cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.1282594.v2
title: Effects of fine particles on children’s hospital admissions for respiratory health in Seville, Spain

description: This study analyzes the influence of fine particles PM<sub>2.5</sub> on nonprogrammed children’s hospital admissions that occurred in the city of Seville between 2007 and 2011, and makes an economic assessment of the cost of the children’s hospital admissions for respiratory causes due to particle pollution. The PM<sub>2.5</sub> dose-response functions for each type of hospital admission were used to quantify the cost of the hospital admissions. It can be concluded that the PM<sub>2.5</sub> concentrations have negative effects on bronchiolitis, pneumonia, asthma, and bronchitis and other causes. A reduction of the daily average annual PM<sub>2.5</sub> concentration from the existing levels to 10 µg/m<sup>3</sup> would show an annual average reduction of children’s hospital admissions due to respiratory diseases of 0.09 cases. This paper shows that the daily average cost for children hospital admissions due to respiratory reasons in the city of Seville, associated with daily average annual levels of PM<sub>2.5</sub> above 10 µg/m<sup>3</sup>, was almost 200€.Implications: <i>Elevated PM<sub>2.5</sub> concentrations in Seville have negative effects on children’s bronchiolitis, pneumonia, asthma, and bronchitis and other causes. A reduction of the daily average annual PM<sub>2.5</sub> concentration from the existing levels to 10 μg/m<sup>3</sup> would suppose an annual mean reduction of children’s hospital admissions due to respiratory diseases of 0.09 cases.</i>
DOI: 10.6084/m9.figshare.1283852.v4
title: NATIONAL SUMMARY DATA

description: This file contains summaries of data around circumcision practice and complications in England and Scotland.
DOI: 10.6084/m9.figshare.1283854.v5
title: LONDON CIRCUMCISION REPORTS AND SUMMARIES

description: Folder contains files received from London NHS funders and hospital trusts with data on circumcisions performed and complications treated. Includes data from the large and long running circumcision scheme in Tower Hamlets, contracted to a GP in the area, showing the rate of early complications and later recircumcisions (no data on other surgical follow ups such as for meatal stenosis). 16/290 babies cut in 2009 in this scheme had experienced a complication within 7 days of which 10 visited the GP and 6 went to A&E. Excluding the 2 who went to the GP and did not get treatment this would be a 4.8% complication rate in one week, trouncing the American assertion that infant circumcision complications affect only 2 per thousand and also the NHS Choice claim that circumcision complications are 'rare' (which would also mean &lt;1%). Tower Hamlets advise that 2005-2009 1492 baby boys were cut religiously by the NHS but apparently none got meatal stenosis treatment as a result. With Iranian research showing 20% of boys will suffer undiagnosed severe meatal stenosis post infant cutting (see link) this indicates a poor attitude to the safety of religious circumcision on the NHS. Or maybe it was just an untruth - Tower Hamlets also said no one got meatal stenosis treatment in the borough in 2009 ...which is vanishingly unlikely. They did admit that of the 1492 cut babies (2005-2009) 11 suffered a second circumcision, a rate of just over 0.7%.
DOI: 10.6084/m9.figshare.1283854.v4
title: LONDON CIRCUMCISION REPORTS AND SUMMARIES

description: Folder contains files received from London NHS funders and hospital trusts with data on circumcisions performed and complications treated. Includes data from the large and long running circumcision scheme in Tower Hamlets, contracted to a GP in the area, showing the rate of early complications and later recircumcisions (no data on other surgical follow ups such as for meatal stenosis). 16/290 babies cut in 2009 in this scheme had experienced a complication within 7 days of which 10 visited the GP and 6 went to A&E. Excluding the 2 who went to the GP and did not get treatment this would be a 4.8% complication rate in one week, absolutely trouncing the American medical assertion that infant circumcision complications affect only 2 per thousand and also the NHS Choice suggestion that complications are 'rare' (which would also mean &lt;1%). Tower Hamlets advise that 2005-2009 1492 baby boys were cut religiously by the NHS but apparently none got meatal stenosis treatment as a result. With Iranian research showing 20% will suffer undiagnosed severe meatal stenosis post infant cutting (see bwlo link) this indicates a poor attitude to tracking and tackling circ complications on the NHS. Or maybe it was just an untruth - Tower Hamlets also said no one got meatal stenosis treatment in the borough in 2009 which is vanishingly unlikely. They did admit that of the 1492 cut babies (2005-2009) 11 suffered a second circumcision
DOI: 10.6084/m9.figshare.1283852.v5
title: NATIONAL SUMMARY DATA

