Entamoeba histolytica induces human neutrophils to form NETs

Entamoeba histolytica invades the intestine and other organs during the pathogenesis of amoebiasis. In the early stages, the host organism responds with an inflammatory infiltrate composed mostly of neutrophils. It has been reported that these immune cells, activated by E. histolytica, exert a protective role by releasing proteolytic enzymes and generating reactive oxygen/nitrogen species (ROS/RNS) and antimicrobial peptides. It is now known that neutrophils also produce neutrophil extracellular traps (NETs), which are able to damage and kill pathogens. Studies have shown that intracellular protozoan pathogens, including Toxoplasma gondi, Plasmodium falciparum and Leishmania spp, induce neutrophils to release NETs and are damaged by them. However, the action of this mechanism has not been explored in relation to E. histolytica trophozoites. Through scanning electron, epifluorescence microscopy and viability assays, we show for first time that during in vitro interaction with E. histolytica trophozoites, human neutrophils released NETs that covered amoebas and reduced amoebic viability. These NETs presented histones, myeloperoxidase and decondensed chromatin. The results suggest that NETs participate in the elimination of the parasite.     

Abstracts from other journals

The aim of the present study was to clinically evaluate fissure sealants on the occlusal fissures and buccal pits of permanent first and second molars after 20 and 15 years, respectively. The population consisted of 72 children, each of whom had had their four first molars sealed between 1977 and 1980. At the annual examinations, all caries-free, newly erupted second molars were sealed. When sealant was applied to the second molars, the first molars were checked and sealant was reapplied to those that had deficient sealants. At the follow-up, when the subjects were 26–27 years of age, 27 in the original group had moved from the community. Thus, the present result is based on 45 subjects. One hundred and fifty-three sealed first molars and 161 sealed second molars were available for inspection. At the follow-up examination of the first molars 20 years after sealant had been applied, 65% showed complete retention, 22% partial retention without caries, and 1306 caries or restoration in the occlusal fissures or buccal pits. At the 15-year follow-up of the second molars, the corresponding figures were 65%, 30% and 5%, respectively. Of the restored or carious molars, significantly more were found in the mandible than in the maxilla ( P  < 0.001). This longitudinal study showed that pit and fissure sealants, applied during childhood, have a long-lasting, caries-preventive effect.     

Trichinella infection and clinical disease

Trichinellosis is caused by ingestion of insufficiently cooked meat contaminated with infective larvae of <it>Trichinella</it> species. The clinical course is highly variable, ranging from no apparent infection to severe and even fatal disease. We report two illustrative cases of trichinellosis. Returning to Denmark a few days after having eaten roasted pork in the Republic of Serbia, a female patient suffered from severe vomiting, epigastric pain, diarrhoea, and later myalgia, generalized oedema, and prostration. A biopsy showed heavy infestation with <it>Trichinella spiralis</it>, 2000 larvae/g of muscle. Life-threatening cardiopulmonary, renal and central nervous system complications developed. The patient recovered after several months. Her husband, who also ate the pork, did not have clinical symptoms, but an increased eosinophil count and a single larva in a muscle biopsy confirmed infection. The epidemiology, clinical manifestations, diagnosis, treatment and prevention of trichinellosis are reviewed.      

JMH variants: serologic, clinical, and biochemical analyses in two cases

BACKGROUND: JMH is a high-frequency red cell blood group antigen that resides on a 76- to 80-kDa glycosylphosphatidylinositol-linked protein also known as CDw108. Antibodies with JMH specificity are often autoimmune and are usually, if not always, clinically benign. Some individuals with JMH-variant antigen produce alloantibodies to JMH, but little evidence concerning their clinical significance is available. This article reports on two patients who express a JMH-variant antigen and produced alloanti-JMH. STUDY DESIGN AND METHODS: Murine monoclonal antibodies and human antibodies to JMH were used in hemagglutination, radioimmunoassay, and Western blot testing of red cells from two JMH- variant patients; antiserum from one of these patients was also used in biochemical studies. In addition, in vivo survival of JMH-positive red cells was studied in the same patient. RESULTS: Biochemically, both examples of red cells with the JMH-variant phenotype expressed a JMH protein with a molecular weight similar to that of the normal JMH protein. For both patients, family studies suggested an autosomal recessive pattern of inheritance. Survival study demonstrated reduced in vivo red cell survival in one patient. CONCLUSION: JMH-variant phenotypes express a protein of normal molecular weight and are inherited in an autosomal recessive pattern. Furthermore, individuals with this phenotype can produce clinically significant antibodies.     

成人型胆管囊肿及其合并症的超声与核磁及胰胆管水成像诊断

目的　探讨成人胆管囊肿及其合并症的超声、核磁及胰胆管水成像 (MR/ MRCP)的影像表现。方法　选取胆管扩张病例进行超声及核磁检查 ,观察胆胰管内径、胆管扩张形态、管壁厚度、回声 ,并进行彩色多普勒血流检测及核磁胰胆管水成像 (MR/ MRCP)检查 ,两者结果与术后病理对照。结果　经手术证实胆管囊肿 2 0例 ,包括 :Caroli's病 2例 , 型胆总管囊肿 14例 ,呈囊性、梭形、圆柱形扩张 ;肝门部胆管囊肿 (囊肿型 ) 3例 ,胆总管上段憩室 1例 ( 型 )。合并胆囊结石 10例 ,肝内胆管、胆总管结石 8例 ;合并肝局灶性炎 3例 ,肝脓肿 1例 ;合并癌变 5例 (高、低分化腺癌 3例 ,黏液腺癌 1例 ,类癌 1例 ) ;共同管过长 (>1.5 cm) 6例。超声与 MRCP对胆管囊肿全部诊断。合并症中超声对炎变、结石、癌变诊断分别为 95 % ,10 0 % ,95 % ,而 MRCP/MR为 10 0 % ,90 % ,95 %。超声对结石、癌变及管壁的微细结构观察优于 MRCP,MRCP对胆管全程显示优于超声 ,结合平扫及增强扫描诊断炎变符合率 10 0 %。结论　超声与 MR成像在成人胆管囊肿及其合并症中的诊断意义重大 ,联合应用有利于对该病的全面认识 ,便于指导临床。     

GE Signa Twinspeed 1.5T磁共振肝脏扩散加权成像的技术探讨

目的探讨高场强双梯度磁共振机(GE Signa Twinspeed 1.5T)的肝脏扩散加权成像技术(DWI).方法对20例正常肝脏进行扩散加权成像研究,分别改变重复时间(TR)及扩散敏感系数(b值),测定ADC值、信噪比、图像质量等.结果 b值固定,TR值改变,正常肝组织平均ADC值差异不显著(P>0.05);TR值固定,b值改变,ADC值随b值增大而减小(P<0.05,差异有显著性).b值越大,图像质量越差;b≥800 s/mm2时,图像几乎难以观察.结论 ADC值随b值的增大而减小.行肝脏扩散加权成像时,可适当减小TR值,以缩短扫描时间及患者的屏气时间,减少呼吸运动伪影.