肝外胆管癌术后辅助放化疗治疗进展

肝外胆管癌（ECC）是一种恶性程度较高的肿瘤,即使在病变早期进行根治性切除手术,患者术后仍有较高的复发率,总体生存率低。近几年来,ECC术后辅助治疗的研究逐渐开展,以吉西他滨、氟尿嘧啶等为基础的辅助化疗或联合放、化疗可使ECC患者术后获益,延长患者的总生存期。然而现有的辅助治疗方案各异,缺少ECC术后辅助治疗的标准方案。本文结合最新发表的研究结果,讨论ECC术后辅助治疗的现状和主要措施。     

腹腔镜低位直肠癌根治腹部无切口经肛切除套入式吻合102例经验

目的探讨腹部无切口经肛门切除标本的腹腔镜低位直肠癌根治套入式吻合术的安全性和可行性及临床疗效。 方法从2010年3月至2017年12月对102例低位直肠癌行腹腔镜下根治经肛门切除行套入式吻合保肛术,男43例,女59例。年龄36～81岁(平均59.6岁)。肿瘤距肛缘5～7 cm 85例,4 cm 17例,术前评估T₁N₀M₀ 79例,T₂N₀M₀ 23例。采用中间入路用超声刀沿乙状结肠系膜根部游离并裸化肠系膜下动静脉根部后,施夹并切断。按TME原则,游离直肠至肛管直肠环达肿瘤远端3～5 cm。会阴部手术距齿状线上2 cm处环型切开,沿黏膜下锐性向上剥离至提肛肌平面切断直肠,将直肠及远端乙状结肠一并从肛门移出体外切除,行套入式近端结肠全层与直肠黏膜及肠黏膜下吻合。 结果本组102例,手术平均时间为179 min,平均检出淋巴结13枚,术后发生吻合口漏3例(2.9%)行临时结肠造口,3个月后还纳愈合。吻合口狭窄2例(1.9%),经扩张后狭窄解除。术后病理为T₁～T₂N₀M₀ 49例,T₂N₁M₀ 53例。术后12个月肛门功能,Kirwan分级1级占94.1%,肛门功能基本恢复到正常。术后随访6～84月,平均45个月,局部肿瘤复发4例(3.9%),生存满3年以上67例。 结论腹腔镜低位直肠癌根治腹部无切口经肛门切除套入式吻合保肛术,是安全可行,真正达到腹部无手术切口、无瘢痕、美容美观、完全微创的最佳效果,其远期疗效待进一步随访观察。     

肝细胞癌组织miRNA-155水平变化及其对预后的影响

目的 观察肝细胞癌（HCC）组织miRNA-155水平变化,并分析其对患者预后的意义。方法 2013年1月~2014年5月我院诊治的50例HCC患者,取手术切除的癌组织,另取50例正常肝组织作为对照组,采用荧光定量PCR法检测组织miRNA-155水平。结果 正常肝组织miRNA-155水平（1.06±0.1）明显低于HCC癌组织,10例Ⅰ级、15例Ⅱ级、12例Ⅲ级和13例Ⅳ级HCC 组织miRNA-155水平分别为（2.04±0.82）、（3.02±1.20）、（4.20±1.84）和（6.24±2.36）;miRNA-155低水平HCC患者生存率（24.00%）明显高于miRNA-155高水平患者（9.24%,P<0.05）;在不同分级HCC（14.26月对9.02月）、不同肿瘤大小（15.68 月对10.02月）、肿瘤是否转移（8.20 月对14.46月）、是否静脉侵犯（9.36 月对14.36月）、肿瘤分化程度（15.20月对7.84月）和miRNA-155水平高低（7.86月对16.32月）患者间生存期均存在明显差异（P<0.05）;肿瘤大小（>5 cm,HR=1.46,P=0.038）、肿瘤转移（是,HR=1.72,P=0.026）、静脉侵犯（是,HR=1.46,P<0.001）、肿瘤分化（高分化,HR=1.33,P=0.012）和miRNA-155（高水平,HR=1.65,P<0.001）均为影响HCC患者预后的独立危险因素（P<0.05）。结论 肝癌组织miRNA-155水平明显高于正常肝组织,且高水平的miRNA-155为HCC患者预后的独立危险因素。结果表明,miRNA-155水平高低可评估HCC患者预后,可考虑将其作为评估HCC患者预后的独立预测因子之一。     

Astrocyte morphology: Diversity,plasticity, and role in neurological diseases

Astrocytes are the most abundant glial cells in the central nervous system (CNS) and participate in synaptic, circuit, and behavioral functions. The well‐developed protoplasmic astrocytes contain numerous processes forming well‐delineated bushy territories that overlap by as little as 5% at their boundaries. This highly complex morphology, with up to approximately 80% of the cell's membrane constituted by fine processes with dimensions on the tens of nanometer scale and high surface area to volume ratios, comes in contact with synapses, blood vessels, and other glial cells. Recent progress is challenging the conventional view that astrocytes are morphologically homogeneous throughout the brain; instead, they display circuit‐ and region‐specific morphological diversity that may contribute to the heterogeneous astrocyte‐neuron spatiotemporal interplay in different brain areas. Further, the fine structure of astrocytes is found to be highly plastic and activity‐dependent. We are beginning to understand how astrocyte structural plasticity contributes to brain functions. The change/loss of astrocyte morphology, traditionally known as a hallmark for reactive astrogliosis, is a common pathological feature in many neurological disorders. However, recent data suggest the fine structural deficits preceding reactive astrogliosis may drive disease progression. This review summarizes recent advances in astrocyte morphological diversity, plasticity, and disease‐related deficits.     

