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  • 1
    Online Resource
    Online Resource
    Human-modified landscapes: patterns of fine-scale woody vegetation structure in communal savannah rangelands
    Cambridge University Press (CUP) ; 2012
    In:  Environmental Conservation Vol. 39, No. 1 ( 2012-03), p. 72-82
    Details
    In: Environmental Conservation, Cambridge University Press (CUP), Vol. 39, No. 1 ( 2012-03), p. 72-82
    Abstract: Despite electrification, over 90% of rural households in certain areas of South Africa continue to depend on fuelwood, and this affects woody vegetation structure, with associated cascading effects on biodiversity within adjacent lands. To promote sustainable use, the interactions between anthropogenic and environmental factors affecting vegetation structure in savannahs need to be understood. Airborne light detection and ranging (LiDAR) data collected over 4758 ha were used to examine woody vegetation structure in five communal rangelands around 12 settlements in Bushbuckridge, a municipality in the Kruger to Canyons Biosphere Reserve (South Africa). The importance of underlying abiotic factors was evaluated by measuring size class distributions across catenas and using canonical correspondence analysis. Landscape position was significant in determining structure, indicating the importance of underlying biophysical factors. Differences in structure were settlement-specific, related to mean annual precipitation at one site, and human population density and intensity of use at the other four sites. Size class distributions of woody vegetation revealed human disturbance gradients around settlements. Intensity of use affected the amplitude, not the shape, of the size class distribution, suggesting the same height classes were being harvested across settlements, but amount harvested varied between settlements. Highly used rangelands result in a disappearance of disturbance gradients, leading to homogeneous patches of low woody cover around settlements with limited rehabilitation options. Reductions in disturbance gradients can serve as early warning indicators of woodland degradation, a useful tool in planning for conservation and sustainable development.
    Type of Medium: Online Resource
    ISSN: 0376-8929 , 1469-4387
    URL: Article
    DOI: 10.1017/S0376892911000592
    Language: English
    Publisher: Cambridge University Press (CUP)
    Publication Date: 2012
    detail.hit.zdb_id: 1470226-5
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    A.3 A novel recessive TNNT1 congenital core-rod myopathy in French Canadians
    Cambridge University Press (CUP) ; 2022
    In:  Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques Vol. 49, No. s1 ( 2022-06), p. S3-S3
    Details
    In: Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques, Cambridge University Press (CUP), Vol. 49, No. s1 ( 2022-06), p. S3-S3
    Abstract: Background: Mutations in the slow skeletal muscle troponin T ( TNNT1 ) gene cause a congenital nemaline myopathy resulting in death from respiratory insufficiency in early infancy. We report on four French Canadians with a novel congenital TNNT1 myopathy. Methods: Patients underwent lower extremity and paraspinal MRI, quadriceps biopsy and genetic testing. TNNT1 expression in muscle was assessed by quantitative PCR and immunoblotting. Wild type or mutated TNNT1 mRNAs were co-injected with morpholinos in a zebrafish knockdown model to assess for rescue of the morphant phenotype. Results: Four patients shared a novel missense homozygous mutation in TNNT1 . They developed from childhood slowly progressive limb-girdle weakness with spinal rigidity and contractures. They suffered from restrictive lung disease and recurrent episodes of rhabdomyolysis. Older patients remained ambulatory into their sixties. Lower extremity MRI showed symmetrical myopathic changes. Paraspinal MRI showed diffuse fibro-fatty involution. Biopsies showed multi-minicores. Nemaline rods were seen in half the patients. TNNT1 mRNA expression was similar in controls and patients, while levels of TNNT1 protein were reduced in patients. Wild type TNNT1 mRNA rescued the zebrafish morphants but mutant transcripts failed to do so. Conclusions: This study expands the spectrum of TNNT1 -related myopathy to include a milder clinical phenotype caused by a functionally-confirmed novel mutation.
