Volume 129 · Issue 14 · 2016

重症监护病房（ICU）重症患者感染发生率和病死率分别高达53.9%和30.0%。^[1]在美国，死于医院感染的患者人数超过10万，单项费用高达250亿美元^[2]每年。一项研究表明，条件性外源性病原体在肠道内的定植是重症ICU患者医院获得性感染的重要病理基础。^[3]肠道居住着种类最多的细菌。一方面，共生菌可以抑制条件性外源性病原体在肠道的定植，另一方面，肠道菌群在免疫、代谢和营养等方面发挥着重要作用。在这里，我们讨论了肠道细菌的组成，肠道中病原体去定植的潜在机制，病理条件下肠道微生态环境的变化，以及肠道去定植病原微生物群的能力的维持。

Over the years, the mechanical ventilation (MV) strategy has changed worldwide. The aim of the present study was to describe the ventilation practices, particularly lung-protective ventilation (LPV), among brain-injured patients in China.

This study was a multicenter, 1-day, cross-sectional study in 47 Intensive Care Units (ICUs) across China. Mechanically ventilated patients (18 years and older) with brain injury in a participating ICU during the time of the study, including traumatic brain injury, stroke, postoperation with intracranial tumor, hypoxic-ischemic encephalopathy, intracranial infection, and idiopathic epilepsy, were enrolled. Demographic data, primary diagnoses, indications for MV, MV modes and settings, and prognoses on the 60^th day were collected. Multivariable logistic analysis was used to assess factors that might affect the use of LPV.

A total of 104 patients were enrolled in the present study, 87 (83.7%) of whom were identified with severe brain injury based on a Glasgow Coma Scale ≤8 points. Synchronized intermittent mandatory ventilation (SIMV) was the most frequent ventilator mode, accounting for 46.2% of the entire cohort. The median tidal volume was set to 8.0 ml/kg (interquartile range [IQR], 7.0-8.9 ml/kg) of the predicted body weight; 50 (48.1%) patients received LPV. The median positive end-expiratory pressure (PEEP) was set to 5 cmH₂O (IQR, 5-6 cmH₂O). No PEEP values were higher than 10 cmH₂O. Compared with partially mandatory ventilation, supportive and spontaneous ventilation practices were associated with LPV. There were no significant differences in mortality and MV duration between patients subjected to LPV and those were not.

Among brain-injured patients in China, SIMV was the most frequent ventilation mode. Nearly one-half of the brain-injured patients received LPV. Patients under supportive and spontaneous ventilation were more likely to receive LPV.

ClinicalTrials.org NCT02517073 https://clinicaltrials.gov/ct2/show/NCT02517073.

Stress index at post-recruitment maneuvers could be a method of positive end-expiratory pressure (PEEP) titration in acute respiratory distress syndrome (ARDS) patients. However, airway pressure (P_aw) stress index may not reflect lung mechanics in the patients with high chest wall elastance. This study was to evaluate the P_aw stress index on lung mechanics and the correlation between P_aw stress index and transpulmonary pressure (P_L) stress index in acute respiratory failure (ARF) patients.

Twenty-four ARF patients with mechanical ventilation (MV) were consecutively recruited from July 2011 to April 2013 in Zhongda Hospital, Nanjing, China and Ospedale S. Giovanni Battista-Molinette Hospital, Turin, Italy. All patients underwent MV with volume control (tidal volume 6 ml/kg) for 20 min. PEEP was set according to the ARDSnet study protocol. The patients were divided into two groups according to the chest wall elastance/respiratory system elastance ratio. The high elastance group (H group, n= 14) had a ratio ≥30%, and the low elastance group (L group, n= 10) had a ratio <30%. Respiratory elastance, gas-exchange, P_aw stress index, and P_L stress index were measured. Student's t-test, regression analysis, and Bland-Altman analysis were used for statistical analysis.

