2023年 · 第136卷第24期

Recent decades have seen the remarkable development of China in medical accessibility and quality index, and the application of a number of new advanced cardiovascular technologies benefits more patients. However, according to the Annual Report on Cardiovascular Health and Diseases in China published in this article, which was organized and summarized by National Center for Cardiovascular Diseases, there is still a huge population living with risk factors of cardiovascular diseases (CVD), and the morbidity and mortality of CVD are increasing. It is estimated that there are around 330 million patients suffering from CVD currently, including 245 million of hypertension, 13 million of stroke, 45.3 million of peripheral artery disease, 11.39 million of coronary heart disease (CHD), 8.9 million of heart failure, 5 million of pulmonary heart disease, 4.87 million of atrial fibrillation, 2.5 million of rheumatic heart disease, and 2 million of congenital heart disease. Tobacco use, diet and nutrition factors, physical activity, overweight and obesity, and psychological factors are what affect cardiovascular health, while hypertension, dyslipidemia, diabetes, chronic kidney disease, metabolic syndrome, and air pollution are the risk factors for CVD. In this article, in addition to risk factors for CVD, we also report the epidemiological trends of CVD, including CHD, cerebrovascular disease, arrhythmias, valvular heart disease, congenital heart disease, cardiomyopathy, heart failure, pulmonary vascular disease and venous thromboembolism, and aortic and peripheral artery diseases, as well as the basic research and medical device development in CVD. In a word, China has entered a new stage of transforming from high-speed development focusing on scale growth to high-quality development emphasizing on strategic and key technological development to curb the trend of increasing incidence and mortality of CVD.

原发性肝癌在中国是一个重大的健康问题，在所有恶性肿瘤中发病率排名第四，死亡率排名第二。^[1,2,3,4]2012-2015年中国肝癌患者的5年总生存率男性仅为12.2%，女性仅为13.1%。^[5]肝细胞癌（HCC）占原发性肝癌的75-85%。^[6]此外，大多数肝癌在诊断时是不可切除的。为了对抗这种情况，使用转换疗法，其涉及系统治疗，如抗血管生成药物或分子靶向治疗与免疫治疗相结合，以及局部治疗，如经导管动脉化疗栓塞(TACE)、肝动脉灌注化疗(HAIC)、消融治疗和放射治疗。目标是消除不可切除状态，增加手术机会。据报道，肿瘤降级后补救手术后的5年生存率在24.9-57%之间。^[7]然而，部分晚期肝癌患者由于基线肝功能较差或治疗相关不良反应导致肝损害，仍不能耐受转换治疗，导致治疗终止或出现危及生命的后遗症。^[8]此外，没有关于在整个治疗过程中评估和管理肝功能的包罗万象的指南。针对这一问题，中国医药保健国际交流与促进会（CPAM）肝脏肿瘤分会联合肝胆外科、介入、肝病学、肿瘤学领域专家，制定了《肝癌转换治疗期间肝功能综合管理中国专家共识（2022版）》。补充图1显示了肝癌转换治疗期间肝功能总体管理的流程图，http://links.lww.com/CM9/B835。

Severe ischemic stroke carries a high rate of disability and death. The severity of stroke is often assessed by the degree of neurological deficits or the extent of brain infarct, defined as severe stroke and large infarction, respectively. Critically severe stroke is a life-threatening condition that requires neurocritical care or neurosurgical intervention, which includes stroke with malignant brain edema, a leading cause of death during the acute phase, and stroke with severe complications of other vital systems. Early prediction of high-risk patients with critically severe stroke would inform early prevention and treatment to interrupt the malignant course to fatal status. Selected patients with severe stroke could benefit from intravenous thrombolysis and endovascular treatment in improving functional outcome. There is insufficient evidence to inform dual antiplatelet therapy and the timing of anticoagulation initiation after severe stroke. Decompressive hemicraniectomy (DHC) <48 h improves survival in patients aged <60 years with large hemispheric infarction. Studies are ongoing to provide evidence to inform more precise prediction of malignant brain edema, optimal indications for acute reperfusion therapies and neurosurgery, and the individualized management of complications and secondary prevention. We present an evidence-based review for severe ischemic stroke, with the aims of proposing operational definitions, emphasizing the importance of early prediction and prevention of the evolution to critically severe status, summarizing specialized treatment for severe stroke, and proposing directions for future research.

