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Intraductal papillary neoplasms of the bile duct. 胆管内乳头状肿瘤。
IF 1.8 Q3 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2014-01-01 Epub Date: 2014-05-18 DOI: 10.1155/2014/459091
Masayuki Ohtsuka, Hiroaki Shimizu, Atsushi Kato, Hideyuki Yoshitomi, Katsunori Furukawa, Toshio Tsuyuguchi, Yuji Sakai, Osamu Yokosuka, Masaru Miyazaki

Intraductal papillary neoplasm of the bile duct (IPNB) is a rare variant of bile duct tumors characterized by papillary growth within the bile duct lumen and is regarded as a biliary counterpart of intraductal papillary mucinous neoplasm of the pancreas. IPNBs display a spectrum of premalignant lesion towards invasive cholangiocarcinoma. The most common radiologic findings for IPNB are bile duct dilatation and intraductal masses. The major treatment of IPNB is surgical resection. Ultrasonography, computed tomography, magnetic resonance image, and cholangiography are usually performed to assess tumor location and extension. Cholangioscopy can confirm the histology and assess the extent of the tumor including superficial spreading along the biliary epithelium. However, pathologic diagnosis by preoperative biopsy cannot always reflect the maximum degree of atypia, because IPNBs are often composed of varying degrees of cytoarchitectural atypia. IPNBs are microscopically classified into four epithelial subtypes, such as pancreatobiliary, intestinal, gastric, and oncocytic types. Most cases of IPNB are IPN with high-grade intraepithelial neoplasia or with an associated invasive carcinoma. The histologic types of invasive lesions are either tubular adenocarcinoma or mucinous carcinoma. Although several authors have investigated molecular genetic changes during the development and progression of IPNB, these are still poorly characterized and controversial.

