Intracorporeal and extracorporeal anastomosis for robotic-assisted and laparoscopic right colectomy: Short-term outcomes of a multi-center prospective trial

BACKGROUND: Studies to date show contrasting conclusions when comparing intracorporeal and extracorporeal anastomoses for minimally invasive right colectomy. Large multi-center prospective studies comparing perioperative outcomes between these two techniques are needed. The purpose of this study was to compare intracorporeal and extracorporeal anastomoses outcomes for robotic assisted and laparoscopic right colectomy. METHODS: Multi-center, prospective, observational study of patients with malignant or benign disease scheduled for laparoscopic or robotic-assisted right colectomy. Outcomes included conversion rate, gastrointestinal recovery, and complication rates. RESULTS: There were 280 patients: 156 in the robotic assisted and laparoscopic intracorporeal anastomosis (IA) group and 124 in the robotic assisted and laparoscopic extracorporeal anastomosis (EA) group. The EA group was older (mean age 67 vs. 65 years, p = 0.05) and had fewer white (81% vs. 90%, p = 0.05) and Hispanic (2% vs. 12%, p = 0.003) patients. The EA group had more patients with comorbidities (82% vs. 72%, p = 0.04) while there was no significant difference in individual comorbidities between groups. IA was associated with fewer conversions to open and hand-assisted laparoscopic approaches (p = 0.007), shorter extraction site incision length (4.9 vs. 6.2 cm; p ≤ 0.0001), and longer operative time (156.9 vs. 118.2 min). Postoperatively, patients with IA had shorter time to first flatus, (1.5 vs. 1.8 days; p ≤ 0.0001), time to first bowel movement (1.6 vs. 2.0 days; p = 0.0005), time to resume soft/regular diet (29.0 vs. 37.5 h; p = 0.0014), and shorter length of hospital stay (median, 3 vs. 4 days; p ≤ 0.0001). Postoperative complication rates were comparable between groups. CONCLUSION: In this prospective, multi-center study of minimally invasive right colectomy across 20 institutions, IA was associated with significant improvements in conversion rates, return of bowel function, and shorter hospital stay, as well as significantly longer operative times compared to EA. These data validate current efforts to increase training and adoption of the IA technique for minimally invasive right colectomy

Characterisation of the Cullin-3 mutation that causes a severe form of familial hypertension and hyperkalaemia

Deletion of exon 9 from Cullin‐3 (CUL3, residues 403–459: CUL3Δ403–459) causes pseudohypoaldosteronism type IIE (PHA2E), a severe form of familial hyperkalaemia and hypertension (FHHt). CUL3 binds the RING protein RBX1 and various substrate adaptors to form Cullin‐RING‐ubiquitin‐ligase complexes. Bound to KLHL3, CUL3‐RBX1 ubiquitylates WNK kinases, promoting their ubiquitin‐mediated proteasomal degradation. Since WNK kinases activate Na/Cl co‐transporters to promote salt retention, CUL3 regulates blood pressure. Mutations in both KLHL3 and WNK kinases cause PHA2 by disrupting Cullin‐RING‐ligase formation. We report here that the PHA2E mutant, CUL3Δ403–459, is severely compromised in its ability to ubiquitylate WNKs, possibly due to altered structural flexibility. Instead, CUL3Δ403–459 auto‐ubiquitylates and loses interaction with two important Cullin regulators: the COP9‐signalosome and CAND1. A novel knock‐in mouse model of CUL3WT/Δ403–459 closely recapitulates the human PHA2E phenotype. These mice also show changes in the arterial pulse waveform, suggesting a vascular contribution to their hypertension not reported in previous FHHt models. These findings may explain the severity of the FHHt phenotype caused by CUL3 mutations compared to those reported in KLHL3 or WNK kinases

Cultural Identity and Social and Emotional Wellbeing in Aboriginal and Torres Strait Islander Children

Connection with Country, community, and culture lies at the heart of Aboriginal and Torres Strait Islander peoples’ health and wellbeing. Although there is some evidence on the role of cultural identity on the mental health of Indigenous adults, this relationship is relatively unexplored in the context of Indigenous Australian children. Robust empirical evidence on the role of cultural identity for social and emotional wellbeing is necessary to design and develop effective interventions and approaches for improving the mental health outcomes for Indigenous Australian children. Drawing on data from the Longitudinal Study of Indigenous Children (LSIC), we explore social and emotional wellbeing in Indigenous Australian children and assesses whether cultural identity protects against social-emotional problems in Indigenous children. The results show that Indigenous children with strong cultural identity and knowledge are less likely to experience social and emotional problems than their counterparts. Our work provides further evidence to support the change from a deficit narrative to a strengths-based discourse for improved health and wellbeing of Indigenous Australian children