description: This file contains summaries of data around circumcision practice and complications in England and Scotland. The A&E datasets are without denominator but there are also datasets from hospitals which have provided full admission details from their own circumcisions (including therapeutic coded and Z412 Ritual/Routine coded) in some cases for up to 90 days. Readmission diagnosis has allowed the weeding out of non relevant readmissions. All this data is important - it reveals that NHS Choices is not telling the truth in saying that complications of male circumcision are 'rare'. My data suggests that even within 30 days you can expect a relevant readmissions rate in children of &gt;4% following circumcision - it can run much higher.The data is from freedom of info requests, mostly generated through queries of hospital/funder databases - it's good quality and it's useful to note it matches findings from more mainstream/commercial sources such as Dr Foster, as well as many published series. The widely varying incidence of therapeutic circumcision indicates there is a real problem with bad practice in this area - admitted verbally by paediatric urologists and in print by urology associations. The complication rates simply underline how important it is that this gets addressed: unnecessary surgery has a financial toll on the NHS as well as a presumed personal toll on the child and their family. A concern of mine is why does the NHS lie about the complication rates on NHS Choices? I was first concerned about this some years ago when making a complaint about their assertion (via Leeds urologist Benjamiin Squires) that child circumcision does not require anaesthetic. This concern was taken seriously and the claim removed - but the question remains in my mind (and I hope will in yours) about whether there is bias being allowed to creep into NHS Choices editorial?
DOI: 10.6084/m9.figshare.1283852.v7
title: NATIONAL SUMMARY DATA

description: This file contains summaries of data around circumcision practice and complications in England and Scotland. The A&E datasets are without denominator but there are also datasets from hospitals which have provided full admission details from their own circumcisions (including therapeutic coded and Z412 Ritual/Routine coded) in some cases for up to 90 days. Readmission diagnosis has allowed the weeding out of non relevant readmissions. All this data is important - it reveals that NHS Choices is not telling the truth in saying that complications of male circumcision are 'rare'. My data suggests that even within 30 days you can expect a relevant readmissions rate in children of &gt;4% following circumcision - it can run much higher.The data is from freedom of info requests, mostly generated through queries of hospital/funder databases - it's good quality and it's useful to note it matches findings from more mainstream/commercial sources such as Dr Foster, as well as many published series. The widely varying incidence of therapeutic circumcision indicates there is a real problem with bad practice in this area - admitted verbally by paediatric urologists and in print by urology associations. The complication rates simply underline how important it is that this gets addressed: unnecessary surgery has a financial toll on the NHS as well as a presumed personal toll on the child and their family. A concern of mine is why does the NHS lie about the complication rates on NHS Choices? I was first concerned about this some years ago when making a complaint about their assertion (via Leeds urologist Benjamiin Squires) that child circumcision does not require anaesthetic. This concern was taken seriously and the claim removed - but the question remains in my mind (and I hope will in yours) about whether there is bias being allowed to creep into NHS Choices editorial? PS my use of the phrase 't or not t coding' on the 2011 dataset on child circumcisions could be misleading. 'T' diagnostic coding would normally refer to a complication of a procedure - here I mean it to stand for 'therapeutic'. Normally the diagnostic coding for a non therapeutic procedure begins with 'Z' and so I should probably have used that terminology. The point remains that there is a significant issue either a/ with non therapeutic genital cutting being hidden (and thus possibly being made fundable) by a false therapeutic diagnosis or b/ wilful ignorance of issues around the normal development of the male body in childhood.
DOI: 10.6084/m9.figshare.1283852.v6
title: NATIONAL SUMMARY DATA