胆管导管内乳头状肿瘤(IPNB)是一种罕见的胆管肿瘤,其特征是胆管腔内乳头状生长,被认为是胰腺导管内乳头状粘液瘤的胆道对应体。IPNBs显示了向侵袭性胆管癌的癌前病变谱。IPNB最常见的影像学表现是胆管扩张和管内肿块。IPNB的主要治疗方法是手术切除。超声检查、计算机断层扫描、磁共振成像和胆管造影通常用于评估肿瘤的位置和范围。胆道镜检查可以确认组织学和评估肿瘤的范围,包括沿胆道上皮的浅表扩散。然而,术前活检的病理诊断并不总是反映最大程度的异型性,因为ipnb通常由不同程度的细胞结构异型性组成。IPNBs在显微镜下可分为四种上皮亚型,如胰胆管型、肠型、胃型和嗜瘤细胞型。大多数IPNB病例为IPN伴高级别上皮内瘤变或伴浸润性癌。浸润性病变的组织学类型为管状腺癌或粘液癌。尽管一些作者已经研究了IPNB发生和发展过程中的分子遗传变化,但这些变化仍然缺乏特征和争议。
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引用次数: 125
What are the precursor and early lesions of peripheral intrahepatic cholangiocarcinoma? 外周肝内胆管癌的前兆和早期病变是什么?
IF 1.8 Q3 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2014-01-01 Epub Date: 2014-04-22 DOI: 10.1155/2014/805973
Yasuni Nakanuma, Akemi Tsutsui, Xiang Shan Ren, Kenichi Harada, Yasunori Sato, Motoko Sasaki
Cholangiocarcinoma (CC) is divided into distal, perihilar, and intrahepatic CCs (ICCS), and are further subdivided into large bile duct ICC and peripheral ICC. In distal and perihilar CC and large duct ICC, biliary intraepithelial neoplasm (BilIN) and intraductal papillary neoplasm (IPN) have been proposed as precursor lesions. Peripheral ICC, bile duct adenoma (BDA), biliary adenofibroma (BAF), and von Meyenburg complexes (VMCs) are reportedly followed by development of ICCs. Herein, we surveyed these candidate precursor lesions in the background liver of 37 cases of peripheral ICC and controls (perihilar CC, 34 cases; hepatocellular carcinoma, 34 cases and combined hepatocellular cholangiocarcinoma, 25 cases). In the background liver of peripheral ICC, BDA and BAF were not found, but there were not infrequently foci of BDA-like lesions and atypical bile duct lesions involving small bile ducts (32.4% and 10.8%, resp.). VMCs were equally found in peripheral CCs and also control CCs. In conclusion, BDA, BAF, and VMCs are a possible precursor lesion of a minority of peripheral CCs, and BDA-like lesions and atypical bile duct lesions involving small bile ducts may also be related to the development of peripheral ICC. Further pathologic studies on these lesions are warranted for analysis of development of peripheral ICCs.
胆管癌(CC)分为远端胆管癌、肝门周围胆管癌和肝内胆管癌(ICCS),并进一步细分为大胆管胆管癌和周围胆管胆管癌。在远端和门周CC和大导管ICC中,胆道上皮内肿瘤(BilIN)和导管内乳头状肿瘤(IPN)被认为是前体病变。外周ICC、胆管腺瘤(BDA)、胆管腺纤维瘤(BAF)和von Meyenburg复合物(vmc)据报道随后发展为ICC。在此,我们调查了37例周围型ICC和对照组(周围型CC, 34例;肝细胞性肝癌34例,合并肝细胞性胆管癌25例。外周ICC背景肝未发现BDA和BAF,但BDA样病变灶和不典型胆管病变累及小胆管的情况并不少见(分别为32.4%和10.8%)。外周细胞癌和对照细胞癌均可见vmc。综上所述,BDA、BAF和vmc可能是少数外周型cc的前体病变,BDA样病变和累及小胆管的非典型胆管病变也可能与外周型ICC的发生有关。对这些病变进行进一步的病理研究是分析周围icc发展的必要条件。
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引用次数: 45
Clinical features of adult patients with acute hepatitis B virus infection progressing to chronic infection. 成人急性乙型肝炎病毒感染进展为慢性感染的临床特征
IF 1.8 Q3 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2014-01-01 Epub Date: 2014-10-02 DOI: 10.1155/2014/358206
Kojiro Michitaka, Atsushi Hiraoka, Yoshio Tokumoto, Keiko Ninomiya, Tomoyuki Ninomiya, Norio Horiike, Masanori Abe, Yoichi Hiasa

Background. Information regarding the progression of acute hepatitis B virus (HBV) infection to chronic infection in adults is scarce. Methods. Twenty-five adult patients with acute HBV infection (14 men and 11 women, 18-84 years old), whose clinical features progressed to those of chronic infection (group A) or did not (group B), were studied retrospectively. Results. There were 3 and 22 patients in groups A and B, respectively. Two of the 3 patients of group A lacked the typical symptoms of acute hepatitis. No differences were found between groups with respect to age, sex, or HBV genotypes. However, total bilirubin and alanine aminotransaminase levels were significantly lower in group A. Conclusions. Three of the 25 adult patients with acute HBV infection progressed to chronic infection. Hepatitis was mild in these patients. Patients with mild acute hepatitis B or unapparent HBV infection may have a higher risk of progressing to chronic infection.

背景。关于成人急性乙型肝炎病毒(HBV)感染进展为慢性感染的信息很少。方法。回顾性研究25例成年急性HBV感染患者(男14例,女11例,年龄18-84岁),其临床特征进展为慢性感染(A组)或未进展为慢性感染(B组)。结果。A组3例,B组22例。A组3例患者中2例无典型急性肝炎症状。各组之间在年龄、性别或HBV基因型方面没有发现差异。然而,a组总胆红素和丙氨酸转氨酶水平明显降低。25例急性HBV感染的成人患者中有3例进展为慢性感染。这些患者的肝炎症状较轻。轻度急性乙型肝炎或不明显HBV感染的患者可能有更高的发展为慢性感染的风险。
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引用次数: 6
Circulating MicroRNAs in Plasma of Hepatitis B e Antigen Positive Children Reveal Liver-Specific Target Genes. 乙型肝炎e抗原阳性儿童血浆循环microrna揭示肝脏特异性靶基因
IF 1.8 Q3 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2014-01-01 Epub Date: 2014-12-17 DOI: 10.1155/2014/791045
Thilde Nordmann Winther, Kari Stougaard Jacobsen, Aashiq Hussain Mirza, Ida Louise Heiberg, Claus Heiner Bang-Berthelsen, Flemming Pociot, Birthe Hogh

