Evaluation of parasitological and molecular techniques for the diagnosis and assessment of cure of schistosomiasis mansoni in a low transmission area

This study evaluated parasitological and molecular techniques for the diagnosis and assessment of cure of schistosomiasis mansoni. A population-based study was performed in 201 inhabitants from a low transmission locality named Pedra Preta, municipality of Montes Claros, state of Minas Gerais, Brazil. Four stool samples were analysed using two techniques, the Kato-Katz® (KK) technique (18 slides) and the TF-Test®, to establish the infection rate. The positivity rate of 18 KK slides of four stool samples was 28.9% (58/201) and the combined parasitological techniques (KK+TF-Test®) produced a 35.8% positivity rate (72/201). Furthermore, a polymerase chain reaction (PCR)-ELISA assay produced a positivity rate of 23.4% (47/201) using the first sample. All 72 patients with positive parasitological exams were treated with a single dose of Praziquantel® and these patients were followed-up 30, 90 and 180 days after treatment to establish the cure rate. Cure rates obtained by the analysis of 12 KK slides were 100%, 100% and 98.4% at 30, 90 and 180 days after treatment, respectively. PCR-ELISA revealed cure rates of 98.5%, 95.5% and 96.5%, respectively. The diagnostic and assessment of cure for schistosomiasis may require an increased number of KK slides or a test with higher sensitivity, such as PCR-ELISA, in situations of very low parasite load, such as after therapeutic interventions.

Mass trapping with MosquiTRAPs does not reduce Aedes aegypti abundance

The objective of this study was to evaluate the effectiveness of Aedes aegyptimass trapping using the sticky trap MosquiTRAP (MQT) by performing a cluster randomised controlled trial in Manaus, state of Amazonas, Brazil. After an initial questionnaire and baseline monitoring of adultAe. aegyptiabundance with BG-Sentinel (BGS) traps in six clusters, three clusters were randomly assigned to the intervention arm where each participating household received three MQTs for mass trapping during 17 months. The remaining three clusters (control arm) did not receive traps. The effect of mass trapping on adult Ae. aegyptiabundance was monitored fortnightly with BGS traps. During the last two months of the study, a serological survey was conducted. After the study, a second questionnaire was applied in the intervention arm. Entomological monitoring indicated that MQT mass trapping did not reduce adult Ae. aegyptiabundance. The serological survey indicated that recent dengue infections were equally frequent in the intervention and the control arm. Most participants responded positively to questions concerning user satisfaction. According to the results, there is no evidence that mass trapping with MQTs can be used as a part of dengue control programs. The use of this sticky trap is only recommendable for dengue vector monitoring.

Open minded and open access: introducing NeoBiota, a new peer-reviewed journal of biological invasions

The Editorial presents the focus, scope, policies, and the inaugural issue of NeoBiota, a new open access peer-reviewed journal of biological invasions. The new journal NeoBiota is a continuation of the former NEOBIOTA publication series. The journal will deal with all aspects of invasion biology and impose no restrictions on manuscript size neither on use of color. NeoBiota implies an XML-based editorial workflow and several cutting-edge innovations in publishing and dissemination, such as semantic markup of and enhancements to published texts, data publication, and extensive cross-linking within the journal and to external sources

Vitae sanctorum.

