of 3980 patients were used. The data were from 3-month re-evaluation records of an electronic periodontal charting record system in the Department of Periodontology of Peking University School and Hospital of Stomatology from June 2008 to January 2015. Descriptive analyses included changes in probing depth (PD) and the Mazza bleeding index (BI). Two-level (patient and tooth) logistic regression models and three-level (patient, tooth, and site) linear regression models were constructed to analyze the influence of LA on PD for all teeth/sites and teeth/sites with an initial PD ≥ 5 mm. Decreases in PD and BI at sites under LA using the initial PD were also compared.

A significantly higher mean decrease in PD after NSPT was found in the LA group than in the no local anesthesia (NLA) group (0.98 vs. 0.54 mm, t = 24.12, P < 0.001). A significantly higher probability of decreases was found in the LA group in BI (percentages of teeth with BI > 1 and BI > 2) for all teeth (16.7% vs. 13.8%, t=3.75, P < 0.001; 34.7% vs. 28.1%, t = 6.73, P < 0.001) and PD for teeth with PD ≥ 5 mm (32.3% vs. 17.3%, t = 28.48, P < 0.001). The difference in PD between the LA and NLA groups increased as the initial PD increased. The difference between the two groups was 0.12 to 0.22 mm for sites with a baseline PD < 7 mm; however, it increased to 0.41 to 1.37 mm for sites with a baseline PD ≥ 7 mm.

LA improved the decrease in PD after NSPT. Root debridement at sites with initial PD ≥ 7 mm should be performed under routine LA.

Due to airway remodeling and emphysematous destruction in the lung, the two classical clinical phenotypes of chronic obstructive pulmonary disease (COPD) are emphysema and bronchiolitis. The present study was designed to investigate the levels of small airway immunoglobulin A (IgA) in COPD with "emphysema phenotype." The study also evaluated the associations between the small airway IgA levels and the severity of disease by the extent of emphysema versus airflow limitation.

Thirty patients (20 with COPD and ten healthy smokers) undergoing lung resection surgery for a solitary peripheral nodule were included. The study was conducted from January 2015 to December 2018 in the Shanxi Dayi Hospital. The presence of small airway IgA expression was determined in the lung by immunohistochemistry. In vivo, Wistar rats were exposed to silica by intratracheal instillation. Rats were sacrificed at 15 and 30 days after exposure of silica (n = 10 for each group). We also evaluated airway IgA from rats.

Small airway secretory IgA (sIgA), dimeric IgA (dIgA), and dIgA/sIgA of Global Initiative for Chronic Obstructive Lung Disease grade 1-2 COPD patients showed no difference compared with smoking control subjects (5.15±1.53 vs. 6.03±0.85; 1.94±0.66 vs. 1.67±0.04; 41.69±21.02 vs. 28.44±9.45, all P > 0.05). dIgA/sIgA level in the lung of COPD patients with emphysema showed higher levels than that of COPD patients without emphysema (51.89±24.81 vs. 31.49±9.28, P=0.03). The percentage of low-attenuation area below 950 Hounsfield units was positively correlated with dIgA/sIgA levels (r=0.45, P=0.047), but not associated with the severity of disease by spirometric measurements (forced expiratory volume in the first second %pred, P>0.05). Likewise, in the rat study, significant differences in sIgA, dIgA, dIgA/sIgA, mean linear intercept, mean alveoli number, and mean airway thickness of bronchioles (VV airway, all P < 0.01) were only observed between control rats and those exposed for 30 days. However, in the group exposed for 15 days, although the VV airway was higher than that in normal rats (27.61±2.26 vs. 20.39±1.99, P<0.01), there were no significant differences in IgA and emphysema parameters between the two groups (all P>0.05).

Airway IgA concentrations in mild and moderate COPD patients are directly associated with the severity of COPD with "emphysema phenotype" preceding severe airway limitation. This finding suggests that small airway IgA might play an important role in the pathophysiology of COPD, especially emphysema phenotype.