    Type of Medium: Online Resource
    ISSN: 0317-1671 , 2057-0155
    URL: Article
    DOI: 10.1017/cjn.2022.93
    RVK:
    XA 10000
    Language: English
    Publisher: Cambridge University Press (CUP)
    Publication Date: 2022
    detail.hit.zdb_id: 2577275-2
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  • 3
    Online Resource
    Online Resource
    New Homogeneous v sin i Determinations for B Stars in Galactic Open Clusters
    Cambridge University Press (CUP) ; 2004
    In:  Symposium - International Astronomical Union Vol. 215 ( 2004), p. 69-70
    Details
    In: Symposium - International Astronomical Union, Cambridge University Press (CUP), Vol. 215 ( 2004), p. 69-70
    Abstract: We present new observations of projected rotational velocities of main sequence B stars in the galactic clusters NGC 2439, NGC 3293, NGC 3766, NGC 4755, NGC 7160 and h & χ Persei. 257 stars have been observed with three instruments, 207 of which are presented here. Projected rotational velocities have been determined by least-squares fit to synthetic spectra. Our v sin i scale is compared with that of Slettebak et al. (1975).
    Type of Medium: Online Resource
    ISSN: 0074-1809
    URL: Article
    DOI: 10.1017/S0074180900195245
    Language: English
    Publisher: Cambridge University Press (CUP)
    Publication Date: 2004
    SSG: 16,12
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  • 4
    Online Resource
    Online Resource
    P.028 A milder congenital myopathy in the french canadians caused by a novel TNNT1 homozygous missense mutation
    Cambridge University Press (CUP) ; 2019
    In:  Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques Vol. 46, No. s1 ( 2019-06), p. S21-
    Details
    In: Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques, Cambridge University Press (CUP), Vol. 46, No. s1 ( 2019-06), p. S21-
    Abstract: Background: Mutations of the slow skeletal muscle troponin-T1 ( TNNT1 ) gene are a rare cause of nemaline myopathy. The phenotype is characterized by severe amyotrophy and contractures. Death from respiratory insufficiency occurs in infancy. We report on four French Canadians with a novel congenital TNNT1 -related myopathy. Methods: Patients underwent MRI of leg muscles, quadriceps biopsy and genetic testing. Wild type or mutated human TNNT1 mRNAs were co-injected with morpholinos in a zebrafish knockdown model to assess their relative abilities to rescue the morphant phenotype. Results: Three adults and one child shared a novel missense homozygous pathogenic variant in the TNNT1 gene. They developed from childhood slowly progressive limb-girdle weakness with spinal rigidity and contractures. They suffered from restrictive lung disease and recurrent episodes of infection-triggered rhabdomyolysis, which were relieved by dantrolene in one patient. Older patients remained ambulatory into their sixties. MRI of leg muscles showed symmetrical atrophy and fatty infiltration in a proximal-to-distal gradient. Biopsies showed multi-minicores, while nemaline rods were seen in half the patients. Wild type TNNT1 mRNA rescued the zebrafish morphants but mutant transcripts failed to rescue the morphants. Conclusions: This study expands the spectrum of TNNT1 -related myopathy to include a milder clinical phenotype caused by a functionally-confirmed novel missense mutation.
    Type of Medium: Online Resource
    ISSN: 0317-1671 , 2057-0155
    URL: Article
    DOI: 10.1017/cjn.2019.128
    RVK:
    XA 10000
    Language: English
    Publisher: Cambridge University Press (CUP)
    Publication Date: 2019
    detail.hit.zdb_id: 2577275-2
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  • 5
    Online Resource
    Online Resource
    The Canadian Geophysical Long Baseline Interferometer
    Cambridge University Press (CUP) ; 1988
    In:  Symposium - International Astronomical Union Vol. 129 ( 1988), p. 489-490
    Details
    In: Symposium - International Astronomical Union, Cambridge University Press (CUP), Vol. 129 ( 1988), p. 489-490
    Abstract: A new VLBI system has been developed and put into operation. The system has three distinctive characteristics as compared with current VLBI practice, namely, the use of a wavefront clock at each station, the capability of a burst mode operation with high speed sampling, and the use of multiple 12 Mb/s data recording channels on commercial VCR's. The main use of the system is to be in geophysical investigations where these new features may prove of value.
