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An unusual case of mesenteric fibromatosis. 肠系膜纤维瘤病的一个不寻常病例。
Pub Date : 2024-05-01 Epub Date: 2024-03-01 DOI: 10.1002/kjm2.12817
Yu-Cheng Chiang, Po-Hsuan Wu
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引用次数: 0
Clinical outcome of bevacizumab or ramucirumab combined with epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors as the first line therapy in susceptible EGFR-mutated advanced non-small-cell lung. 贝伐珠单抗或雷莫芦单抗联合表皮生长因子受体(EGFR)酪氨酸激酶抑制剂作为易受 EGFR 突变影响的晚期非小细胞肺癌一线疗法的临床疗效。
Pub Date : 2024-05-01 Epub Date: 2024-03-25 DOI: 10.1002/kjm2.12822
Chia-Yu Kuo, Ming-Ju Tsai, Jen-Yu Hung, Mei-Hsuan Lee, Kuan-Li Wu, Yu-Chen Tsai, Cheng-Hao Chuang, Chung-Wen Huang, Chin-Ling Chen, Chih-Jen Yang, Inn-Wen Chong

Combining epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) with an anti- vascular endothelial growth factor (VEGF) agent, bevacizumab or ramucirumab, is indicated for advanced lung adenocarcinoma harboring EGFR mutation. This study aimed to show the real-world data of combination therapy and compare the effectiveness between bevacizumab and ramucirumab in combination with an EGFR-TKI. This retrospective study enrolled 47 patients diagnosed of stage IV lung adenocarcinoma with exon 19 deletion or L858R point mutation, receiving a first-line EGFR-TKI with anti-VEGF agent, including 34 (72%) and 13 (28%) patients receiving bevacizumab and ramucirumab, respectively. The response rate was similar in both groups (p = 0.38). Patients receiving bevacizumab had similar progression free survival (PFS) as those receiving ramucirumab (median PFS: 21.9 vs. 24.2 months, p = 0.4871); similar finding was noted in overall survival (OS) (median OS: 33.5 months vs. not reached, p = 0.4618). Patients receiving ramucirumab experienced a significantly high-grade hypertension compared to those receiving bevacizumab (p = 0.0351). Multivariable Cox regression analysis found independent risk factors for worse PFS included poorer ECOG performance status, multiple (≥3) metastatic sites, brain metastasis, and pleural metastasis/effusion, while the type of anti-VEGF agent was not a risk factor. Pericardial metastasis/effusion was the only one independent risk factor for worse OS. In summary, ramucirumab may have similar effectiveness as bevacizumab in combination with an EGFR-TKI as first line therapy for advanced lung adenocarcinoma harboring susceptible EGFR mutation. Further large-scale registry-based cohort studies may be needed to validate our findings.

表皮生长因子受体(EGFR)酪氨酸激酶抑制剂(TKI)与抗血管内皮生长因子(VEGF)药物贝伐珠单抗(bevacizumab)或雷木单抗(ramucirumab)联合治疗表皮生长因子受体(EGFR)突变的晚期肺腺癌。本研究旨在展示联合治疗的实际数据,并比较贝伐单抗和雷莫芦单抗与 EGFR-TKI 联合治疗的疗效。这项回顾性研究共纳入了47例确诊为外显子19缺失或L858R点突变的IV期肺腺癌患者,他们均接受了一线EGFR-TKI联合抗血管内皮生长因子药物治疗,其中34例(72%)和13例(28%)患者分别接受了贝伐单抗和雷莫芦单抗治疗。两组患者的应答率相似(P = 0.38)。接受贝伐珠单抗治疗的患者与接受拉莫单抗治疗的患者的无进展生存期(PFS)相似(中位PFS:21.9个月 vs. 24.2个月,p = 0.4871);总生存期(OS)也相似(中位OS:33.5个月 vs. 未达到,p = 0.4618)。与接受贝伐珠单抗治疗的患者相比,接受雷莫芦单抗治疗的患者出现明显的高血压(p = 0.0351)。多变量考克斯回归分析发现,PFS较差的独立风险因素包括较差的ECOG表现状态、多个(≥3个)转移部位、脑转移和胸膜转移/渗出,而抗VEGF药物的类型不是风险因素。心包转移/浸润是唯一一个导致OS恶化的独立危险因素。总之,ramucirumab与贝伐珠单抗联合EGFR-TKI作为携带易感EGFR突变的晚期肺腺癌的一线疗法,可能具有与贝伐珠单抗相似的疗效。要验证我们的研究结果,可能还需要进一步开展基于登记的大规模队列研究。
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引用次数: 0
Precursor B-cell lymphoblastic lymphoma presenting as concurrent enlarging masses on the scalp and postauricular region in a 13-year-old boy. 一名 13 岁男孩头皮和耳后区域同时出现增大肿块的前体 B 细胞淋巴母细胞淋巴瘤。
Pub Date : 2024-05-01 Epub Date: 2024-02-16 DOI: 10.1002/kjm2.12811
Wei-Yao Wang, Sheau-Fang Yang, Yu-Wen Cheng, Yang-Yi Chen
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引用次数: 0
Correction to "Circ-MALAT1 accelerates cell proliferation and epithelial mesenchymal transformation of colorectal cancer through regulating miR-506-3p/KAT6B axis". Correction to "Circ-MALAT1 accelerates cell proliferation and ephelial mesenchymal transformation of colorectal cancer through regulating miR-506-3p/KAT6B axis".
