Volume 134 · Issue 18 · 2021

对于早期诊断为乳腺癌的合格患者，保乳手术（BCS）联合放疗是主要同意的手术选择。2019年，由中国乳腺外科学会（CSBrS）召集的中国专家小组制定了中国早期乳腺癌BCS专家共识（2019版），旨在规范中国的BCS。随后，CSBrS对已发表的报告和专家之间的讨论进行了审查，以确定早期乳腺癌患者BCS临床实践指南的关键临床问题。本集团使用分级建议评估、发展和评价系统对相关证据进行评估，并制定了早期乳腺癌患者BCS临床实践指南（2021版），旨在为中国乳腺外科医生提供临床实践指导。

乳腺癌是我国女性最常见的癌症。自从霍尔斯特德引入乳腺癌根治术以来，手术一直是乳腺癌治疗的基石。在进行此类手术之前，应进行全面和规范的评估。这应包括识别可能增加手术或偏见恢复风险的因素，以及可能影响疾病后续病程的因素。中国乳腺外科学会（CSBrS）进行了文献综述，专家讨论了与规范乳腺癌患者术前评估相关的关键临床问题；参考建议评估、开发和评估系统的分级评估相关证据；结合了中国国情下的可及性；并制定了以下书面的乳腺癌术前评估临床实践指南（2021版），旨在为中国乳腺外科医生提供参考。

急性胰腺炎（AP）是一种复杂的腹部疾病，具有较高的发病率和死亡率，涉及强烈的局部和全身炎症反应。当AP发展为重症急性胰腺炎（SAP）时，易导致多器官功能障碍综合征，这也是导致SAP患者死亡的主要原因之一。^[1]在过去的十年中，我们对AP的病理生理机制的理解取得了实质性的进展。钙介导的腺泡细胞损伤和死亡的机制已经阐明。已经显示了未折叠蛋白反应和自噬在防止持续内质网应激、凋亡和坏死中的细胞保护作用。不饱和脂肪酸在引起胰腺器官衰竭中的中心作用也已得到证实。相比之下，我们对实质细胞死亡的机制知之甚少。^[2]早期有效调控胰腺腺泡细胞死亡可能是治疗AP的有效方法。近年来，一种称为焦亡的新型细胞死亡已成为炎症和免疫疾病领域的重要研究课题。近年来的研究表明，上睑下垂参与了胰腺实质细胞死亡的发病机制。抑制上睑下垂可减轻胰腺损伤，对AP的进展有重要影响。^[3,4]本文综述了AP上睑下垂的研究进展，重点是了解AP的发病机制，为确定新的治疗靶点提供参考[补充图1，http://links.lww.com/CM9/A630]。

临床试验是在一个或多个人类受试者中进行的系统调查或研究，旨在评估医疗器械的安全性、临床性能和/或有效性。^[1]在本文中，“境外临床试验数据”是指在外国或司法管辖区进行的临床试验产生的数据，拟用作中国上市前注册申请的临床证据。

The effectiveness of bronchial thermoplasty (BT) has been reported in patients with severe asthma. This study compared the effects of BT and cryoballoon ablation (CBA) therapy on the airway smooth muscle (ASM).

Eight healthy male beagle dogs were included in this experiment. In the preliminary experiment, one dog received BT treatment for both lower lobe bronchus, another dog received CBA treatment for 7 s on the upper and lower lobe of right bronchus, and 30 s on the left upper and lower lobe. The treatments were performed twice at an interval of 1 month. In subsequent experiments, the right lower lobe bronchus was treated with BT, and the left lower lobe bronchus was treated with CBA. The effects of treatment were observed after 1 (n = 3) month and 6 months (n = 3). Hematoxylin-eosin staining, Masson trichrome staining, and immunohistochemical staining were used to compare the effects of BT and CBA therapy on the ASM thickness, collagen fibers synthesis, and M3 receptor expression after treatment. One-way analysis of variance with Dunnett post hoc test was used to analyze the differences among groups.