Pneumonia was the major cause of respiratory failure (71.0%). Compared with the L group, PEEP was lower in the H group (5.7 ± 1.7 cmH²O vs. 9.0 ± 2.3 cmH_2O, P < 0.01). Compared with the H group, lung elastance was higher (20.0 ± 7.8 cmH_2O/L vs. 11.6 ± 3.6 cmH₂O/L, P < 0.01), and stress was higher in the L group (7.0 ± 1.9 vs. 4.9 ± 1.9, P = 0.02). A linear relationship was observed between the P_aw stress index and the P_L stress index in H group (R² = 0.56, P < 0.01) and L group (R² = 0.85, P < 0.01).

In the ARF patients with MV, P_aw stress index can substitute for P_L to guide ventilator settings.

ClinicalTrials.gov NCT02196870 (https://clinicaltrials.gov/ct2/show/NCT02196870).

Previous studies have suggested that β1-receptor blockers benefit septic shock patients. This study aimed to determine whether β1-receptor blockers benefit tissue perfusion in sepsis and to identify parameters to reduce the risk of this drug in sepsis.

Consecutive septic shock patients were recruited from the Intensive Care Unit of Peking Union Medical College Hospital within 48 h of diagnosis. All patients were hemodynamically stable and satisfactorily sedated with a heart rate (HR) >100 beats/min. Esmolol therapy achieved the target HR of 10-15% lower than the baseline HR. Clinical and physiological data of patients were collected prospectively within 1 h prior to esmolol therapy and 2 h after achieving the targeted HR.

Sixty-three patients were recruited. After esmolol therapy, blood pressure was unaltered, whereas stroke volume (SV) was increased compared with before esmolol therapy (43.6 ± 22.7 vs. 49.9 ± 23.7 ml, t = -2.3, P = 0.047). Tissue perfusion, including lactate levels (1.4 ± 0.8 vs. 1.1 ± 0.6 mmol/L, t = 2.6, P = 0.015) and the central venous-to-arterial carbon dioxide difference (5.6 ± 3.3 vs. 4.3 ± 2.2 mmHg, t = 2.6 P = 0.016), was also significantly decreased after esmolol therapy. For patients with increased SV (n = 42), cardiac efficiency improved, and esmolol therapy had a lower risk for a decrease in cardiac output (CO). Therefore, pretreatment cardiac systolic and diastolic parameters with (n = 42)/without (n = 21) an increase in SV were compared. Mitral lateral annular plane systolic excursion (MAPSElat) in patients with increased SV was significantly higher than that in those without increased SV (1.3 ± 0.3 vs. 1.1 ±0.2 cm, t = 2.4, P = 0.034).

SV of septic shock patients is increased following esmolol therapy. Although CO is also decreased with HR, tissue perfusion is not worse. MAPSElat can be used to predict an increase in SV before esmolol use.

ClinicalTrials.gov, NCT01920776; https://clinicaltrials.gov/ct2/show/NCT01920776?term=NCT01920776&amp;rank=l.

Early goal-directed therapy (EGDT) has become an important therapeutic management in early salvage stage of septic shock. However, splenic organs possibly remained hypoperfused and hypoxic despite fluid resuscitation. This study aimed to evaluate the effect of EGDT on hepatic perfusion in septic shock patients.

A prospective observational study was carried out in early septic shock patients who were admitted to Intensive Care Unit within 24 h after onset and who met all four elements of the EGDT criteria after treatment with the standard EGDT procedure within 6 h between December 1, 2012 and November 30, 2013. The hemodynamic data were recorded, and oxygen metabolism and hepatic functions were monitored. An indocyanine green clearance test was applied to detect the hepatic perfusion. The patients' characteristics were compared before treatment (T0), immediately after EGDT (T1), and 24 h after EGDT (T2). This study is registered at ClinicalTrials.org, NCT02060773.