Uveal melanoma (UM) is the most common primary intraocular malignancy in adults. It has been demonstrated that microRNA-145 (miR-145) is correlated with the progression of various cancers by regulating the expression of multiple target genes, especially a number of genes that regulate angiogenesis and proliferation. However, the underlying mechanisms of miR-145 in tumor angiogenesis of UM are still not well illustrated. Thus, we aimed to explore the potential target genes or pathways regulated by miR-145 in UM and the effect of miR-145 on invasion and angiogenesis.

Totally, 24 choroid samples were collected in our study, including 12 UM samples and 12 normal uveal tissues. The expression of neuroblastoma RAS viral oncogene homolog (N-RAS), phosphorylated protein kinase B (p-AKT), and vascular endothelial growth factor (VEGF) in UM tissues and normal uveal tissues was analyzed using Western blotting analysis. Lentivirus expression system was used to construct MUM-2B and OCM-1 cell lines with stable overexpression of miR-145. Transwell and endothelial cell tube formation assay were used to measure the effects of miR-145 on the invasion and angiogenesis of UM in vitro. The downstream target genes of miR-145 were predicted by bioinformatics and confirmed using a luciferase assay. BALB/c nude mice models were established to investigate the mechanisms of miR-145 on tumor growth and angiogenesis in vivo. Group data comparisons were performed using analysis of Student’s t test. A two-tailed P < 0.05 was considered as statistically significant.

The results of Western blotting analysis indicated that the expressions of N-RAS (1.10 ± 0.35 vs. 0.41 ± 0.36, t = 3.997, P = 0.012), p-AKT (1.16 ± 0.22 vs. 0.57 ± 0.03, t = 7.05, P = 0.001), and VEGF (0.97 ± 0.32 vs. 0.45 ± 0.21, t = 3.314, P = 0.008) in UM tumor tissues were significantly higher than those in normal uveal tissue. Luciferase assay demonstrated N-RAS and VEGF as downstream targets of miR-145. Moreover, tube formation assay revealed that miR-145-transfected human microvascular endothelial cell line formed shorter tube length (36.10 ± 1.51 mm vs. 42.91 ± 0.94 mm, t = 6.603, P = 0.003) and less branch points (350.00 ± 19.97 vs. 406.67 ± 17.62, t = 3.685, P = 0.021) as compared with controls. In addition, the numbers of invaded MUM-2B and OCM-1 cells with miR-145 overexpression were significantly lower than the controls (35.7 ± 3.3 vs. 279.1 ± 4.9, t = 273.75, P < 0.001 and 69.5 ± 4.4 vs. 95.6 ± 4.7, t = 21.27, P < 0.001, respectively). In vivo, xenografts expressing miR-145 had smaller sizes (miR-145 vs. miR-scr, 717.41 ± 502.62 mm³vs. 1694.80 ± 904.33 mm³, t = 2.314, P = 0.045) and lower weights (miR-145 vs. miR-scr, 0.74 ± 0.46 g vs. 1.65 ± 0.85 g, t = 2.295, P = 0.045).

Our results indicated that miR-145 is an important tumor suppressor and the inhibitory strategies against N-RAS/VEGF signaling pathway might be potential therapeutic applications for UM in the future.

Pulmonary deportation of hydatidiform mole is an exceedingly rare entity. The underlying mechanisms and proper management strategies remain unclear based on sporadic case reports over the past six decades. This study aimed to investigate the clinical features and rational treatment of patients with benign molar pregnancies with pulmonary deportation based on our experience.

Medical records of 20 cases of hydatidiform mole with pulmonary deportation were retrospectively reviewed at Peking Union Medical College Hospital from November 2006 to May 2019. The detailed information of all patients was recorded and analyzed. Patients were divided into different groups according to their characteristics and Mann-Whitney U test was used to compare the duration to achieve a normal β-human chorionic gonadotrophin (β-hCG) level after the first evacuation among groups.