Pub Date : 2024-05-01 DOI: 10.1002/kjm2.12846
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引用次数: 0
Takayasu's arteritis presented with empyema and acute heart failure with left ventricular thrombus in a 25‐year‐old woman 一名 25 岁女性因左心室血栓引发的高安氏动脉炎并发肺水肿和急性心力衰竭
Pub Date : 2024-04-30 DOI: 10.1002/kjm2.12839
Yu‐Jen Chen, Chia‐Wei Hsieh, Chih‐Hung Lai, Shih‐Ting Huang
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引用次数: 0
Proteasome inhibitor bortezomib prevents proliferation and migration of pulmonary arterial smooth muscle cells 蛋白酶体抑制剂硼替佐米能防止肺动脉平滑肌细胞增殖和迁移
Pub Date : 2024-04-29 DOI: 10.1002/kjm2.12835
Yi‐Ching Liu, Yu‐Hsin Tseng, Yu‐Hsin Kuan, Lin‐Yen Wang, Shang‐En Huang, Siao‐Ping Tsai, Jwu‐Lai Yeh, Jong‐Hau Hsu
Pulmonary vascular remodeling is a key pathological process of pulmonary arterial hypertension (PAH), characterized by uncontrolled proliferation and migration of pulmonary arterial smooth muscle cells (PASMCs). Bortezomib (BTZ) is the first Food and Drug Administration (FDA)‐approved proteasome inhibitor for multiple myeloma treatment. Recently, there is emerging evidence showing its effect on reversing PAH, although its mechanisms are not well understood. In this study, anti‐proliferative and anti‐migratory effects of BTZ on PASMCs were first examined by different inducers such as fetal bovine serum (FBS), angiotensin II (Ang II) and platelet‐derived growth factor (PDGF)‐BB, while potential mechanisms including cellular reactive oxygen species (ROS) and mitochondrial ROS were then investigated; finally, signal transduction of ERK and Akt was examined. Our results showed that BTZ attenuated FBS‐, Ang II‐ and PDGF‐BB‐induced proliferation and migration, with associated decreased cellular ROS production and mitochondrial ROS production. In addition, the phosphorylation of ERK and Akt induced by Ang II and PDGF‐BB was also inhibited by BTZ treatment. This study indicates that BTZ can prevent proliferation and migration of PASMCs, which are possibly mediated by decreased ROS production and down‐regulation of ERK and Akt. Thus, proteasome inhibition can be a novel pharmacological target in the management of PAH.
