Are dementia with Lewy bodies and Parkinson's disease dementia the same disease?
Dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD), which share many clinical, neurochemical, and morphological features, have been incorporated into DSM-5 as two separate entities of major neurocognitive disorders with Lewy bodies. Despite clinical overlap, their diagnosis is based on an arbitrary distinction concerning the time of onset of motor and cognitive symptoms, namely as early cognitive impairment in DLB and later onset following that of motor symptoms in PDD. Their morphological hallmarks – cortical and subcortical α-synuclein/Lewy body plus β-amyloid and tau pathologies – are similar, but clinical differences at onset suggest some dissimilar profiles. Based on recent publications, including the fourth consensus report of the DLB Consortium, a critical overview is provided herein.
The clinical constellations of DLB and PDD include cognitive impairment, parkinsonism, visual hallucinations, and fluctuating attention. Intravitam PET and postmortem studies have revealed a more pronounced cortical atrophy, elevated cortical and limbic Lewy body pathologies, higher Aβ and tau loads in cortex and striatum in DLB compared to PDD, and earlier cognitive defects in DLB. Conversely, multitracer PET studies have shown no differences in cortical and striatal cholinergic and dopaminergic deficits. Clinical management of both DLB and PDD includes cholinesterase inhibitors and other pharmacologic and non-drug strategies, yet with only mild symptomatic effects. Currently, no disease-modifying therapies are available.
DLB and PDD are important dementia syndromes that overlap in many clinical features, genetics, neuropathology, and management. They are currently considered as subtypes of an α-synuclein-associated disease spectrum (Lewy body diseases), from incidental Lewy body disease and non-demented Parkinson's disease to PDD, DLB, and DLB with Alzheimer's disease at the most severe end. Cognitive impairment in these disorders is induced not only by α-synuclein-related neurodegeneration but by multiple regional pathological scores. Both DLB and PDD show heterogeneous pathology and neurochemistry, suggesting that they share important common underlying molecular pathogenesis with Alzheimer's disease and other proteinopathies. While we prefer to view DLB and PDD as extremes on a continuum, there remains a pressing need to more clearly differentiate these syndromes and to understand the synucleinopathy processes leading to either one.
The nosologic relationship, as defined by DSM-5 [1, 2], between dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD), both of which are major neurocognitive disorders with α-synuclein (αSyn) deposition/Lewy bodies (LB), is continuously being debated [3–22].
The clinical features of DLB and PDD are similar and include dementia, cognitive fluctuations, and (visual) hallucinations in the setting of clinical or latent parkinsonism. The cognitive domains of both disorders overlap, with progressive executive dysfunctions, visual-spatial abnormalities, and memory disorders . Based on international consensus, DLB is diagnosed when cognitive impairment precedes parkinsonian motor signs or begins within 1 year from its onset , whereas in PDD, cognitive impairment develops in the setting of well-established Parkinson's disease (PD) . DLB patients will also develop parkinsonism of increasing severity over the years, although 25% of them never develop parkinsonian symptoms . Despite different temporal sequences of motor and cognitive deficits and several quantitative clinical differences, both disorders show largely convergent, albeit locally and quantitatively divergent neuropathological lesions, associated with increased Aβ and tau loads in DLB [9, 26–30]. The overlap of clinical and morphological features has led to the debate of whether DLB and PDD are the same disease , different phenotypic expressions of the same αSyn/Lewy body disease (LBD) spectrum, or distinct 'diseases' [3, 31] sharing genetic risk features with PD and Alzheimer's disease (AD) [10, 32], despite recent studies indicating a regional overlap of pathologies [33–37]. The present paper will critically review the major current findings in DLB and PDD, their possible nosologic interrelations, and the available biological markers and therapies. Of note, this review does not include mild cognitive impairment in LBD (see [8, 38–46]).
The presenting features of DLB can be broadly placed into three categories, namely cognitive impairment, behavioral/psychiatric phenomena, and physical symptoms . Essential for its diagnosis are dementia with moderate memory impairment, deficits in attention, executive dysfunction and visuoperceptual ability, fluctuating cognition (presumably related to thalamic damage and cholinergic imbalance ), and recurrent visual hallucinations that are well formed and detailed . Hallucinations in DLB may occur spontaneously, independent of visuospatial and perceptional impairment , and possibly related to LBs in the temporal lobe , while in PDD they typically occur after dopaminergic therapy [10, 23, 51]. Nevertheless, hallucinations had been reported prior to the levodopa era  as well as in drug-naive PD patients even in the premotor phase . Language impairment tends to be mild, with verbal and semantic fluency deficits. Spontaneous parkinsonian features, such as bradykinesia and rigidity, are common in DLB (over 85%) , while rest tremor is less frequent . REM sleep behavior disorder (RBD), which shows a high prevalence in DLB and may precede cognitive decline by decades, is now included as a core clinical feature . RBD may reflect a distinct subtype of DLB with earlier disease onset , associated with severe brain metabolic decreases ; however, as an early manifestation, it is not specific to DLB [58, 59]. The pattern of initial cognitive dysfunction differs between DLB and PDD , with greater deficiencies of attention, executive function, and constructive abilities, as well as significantly lower ratings in episodic verbal memory tasks, in DLB [61, 62]. Further, the rate of cognitive decline is reportedly faster in DLB than in PDD and AD [63, 64] (Table 1).