In the preliminary experiment, the ASM ablation effect of 30-s CBA was equivalent to that of 7-s CBA (ASM thickness: 30.52 ± 7.75 μm vs. 17.57 ± 15.20 μm, P = 0.128), but the bronchial mucociliary epithelium did not recover, and large numbers of inflammatory cells had infiltrated the mucosal epithelium at 1-month post-CBA with 30-s freezing. Therefore, we chose 7 s as the CBA treatment time in our follow-up experiments. Compared with the control group (35.81 ± 11.02 μm), BT group and CBA group (13.41 ± 4.40 μm and 4.81 ± 4.44 μm, respectively) had significantly decreased ASM thickness after 1 month (P < 0.001). Furthermore, the ASM thickness was significantly lower in the 1-month post-CBA group than in the 1-month post-BT group (P = 0.015). There was no significant difference in ASM thickness between the BT and CBA groups after six months (9.92 ± 4.42 μm vs. 7.41 ± 7.20 μm, P = 0.540). Compared with the control group (0.161 ± 0.013), the average optical density of the ASM M3 receptor was significantly decreased in 6-month post-BT, 1-month post-CBA, and 6-month post-CBA groups (0.070 ± 0.022, 0.072 ± 0.012, 0.074 ± 0.008, respectively; all P < 0.001). There was no significant difference in the average optical density of ASM M3 receptor between the BT and CBA therapy groups after six months (P = 0.613).

CBA therapy effectively ablates the ASM, and its ablation effect is equivalent to that of BT with a shorter onset time. A neural mechanism is involved in both BT and CBA therapy.

Macrophages are involved in the pathogenesis of idiopathic pulmonary fibrosis, partially by activating lung fibroblasts. However, how macrophages communicate with lung fibroblasts is largely unexplored. Exosomes can mediate intercellular communication, whereas its role in lung fibrogenesis is unclear. Here we aim to investigate whether exosomes can mediate the crosstalk between macrophages and lung fibroblasts and subsequently induce fibrosis.

In vivo, bleomycin (BLM)-induced lung fibrosis model was established and macrophages infiltration was examined. The effects of GW4869, an exosomes inhibitor, on lung fibrosis were assessed. Moreover, macrophage exosomes were injected into mice to observe its pro-fibrotic effects. In vitro, exosomes derived from angiotensin II (Ang II)-stimulated macrophages were collected. Then, lung fibroblasts were treated with the exosomes. Twenty-four hours later, protein levels of α-collagen I, angiotensin II type 1 receptor (AT1R), transforming growth factor-β (TGF-β), and phospho-Smad2/3 (p-Smad2/3) in lung fibroblasts were examined. The Student’s t test or analysis of variance were used for statistical analysis.

In vivo, BLM-treated mice showed enhanced infiltration of macrophages, increased fibrotic alterations, and higher levels of Ang II and AT1R. GW4869 attenuated BLM-induced pulmonary fibrosis. Mice with exosomes injection showed fibrotic features with higher levels of Ang II and AT1R, which was reversed by irbesartan. In vitro, we found that macrophages secreted a great number of exosomes. The exosomes were taken by fibroblasts and resulted in higher levels of AT1R (0.22 ± 0.02 vs. 0.07 ± 0.02, t = 8.66, P = 0.001), TGF-β (0.54 ± 0.05 vs. 0.09 ± 0.06, t= 10.00, P < 0.001), p-Smad2/3 (0.58 ± 0.06 vs. 0.07 ± 0.03, t= 12.86, P < 0.001) and α-collagen I (0.27 ± 0.02 vs. 0.16 ± 0.01, t = 7.01, P = 0.002), and increased Ang II secretion (62.27 ± 7.32 vs. 9.56 ± 1.68, t= 12.16, P < 0.001). Interestingly, Ang II increased the number of macrophage exosomes, and the protein levels of Alix (1.45 ± 0.15 vs. 1.00 ± 0.10, t = 4.32, P = 0.012), AT1R (4.05 ± 0.64 vs. 1.00 ± 0.09, t = 8.17, P = 0.001), and glyceraldehyde-3-phosphate dehydrogenase (2.13 ± 0.36 vs. 1.00 ± 0.10, t = 5.28, P = 0.006) were increased in exosomes secreted by the same number of macrophages, indicating a positive loop between Ang II and exosomes production.