Initial pulmonary computed tomography scans showed suspected bilateral, left and right chest deportation of hydatidiform mole in 12, four, and four patients, respectively, with the maximum nodular diameter ranging from 0.6 to 1.2 cm. Ten patients achieved lesion resolution while the remaining ten patients achieved decreases in the size of their pulmonary lesions. The median duration to achieve a normal β-hCG level after the first evacuation was 15.5 (13.0, 21.9) weeks. There was no significant difference in the duration to achieve a normal β-hCG level after the first evacuation between two groups based on age (≥40 years vs. < 40 years: 15.8 [12.2, 21.5] weeks vs. 15.5 [12.9, 23.0] weeks, Z = 0.094, P = 0.925), type of antecedent mole (partial mole vs. complete mole: 15.2 [12.5, 27.4] weeks vs. 15.9 [12.9, 21.5] weeks, Z = 0.165, P = 0.869), distribution of pulmonary nodules (bilateral lungs vs. unilateral lung: 15.2 [12.8, 22.5] weeks vs. 15.9 [13.2, 22.2] weeks, Z = 0.386, P = 0.700), maximum size of pulmonary nodules (>0.5 cm vs. ≤0.5 cm: 13.0 [11.3, 17.2] weeks vs. 16.0 [14.5, 23.8] weeks, Z = 1.815, P = 0.070), and number of uterine evacuations (once vs. twice or three times: 15.0 [13.0, 16.3] weeks vs. 16.0 [12.8, 23.9] weeks, Z = 0.832, P = 0.405). The post-molar cohort was followed up for 17 to 139 months, and no gestational trophoblastic neoplasia was observed.

No surgeries other than uterine evacuation and no chemotherapy regimens are recommended for such patients if they achieve satisfactory decreases in the level of hCG and gradual decrease or disappearance of pulmonary deportation nodules. Patients should be informed about the necessity of long-term follow-up. More collaborative international studies on this exceedingly rare condition may guide decisions regarding optimal management strategies.

The casein kinase 2-interacting protein-1 (CKIP-1) is important in the development of osteoblasts and cardiomyocytes. However, the effects of CKIP-1 on osteoblast precursor mesenchymal stem cells (MSCs) remain unclear. This study aimed to determine whether CKIP-1 affects osteogenic differentiation in MSCs and explore the relationship of CKIP-1 and inflammation.

Bone marrow MSCs of CKIP-1 wild type (WT) and knockout (KO) mice were cultivated in vitro. Cell phenotype was analyzed by flow cytometry, colony formation was detected to study the proliferative ability. Osteogenic and adipogenic induction were performed. The osteogenic ability was explored by alizarin red staining, alkaline phosphatase (ALP) staining and ALP activity detection. Quantitative real-time polymerase chain reaction (qRT-PCR) was carried out to determine the mRNA expression levels of osteoblast marker genes. The adipogenic ability was detected by oil red O staining. Content of the bone was analyzed to observe the differences of bone imaging parameters including trabecular bone volume/tissue volume (BV/TV), bone surface area fraction/trabecular BV, trabecular number (Tb.N), and trabecular spacing (Tb.sp). Interleukin (IL)-1β was injected on WT mice of 2 months old and 18 months old, respectively. Difference in CKIP-1 expression was detected by RT-PCR and western blot. The relationship between CKIP-1 and inflammation was explored by RT-PCR and western blot.

ALP assays, alizarin red staining, and qRT-PCR showed that MSCs derived from CKIP-1 KO mice exhibited a stronger capability for osteogenesis. Micro-computed tomography detection showed that among 18-month-old mice, CKIP-1 KO mice presented significantly higher bone mass compared with WT mice (P = 0.02). No significant difference was observed in 2-month-old mice. In vivo data showed that expression of CKIP-1 was higher in the bone marrow of aging mice than in young mice (4.3-fold increase at the mRNA level, P = 0.04). Finally, the expression levels of CKIP-1 in bone marrow (3.2-fold increase at the mRNA level, P = 0.03) and cultured MSCs were up-regulated on chronic inflammatory stimulation by IL-1β.