Supporting clinical features for the diagnosis of probable or possible DLB are repeated falls, syncopes, hyposmia, severe autonomic dysfunction, hypersomnia, hallucinations in non-visual modalities, apathy, depression, and severe sensitivity to antipsychotic agents [2, 65]. However, since these changes also occur in advanced PD, they cannot differentiate DLB from PDD, e.g., the prevalence of neuroleptic sensitivity does not differ significantly between them .
A diagnosis of clinically probable DLB requires (1) two or more core clinical features to be present, with or without indicative biomarkers, or (2) the presence of only one core clinical feature but with one or more indicative biomarkers . Although the diagnostic specificity of these criteria is high (range 79–100%), the sensitivity can be low (12–88%), improving with additional supporting features such as biomarkers [67–70]. A recent meta-analysis reported a pooled sensitivity, specificity, and accuracy of 60.2% (95% CI 30.9–83.7%), 93.8% (83.8–97.6%), and 79.7% (62.6–90.7%), respectively, for the diagnostic  criteria of DLB . Thus, currently, approximately 20% of DLB diagnoses are incorrect [68, 69].
The clinical features of PDD are in many respects similar to those seen in DLB, although, by definition [23, 71], the occurrence of parkinsonism distinguishes one from the other. Rigidity and akinesia occur both in PDD and DLB . Cognitive impairments in PDD are common and are similar in quality to those of DLB . However, the timing, profile, and rate of cognitive decline vary widely; indeed, the average time to dementia after PD diagnosis is almost 10 years, but may be as long as 20 years . Consensus criteria for PDD [24, 72, 73] require cognitive impairment across multiple domains, mood disturbances, and visual-spatial impairment similar to that seen in DLB. Attentional fluctuations, which are characteristic of DLB, are less frequent in PDD  but are clinically indistinguishable in the two conditions . Executive functions are probably more impaired in PDD, while language deficits are rare . Visual symptoms, common in PDD  likely due to a reduced metabolism in both dorsal and ventral visual pathways , include visual hallucinations, although they are less common than in DLB ; yet, the phenomenology of hallucinations is similar in both disorders . Other non-motor features, including autonomic dysfunctions and sleep disorders, may occur disproportionally to the severity of dementia [24, 72], while mood disturbances have a similar frequency as in DLB. The psychosis spectrum of PD has recently been reviewed . RBD can evolve in PDD and DLB  in up to 90% of patients after > 10 years . Finally, clinical validation efforts for PDD have shown variable diagnostic sensitivity and specificity [82, 83] and should be considered using the Movement Disorder Society criteria for the diagnosis of PDD .
Approximately 1–2% of those aged above 65 years are diagnosed with DLB worldwide , affecting approximately 5% of all dementia cases in those over the age of 75 . Its incidence is 0.7–1.4 new cases/100,000 person-years  or 3.5/100,000 person-years . For PDD, the cumulative prevalence is of 75% of PD patients surviving more than 10 years , 83% after 20 years , and up to 95% by age 90 years , with an overall prevalence of 31.1% (95% CI 20.1–42.1) and incidence rates from 0.43 to 1.13/100,000 person-years , indicating that, annually, approximately 10% of a PD population will develop dementia . The data concerning age at disease or dementia onset are highly variable. Whereas in the Olmsted County study  DLB patients were younger at symptom onset than those with PDD and had more hallucinations and cognitive fluctuations, others have reported younger age at disease onset in PDD [27, 90, 91], or no essential differences between disorders [14, 37, 92, 93].
Individuals with DLB or PDD have an increased mortality compared with the general population . DLB patients with a cerebrospinal fluid (CSF) AD profile and structural MRI changes (hippocampal atrophy) have a shorter survival [95, 96]; similarly, dementia and/or neuritic AD pathology in PD are related to a significantly shorter survival . PDD is associated with high mortality, advancing death by approximately 4 years . For typical DLB, the average survival time from the beginning of symptoms is 5–8 years , while rapidly progressing cases have a mean duration of 9 months . In both disorders, older age, hallucinations, and fluctuating dementia at onset are the best predictors of poor outcome [101, 102].
