14 research outputs found
Optimizing project efficiency: impact of cloud computing solution in modern construction project management
No full textThe study is intended to determine the effect of introducing cloud computing platforms on the efficiency of current construction project management. Working with construction engineers and using SPSS statistics, this study gets the desired results of better interactions, collaboration in work, a scalability, flexibility, workflow optimization, and payroll cuts. The fact that cloud technology allows for faster sharing of data, improved resource allocation, and streamlined implementation of projects helps in the project execution and with reduced costs. The data we collected support the Thought Acceptance Model (TAM), the core of which lies in both perceived usefulness and ease of usage. Even though the limitations of the small sample size and the regional perspective were identified, this study recommends the future of research needs to go wider encompassing the cloud computing family of technologies and compare it with emerging technologies as well. The study ends by providing suggestions to industrial players so that they integrate cloud solutions to get better from the projects they conduct
White paper on high-throughput process development for integrated continuous biomanufacturing
No full textContinuous manufacturing is an indicator of a maturing industry, as can be seen by the example of the petrochemical industry. Patent expiry promotes a price competition between manufacturing companies, and more efficient and cheaper processes are needed to achieve lower production costs. Over the last decade, continuous biomanufacturing has had significant breakthroughs, with regulatory agencies encouraging the industry to implement this processing mode. Process development is resource and time consuming and, although it is increasingly becoming less expensive and faster through high-throughput process development (HTPD) implementation, reliable HTPD technology for integrated and continuous biomanufacturing is still lacking and is considered to be an emerging field. Therefore, this paper aims to illustrate the major gaps in HTPD and to discuss the major needs and possible solutions to achieve an end-to-end Integrated Continuous Biomanufacturing, as discussed in the context of the 2019 Integrated Continuous Biomanufacturing conference. The current HTPD state-of-the-art for several unit operations is discussed, as well as the emerging technologies which will expedite a shift to continuous biomanufacturing.BT/Bioprocess Engineerin
Author Correction: Oncolytic DNX-2401 virotherapy plus pembrolizumab in recurrent glioblastoma: a phase 1/2 trial.
No full textAuthor Correction: Oncolytic DNX-2401 virotherapy plus pembrolizumab in recurrent glioblastoma: a phase 1/2 trial
No full textCorrection to: Oncolytic DNX-2401 virotherapy plus pembrolizumab in recurrent glioblastoma: a phase 1/2 tria
Copy Number Variation and Haplotype Analysis of 17q21.31 Reveals Increased Risk Associated with Progressive Supranuclear Palsy and Gene Expression Changes in Neuronal Cells
No full textBackground: The 17q21.31 region with various structural forms characterized by the H1/H2 haplotypes and three large copy number variations (CNVs) represents the strongest risk locus in progressive supranuclear palsy (PSP)
Objective:To investigate the association between CNVs and structural forms on 17q.21.31 with the risk of PSP.
Methods: Utilizing whole genome sequencing data from 1684 PSP cases and 2392 controls, the three large CNVs (α, β, and γ) and structural forms within 17q21.31 were identified and analyzed for their association with PSP.
Results: We found that the copy number of γ was associated with increased PSP risk (odds ratio [OR] = 1.10, P = 0.0018). From H1β1γ1 (OR = 1.21) and H1β2γ1 (OR = 1.24) to H1β1γ4 (OR = 1.57), structural forms of H1 with additional copies of γ displayed a higher risk for PSP. The frequency of the risk sub-haplotype H1c rises from 1% in individuals with two γ copies to 88% in those with eight copies. Additionally, γ duplication up-regulates expression of ARL17B, LRRC37A/LRRC37A2, and NSFP1, while down-regulating KANSL1. Single-nucleus RNA-seq of the dorsolateral prefrontal cortex analysis reveals γ duplication primarily up-regulates LRRC37A/LRRC37A2 in neuronal cells.