CKIP-1 is responsible for negative regulation of MSC osteogenesis with age-dependent effects. Increasing levels of inflammation with aging may be the primary factor responsible for higher expression levels of CKIP-1 but may not necessarily affect MSC aging.

Hematopoietic stem cells (HSCs) have the ability to differentiate into all subsets of blood cells and self-renew. Large tumor suppressor 1 (LATS1) and large tumor suppressor 2 (LATS2) kinases are essential for cell cycle regulation, organism fitness, genome integrity, and cancer prevention. Here, we investigated whether Lats1 and Lats2 are critical for the maintenance of the self-renewal and quiescence capacities of HSCs in mice.

Quantitative reverse transcription-polymerase chain reaction was used to determine the expression levels of Lats1 and Lats2 in subsets of progenitor cells and mature bone marrow cells. A clustered regularly interspaced short palindromic repeats system was used to generate Lats1 or Lats2 knockout mice. Complete blood cell counts were used to compare the absolute number of white blood cells, lymphocytes, monocytes, neutrophils, and platelets between Lats1 or Lats2 heterozygotes and littermates. Flow cytometry was used to assess the size of hematopoietic progenitor cells (HPCs) and HSC pools in Lats1 or Lats2 heterozygotes and littermates. The comparison between the two groups was analyzed using Student’s t test.

Lats1 and Lats2 were widely expressed in hematopoietic cells with higher expression levels in primitive hematopoietic cells than in mature cells. Lats1 or Lats2 knockout mice were generated, with the homozygotes showing embryonic lethality. The size of the HPC and HSC pools in Lats1 (HPC: wild-type [WT] vs. heterozygote, 220,426.77 ± 54,384.796 vs. 221,149.4 ± 42,688.29, P = 0.988; HSC: WT vs. heterozygote, 2498.932 ± 347.856 vs. 3249.763 ± 370.412, P = 0.105) or Lats2 (HPC: WT vs. heterozygote, 425,540.52 ± 99,721.86 vs. 467,127.8 ± 89,574.48, P = 0.527; HSC: WT vs. heterozygote, 4760.545 ± 1518.01 vs. 5327.437 ± 873.297, P = 0.502) heterozygotes were not impaired. Moreover, the depletion of Lats1 or Lats2 did not affect the overall survival of the heterozygotes (Lats1: P = 0.654; Lats2: P = 0.152).

These results indicate that a single allele of Lats1 or Lats2 may be sufficient for normal hematopoiesis.

Electrical stimulation has been recommended as an effective therapy to prevent muscle atrophy after nerve injury. However, the effect of electrical stimulation on the proliferation of satellite cells in denervated muscles has not yet been fully elucidated. This study was aimed to evaluate the changes in satellite cell proliferation after electrical stimulation in nerve injury and to determine whether these changes are related to the restoration of myofiber cross-section area (CSA).

Sciatic nerve crush injury was performed in 48 male Sprague-Dawley rats. In half (24/48) of the rats, the gastrocnemius was electrically stimulated transcutaneously on a daily basis after injury, while the other half were not stimulated. Another group of 24 male Sprague-Dawley rats were used as sham operation controls without injury or stimulation. The rats were euthanized 2, 4, and 6 weeks later. After 5-bromo-2’-deoxyuridine (BrdU) labeling, the gastrocnemia were harvested for the detection of paired box protein 7 (Pax7), BrdU, myofiber CSA, and myonuclei number per fiber. All data were analyzed using two-way analysis of variance and Bonferroni post-hoc test.