Twenty-one patients were included in the study; however, the hepatic perfusion data were not included in the analysis for two patients; therefore, 19 patients were eligible for the study. Hemodynamics data, as monitored by pulse-indicator continuous cardiac output, were obtained from 16 patients. There were no significant differences in indocyanine green plasma disappearance rate (ICG-PDR) and 15-min retention rate (R15) at T0 (11.9 ± 5.0%/min and 20.0 ± 13.2%), T1 (11.4 ± 5.1%/min and 23.6 ± 14.9%), and T2 (11.0 ± 4.5%/min and 23.7 ± 15.3%) (all P > 0.05). Both of the alterations of ICG-PDR and R15 showed no differences at T0, T1, and T2 in the patients of different subgroups that achieved different resuscitation goal numbers when elected (P > 0.05).

There were no hepatic perfusion improvements after EGDT in the early phase of patients with septic shock.

Clinicaltrials.gov NCT02060773 (https://clinicaltrials.gov/ct2/show/NCT02060773).

Despite its high prevalence, morbidity, and mortality, sepsis-associated encephalopathy (SAE) is still poorly understood. The aim of this prospective and observational study was to investigate the clinical significance of calcium-binding protein A8 (S100A8) in serum and tumor necrosis factor receptor-associated factor 6 (TRAF6) in peripheral blood mononuclear cells (PBMCs) in diagnosing SAE and predicting its prognosis.

Data of septic patients were collected within 24 h after Intensive Care Unit admission from July 2014 to March 2015. Healthy medical personnel served as the control group. SAE was defined as cerebral dysfunction in the presence of sepsis that fulfilled the exclusion criteria. The biochemical indicators, Glasgow Coma Scale, Acute Physiology and Chronic Health Evaluation score II, TRAF6 in PBMC, serum S100A8, S100β, and neuron-specific enolase were evaluated in SAE patients afresh. TRAF6 and S100A8 were also measured in the control group.

Of the 57 enrolled patients, 29 were diagnosed with SAE. The S100A8 and TRAF6 concentrations in SAE patients were both significantly higher than that in no-encephalopathy (NE) patients, and higher in NE than that in controls (3.74 ± 3.13 vs. 1.08 ± 0.75 vs. 0.37 ± 0.14 ng/ml, P< 0.01; 3.18 ± 1.55 vs. 1.02 ± 0.63 vs. 0.47 ± 0.10, P< 0.01). S100A8 levels of 1.93 ng/ml were diagnostic of SAE with 92.90% specificity and 69.00% sensitivity in the receiver operating characteristic (ROC) curve, and the area under the curve was 0.86 (95% confidence interval [CI]: 0.76-0.95). TRAF6-relative levels of 1.44 were diagnostic of SAE with 85.70% specificity and 86.20% sensitivity, and the area under the curve was 0.94 (95% CI: 0.88-0.99). In addition, S100A8 levels of 2.41 ng/ml predicted 28-day mortality of SAE with 90.00% specificity and 73.70%sensitivity in the ROC curve, and the area under the curve was 0.88. TRAF6 relative levels of 2.94 predicted 28-day mortality of SAE with 80.00% specificity and 68.40% sensitivity, and the area under the curve was 0.77. Compared with TRAF6, the specificity of serum S100A8 in diagnosing SAE and predicting mortality was higher, although the sensitivity was low. In contrast, the TRAF6 had higher sensitivity for diagnosis.

Peripheral blood levels of S100A8 and TRAF6 in SAE patients were elevated and might be related to the severity of SAE and predict the outcome of SAE. The efficacy and specificity of S100A8 for SAE diagnosis were superior, despite its weak sensitivity. S100A8 might be a better biomarker for diagnosis of SAE and predicting prognosis.

It is unclear that how to decide the calcium infusion rate during continuous veno-venous hemofiltration (CVVH) with regional citrate anticoagulation (RCA). This study aimed to assess the determinants of calcium infusion rate during CVVH with RCA in critically ill patients with acute kidney injury (AKI).

