A Systematic Review and Meta-Analysis of Outcomes for Type 1 Diabetes after Bariatric Surgery

Background. The utility of bariatric surgery in type 1 diabetes remains controversial. The aim of the present study is to evaluate glycemic control outcomes in obese patients with type 1 diabetes after bariatric surgery. Methods. A comprehensive search of electronic databases was completed. Inclusion criteria included human adult subjects with BMI ≥35 kg/m2 and a confirmed diagnosis of type 1 diabetes who underwent a bariatric surgical procedure. Results. Thirteen primary studies (86 patients) were included. Subjects had a mean age of 41.16±6.76 years with a mean BMI of 42.50±2.65 kg/m2. There was a marked reduction in BMI postoperatively at 12 months and at study endpoint to 29.55±1.76 kg/m2 (P<0.00001) and 30.63±2.09 kg/m2 (P<0.00001), respectively. Preoperative weighted mean total daily insulin requirement was 98±26 IU/d, which decreased significantly to 36±15 IU/d (P<0.00001) and 42±11 IU/d (P<0.00001) at 12 months and at study endpoint, respectively. An improvement in HbA1c was also seen from 8.46±0.78% preoperatively to 7.95±0.55% (P=0.01) and 8.13±0.86% (P=0.03) at 12 months and at study endpoint, respectively. Conclusion. Bariatric surgery in patients with type 1 diabetes leads to significant reductions in BMI and improvements in glycemic control

A Systematic Review and Meta-Analysis of Outcomes for Type 1 Diabetes after Bariatric Surgery

Background. The utility of bariatric surgery in type 1 diabetes remains controversial. The aim of the present study is to evaluate glycemic control outcomes in obese patients with type 1 diabetes after bariatric surgery. Methods. A comprehensive search of electronic databases was completed. Inclusion criteria included human adult subjects with BMI ≥35 kg/m 2 and a confirmed diagnosis of type 1 diabetes who underwent a bariatric surgical procedure. Results. Thirteen primary studies (86 patients) were included. Subjects had a mean age of 41.16 ± 6.76 years with a mean BMI of 42.50 ± 2.65 kg/m 2 . There was a marked reduction in BMI postoperatively at 12 months and at study endpoint to 29.55 ± 1.76 kg/m 2 ( &lt; 0.00001) and 30.63 ± 2.09 kg/m 2 ( &lt; 0.00001), respectively. Preoperative weighted mean total daily insulin requirement was 98 ± 26 IU/d, which decreased significantly to 36 ± 15 IU/d ( &lt; 0.00001) and 42 ± 11 IU/d ( &lt; 0.00001) at 12 months and at study endpoint, respectively. An improvement in HbA1c was also seen from 8.46 ± 0.78% preoperatively to 7.95 ± 0.55% ( = 0.01) and 8.13 ± 0.86% ( = 0.03) at 12 months and at study endpoint, respectively. Conclusion. Bariatric surgery in patients with type 1 diabetes leads to significant reductions in BMI and improvements in glycemic control

A model for describing and maximising Security Knowledge Sharing to enhance security awareness

Employees play a crucial role in enhancing information security in the workplace, and this requires everyone having the requisite security knowledge and know-how. To maximise knowledge levels, organisations should encourage and facilitate Security Knowledge Sharing (SKS) between employees. To maximise sharing, we need first to understand the mechanisms whereby such sharing takes place and then to encourage and engender such sharing. A study was carried out to test the applicability of Transactive Memory Systems Theory in describing knowledge sharing in this context, which confirmed its applicability in this domain. To encourage security knowledge sharing, the harnessing of Self-Determination Theory was proposed— satisfying employee autonomy, relatedness and competence needs to maximise sharing. Such sharing is required to improve and enhance employee security awareness across organisations. We propose a model to describe the mechanisms for such sharing as well as the means by which it can be encouraged

Defining the Molecular Basis of Tumor Metabolism: a Continuing Challenge Since Warburg's Discovery