description: This file contains summaries of data around circumcision practice and complications in England and Scotland. The A&E datasets are without denominator but there are also datasets from hospitals which have provided full admission details from their own circumcisions (including therapeutic coded and Z412 Ritual/Routine coded) in some cases for up to 90 days. Readmission diagnosis has allowed the weeding out of non relevant readmissions. All this data is important - it reveals that NHS Choices is not telling the truth in saying that complications of male circumcision are 'rare'. My data suggests that even within 30 days you can expect a relevant readmissions rate in children of &gt;4% following circumcision - it can run much higher.The data is from freedom of info requests, mostly generated through queries of hospital/funder databases - it's good quality and it's useful to note it matches findings from more mainstream/commercial sources such as Dr Foster, as well as many published series. The widely varying incidence of therapeutic circumcision indicates there is a real problem with bad practice in this area - admitted verbally by paediatric urologists and in print by urology associations. The complication rates simply underline how important it is that this gets addressed: unnecessary surgery has a financial toll on the NHS as well as a presumed personal toll on the child and their family. A concern of mine is why does the NHS lie about the complication rates on NHS Choices? I was first concerned about this some years ago when making a complaint about their assertion (via Leeds urologist Benjamiin Squires) that child circumcision does not require anaesthetic. This concern was taken seriously and the claim removed - but the question remains in my mind (and I hope will in yours) about whether there is bias being allowed to creep into NHS Choices editorial?
DOI: 10.6084/m9.figshare.1282587
title: Cell-cycle fate-monitoring distinguishes individual chemosensitive and chemoresistant cancer cells in drug-treated heterogeneous populations demonstrated by real-time FUCCI imaging

description: Essentially every population of cancer cells within a tumor is heterogeneous, especially with regard to chemosensitivity and resistance. In the present study, we utilized the fluorescence ubiquitination-based cell cycle indicator (FUCCI) imaging system to investigate the correlation between cell-cycle behavior and apoptosis after treatment of cancer cells with chemotherapeutic drugs. HeLa cells expressing FUCCI were treated with doxorubicin (DOX) (5 μM) or cisplatinum (CDDP) (5 μM) for 3 h. Cell-cycle progression and apoptosis were monitored by time-lapse FUCCI imaging for 72 h. Time-lapse FUCCI imaging demonstrated that both DOX and CDDP could induce cell cycle arrest in S/G<sub>2</sub>/M in almost all the cells, but a subpopulation of the cells could escape the block and undergo mitosis. The subpopulation which went through mitosis subsequently underwent apoptosis, while the cells arrested in S/G<sub>2</sub>/M survived. The present results demonstrate that chemoresistant cells can be readily identified in a heterogeneous population of cancer cells by S/G<sub>2</sub>/M arrest, which can serve in future studies as a visible target for novel agents that kill cell-cycle-arrested cells.
DOI: 10.6084/m9.figshare.1282588.v1
title: Multiple functions of the SNARE protein Snap29 in autophagy, endocytic, and exocytic trafficking during epithelial formation in <i>Drosophila</i>

