Pattern of lateral neck metastases in N0 papillary thyroid carcinoma

<p>Abstract</p> <p>Background</p> <p>Indication and extent of lateral prophylactic neck dissection (PLND) in papillary thyroid carcinoma (PTC) is very controversial.</p> <p>Methods</p> <p>We retrospectively analysed 131 patients who underwent thyroidectomy and prophylactic lateral neck dissection from level II to V for PTC.</p> <p>Results</p> <p>140 PLND were performed. The occult lymph node metastases (OLNM) overall rate was 18.6%. The incidence of node involvement was 10% at level III and 6.4% at level IIa. Level IV and level Vb were both concerned by 5.7% OLNM. Only 2.9% of level IIb contained OLNM. None of the level Va ND revealed OLNM.</p> <p>Conclusions</p> <p>OLNM from PTC occurs commonly in level IIa, III, IV and Vb. Incidence in other levels is low. For surgeons that usually perform PLND, we believe that a selective neck dissection of levels IIa, III, IV and Vb in N0 neck PTC is sufficient for the clearance of occult metastases.</p

A Large Gene Network in Immature Erythroid Cells Is Controlled by the Myeloid and B Cell Transcriptional Regulator PU.1

PU.1 is a hematopoietic transcription factor that is required for the development of myeloid and B cells. PU.1 is also expressed in erythroid progenitors, where it blocks erythroid differentiation by binding to and inhibiting the main erythroid promoting factor, GATA-1. However, other mechanisms by which PU.1 affects the fate of erythroid progenitors have not been thoroughly explored. Here, we used ChIP-Seq analysis for PU.1 and gene expression profiling in erythroid cells to show that PU.1 regulates an extensive network of genes that constitute major pathways for controlling growth and survival of immature erythroid cells. By analyzing fetal liver erythroid progenitors from mice with low PU.1 expression, we also show that the earliest erythroid committed cells are dramatically reduced in vivo. Furthermore, we find that PU.1 also regulates many of the same genes and pathways in other blood cells, leading us to propose that PU.1 is a multifaceted factor with overlapping, as well as distinct, functions in several hematopoietic lineages

Kinetic and mechanistic aspects of ultrafiltration membrane fouling by nano- and microplastics

The mechanical and chemical breakdown of plastic litter increases the release of nano- and microplastics, which have the potential to impact the performance of membranes processes used in water treatment plants. In this work, the extent of fouling of a commercial ultrafiltration poly(sulfone) membrane induced by nano- and microplastics ranging from 13 to 690 nm in size was investigated. The cross-flow filtration of the plastic particles over 48 h at a 1 bar pressure reduced the permeate water flux by 38 % compared to pure water filtration. Over 25 % of the nano- and microplastics initially present in the feed were absorbed onto the membrane surface within the 48 h of filtration. Particulate fouling mechanism was sequentially modelled into intermediate and complete pore blockage, followed by cake layer formation. Hydrophobic interactions and surface repulsion forces were found to dictate the adsorption rate of the nano- and microplastics onto the membrane surface. This work opens the understanding of NPs/MPs interactions with water filtration processes and demonstrates the need to develop solutions limiting the impact of NPs/MPs on current treating units

Kinetic and mechanistic aspects of ultrafiltration membrane fouling by nano- and microplastics

The mechanical and chemical breakdown of plastic litter increases the release of nano- and microplastics, which have the potential to impact the performance of membranes processes used in water treatment plants. In this work, the extent of fouling of a commercial ultrafiltration poly(sulfone) membrane induced by nano- and microplastics ranging from 13 to 690 nm in size was investigated. The cross-flow filtration of the plastic particles over 48 h at a 1 bar pressure reduced the permeate water flux by 38 % compared to pure water filtration. Over 25 % of the nano- and microplastics initially present in the feed were absorbed onto the membrane surface within the 48 h of filtration. Particulate fouling mechanism was sequentially modelled into intermediate and complete pore blockage, followed by cake layer formation. Hydrophobic interactions and surface repulsion forces were found to dictate the adsorption rate of the nano- and microplastics onto the membrane surface. This work opens the understanding of NPs/MPs interactions with water filtration processes and demonstrates the need to develop solutions limiting the impact of NPs/MPs on current treating units