Exosomes mediate intercellular communication between macrophages and fibroblasts plays an important role in BLM-induced pulmonary fibrosis.

Pregnancy-associated breast cancer (PABC) is a special type of breast cancer that occurs during pregnancy and within 1 year after childbirth. With the rapid social development and the adjustment of reproductive policies in China, the average age of females at first childbirth is increasing, which is expected to lead to an increase in the incidence of PABC. This study aimed to accumulate clinical experience and to investigate and summarize the prevalence, diagnosis, and treatment of PABC based on large multicenter samples in China.

According to the Chinese Society of Breast Surgery, a total of 164 patients with PABC in 27 hospitals from January 2016 to December 2018 were identified. The pregnancy status, clinicopathological features, comprehensive treatment methods, and outcomes were retrospectively analyzed. Survival curves were plotted using the Kaplan-Meier method.

A total of 164 patients of PABC accounted for 0.30% of the total number of cases in the same period; of which, 83 patients were diagnosed during pregnancy and 81 patients during lactation. The median age of PABC was 33 years (24-47 years). Stage I patients accounted for 9.1% (15/164), stage II 54.9% (90/164), stage III 24.4% (40/164), and stage IV 2.4% (4/164). About 9.1% (15/164) of patients were luminal A. Luminal B patients accounted the most (43.3% [71/164]). About 15.2% (25/164) of patients were human epidermal growth factor receptor 2 (Her-2) overexpression and 18.9% (31/164) of patients were triple-negative breast cancer. For pregnancy breast cancer, 36.1% (30/83) of patients received direct surgery and 20.5% (17/83) received chemotherapy during pregnancy. About 31.3% (26/83) chose abortion or induction of labor. The median follow-up time was 36 months (3-59 months); 11.0% (18/164) patients had local recurrence or distant metastasis and 3.0% (5/164) died.

It is safe and feasible to standardize surgery and chemotherapy for PABC.

Previous studies have demonstrated different predominant sites of distant metastasis between patients with and without neoadjuvant chemoradiotherapy (NCRT). This study aimed to explore whether NCRT could influence the metastasis pattern of rectal cancer through a propensity score-matched analysis.

In total, 1296 patients with NCRT or post-operative chemoradiotherapy (PCRT) were enrolled in this study between January 2008 and December 2015. Propensity score matching was used to correct for differences in baseline characteristics between the two groups. After propensity score matching, the metastasis pattern, including metastasis sites and timing, was compared and analyzed.

After propensity score matching, there were 408 patients in the PCRT group and 245 patients in the NCRT group. NCRT significantly reduced local recurrence (4.1% vs. 10.3%, P = 0.004), but not distant metastases (28.2% vs. 27.9%, P= 0.924) compared with PCRT. In both the NCRT and PCRT groups, the most common metastasis site was the lung, followed by the liver. The NCRT group developed local recurrence and distant metastases later than the PCRT group (median time: 29.2 [18.8, 52.0] months vs. 18.7 [13.3, 30.0] months, Z=-2.342, P= 0.019; and 21.2 [12.2, 33.8] vs. 16.4 [9.3, 27.9] months, Z=-1.765, P = 0.035, respectively). The distant metastases occurred mainly in the 2nd year after surgery in both the PCRT group (39/114, 34.2%) and NCRT group (21/69, 30.4%). However, 20.3% (14/69) of the distant metastases appeared in the 3rd year in the NCRT group, while this number was only 13.2% (15/114) in the PCRT group.

The predominant site of distant metastases was the lung, followed by the liver, for both the NCRT group and PCRT group. NCRT did not influence the predominant site of distant metastases, but the NCRT group developed local recurrence and distant metastases later than the PCRT group. The follow-up strategy for patients with NCRT should be adjusted and a longer intensive follow-up is needed.