description: How autophagic degradation is linked to endosomal trafficking routes is little known. Here we screened a collection of uncharacterized <i>Drosophila</i> mutants affecting membrane transport to identify new genes that also have a role in autophagy. We isolated a loss of function mutant in <i>Snap29</i> (<i>Synaptosomal-associated protein 29 kDa</i>)<i>,</i> the gene encoding the <i>Drosophila</i> homolog of the human protein SNAP29 and have characterized its function <i>in vivo</i>. Snap29 contains 2 soluble NSF attachment protein receptor (SNARE) domains and a asparagine-proline-phenylalanine (NPF motif) at its N terminus and rescue experiments indicate that both SNARE domains are required for function, whereas the NPF motif is in part dispensable. We find that Snap29 interacts with SNARE proteins, localizes to multiple trafficking organelles, and is required for protein trafficking and for proper Golgi apparatus morphology. Developing tissue lacking Snap29 displays distinctive epithelial architecture defects and accumulates large amounts of autophagosomes, highlighting a major role of Snap29 in autophagy and secretion. Mutants for autophagy genes do not display epithelial architecture or secretion defects, suggesting that the these alterations of the <i>Snap29</i> mutant are unlikely to be caused by the impairment of autophagy. In contrast, we find evidence of elevated levels of hop-Stat92E (hopscotch-signal transducer and activator of transcription protein at 92E) ligand, receptor, and associated signaling, which might underlie the epithelial defects. In summary, our findings support a role of Snap29 at key steps of membrane trafficking, and predict that signaling defects may contribute to the pathogenesis of cerebral dysgenesis, neuropathy, ichthyosis, and palmoplantar keratoderma (CEDNIK), a human congenital syndrome due to loss of Snap29.
DOI: 10.6084/m9.figshare.1282589.v1
title: Loss of functional MYO1C/myosin 1c, a motor protein involved in lipid raft trafficking, disrupts autophagosome-lysosome fusion

description: MYO1C, a single-headed class I myosin, associates with cholesterol-enriched lipid rafts and facilitates their recycling from intracellular compartments to the cell surface. Absence of functional MYO1C disturbs the cellular distribution of lipid rafts, causes the accumulation of cholesterol-enriched membranes in the perinuclear recycling compartment, and leads to enlargement of endolysosomal membranes. Several feeder pathways, including classical endocytosis but also the autophagy pathway, maintain the health of the cell by selective degradation of cargo through fusion with the lysosome. Here we show that loss of functional MYO1C leads to an increase in total cellular cholesterol and its disrupted subcellular distribution. We observe an accumulation of autophagic structures caused by a block in fusion with the lysosome and a defect in autophagic cargo degradation. Interestingly, the loss of MYO1C has no effect on degradation of endocytic cargo such as EGFR, illustrating that although the endolysosomal compartment is enlarged in size, it is functional and contains active hydrolases and the correct pH. Our results highlight the importance of correct lipid composition in autophagosomes and lysosomes to enable them to fuse. Ablating MYO1C function causes abnormal cholesterol distribution, which has a major selective impact on the autophagy pathway.
DOI: 10.6084/m9.figshare.1282585
title: Mir-23a and mir-125b regulate neural stem/progenitor cell proliferation by targeting Musashi1

description: Musashi1 is an RNA binding protein that controls the neural cell fate, being involved in maintaining neural progenitors in their proliferative state. In particular, its downregulation is needed for triggering early neural differentiation programs. In this study, we profiled microRNA expression during the transition from neural progenitors to differentiated astrocytes and underscored 2 upregulated microRNAs, miR-23a and miR-125b, that sinergically act to restrain Musashi1 expression, thus creating a regulatory module controlling neural progenitor proliferation.
DOI: 10.6084/m9.figshare.1282588.v2
title: Multiple functions of the SNARE protein Snap29 in autophagy, endocytic, and exocytic trafficking during epithelial formation in <i>Drosophila</i>

description: How autophagic degradation is linked to endosomal trafficking routes is little known. Here we screened a collection of uncharacterized <i>Drosophila</i> mutants affecting membrane transport to identify new genes that also have a role in autophagy. We isolated a loss of function mutant in <i>Snap29</i> (<i>Synaptosomal-associated protein 29 kDa</i>)<i>,</i> the gene encoding the <i>Drosophila</i> homolog of the human protein SNAP29 and have characterized its function <i>in vivo</i>. Snap29 contains 2 soluble NSF attachment protein receptor (SNARE) domains and a asparagine-proline-phenylalanine (NPF motif) at its N terminus and rescue experiments indicate that both SNARE domains are required for function, whereas the NPF motif is in part dispensable. We find that Snap29 interacts with SNARE proteins, localizes to multiple trafficking organelles, and is required for protein trafficking and for proper Golgi apparatus morphology. Developing tissue lacking Snap29 displays distinctive epithelial architecture defects and accumulates large amounts of autophagosomes, highlighting a major role of Snap29 in autophagy and secretion. Mutants for autophagy genes do not display epithelial architecture or secretion defects, suggesting that the these alterations of the <i>Snap29</i> mutant are unlikely to be caused by the impairment of autophagy. In contrast, we find evidence of elevated levels of hop-Stat92E (hopscotch-signal transducer and activator of transcription protein at 92E) ligand, receptor, and associated signaling, which might underlie the epithelial defects. In summary, our findings support a role of Snap29 at key steps of membrane trafficking, and predict that signaling defects may contribute to the pathogenesis of cerebral dysgenesis, neuropathy, ichthyosis, and palmoplantar keratoderma (CEDNIK), a human congenital syndrome due to loss of Snap29.
DOI: 10.6084/m9.figshare.1282587.v1
title: Cell-cycle fate-monitoring distinguishes individual chemosensitive and chemoresistant cancer cells in drug-treated heterogeneous populations demonstrated by real-time fucci imaging