Conclusions: The copy number of γ is associated with the risk of PSP after adjusting for H1/H2, indicating that the complex structure at 17q21.31 is an important consideration when evaluating the genetic risk of PSP. © 2025 The Author(s). Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society
Copy Number Variation and Haplotype Analysis of 17q21.31 Reveals Increased Risk Associated with Progressive Supranuclear Palsy and Gene Expression Changes in Neuronal Cells
No full textBackground:
The 17q21.31 region with various structural forms characterized by the H1/H2 haplotypes and three large copy number variations (CNVs) represents the strongest risk locus in progressive supranuclear palsy (PSP).
//
Objective:
To investigate the association between CNVs and structural forms on 17q.21.31 with the risk of PSP.
//
Methods:
Utilizing whole genome sequencing data from 1684 PSP cases and 2392 controls, the three large CNVs (α, β, and γ) and structural forms within 17q21.31 were identified and analyzed for their association with PSP.
//
Results:
We found that the copy number of γ was associated with increased PSP risk (odds ratio [OR] = 1.10, P = 0.0018). From H1β1γ1 (OR = 1.21) and H1β2γ1 (OR = 1.24) to H1β1γ4 (OR = 1.57), structural forms of H1 with additional copies of γ displayed a higher risk for PSP. The frequency of the risk sub-haplotype H1c rises from 1% in individuals with two γ copies to 88% in those with eight copies. Additionally, γ duplication up-regulates expression of ARL17B, LRRC37A/LRRC37A2, and NSFP1, while down-regulating KANSL1. Single-nucleus RNA-seq of the dorsolateral prefrontal cortex analysis reveals γ duplication primarily up-regulates LRRC37A/LRRC37A2 in neuronal cells.
//
Conclusions:
The copy number of γ is associated with the risk of PSP after adjusting for H1/H2, indicating that the complex structure at 17q21.31 is an important consideration when evaluating the genetic risk of PSP. © 2025 The Author(s). Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society
Copy number variation and haplotype analysis of 17q21.31 reveals increased risk associated with progressive supranuclear palsy and gene expression changes in neuronal cells
No full textAbstract: Background: The 17q21.31 region with various structural forms characterized by the H1/H2 haplotypes and three large copy number variations (CNVs) represents the strongest risk locus in progressive supranuclear palsy (PSP). Objective: To investigate the association between CNVs and structural forms on 17q.21.31 with the risk of PSP. Methods Utilizing whole genome sequencing data from 1684 PSP cases and 2392 controls, the three large CNVs (alpha, beta, and gamma) and structural forms within 17q21.31 were identified and analyzed for their association with PSP. Results: We found that the copy number of gamma was associated with increased PSP risk (odds ratio [OR] = 1.10, P = 0.0018). From H1 beta 1 gamma 1 (OR = 1.21) and H1 beta 2 gamma 1 (OR = 1.24) to H1 beta 1 gamma 4 (OR = 1.57), structural forms of H1 with additional copies of gamma displayed a higher risk for PSP. The frequency of the risk sub-haplotype H1c rises from 1% in individuals with two gamma copies to 88% in those with eight copies. Additionally, gamma duplication up-regulates expression of ARL17B, LRRC37A/LRRC37A2, and NSFP1, while down-regulating KANSL1. Single-nucleus RNA-seq of the dorsolateral prefrontal cortex analysis reveals gamma duplication primarily up-regulates LRRC37A/LRRC37A2 in neuronal cells. Conclusions: The copy number of gamma is associated with the risk of PSP after adjusting for H1/H2, indicating that the complex structure at 17q21.31 is an important consideration when evaluating the genetic risk of PSP. (c) 2025 The Author(s). Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society
Erratum: Global, regional, and national comparative risk assessment of 84 behavioural, environmental and occupational, and metabolic risks or clusters of risks for 195 countries and territories, 1990–2017: a systematic analysis for the Global Burden of Disease Study 2017
