Which forest bird species are the main hosts of the tick,Ixodes ricinus,the vector of Borrelia burgdorferi sensu lato,during the breeding season?

Wild birds are important hosts for vector-borne pathogens, especially those borne by ticks. However, few studies have been conducted on the role of different bird species within a community as hosts of vector-borne pathogens. This study addressed individual and species factors that could explain the burden of Ixodes ricinus on forest birds during the reproductive periods of both vectors and hosts. The goal was to identify which bird species contribute the most to the tick population at the community level. Birds were mist-netted on four plots in 2008 and on seven plots in 2009 in two forests (Sénart and Notre Dame, near Paris, France). The dependence of the tick load per bird upon environmental conditions (questing nymph density, year and plot) and on host species traits (species, age, sex, body size, vertical space use, level of innate and acquired immunity) was analysed. Finally, the relative contribution of each bird species to the local dynamics of ticks was estimated, while accounting for their respective abundance. Tick burden differed markedly between bird species and varied according to questing nymph density. Bird species with a high body mass, those that forage low in the vegetation, and those that had a high innate immune response and a high spleen mass were more likely to have a high tick burden. Four species (the Common Blackbird, Turdus merula, the European Robin, Erithacus rubecula, the Song Thrush, Turdus philomelos, and the Winter Wren, Troglodytes troglodytes) hosted more than 90% of the ticks in the local bird community. These species, and particularly T. merula which was host to a high proportion of the nymphs, are likely to contribute significantly to the circulation of pathogens for which they are competent, such as the agent of Lyme borreliosis.     

Sperm ultrastructure of Helicometra epinepheli (Platyhelminthes, Digenea, Opecoelidae), parasite of Epinephelus fasciatus (Pisces, Teleostei)

This paper describes the ultrastructure of the mature spermatozoon of the digenean Helicometra epinepheli. The ultrastructural elements observed are: two axonemes with a 9+"1" pattern of Trepaxonemata, four attachment zones, a nucleus, two mitochondria, external ornamentation of the plasma membrane, spine-like bodies and cortical microtubules. A particularity of this spermatozoon is the presence of an apical cone. However, the spermatozoon presents the general pattern of the Opecoelidae and thus differs from Helicometra fasciata (which appears as an exception in this family) by several ultrastructural features: the presence of external ornamentation and spine-like bodies and the arrangement of cortical microtubules around the first mitochondrion in the region of the ornamentation. Each ultrastructural feature is discussed and compared with the literature to highlight characters which could be useful for phylogeny.     

Autophagy protein p62/SQSTM1 is involved in HAMLET-induced cell death by modulating apotosis in U87MG cells

HAMLET is a complex of oleic acids and decalcified α-lactalbumin that was discovered to selectively kill tumor cells both in vitro and in vivo. Autophagy is an important cellular process involved in drug-induced cell death of glioma cells. We treated U87MG human glioma cells with HAMLET and found that the cell viability was significantly decreased and accompanied with the activation of autophagy. Interestingly, we observed an increase in p62/SQSTM1, an important substrate of autophagosome enzymes, at the protein level upon HAMLET treatment for short periods. To better understand the functionality of autophagy and p62/SQSTM1 in HAMLET-induced cell death, we modulated the level of autophagy or p62/SQSTM1 with biochemical or genetic methods. The results showed that inhibition of autophagy aggravated HAMLET-induced cell death, whereas activation of authophagy attenuated this process. Meanwhile, we found that overexpression of wild-type p62/SQSTM1 was able to activate caspase-8, and then promote HAMLET-induced apoptosis, whereas knockdown of p62/SQSTM1 manifested the opposite effect. We further demonstrated that the function of p62/SQSTM1 following HAMLET treatment required its C-terminus UBA domain. Our results indicated that in addition to being a marker of autophagy activation in HAMLET-treated glioma cells, p62/SQSTM1 could also function as an important mediator for the activation of caspase-8-dependent cell death.     

Radiosensitization by a novel Bcl-2 and Bcl-XL inhibitor S44563 in small-cell lung cancer