Melanoma accounts for a small proportion of skin cancers diagnosed each year, but it has a high degree of malignancy and rapid progression, resulting in a short survival period for patients. The incidence of melanoma continues to rise, and now melanoma accounts for 1.7% of cancer diagnoses worldwide and is the fifth most common cancer in the United States. With the development of high-throughput sequencing technologies, the understanding of the pathophysiology of melanoma had also been improved. The most common activating mutations in melanoma cells are BRAF, NRAS, and KIT mutations, which disrupt cell signaling pathways related to tumor proliferation. The progress has led to the emergence of molecularly targeted drugs, which extends the survival of patients with advanced melanoma. A large number of clinical trials have been conducted to confirm that targeted therapy for patients with advanced melanoma can improve progression-free survival and overall survival, and for stage III patients after radical tumor resection targeted therapy can reduce the recurrence of melanoma. Patients who were originally stage III or IV inoperable have the opportunity to achieve tumor radical resection after targeted therapy. This article reviewed the clinical trial data and summarized the clinical benefits and limitations of these therapies.

This study aimed to determine the reasons for conversion and elucidate the safety and efficacy of transition to tenofovir alafenamide/emtricitabine/bictegravir sodium (TAF/FTC/BIC) in highly active antiretroviral therapy (HAART)-experienced HIV-infected patients in real-world settings.

We conducted a retrospective cohort study. The treatment conversion rationales, safety, and effectiveness in 1684 HIV-infected patients with previous HAART experience who switched to TAF/FTC/BIC were evaluated at Beijing Ditan Hospital from September 2021 to Auguest 2022.

Regimen simplification (990/1684, 58.79%) was the most common reason for switching, followed by osteoporosis or osteopenia (375/1684, 22.27%), liver dysfunction (231/1684, 13.72%), decline in tenofovir alafenamide/emtricitabine/elvitegravir/cobicistat (TAF/FTC/EVG/c) with food restriction (215/1684, 12.77%), virological failure (116/1684, 6.89%), and renal dysfunction (90/1684, 5.34%). In patients receiving non-nucleotide reverse transcriptase inhibitors (NNRTI)-containing regimens, lipid panel changes 1 year after switching indicated a difference of 3.27 ± 1.10 mmol/L vs. 3.40 ± 1.59 mmol/L in triglyceride (P = 0.014), 4.82 ± 0.74 mmol/L vs. 4.88 ± 0.72 mmol/L in total cholesterol (P = 0.038), 3.09 ± 0.70 mmol/L vs. 3.18 ± 0.66 mmol/L in low-density lipoprotein (P <0.001), and 0.99 ± 0.11 mmol/L vs. 0.95 ± 0.10 mmol/L in high-density lipoprotein (P <0.001). Conversely, among patients receiving booster-containing regimens, including TAF/FTC/EVG/c and lopinavir/ritonavir (LPV/r), lipid panel changes presented decreased trends. We also observed an improved trend in viral load suppression, and alanine transaminase (ALT), aspartate transaminase (AST), estimated glomerular filtration rate (eGFR), and serum creatinine levels after the transition (P <0.001).

The transition to TAF/FTC/BIC demonstrated good treatment potency. Furthermore, this study elucidates the motivations behind the adoption of TAF/FTC/BIC in real-world scenarios, providing clinical evidence supporting the stable conversion to TAF/FTC/BIC for HAART-experienced patients.

T-cell immunoreceptor with immunoglobulin and immunoreceptor tyrosine-based inhibition motif domains (TIGIT), an inhibitory receptor expressed on T cells, plays a dysfunctional role in antiviral infection and antitumor activity. However, it is unknown whether TIGIT expression on T cells influences the immunological effects of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) inactivated vaccines.

Forty-five people living with HIV (PLWH) on antiretroviral therapy (ART) for more than two years and 31 healthy controls (HCs), all received a third dose of a SARS-CoV-2 inactivated vaccine, were enrolled in this study. The amounts, activation, proportion of cell subsets, and magnitude of the SARS-CoV-2-specific immune response of TIGIT⁺CD4⁺ and TIGIT⁺CD8⁺ T cells were investigated before the third dose but 6 months after the second vaccine dose (0W), 4 weeks (4W) and 12 weeks (12W) after the third dose.