Hyperbaric oxygen treatment (HBOT) has been demonstrated to influence the keloid recurrence rate after surgery and to relieve keloid symptoms and other pathological processes in keloids. To explore the mechanism of the effect of HBOT on keloids, tumor immune gene expression and immune cell infiltration were studied in this work.

From February 2021 to April 2021, HBOT was carried out on keloid patients four times before surgery. Keloid tissue samples were collected and divided into an HBOT group (keloid with HBOT before surgery [HK] group, n = 6) and a non-HBOT group (K group, n = 6). Tumor gene expression was analyzed with an Oncomine Immune Response Research Assay kit. Data were mined with R package. The differentially expressed genes between the groups were compared. Hub genes between the groups were determined and verified with Quantitative Real-time PCR. Immune cell infiltration was analyzed based on CIBERSORT deconvolution algorithm analysis of gene expression and verified with immunohistochemistry (IHC).

Inflammatory cell infiltration was reduced in the HK group. There were 178 upregulated genes and 217 downregulated genes. Ten hub genes were identified, including Integrin Subunit Alpha M (ITGAM), interleukin (IL)-4, IL-6, IL-2, Protein Tyrosine Phosphatase Receptor Type C (PTPRC), CD86, transforming growth factor (TGF), CD80, CTLA4, and IL-10. CD80, ITGAM, IL-4, and PTPRC with significantly downregulated expression were identified. IL-10 and IL-2 were upregulated in the HK group but without a significant difference. Infiltration differences of CD8 lymphocyte T cells, CD4 lymphocyte T-activated memory cells, and dendritic resting cells were identified with gene CIBERSORT deconvolution algorithm analysis. Infiltration levels of CD4 lymphocyte T cell in the HK group were significantly higher than those of the K group in IHC verification.

HBOT affected tumor gene expression and immune cell infiltration in keloids. CD4 lymphocyte T cell, especially activated memory CD4⁺T, might be the key regulatory immune cell, and its related gene expression needs further study.

Accumulating evidence suggests that lithium influences mesenchymal stem cell (MSC) proliferation and osteogenic differentiation. As decreased bone formation in femoral heads is induced by glucocorticoids (GCs), we hypothesized that lithium has a protective effect on GC-induced osteonecrosis of femoral heads (ONFH).

A rat ONFH model was induced by methylprednisolone (MP) and the effect of lithium chloride on the models was evaluated. Micro-computed tomography (CT)-based angiography and bone scanning were performed to analyze the vessels and bone structure in the femoral heads. Hematoxylin and eosin and immunohistochemical staining were performed to evaluate the trabecular structure and osteocalcin (OCN) expression, respectively. Bone marrow-derived MSCs were isolated from the models, and their proliferative and osteogenic ability was evaluated. Western blotting and quantitative real-time polymerase chain reaction were performed to detect osteogenic-related proteins including Runx2, alkaline phosphatase, and Collagen I.

Micro-CT analysis showed a high degree of osteonecrotic changes in the rats that received only MP injection. Treatment with lithium reduced this significantly in rats that received lithium (MP + Li group); while 18/20 of the femoral heads in the MP showed severe osteonecrosis, only 5/20 in the MP + Li showed mild osteonecrotic changes. The MP + Li group also displayed a higher vessel volume than the MP group (0.2193 mm³vs. 0.0811 mm³, P < 0.05), shown by micro-CT-based angiography. Furthermore, histological analysis showed better trabecular structures and more OCN expression in the femoral heads of the MP + Li group compared with the MP group. The ex vivo investigation indicated higher proliferative and osteogenic ability and upregulated osteogenic-related proteins in MSCs extracted from rats in the MP + Li group than that in the MP group.

We concluded that lithium chloride has a significant protective effect on GC-induced ONFH in rats and that lithium also enhances MSC proliferation and osteogenic differentiation in rats after GC administration.

Although congenital hypothyroidism (CH) has been widely studied in Western countries, CH incidence at different administrative levels in China during the past decade remains unknown. This study aimed to update the incidence and revealed the spatial pattern of CH incidence in the mainland of China, which could be helpful in the planning and implementation of preventative measures.