The percentages of Pax7-positive nuclei (10.81 ± 0.56%) and BrdU-positive nuclei (34.29 ± 3.87%) in stimulated muscles were significantly higher compared to those in non-stimulated muscles (2.58 ± 0.33% and 1.30 ± 0.09%, respectively, Bonferroni t = 15.91 and 18.14, P < 0.05). The numbers of myonuclei per fiber (2.19 ± 0.24) and myofiber CSA (1906.86 ± 116.51 μm²) were also increased in the stimulated muscles (Bonferroni t = 3.57 and 2.73, P < 0.05), and both were positively correlated with the Pax7-positive satellite cell content (R² = 0.52 and 0.60, P < 0.01). There was no significant difference in the ratio of myofiber CSA/myonuclei number per fiber among the three groups.

Our results indicate that satellite cell proliferation is promoted by electrical stimulation after nerve injury, which may be correlated with an increase in myonuclei number and myofiber CSA.

现在，一场新型冠状病毒疫情已经对人类健康构成重大威胁。医务人员在流行病的早期阶段面临很高的职业暴露风险。一旦医护人员被感染，将极大影响医疗机构的“战斗力”，更有助于病毒在医院内部传播。这些问题强烈表明了医院管理、预防和控制系统在抗击传染病中的关键作用。

磁外科被定义为利用磁技术进行的外科治疗，包括磁性装置和载体。磁性技术包括压缩、导航、悬浮、锚定和递送。^[1]在过去的十年中，由于磁外科手术促进微创手术的潜力，人们对磁外科手术的兴趣有所增加。因此，需要建立在外科手术中使用磁性技术的指南。

2019年12月，我国武汉市爆发高传染性2019新型冠状病毒病（COVID-19）。病原体被鉴定为2019新型冠状病毒（2019新型冠状病毒）。^[1]2019新型冠状病毒有能力造成全身损伤，包括除肺炎外的肾损伤。^[2]血管紧张素转换酶2（ACE2）作为2019新型冠状病毒病的细胞进入受体。^[1]ACE2表达在肾脏内的近端小管中占主导地位。在这项研究中，回顾性分析了住院患者入院时的临床数据，以确定是否有任何近端小管损伤的证据。

冠状病毒疾病2019（新冠肺炎）由严重急性呼吸综合征冠状病毒-2（新型冠状病毒）引起，可导致肺炎和严重急性呼吸综合征，继续在全球传播。^[1]由于采取了严格的防范措施，新冠肺炎疫情在我国已得到初步控制。然而，在其他国家，新冠肺炎确诊阳性病例和死亡人数正在增加。事实上，新型冠状病毒比严重急性呼吸综合征冠状病毒（SARS-CoV）更具传染性^[2]和中东呼吸综合征冠状病毒（MERS-CoV）。^[3]因此，快速、准确地鉴定致病病毒对控制流行病起着至关重要的作用。计算机断层扫描成像和一些血液学参数是COVID-19感染的初始标志物，^[4,5]而逆转录-聚合酶链反应检测病毒核酸作为疑似病例临床诊断的金标准。^[1]然而，核酸检测耗时长，需要经过认证的实验室和训练有素的技术人员，结果容易受到标本质量的影响。使用胶体金免疫层析法（GICA）检测血清特异性抗体是快速和高度灵敏诊断病毒感染的另一种关键方法。更重要的是，这种方法不需要特殊的设备和试剂，非常适合即时检测。

抗凝剂通常在房颤（AF）导管消融后的最初几周内开出。非维生素K拮抗剂口服抗凝剂（NOACs）因其优越性而被推荐优于华法林。不像华法林需要定期临床访视进行血液检查，NOACs对患者更友好。但是缺乏常规的医疗接触可能会导致依从性差。严格坚持抗凝治疗对疗效和安全性都至关重要。考虑到NOAC在中国的应用越来越普遍，因此有必要评估房颤导管消融后NOAC的依从性。本研究的目的是调查治疗依从性并确定可以提高抗凝质量的因素。