A total of 18 patients with AKI requiring CVVH were prospectively analyzed. Postdilution CVVH was performed with a fixed blood flow rate of 150 ml/min and a replacement fluid flow rate of 2000 ml/h for each new circuit. The infusion of 4% trisodium citrate was started at a rate of 29.9 mmol/h prefilter and adjusted according to postfilter ionized calcium. The infusion of 10% calcium gluconate was initiated at a rate of 5.5 mmol/h and adjusted according to systemic ionized calcium. The infusion rate of trisodium citrate and calcium gluconate as well as ultrafiltrate flow rate were recorded at 1,2, 4, 6, 12, and 24 h after starting CVVH, respectively. The calcium loss rate by CVVH was also calculated.

Fifty-seven sessions of CVVH were performed in 18 AKI patients. The citrate infusion rate, calcium loss rate by CVVH, and calcium infusion rate were 31.30 (interquartile range: 2.70), 4.60 ± 0.48, and 5.50 ± 0.35 mmol/h, respectively. The calcium infusion rate was significantly higher than that of calcium loss rate by CVVH (P < 0.01). The correlation coefficient between the calcium and citrate infusion rates, and calcium infusion and calcium loss rates by CVVH was -0.031 (P > 0.05) and 0.932 (P < 0.01), respectively. In addition, calcium infusion rate (mmol/h) = 1.77 + 0.8× (calcium loss rate by CVVH, mmol/h).

The calcium infusion rate correlates significantly with the calcium loss rate by CVVH but not with the citrate infusion rate in a fixed blood flow rate during CVVH with RCA.

There has been no external validation of survival prediction models for severe adult respiratory distress syndrome (ARDS) with extracorporeal membrane oxygenation (ECMO) therapy in China. The aim of study was to compare the performance of multiple models recently developed for patients with ARDS undergoing ECMO based on Chinese single-center data.

A retrospective case study was performed, including twenty-three severe ARDS patients who received ECMO from January 2009 to July 2015. The PRESERVE (Predicting death for severe ARDS on VV-ECMO), ECMOnet, Respiratory Extracorporeal Membrane Oxygenation Survival Prediction (RESP) score, a center-specific model developed for inter-hospital transfers receiving ECMO, and the classical risk-prediction scores of Acute Physiology and Chronic Health Evaluation (APACHE) II and Sequential Organ Failure Assessment (SOFA) were calculated. In-hospital and six-month mortality were regarded as the endpoints and model performance was evaluated by comparing the area under the receiver operating characteristic curve (AUC).

The RESP and APACHE II scores showed excellent discriminate performance in predicting survival with AUC of 0.835 (95%confidence interval [CI], 0.659-1.010, P = 0.007) and 0.762 (95% CI, 0.558-0.965, P = 0.035), respectively. The optimal cutoff values were risk class 3.5 for RESP and 35.5 for APACHE II score, and both showed 70.0% sensitivity and 84.6% specificity. The excellent performance of these models was also evident for the pneumonia etiological subgroup, for which the SOFA score was also shown to be predictive, with an AUC of 0.790 (95% CI, 0.571-1.009, P = 0.038). However, the ECMOnet and the score developed for externally retrieved ECMO patients failed to demonstrate significant discriminate power for the overall cohort. The PRESERVE model was unable to be evaluated fully since only one patient died six months postdischarge.

The RESP, APCHAE II, and SOFA scorings systems show good predictive value for intra-hospital survival of ARDS patients treated with ECMO in our single-center evaluation. Future validation should include a larger study with either more patients' data at single-center or by integration of domestic multi-center data. Development of a scoring system with national characteristics might be warranted.

Osteoporosis is a common complication of chronic obstructive pulmonary disease (COPD). Recent clinical and biological researches have increasingly delineated the biomolecular pathways of bone metabolism regulation in COPD. We extended this work by examining the specific association and potential contribution of the osteoprotegerin (OPG)/receptor activator of nuclear factor-κB ligand (RANKL) axis to the pathogenesis of osteoporosis in advanced COPD. The aim of this study was to assess the relationships of serum OPG, RANKL, and tumor necrosis factor-alpha (TNF-α) with bone turnover in men with very severe COPD.

