巨幼细胞性贫血与脾大的临床相关性分析

目的:分析巨幼细胞性贫血脾肿大的超声表现及临床结果的相关性。方法:①选择2008年至2011年在哈尔滨医科大学第二临床医院血液内科住院的巨幼细胞性贫血患者239例。②按贫血程度将患者设为重度贫血组108例(血红蛋白>30 g/L);中度贫血组78例(血红蛋白>60 g/L);轻度贫血组53例(血红蛋白>90 g/L)。③超声检查显示脾厚度超过4 cm或长度超过8 cm,最大长径超过11 cm以及左肋缘下探及脾,均可判定为脾大。④率的资料比较采用卡方检验,相关性分析采用Pearson相关。结果:对不同贫血程度的脾大发生率进行比较分析,采用卡方检验(x2=22.873,P<0.01)。贫血程度与脾大进行Pearson相关性分析(r=0.309,P<0.01)。结论:①巨幼细胞性贫血可导致脾肿大。②脾大与贫血程度有关系。     

Trypanoplasma salmositica: experimental infections in rainbow trout, Salmo gairdneri.

Trypanoplasma salmositica was successfully cultured in Hanks' medium with 10% heated fetal calf serum. The culture forms were morphologically similar to blood forms and were infective to rainbow trout by inoculation. T. salmositica produced a disease in experimentally infected rainbow trout (Salmo gairdneri). The clinical signs were anemia, exophthalmia, abdominal distension with ascites, and splenomegaly. These clinical signs were observed in fish that were infected with three substrains (field substrain, cultured substrain, and cloned substrain) thus satisfying Koch's postulates. The anemia was microcytic and hypochromic and was coincident with increasing parasite number in the blood. The hemoglobin in the infected fish dropped from a normal of about 6 g% to about 1 g% in the first 10 weeks postinfection. Similarly, the hematocrit and red cell count declined as the infection progressed. Abdominal distension and exophthalmia was obvious 10 weeks postinfection. Up to 5 ml ascites fluid were recovered from each of three fish. The fluid contained large numbers of Trypanoplasma and macrophages. Some of the macrophages were engulfing the Trypanoplasma. At about this time the spleen in the infected fish was enlarged 5 to 10 times over that of control fish. The hematocrit centrifuge technique was less sensitive than wet mount examinations for the detection of the organism in blood. Fluctuations in parasite number during the course of infection may be due to antigenic change by the parasite to evade the host immune system.     

Splenic extramedullary hemopoiesis caused by a dysfunctional mutation in the NF-κB-inducing kinase gene

NF-κB-inducing kinase (NIK) plays critical roles in the development of lymph nodes and Peyer’s patches, and microarchitecture of the thymus and spleen via NF-κB activation. Alymphoplasia (aly/aly) mice have a point mutation in the NIK gene that causes a defect in the activation of an NF-κB member RelB. Here, we developed a novel method to determine the aly mutation by genetic typing using PCR. This method facilitated the easy establishment of a congeneic aly/aly mouse line. Indeed, we generated a mouse line with aly mutation on a BALB/cA background (BALB/cA-aly/aly). BALB/cA-aly/aly mice showed significant splenomegaly with extramedullary hemopoiesis, which was not significant in aly/aly mice on a C57BL/6 background. Interestingly, the splenomegaly and extramedullary hemopoiesis caused by the aly mutation was gender-dependent. These data together with previous reports on extramedullary hemopoiesis in RelB-deficient mice suggest that NIK–RelB signaling may be involved in the suppression of extramedullary hemopoiesis in adult mice.     

Proteomic changes at 8 weeks after infection are associated with chronic liver pathology in experimental schistosomiasis

Chronic Schistosoma mansoni infection can present as a moderate or severe disease, termed intestinal or hepatosplenic schistosomiasis, respectively. Similarly, either moderate splenomegaly or hypersplenomegaly syndrome develops in CBA/J mice by 20 weeks of infection and is similar to intestinal or hepatosplenic schistosomiasis respectively. Using this mouse model and two-dimensional differential in gel electrophoresis, the liver proteomic signatures of uninfected mice and mice infected for 6, 8, 12, or 20 weeks were compared, and significant protein spots identified using mass spectrometry. We found the greatest number of changes at 12 weeks suggesting that this period represents the peak time of change. Pathway analysis identified specific proteins and pathways that correlated to the pathological changes indicative of severe disease, and these pathways were involved as early as 8 weeks after infection. These findings provide insight into the development of severe liver pathology in schistosomiasis and may aid in developing biomarkers for hepatosplenic schistosomiasis.     

Effects of repeated praziquantel treatment on schistosomiasis mekongi morbidity as detected by ultrasonography

Schistosomiasis mekongi is endemic in the Mekong River basin; about 80,000 people are at risk of infection in Cambodia. We conducted ultrasonographic studies of patients with schistosomiasis mekongi in Kratie province, Cambodia, focusing especially on the relationship between the frequency of praziquantel treatment and findings of ultrasonographic imaging. The frequency of praziquantel treatment in the period from 1995 to 2002 was classified into four groups: 1–2, 3–4, 5–6, and 7–8 times. Ultrasonographic images were examined to determine the presence of thickening of the portal vein wall and formation of meandering collateral circulation of the splenic vein. We selected these parameters because they are unaffected by interobserver bias. The results showed that thickening of the portal vein wall may have potential to improve with frequent praziquantel treatment. On the other hand, established hard splenomegaly and meandering collateral circulation of the splenic vein, improved very little with praziquantel treatment.     

Role of chemokines in regulation of immunity against leishmaniasis

Successful immunity to Leishmania depends on recruitment of appropriate immune effector cells to the site of infection and chemokines play a crucial role in the process. At the same time, Leishmania parasites possess the ability to modify the chemokine profiles of their host thereby facilitating establishment of progressive infection. Therapeutic and prophylactic strategies targeted at chemokines and their receptors provide a promising area for further research. This review highlights our current knowledge concerning the role of chemokines and their receptors in modulating leishmaniasis in both clinical settings and experimental disease models.