Grupos de pesquisa em enfermagem no Brasil: comparação dos perfis de 2006 e 2016

RESUMO Objetivos Comparar o perfil dos grupos de pesquisa em Enfermagem cadastrados no Diretório do CNPq em 2006 e 2016. Métodos Estudo descritivo documental. A coleta de dados aconteceu em 2006 e 2016 a partir de consulta parametrizada com o termo Enfermagem no Diretório dos Grupos de Pesquisa, na página online do CNPq, sendo realizada a análise descritiva. Os dados foram organizados em planilha do Excel. Resultados O número de Grupos de Pesquisa aumentou de 251 em 2006 para 617 em 2016, com incremento no número de participantes. Houve redução do número de grupos sem estudantes, embora 22% permaneçam sem participação de alunos de graduação. Conclusões Os grupos de pesquisa em Enfermagem refletem avanços estruturais e políticos na geração de ciência, tecnologia e inovação da área, entretanto ainda deve ser incentivada a participação de alunos de graduação e pesquisadores estrangeiros, bem como a ampliação de recursos tecnológicos e das parcerias interinstitucionais

Wireless aquatic navigator for detection and analysis (WANDA)

The cost of monitoring and detecting pollutants in natural waters is of major concern. Current and forthcoming bodies of legislation will continue to drive demand for spatial and selective monitoring of our environment, as the focus increasingly moves towards effective enforcement of legislation through detection of events, and unambiguous identification of perpetrators. However, these monitoring demands are not being met due to the infrastructure and maintenance costs of conventional sensing models. Advanced autonomous platforms capable of performing complex analytical measurements at remote locations still require individual power, wireless communication, processor and electronic transducer units, along with regular maintenance visits. Hence the cost base for these systems is prohibitively high, and the spatial density and frequency of measurements are insufficient to meet requirements. In this paper we present a more cost effective approach for water quality monitoring using a low cost mobile sensing/communications platform together with very low cost stand-alone ‘satellite’ indicator stations that have an integrated colorimetric sensing material. The mobile platform is equipped with a wireless video camera that is used to interrogate each station to harvest information about the water quality. In simulation experiments, the first cycle of measurements is carried out to identify a ‘normal’ condition followed by a second cycle during which the platform successfully detected and communicated the presence of a chemical contaminant that had been localised at one of the satellite stations

Role of transcript and interplay between transcription and replication in triplet-repeat instability in mammalian cells

Triplet-repeat expansions cause several inherited human diseases. Expanded triplet-repeats are unstable in somatic cells, and tissue-specific somatic instability contributes to disease pathogenesis. In mammalian cells instability of triplet-repeats is dependent on the location of the origin of replication relative to the repeat tract, supporting the ‘fork-shift’ model of repeat instability. Disease-causing triplet-repeats are transcribed, but how this influences instability remains unclear. We examined instability of the expanded (GAA•TTC)n sequence in mammalian cells by analyzing individual replication events directed by the SV40 origin from five different locations, in the presence and absence of doxycycline-induced transcription. Depending on the location of the SV40 origin, either no instability was observed, instability was caused by replication with no further increase due to transcription, or instability required transcription. Whereas contractions accounted for most of the observed instability, one construct showed expansions upon induction of transcription. These expansions disappeared when transcript stability was reduced via removal or mutation of a spliceable intron. These results reveal a complex interrelationship of transcription and replication in the etiology of repeat instability. While both processes may not be sufficient for the initiation of instability, transcription and/or transcript stability seem to further modulate the fork-shift model of triplet-repeat instability

Mode Properties of Flat-top Silver Nano-ridge Surface Plasmon Waveguides

We investigate surface plasmon modes supported by flat-top silver nano-ridges. We calculate the mode electromagnetic field distribution, the dispersion curve, the travel range, and the figure-of-merit of the nano-ridge mode. We find that the nano-ridge surface plasmon modes are quasi-TEM modes with longitudinal field components three orders of magnitude smaller than the transverse field components. The quasi-TEM nature of mode profiles reveals that the propagation of free electron oscillations on the top of the nano-ridge contributes mainly to the tightly confined ridge mode. We also find that as the width of the nano-ridge decreases, the ridge mode becomes more tightly confined on the ridge top. As the width of the nano-ridge increases, the nano-ridge mode approaches two decoupled right-angle wedge plasmon modes.Comment: 23 pages, 9 figures, journal articl