    Type of Medium: Online Resource
    ISSN: 0074-1809
    URL: Article
    DOI: 10.1017/S0074180900135363
    Language: English
    Publisher: Cambridge University Press (CUP)
    Publication Date: 1988
    SSG: 16,12
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  • 6
    Online Resource
    Online Resource
    Spectral broadening for multi-Joule pulse compression in the APOLLON Long Focal Area facility
    Cambridge University Press (CUP) ; 2022
    In:  High Power Laser Science and Engineering Vol. 10 ( 2022)
    Details
    In: High Power Laser Science and Engineering, Cambridge University Press (CUP), Vol. 10 ( 2022)
    Abstract: Spectral-broadening of the APOLLON PW-class laser pulses using a thin-film compression technique within the long-focal-area interaction chamber of the APOLLON laser facility is reported, demonstrating the delivery of the full energy pulse to the target interaction area. The laser pulse at 7 J passing through large aperture, thin glass wafers is spectrally broadened to a bandwidth that is compatible with a 15-fs pulse, indicating also the possibility to achieve sub-10-fs pulses using 14 J. Placing the post-compressor near the interaction makes for an economical method to produce the shortest pulses by limiting the need for high damage, broadband optics close to the final target rather than throughout the entire laser transport system.
    Type of Medium: Online Resource
    ISSN: 2095-4719 , 2052-3289
    URL: Article
    DOI: 10.1017/hpl.2021.61
    Language: English
    Publisher: Cambridge University Press (CUP)
    Publication Date: 2022
    detail.hit.zdb_id: 2723155-0
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  • 7
    Online Resource
    Online Resource
    A.4 A Novel Recessive TNNT1 Congenital Core-Rod Myopathy in French Canadians
    Cambridge University Press (CUP) ; 2021
    In:  Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques Vol. 48, No. s3 ( 2021-11), p. S14-S15
    Details
    In: Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques, Cambridge University Press (CUP), Vol. 48, No. s3 ( 2021-11), p. S14-S15
    Abstract: Background: Mutations in the slow skeletal muscle troponin T ( TNNT1 ) gene cause a congenital nemaline myopathy resulting in death from respiratory insufficiency in early infancy. We report on four French Canadians with a novel congenital TNNT1 myopathy. Methods: Patients underwent lower extremity and paraspinal MRI, quadriceps biopsy and genetic testing. TNNT1 expression in muscle was assessed by quantitative PCR and immunoblotting. Wild type or mutated TNNT1 mRNAs were co-injected with morpholinos in a zebrafish knockdown model to assess for rescue of the morphant phenotype. Results: Four patients shared a novel missense homozygous mutation in TNNT1 . They developed from childhood slowly progressive limb-girdle weakness with spinal rigidity and contractures. They suffered from restrictive lung disease and recurrent episodes of rhabdomyolysis. Older patients remained ambulatory into their sixties. Lower extremity MRI showed symmetrical myopathic changes. Paraspinal MRI showed diffuse fibro-fatty involution. Biopsies showed multi-minicores. Nemaline rods were seen in half the patients. TNNT1 mRNA expression was similar in controls and patients, while levels of TNNT1 protein were reduced in patients. Wild type TNNT1 mRNA rescued the zebrafish morphants but mutant transcripts failed to do so. Conclusions: This study expands the spectrum of TNNT1 -related myopathy to include a milder clinical phenotype caused by a functionally-confirmed novel mutation.
    Type of Medium: Online Resource
    ISSN: 0317-1671 , 2057-0155
    URL: Article
    DOI: 10.1017/cjn.2021.266
    RVK:
    XA 10000
    Language: English
    Publisher: Cambridge University Press (CUP)
    Publication Date: 2021
    detail.hit.zdb_id: 2577275-2
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  • 8
    Online Resource
    Online Resource
    Diversity of ARSACS Mutations in French-Canadians
    Cambridge University Press (CUP) ; 2013
    In:  Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques Vol. 40, No. 1 ( 2013-01), p. 61-66
    Details
    In: Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques, Cambridge University Press (CUP), Vol. 40, No. 1 ( 2013-01), p. 61-66
    Abstract: The growing number of spastic ataxia of Charlevoix-Saguenay ( SACS ) gene mutations reported worldwide has broadened the clinical phenotype of autosomal recessive spastic ataxia of Charlevoix-Saguenay (ARSACS). The identification of Quebec ARSACS cases without two known SACS mutation led to the development of a multi-modal genomic strategy to uncover mutations in this large gene and explore phenotype variability. Methods: Search for SACS mutations by combining various methods on 20 cases with a classical French-Canadian ARSACS phenotype without two mutations and a group of 104 sporadic or recessive spastic ataxia cases of unknown cause. Western blot on lymphoblast protein from cases with different genotypes was probed to establish if they still expressed sacsin. Results: A total of 12 mutations, including 7 novels, were uncovered in Quebec ARSACS cases. The screening of 104 spastic ataxia cases of unknown cause for 98 SACS mutations did not uncover carriers of two mutations. Compounds heterozygotes for one missense SACS mutation were found to minimally express sacsin. Conclusions: The large number of SACS mutations present even in Quebec suggests that the size of the gene alone may explain the great genotypic diversity. This study does not support an expanding ARSACS phenotype in the French-Canadian population. Most mutations lead to loss of function, though phenotypic variability in other populations may reflect partial loss of function with preservation of some sacsin expression. Our results also highlight the challenge of SACS mutation screening and the necessity to develop new generation sequencing methods to ensure low cost complete gene sequencing.