Compared to that in HCs, the frequency of TIGIT⁺ CD8⁺T cells in the peripheral blood of PLWH increased at 12W after the third dose of the inactivated vaccine, and the immune activation of TIGIT⁺CD8⁺ T cells also increased. A decrease in the ratio of both T naïve (T_N) and central memory (T_CM) cells among TIGIT⁺CD8⁺T cells and an increase in the ratio of the effector memory (T_EM) subpopulation were observed at 12W in PLWH. Interestingly, particularly at 12W, a higher proportion of TIGIT⁺CD8⁺ T cells expressing CD137 and CD69 simultaneously was observed in HCs than in PLWH based on the activation-induced marker assay. Compared with 0W, SARS-CoV-2-specific TIGIT⁺CD8⁺ T-cell responses in PLWH were not enhanced at 12W but were enhanced in HCs. Additionally, at all time points, the SARS-CoV-2-specific responses of TIGIT⁺CD8⁺ T cells in PLWH were significantly weaker than those of TIGIT^-CD8⁺ T cells. However, in HCs, the difference in the SARS-CoV-2-specific responses induced between TIGIT⁺CD8⁺ T cells and TIGIT^-CD8⁺ T cells was insignificant at 4W and 12W, except at 0W.

TIGIT expression on CD8⁺ T cells may hinder the T-cell immune response to a booster dose of an inactivated SARS-CoV-2 vaccine, suggesting weakened resistance to SARS-CoV-2 infection, especially in PLWH. Furthermore, TIGIT may be used as a potential target to increase the production of SARS-CoV-2-specific CD8⁺ T cells, thereby enhancing the effectiveness of vaccination.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccine can induce a potent cellular and humoral immune response to protect against SARS-CoV-2 infection. However, it was unknown whether SARS-CoV-2 vaccination can induce effective natural killer (NK) cell response in people living with human immunodeficiency virus (PLWH) and healthy individuals.

Forty-seven PLWH and thirty healthy controls (HCs) inoculated with SARS-CoV-2 inactivated vaccine were enrolled from Beijing Youan Hospital in this study. The effect of SARS-CoV-2 vaccine on NK cell frequency, phenotype, and function in PLWH and HCs was evaluated by flow cytometry, and the response of NK cells to SARS-CoV-2 Omicron Spike (SARS-2-OS) protein stimulation was also evaluated.

SARS-CoV-2 vaccine inoculation elicited activation and degranulation of NK cells in PLWH, which peaked at 2 weeks and then decreased to a minimum at 12 weeks after the third dose of vaccine. However, in vitro stimulation of the corresponding peripheral blood monocular cells from PLWH with SARS-2-OS protein did not upregulate the expression of the aforementioned markers. Additionally, the frequencies of NK cells expressing the activation markers CD25 and CD69 in PLWH were significantly lower than those in HCs at 0, 4 and 12 weeks, but the percentage of CD16⁺ NK cells in PLWH was significantly higher than that in HCs at 2, 4 and 12 weeks after the third dose of vaccine. Interestingly, the frequency of CD16⁺ NK cells was significantly negatively correlated with the proportion of CD107a⁺ NK cells in PLWH at each time point after the third dose. Similarly, this phenomenon was also observed in HCs at 0, 2, and 4 weeks after the third dose. Finally, regardless of whether NK cells were stimulated with SARS-2-OS or not, we did not observe any differences in the expression of NK cell degranulation markers between PLWH and HCs.

SARS-CoV-2 vaccine elicited activation and degranulation of NK cells, indicating that the inoculation of SARS-CoV-2 vaccine enhances NK cell immune response.

The KangDuo-Surgical Robot-01 (KD-SR-01) system is a new surgical robot recently developed in China. The aim of this study was to present our single-center experience and mid-term outcomes of urological procedures using the KD-SR-01 system.

From August 2020 to April 2023, consecutive urologic procedures were performed at Peking University First Hospital using the KD-SR-01 system. The clinical features, perioperative data, and follow-up outcomes were prospectively collected and analyzed.

A total of 110 consecutive patients were recruited. Among these patients, 28 underwent partial nephrectomy (PN), 41 underwent urinary tract reconstruction (26 underwent pyeloplasty, 3 underwent ureteral reconstruction and 12 underwent ureterovesical reimplantation [UR]), and 41 underwent radical prostatectomy (RP). The median operative time for PN was 112.5 min, 157.0 min for pyeloplasty, 151.0 min for ureteral reconstruction, 142.5 min for UR, and 138.0 min for RP. The median intraoperative blood loss was 10 mL for PN, 10 mL for pyeloplasty, 30 mL for ureteral reconstruction, 20 mL for UR, and 50 mL for RP. All procedures were successfully completed without conversion, and there were no major complications in any patient. The median warm ischemia time of PN was 17.3 min, and positive surgical margin was not noted in any patient. The overall positive surgical margin rate of RP was 39% (16/41), and no biochemical recurrence was observed in any RP patient during the median follow-up of 11.0 months. The surgical success rates of pyeloplasty and UR were 96% (25/26) and 92% (11/12) during the median follow-up of 29.5 months and 11.5 months, respectively.

