| 1. |
- Li, T, et al.
(författare)
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Systemic hypothermia induced within 10 hours after birth improved neurological outcome in newborns with hypoxic-ischemic encephalopathy
- 2009
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Ingår i: Hospital Practice. - : Informa UK Limited. - 0018-5809 .- 2154-8331 .- 2377-1003. ; 37:1, s. 1-6
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Tidskriftsartikel (refereegranskat)abstract
- Objective: To evaluate the efficacy of systemic hypothermia when applied within 10 hours after birth to neonates with hypoxic-ischemic encephalopathy (HIE). Study Design: Ninety-three term infants with moderate-to-severe HIE were randomly assigned to either systemic hypothermia (n = 46) or conventional treatment (n = 47). Hypothermia was induced within 10 hours after birth, decreasing rectal temperature to 33.5°C for 72 hours, followed by slow rewarming to 36.5°C. Neurodevelopmental outcome was assessed at 18 months old. The primary outcome was death or moderate-to-severe disability. Results: Outcome data were available for 82 infants. Death or moderate-to-severe disability occurred in 21 of 44 infants (47.7%) in the control group and in 7 of 38 infants (18.4%) in the hypothermia group (P = 0.01) at 18 months. The primary outcome was not different whether hypothermia was started within 6 hours or 6 to 10 hours after birth. Subgroup analysis suggested that systemic hypothermia improved long-term outcome only in infants with moderate HIE (P = 0.009), but not in those with severe HIE. No severe hypothermia-related adverse events were observed. Conclusion: Systemic hypothermia reduced the risk of disability in infants with moderate HIE, in accordance with earlier studies. Hypothermia was induced within 6 hours in most infants, but delaying the onset to 6 to 10 hours after birth did not negatively affect primary outcome. Further studies with a large number of patients are needed to confirm that delayed cooling is equally effective.
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| 2. |
- Cheng, Q, et al.
(författare)
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Clinical features of patients with multiple sclerosis from a survey in Shanghai, China
- 2008
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Ingår i: Multiple sclerosis (Houndmills, Basingstoke, England). - : SAGE Publications. - 1352-4585 .- 1477-0970. ; 14:5, s. 671-678
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Tidskriftsartikel (refereegranskat)abstract
- Objective To describe clinical features of patients with multiple sclerosis (MS) in Shanghai, China. Methods Prevalent patients with MS were identified and investigated by a network of physicians in 11 districts of Shanghai during the period from 1 September 2004 to 31 August 2005. Admission registries of each hospital in the study area were checked systematically for patients with a diagnosis of MS, neuromyelitis optica or other demyelinating disorders. All patients with collected information were evaluated by four senior neurologists according to the McDonald criteria. Results There were 249 (146 female and 103 male) patients with a confirmed MS diagnosis, at a female-to-male ratio of 1.4. The mean age at onset of MS was 37.4 years for the 249 patients with MS and, on the prevalence day, 42.7 years. The most frequent location of clinical MS lesions in the central nervous system was the spinal cord (61%), followed by the cerebrum (55%) and optic nerves (41%). Nearly all (96%) of the patients with MS had been examined by magnetic resonance imaging, and 226 (94%) patients of those examined were suggestive of MS. No family history of MS was found in any of the patients. Most (86%) of the patients had no or mild disability on the prevalence day (31 December 2004). Almost all (96%) patients with MS had been treated with corticosteroids. Conclusion Clinical features of patients with MS are described based on the information from the largest case series reported among Chinese. Comparisons and discussions are made with findings from the other populations.
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| 3. |
- Dong, X.-P., et al.