肺血管重塑是肺动脉高压(PAH)的一个关键病理过程,其特点是肺动脉平滑肌细胞(PASMC)增殖和迁移失控。硼替佐米(BTZ)是美国食品药品管理局(FDA)批准用于多发性骨髓瘤治疗的第一种蛋白酶体抑制剂。最近,有新的证据显示其具有逆转 PAH 的作用,尽管其机制尚不十分清楚。本研究首先通过胎牛血清(FBS)、血管紧张素II(Ang II)和血小板衍生生长因子(PDGF)-BB等不同诱导剂检测了BTZ对PASMCs的抗增殖和抗迁移作用,然后研究了包括细胞活性氧(ROS)和线粒体ROS在内的潜在机制,最后检测了ERK和Akt的信号转导。我们的研究结果表明,BTZ 可抑制 FBS、Ang II 和 PDGF-BB 诱导的增殖和迁移,同时减少细胞 ROS 和线粒体 ROS 的产生。此外,BTZ 还能抑制 Ang II 和 PDGF-BB 诱导的 ERK 和 Akt 磷酸化。这项研究表明,BTZ 可阻止 PASMCs 的增殖和迁移,而增殖和迁移可能是通过减少 ROS 的产生以及下调 ERK 和 Akt 来实现的。因此,蛋白酶体抑制可以成为治疗 PAH 的一个新的药物靶点。
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引用次数: 0
Extracellular vesicles of Bifidobacterium longum reverse the acquired carboplatin resistance in ovarian cancer cells via p53 phosphorylation on Ser15 长双歧杆菌的胞外囊泡通过 p53 在 Ser15 上的磷酸化逆转卵巢癌细胞的卡铂获得性耐药性
Pub Date : 2024-04-22 DOI: 10.1002/kjm2.12837
Yun‐Long Fan, Jia‐Xi Jin, Jun Zhu, Hai‐Bo Ruan, Jin‐Qun Huang
We previously found that the relative abundance of Bifidobacterium was increased after chemotherapy; however, the role of Bifidobacterium longum in chemotherapeutic drug resistance in ovarian cancer (OVC) remains unclear. This study aimed to understand the potential effects and mechanism of B. longum extracellular vesicles (B. longum‐EVs) on carboplatin (CBP) resistance in OVC. Eight normal and 11 ovarian tissues were collected and the expression of B. longum genomic DNA and its association with acquired CBP resistance in OVC patients was determined. After isolating EVs by ultracentrifugation from B. longum (ATCC 15707), CBP‐resistant A2780 cells were treated with PBS, CBP, B. longum‐EVs, or CBP + B. longum‐EVs, and subsequently analyzed by CCK‐8, Edu staining, Annexin V/PI double staining, wound healing, and Transwell assays to detect cell viability, proliferation, apoptosis, migration, and invasion, respectively. MRP1, ATP7A, ATP7B, and p53 expression as well as p53 phosphorylation were measured by western blot analysis. S15A mutation of p53 was assessed to examine the potential role of p53 Ser15 phosphorylation in CBP‐resistant OVC. B. longum levels were elevated and positively associated with CBP resistance in OVC patients. Only high concentrations of B. longum‐EVs attenuated A2780 cell proliferation, apoptosis, migration, and invasion. B. longum‐EVs exposure significantly enhanced the sensitivity of CBP‐resistant A2780 cells to CBP and decreased the expression of drug resistance‐related proteins. The effect of B. longum‐EVs on reversing CBP resistance was completely inhibited by S15A mutation of p53. B. longum‐EVs enhanced the sensitivity of OVC cells to CBP through p53 phosphorylation on Ser15.
我们以前曾发现,化疗后双歧杆菌的相对丰度会增加;然而,长双歧杆菌在卵巢癌(OVC)化疗耐药性中的作用仍不清楚。本研究旨在了解长双歧杆菌胞外囊泡(B. longum-EVs)对卵巢癌患者卡铂(CBP)耐药性的潜在影响和机制。研究收集了8例正常卵巢组织和11例卵巢组织,并测定了长春花酵母菌基因组DNA的表达及其与卵巢癌患者获得性CBP耐药性的关系。通过超速离心从长殖菌(ATCC 15707)中分离出EVs后,用PBS、CBP、长殖菌-EVs或CBP + 长殖菌-EVs处理CBP耐药的A2780细胞,然后用CCK-8、Edu染色、Annexin V/PI双重染色、伤口愈合和Transwell试验分别检测细胞活力、增殖、凋亡、迁移和侵袭。MRP1、ATP7A、ATP7B 和 p53 的表达以及 p53 磷酸化均通过 Western 印迹分析进行检测。评估了 p53 的 S15A 突变,以研究 p53 Ser15 磷酸化在 CBP 抗性 OVC 中的潜在作用。OVC患者体内长春花酵母菌水平升高,并与CBP耐药性呈正相关。只有高浓度的长春花酵母菌-EVs能抑制A2780细胞的增殖、凋亡、迁移和侵袭。B.longum-EVs暴露能显著增强对CBP耐药的A2780细胞对CBP的敏感性,并降低耐药相关蛋白的表达。p53的S15A突变完全抑制了B. longum-EVs逆转CBP耐药性的作用。B. longum-EVs通过p53在Ser15上的磷酸化增强了OVC细胞对CBP的敏感性。
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引用次数: 0