Cancer cells are the product of genetic disorders that alter crucial intracellular signaling pathways associated with the regulation of cell survival, proliferation, differentiation and death mechanisms. the role of oncogene activation and tumor suppressor inhibition in the onset of cancer is well established. Traditional antitumor therapies target specific molecules, the action/expression of which is altered in cancer cells. However, since the physiology of normal cells involves the same signaling pathways that are disturbed in cancer cells, targeted therapies have to deal with side effects and multidrug resistance, the main causes of therapy failure. Since the pioneering work of Otto Warburg, over 80 years ago, the subversion of normal metabolism displayed by cancer cells has been highlighted by many studies. Recently, the study of tumor metabolism has received much attention because metabolic transformation is a crucial cancer hallmark and a direct consequence of disturbances in the activities of oncogenes and tumor suppressors. in this review we discuss tumor metabolism from the molecular perspective of oncogenes, tumor suppressors and protein signaling pathways relevant to metabolic transformation and tumorigenesis. We also identify the principal unanswered questions surrounding this issue and the attempts to relate these to their potential for future cancer treatment. As will be made clear, tumor metabolism is still only partly understood and the metabolic aspects of transformation constitute a major challenge for science. Nevertheless, cancer metabolism can be exploited to devise novel avenues for the rational treatment of this disease. Copyright (C) 2011 S. Karger AG, BaselFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Univ Fed ABC UFABC, CCNH, Santo Andre, BrazilUniversidade Federal de São Paulo UNIFESP, Dept Ciencias Biol, São Paulo, BrazilUniversidade Federal de São Paulo UNIFESP, Dept Bioquim, São Paulo, BrazilUniv Fed Sao Carlos UFSCar, DFQM, Sorocaba, BrazilUniversidade Federal de São Paulo UNIFESP, Dept Ciencias Biol, São Paulo, BrazilUniversidade Federal de São Paulo UNIFESP, Dept Bioquim, São Paulo, BrazilFAPESP: 10/16050-9FAPESP: 10/11475-1FAPESP: 08/51116-0Web of Scienc

Improvement of attention span and reaction time with hyperbaric oxygen treatment in patients with toxic injury due to mold exposure

It is, by now, well established that mold toxins (mycotoxins) can cause significant adverse health effects. In this study, 15 subjects who developed an attention deficit disorder (ADD) and slowing of reaction time at the time of exposure to mold toxins were identified. Deficits in attention span and reaction time were documented not only by taking a careful history, but also by performing a Test of Variables of Attention (TOVA). The TOVA test provides an objective measure of these two variables. It was found that mold-exposed subjects show statistically significant decreases in attention span and significant increases in reaction time to stimuli compared to controls. After ten sessions of hyperbaric oxygen treatment (HBOT), a statistically significant improvement was seen in both measures. This preliminary study suggests promising outcomes in treating mold-exposed patients with hyperbaric oxygen

Identification of ORC1/CDC6-Interacting Factors in Trypanosoma brucei Reveals Critical Features of Origin Recognition Complex Architecture

DNA Replication initiates by formation of a pre-replication complex on sequences termed origins. In eukaryotes, the pre-replication complex is composed of the Origin Recognition Complex (ORC), Cdc6 and the MCM replicative helicase in conjunction with Cdt1. Eukaryotic ORC is considered to be composed of six subunits, named Orc1–6, and monomeric Cdc6 is closely related in sequence to Orc1. However, ORC has been little explored in protists, and only a single ORC protein, related to both Orc1 and Cdc6, has been shown to act in DNA replication in Trypanosoma brucei. Here we identify three highly diverged putative T. brucei ORC components that interact with ORC1/CDC6 and contribute to cell division. Two of these factors are so diverged that we cannot determine if they are eukaryotic ORC subunit orthologues, or are parasite-specific replication factors. The other we show to be a highly diverged Orc4 orthologue, demonstrating that this is one of the most widely conserved ORC subunits in protists and revealing it to be a key element of eukaryotic ORC architecture. Additionally, we have examined interactions amongst the T. brucei MCM subunits and show that this has the conventional eukaryotic heterohexameric structure, suggesting that divergence in the T. brucei replication machinery is limited to the earliest steps in origin licensing

SPARC 2017 retrospect & prospects : Salford postgraduate annual research conference book of abstracts