Characterisation of the Cullin-3 mutation that causes a severe form of familial hypertension and hyperkalaemia

This is the final version of the article. Available from the publisher via the DOI in this record.Deletion of exon 9 from Cullin‐3 (CUL3, residues 403–459: CUL3Δ403–459) causes pseudohypoaldosteronism type IIE (PHA2E), a severe form of familial hyperkalaemia and hypertension (FHHt). CUL3 binds the RING protein RBX1 and various substrate adaptors to form Cullin‐RING‐ubiquitin‐ligase complexes. Bound to KLHL3, CUL3‐RBX1 ubiquitylates WNK kinases, promoting their ubiquitin‐mediated proteasomal degradation. Since WNK kinases activate Na/Cl co‐transporters to promote salt retention, CUL3 regulates blood pressure. Mutations in both KLHL3 and WNK kinases cause PHA2 by disrupting Cullin‐RING‐ligase formation. We report here that the PHA2E mutant, CUL3Δ403–459, is severely compromised in its ability to ubiquitylate WNKs, possibly due to altered structural flexibility. Instead, CUL3Δ403–459 auto‐ubiquitylates and loses interaction with two important Cullin regulators: the COP9‐signalosome and CAND1. A novel knock‐in mouse model of CUL3WT/Δ403–459 closely recapitulates the human PHA2E phenotype. These mice also show changes in the arterial pulse waveform, suggesting a vascular contribution to their hypertension not reported in previous FHHt models. These findings may explain the severity of the FHHt phenotype caused by CUL3 mutations compared to those reported in KLHL3 or WNK kinases.This work was supported by the British Heart Foundation (a PhD studentship to KS and PG 13 89 30577), Medical Research Council, and an ERC Starting Investigator Grant (to TK), as well as the pharmaceutical companies supporting the Division of Signal Transduction Therapy Unit (AstraZeneca, Boehringer Ingelheim, GlaxoSmithKline, Merck, Janssen Pharmaceutica and Pfizer). The Human Research Tissue Bank is supported by the NIHR Cambridge Biomedical Research Centre

Mechanical analysis of end-to-end silk-sutured anastomosis for robot-assisted surgery

Background Robot-assisted anastomosis holds great promise for the future. To secure surgery quality, some key process factors, such as the force arrangement of sutures, should be provided because of the lack of haptic feedback in robotics systems Methods A model of anastomosis is presented to establish the mechanical relationship between vessel and sutures. Stress distribution of the vessel loaded by the suture was then achieved through finite-element simulations, based on the material property test results. Further, experiments were performed to validate the reliability of the FEM simulation of the anastomosis process. Results To avoid blood osmosis, the allowable lower limit of the suture tension was 0.05 N. To keep the tissue free from injury, the allowable upper limit of tension on the suture was 0.4 N. Conclusions The study provided meaningful results for directing the robot-assisted anastomosis procedure and design of the surgical tools. Copyright © 2009 John Wiley & Sons, Ltd.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/64523/1/276_ftp.pd

Replication in mammalian cells recapitulates the locus-specific differences in somatic instability of genomic GAA triplet-repeats

Friedreich ataxia is caused by an expanded (GAA·TTC)(n) sequence in intron 1 of the FXN gene. Small pool PCR analysis showed that pure (GAA·TTC)(44+) sequences at the FXN locus are unstable in somatic cells in vivo, displaying both expansions and contractions. On searching the entire human and mouse genomes we identified three other genomic loci with pure (GAA·TTC)(44+) sequences. Alleles at these loci showed mutation loads of <1% compared with 6.3–30% for FXN alleles of similar length, indicating that somatic instability in vivo is regulated by locus-specific factors. Since distance between the origin of replication and the (CTG·CAG)(n) sequence modulates repeat instability in mammalian cells, we tested if this could also recapitulate the locus-specific differences for genomic (GAA·TTC)(n) sequences. Repeat instability was evaluated following replication of a (GAA·TTC)(115) sequence in transfected COS1 cells under the control of the SV40 origin of replication located at one of five different distances from the repeat. Indeed, depending on the location of the SV40 origin relative to the (GAA·TTC)(n) sequence, we noted either no instability, predominant expansion or both expansion and contraction. These data suggest that mammalian DNA replication is a possible mechanism underlying locus-specific differences in instability of GAA triplet-repeat sequences