Background and Aim. Hepatitis B e antigen positive (HBeAg-positive) children are at high risk of severe complications such as hepatocellular carcinoma and cirrhosis. Liver damage is caused by the host immune response to infected hepatocytes, and we hypothesise that specific microRNAs play a role in this complex interaction between virus and host. The study aimed to identify microRNAs with aberrant plasma expressions in HBeAg-positive children and with liver-specific target genes. Methods. By revisiting our previous screen of microRNA plasma levels in HBeAg-positive and HBeAg-negative children with chronic hepatitis B (CHB) and in healthy controls, candidate microRNAs with aberrant plasma expressions in HBeAg-positive children were identified. MicroRNAs targeting liver-specific genes were selected based on bioinformatics analysis and validated by qRT-PCR using plasma samples from 34 HBeAg-positive, 26 HBeAg-negative, and 60 healthy control children. Results. Thirteen microRNAs showed aberrant plasma expressions in HBeAg-positive children and targeted liver-specific genes. In particular, three microRNAs were upregulated and one was downregulated in HBeAg-positive children compared to HBeAg-negative and healthy control children, which showed equal levels. Conclusion. The identified microRNAs might impact the progression of CHB in children. Functional studies are warranted, however, to elucidate the microRNAs' role in the immunopathogenesis of childhood CHB.

背景和目的。乙型肝炎e抗原阳性(hbeag阳性)的儿童发生严重并发症(如肝细胞癌和肝硬化)的风险很高。肝损伤是由宿主对感染肝细胞的免疫反应引起的,我们假设特定的microrna在病毒和宿主之间复杂的相互作用中起作用。该研究旨在鉴定hbeag阳性儿童和肝脏特异性靶基因中异常血浆表达的microrna。方法。通过回顾我们之前对hbeag阳性和hbeag阴性的慢性乙型肝炎(CHB)儿童以及健康对照者的血浆microRNA水平的筛查,我们确定了hbeag阳性儿童血浆表达异常的候选microRNA。基于生物信息学分析选择靶向肝脏特异性基因的microrna,并通过qRT-PCR对34名hbeag阳性、26名hbeag阴性和60名健康对照儿童的血浆样本进行验证。结果。13个microrna在hbeag阳性儿童和靶向肝脏特异性基因中表现出异常的血浆表达。特别是,与hbeag阴性和健康对照儿童相比,hbeag阳性儿童中有3个microrna上调,1个microrna下调,两者水平相同。结论。鉴定的microrna可能影响儿童CHB的进展。然而,功能研究是有必要的,以阐明microrna在儿童慢性乙型肝炎免疫发病机制中的作用。
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引用次数: 14
Serum Cytokeratin-18 Is Associated with NOX2-Generated Oxidative Stress in Patients with Nonalcoholic Fatty Liver. 非酒精性脂肪肝患者血清细胞角蛋白-18与nox2产生的氧化应激相关
IF 1.8 Q3 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2014-01-01 Epub Date: 2014-01-29 DOI: 10.1155/2014/784985
M Del Ben, L Polimeni, F Baratta, S Bartimoccia, R Carnevale, L Loffredo, P Pignatelli, F Violi, F Angelico

