SummaryA region growing algorithm for segmentation of human intestinal gland images is presented. The initial seeding regions are identified based on the large vacant regions (lumen) inside the intestinal glands by fitting with a very large moving window. The seeding regions are then expanded by repetitive application of a morphological dilate operation with a much smaller round window structure set. False gland regions (nongland regions initially misclassified as gland regions) are removed based on either their excessive ages of active growth or inadequate thickness of dams formed by the strings of goblet cell nuclei sitting immediately outside the grown regions. The goblet cell nuclei are then identified and retained in the image. The gland contours are detected by applying a large moving round window fitting to the enormous empty exterior of the goblet cell nucleus chains in the image. The assumptions based on real intestinal gland images include the closed chain structured goblet cell nuclei that sit side-by-side with only small gaps between the neighbouring nuclei and that the lumens enclosed by the goblet cell nucleus chains are most vacant with only occasional run-away nuclei. The method performs well for most normal and abnormal intestinal gland images although it is less applicable to cancer cases. The experimental results show that the segmentations of the real microscopic intestinal gland images are satisfactorily accurate based on the visual evaluations.

A method for the selective capture and analysis of peptides containing neither histidine nor arginine is evaluated. It is based on the reversible modification of alpha- and epsilon-amino groups of peptides and the relatively easy separation of charged and noncharged peptides by cation exchange chromatography. The simplicity of the method and the results obtained in silico and with standard proteins, anticipate the utility of the SCAPE approach for proteome analyses.

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This work presents the results from a study of the protein composition of outer membrane vesicles from VA-MENGOC-BC (Finlay Institute, Cuba), an available vaccine against serogroup B Neisseria meningitidis. Proteins were identified by means of SCAPE, a 2DE-free method for proteome studies. More than one hundred proteins were detected by tandem liquid chromatographymass spectrometry analysis of fractions enriched in peptides devoid of histidine or arginine residues, providing a detailed description of the vaccine. A bioinformatic analysis of the identified components resulted in the identification of 31 outer membrane proteins and three conserved hypothetical proteins, allowing the cloning, expression, purification and immunological study of two of them (NMB0088 and NMB1796) as new antigens.

We report the first case of T-cell gamma delta+ hepatosplenic malignant lymphoma in childhood. Tumour-specific oligoprobes were developed against the single V1-J1 rearrangement of the delta T-cell receptor (TCR) gene in order to perform minimal residual disease (MRD) studies. Molecular analysis in serial bone marrow samples proved to be of predictive value concerning the clinical outcome. Clonotypic DNA was not detected in peripheral blood during the course of the disease until a refractory terminal leukaemic phase took place 18 months after the diagnosis. This case demonstrates the usefulness of MRD studies to monitor the course of disease in at least some subsets of peripheral T-cell lymphomas.

Huntington's disease (HD) is a neurodegenerative disorder caused by CAG expansions in the huntingtin (HTT) gene. Modelling HD has remained challenging, as rodent and cellular models poorly recapitulate the disease. To address this, we generated induced neurons (iNs) through direct reprogramming of human skin fibroblasts, which retain age-dependent epigenetic characteristics. HD-iNs displayed profound deficits in autophagy, characterised by reduced transport of late autophagic structures from the neurites to the soma. The neurite-specific alterations in autophagy resulted in shorter, thinner and fewer neurites presented by HD-iNs. CRISPRi-mediated silencing of HTT did not rescue this phenotype but rather resulted in additional autophagy alterations in ctrl-iNs, highlighting the importance of wild type HTT in neuronal autophagy. In summary, our work identifies a distinct subcellular autophagy impairment in aged patient derived HD-neurons and provides a new rational for future development of autophagy activation therapies.

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The online version of this article contains the full text of the retracted article as electronic supplementary material.