13 research outputs found
δ-Catenin promotes prostate cancer cell growth and progression by altering cell cycle and survival gene profiles
Background: delta-Catenin is a unique member of delta-catenin/armadillo domain superfamily proteins and its primary expression is restricted to the brain. However, delta-catenin is upregulated in human prostatic adenocarcinomas, although the effects of delta-catenin overexpression in prostate cancer are unclear. We hypothesized that delta-catenin plays a direct role in prostate cancer progression by altering gene profiles of cell cycle regulation and cell survival.
Results: We employed gene transfection and small interfering RNA to demonstrate that increased delta-catenin expression promoted, whereas its knockdown suppressed prostate cancer cell viability. delta-Catenin promoted prostate cancer cell colony formation in soft agar as well as tumor xenograft growth in nude mice. Deletion of either the amino-terminal or carboxyl-terminal sequences outside the armadillo domains abolished the tumor promoting effects of delta-catenin. Quantitative RT2 Profilerâ„¢ PCR Arrays demonstrated gene alterations involved in cell cycle and survival
regulation. delta-Catenin overexpression upregulated cyclin D1 and cdc34, increased phosphorylated histone-H3, and promoted the entry of mitosis. In addition, delta-catenin overexpression resulted in increased expression of cell survival genes Bcl-2 and survivin while reducing the cell cycle inhibitor p21Cip1.
Conclusion: Taken together, our studies suggest that at least one consequence of an increased expression of delta-catenin in human prostate cancer is the alteration of cell cycle and survival gene profiles, thereby promoting tumor progression.
Originally published Molecular Cancer, Vol. 8, No. 19, Mar 200
Reducing the environmental impact of surgery on a global scale: systematic review and co-prioritization with healthcare workers in 132 countries
Abstract
Background
Healthcare cannot achieve net-zero carbon without addressing operating theatres. The aim of this study was to prioritize feasible interventions to reduce the environmental impact of operating theatres.
Methods
This study adopted a four-phase Delphi consensus co-prioritization methodology. In phase 1, a systematic review of published interventions and global consultation of perioperative healthcare professionals were used to longlist interventions. In phase 2, iterative thematic analysis consolidated comparable interventions into a shortlist. In phase 3, the shortlist was co-prioritized based on patient and clinician views on acceptability, feasibility, and safety. In phase 4, ranked lists of interventions were presented by their relevance to high-income countries and low–middle-income countries.
Results
In phase 1, 43 interventions were identified, which had low uptake in practice according to 3042 professionals globally. In phase 2, a shortlist of 15 intervention domains was generated. In phase 3, interventions were deemed acceptable for more than 90 per cent of patients except for reducing general anaesthesia (84 per cent) and re-sterilization of ‘single-use’ consumables (86 per cent). In phase 4, the top three shortlisted interventions for high-income countries were: introducing recycling; reducing use of anaesthetic gases; and appropriate clinical waste processing. In phase 4, the top three shortlisted interventions for low–middle-income countries were: introducing reusable surgical devices; reducing use of consumables; and reducing the use of general anaesthesia.
Conclusion
This is a step toward environmentally sustainable operating environments with actionable interventions applicable to both high– and low–middle–income countries
δ-Catenin promotes prostate cancer cell growth and progression by altering cell cycle and survival gene profiles
Abstract Background δ-Catenin is a unique member of β-catenin/armadillo domain superfamily proteins and its primary expression is restricted to the brain. However, δ-catenin is upregulated in human prostatic adenocarcinomas, although the effects of δ-catenin overexpression in prostate cancer are unclear. We hypothesized that δ-catenin plays a direct role in prostate cancer progression by altering gene profiles of cell cycle regulation and cell survival. Results We employed gene transfection and small interfering RNA to demonstrate that increased δ-catenin expression promoted, whereas its knockdown suppressed prostate cancer cell viability. δ-Catenin promoted prostate cancer cell colony formation in soft agar as well as tumor xenograft growth in nude mice. Deletion of either the amino-terminal or carboxyl-terminal sequences outside the armadillo domains abolished the tumor promoting effects of δ-catenin. Quantitative RT2 Profiler™ PCR Arrays demonstrated gene alterations involved in cell cycle and survival regulation. δ-Catenin overexpression upregulated cyclin D1 and cdc34, increased phosphorylated histone-H3, and promoted the entry of mitosis. In addition, δ-catenin overexpression resulted in increased expression of cell survival genes Bcl-2 and survivin while reducing the cell cycle inhibitor p21Cip1. Conclusion Taken together, our studies suggest that at least one consequence of an increased expression of δ-catenin in human prostate cancer is the alteration of cell cycle and survival gene profiles, thereby promoting tumor progression.</p
delta-Catenin promotes prostate cancer cell growth and progression by altering cell cycle and survival gene profiles