Radiotherapy has a critical role in the treatment of small-cell lung cancer (SCLC). The effectiveness of radiation in SCLC remains limited as resistance results from defects in apoptosis. In the current study, we investigated whether using the Bcl-2/Bcl-X_L inhibitor S44563 can enhance radiosensitivity of SCLC cells in vitro and in vivo. In vitro studies confirmed that S44563 caused SCLC cells to acquire hallmarks of apoptosis. S44563 markedly enhanced the sensitivity of SCLC cells to radiation, as determined by a clonogenic assay. The combination of S44563 and cisplatin-based chemo-radiation showed a significant tumor growth delay and increased overall survival in mouse xenograft models. This positive interaction was greater when S44563 was given after the completion of the radiation, which might be explained by the radiation-induced overexpression of anti-apoptotic proteins secondary to activation of the NF-κB pathway. These data underline the possibility of combining IR and Bcl-2/Bcl-X_L inhibition in the treatment of SCLC as they underscore the importance of administering conventional and targeted therapies in an optimal sequence.Identifying the mechanisms leading to radioresistance including resistance to apoptosis is essential to improve clinical outcome in cancer patients. Disabled apoptosis has been catalogued among the fundamental hallmarks of cancer¹ and the proteins of the Bcl-2 family play a fundamental role in regulating this modality of cell death. The Bcl-2 family comprises both pro- and anti-apoptotic members; the latter (Bcl-2, Bcl-X_L and Mcl-1) are often overexpressed in cancer cells to facilitate the survival of cells that under normal circumstances should have undergone apoptosis.² The molecular interactions between pro- and anti-apoptotic Bcl-2 family members determine cellular sensitivity to multiple lethal triggers, including many standard chemotherapeutic agents and ionizing radiation (IR).^{3, 4} Overexpression of Bcl-2 is known to increase clonogenic survival and inhibit IR-induced apoptosis.^{3, 4} Bcl-X_L expression also shows a strong correlation with resistance to cytotoxic anticancer therapies including IR.^{5, 6}Lung cancer is the leading cause of cancer deaths in western countries.⁷ Small-cell lung cancer (SCLC) accounts for 15% of all lung cancer cases and is distinguished from non-SCLC by its characteristic cytomorphology, rapid proliferation and early dissemination to metastatic sites.⁸ The standard of care to patients with limited-stage SCLC and good performance status is based on a combination of IR and cisplatin-based chemotherapy, resulting in a complete response rate as high as 50–80% coupled to a deceptive 12–20% 5-year survival.⁹ Initially, SCLC is responsive to chemo- and radiotherapy. However, SCLC recurs within the first 12 months.¹⁰ To date, the pathways mediating chemo- and radioresistance in SCLC are largely unknown.Deletion of pro-apoptotic gene and amplification of anti-apoptotic gene are frequently observed in SCLC, especially amplification of the BCL2L1 and BCL2L2 genes.¹¹ At the protein level, increased expression of Bcl-2 has been reported in up to 90% of metastatic SCLC. Bcl-2 overexpression, downregulation of the pro-apoptotic Bcl-2 antagonist Bax and a shift in the Bcl-2/Bax ratio to levels >1 are correlated with lower apoptotic index in tumors¹² and are associated with chemotherapeutic resistance in SCLC cell lines.¹³ In contrast with most solid tumor cell lines, where apoptosis does not appear as a predominant cell death mechanism after IR,¹⁴ overexpression of Bcl-2 can abrogate chemotherapy-induced apoptosis in SCLC cell lines.¹³ Apoptosis may be one of the mechanisms that cause SCLC cells to die in response to radiotherapy.^{15, 16}Recently, a small synthetic compound ABT-737 and its orally bioavailable form ABT-263 (Navitoclax) were shown to efficiently antagonize Bcl-2 and Bcl-X_L by binding to their BH3 receptor domain. ABT737 or its derivatives mediate antitumoral effects in chronic lymphocytic leukemia (CLL) and SCLC in preclinical and early clinical trials.^{17, 18} However, there is no published study that evaluates the combination of new Bcl-2/Bcl-X_L inhibitors, IR and chemo-radiotherapy.     

Toxoplasma gondii infection in pregnant women in China

Toxoplasmosis, caused by the protozoan parasite Toxoplasma gondii, is one of the most common parasitic infections in humans. Primary infection in pregnant women can be transmitted to the fetus leading to miscarriage or congenital toxoplasmosis. Carefully designed nationwide seroprevalence surveys and case-control studies of risk factors conducted primarily in Europe and America, have shaped our view of the global status of maternal and congenital infection, directing approaches to disease prevention. However, despite encompassing 1 in 5 of the world's population, information is limited on the status of toxoplasmosis in China, partly due to the linguistic inaccessibility of the Chinese literature to the global scientific community. By selection and analysis of studies and data, reported within the last 2 decades in China, this review summarizes and renders accessible a large body of Chinese and other literature and aims to estimate the seroprevalence in Chinese pregnant women. It also reviews the prevalence trends, risk factors, and clinical manifestations. The key findings are (1) the majority of studies show that the overall seroprevalence in Chinese pregnant women is less than 10%, considerably lower than a recently published global analysis; and (2) the few available appropriate studies on maternal acute infection suggested an incidence of 0·3% which is broadly comparable to studies from other countries.     

Microdeletion on 17p11.2 in a Smith-Magenis syndrome patient with mental retardation and congenital heart defect: first report from China

Smith-Magenis syndrome (SMS) is a rare syndrome with multiple congenital malformations, including development and mental retardation, behavioral problems and a distinct facial appearance. SMS is caused by haploinsufficiency of RAI1 (deletion or mutation of RAI1). We describe an eight-year-old female Chinese patient with multiple malformations, congenital heart defect, mental retardation, and behavioral problems (self hugging, sleeping disturbance). High-resolution genome wide single nucleotide polymorphism array revealed a 3.7-Mb deletion in chromosome region 17p11.2. This chromosome region contains RAI1, a critical gene involved in SMS. To the best of our knowledge, this is the first report of an SMS patient in mainland China.     

Genome-wide prediction models that incorporate de novo GWAS are a powerful new tool for tropical rice improvement

To address the multiple challenges to food security posed by global climate change, population growth and rising incomes, plant breeders are developing new crop varieties that can enhance both agricultural productivity and environmental sustainability. Current breeding practices, however, are unable to keep pace with demand. Genomic selection (GS) is a new technique that helps accelerate the rate of genetic gain in breeding by using whole-genome data to predict the breeding value of offspring. Here, we describe a new GS model that combines RR-BLUP with markers fit as fixed effects selected from the results of a genome-wide-association study (GWAS) on the RR-BLUP training data. We term this model GS + de novo GWAS. In a breeding population of tropical rice, GS + de novo GWAS outperformed six other models for a variety of traits and in multiple environments. On the basis of these results, we propose an extended, two-part breeding design that can be used to efficiently integrate novel variation into elite breeding populations, thus expanding genetic diversity and enhancing the potential for sustainable productivity gains.