阿奇霉素序贯疗法治疗小儿支原体肺炎的临床疗效及其安全性

目的 探讨阿奇霉素序贯疗法治疗小儿支原体肺炎的临床疗效及其安全性.方法 选取抚州市东乡区人民医院2017—2019年收治的支原体肺炎患儿60例,按照就诊序号单双号分成对照组和研究组,每组30例.对照组给予布地奈德、奥司他韦进行常规治疗,研究组在对照组基础上给予阿奇霉素序贯治疗.比较2组临床疗效,咳嗽、发热及肺啰音消失时...     

肝癌TACE中化疗和栓塞与肿瘤抑制和肝损伤关系的临床研究

目的 研究肝癌TACE中化疗与栓塞的并用与否对肿瘤抑制和肝损伤的影响.方法 回顾性分析152例HCC患者接受化疗灌注(A组30例)、栓塞(B组29例)或化疗栓塞(C组93例)后1天和4天,AFP下降及肝功能各指标变化.结果 (1)AFP下降人数,B组(56.5%,78.3%)和C组(67%,80.7%)显著大于A组(25%,25%)(P＜0.001).(2)肝功能异常人数增幅表现为:TBil,A、C组明显高于B组(P＜0.001).ALT及ALB,B、C组明显大于A组(P＜0.005).PA,C组明显高于A、B组(P＜0.005).结论 TACE对肿瘤的抑制主要归功于肿瘤供血血管的栓塞作用;加用肝动脉化疗灌注后,肝损伤的增加明显大于对肿瘤的抑制.     

不同诊断标准对上海市浦东新区40岁以上社区人群糖代谢类型分布的影响

目的比较不同诊断标准对社区自然人群糖代谢类型分布的影响。方法抽取2002年上海市浦东新区社区自然人群糖尿病调查数据库中40岁以上人群1716例,分别按照1999年世界卫生组织(WHO)和 2003年美国糖尿病学会(ADA)糖尿病诊断标准划分人群糖代谢类型。结果 40岁以上人群中,糖尿病患病率为 10．4％。与WHO标准相比,ADA标准所诊断的糖调节受损患病率升高8．9％(从21.3％至30．2％),而正常葡萄糖耐量下降8．9％(从68．3％至59．4％)。ADA标准新确定的空腹葡萄糖受损与正常葡萄糖耐量比较,其体重指数(40～49岁)和腰臀比(50～59岁)明显增加,而与WHO标准确定的空腹葡萄糖受损的差异无显著性。结论上海市浦东新区40岁以上社区自然人群糖代谢异常患病率较高,不同诊断标准对糖代谢类型比例有明显的影响,ADA新的诊断标准比WHO标准更有利于早期发现高危糖尿病人群。     

Sea-blue histiocyte syndrome in bone marrow secondary to total parenteral nutrition including fat-emulsion sources: a clinicopathologic study of seven cases

Bone marrow examination revealed a lipid-laden histiocytosis in seven patients undergoing long-term total parenteral nutrition necessitated by extensive short-bowel surgical resection. Clinical abnormalities occurred during this treatment which required bone marrow examination. These included hepatosplenomegaly and peripheral blood cytopenia; the median time to the detection of these abnormalities was 64 months.   The most striking change within the bone marrow was the presence of many pigment-laden histiocytes which had the typical morphology of sea-blue histiocytes seen in the so-called idiopathic sea-blue histiocyte syndrome. The occurrence of sea-blue histiocytosis in the bone marrow in association with long-term parenteral nutrition for short-bowel syndrome has not, to our knowledge, been reported previously and should now be considered in the differential diagnosis of bone marrow sea-blue histiocytosis.     

Further delineation of the KBG syndrome caused by ANKRD11 aberrations

Loss-of-function variants in ANKRD11 were identified as the cause of KBG syndrome, an autosomal dominant syndrome with specific dental, neurobehavioural, craniofacial and skeletal anomalies. We present the largest cohort of KBG syndrome cases confirmed by ANKRD11 variants reported so far, consisting of 20 patients from 13 families. Sixteen patients were molecularly diagnosed by Sanger sequencing of ANKRD11, one familial case and three sporadic patients were diagnosed through whole-exome sequencing and one patient was identified through genomewide array analysis. All patients were evaluated by a clinical geneticist. Detailed orofacial phenotyping, including orthodontic evaluation, intra-oral photographs and orthopantomograms, was performed in 10 patients and revealed besides the hallmark feature of macrodontia of central upper incisors, several additional dental anomalies as oligodontia, talon cusps and macrodontia of other teeth. Three-dimensional (3D) stereophotogrammetry was performed in 14 patients and 3D analysis of patients compared with controls showed consistent facial dysmorphisms comprising a bulbous nasal tip, upturned nose with a broad base and a round or triangular face. Many patients exhibited neurobehavioural problems, such as autism spectrum disorder or hyperactivity. One-third of patients presented with (conductive) hearing loss. Congenital heart defects, velopharyngeal insufficiency and hip anomalies were less frequent. On the basis of our observations, we recommend cardiac assessment in children and regular hearing tests in all individuals with a molecular diagnosis of KBG syndrome. As ANKRD11 is a relatively common gene in which sequence variants have been identified in individuals with neurodevelopmental disorders, it seems an important contributor to the aetiology of both sporadic and familial cases.     