No full textInterpretation: By quantifying levels and trends in exposures to risk factors and the resulting disease burden, this assessment offers insight into where past policy and programme efforts might have been successful and highlights current priorities for public health action. Decreases in behavioural, environmental, and occupational risks have largely offset the effects of population growth and ageing, in relation to trends in absolute burden. Conversely, the combination of increasing metabolic risks and population ageing will probably continue to drive the increasing trends in non-communicable diseases at the global level, which presents both a public health challenge and opportunity. We see considerable spatiotemporal heterogeneity in levels of risk exposure and risk-attributable burden. Although levels of development underlie some of this heterogeneity, O/E ratios show risks for which countries are overperforming or underperforming relative to their level of development. As such, these ratios provide a benchmarking tool to help to focus local decision making. Our findings reinforce the importance of both risk exposure monitoring and epidemiological research to assess causal connections between risks and health outcomes, and they highlight the usefulness of the GBD study in synthesising data to draw comprehensive and robust conclusions that help to inform good policy and strategic health planning.Stanaway, Jeffrey D-2520fbe1e553ab7130a3e14d339cc29e-0Afshin, Ashkan-4062fbc2d605ce12060facaec6d95b23-0Gakidou, Emmanuela-f92c7e1014d29cebdcab875927db3eac-0Lim, Stephen S-2dfacd56ccc922d1b607c443c3aed8b3-0Abate, Degu-4c9c9907f2717c0bf18a360b4adc23fa-0Abate, Kalkidan Hassen-c29aa366a14f60e18d131235548e6764-0Abbafati, Cristiana-f12d1252183d734ef769098209e59c75-0Abbasi, Nooshin-fe10e2a9e12733c5a369e08cac0cc626-0Abbastabar, Hedayat-db4b6e4e6a8f2f22ec5b2ef0001c80f7-0Abd-Allah, Foad-315bbcdbb313ea1850a4c83707cf22e4-0Abdela, Jemal-ea18b0db074176a0a8843cf7b6f4b574-0Abdelalim, Ahmed-729ff719b4f2e616be01aca670300fc6-0Abdollahpour, Ibrahim-01b160c436c07eb954f4720675e6bd23-0Abdulkader, Rizwan Suliankatchi-82f3def17146f3217d67e5d420a09d2f-0Abebe, Molla-f069369cc88f0ff20184f65022e52404-0Abebe, Zegeye-dc8063f4c2383f9646ee0c6014901e04-0Abera, Semaw Ferede-28fd674f722c27f0a3d66100a57fce74-0Abil, Olifan Zewdie-62e69e9e8589dc80140e0c9c76b2a743-0Abraha, Haftom Niguse-6f45c1da5e4fdda97c3adc3da2d477a6-0Roba, Aklilu Abrham-f97be0b52463568f84c9fa9affff2463-0Abu Raddad, Laith J-87179b55a3abe08d15357d22d77b0c9f-0Abun Rmeileh, Niveen M.E-e394ad81f593042412c8643ab8a7a4f9-0Accrombessi, Manfred Mario Kokou-1b088b3416d0f6ec3a7e9c864680942d-0Acharya, Dilaram-240b7a14aa142c99753566d79c7f3b22-0Acharya, Pawan-01cb4a54739afb677b91e0c05c7bface-0Adamu, Abdu Abdullahi-e39e3857e02d33a997368b54498ac2c0-0Adane, Akilew Awoke-15c0422bbf6693d459926fee9fc4d9c1-0Adebayo, Oladimeji-4c0a9d75950ff513bd301db5f932d7d9-0Adedoyin, Rufus Adesoji-84fc0bb933bb9ff247cda9f35406ff61-0Adekanmbi, Victor T-e61819d7aa2c70a57ded8f98f24e51c4-0Ademi, Zanfina-244384081418339dd051b719eea79eb7-0Adetokunboh, Olatunji O-adc3c1a0fbe4e0fcc186e9c39f20aab6-0Adib, Mina G-5e2e4a2b955c99a7148bf2835df4da1e-0Admasie, Amha-3886ac12611046939e2700837619b6cb-0Adsuar, Jose C-baf85df62abf1a7c7551a6af0dc965f5-0Afanvi, Kossivi Agbélénko-8ab9da633de1822d6740ff2bd12e2e8a-0Afarideh, Mohsen-16092959beee378428077dd5e6d04832-0Agarwal, Gina-264b1b6b950696d5c41cdcd383a30c3e-0Aggarwal, Anju-f8be93a84e70ebfb86441e91f9451992-0Aghayan, Sargis A-58cc18e7d481a0d431f2a3c93ee71b4e-0Agrawal, Anurag-509f342b1575b999d5ec6bd3f612df26-0Agrawal, Sutapa-f12c5d24e93e2c07c6321cb7dce96069-0Ahmadi, Alireza-219a6a30c7460d2b398c05ca35d5a1e1-0Ahmadi Moghadam, M-094a65b0c8189b7125eca1b8f5afae2e-0Ahmadieh, Hamid-6f9d23d4531563d07e9d3039d16294bc-0Ahmed, Muktar Beshir-827a98e28bbeb4ad75edaadbc87a6956-0Aichour, Amani Nidhal-84ac126cb31640764728380f61311b50-0Aichour, Ibtihel-984dfc4e36d078e7665d8d90220e472f-0Aichour, Miloud Taki Eddine-8ea68860413c6b03f5c2f7f808fc3e59-0Akbari, Mohammad Esmaeil-f41dc784812f38441d1a970abcd1e76f-0Akinyemiju, Tomi F.-aa496f0e0203c38d494058c117171fd1-0Akseer, Nadia-a208855455ad6ca542b60f1c9d6f0076-0Al Aly, Ziyad-5727374838f3b814fee2209100046f1f-0Al Eyadhy, Ayman A-4e6eed03ca8f2b345b91a02928d77d95-0Al Mekhlafi, H. 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Dedicated anticoagulation management protocols in fragility femoral fracture care – a source of significant variance and limited effectiveness in improving time to surgery: The hip and femoral fracture anticoagulation surgical timing evaluation (HASTE) study