(författare)
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The type IV mucolipidosis-associated protein TRPML1 is an endolysosomal iron release channel
- 2008
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Ingår i: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 455:7215, s. 992-996
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Tidskriftsartikel (refereegranskat)abstract
- TRPML1 (mucolipin 1, also known as MCOLN1) is predicted to be an intracellular late endosomal and lysosomal ion channel protein that belongs to the mucolipin subfamily of transient receptor potential (TRP) proteins. Mutations in the human TRPML1 gene cause mucolipidosis type IV disease (ML4). ML4 patients have motor impairment, mental retardation, retinal degeneration and iron-deficiency anaemia. Because aberrant iron metabolism may cause neural and retinal degeneration, it may be a primary cause of ML4 phenotypes. In most mammalian cells, release of iron from endosomes and lysosomes after iron uptake by endocytosis of Fe3+-bound transferrin receptors, or after lysosomal degradation of ferritin-iron complexes and autophagic ingestion of iron-containing macromolecules, is the chief source of cellular iron. The divalent metal transporter protein DMT1 (also known as SLC11A2) is the only endosomal Fe2+ transporter known at present and it is highly expressed in erythroid precursors. Genetic studies, however, suggest the existence of a DMT1-independent endosomal and lysosomal Fe2+ transport protein. By measuring radiolabelled iron uptake, by monitoring the levels of cytosolic and intralysosomal iron and by directly patch-clamping the late endosomal and lysosomal membrane, here we show that TRPML1 functions as a Fe2+ permeable channel in late endosomes and lysosomes. ML4 mutations are shown to impair the ability of TRPML1 to permeate Fe2+ at varying degrees, which correlate well with the disease severity. A comparison of TRPML1-/-ML4 and control human skin fibroblasts showed a reduction in cytosolic Fe2+ levels, an increase in intralysosomal Fe 2+ levels and an accumulation of lipofuscin-like molecules in TRPML1-/- cells. We propose that TRPML1 mediates a mechanism by which Fe2+ is released from late endosomes and lysosomes. Our results indicate that impaired iron transport may contribute to both haematological and degenerative symptoms of ML4 patients. ©2008 Macmillan Publishers Limited. All rights reserved.
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| 5. |
- Das, Indra J., et al.
(författare)
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Accelerator beam data commissioning equipment and procedures : report of the TG-106 of the Therapy Physics Committee of the AAPM
- 2008
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Ingår i: Medical physics (Lancaster). - : Wiley. - 0094-2405. ; 35:9, s. 4186-4215
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Forskningsöversikt (refereegranskat)abstract
- For commissioning a linear accelerator for clinical use, medical physicists are faced with many challenges including the need for precision, a variety of testing methods, data validation, the lack of standards, and time constraints. Since commissioning beam data are treated as a reference and ultimately used by treatment planning systems, it is vitally important that the collected data are of the highest quality to avoid dosimetric and patient treatment errors that may subsequently lead to a poor radiation outcome. Beam data commissioning should be performed with appropriate knowledge and proper tools and should be independent of the person collecting the data. To achieve this goal, Task Group 106 (TG-106) of the Therapy Physics Committee of the American Association of Physicists in Medicine was formed to review the practical aspects as well as the physics of linear accelerator commissioning. The report provides guidelines and recommendations on the proper selection of phantoms and detectors, setting up of a phantom for data acquisition (both scanning and no-scanning data), procedures for acquiring specific photon and electron beam parameters and methods to reduce measurement errors (<1%), beam data processing and detector size convolution for accurate profiles. The TG-106 also provides a brief.discussion on the emerging trend in Monte Carlo simulation techniques in photon and electron beam commissioning. The procedures described in this report should assist a qualified medical physicist in either measuring a complete set of beam data, or in verifying a subset of data before initial use or for periodic quality assurance measurements. By combining practical experience with theoretical discussion, this document sets a new standard for beam data commissioning.
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| 7. |
- Fan, Yi, et al.