盆腔器官脱垂（POP）是一种通常不会危及生命但会严重影响患者生活质量的疾病。目前认为POP与宫颈延长有显著相关性。^[1]在POP手术中，宫颈长度对手术入路的选择和子宫保留的决策有关键影响。目前尚不清楚术前如何评估子宫颈的长度。特别是，缺乏中国POP妇女的宫颈长度数据。

沙门氏菌阿伯丁是一种普遍存在的病原体，可引起严重的胃肠炎，在食源性疾病和国际食品贸易争端中起着重要作用。^[1]然而，对该生物的分子生物学特性研究较少。本研究是根据《赫尔辛基宣言》进行的，旨在评估由沙门氏菌阿伯丁。此外，对暴发分离株的分子生物学特征进行了检测和分析。2018年6月10日至12日，中国山东省烟台市福山区发生肠炎疫情，影响75名员工，其中男性33人，女性42人。患者的平均年龄为34.2±5.3岁。流行病学调查显示，所有感染员工都曾于2018年6月9日食用过某餐饮公司提供的午餐。共收集了22个样本，包括4个粪便样本、5个剩余食物样本、8个餐饮公司使用的炊具，以及5个来自购买食品原料的市场的鸡肉和鸡蛋样本。^[2]在22份样本中，6份（27.2%）检测呈阳性沙门氏菌阿伯丁（O11：Hi；1, 2），包括来自粪便的三个分离物（3/4，75%）和来自剩余食物的三个分离物（3/5，60%）。脉冲场凝胶电泳（PFGE）结果显示分离株之间高度密切的相关性，根据PulseNet标准化PFGE方案，使用限制性内切酶核酸酶XbaI（96.8%）和BlnI（100%）（Takara，大连，辽宁，中国）消化。^[3]使用Bionumerics 6.0版（Applied Maths，Kortrijk，Belgium）分析PFGE模式。

致编辑：随着脐带血临床研究和应用的发展，脐带血（UCB）的临床价值越来越引起人们的重视。UCB已越来越多地应用于儿童和成人的血液疾病、自身免疫性疾病和恶性肿瘤的治疗^[1]并获得了较高的总生存率。^[1,2,3]UCB含有大量的各种干细胞，包括造血干细胞(HSC)、间充质干细胞、内皮祖细胞等^[4];其中，HSC在研究和临床应用中应用最为广泛。将UCB HSC植入患者体内的移植需要在手术前破坏免疫系统和造血系统。另一种治疗方法是UCB输注，其中UCB被视为营养物，以改善外周血HSC移植的结果^[5]或通过UCB干细胞旁分泌途径的症状。^[6]除异体UCB的应用外，自体UCB也已应用于临床治疗研究。自体UCB不仅限于治疗血液病，还可用于治疗非遗传代谢疾病、免疫疾病、神经系统损伤等。^[6]

致编辑：怀孕期间首次感染水痘-带状疱疹病毒（VZV）可导致母亲和胎儿严重的全身性疾病。尽管如此，母体带状疱疹（HZ）不会增加胎儿死亡率，水痘带状疱疹病毒很少传播给胎儿。虽然HZ感染对胎儿的影响很小，但母体HZ会给母亲带来严重的并发症。^[1]

致编辑：本研究报告1例费城染色体阳性B型急性淋巴细胞白血病⁺B-ALL）在CD19嵌合抗原受体（CAR）修饰的T（CAR-T）细胞治疗后经历了向急性髓性白血病（AML）的谱系转换。该研究由南京医科大学第一附属医院伦理委员会审查批准（编号：2020-QT-06）。患者女，46岁，有胸痛病史1个月，于2014年1月24日收治于我院。实验室检查结果如下：（i）白细胞计数12.01 × 10⁹/L；血红蛋白92克/升；血小板计数47 × 10⁹/L；（ii）骨髓（BM）涂片显示大量原始细胞浸润（95.2%）；③流式细胞术（FCM）免疫表型分析显示原始细胞占66.3%，CD34、CD10、CD19、CD20、CD22、CD38、人白细胞抗原DR均呈阳性；（iv）核型分析显示无有丝分裂期；(v)荧光原地杂交显示费城染色体阳性（BCR-ABL融合基因)；（六）BM定量实时聚合酶链反应（qRT-PCR）检出阳性BCR-ABLp190转录物（BCR-ABL, 184.1%).因此她被诊断为Ph⁺全部。