Background & Aims. Hepatocyte apoptosis may play a role in progression of nonalcoholic fatty liver and oxidative stress seems one of the key mechanisms responsible for liver damage. The aim was to determine the association of oxidative stress with cytokeratin-18 M30 fragment levels, a marker of hepatocyte apoptosis. Methods. Steatosis severity was defined according to Hamaguchi's echographic criteria in 209 patients with nonalcoholic fatty liver. Serum cytokeratin-18, urinary 8-iso-prostaglandin F2 α , soluble NOX2-derived peptide, and adiponectin were measured. Results. Serum cytokeratin-18 progressively increased with steatosis severity (from 169.5 (129.3/183.8) to 176 (140/190) and 180 (169.5/192.5) μ IU/mL in mild, moderate, and severe steatosis, respectively; P < 0.01). After stratification by cytokeratin-18 tertiles, a significant progression of body mass index, HOMA-IR, triglycerides, urinary 8-iso-PGF2 α , soluble NOX2-derived peptide, and of the prevalence of diabetes and severe steatosis was found, while HDL-cholesterol and adiponectin progressively decreased. A positive correlation between cytokeratin-18 and body mass index, HOMA-IR, Hamaguchi's score, urinary 8-iso-PGF2 α , and soluble NOX2-derived peptide and a negative correlation between cytokeratin-18 and HDL-cholesterol and adiponectin were found. Body mass index, adiponectin, and soluble NOX2-derived peptide were independent predictors of serum cytokeratin-18 levels (adjusted R (2) = 0.36). Conclusion. We support an association between oxidative stress and severity of liver damage in patients with nonalcoholic fatty liver.

背景与目的肝细胞凋亡可能在非酒精性脂肪肝的进展中起作用,氧化应激似乎是导致肝损伤的关键机制之一。目的是确定氧化应激与细胞角蛋白-18 M30片段水平的关系,细胞角蛋白-18 M30片段是肝细胞凋亡的标志。方法。209例非酒精性脂肪肝患者根据Hamaguchi超声标准确定脂肪变性严重程度。测定血清细胞角蛋白-18、尿8-异前列腺素F2 α、可溶性nox2衍生肽和脂联素。结果。血清细胞角蛋白-18随脂肪变性严重程度逐渐升高(轻度、中度和重度脂肪变性患者分别从169.5(129.3/183.8)到176(140/190)和180 (169.5/192.5)μ IU/mL;P < 0.01)。经细胞角蛋白-18分层后,发现体重指数、HOMA-IR、甘油三酯、尿8-iso-PGF2 α、可溶性nox2衍生肽、糖尿病和严重脂肪变性的患病率显著上升,而hdl -胆固醇和脂联素逐渐下降。细胞角蛋白18与体重指数、HOMA-IR、Hamaguchi评分、尿8-iso-PGF2 α、可溶性nox2衍生肽呈正相关,与hdl -胆固醇、脂联素呈负相关。体重指数、脂联素和可溶性nox2衍生肽是血清细胞角蛋白-18水平的独立预测因子(调整后R(2) = 0.36)。结论。我们支持氧化应激与非酒精性脂肪肝患者肝损伤严重程度之间的关联。
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引用次数: 18
Genetic diseases that predispose to early liver cirrhosis. 容易导致早期肝硬化的遗传疾病。
IF 1.8 Q3 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2014-01-01 Epub Date: 2014-07-14 DOI: 10.1155/2014/713754
Manuela Scorza, Ausilia Elce, Federica Zarrilli, Renato Liguori, Felice Amato, Giuseppe Castaldo

Inherited liver diseases are a group of metabolic and genetic defects that typically cause early chronic liver involvement. Most are due to a defect of an enzyme/transport protein that alters a metabolic pathway and exerts a pathogenic role mainly in the liver. The prevalence is variable, but most are rare pathologies. We review the pathophysiology of such diseases and the diagnostic contribution of laboratory tests, focusing on the role of molecular genetics. In fact, thanks to recent advances in genetics, molecular analysis permits early and specific diagnosis for most disorders and helps to reduce the invasive approach of liver biopsy.