Background: delta-Catenin is a unique member of delta-catenin/armadillo domain superfamily proteins and its primary expression is restricted to the brain. However delta-catenin is upregulated in human prostatic adenocarcinomas although the effects of delta-catenin overexpression in prostate cancer are unclear. We hypothesized that delta-catenin plays a direct role in prostate cancer progression by altering gene profiles of cell cycle regulation and cell survival. esults: We employed gene transfection and small interfering RNA to demonstrate that increased delta-catenin expression promoted whereas its knockdown suppressed prostate cancer cell viability. delta-Catenin promoted prostate cancer cell colony formation in soft agar as well as tumor xenograft growth in nude mice. Deletion of either the amino-terminal or carboxyl-terminal sequences outside the armadillo domains abolished the tumor promoting effects of delta-catenin. Quantitative RT2 Profilerâ„¢ PCR Arrays demonstrated gene alterations involved in cell cycle and survival egulation. delta-Catenin overexpression upregulated cyclin D1 and cdc34 increased phosphorylated histone-H3 and promoted the entry of mitosis. In addition delta-catenin overexpression resulted in increased expression of cell survival genes Bcl-2 and survivin while reducing the cell cycle inhibitor p21Cip1. onclusion: Taken together our studies suggest that at least one consequence of an increased expression of delta-catenin in human prostate cancer is the alteration of cell cycle and survival gene profiles thereby promoting tumor progression. riginally published Molecular Cancer Vol. 8 No. 19 Mar 200
Iron mineralization and core dissociation in mammalian homopolymeric H-ferritin: Current understanding and future perspectives
Molecular Cancer BioMed Central
δ-Catenin promotes prostate cancer cell growth and progression by altering cell cycle and survival gene profile
Semi-empirical correlation of solid solute solubility in supercritical carbon dioxide: Comparative study and proposition of a novel density-based model
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Climate, Ticks and Disease
This book brings together expert opinions from scientists to consider the evidence for climate change and its impacts on ticks and tick-borne infections. It considers what is meant by 'climate change', how effective climate models are in relation to ecosystems, and provides predictions for changes in climate at global, regional and local scales relevant for ticks and tick-borne infections. It examines changes to tick distribution and the evidence that climate change is responsible. The effect of climate on the physiology and behaviour of ticks is stressed, including potentially critical impacts on the tick microbiome. Given that the notoriety of ticks derives from pathogens they transmit, the book considers whether changes in climate affect vector capacity. Ticks transmit a remarkable range of micro- and macro-parasites many of which are pathogens of humans and domesticated animals. The intimacy between a tick-borne agent and a tick vector means that any impacts of climate on a tick vector will impact tick-borne pathogens. Most obviously, such impacts will be apparent as changes in disease incidence and prevalence. The evidence that climate change is affecting diseases caused by tick-borne pathogens is considered, along with the potential to make robust predictions of future events. This book contains: Expert opinions and predictions. Global coverage of trends in ticks and disease. In-depth examination of climate change and tick distribution links.This book is suitable for researchers and students studying zoology, biological sciences, medical entomology, animal health, veterinary medicine, epidemiology, parasitology, and climate change impacts; and for those concerned with public health planning or livestock management where ticks and tick-borne pathogens pose a threat
SARS-CoV-2 vaccination modelling for safe surgery to save lives: data from an international prospective cohort study
Background: Preoperative SARS-CoV-2 vaccination could support safer elective surgery. Vaccine numbers are limited so this study aimed to inform their prioritization by modelling.
Methods: The primary outcome was the number needed to vaccinate (NNV) to prevent one COVID-19-related death in 1 year. NNVs were based on postoperative SARS-CoV-2 rates and mortality in an international cohort study (surgical patients), and community SARS-CoV-2 incidence and case fatality data (general population). NNV estimates were stratified by age (18-49, 50-69, 70 or more years) and type of surgery. Best- and worst-case scenarios were used to describe uncertainty.
Results: NNVs were more favourable in surgical patients than the general population. The most favourable NNVs were in patients aged 70 years or more needing cancer surgery (351; best case 196, worst case 816) or non-cancer surgery (733; best case 407, worst case 1664). Both exceeded the NNV in the general population (1840; best case 1196, worst case 3066). NNVs for surgical patients remained favourable at a range of SARS-CoV-2 incidence rates in sensitivity analysis modelling. Globally, prioritizing preoperative vaccination of patients needing elective surgery ahead of the general population could prevent an additional 58 687 (best case 115 007, worst case 20 177) COVID-19-related deaths in 1 year.
Conclusion: As global roll out of SARS-CoV-2 vaccination proceeds, patients needing elective surgery should be prioritized ahead of the general population