The data used in our study were derived from 245 newborns screening centers that cover 30 provinces of the Chinese Newborn Screening Information System. Spatial auto-correlation was analyzed by Global Moran I and Getis-Ord Gi statistics at the provincial level. Kriging interpolation methods were applied to estimate a further detailed spatial distribution of CH incidence at city level throughout the mainland of China, and Kulldorff space scanning statistical methods were used to identify the spatial clusters of CH cases at the city level.

A total of 91,921,334 neonates were screened from 2013 to 2018 and 42,861 cases of primary CH were identified, yielding an incidence of 4.66 per 10,000 newborns screened (95% confidence interval [CI]: 4.62-4.71). Neonates in central (risk ratio [RR] = 0.84, 95% CI: 0.82-0.85) and western districts (RR = 0.71, 95% CI: 0.69-0.73) had lower probability of CH cases compared with the eastern region. The CH incidence indicated a moderate positive global spatial autocorrelation (Global Moran I value = 0.394, P < 0.05), and the CH cases were significantly clustered in spatial distribution. A most likely city-cluster (log-likelihood ratio [LLR]= 588.82, RR = 2.36, P < 0.01) and 25 secondary city-clusters of high incidence were scanned. The incidence of each province and each city in the mainland of China was estimated by kriging interpolation, revealing the most affected province and city to be Zhejiang Province and Hangzhou city, respectively.

This study offers an insight into the space clustering of CH incidence at provincial and city scales. Future work on environmental factors need to focus on the effects of CH occurrence.

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder associated with loss of motor neurons. Our objective was to explore the epidemiology, clinical features, and survival factors of 1809 patients with ALS.

We analyzed 1809 ALS patients, who were recruited from the Peking University Third Hospital from January 2005 to December 2015. Demographic data and disease-related parameters were collected. Kaplan-Meier curves were used to compare survival time. Cox proportional hazards function and the hazard ratio were used to identify adjusted prognostic predictors.

The results showed that the average annual incidence in Beijing alone was 0.38 cases/100,000 person-years and the mean age of onset was 48.88 ± 11.35 (95% confidence interval [CI]: 48.17-49.85) years. The median survival time from onset to death/tracheostomy was 58.89 ± 33.03 (95% CI: 51.46-63.84) months. In the adjusted Cox proportional hazard model, age of onset, diagnosis delay, rate of disease progression (Amyotrophic Lateral Sclerosis Functional Rating Scale Revised decline [points/month]), and body mass index all had an independent effect on survival in ALS.

Our study provides information on epidemiology, clinical features, and survival factors of patients with ALS in China. These results can be helpful in clinical practice, clinical trial design, and validation of new tools to predict disease progression.

致编辑：阻塞性睡眠呼吸暂停（OSA）是一种常见的睡眠呼吸障碍。既往研究报道，中国OSA患者日间高碳酸血症的发生率为26.2%^[1]日本为14%。^[2]然而，Weitzenblum等人^[3]证明OSA患者的日间高碳酸血症可能不是继发于睡眠呼吸暂停/呼吸不足，但可能是由于合并症，如慢性阻塞性肺疾病或严重肥胖。肥胖通气不足综合征(OHS)被定义为肥胖（体重指数[BMI]≥30kg/m²）、日间高碳酸血症（动脉血中二氧化碳分压[PaCO₂]≥45 mmHg）和睡眠呼吸障碍，在排除其他原因导致肺泡通气不足后。^[4]由于在以前的研究中没有完全排除OHS患者，^[1,2]我们假设中国OSA患者日间高碳酸血症的发生率可能较低。

致编辑：阻塞性睡眠呼吸暂停低通气综合征（OSAHS）是一种常见的睡眠障碍性呼吸疾病，具有一系列有害后遗症。作为一种涉及多个系统的综合征，^[1]OSAHS的临床表现具有很大的异质性。在2019年世界睡眠大会上，一系列关于冰岛睡眠呼吸暂停队列的聚类分析^[2]进行了详细介绍。然而，由于相关研究较少，中国的数据缺失。此外，尽管OSAHS和认知障碍之间的关系在20世纪80年代得到证实，但尚未探索评估认知功能的所有变量。