Abdo et Sennes (262-263v) ; Acisclus et Victoria (163-165) ; Adrianus (72v-77) ; Affra (45v) ; Amancius (122-125v) ; Andochius (90v-92v) ; Andreas (186-194v) ; Antoninus (68v-70v, 221v) ; Apollinaris (1bis-1bis v); Audardus (254-259) ; Augustinus (231-232v) ; Bartholomeus (55v-59v) ; Bricius Turonensis (162v-163) ; Caprasius (107-108) ; Caprasius et Fides (218-219v) ; Cassianus (48v) ; Cecilia (168v-174v) ; Christina (12-16v) ; Christoforus (22-24) ; Ciricus et Julita (2v-6, 260v-262) ; Cirillus (2-2v) ; Ciprianus (47v-48v) ; Claudius, Asterius, Neo (54v-55v) ; Clemens (174v-176) ; Cosmas et Damianus (97v-98v) ; Crisantus et Daria (179-182v) ; Crucis exaltatio (83-84) ; Cucufas (24-25) ; Dalmacius Rutenae urbis (131-132v) ; Desiderius Caturcensis (207v-217v) ; Dionisius (105-106v) ; Donatus (263v-265v) ; Eleazarus (38-38v) ; Eptadius (59v-61v) ; Eufemia (84-86) ; Eugenia (78-83) ; Eulalia (195v-199) ; Eustachius (125v-129v) ; Fabius (34v-36v) ; Fausta (52-53v) ; Faustus, Januarius et Marcialis (106v-107) ; Felix (36v-38) ; Felix Nolensis ep. (25-27) ; Filibertus (227v-231) ; Genesius Arelatensis (61v-62v) ; Germanus Autissiodorensis (33-34) ; Gervasius et Protasius (259v-260v) ; Gregorius papa (222-224v) ; Grisogonus (176v-178) ; Jacobus major (20v-21v) ; Jeronimus (100-102) ; Johannis Baptistae decollatio (66v-68v) ; Johannes et Paulus (227-227v) ; Julia (11-12) ; Julianus (64-64v) ; Julianus, auct. Gregorio Turonense (265v-272) ; Julius (178-178v) ; Justa et Rufina (6v-7) ; Justina et Ciprianus (92v-97v) ; Justus et Pastor (44v-45) ; Laurianus (167v-168v) ; Leochadia (195-195v) ; Leodegarius (102-104v) ; Licerius (62v-64) ; Longinus (195) ; Lucia (199-200v) ; Machabei (34-34v) ; Mammes (45v-47v) ; Marcellinus et Petrus (259-259v) ; Marcellus (114) ; Marcellus Cavalonis (219v-220) ; Marcellus Kavilonensis (1v-1bis) ; Marcus (224v-225) ; Marciana (129v-131) ; Marcianus (206-206v) ; Margarita (7-11) ; Mariae assumptio (48v-51) ; Martinus, auct. Sulpicio Severo (133-160v) ; Matheus (86-89) ; Mauricius (89-90v) ; Mauricius, Exuperius, Candidus, Innocentius, Victor cum sociis eorum (272-272v) ; Maurinus (245-247v) ; Maximus (241-244v) ; Medardus (225-227) ; Mennas (160v-162v) ; Michael (98v-100) ; Mimius (39v-40) ; Nazarius et Celsus (27-31v) ; Omnes Sancti (118v-122) ; Pantaleo (31v-32v) ; Petri cathedra (220-221v, 249-250) ; Petrus, ep. Alexandriae (248-249) ; Procopius (39-39v) ; Quintinus (114-118v) ; Regina (70v-72v) ; Reparata (104v-105) ; Romanus (165-167) ; Sabina (64v-66v) ; Salvius (77-78) ; Saturninus et Sisinnius (178v) ; Saturninus Tolosanensis (182v-185v, 232v-239) ; Segolena (16v-20v) ; Servandus et Germanus (108-109) ; Sixtus, Laurentius et Ypolitus (40-44v); Symo et Judas (109-112v) ; Symphorianus (53v-54v) ; Teodota (38v-39) ; Terencianus (239-241) ; Theodardus Narbonensis (250-254) ; Thomas (200v-206) ; Valerianus (206v-207) ; Vamnes (51-52) ; Vincentius et Savina (112v-114). Le f. 220v contient un catalogue ancien de la bibliothèque de Moissac.

Association of NTRK3 and its interaction with NGF suggest an altered cross-regulation of the neurotrophin signaling pathway in eating disorders

Eating disorders (EDs) are complex psychiatric diseases that include anorexia nervosa and bulimia nervosa, and have higher than 50% heritability. Previous studies have found association of BDNF and NTRK2 to ED, while animal models suggest that other neurotrophin genes might also be involved in eating behavior. We have performed a family-based association study with 151 TagSNPs covering 10 neurotrophin signaling genes: NGFB, BDNF, NTRK1, NGFR/p75, NTF4/5, NTRK2, NTF3, NTRK3, CNTF and CNTFR in 371 ED trios of Spanish, French and German origin. Besides several nominal associations, we found a strong significant association after correcting for multiple testing (P = 1.04 × 10−4) between ED and rs7180942, located in the NTRK3 gene, which followed an overdominant model of inheritance. Interestingly, HapMap unrelated individuals carrying the rs7180942 risk genotypes for ED showed higher levels of expression of NTRK3 in lymphoblastoid cell lines. Furthermore, higher expression of the orthologous murine Ntrk3 gene was also detected in the hypothalamus of the anx/anx mouse model of anorexia. Finally, variants in NGFB gene appear to modify the risk conferred by the NTRK3 rs7180942 risk genotypes (P = 4.0 × 10−5) showing a synergistic epistatic interaction. The reported data, in addition to the previous reported findings for BDNF and NTRK2, point neurotrophin signaling genes as key regulators of eating behavior and their altered cross-regulation as susceptibility factors for EDs.