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| 2. |
- Ng, B. S., et al.
(författare)
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Characterisation of a duplex TiO2/CaP coating on Ti6Al4V for hard tissue replacement
- 2005
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Ingår i: Biomaterials. - : Elsevier BV. - 0142-9612 .- 1878-5905. ; 26:10, s. 1087-1095
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Tidskriftsartikel (refereegranskat)abstract
- An initial TiO2 coating was applied on Ti6Al4V by electrochemical anodisation in two dissimilar electrolytes. The secondary calcium phosphate (CaP) coating was subsequently applied by immersing the substrates in a simulated body fluid (SBF) with three times concentration (SBF×3), mimicking biomineralisation of biological bone. Electrochemical impedance spectroscopy and potentiodynamic polarisation assessments in SBF revealed that the anodic TiO2 layer is compact, exhibiting up to four-folds improvement in in vitro corrosion resistance over unanodised Ti6Al4V. X-ray photoelectron spectroscopy analysis indicates that the anodic Ti oxide is thicker than air-formed ones with a mixture of TiO2-x compound between the TiO2/Ti interfaces. The morphology of the dense CaP film formed, when observed using scanning electron microscopy, is made up of linked globules 0.1-0.5ÎŒm in diameter without observable delamination. Fourier transform infrared spectrometry with an attenuated total internal reflection analysis revealed that this film is an amorphous/poorly crystallised calcium-deficient-carbonated CaP system. The calculated Ca:P ratios of all samples (1.14-1.28) are lower than stoichiometric hydroxyapatite (1.67). These results show that a duplex coating consisting of (1) a compact TiO2 with enhanced in vitro corrosion resistance and (2) bone-like apatite coating can be applied on Ti6Al4V by anodisation and subsequent immersion in SBF. © 2004 Elsevier Ltd. All rights reserved.
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| 3. |
- Ekström, Ulf, et al.
(författare)
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An individual with a healthy phenotype in spite of a pathogenic LDL receptor mutation (C240F)
- 1999
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Ingår i: Clinical Genetics. - : Wiley. - 0009-9163. ; 55:5, s. 332-339
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Tidskriftsartikel (refereegranskat)abstract
- Familial hypercholesterolemia (FH) is caused by a defect in the function of the low density lipoprotein (LDL) receptor and inherited in an autosomal, codominant way. In this study we present a 13-year-old girl, compound heterozygote for the LDL receptor mutations C240F and Y167X. Fibroblasts from the patient showed very low cholesterol esterification rate, LDL uptake, and degradation compared to normal fibroblasts (< 2%, 8%, and < 2%, respectively). The C240F mutant was expressed in LDL receptor deficient CHOMldlA7 cells. Analysis of cell extracts by immunoblotting demonstrated delayed processing of the mutated LDL receptor, which was accumulated as a precursor protein of normal size. A high molecular weight form of the receptor was also detectable in these cells, which probably reflects cross-linking through the unpaired cysteine residue in the binding domain. Cells expressing the C240F mutant protein were unable to mediate uptake and degradation of LDL. The two siblings of the index case also carried the C240F mutation, but surprisingly one of them (a 17-year-old brother) showed no signs of hypercholesterolemia. This observation is consistent with the view that there may be cholesterol lowering mechanisms that can be activated, perhaps by mutations in known or hitherto unknown genes.
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| 4. |
- Ekström, Ulf, et al.
(författare)
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Expression of an LDL receptor allele with two different mutations (E256K and I402T)
- 2000
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Ingår i: Molecular Pathology. - 1366-8714. ; 53:1, s. 31-36
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Tidskriftsartikel (refereegranskat)abstract
- AIMS: To investigate the disease causing event in patients with familial hypercholesterolaemia, carrying two mutations each, E256K in exon 6 and I402T in exon 9, of the gene encoding the low density lipoprotein (LDL) receptor. It was not known whether the mutations were positioned in cis or trans, or if they were each pathogenic separately or only when present together. METHODS: Polymerase chain reaction, denaturing gradient gel electrophoresis and sequencing were used to characterise the LDL receptor locus of the patients and family members. The different LDL receptor mutants, constructed in vitro by oligonucleotide directed mutagenesis, were expressed in LDL receptor deficient Chinese hamster ovary (CHO1d1A7) cells, to determine the effects of the mutations on LDL receptor function. RESULTS: The two mutations were located on the same allele of the LDL receptor gene. All mutant constructs resulted in the production of a detectable protein in CHO cells. The cells expressing only the I402T mutation, or the combination of I402T and E256K mutations, were seriously affected in mediating uptake and degradation of LDL. Contrary to initial predictions, the cells expressing only the E256K mutation showed essentially the same binding, uptake, and degradation of 125I labelled LDL as cells transfected with normal LDL receptor cDNA. These results suggest that the pathogenic mutation in the patients heterozygous for the E256K/I402T allele is the I402T mutation, and that E256K alone is a rare sequence variation, which does not affect LDL receptor protein function. E256K was not detected either in DNA from a healthy population or in DNA from other hypercholesterolaemic patients studied. CONCLUSIONS: Despite the information available on the structure-function relations between the LDL receptor and LDL receptor like proteins, predictions about the disease causing potential of a mutation are not reliable. These results suggest that the I402T mutation is pathogenic and that the substitution of E256K alone is a rare sequence variation, without a detectable phenotype modulating effect.
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| 5. |
- Rodriguez Lorenzo, Andres, et al.
(författare)
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Anatomy of the motor nerve to the gracilis muscle and its implications in a one-stage microneurovascular gracilis transfer for facial reanimation
- 2010
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Ingår i: Journal of Plastic, Reconstructive & Aesthetic Surgery. - : Elsevier BV. - 1748-6815 .- 1878-0539. ; 63:1, s. 54-58
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND:The present study was conducted to investigate the anatomy of the motor nerve to the gracilis muscle (MNG) to provide the anatomical basis for harvesting a one-stage gracilis transfer with a long nerve for re-animation of the paralysed face.METHODS:An anatomical study was performed on 24 lower-limb specimens (from the pelvis down to the knee) from 12 embalmed cadavers. The MNG was dissected from the surface of the muscle to the obturator foramen. Two anatomical regions were defined in the course of the nerve. The first region includes the part of the nerve that can easily be reached through a standard incision in the medial aspect of the thigh, that is, from the surface of the muscle to the posterior border of the adductor brevis muscle and the second region from there to the obturator foramen. Measurements of both anatomical regions and the maximum length of the nerve were taken with a calliper. The anatomical relations of the nerve were also noted and photo-documented.RESULTS:The median maximum length of the MNG from the surface of gracilis to the posterior border of adductor brevis ('first anatomical region') was 7.7 cm (Range 6.3-10.5 cm); from there to the obturator foramen ('second anatomical region') the length was 3.7 cm (Range 2-6 cm), giving a median length of dissection of the nerve as 11.5 cm (Range 9.9-13.6 cm). Intraneural dissection of the MNG has to be performed proximally in the course of the nerve (the part corresponding to the second anatomical region), just where it runs inside the fascia over the obturator externus muscle.CONCLUSIONS:Over 10-cm length of the MNG can be obtained when dissected along the course of the nerve up to the obturator foramen. To achieve the maximum length, intraneural dissection must normally be performed after the nerve passes the posterior border of the adductor brevis. An endoscopic approach or extended proximal incision is recommended to easily reach the proximal part of the nerve as far as the obturator foramen.
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