致编辑：2型糖尿病（T2D）是一种由多种病因引起的以高血糖为特征的代谢性疾病。^[1]长期高血糖引起T2D患者微血管和大血管损伤及脂质代谢紊乱，可导致动脉粥样硬化。^[1]大约三分之二的T2D患者死于心血管并发症，主要是动脉粥样硬化性心血管疾病。^[2]T2D大血管并发症的总体患病率约为32%。^[3]目前尚无能准确预测T2D心血管并发症的临床指标。早期检测T2D患者致动脉粥样硬化性血脂异常的生物标志物，可实现糖尿病大血管病变的早期识别，对早期干预、改善临床预后、降低致残死亡率和经济负担具有重要意义。成纤维细胞生长因子19（FGF19）是由远端小肠分泌的调节脂质和葡萄糖代谢的激素。然而，尚不清楚FGF19是否在T2D向致动脉粥样硬化性血脂异常的进展中发挥作用。在人类中，一些研究调查了循环FGF19与冠状动脉疾病（CAD）存在之间的关系，也证明了FGF19与稳定型CAD中主要心血管不良事件发展之间的关联。^[4,5]我们之前的研究也表明，FGF19可以预测T2D男性亚临床动脉粥样硬化的进展。^[6]在这项研究中，我们旨在调查FGF19与T2D患者致动脉粥样硬化性血脂异常风险之间的关系，并探索FGF19是否可以作为T2D患者致动脉粥样硬化性血脂异常早期诊断的生物标志物。

致编辑：糖尿病流行日益成为世界范围内的主要公共卫生问题。2014年，尽管中国当时仅占全球人口的18.7%，但中国有1.029亿成年糖尿病患者，占全球糖尿病人口的24.4%。^[1]此外，糖尿病和糖尿病前期的估计总体患病率分别为10.9%和35.7%，表明中国是世界上糖尿病患病率最高的国家之一。^[2]尽管包括久坐不动的生活方式和高能量饮食在内的因素推动了糖尿病的流行，但遗传结构也可能有助于个体对环境挑战的反应的易感性。醛脱氢酶（ALDH）2是通过催化有毒醛氧化成非反应性酸来消除有毒醛的关键酶。新的证据表明，患有ALDH2除了酒精不耐受、硝酸甘油耐受和癌症之外，缺乏还会增加心血管和代谢疾病的风险。^[3]值得注意的是，一个独特的ALDH2功能丧失等位基因、ALDH2*2，在大约50%的东亚人口和8%的全球人口中发现。有报道称，这ALDH2突变与冠状动脉疾病（CAD）患者糖尿病患病率较高相关，并伴有C反应蛋白（CRP）水平升高。^[4]ALDH2突变也与各种糖尿病危险因素有关，但直接相关性仍然难以捉摸。在此，我们探讨了潜在的致病性和机制ALDH2实验室和临床环境中2型糖尿病发展的缺陷。

致编辑：先兆子痫是孕产妇发病率和死亡率的主要原因。尽管先兆子痫的病因和进展尚不完全清楚，但已经证明分娩是最终的治疗方法。然后，临床医生面临何时以及如何进行递送的决定。根据指南，先兆子痫不是剖宫产的指征，正如预期的那样，会有一些严重的并发症。这意味着患有先兆子痫的孕妇可以进行阴道试验。然而，目前大多数先兆子痫孕妇选择直接剖宫产。尝试阴道分娩后进行剖宫产是否会影响母婴结局及其相关风险因素仍不清楚。本研究的目的是调查在阴道分娩期间接受转移剖宫产的重度子痫前期患者的危险因素和母婴结局。