PU.1/Spi-1 binds to the human TAL-1 silencer to mediate its activity

The TAL-1/SCL gene encodes a basic helix-loop-helix (bHLH) transcription factor essential for primitive hematopoiesis and for adult erythroid and megakaryocytic development. Activated transcription of TAL-1 as a consequence of chromosomal rearrangements is associated with a high proportion of human T cell acute leukemias, showing that appropriate control of TAL-1 is crucial for the formation and subsequent fate of hematopoietic cells. Hence, the knowledge of the mechanisms, which govern the pattern of TAL-1 expression in hematopoiesis, is of great interest. We previously described a silencer in the 3'-untranslated region of human TAL-1, the activity of which is mediated through binding of a tissue-specific 40 kDa nuclear protein to a new DNA recognition motif, named tal-RE. Here, we show that tal-RE-binding activity, high in immature human hematopoietic progenitors is down regulated upon erythroid and megakaryocytic differentiation. This expression profile helped us to identify that PU.1/Spi-1 binds to the tal-RE sequences in vitro and occupies the TAL-1 silencer in vivo. By expressing a mutant protein containing only the ETS domain of PU.1 in human erythroleukemic HEL cells, we demonstrated that PU.1 mediates the transcriptional repression activity of the silencer. We found that ectopic PU.1 is not able to induce silencing activity in PU.1-negative Jurkat T cells, indicating that PU.1 activity, although necessary, is not sufficient to confer transcriptional repression activity to the TAL-1 silencer. Finally, we showed that the silencer is also active in TAL-1-negative myeloid HL60 cells that express PU.1 at high levels. In summary, our study shows that PU.1, in addition to its positive role in TAL-1 expression in early hematopoietic progenitors, may also act as a mediator of TAL-1 silencing in some hematopoietic lineages

PU.1/Spi-1 binds to the human TAL-1 silencer to mediate its activity

The TAL-1/SCL gene encodes a basic helix-loop-helix (bHLH) transcription factor essential for primitive hematopoiesis and for adult erythroid and megakaryocytic development. Activated transcription of TAL-1 as a consequence of chromosomal rearrangements is associated with a high proportion of human T cell acute leukemias, showing that appropriate control of TAL-1 is crucial for the formation and subsequent fate of hematopoietic cells. Hence, the knowledge of the mechanisms, which govern the pattern of TAL-1 expression in hematopoiesis, is of great interest. We previously described a silencer in the 3'-untranslated region of human TAL-1, the activity of which is mediated through binding of a tissue-specific 40 kDa nuclear protein to a new DNA recognition motif, named tal-RE. Here, we show that tal-RE-binding activity, high in immature human hematopoietic progenitors is down regulated upon erythroid and megakaryocytic differentiation. This expression profile helped us to identify that PU.1/Spi-1 binds to the tal-RE sequences in vitro and occupies the TAL-1 silencer in vivo. By expressing a mutant protein containing only the ETS domain of PU.1 in human erythroleukemic HEL cells, we demonstrated that PU.1 mediates the transcriptional repression activity of the silencer. We found that ectopic PU.1 is not able to induce silencing activity in PU.1-negative Jurkat T cells, indicating that PU.1 activity, although necessary, is not sufficient to confer transcriptional repression activity to the TAL-1 silencer. Finally, we showed that the silencer is also active in TAL-1-negative myeloid HL60 cells that express PU.1 at high levels. In summary, our study shows that PU.1, in addition to its positive role in TAL-1 expression in early hematopoietic progenitors, may also act as a mediator of TAL-1 silencing in some hematopoietic lineages

Distinct Cortical Areas for Names of Numbers and Body Parts Independent Of Language and Input Modality

INTRODUCTION The goal of the present work is to examine whether the semantic representations of numbers and body parts are associated with partially distinct cortical territories. Clinical and cognitive neuropsychology studies associate semantic deficits in both domains to lesions coarsely localized to the left parietal lobe (McCarthy and Warrington, 1990). Furthermore, patients with left inferior parietal lesions often exhibit simultaneous deficits for numbers and body parts (Benton, 1992; Gerstmann, 1940). Such an association of neuropsychological deficits is however notoriously ambiguous, and has been the subject of much debate. It might suggest that there is a shared substrate for numbers and body parts in the left parietal region, perhaps based on a common functional system for spatial representation and manipulation (Gerstmann, 1940) or on the crucial role that finger counting plays in numerical development (Butterworth, 1999). However, it might also reflect the existence of di