致编辑：2016年9月，一名来自云南省的26岁农民，无病史或药物史，胸部出现无痛性皮肤结节。后来他的四肢、面部、躯干逐渐出现结节。半月后出现中高热（39.5℃），四肢麻木。他报告没有咳嗽、腹泻、关节痛和肌痛。他的家族没有类似的疾病。当地医院的实验室检查显示白细胞和中性粒细胞计数升高。感染的血清学检查为阴性。抗中性粒细胞胞浆抗体（ANCA）和髓过氧化物酶ANCA（MPO-ANCA）阳性。胸部计算机断层扫描正常。根据临床和实验室表现，诊断为ANCA相关性血管炎（AAV），最初在当地医院静脉滴注甲泼尼龙80mg/天和环磷酰胺（0.4 g/2周）治疗4次。在治疗过程中，发热和皮肤结节暂时缓解，但当泼尼松减量至20~30mg/天时又复发。反复发热、皮肤结节、四肢麻木已持续2年，转诊至四川大学华西医院。

致编辑：一名59岁的中国女性因疲劳和发热1个月入院。3年前，由于间歇性发热和记录的EB病毒血清学阳性，她被诊断为慢性活动性EB病毒（CAEBV）感染。体检时，她的脾脏、肝脏和浅表淋巴结不可触及。没有肺部感染的迹象。初步实验室检查如下：白细胞计数0.92 × 10⁹/L，血红蛋白66 g/L，血小板计数15 × 10⁹/L。血清生化：丙氨酸转氨酶44 U/L，天冬氨酸转氨酶142 U/L，白蛋白26.7 g/L，甘油三酯3.02 mmol/L，乳酸脱氢酶1166 U/L。凝血指标如下：凝血酶原时间14.3 s，活化凝血活酶原时间65.9 s，凝血酶时间32.2 s，D-二聚体18.35 mg/L，纤维蛋白原0.81 g/L。血清铁蛋白水平显著升高至高达8500 ng/mL，血清可溶性白细胞介素-2受体（sIL-2R）为13,200 U/mL。入院时，其血清EBV-DNA载量为1.99 × 10³拷贝数/mL。计算机断层扫描未发现任何肿大的淋巴结，脾脏和肝脏大小正常。骨髓形态和病理学显示没有淋巴瘤的迹象，但轻微的噬血细胞增多。骨髓抽吸物的流式细胞术未发现克隆性淋巴增生。因此，由于发热、全血细胞减少、甘油三酯升高、肝功能障碍、凝血障碍以及血清铁蛋白和sIL-2R明显升高，患者被诊断为EBV相关的噬血细胞性淋巴组织细胞增多症（HLH）。我们启动了HLH-2004方案，在诊断后立即控制她的HLH。除地塞米松、依托泊苷、环孢素A外，每隔一天皮下注射重组人干扰素（IFN）-α 2b 3亿单位。她的体温很快恢复正常，实验室指标在2周内迅速改善。她的全血细胞计数、血清生化和凝血试验在4周内完全正常化，尽管她的血清EBV-DNA载量保持在1.02 × 10的低水平²拷贝数/mL。我们逐渐减少化疗，六周后完全停用依托泊苷、地塞米松和环孢素A。IFN-α 2b作为唯一的维持治疗持续给予，6个月后逐渐减少至每周一次。该患者随访3年。她保持完全缓解，即使她的血清EBV-DNA总是可以在10至100拷贝/mL之间检测到。