遗传性肝病是一组代谢和遗传缺陷,通常会导致早期慢性肝脏受累。大多数遗传性肝病是由于酶/转运蛋白缺陷引起的,这种缺陷会改变代谢途径,并主要在肝脏中发挥致病作用。发病率各不相同,但大多数都是罕见病。我们回顾了这类疾病的病理生理学和实验室检测对诊断的贡献,重点是分子遗传学的作用。事实上,由于遗传学的最新进展,分子分析可以对大多数疾病进行早期和特异性诊断,并有助于减少肝活检的侵入性方法。
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引用次数: 0
Central portalization correlates with fibrosis but not with risk factors for nonalcoholic steatohepatitis in steatotic chronic hepatitis C. 中枢性门化与慢性丙型肝炎非酒精性脂肪性肝炎的纤维化相关,但与危险因素无关。
IF 1.8 Q3 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2014-01-01 Epub Date: 2014-11-30 DOI: 10.1155/2014/329297
Hwajeong Lee, Sanaz Ainechi, Karen Dresser, Elizabeth M Kurian

Concomitant steatosis in chronic hepatitis C is associated with fibrosis and unfavorable treatment outcome. Central zone injury in nonalcoholic steatohepatitis (NASH) manifests as central portalization, with centrizonal microvessels and ductular reaction. We investigated whether central portalization in steatotic HCV biopsies would identify patients with metabolic risk factors for NASH. Liver biopsies with chronic hepatitis C and >10% steatosis (n = 65) were evaluated for the degree of steatosis, zonation of steatosis, fibrosis, and nonalcoholic fatty liver disease (NAFLD) activity score. The presence of centrizonal microvessels, sinusoidal capillarization, ductular reaction, and CK7 positive intermediate-phenotype hepatocytes were evaluated by CD34 and CK7 immunostain. The degree of steatosis and fibrosis showed a positive correlation. Additional positive correlations were noted between centrizonal angiogenesis and NAFLD activity score and central portalization and fibrosis. However, neither central portalization nor zonation of steatosis identified patients with metabolic risk factors for NASH. Therefore, central portalization cannot be used as a surrogate marker to identify patients with metabolic risk factors for NASH in steatotic HCV biopsies. The mechanism of centrizonal injury in steatotic HCV hepatitis is not solely attributable to the metabolic risk factors for NASH.

慢性丙型肝炎伴发脂肪变性与纤维化和不良治疗结果相关。非酒精性脂肪性肝炎(NASH)中央区损伤表现为中央性门化,伴有中央性微血管和导管反应。我们研究了脂肪变性HCV活检中的中枢门化是否能识别出NASH的代谢危险因素。对慢性丙型肝炎和>10%脂肪变性患者(n = 65)进行肝活检,评估脂肪变性程度、脂肪变性分带、纤维化和非酒精性脂肪性肝病(NAFLD)活动性评分。通过CD34和CK7免疫染色评估中心微血管、窦状毛细血管、导管反应和CK7阳性中表型肝细胞的存在。脂肪变性程度与纤维化程度呈正相关。中心血管生成和NAFLD活动评分与中心门化和纤维化之间存在额外的正相关。然而,中枢门化和脂肪变性分带都不能确定NASH患者的代谢危险因素。因此,在脂肪变性HCV活检中,中枢门化不能作为识别NASH代谢危险因素患者的替代标志物。脂肪变性HCV肝炎中枢性损伤的机制并不能完全归因于NASH的代谢危险因素。
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引用次数: 3
Effect of Platelet-Rich Plasma on CCl4-Induced Chronic Liver Injury in Male Rats. 富血小板血浆对ccl4诱导的雄性大鼠慢性肝损伤的影响。
IF 1.8 Q3 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2014-01-01 Epub Date: 2014-02-23 DOI: 10.1155/2014/932930
Zahra Hesami, Akram Jamshidzadeh, Maryam Ayatollahi, Bita Geramizadeh, Omid Farshad, Akbar Vahdati