The KD-SR-01 system appears feasible, safe, and effective for most urological procedures, based on our single-center experience.

In light of the significant clinical benefits of antibody-drug conjugates in clinical trials, the human epidermal growth factor receptor 2 (HER2)-low category in breast cancers has gained increasing attention. Therefore, we studied the clinicopathological characteristics of Chinese patients with hormone receptor (HR)-positive/HER2-low early-stage breast cancer and developed a recurrence risk prediction model.

Female patients with HR-positive/HER2-low early-stage breast cancer treated in 29 hospitals of the Chinese Society of Breast Surgery (CSBrS) from Jan 2015 to Dec 2016 were enrolled. Their clinicopathological data and prognostic information were collected, and machine learning methods were used to analyze the prognostic factors.

In total, 25,096 patients were diagnosed with breast cancer in 29 hospitals of CSBrS from Jan 2015 to Dec 2016, and clinicopathological data for 6486 patients with HER2-low early-stage breast cancer were collected. Among them, 5629 patients (86.79%) were HR-positive. The median follow-up time was 57 months (4, 76 months); the 5-year disease-free survival (DFS) rate was 92.7%, and the 5-year overall survival (OS) rate was 97.7%. In total, 412 cases (7.31%) of metastasis were observed, and 124 (2.20%) patients died. Multivariate Cox regression analysis revealed that T stage, N stage, lymphovascular thrombosis, Ki-67 index, and prognostic stage were associated with recurrence and metastasis (P <0.05). A recurrence risk prediction model was established using the random forest method and exhibited a sensitivity of 81.1%, specificity of 71.7%, positive predictive value of 74.1%, and negative predictive value of 79.2%.

Most of patients with HER2-low early-stage breast cancer were HR-positive, and patients had favorable outcome; tumor N stage, lymphovascular thrombosis, Ki-67 index, and tumor prognostic stage were prognostic factors. The HR-positive/HER2-low early-stage breast cancer recurrence prediction model established based on the random forest method has a good reference value for predicting 5-year recurrence events.

ChiCTR.org.cn, ChiCTR2100046766

High-grade serous ovarian cancer (HGSOC) is the biggest cause of gynecological cancer-related mortality because of its extremely metastatic nature. This study aimed to explore and evaluate the characteristics of candidate factors associated with the metastasis and progression of HGSOC.

Transcriptomic data of HGSOC patients’ samples collected from primary tumors and matched omental metastatic tumors were obtained from three independent studies in the National Center for Biotechnology Information (NCBI) Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were selected to evaluate the effects on the prognosis and progression of ovarian cancer using data from The Cancer Genome Atlas (TCGA) database. Hub genes’ immune landscapes were estimated by the Tumor Immune Estimation Resource (TIMER) database. Finally, using 25 HGSOC patients' cancer tissues and 10 normal fallopian tube tissues, immunohistochemistry (IHC) was performed to quantify the expression levels of hub genes associated with International Federation of Gynecology and Obstetrics (FIGO) stages.

Fourteen DEGs, ADIPOQ, ALPK2, BARX1, CD37, CNR2, COL5A3, FABP4, FAP, GPR68, ITGBL1, MOXD1, PODNL1, SFRP2, and TRAF3IP3, were upregulated in metastatic tumors in every database while CADPS, GATA4, STAR, and TSPAN8 were downregulated. ALPK2, FAP, SFRP2, GATA4, STAR, and TSPAN8 were selected as hub genes significantly associated with survival and recurrence. All hub genes were correlated with tumor microenvironment infiltration, especially cancer-associated fibroblasts and natural killer (NK) cells. Furthermore, the expression of FAP and SFRP2 was positively correlated with the International Federation of Gynecology and Obstetrics (FIGO) stage, and their increased protein expression levels in metastatic samples compared with primary tumor samples and normal tissues were confirmed by IHC (P = 0.0002 and P = 0.0001, respectively).

This study describes screening for DEGs in HGSOC primary tumors and matched metastasis tumors using integrated bioinformatics analyses. We identified six hub genes that were correlated with the progression of HGSOC, particularly FAP and SFRP2, which might provide effective targets to predict prognosis and provide novel insights into individual therapeutic strategies for HGSOC.