Activation of ASIC3/ERK pathway by paeoniflorin improves intestinal fluid metabolism and visceral sensitivity in slow transit constipated rats 芍药苷激活 ASIC3/ERK 通路可改善慢速便秘大鼠的肠液代谢和内脏敏感性
Pub Date : 2024-04-18 DOI: 10.1002/kjm2.12829
Yuan Deng, Qiong Zhao, Hong‐Yun Zhou, Zi‐Qi Zhang, Yu Zhan
Slow transit constipation (STC) is one of the most common gastrointestinal disorders in children and adults worldwide. Paeoniflorin (PF), a monoterpene glycoside compound extracted from the dried root of Paeonia lactiflora, has been found to alleviate STC, but the mechanisms of its effect remain unclear. The present study aimed to investigate the effects and mechanisms of PF on intestinal fluid metabolism and visceral sensitization in rats with compound diphenoxylate‐induced STC. Based on the evaluation of the laxative effect, the abdominal withdrawal reflex test, enzyme‐linked immunosorbent assay, quantitative real‐time polymerase chain reaction, western blot, and immunohistochemistry were used to detect the visceral sensitivity, fluid metabolism‐related proteins, and acid‐sensitive ion channel 3/extracellular signal‐regulated kinase (ASIC3/ERK) pathway‐related molecules. PF treatment not only attenuated compound diphenoxylate‐induced constipation symptoms and colonic pathological damage in rats but also ameliorated colonic fluid metabolic disorders and visceral sensitization abnormalities, as manifested by increased colonic goblet cell counts and mucin2 protein expression, decreased aquaporin3 protein expression, improved abdominal withdrawal reflex scores, reduced visceral pain threshold, upregulated serum 5‐hydroxytryptamine, and downregulated vasoactive intestinal peptide levels. Furthermore, PF activated the colonic ASIC3/ERK pathway in STC rats, and ASIC3 inhibition partially counteracted PF's modulatory effects on intestinal fluid and visceral sensation. In conclusion, PF alleviated impaired intestinal fluid metabolism and abnormal visceral sensitization in STC rats and thus relieved their symptoms through activation of the ASIC3/ERK pathway.
慢传输性便秘(STC)是全球儿童和成人最常见的胃肠道疾病之一。芍药苷(PF)是从芍药的干根中提取的一种单萜烯苷化合物,已被发现能缓解慢传输性便秘,但其作用机制仍不清楚。本研究旨在探讨 PF 对复方地芬诺酯诱导的 STC 大鼠肠液代谢和内脏敏感性的影响和机制。在评估通便效果的基础上,采用腹部退缩反射试验、酶联免疫吸附试验、实时定量聚合酶链反应、Western 印迹和免疫组织化学方法检测内脏敏感性、体液代谢相关蛋白和酸敏感离子通道 3/ 细胞外信号调节激酶(ASIC3/ERK)通路相关分子。PF 治疗不仅减轻了复合二苯氧胺诱导的大鼠便秘症状和结肠病理损伤,还改善了结肠液体代谢紊乱和内脏敏感性异常,具体表现为结肠小管细胞数量和粘蛋白 2 蛋白表达增加,水肿素 3 蛋白表达减少,腹部退缩反射评分提高,内脏痛阈降低,血清 5- 羟色胺上调,血管活性肠肽水平下调。此外,PF 还激活了 STC 大鼠结肠的 ASIC3/ERK 通路,而 ASIC3 抑制则部分抵消了 PF 对肠液和内脏感觉的调节作用。总之,PF 通过激活 ASIC3/ERK 通路,缓解了 STC 大鼠受损的肠液代谢和异常的内脏敏感性,从而缓解了它们的症状。
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引用次数: 0
Esophageal cancer localization by sagittal computed tomography images and endoscopic measurement 通过矢状面计算机断层扫描图像和内窥镜测量进行食管癌定位
Pub Date : 2024-04-17 DOI: 10.1002/kjm2.12834
Jen Yang, Wei‐Lun Chang, Forn‐Chia Lin, Nan‐Tsing Chiu
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引用次数: 0
Predictive effects of the interactions among cesarean section, birth weight, and preterm birth on the risk of atopic dermatitis in children 剖腹产、出生体重和早产之间的相互作用对儿童患特应性皮炎风险的预测作用
Pub Date : 2024-04-17 DOI: 10.1002/kjm2.12826
Chih‐Kai Wong, Cheng‐Fang Yen, Yi‐Lung Chen
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引用次数: 0
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The Kaohsiung journal of medical sciences
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