致编辑：膜性肾病(MN)是一种自身免疫性疾病，是成人肾病综合征的最常见原因。在中国，MN的发病率估计约为每年12/百万，平均年龄在50至60岁之间，男性占优势的比例为2：1。在10年的肾活检分析中，MN（29.1%）是最常见的病理疾病。^[1]

致编辑：肝纤维化是导致肝功能障碍的关键阶段，在门静脉高压症、胆汁性肝硬化和肝细胞癌的进展中可能很重要。因此，肝纤维化的准确评估仍然是医生临床关注的问题。在最近的研究中，肝活检多年来一直被认为是诊断和评估肝纤维化的金标准。然而，由于其侵入性实践、采样变异性以及病理学解释的评估者间和评估者内的变异性，肝活检在许多情况下在患者和临床医生中并不受欢迎。因此，肝纤维化评估的多种非侵入性检测已被开发为肝活检的替代策略，因为它们可以通过医学成像信息提供方便的操作和可接受的诊断准确性。通过临床影像学早期发现肝纤维化可以减少肝衰竭并防止其进展。医学影像信息的判读和分析通常由临床专家进行。受益于计算机辅助诊断的快速发展，特别是人工智能深度学习的改进算法，医生可以提取更准确的评估，用于诊断和治疗的临床决策。^[1]

致编辑：在脓毒症中，细菌内毒素通过诱导炎性介质和细胞因子的失调和过度释放发挥中心作用，通常被描述为“细胞因子风暴”或“细胞因子血症”^[1]内毒素和细胞因子都与器官功能障碍的发展有关，包括急性肾损伤（AKI）。^[2]从循环中去除循环内毒素和过量细胞因子可恢复趋化梯度，将免疫应答定位于主要感染部位并重新建立受调节的免疫应答。^[1,3]因此，与传统的连续肾脏替代疗法(CRRT)过滤器相比，使用具有增强的内毒素和细胞因子吸附特性的血液过滤器可以提供额外的治疗益处。

致编辑：创伤性脑损伤（TBI）是指头部或身体受到打击或脑震荡后正常功能的破坏。根据格拉斯哥昏迷量表的标准，基于患者的运动和言语反应以及睁眼情况，将TBI的严重程度分为轻度、中度和重度。^[1]最近，研究表明，10%至30%耐受头部损伤的个体可能会在数月至数年后出现延迟症状和损伤。^[2]

致编辑：确定颅内压（ICP）升高在神经外科和神经系统疾病的管理中非常重要，因为ICP升高与不良结局（如脑疝和死亡）相关。尽管脑实质内或脑室内侵入性方法仍然是ICP测量的金标准，但由于缺乏足够数量的神经外科医生，它们不能常规使用。此外，由于禁忌症（如凝血障碍和严重血小板障碍）和并发症（如感染和出血），侵入性方法并不总是可能的。^[1]因此，在临床实践中需要准确的非侵入性方法来估计ICP。大量研究表明，视神经鞘直径（ONSD）是ICP的间接标志，两参数之间存在线性关系。^[1,2]因此，ONSD及其精确测量方法越来越受到学者的关注。

致编辑：在紧急情况下，可以使用声门上气道装置（SAD）代替气管导管（ET）。SAD有两种类型，翻边和非翻边，它们的易用性和成功率是相似的。与ET插入相比，SAD插入快速简单，同时提供相当的通气量。2019年美国心脏协会指南建议在紧急情况下插入SAD，如院外心脏骤停。^[1,2]然而，SAD插入的成功不容易确定。根据一项研究，当在紧急医疗服务（EMS）环境中使用SAD时，13.8%的患者未识别出气道衰竭。^[3]SAD的不正确定位表现为咬合块与门牙对齐不良和气体交换无效（其特征是胸部和“颈前”偏移、潮气量不足、动脉血氧饱和度低[SpO₂]、二氧化碳描记图描记不良、气道压力高和漏气）。^[1,4]未能将SAD插入到适当的深度通常是由于下咽周围结构的阻力造成的。^[5]在这项研究中，我们介绍了甲状软骨抬高（TCE）操作，这是一种简单而新颖的方法，有助于SAD的正确插入。