Posttraumatic stress disorder (PTSD) and depression are highly comorbid. Psilocybin exerts substantial therapeutic effects on depression by promoting neuroplasticity. Fear extinction is a key process in the mechanism of first-line exposure-based therapies for PTSD. We hypothesized that psilocybin would facilitate fear extinction by promoting hippocampal neuroplasticity.

First, we assessed the effects of psilocybin on percentage of freezing time in an auditory cued fear conditioning (FC) and fear extinction paradigm in mice. Psilocybin was administered 30 min before extinction training. Fear extinction testing was performed on the first day; fear extinction retrieval and fear renewal were tested on the sixth and seventh days, respectively. Furthermore, we verified the effect of psilocybin on hippocampal neuroplasticity using Golgi staining for the dendritic complexity and spine density, Western blotting for the protein levels of brain derived neurotrophic factor (BDNF) and mechanistic target of rapamycin (mTOR), and immunofluorescence staining for the numbers of doublecortin (DCX)- and bromodeoxyuridine (BrdU)-positive cells.

A single dose of psilocybin (2.5 mg/kg, i.p.) reduced the increase in the percentage of freezing time induced by FC at 24 h, 6th day and 7th day after administration. In terms of structural neuroplasticity, psilocybin rescued the decrease in hippocampal dendritic complexity and spine density induced by FC; in terms of neuroplasticity related proteins, psilocybin rescued the decrease in the protein levels of hippocampal BDNF and mTOR induced by FC; in terms of neurogenesis, psilocybin rescued the decrease in the numbers of DCX- and BrdU-positive cells in the hippocampal dentate gyrus induced by FC.

A single dose of psilocybin facilitated rapid and sustained fear extinction; this effect might be partially mediated by the promotion of hippocampal neuroplasticity. This study indicates that psilocybin may be a useful adjunct to exposure-based therapies for PTSD and other mental disorders characterized by failure of fear extinction.

致编辑：青蒿素是从药用植物中提取分离得到的具有过氧化物桥结构的倍半萜内酯化合物，黄花蒿多年来，现有研究揭示了青蒿素化合物在抗肿瘤、免疫调节、预防骨质疏松症、抗菌和抗病毒作用方面的广泛潜在应用，使其对一系列其他疾病有效，这拓宽了青蒿素的临床应用。在此，我们更新了青蒿素及其衍生物对多种病毒的抗病毒活性的当前知识，例如冠状病毒,疱疹病毒，和黄病毒对青蒿素类化合物抗病毒作用的研究可以为对抗新出现的尚无有效抗病毒药物的病毒性疾病提供新的思路。

致编辑：中性粒细胞作为先天细胞，在针对入侵病原体的免疫防御反应中发挥重要作用，并为T和B细胞的增殖和活化提供信号以启动适应性免疫。^[1]来自人类免疫缺陷病毒(HIV)-1患者的中性粒细胞表现出多种功能缺陷，例如抗微生物杀伤活性受损和活性氧(ROS)产生受损以及表型改变。^[2]CD177⁺中性粒细胞被鉴定为功能性活化的细胞群。^[3]与CD177相比，它释放高水平的ROS和抗菌肽^-炎症状态下的中性粒细胞。这种增加的炎性细胞因子产生和ROS产生可能对刺激部位产生有害影响，导致组织损伤，例如导致微生物易位的上皮屏障损伤，这是HIV-1感染期间慢性免疫激活的关键因素。

致编辑：约占人类免疫缺陷病毒(HIV)感染个体的10-40%的免疫无应答者(INR)已接受有效治疗并表现出对病毒复制的持续抑制，但其CD4⁺T细胞计数未恢复。与免疫应答者（IRs）相比，他们可能具有增加的非获得性免疫缺陷综合征（AIDS）相关发病率和死亡率的风险。^[1]CD8⁺T细胞在病毒感染中起重要作用，循环CD8的功能特性⁺T细胞与HIV的免疫控制有关。高CD8⁺在长期抗逆转录病毒治疗（ART）期间，T细胞计数有利于免疫恢复患者的持续病毒衰变和CD4 T细胞恢复。^[2]CD8的两个亚群⁺已经根据其CD8表达强度鉴定T细胞：CD8^bri和CD8^昏暗的T淋巴细胞。证明CD3⁺CD8^昏暗的T细胞，功能弱于CD3⁺CD8^briT细胞与HIV感染期间的疾病进展相关。^[3]然而，CD8数量的动态变化^bri和CD8^昏暗的ART前后INR和IRs中的T细胞尚未见报道。

