Impregnated netting slows infestation by Triatoma infestans

We used sentinel animal enclosures to measure the rate of infestation by the Chagas disease vector, Triatoma infestans, in an urban community of Arequipa, Peru, and to evaluate the effect of deltamethrin-impregnated netting on that rate. Impregnated netting decreased the rate of infestation of sentinel enclosures (rate ratio, 0.23; 95% confidence interval, 0.13-0.38; P < 0.001), controlling for the density of surrounding vector populations and the distance of these to the sentinel enclosures. Most migrant insects were early-stage nymphs, which are less likely to carry the parasitic agent of Chagas disease, Trypanosoma cruzi. Spread of the vector in the city therefore likely precedes spread of the parasite. Netting was particularly effective against adult insects and late-stage nymphs; taking into account population structure, netting decreased the reproductive value of migrant populations from 443.6 to 40.5. Impregnated netting can slow the spread of T. infestans and is a potentially valuable tool in the control of Chagas disease.     

A classification of ductal plate malformations based on distinct pathogenic mechanisms of biliary dysmorphogenesis

Ductal plate malformations (DPMs) are developmental anomalies considered to result from lack of ductal plate remodeling during bile duct morphogenesis. In mice, bile duct development is initiated by the formation of primitive ductal structures lined by two cell types, namely ductal plate cells and hepatoblasts. During ductal plate remodeling, the primitive ductal structures mature to ducts as a result from differentiation of the ductal plate cells and hepatoblasts to cholangiocytes. Here, we report this process is conserved in human fetal liver. These findings prompted us to evaluate how DPMs develop in three mouse models, namely mice with livers deficient in hepatocyte nuclear factor 6 (HNF6), HNF1β, or cystin-1 (cpk [congenital polycystic kidney] mice). Human liver from a patient with a HNF1B/TCF2 mutation, and from fetuses affected with autosomal recessive polycystic kidney disease (ARPKD) were also analyzed. Despite the epistatic relationship between HNF6, HNF1β, and cystin-1, the three mouse models displayed distinct morphogenic mechanisms of DPM. They all developed biliary cysts lined by cells with abnormal apicobasal polarity. However, the absence of HNF6 led to an early defect in ductal plate cell differentiation. In HNF1β-deficient liver, maturation of the primitive ductal structures was impaired. Normal differentiation and maturation but abnormal duct expansion was apparent in cpk mouse livers and in human fetal ARPKD. CONCLUSION: DPM is the common endpoint of distinct defects initiated at distinct stages of bile duct morphogenesis. Our observations provide a new pathogenic classification of DPM.     

Stage-specific effects of diflubenzuron on ecdysteroid titers during the development of Tenebrio molitor: evidence for a change in hormonal source

The effects of the insect growth regulator diflubenzuron (DFB) were observed on the larval-larval and larval-pupal moulting cycles of Tenebrio molitor, after treatment at ecdysis. In both cases, the first parts of the cycles, from ecdysis to apolysis, were apparently not affected, but the pharate periods were lengthened; treated animals were generally unable to perform ecdysis and died at this step. The ecdysteroid titers in the hemolymph of treated animals were measured with a radioimmunoassay and compared to controls. During larval-larval cycles, the single ecdysteroid increase was not affected by DFB treatment. On the contrary, during larval-pupal development, a significant modification was observed; whereas two ecdysteroid peaks occurred in controls, the second peak of treated animals was significantly reduced and slightly delayed; however, the first peak was not modified. Taking into account that previous observations demonstrated a complete inhibition of the ecdysteroid peak in Tenebrio pupae, these stage-specific differences could reveal either a change in the DFB sensitivity of a sole endocrine source (i.e., prothoracic gland) or a change in hormone origin during metamorphosis. Ligation experiments during the last larval stage, in combination or not with DFB applications, clearly demonstrated the change in the moulting hormone source at the end of larval development in Tenebrio.     

Shunting the intervillous space: new concepts in human uteroplacental vascularization

OBJECTIVE: It is supposed that the intervillous space is not perfused by maternal blood during the first trimester, suggesting vascular shunts in the myometrium. We therefore attempted to provide arguments for a functional vascular anastomotic network located in the placental bed during human pregnancy. STUDY DESIGN: Three-dimensional (3D) sonography, laboratory analyses, and anatomic studies (hysterectomy specimens, uteroplacental vascular cast) were performed. RESULTS: Color Doppler showed a vascular network with anastomotic aspect located in the placental bed. A vascular cast of a uterus, obtained after postpartum hemorrhage, demonstrated a vascular anastomotic network in the myometrium. Higher PO2 levels in the uterine vein compared with the intervillous space confirmed the functional nature of this shunt. Low resistances in the uterine arteries during the first week after delivery suggested that this vascular network remains functional after placental expulsion. CONCLUSION: Our studies have yielded functional and anatomic evidence of an arteriovenous shunt located in the subplacental myometrium.     

Congenital absence of the left pericardium and diaphragmatic defect in sibs

Congenital absence of the left pericardium (allowing communication between pericardial and pleural cavities) is a rare developmental defect that results from faulty partitioning of the pleuropericardic cavity during the 5th week of development. It occurs sporadically in most instances, and may be associated with other malformations of the thoracic viscera. We report here two sibs born to consanguineous parents with absent left fibrous pericardium and developmental defects of the septum transversum: left posterolateral diaphragmatic hernia in one child, left diaphragmatic eventration in the other sib. This appears to be the first familial report of this rare association.     

Distribution of varicella-zoster virus DNA and gene products in tissues of a first-trimester varicella-infected fetus

Precise information about varicella-zoster virus (VZV) infection in first-trimester fetuses remains sketchy. After varicella infection was diagnosed in a woman, her 12-week-old fetus was aborted and was investigated, by histological examination, virus culturing, polymerase chain reaction, in situ hybridization (ISH), and immunohistochemistry (IHC), for the presence of VZV infection. Only the results of the histological examination suggested the presence of alpha -herpesvirus infection, in the gastrointestinal tract and liver; results of ISH were positive for VZV, and results of IHC staining were positive for intermediate early protein 63 (IE63) but negative for glycoprotein E (gE), in the dorsal root ganglia (DRG), meninges, gastrointestinal tract, pancreas, smooth muscle, liver, and placental trophoblast, indicating the presence of a nonproductive, latency-like VZV infection. Only the gastrointestinal tract and liver exhibited simultaneous staining for IE63 and gE, a result suggesting that active replication of VZV was present. In conclusion, widespread nonproductive VZV infection in the absence of histological clues is an early event in VZV infection in fetuses. The observed gene-expression pattern in most tissues resembles that of latent VZV infection in DRG. Latency-like infection in nonneural cell types may potentially reactivate, leading to multifocal necrosis, fibrosis, and dystrophic calcifications, as observed in advanced congenital varicella syndrome.