Sail–sail and sail–hull interaction effects of hybrid-sail assisted bulk carrier

In a previously reported study, wind tunnel experiments were undertaken to investigate the aerodynamic characteristics of hybrid-sails in isolation. Such sails are seen as providing a worthwhile reduction in the delivered power to the propeller and hence the engine generated thrust, with a corresponding reduction in the CO2 production of diesel engine exhaust. In this paper, wind tunnel testing is used to investigate sail–sail interaction effects for two sets of four identical hybrid-sails, and the sail–hull interaction effects for the same two sets of four identical sails in the presence of a bulk carrier hullform. The analysis presented suggests that to build a sail-assisted ship requires an appreciation of the sail–sail and sail–hull interaction effects

Steady sailing performance of a hybrid-sail assisted bulk carrier

The steady sailing performance of a sail-assisted bulk carrier is investigated utilising towing-tank derived hydrodynamic derivatives and wind tunnel measured aerodynamic properties of the sails and the ship. The aerodynamic characteristics investigated include the ship hull at the fully-loaded draught, the sail–sail interaction effects for two sets of four identical hybrid-sails, and the sail–hull interaction effects for the same two sets of identical sails in the presence of the selected bulk carrier hull-form. This is in addition to lift–drag measurements of single isolated sails of each shape. The form of the two sets of soft sails was rectangular and triangular. This paper is concerned with assessing the benefits of a sail-assisted ship operation, and hence a steady-state rather than complete time-domain integrations of the governing equations are reported. The results of the completed analysis suggest that the benefits of the derived sail generated driving force are greater than the overhead of equipping the ship with a selected system of hybrid-sails. Sail-assisted ships could represent an important contribution to an improving global environment by reducing the demands for a driving force through the propeller

[11C]PBB3 PET detects tau pathology in corticobasal syndrome and progressive supranuclear palsy.

Objective:[11C]PBB3 has been recently introduced as a tau imaging PET ligand that has high affinity and selectivity for tau deposits. The aim of the present study is to investigate distribution of tau-pathology in progressive supranuclar palsy (PSP) and corticobasal degeneration (CBD) by [11C]PBB3 PET. Methods:Twelve patients with PSP, 8 patients with corticobasal syndrome (CBS), and 25 age-matched healthy controls (HCs) participated in this study. Seventeen patients with Alzheimer’s disease (AD) also took part in as disease control. Sequential PET scans were performed for 70 min following intravenous injection of [11C]PBB3. Standardized uptake value ratio (SUVR) at 30-50 min was calculated using the cerebellar cortex as reference region. Cerebral beta-amyloid depositions were estimated using [11C]Pittsburgh compound B PET. Results:All patients and HCs were PIB-negative except one patient with CBS and 4 HCs. SPM analysis showed high [11C]PBB3 binding in globus pallidus, putamen, thalamus, midbrain, pons, and peri-rolandic areas in PSP patients compared with 21 HCs. Seven PIB-negative CBS patients showed high [11C]PBB3 binding in peri-rolandic areas, supplementary motor area, and midbrain compared with 21 HCs. One PIB-positive patient with CBS showed high [11C]PBB3 binding in the whole cerebral cortex including limbic cortex like AD patients. Conclusion:The distribution of [11C]PBB3 binding in the patients was mostly in agreement with the known distribution of tau pathology in PSP and CBD, suggesting that [11C]PBB3-PET may be useful for the diagnosis of these disorders and therapeutic monitoring of anti-tau therapy.12th International conference on Alzheimer’s disease and Parkinson’s disease and related neurological disorder

Association between Aβ and tau accumulations and their influence on clinical features in aging and Alzheimer’s disease spectrum brains: A [11C]PBB3-PET study

INTRODUCTION:Amyloid-β (Aβ) and tau accumulations may occur independently and concurrently as exemplified by primary age-related tauopathy and Alzheimer\u27s disease (AD), respectively. Interactions between Aβ and tau accumulations and their influence on clinical features, however, are still unclear.METHODS:Associations among clinical symptoms, gray-matter volume, regional tau, and Aβ deposition assessed by positron emission tomography with [11C]pyridinyl-butadienyl-benzothiazole 3 (PBB3) and [11C]Pittsburgh compound-B (PiB), were evaluated in 17 AD, 9 mild cognitive impairment due to AD, and 28 PiB(-)-cognitive healthy controls (HCs).RESULTS:High tau burden was associated with aging and low-level education in PiB(-)-HC and AD-spectrum groups, and with high Aβ burden and low-level education in all subjects. It was not Aβ but tau accumulation that showed significant associations with cognitive performance even in PiB(-)-HC.DISCUSSION:The present study indicated aging and low-level education after Aβ would be enhancers for tau pathology, associated with neurodegeneration and cognitive impairment in healthy and diseased elderly individuals

Tau accumulation in patients with MAPT gene mutation measured by [11C]PBB3 PET

ファイル参照第56回日本神経学会学術大

The Association Between Aβ and Tau Accumulation And Its Influence On Clinical Features In Aging And Alzheimer\u27s Disease Spectrum Brains: [11C]PBB3 PET Study

関連ファイル参照Alzheimer”s Association International Conference 201

Tau-induced focal neurotoxicity and network disruption related to apathy in Alzheimer\u27s disease

Objective A pathy is a common neuropsychologicalsymptom in Alzheimer’s disease (AD), and previousstudies demonstrated that neuronal loss and networkdisruption in some brain regions play pivotal roles in thepathogenesis of apathy. However, contributions of tauand amyloid-β (Aβ) depositions, pathological hallmarksof AD, to the manifestation of apathy remain elusive.Methods S eventeen patients with AD underwentpositron emission tomography (PET) with 11C-pyridinylbutadienyl-benzothiazole 3 (11C-PBB3) and11C-Pittsburgh compound-B (11C-PiB) to estimate tauand Aβ accumulations using standardised uptake valueratio (SUVR) images. 11C-PBB3 and 11C-PiB SUVR werecompared between AD patients with high and lowApathy Scale (AS) scores. Additionally, volumetric anddiffusion tensor MRI was performed in those areas whereany significant difference was observed in PET analyses.Correlation and path analyses among AS and estimatedimaging parameters were also conducted.Results A D patients with high AS scores showed higher11C-PBB3 SUVR in the orbitofrontal cortex (OFC) thanthose with low AS scores, while 11C-PiB SUVR in anybrain regions did not differ between them. Elevated11C-PBB3 SUVR in OFC, decreased OFC thickness anddecreased fractional anisotropy (FA) in the uncinatefasciculus (UNC), which is structurally connected to OFC,correlated significantly with increased scores of the AS.Path analysis indicated that increased 11C-PBB3 SUVR inOFC affects apathy directly and through reduction of OFCthickness and subsequent decrease of FA in UNC.Conclusions The present findings suggested that taupathology in OFC may provoke focal neurotoxicity in OFCand the following disruption of the OFC-UNC network,leading to the emergence and progression of apathy inAD