In vivo treatment with recombinant IL-12 protects C57BL/6J mice against secondary alveolar echinococcosis

Using an experimental model of hepatic Echinococcus multilocularis infection in C57BL/6J mice, intraperitoneal administration of 0.8 μg of recombinant IL-12 to mice with an established infection was shown to reduce the parasite burden as soon as two weeks after the end of treatment. At that time, in vitro Echinococcus multilocularis -induced spleen T cell proliferative responses as well as IFN-γ and IL-5 production were higher in IL-12 treated mice than in untreated mice. Administration of 0.8 μg of IL-12 at the time of infection was shown to be without effect on the parasite establishment. However, this treatment greatly inhibited the subsequent metacestode development. Indeed, ten weeks after infection, it induced a complete healing in 37.5% of mice. At that time, the development of metastases was inhibited in 68.75% of IL-12-treated mice. This reduction of parasite burden was mainly associated with a strong proliferation of spleen cells to E. multilocularis antigen and with a high IFN-γ production. Altogether, our results show that IL-12 is of crucial importance in inhibiting the larval growth after the metacestode establishment in the liver and suggest that this cytokine could be of potential value in the treatment of human alveolar echinococcosis .     

RP-HPLC法测定β-司他夫定的有关物质

目的:建立了β-司他夫定原料有关物质的RP-HPLC测定方法和水解破坏制备系统适用性试验溶液方法。方法:采用Agilent 1100型高效液相色谱仪,使用SUPELCOSIL LC-18-DB(4.6 mm×250 mm,5μm)色谱柱,以0.01 mol·L-1醋酸铵溶液-乙腈(96.5∶3.5)和0.01 mol·L-1醋酸铵溶液-乙腈(75∶25)为流动相,梯度洗脱,检测波长254 nm,柱温25℃。结果:β-司他夫定和4种已知杂质及其他未知杂质均能达到有效分离;经水解破坏产生的α-司他夫定与β-司他夫定的分离度均达2.8;β-司他夫定、胸腺嘧啶、β-胸苷与5-O’-苯甲酰-司他夫定线性范围分别为0.51~26μg·m L-1(r=1.000)、0.13~27μg·m L-1(r=1.000)、0.50~25μg·m L-1(r=1.000)、1.7~6.3μg·m L-1(r=1.000),已知杂质胸腺嘧啶、β-胸苷与5-O’-苯甲酰-司他夫定的平均加样回收率(n=9)分别为102.8%(RSD=1.5%)、100.6%(RSD=0.9%)、101.9%(RSD=2.1%);β-司他夫定与3种已知杂质的最小检出量均在2.5 ng以下;经水解破坏制备的系统适用性溶液的重复性良好;供试品溶液在4℃下的30 h内基本稳定。结论:本方法灵敏、准确、可靠,专属性强,可用于β-司他夫定原料的有关物质测定。     

Vaccine Protection against Bacillus cereus-Mediated Respiratory Anthrax-Like Disease in Mice

Bacillus cereus strains harboring a pXO1-like virulence plasmid cause respiratory anthrax-like disease in humans, particularly in welders. We developed mouse models for intraperitoneal as well as aerosol challenge with spores of B. cereus G9241, harboring pBCXO1 and pBC218 virulence plasmids. Compared to wild-type B. cereus G9241, spores with a deletion of the pBCXO1-carried protective antigen gene (pagA1) were severely attenuated, whereas spores with a deletion of the pBC218-carried protective antigen homologue (pagA2) were not. Anthrax vaccine adsorbed (AVA) immunization raised antibodies that bound and neutralized the pagA1-encoded protective antigen (PA1) but not the PA2 orthologue encoded by pagA2. AVA immunization protected mice against a lethal challenge with spores from B. cereus G9241 or B. cereus Elc4, a strain that had been isolated from a fatal case of anthrax-like disease. As the pathogenesis of B. cereus anthrax-like disease in mice is dependent on pagA1 and PA-neutralizing antibodies provide protection, AVA immunization may also protect humans from respiratory anthrax-like death.