    Type of Medium: Online Resource
    ISSN: 0317-1671 , 2057-0155
    URL: Article
    DOI: 10.1017/S0317167100012968
    RVK:
    XA 10000
    Language: English
    Publisher: Cambridge University Press (CUP)
    Publication Date: 2013
    detail.hit.zdb_id: 2577275-2
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  • 9
    Online Resource
    Online Resource
    GR.2 A deep intronic FGF14 GAA repeat expansion causes late-onset cerebellar ataxia
    Cambridge University Press (CUP) ; 2023
    In:  Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques Vol. 50, No. s2 ( 2023-06), p. S46-S46
    Details
    In: Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques, Cambridge University Press (CUP), Vol. 50, No. s2 ( 2023-06), p. S46-S46
    Abstract: Background: The late-onset cerebellar ataxias (LOCAs) have until recently resisted molecular diagnosis. Contributing to this diagnostic gap is that non-coding structural variations, such as repeat expansions, are not fully accessible to standard short-read sequencing analysis. Methods: We combined bioinformatics analysis of whole-genome sequencing and long-read sequencing to search for repeat expansions in patients with LOCA. We enrolled 66 French-Canadian, 228 German, 20 Australian and 31 Indian patients. Pathogenic mechanisms were studied in post-mortem cerebellum and induced pluripotent stem cell (iPSC)-derived motor neurons from 2 patients. Results: We identified 128 patients who carried an autosomal dominant GAA repeat expansion in the first intron of the FGF14 gene. The expansion was present in 61%, 18%, 15% and 10% of patients in the French-Canadian, German, Australian and Indian cohorts, respectively. The pathogenic threshold was determined to be (GAA) ≥250 , although incomplete penetrance was observed in the (GAA) 250-300 range. Patients developed a slowly progressive cerebellar syndrome at an average age of 59 years. Patient-derived post-mortem cerebellum and induced motor neurons both showed reduction in FGF14 RNA and protein expression compared to controls. Conclusions: This intronic, dominantly inherited GAA repeat expansion in FGF14 represents one of the most common genetic causes of LOCA uncovered to date.
    Type of Medium: Online Resource
    ISSN: 0317-1671 , 2057-0155
    URL: Article
    DOI: 10.1017/cjn.2023.71
    RVK:
    XA 10000
    Language: English
    Publisher: Cambridge University Press (CUP)
    Publication Date: 2023
    detail.hit.zdb_id: 2577275-2
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  • 10
    Online Resource
    Online Resource
    On the application of successive plane strains to grid-generated turbulence
    Cambridge University Press (CUP) ; 1979
    In:  Journal of Fluid Mechanics Vol. 93, No. 3 ( 1979-08), p. 501-513
    Details
    In: Journal of Fluid Mechanics, Cambridge University Press (CUP), Vol. 93, No. 3 ( 1979-08), p. 501-513
    Abstract: A grid-generated turbulence is subjected to a pure plane strain and the principal axes of the Reynolds stress tensor become those of the strain. This ‘oriented’ homogeneous turbulence is then submitted to a new strain the principal axes of which have a different orientation. We show that in such a situation it is possible to observe a transfer of energy from the fluctuating motion to the mean one. Such transfer is necessarily associated with a forced decay of the anisotropy of the motion. A detailed analysis of the reorientation of the principal axes of the Reynolds stress tensor in the frame of those of the second strain gives an explanation of the evolution of the principal axes of the Reynolds stress tensor in a shear flow.
    Type of Medium: Online Resource
    ISSN: 0022-1120 , 1469-7645
    URL: Article
    DOI: 10.1017/S0022112079002627
    Language: English
    Publisher: Cambridge University Press (CUP)
    Publication Date: 1979
    detail.hit.zdb_id: 1472346-3
    detail.hit.zdb_id: 218334-1
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