Platelet-rich plasma (PRP) has been of great concern to the scientists and doctors who are involved in wound healing and regenerative medicine which focuses on repairing and replacing damaged cells and tissues. Growth factors of platelet-rich plasma are cost-effective, available, and is more stable than recombinant human growth factors. Given these valuable properties, we decided to assess the effect of PRP on CCl4-induced hepatotoxicity on rats. The rats received CCl4 (1 mL/kg, i.p. 1 : 1 in olive oil) twice per week for 8 weeks. Five weeks after CCl4 injection, the rats also received PRP (0.5 mL/kg, s.c.) two days a week for three weeks. Twenty-four hours after last CCl4 injection, the animals bled and their livers dissected for biochemical and histopathological studies. Blood analysis was performed to evaluate enzyme activity. The results showed that PRP itself was not toxic for liver and could protect the liver from CCl4-induced histological damages and attenuated oxidative stress by increase in glutathione content and decrease in lipid peroxidative marker of liver tissue. The results of the present study lend support to our beliefs in hepatoprotective effects of PRP.

富血小板血浆(PRP)一直是从事伤口愈合和再生医学的科学家和医生非常关注的问题,再生医学侧重于修复和替换受损的细胞和组织。富血小板血浆生长因子具有成本效益,可获得,并且比重组人生长因子更稳定。鉴于这些有价值的特性,我们决定评估PRP对ccl4诱导的大鼠肝毒性的影响。大鼠每周2次给予CCl4 (1 mL/kg, 1∶1橄榄油),连续8周。注射CCl4 5周后,大鼠同时给予PRP (0.5 mL/kg, s.c),每周2天,连续3周。最后一次注射CCl4 24小时后,大鼠放血并解剖肝脏进行生化和组织病理学研究。进行血液分析以评估酶活性。结果表明,PRP本身对肝脏无毒性,可通过增加肝组织谷胱甘肽含量、降低肝组织脂质过氧化标志物来保护肝脏免受ccl4诱导的组织损伤和减轻氧化应激。本研究的结果支持了我们对PRP具有肝保护作用的看法。
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引用次数: 39
Patterns of antimicrobial resistance in the causative organisms of spontaneous bacterial peritonitis: a single centre, six-year experience of 1981 samples. 自发性细菌性腹膜炎病原菌的抗微生物药物耐药性模式:单一中心,1981年样本的六年经验。
IF 1.8 Q3 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2014-01-01 Epub Date: 2014-03-20 DOI: 10.1155/2014/917856
Sara Sheikhbahaei, Alireza Abdollahi, Nima Hafezi-Nejad, Elham Zare

Background/Aims. Spontaneous bacterial peritonitis (SBP) is one of the leading causes of morbidity and mortality in patients with cirrhosis. This study aims to determine the microbial agents of SBP and the pattern of antibiotic resistance, in a large number of ascitic samples. Methodology. In a cross-sectional, single center, hospital based study, 1981 consecutive ascitic fluid samples were recruited from 2005 to 2011. Samples were dichotomized into three-year periods, in order to assess the trend of resistance to the first-line empirical antibiotics. Results. SBP was found in 482 (24.33%) of samples, of which 314 (65.15%) were culture positive. The most prevalent isolated pathogen was E. coli (33.8%), followed by staphylococcus aureus (8.9%) and Enterococcus (8.6%). No significant changes in the proportion of gram-negative/gram-positive infections occurred during this period. A percentage of resistant strains to cefotaxime (62.5%, 85.7%), ceftazidim (73%, 82.1%), ciprofloxacin (30, 59.8%), ofloxacin (36.8%, 50%), and oxacilin (35%, 51.6%) were significantly increased. E. coli was most sensitive to imipenem, piperacillin-tazobactam, amikacin, ceftizoxime, and gentamicin. Conclusions. The microbial aetiology of SBP remains relatively constant. However, the resistance rate especially to the first-line recommended antibiotics was significantly increased. This pattern must be watched closely and taken into account in empirical antibiotic treatment.