description: Essentially every population of cancer cells or tumor is heterogeneous, especially with regard to chemosensitivity and resistance. In the present study, we utilized the fluorescent ubiquitination-based cell cycle indicator (FUCCI) imaging system to investigate the correlation between cell cycle behavior and apoptosis after treatment of cancer cells with chemotherapeutic drugs. HeLa cells expressing FUCCI were treated with doxorubicin (DOX) (5 μM) or cisplatinum (CDDP) (5 μM) for 3 h. Cell cycle progression and apoptotic changes were monitored by time-lapse FUCCI imaging for 72 h. Time-lapse FUCCI imaging demonstrated that both DOX and CDDP could induce cell cycle arrest in S/G<sub>2</sub>/M in almost all the cells, but a subpopulation of the cells could escape the block and undergo mitosis. The subpopulation which went through mitosis subsequently underwent apoptosis while the cells arrested in S/G<sub>2</sub>/M survived. The present results demonstrate that chemoresistant cells can be readily identified in a heterogeneous population of cancer cells by S/G<sub>2</sub>/M arrest which can serve in future studies as a visible target for novel agents that kill cell-cycle-arrested cells.
DOI: 10.6084/m9.figshare.1282588
title: Multiple functions of the SNARE protein Snap29 in autophagy, endocytic, and exocytic trafficking during epithelial formation in <i>Drosophila</i>

description: How autophagic degradation is linked to endosomal trafficking routes is little known. Here we screened a collection of uncharacterized <i>Drosophila</i> mutants affecting membrane transport to identify new genes that also have a role in autophagy. We isolated a loss of function mutant in <i>Snap29</i> (<i>Synaptosomal-associated protein 29 kDa</i>)<i>,</i> the gene encoding the <i>Drosophila</i> homolog of the human protein SNAP29 and have characterized its function <i>in vivo</i>. Snap29 contains 2 soluble NSF attachment protein receptor (SNARE) domains and a asparagine-proline-phenylalanine (NPF motif) at its N terminus and rescue experiments indicate that both SNARE domains are required for function, whereas the NPF motif is in part dispensable. We find that Snap29 interacts with SNARE proteins, localizes to multiple trafficking organelles, and is required for protein trafficking and for proper Golgi apparatus morphology. Developing tissue lacking Snap29 displays distinctive epithelial architecture defects and accumulates large amounts of autophagosomes, highlighting a major role of Snap29 in autophagy and secretion. Mutants for autophagy genes do not display epithelial architecture or secretion defects, suggesting that the these alterations of the <i>Snap29</i> mutant are unlikely to be caused by the impairment of autophagy. In contrast, we find evidence of elevated levels of hop-Stat92E (hopscotch-signal transducer and activator of transcription protein at 92E) ligand, receptor, and associated signaling, which might underlie the epithelial defects. In summary, our findings support a role of Snap29 at key steps of membrane trafficking, and predict that signaling defects may contribute to the pathogenesis of cerebral dysgenesis, neuropathy, ichthyosis, and palmoplantar keratoderma (CEDNIK), a human congenital syndrome due to loss of Snap29.