Welcome to the Book of Abstracts for the 2017 SPARC conference. This year we not only celebrate the work of our PGRs but also the 50th anniversary of Salford as a University, which makes this year’s conference extra special. Once again we have received a tremendous contribution from our postgraduate research community; with over 130 presenters, the conference truly showcases a vibrant PGR community at Salford. These abstracts provide a taster of the research strengths of their works, and provide delegates with a reference point for networking and initiating critical debate. With such wide-ranging topics being showcased, we encourage you to exploit this great opportunity to engage with researchers working in different subject areas to your own. To meet global challenges, high impact research inevitably requires interdisciplinary collaboration. This is recognised by all major research funders. Therefore engaging with the work of others and forging collaborations across subject areas is an essential skill for the next generation of researchers

Global, regional, and national prevalence and mortality burden of sickle cell disease, 2000-2021: a systematic analysis from the Global Burden of Disease Study 2021

BACKGROUND: Previous global analyses, with known underdiagnosis and single cause per death attribution systems, provide only a small insight into the suspected high population health effect of sickle cell disease. Completed as part of the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2021, this study delivers a comprehensive global assessment of prevalence of sickle cell disease and mortality burden by age and sex for 204 countries and territories from 2000 to 2021. METHODS: We estimated cause-specific sickle cell disease mortality using standardised GBD approaches, in which each death is assigned to a single underlying cause, to estimate mortality rates from the International Classification of Diseases (ICD)-coded vital registration, surveillance, and verbal autopsy data. In parallel, our goal was to estimate a more accurate account of sickle cell disease health burden using four types of epidemiological data on sickle cell disease: birth incidence, age-specific prevalence, with-condition mortality (total deaths), and excess mortality (excess deaths). Systematic reviews, supplemented with ICD-coded hospital discharge and insurance claims data, informed this modelling approach. We employed DisMod-MR 2.1 to triangulate between these measures-borrowing strength from predictive covariates and across age, time, and geography-and generated internally consistent estimates of incidence, prevalence, and mortality for three distinct genotypes of sickle cell disease: homozygous sickle cell disease and severe sickle cell β-thalassaemia, sickle-haemoglobin C disease, and mild sickle cell β-thalassaemia. Summing the three models yielded final estimates of incidence at birth, prevalence by age and sex, and total sickle cell disease mortality, the latter of which was compared directly against cause-specific mortality estimates to evaluate differences in mortality burden assessment and implications for the Sustainable Development Goals (SDGs). FINDINGS: Between 2000 and 2021, national incidence rates of sickle cell disease were relatively stable, but total births of babies with sickle cell disease increased globally by 13·7% (95% uncertainty interval 11·1-16·5), to 515 000 (425 000-614 000), primarily due to population growth in the Caribbean and western and central sub-Saharan Africa. The number of people living with sickle cell disease globally increased by 41·4% (38·3-44·9), from 5·46 million (4·62-6·45) in 2000 to 7·74 million (6·51-9·2) in 2021. We estimated 34 400 (25 000-45 200) cause-specific all-age deaths globally in 2021, but total sickle cell disease mortality burden was nearly 11-times higher at 376 000 (303 000-467 000). In children younger than 5 years, there were 81 100 (58 800-108 000) deaths, ranking total sickle cell disease mortality as 12th (compared to 40th for cause-specific sickle cell disease mortality) across all causes estimated by the GBD in 2021. INTERPRETATION: Our findings show a strikingly high contribution of sickle cell disease to all-cause mortality that is not apparent when each death is assigned to only a single cause. Sickle cell disease mortality burden is highest in children, especially in countries with the greatest under-5 mortality rates. Without comprehensive strategies to address morbidity and mortality associated with sickle cell disease, attainment of SDG 3.1, 3.2, and 3.4 is uncertain. Widespread data gaps and correspondingly high uncertainty in the estimates highlight the urgent need for routine and sustained surveillance efforts, further research to assess the contribution of conditions associated with sickle cell disease, and widespread deployment of evidence-based prevention and treatment for those with sickle cell disease. FUNDING: Bill & Melinda Gates Foundation