致编辑：在接受或未接受抗逆转录病毒治疗(ART)的HIV感染个体分离的循环单核细胞中检测到人类免疫缺陷病毒(HIV)DNA。^[1]在循环单核细胞中检测到罕见且低水平的HIV DNA。^[2]在接受ART的患者中，单核细胞含有复制能力的非潜伏性HIV-1。早期对循环单核细胞的研究揭示了与T细胞相比不同的病毒群体和遗传特征。^[3,4]然而，目前没有简单的方法来清楚地区分单核细胞中的病毒和T细胞中的病毒。

致编辑：袖状切除术是一种切除和重建支气管和/或肺动脉的手术，被认为是中心位置肺癌的有效治疗方法。随着综合治疗理念的确立和发展，针对局部晚期分期的中心部位肺癌应用新辅助免疫治疗等新辅助治疗是有效的。新辅助治疗可能会缩小肿瘤大小，以增加完全切除的机会，并实现保留实质的袖状切除手术。一般来说，袖状切除术改善了术后呼吸功能和生活质量，并实现了较低的术后发病率和死亡率，肿瘤学结局与新辅助治疗后的全肺切除术相似。

致编辑：脊柱是肿瘤转移的常见部位。脊柱转移瘤患者由于肿瘤侵犯脊柱骨而出现疼痛、病理性骨折和脊柱畸形。目前，小鼠模型是脊柱转移相关研究的一个非常重要的工具。^[1]阐明脊柱转移瘤的病理生理机制，完善诊断和治疗指南，开发新的治疗方法至关重要。在本研究中，我们总结了各种小鼠脊髓转移模型及其适用的研究内容。

致编辑：心房颤动（AF）是左心房（LA）结构重塑的公认原因。^[1]LA球形度（LASP）是一种新的基于形状的重塑参数，是房颤消融结果的独立预测因子。^[2,3]LA结构的改善被定义为LA反向重塑（RR）。本研究比较了单次手术联合左心耳（LAA）封堵（LAAC）和导管消融（CA）对左心耳容积（LAV）和LASP的影响。

致编辑：大约2%的>65岁的人患有主动脉瓣狭窄（AS）。^[1]如果不进行干预，AS是一种快速进展的心脏瓣膜病，2年死亡率为50%。^[1]由于首例经导管主动脉瓣置换术(TAVR)是由Cribier进行的等人^[2]2002年，TAVR被认为在各种风险分层的AS患者中是非劣效性的。TAVR术后并发症对于预测患者生存率和改善生活质量至关重要，尤其是在越来越多的低风险患者中进行该手术。^[3]其中，心肌梗死（MI）是一种罕见但危及生命的并发症，通常由冠状动脉口阻塞引起。^[1]相比之下，以心脏标志物升高为主要特征的围手术期心肌损伤是TAVR相对常见的并发症。尽管最近的研究证明了心脏标志物在预测心血管不良事件方面的有希望的结果，但围手术期心肌损伤对短期和长期死亡率的影响尚未确定。

致编辑：隔膜子宫是最常见的子宫异常，与不良生殖结局的风险增加有关。经宫颈鼻中隔切除术（TCRS）广泛用于具有不良生殖结局的患者。的发生率再一次TCRS后的宫内粘连（IUAs）约为5%至25%。^[1]各种抗粘连方法广泛应用于子宫间隔患者的临床处理，包括宫内节育器、Foley球囊、雌激素、抗生素、透明质酸凝胶等。然而，没有足够的证据支持或反对这些方法中的任何一种（C级），^[2]缺乏高级证据。

致编辑：肿瘤免疫治疗近年来进展迅速。然而，免疫检查点阻断（ICB）治疗可能会导致过度进行性疾病（HPD）的临床症状，特别是对于驱动基因发生改变或扩增的患者，如小鼠双分钟2（MDM2),表皮生长因子受体（EGFR）和成纤维细胞生长因子4（FGF4).近日，镰田等人^[1]研究了HPD的分子机制，以探索免疫检查点抑制是否在临床试验中导致患者发生HPD。在PD-1单抗治疗后，发现HPD患者的Ki67+效应调节性T细胞（eTregs）增加。其他研究也发现，HPD患者肿瘤微环境中的免疫细胞在治疗前后表现出明显的变化。^[2]HPD中的肿瘤微环境变化暗示了癌症免疫治疗后促进肿瘤细胞快速生长的未知基因相互作用的潜在存在。