Pulmonary function, T-score at the lumbar spine (LS) and femoral neck (FN), serum OPG, RANKL, soluble receptor of tumor necrosis factor-alpha-I and II (sTNFR-I, sTNFR-II), osteocalcin (OC), and β-CrossLaps (βCL) levels were measured in 45 men with very severe stage COPD and 36 male non-COPD volunteers. COPD patients and healthy controls were compared using an independent t-test and Mann-Whitney U-test. The Pearson coefficient was used to assess the relationships between variables.

OPG and OC were lower in male COPD patients than in control subjects whereas RANKL, serum βCL, TNF-α, and its receptors were higher. OPG directly correlated with forced expiratory volume in 1 s (FEV1) % predicted (r = 0.46, P < 0.005), OC (r = 0.34, P < 0.05), LS (r = 0.56, P < 0.001), and FN T-score (r = 0.47, P < 0.01). In contrast, serum RANKL inversely associated with LS and FN T-score (r = -0.62, P < 0.001 and r = -0.48, P < 0.001) but directly correlated with βCL (r = 0.48, P < 0.001). In addition, OPG was inversely correlated with RANKL (r = -0.39, P < 0.01), TNF-α (r = -0.56, P < 0.001), and sTNFR-I (r = -0.40, P < 0.01).

Our results suggest that serum OPG and RANKL levels are inversely associated with bone loss in men with advanced stage COPD.

Aspergillosis infection is common in the patients with insufficient immunity. The role of mammalian target of rapamycin (mTOR), T-box expressed in T-cells (T-bet), and eomesodermin (EOMES) in mediating T lymphocytes differentiation in response to Aspergillus fumigatus infection in immunocompromised rats was investigated in this study.

Invasive pulmonary aspergillosis (IPA) of immunosuppressive twenty male rats were established and sacrificed at 24 h (n = 5), 48 h (n = 5), 72 h (n = 5), and 96 h (n = 5) after A. fumigatus infection. In addition, control (n = 5), cyclophosphamide (CTX) (n = 5), and aspergillosis (n = 5) group were also established the tissues and pathology of lung tissue was examined by hematoxylin and eosin staining. CD8⁺ T-cells was sorted by flow cytometry. Serum mTOR, S6K, T-bet, and EOMES were quantified by enzyme-linked immunosorbent assay.

Histology of lung tissue indicated severe lung tissue injury including infiltration of inflammatory cells, alveolar wall damage or degradation, blood congestion, and hemorrhage in the CTX, IPA, and CTX + IPA rats. Hyphae were seen in the IPA, and CTX + IPA groups. The proportion of CD8⁺ T-cells was significantly increased in the animals of CTX + IPA. Memory CD8⁺ T-cells was significantly increased in early stage (24 h and 48 h, P < 0.001), but decreased in the late phase of fungal infection (72 h and 96 h) in the animals of CTX + IPA. In addition, at early stage of fungal infection (24 h and 48 h), serum mTOR (P < 0.001), S6K (P < 0.001), and T-bet (P < 0.05) was significantly higher, while EOMES was significantly lower (P < 0.001), in CTX + IPA group than that in control, CTX alone or IPA alone group. Conversely, serum mTOR, S6K, T-bet, and EOMES showed opposite changed in the late stage (72 h and 96 h). Pearson's correlation analysis indicated that mTOR and S6K were significantly correlated with T-bet (r = 0.901 and 0.91, respectively, P < 0.001), but negatively and significantly correlated with EOMES (r = -0.758 and -0.751, respectively, P < 0.001).

mTOR may regulate transcription factors of EOMES and T-bet, and by which mechanism, it may modulate lymphocytes differentiation in animals with immune suppression and fungal infection.

Inflammation is supposed to play a key role in the pathophysiological processes of intestinal ischemia-reperfusion injury (IIRI), and Candida albicans in human gut commonly elevates inflammatory cytokines in intestinal mucosa. This study aimed to explore the effect of C. albicans on IIRI.