No full text\ua9 2024 The Author(s)Introduction: Approximately 20 % of femoral fragility fracture patients take anticoagulants, typically warfarin or Direct Oral AntiCoagulant (DOAC). These can impact timing of surgery affecting patient survival. Due to several possible approaches and numerous factors to consider in the preoperative workup of anticoagulated patients, potential for variations in clinical practice exist. Some hospitals employ dedicated anticoagulation management protocols to address this issue, and to improve time to surgery. This study aimed to determine the proportion of hospitals with such protocols, compare protocol guidance between hospitals, and evaluate the effectiveness of protocols in facilitating prompt surgery. Methods: Data was prospectively collected through a collaborative, multicentre approach involving hospitals across the UK. Femoral fragility fracture patients aged ≥60 years and admitted to hospital between 1st May to 31st July 2023 were included. Information from dedicated anticoagulation management protocols were collated on several domains relating to perioperative care including administration of reversal agents and instructions on timing of surgery as well as others. Logistic regression was used to evaluate effects of dedicated protocols on time to surgery. Results: Dedicated protocols for management of patients taking warfarin and DOACs were present at 41 (52.6 %) and 43 (55.1 %) hospitals respectively. For patients taking warfarin, 39/41 (95.1 %) protocols specified the dose of vitamin k and the most common was 5 milligrams intravenously (n=21). INR threshold values for proceeding to surgery varied between protocols; 1.5 (n=28), 1.8 (n=6), and 2 (n=6). For patients taking DOACs, 35/43 (81.4 %) and 8/43 (18.6 %) protocols advised timing of surgery based on renal function and absolute time from last dose respectively. Analysis of 10,197 patients from 78 hospitals showed fewer patients taking DOACs received surgery within 36 h of admission at hospitals with a dedicated protocol compared to those without (adjusted OR 0.73, 95% CI 0.54–0.99, p=0.040), while there were no differences among patients taking warfarin (adjusted OR 1.64, 95% CI 0.75–3.57, p=0.219). Conclusions: Around half of hospitals employed a dedicated anticoagulation management protocol for femoral fragility fracture patients, and substantial variation was observed in guidance between protocols. Dedicated protocols currently being used at hospitals were ineffective at improving the defined targets for time to surgery
The use of mobile phones and the risk of brain tumors among children and adolescents
No full textMobile phones experienced a steep rise in popularity among children and adolescents during the last decade. The increase in popularity has been reflected in both increased ownership and increased usage of mobile phones. Most children start to use mobile phones when they are around 9–10 years old, but usage before school age is not uncommon. The increase in mobile phone use has raised concerns about possible adverse health effects. Brain tumors have been a main concern because the brain absorbs most of the radio frequency energy emitted by mobile phones during calls. In addition, it has been hypothesized that children may be more vulnerable to radio frequency electromagnetic fields (RF-EMFs) because their nervous system is developing, their brain tissue is more conductive than that of adults, and RF-EMFs penetrate in to regions that are deeper in their brains. Radio frequency radiation emitted by mobile phones has insufficient energy to directly damage the DNA and the only known effect of RF-EMFs is heating of the tissue. Studies about mobile phone use and brain tumor risk among adults have shown no increased risk for regular users but have been inconclusive regarding long-term (≥10 years) and heavy mobile phone use. The largest case-control study so far, INTERPHONE, found an increased risk for glioma among heavy users (≥1640 lifetime calls). Another study from a Swedish research group reported a five-fold increased risk for astrocytoma for adults who first used mobile phones before the age of 20. No study has addressed the association between mobile phone use and brain tumor risk among children and adolescents so far. The goal of this thesis was to assess whether there is a relationship between mobile phone use and brain tumor risk among children and adolescents or not. In 2006, we set up CEFALO, an international case-control study about the relationship between mobile phone use and brain tumor risk in children and adolescents aged 7–19 years. CEFALO was performed in Denmark, Sweden, Norway, and Switzerland. The study period ranged from 2004 through 2008. Children and adolescents of age 7–19 years who were diagnosed during the study period with a primary brain tumor were eligible. For each case patient, we selected two healthy controls matched by age, sex and geographical region of residence using population registries. Exposure data was collected by face to face interviews with the study participants accompanied by at least one parent. Risk estimates for brain tumors were calculated for various exposure surrogates. We also examined the gender and age-adjusted brain tumor incidence rates among Swedish children and adolescents aged 5–19 years from 1990 to 2008 including hypothetical incidence rate trends based on the risk estimates found in our analyses. Lastly, we compared the self-reported amount of mobile phone use with objectively recorded data by network operators. Regular users of mobile phones were not statistically significantly more likely to have been diagnosed with brain tumors compared with non-regular users (OR=1.36, 95%-CI: 0.92 to 2.02). No clear exposure-response relationship was observed for any exposure surrogate. Moreover, no exposure-response relationship was seen in terms of localization of the tumor. For the study participants for whom operator-recorded data were available, we found a statistically significantly increased risk among users with more than 2.8 years since the start of the first subscription (OR=2.15). The odds ratio for brain tumor risk among ipsilateral regular users of mobile phones was not higher than the odds ratio of contralateral regular users. The risk estimate of 2.15 after 3 years of regular mobile phone use is incompatible with the stable (or even downward) incidence trends observed among Swedish children and adolescents aged 5–19 years from 1990 to 2008. This indicates that short-term use of mobile phones does not cause brain tumors in children and adolescents. In the validation study, cases overestimated their cumulative number of calls by 9% on average and controls by 34%. Cases also overestimated their cumulative duration of calls by 52% on average and controls by 163%. We found little evidence for differential recall errors. CEFALO is the first study to investigate the relationship between mobile phone use and brain tumor risk in children and adolescents. We found no consistent evidence for a causal association between short-term mobile phone use and brain tumor risk among children and adolescents. The lack of an exposure-response relationship either in terms of the amount of mobile phone use or by localization of the brain tumor argues against a causal relationship. These findings are corroborated by the fact that brain tumor incidence rates among children and adolescents have not increased in many countries in recent times. We cannot, however, exclude the possibility of a small increase in brain tumor risk due to mobile phone use. As we found that self-reported mobile phone use is affected with large random and some systematic recall errors, we emphasize the importance of future studies with objective exposure assessment or the use of prospectively collected exposure data. We also recommend the monitoring of time trends in brain tumor incidence rates as increased risks should be reflected in future brain tumor incidence rate trends