背景/目的。自发性细菌性腹膜炎(SBP)是肝硬化患者发病和死亡的主要原因之一。本研究旨在确定大量腹水样本中感染SBP的微生物菌剂及其耐药模式。方法。在一项横断面、单中心、以医院为基础的研究中,从2005年到2011年连续收集了1981份腹水样本。样本以三年为周期进行分类,以评估一线经验性抗生素的耐药趋势。结果。检出收缩压482例(24.33%),培养阳性314例(65.15%)。分离出的病原菌以大肠杆菌(33.8%)最多,其次是金黄色葡萄球菌(8.9%)和肠球菌(8.6%)。在此期间,革兰氏阴性/革兰氏阳性感染的比例没有显著变化。对头孢噻肟(62.5%,85.7%)、头孢他啶(73%,82.1%)、环丙沙星(30,59.8%)、氧氟沙星(36.8%,50%)、恶西林(35%,51.6%)耐药菌比例显著升高。大肠杆菌对亚胺培南、哌拉西林-他唑巴坦、阿米卡星、头孢替肟和庆大霉素最敏感。结论。收缩压的微生物病因学保持相对恒定。然而,耐药率,特别是对一线推荐抗生素的耐药率显著增加。这种模式必须密切关注,并在经验性抗生素治疗中加以考虑。
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引用次数: 29
Targeting interleukin-4 receptor alpha by hybrid Peptide for novel biliary tract cancer therapy. 利用杂交肽靶向白介素-4受体治疗胆道肿瘤。
IF 1.8 Q3 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2014-01-01 Epub Date: 2014-04-27 DOI: 10.1155/2014/584650
Kahori Seto, Junichi Shoda, Tomohisa Horibe, Eiji Warabi, Masayuki Kohno, Toru Yanagawa, Hiroki Bukawa, Yasuni Nakanuma, Koji Kawakami

It is known that the interleukin-4 receptor α (IL-4R α ) is highly expressed on the surface of various human solid tumors. We previously designed novel IL-4R α -lytic hybrid peptide composed of binding peptide to IL-4R α and cell-lytic peptide and reported that the designed IL-4R α -lytic hybrid peptide exhibited cytotoxic and antitumor activity both in vitro and in vivo against the human pancreatic cancer cells expressing IL-4R α . Here, we evaluated the antitumor activity of the IL-4R α -lytic hybrid peptide as a novel molecular targeted therapy for human biliary tract cancer (BTC). The IL-4R α -lytic hybrid peptide showed cytotoxic activity in six BTC cell lines with a concentration that killed 50% of all cells (IC50) as low as 5  μ M. We also showed that IL-4R α -lytic hybrid peptide in combination with gemcitabine exhibited synergistic cytotoxic activity in vitro. In addition, intravenous administration of IL-4R α -lytic hybrid peptide significantly inhibited tumor growth in a xenograft model of human BTC in vivo. Taken together, these results indicated that the IL-4R α -lytic hybrid peptide is a potent agent that might provide a novel therapy for patients with BTC.

白细胞介素-4受体α (IL-4R α)在人类多种实体瘤的表面高度表达。我们设计了一种由IL-4R α结合肽和细胞裂解肽组成的新型IL-4R α裂解杂肽,并报道了所设计的IL-4R α裂解杂肽在体外和体内对表达IL-4R α的人胰腺癌细胞具有细胞毒性和抗肿瘤活性。在这里,我们评估了IL-4R α -裂解杂化肽作为一种新的分子靶向治疗人类胆道癌(BTC)的抗肿瘤活性。IL-4R α -裂解杂肽对6株BTC细胞株具有细胞毒活性,其浓度低至5 μ m,杀伤50%的细胞(IC50)。我们还发现IL-4R α -裂解杂肽与吉西他滨在体外具有协同细胞毒活性。此外,静脉注射IL-4R α -裂解杂交肽可显著抑制人BTC异种移植模型体内肿瘤的生长。综上所述,这些结果表明IL-4R α -裂解杂化肽是一种有效的药物,可能为BTC患者提供一种新的治疗方法。
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引用次数: 6
期刊
International Journal of Hepatology
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