Fifty female Wistar rats were divided into five groups according to the status of C. albicans infection and IIRI operation: group blank and sham; group blank and IIRI; group cefoperazone plus IIRI; group C. albicans plus cefoperazone and IIRI (CCI); and group C. albicans plus cefoperazone and sham. The levels of inflammatory factors tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β, and diamine oxidase (DAO) measured by enzyme-linked immunosorbent assay were used to evaluate the inflammation reactivity as well as the integrity of small intestine. Histological scores were used to assess the mucosal damage, and the C. albicans blood translocation was detected to judge the permeability of intestinal mucosal barrier.

The levels of inflammatory factors TNF-α, IL-6, and IL-1β in serum and intestine were higher in rats undergone both C. albicans infection and IIRI operation compared with rats in other groups. The levels of DAO (serum: 44.13 ± 4.30 pg/ml, intestine: 346.21 ± 37.03 pg/g) and Chiu scores (3.41 ± 1.09) which reflected intestinal mucosal disruption were highest in group CCI after the operation. The number of C. albicans translocated into blood was most in group CCI ([33.80 ± 6.60] ×10² colony forming unit (CFU)/ml).

Intestinal C. albicans infection worsened the IIRI-induced disruption of intestinal mucosal barrier and facilitated the subsequent C. albicans translocation and dissemination.

Aberrant expression of ten-eleven translocation 1 (TET1) plays a critical role in tumor development and progression. We systematically summarized the latest research progress on the role and mechanisms of TET1 in cancer biology.

Relevant articles published in English from 1980 to April 2016 were selected from the PubMed database. The terms "ten-eleven translocation 1," "5mC," "5hmC," "microRNA," "hypoxia," and "embryonic stem cell" were used for the search.

Articles focusing on the role and mechanism of TET1 in tumor were reviewed, including clinical and basic research articles.

TET proteins, the key enzymes converting 5-methylcytosine to 5-hydroxymethylcytosine, play vital roles in DNA demethylation regulation. Recent studies have shown that loss of TET1 is associated with tumorigenesis and can be used as a potential biomarker for cancer therapy, which indicates that TET1 serves as tumor suppressor gene. Moreover, besides its dioxygenase activity, TET1 could induce epithelial-mesenchymal transition and act as a coactivator to regulate gene transcription, such as developmental regulator in embryonic stem cells (ESCs) and hypoxia-responsive gene in cancer. The regulation of TET1 is also correlated with microRNA in a posttranscriptional modification process. Hence, it is complex but critical to comprehend the mechanisms of TET1 in the biology of ESCs and cancer.

TET1 not only serves as a demethylation enzyme but also plays multiple roles during tumorigenesis and progression. More studies should be carried out to elucidate the exact mechanisms of TET1 and its associations with cancer before considering it as a therapeutic tool.

一名16岁女孩因原发性闭经和盆腔实性肿块入院治疗。她身高158厘米，体重55公斤。没有黑棘皮病、痤疮、多毛症、甲状腺肿、库欣样特征或特纳氏圣痕的证据。第二性征检查显示乳房小且发育不良（坦纳氏II期）。没有阴毛，而外生殖器是女性类型，没有阴蒂肥大的证据。盆腔超声检查显示右侧附件区实性肿块直径约9 cm，正常子宫内膜3 mm，左侧卵巢1.5 cm × 1.0 cm。她的血清激素检测显示雌二醇水平低为0.155 nmol/L（卵泡期正常范围：0.200-0.790 nmol/L），而黄体生成素水平升高为25.47 U/L（卵泡期正常范围：2.12-10.89 U/L），卵泡刺激素水平升高为51.36 U/L（卵泡期正常范围：3.85-8.78 U/L），睾酮水平升高为3.97 nmol/L（正常范围：0.35-2.60 nmol/L）。发现她的正常孕酮水平为3.77 nmol/L（卵泡期为0.98-4.83 nmol/L），血清催乳素水平为12.47 ng/ml（3.34-26.72 ng/ml）。术前检测血清肿瘤标志物，结果如下：CA 125 34.20 U/ml（正常范围：0-35.00 U/ml），CA 199 34.11 U/ml（正常范围：0-39.00 U/ml），甲胎蛋白(AFP)>1210.0 ng/ml（正常范围：0-7.0 ng/ml），β-人绒毛膜促性腺激素(β-hCG)12.81 U/L（正常范围：0-2.90 U/L），乳酸脱氢酶(LDH)204U/L（正常范围：109-245 U/L）。她没有给出任何腹痛、恶心或呕吐病史，没有激素摄入、辐射暴露、化疗或任何中枢神经症状，如头痛或视觉障碍。她没有重大创伤或外科手术史。她的家族中没有儿童结核病史或任何先天性异常或遗传性疾病。

