Liotryphon punctulatus (Ratzeburg, 1848) (Hymenoptera: Ichneumonidae) – a parasitoid of Ephestia kuehniella larvae

Until now, there has been no record of Liotrophon punctulatus (Hymenoptera: Ichneumonidae) presence in the anthropogenic environment of mills, bakeries or pasta factories. This is the first report of the species parasitizing Ephestia kuehniella (Lepidoptera: Pyralidae) larvae. The host/parasitoid interaction was validated under laboratory conditions where fourth or fifth instar larvae of Ephestia kuehniella were provided ad libitum to L. punctulatus females. After two filial generations emergence, the validation process was considered to confirm the interaction. Keywords: Liotrophon punctulatus, Parasitoid, Ephestia kuehniell

Specific microRNAs and heart failure: time for the next step toward application?

A number of microRNAs are involved in the pathophysiological events associated with heart disease. In this review, we discuss miR-21, miR-1, miR-23a, miR-142-5p, miR-126, miR-29, miR-195, and miR-499 because they are most often mentioned as important specific indicators of myocardial hypertrophy and fibrosis leading to heart failure. The clinical use of microRNAs as biomarkers and for therapeutic interventions in cardiovascular diseases appears highly promising. However, there remain many unresolved details regarding their specific actions in distinct pathological phenomena. The introduction of microRNAs into routine practice, as part of the cardiovascular examination panel, will require additional clinically relevant and reliable data. Thus, there remains a need for additional research in this area, as well as the optimization and standardization of laboratory procedures which could significantly shorten the determination time, and make microRNA analysis simpler and more affordable. In this review, we aim to summarize the current knowledge about selected microRNAs related to heart failure, including their potential use in diagnosis, prognosis, and treatment, and options for their laboratory determination

Imaging properties of the Medipix2 system exploiting single and dual energy thresholds

Low noise, high resolution and high dose efficiency are the common requirements for most X-ray imaging applications. Especially in medical applications the dose efficiency is a necessity for detector systems. We present the imaging performance of the Medipix2 readout chip bump bonded to a 300 mu m thick Si detector as a function of the detection threshold, a free parameter not available in conventional integrating imaging systems. Spatial resolution has been measured using the modulation transfer function (MTF) and it varies between 8.2 Ip/mm and 11.0 Ip/mm at 70%. An associated measurement of noise power spectrum (NPS) permits us to derive the detective quantum efficiency (DQE) which can be as a high as 25.5 % for a broadband incoming spectrum. The influence of charge diffusion in the sensor together with threshold variation in the readout chip is discussed. Although the Medipix2 system is used in photon counting mode with a single threshold in energy, the system is also capable of counting within a given energy window of down to ~1.4 keV. First measurements and images using this feature reveal capabilities that allow to identify fluorescence and other sources of disturbance

A proteomic survey of microtubule-associated proteins in a R402H TUBA1A mutant mouse.

Microtubules play a critical role in multiple aspects of neurodevelopment, including the generation, migration and differentiation of neurons. A recurrent mutation (R402H) in the α-tubulin gene TUBA1A is known to cause lissencephaly with cerebellar and striatal phenotypes. Previous work has shown that this mutation does not perturb the chaperone-mediated folding of tubulin heterodimers, which are able to assemble and incorporate into the microtubule lattice. To explore the molecular mechanisms that cause the disease state we generated a new conditional mouse line that recapitulates the R402H variant. We show that heterozygous mutants present with laminar phenotypes in the cortex and hippocampus, as well as a reduction in striatal size and cerebellar abnormalities. We demonstrate that homozygous expression of the R402H allele causes neuronal death and exacerbates a cell intrinsic defect in cortical neuronal migration. Microtubule sedimentation assays coupled with quantitative mass spectrometry demonstrated that the binding and/or levels of multiple microtubule associated proteins (MAPs) are perturbed by the R402H mutation including VAPB, REEP1, EZRIN, PRNP and DYNC1l1/2. Consistent with these data we show that the R402H mutation impairs dynein-mediated transport which is associated with a decoupling of the nucleus to the microtubule organising center. Our data support a model whereby the R402H variant is able to fold and incorporate into microtubules, but acts as a gain of function by perturbing the binding of MAPs

Clinical characteristics and outcomes in risk-stratified patients with smoldering multiple myeloma: data from the Czech Republic Registry of Monoclonal Gammopathies

Abstract Smoldering multiple myeloma (SMM) is an asymptomatic precursor to active multiple myeloma (MM). The aim of this study was to report clinical characteristics and outcomes of patients with SMM stratified based on their risk of progression to MM using the Mayo 20/2/20 criteria. Data were leveraged from the Czech Myeloma Group Registry of Monoclonal Gammopathies (RMG). Key outcomes included progression-free survival from SMM diagnosis to active MM diagnosis or death (PFS), progression-free survival from SMM diagnosis to progression on first line (1 L) MM treatment or death (PFS2), and overall survival (OS). Of 498 patients, 174 (34.9%) were classified as high risk and 324 (65.1%) as non–high risk. Median follow-up was approximately 65 months. During follow-up, more patients in the high-risk vs non–high-risk group received 1 L MM treatment (76.4% vs 46.6%, p < 0.001). PFS, PFS2, and OS were significantly shorter in high-risk vs non–high-risk patients (13.2 vs 56.6 months, p < 0.001; 49.9 vs 84.9 months, p < 0.001; 93.2 vs 131.1 months, p = 0.012, respectively). The results of this study add to the growing body of evidence that patients with high-risk vs non–high-risk SMM have significantly worse outcomes, including OS

KIF14 controls ciliogenesis via regulation of Aurora A and is important for Hedgehog signaling

International audiencePrimary cilia play critical roles in development and disease. Their assembly and disassembly are tightly coupled to cell cycle progression. Here, we present data identifying KIF14 as a regulator of cilia formation and Hedgehog (HH) signaling. We show that RNAi depletion of KIF14 specifically leads to defects in ciliogenesis and basal body (BB) biogenesis, as its absence hampers the efficiency of primary cilium formation and the dynamics of primary cilium elongation, and disrupts the localization of the distal appendage proteins SCLT1 and FBF1 and components of the IFT-B complex. We identify deregulated Aurora A activity as a mechanism contributing to the primary cilium and BB formation defects seen after KIF14 depletion. In addition, we show that primary cilia in KIF14-depleted cells are defective in response to HH pathway activation, independently of the effects of Aurora A. In sum, our data point to KIF14 as a critical node connecting cell cycle machinery, effective ciliogenesis, and HH signaling