致编辑：一名来自成都（中国四川省）的15岁女孩于2019年12月来到我院。她的母亲表示，女孩从3岁起身体就很瘦，但没有发现其他异常。她因在过去5个月中出现耳鸣和听力损失而去医院就诊。入院时，发现她皮下脂肪少，面部特征特别，包括下巴小、嘴唇薄、下颌骨发育不良和牙齿拥挤[图1].她的身高为1.50米，体重指数(BMI)为13.3千克/米²双能X射线吸收法（DXA）扫描显示总脂肪量为6.65 kg。计算的脂肪质量指数(FMI)为2.96 kg/m²，表明脂肪不足。甘油三酯水平为1.40 mmol/L，胆固醇水平为3.08 mmol/L，尿酸水平为476 μ mol/L。腹部超声显示脂肪肝。人生长激素水平为0.1 μ g/L，雌二醇为64pg/mL。口服葡萄糖耐量试验显示，空腹血清葡萄糖、餐后1小时血清葡萄糖和餐后2小时血清葡萄糖分别为4.64 mmol/L、7.75 mmol/L和7.12 mmol/L。空腹血清胰岛素、餐后1小时血清胰岛素和餐后2小时血清胰岛素分别为25.7 μ U/mL、253.6 μ U/mL和257.4 μ U/mL。空腹血清C肽、餐后1 h血清C肽、餐后2 h血清C肽分别为25.7 nmol/L、253.6 nmol/L、257.4 nmol/L。这些结果表明葡萄糖耐量正常，胰岛素抵抗增加。内听道磁共振（MRI）平扫显示双侧无明显异常。进一步的耳鼻喉科检查显示感音神经性听力损失。颅脑MRI平扫未发现明确异常，骨密度检查提示骨质疏松。鉴于患者特殊的临床表现，考虑为潜在遗传病。因此，对患者及其父母进行了三重全外显子组测序。结果显示父母双方均无异常，但a再一次DNA聚合酶δ 1催化亚基的变异（POLD1)基因[NM_002691.3：c.1812_1814del，p.(Ser605del)]。根据临床表现和基因检测的结合，该女孩被诊断为下颌骨发育不全、耳聋、早衰样特征和脂肪营养不良（MDPL）综合征。

致编辑：高尿酸血症是我国仅次于糖尿病的第二常见代谢性疾病，其特征是由于尿酸生成过度活跃或排泄不足而导致血清尿酸浓度升高。^[1]最近的研究支持高尿酸血症与肾小管损伤、随后的肾小管间质纤维化和最终的痛风性肾病有关的观点。^[2]然而，由于缺乏合适、稳定的小鼠模型来研究高尿酸血症和痛风性肾病，延缓和限制了机制研究和新药的开发。对高尿酸血症和痛风性肾病发病机制的进一步理解在很大程度上受到缺乏可靠捕获高尿酸血症和痛风性肾病特征表型的临床前动物模型的阻碍。在这项研究中，我们旨在开发一种新的高尿酸血症和痛风性肾病小鼠模型。

致编辑：我们赞赏李撰写的有趣文章“不可预测的慢性应激对不同年龄大鼠行为和海马氨角3（CA3）亚区和齿状回脑源性神经营养因子表达的影响”等人.^[1]作者表明，应激对大鼠的行为反应和海马脑源性神经营养因子（BDNF）表达有年龄依赖性影响。此外，应激和年龄是影响BDNF表达的主要因素。在每个测试时间点，与年轻应激大鼠相比，老年应激大鼠显示出较低的BDNF表达。

文章中，“体外维持大鼠腹股沟脂肪瓣长期生存能力的流动灌注：大规模工程组织研究的新模型”，发表于第212-7页，第2期，第131卷中华医学杂志,^[1]作者列表、通信和资助更改为“杨安^1,2,克斯汀·赖默斯¹,克里斯蒂娜·奥尔梅林¹,刘洁丽¹,安德里亚·拉扎里迪斯¹,莎拉·施特劳斯¹,聂芳菲²,秦泽莲²,彼得·M·沃格特¹