液体激发是帮助医生确定液体反应性的常用诊断方法，这是危重患者液体管理的重要组成部分。^[1]抬起患者的腿诱导包含在静脉储器中的可变量的血液（大约200-300毫升）从肢体转移到中心静脉隔室。根据Franck-Starling曲线，这种前负荷的短暂增加可能会导致未来应答者的心输出量（CO）增加，这是由于他们的前负荷储备状态。许多临床研究已经验证了被动抬腿（PLR），PLR的优势在重症监护室（ICU）具有吸引力。最近，PLR被建议作为预测流体反应性的简单且潜在的方法，其类似于没有一滴流体的“自动流体挑战”。^[2]然而，一项研究揭示了PLR在现实世界中的应用很差。^[3]我们承认，缺乏PLR教育会导致目前的做法。另一方面，PLR在临床实践中的应用可能并不简单，液体反应性的圣杯仍有待发现。^[4]PLR的标准尚未确立，PLR的一些问题值得探讨。

致编者：反向痤疮（AI；OMIM：142690）是一种疼痛的慢性滤泡疾病，其特征是复发性引流窦和脓肿，随后伴有疤痕和慢性渗漏，主要发生在携带终毛和顶汗腺的皮肤褶皱中。它主要影响头皮、颈部、腋窝、会阴和乳房下区域。由于症状的慢性和复发性以及缺乏令人满意的治疗方案，AI显著影响患者的生活质量。

致编者：脑脂肪栓塞（CFE）的症状通常是创伤后12-24小时无症状间隔后的急性呼吸衰竭、意识不清和瘀点皮疹的三联征。尽管自20世纪60年代以来就有CFE病例的报道，但据我们所知，一些报道讨论了皮质类固醇治疗CFE的有益作用，尽管皮质类固醇通常被认为具有预防作用。在此，我们报告一例CFE病例，患者为63岁女性，右胫骨和腓骨骨折，无颅脑外伤。我们从1号开始给她静脉注射地塞米松11天^圣创伤日，患者恢复良好。

致编者：60岁男性，因新发突发性心悸、心前区不适，每日数次，入住我院急诊科。记录了右束支传导阻滞（RBBB）模式（245次/分钟）的持续性单形性室性心动过速（VT），在同步复律后逆转为窦性心律。随后的12导联心电图显示正常窦性心律，V4至V6导联T波倒置，V1至V3导联ST段抬高（78次/分钟）。大约10年前，他被诊断出患有糖尿病，并得到了很好的治疗。无致心律失常性心肌病家族史或心脏病体征或症状。心肌酶水平，包括肌钙蛋白I、肌酸激酶同工酶MB和肌红蛋白，均在正常水平内。血清C反应蛋白和D-二聚体水平正常。经胸二维超声心动图显示左心室（LV）整体收缩功能正常（舒张末期/收缩末期容积150/66 ml，射血分数57%），左心室假性动脉瘤（心尖，4.2 cm × 2.6 cm）[图1]和正常形态的右心室(RV)。冠状动脉造影显示冠状动脉正常。

在题为“阵发性心房颤动引起的双侧急性肾动脉栓塞的介入治疗”的文章中，第10期，第129卷第1244-1245页中华医学杂志^[1]，“资金支持和赞助”部分国家自然科学基金批准号错误地写成了“81355392”，而不是“81370437”。