(författare)
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A study of fluid coolant with carbon nanotube suspension for MicroChannel coolers
- 2008
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Ingår i: 2008 International Conference on Electronic Packaging Technology and High Density Packaging, ICEPT-HDP 2008; Pudong, Shanghai; China; 28 July 2008 through 31 July 2008. - 9781424427406
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Konferensbidrag (refereegranskat)abstract
- In this work, silicon microchannel coolers were made using the Deep Ion Reactive Etching (DIRE) technique. Stable and homogeneous Carbon NanoTube (CNT) suspension was also prepared. Meanwhile, a closed-loop cooling test system was developed to investigate the heat removal of the silicon microchannel cooler with different coolants. The experimental setup included a test module, a minipump for providing controllable flow, and a fan system for cooling the circular fluid. Beside the inlet and outlet of the test module, two thermocouples and pressure gauges were set up to measure the temperature and pressure of the fluids. The heat removal of the silicon microchannel cooler using different CNT volume fraction of suspension coolant was studied. The results show that the microchannel cooler with CNT suspension as coolant could strengthen the heat removal capability of microchannel cooler. In addition to heat transfer enhancement, the microchannel cooler with CNT suspension coolant did not produce extra pressure drop in the present study.
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| 8. |
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| 9. |
- Franzen, L., et al.
(författare)
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Letter to the editor (multiple letter)
- 2005
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Ingår i: Clinical Transplantation. - : Wiley. - 0902-0063 .- 1399-0012. ; 19:4, s. 571-
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 15. |
- Zhou, Qi, et al.
(författare)
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Homogeneous hydroxyethylation of cellulose in NaOH/urea aqueous solution
- 2005
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Ingår i: Polymer Bulletin. - : Springer Science and Business Media LLC. - 0170-0839 .- 1436-2449. ; 53:4, s. 243-248
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Tidskriftsartikel (refereegranskat)abstract
- The 6 wt.% NaOH/4 wt.% urea aqueous solution was proved to be an aqueous nonderivatizing solvent for cellulose by C-13 NMR. O-(2-hydroxyethyl) cellulose (HEC) was prepared by a totally homogeneous hydroxyethylation of cellulose using this new solvent for the first time, and the distribution of substituents within anhydroglucose units (AGU) was examined by C-13 NMR. It was found that the relative reactivity of the hydroxyl groups within AGU and the new hydroxyl group was in the order C-x > C-6 > C-2 > C-3, an analogous functionalization pattern as HEC obtained by the heterogeneous slurry process. The ethylene oxide efficiency in this homogeneous etherification reaction was 20 - 30%.
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| 16. |
- Zhu, Changlian, 1964, et al.
(författare)
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Intraischemic mild hypothermia prevents neuronal cell death and tissue loss after neonatal cerebral hypoxia-ischemia
- 2006
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Ingår i: Eur J Neurosci. ; 23:2, s. 387-93
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Tidskriftsartikel (refereegranskat)abstract
- The effectiveness of hypothermia in preventing ischemic brain damage depends on when it is started. The purpose of this study was to investigate the effects of temperature reduction during a hypoxic-ischemic (HI) insult on brain injury and signalling pathways of neuronal cell death and survival. Seven-day-old mice were subjected to left common carotid artery ligation and hypoxia (10% oxygen) at different temperatures (37, 36 or 34 degrees C) for 50 min. Brain injury at 7 days post-HI was significantly reduced from 67.4% at 37 degrees C to 31.6% at 36 degrees C and 10% at 34 degrees C, with no observable injury in the cortex of the 34 degrees C group. Cytochrome c release, caspase-3 activation and apoptosis-inducing factor translocation from mitochondria to nuclei were all significantly inhibited after intraischemic temperature reduction. Concurrently, the cell survival signalling pathway involving Akt was significantly sustained (the phosphorylated form of Akt was maintained) when the hypoxia temperature was decreased. These results indicate that intraischemic hypothermia diminished apoptosis through inhibition of both caspase-dependent and caspase-independent neuronal cell death pathways and promoted cell survival by inhibition of phosphorylated Akt dephosphorylation in the neonatal brain, thereby preventing neuronal cell death.
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