Bone morphogenetic protein-7 represses hepatic stellate cell activation and liver fibrosis via regulation of TGF-β/Smad signaling pathway

BACKGROUND Liver fibrosis is a refractory disease whose persistence can eventually induce cirrhosis or even liver cancer.Early liver fibrosis is reversible by intervention.As a member of the transforming growth factor-beta(TGF-β)superfamily,bone morphogenetic protein 7(BMP7)has anti-liver fibrosis functions.However,little is known about BMP7 expression changes and its potential regulatory mechanism as well as the relationship between BMP7 and TGF-βduring liver fibrosis.In addition,the mechanism underlying the anti-liver fibrosis function of BMP7 needs to be further explored.AIM To investigate changes in the dynamic expression of BMP7 during liver fibrosis,interactions between BMP7 and TGF-β1,and possible mechanisms underlying the anti-liver fibrosis function of BMP7.METHODS Changes in BMP7 expression during liver fibrosis and the interaction between BMP7 and TGF-β1 in mice were observed.Exogenous BMP7 was used to treat mouse primary hepatic stellate cells(HSCs)to observe its effect on activation,migration,and proliferation of HSCs and explore the possible mechanism underlying the anti-liver fibrosis function of BMP7.Mice with liver fibrosis received exogenous BMP7 intervention to observe improvement of liver fibrosis by using Masson’s trichrome staining and detecting the expression of the HSC activation indicator alpha-smooth muscle actin(α-SMA)and the collagen formation associated protein type I collagen(Col I).Changes in the dynamic expression of BMP7 during liver fibrosis in the human body were further observed.RESULTS In the process of liver fibrosis induced by carbon tetrachloride(CCl4)in mice,BMP7 protein expression first increased,followed by a decrease;there was a similar trend in the human body.This process was accompanied by a sustained increase in TGF-β1 protein expression.In vitro experiment results showed that TGF-β1 inhibited BMP7 expression in a time-and dose-dependent manner.In contrast,high doses of exogenous BMP7 inhibited TGF-β1-induced activation,migration,and proliferation of HSCs;this inhibitory effect was associated with upregulation of pSmad1/5/8 and downregulation of phosphorylation of Smad3 and p38 by BMP7.In vivo experiment results showed that exogenous BMP7 improved liver fibrosis in mice.CONCLUSION During liver fibrosis,BMP7 protein expression first increases and then decreases.This changing trend is associated with inhibition of BMP7 expression by sustained upregulation of TGF-β1 in a time-and dose-dependent manner.Exogenous BMP7 could selectively regulate TGF-β/Smad pathway-associated factors to inhibit activation,migration,and proliferation of HSCs and exert antiliver fibrosis functions.Exogenous BMP7 has the potential to be used as an antiliver fibrosis drug.     

鼻咽癌腮腺淋巴结转移危险因素及高危患者腮腺局部调强放疗的探讨

目的 探讨鼻咽癌腮腺淋巴结转移的高危因素,评价高危者腮腺放疗的可行性。方法 收集2011-2017年江苏省肿瘤医院放疗科收治的440例初诊鼻咽癌患者的临床资料,回顾性分析腮腺淋巴结转移相关的影像特点、治疗及预后。全组采用调强放疗技术,全腮腺或部分腮腺照射、选择性PLN照射,X线和(或)电子线补量,剂量45~60 Gy。χ²检验或Fisher's精确概率法检验和单因素分析,Logistic回归模型多因素分析。Kaplan-Meier法生存分析,Logrank检验差异。结果 腮腺区影像学可见淋巴结者共230例。确诊腮腺转移11例(占2.5%,11/440),其中腮腺淋巴结最大径≥5 mm者占81.8%(9/11)。多因素分析显示Ⅱ区淋巴结包膜外侵为其转移的独立危险因素。将腮腺区淋巴结最大径≥5 mm、Ⅱ区淋巴结包膜外侵者筛选为腮腺淋巴结转移高危组,根据腮腺区是否放疗分为放疗组及未放疗组。生存分析发现,在230例患者中,高危组腮腺区放疗者与未放疗者无局部复发生存率不同(P<0.05),总生存、无远处转移生存、无进展生存均相近(P>0.05)。结论 鼻咽癌腮腺淋巴结转移率低,Ⅱ区淋巴结包膜外侵为其独立高危因素。对于腮腺淋巴结最大径≥5 mm,或腮腺区存在影像学可见淋巴结,即使其最大径<5 mm,但若合并Ⅱ区淋巴结包膜外侵,建议行腮腺区放疗。