Malaria epidemiology, glucose 6-phosphate dehydrogenase deficiency and human settlement in the Vanuatu Archipelago

Vanuatu is located at the southeast margin of the malarious band extending from southeast Asia to eastern Melanesia. We analysed the malaria situation on different islands of Vanuatu, using passive case detection and malariometric survey data from 1985 to 1992, i.e. after the DDT residual programme ceased and before the impregnated bed-nets programme started on a larger scale. Malaria was mainly hypo-mesoendemic but with hyperendemic spots in certain years and on some islands. The transmission was generally more intense in the northern islands than in the south. In the late 1980s, annual parasite incidence per one thousand population (API) was around 180. The overall parasite rate was 11.9% with Plasmodium falciparum, P. vivax and P. malariae rate of 5.2, 6.7, and 0.1%, respectively. There was a seasonal fluctuation of P. falciparum incidence, whereas the P. vivax incidence was rather stable. Vivax malaria was confined to children less than 10 years old, while the prevalence of P. falciparum only changed moderately with age. The mean rate of glucose 6-phosphate dehydrogenase (G6PD) deficiency among male subjects was in 7.4% but with a wide variation of 0–14.3% on different islands. A positive rank-order correlation was found between malaria incidence and G6PD deficiency rate on the different islands. A reasonable hypothesis is that malaria was introduced to the islands with the first human settlement 4000 years ago, with a geographical malaria distribution similar to the present situation. Different malaria endemicities possibly then selected different prevalences of G6PD deficiency over many generations.     

Malaria dispersal among islands: human mediated Plasmodium falciparum gene flow in Vanuatu, Melanesia

A comparison of human and Plasmodium falciparum gene flow patterns in the model island system of Vanuatu, the limit of malaria in the Pacific reveals that human movement is essential for long, but not short distance P. falciparum gene flow. This suggests that long distance movement of humans may accelerate the evolution and spread of drug resistance and therefore exacerbate the global malaria problem.     

青海省玉树市人群定居点周围小型啮齿类动物种群动态及棘球绦虫感染调查

目的　调查青海省玉树市人群定居点周围小型啮齿类动物种群动态及其棘球蚴感染情况。方法　2018年5、8月和10月,在青海省玉树市巴塘乡和隆宝镇牧场布置鼠夹捕捉啮齿类动物,测量捕获的动物体质量和头体长并根据形态学进行种类鉴定。提取动物肝脏组织和病灶组织DNA,PCR扩增棘球绦虫线粒体cox1基因进行虫种鉴定,PCR检测阳性组织样本进行病理观察。计算啮齿类动物棘球蚴感染率,基于棘球绦虫cox1基因序列构建系统进化树。结果　累计捕获小型啮齿类动物285只,其中高原鼠兔143只（50.2%）、青海田鼠141只（49.5%）、高原松田鼠1只（0.3%）,高原鼠兔和田鼠在栖息地选择上表现出明显分离。青海田鼠数量与植被覆盖度呈正相关（r = 0.350,P = 0.264）,在8月达到最高水平;高原鼠兔数量与植被覆盖度呈负相关（r = –0.371,P = 0.235）,在8月活动频率最低、5月活动频率最高。高原鼠兔雌雄性别比例为1∶0.96,田鼠雌雄性别比例为0.82∶1;高原鼠兔体质量（r = 0.519,P < 0.01）和头体长（r = 0.578,P < 0.01）随月份呈逐渐增大趋势,田鼠体质量（r = –0.401,P < 0.01）和头体长（r = –0.570,P < 0.01）随月份呈逐渐下降趋势;田鼠中未发现棘球绦虫感染,高原鼠兔石渠棘球绦虫感染率为2.1%。系统进化树显示,青海省玉树市石渠棘球绦虫和四川省甘孜藏族自治州石渠县境内发现的石渠棘球绦虫cox1基因序列一致。结论　青海省玉树市人群定居点周围小型啮齿类动物主要为高原鼠兔和青海田鼠,高原鼠兔和青海田鼠分别在5月和8月达到最大种群数量;随着玉树市棘球蚴病防治措施的有效实施,人群定居点周围小型啮齿类动物棘球蚴感染率处于较低水平,但仍然存在棘球蚴病传播风险。     

Biological significance of MAPK, AKT and JAK-STAT protein activation by various erythropoietic factors in normal human early erythroid cells

The aim of this study was to identify signal transduction pathways activated by erythropoietin (EpO) and erythropoietin co-stimulatory factors (kit ligand), insulin-like growth factor, thrombopoietin, interleukin 3 and granulocyte-macrophage colony-stimulating factor) in normal human bone marrow CD34(+) cells and d 11 erythroid burst forming unit derived glycophorin+ cells. The activation of these signal transduction pathways was further correlated with various biological effects such as (i) cell proliferation, (ii) inhibition of apoptosis, (iii) activation of adhesion and (iv) secretion of the matrix metalloproteinases (MMPs) MMP-9 and MMP-2, and vascular endothelial growth factor (VEGF). We found that in human CD34(+) cells and erythroblasts erythropoietic factors may activate similar but different signalling pathways, and that activation of each of the JAK-STAT, MAPK p42/44 or PI-3K-AKT axes alone is not sufficient either to stimulate cell proliferation or inhibit apoptosis, suggesting that these processes are regulated by orchestrated activation of multiple signalling cascades. Accordingly, we found that although cell proliferation was more related to simultaneous activation of JAK-STAT and MAPK p42/44, the effect on cell survival correlated with activation of PI-3K-AKT, MAPK p42/44 and JAK-STAT proteins. We also demonstrated that differentiating normal human erythroid cells lose their adhesive properties and secrete angiopoietic factors such as MMP-9, MMP-2 and VEGF, and we postulate that this secretion by early erythroid cells may play a role in their maturation and egress from the haematopoietic niches of the bone marrow.