The neuroimaging characteristics have been reviewed in a quest for multimodal methods able to improve ante mortem diagnosis [103, 104]. Studies using 123I-β-CIT (DaTScan) SPECT or 18Fluorodopa PET demonstrated reduced dopamine transport binding in caudate and posterior putamen in DLB compared to AD, but observed no differences between DLB and PDD [105, 106]. Further, lower 123I–ioflupane-CIT has been observed in caudate nucleus in DLB and a greater asymmetry of uptake was seen in the posterior putamen in PDD [104, 107]. Dopamine uptake in striatum is significantly lower in PDD compared to DLB (P < 0.04), consistent with dopaminergic cell loss in substantia nigra pars compacta and the severity of parkinsonism . The disruption of dopaminergic pathways impacts the modulation of intrinsic brain networks, resulting in poor motor and cognitive performance .
SPECT imaging using 123I–metaiodobenzylguanidine, a marker of postganglionic sympathetic innervation, showed reduced cardiac uptake in both DLB and PDD as compared with AD [110, 111]. The sensitivity, specificity, and accuracy for the diagnosis of probable DLB is 82.4%, 96.3%, and 92.5%, respectively ; yet, although specific data on PDD are not available, 123I–metaiodobenzylguanidine imaging is unlikely to differentiate PDD from DLB.
Voxel-based morphometric MRI studies revealed greater grey matter loss in frontotemporal, occipital, and parietal areas in DLB compared to PDD [113–118]. Decreased grey matter volumes in association areas (left precuneus and inferior temporal lobe) are correlated with visual hallucinations in DLB , and atrophy of caudate, putamen, and pallidum have been observed in DLB but not in PDD [120–123]. However, since greater volume loss in various brain regions has not been statistically confirmed , these differences cannot be used for individual diagnoses.
White matter hyperintensities (WMH) on T2-weighted MRI have been observed in parieto-occipital areas in PDD cases with low CSF Aβ levels , without significant difference of progression between PDD and DLB , but more severe WMHs have been observed in the temporal lobe in DLB . Thus, evaluation of WMH and medial temporal lobe atrophy using MRI may be a powerful diagnostic tool to investigate the progression of AD-related pathology in DLB and perhaps to distinguish DLB from PDD [126, 128]. Magnetic resonance spectroscopy studies found relatively normal N-acetylaspartate/creatinine ratios in DLB, with similar reductions being observed in PDD and AD .
PET, perfusion SPECT, and arterial spin labelling MRI studies showed parietal, frontal, temporal, and occipital hypoperfusion common to both entities [104, 130–135]. Further, 11C PIB-PET imaging showed increased Aβ brain deposition in more than 50% of DLB cases, with more modest and less frequent Aβ accumulation in PDD [106, 136–139], while others reported increased cortical Aβ binding without dissimilarity between PDD and DLB . Tau-PET imaging, along with temporal atrophy, may indicate co-existing AD pathology in DLB with variable cortical tau 18F–AV-1451 uptake, which appears more common than in PDD [141, 142]. Preliminary tau-PET studies suggest a gradient of tau binding from PD/non-demented (minimal) to PDD (low), DLB (intermediate), and AD (highest) . Finally, the recently described additional 18F–AV-1451 binding to (neuro)melanin  deserves further investigation.
EEG abnormalities from posterior leads have been observed in all DLB cases and in three-quarters of those with PDD . Further, a multicenter study supported the validity of quantitative EEG analysis as a tool for diagnosis of both disorders and their distinction from AD [146, 147], although some components may be reduced more in PDD than in DLB . Finally, transcranial sonographic hyperechogenicity was inconclusive in differentiating DLB from PDD ; a comparative electro-oculographic study showed similar impairment in all tasks in both disorders .
Both DLB and PD are primarily sporadic diseases, yet genetic factors may be involved in their causation. Recent studies have uncovered certain genetic differences between PDD and DLB, albeit none of which is diagnostic. There is a substantial genetic contribution to DLB, heritability being estimated at about 36% [151, 152], while different genetic markers within the α-Syn gene (SNCA) may be associated with PDD [153, 154], although this is not unexpected in PD (Table 3). Analyses of SNCA expression in PDD and DLB showed an overlap of αSyn biology, indicating that they have distinct genetic etiologies and predicting that several mechanisms may be specific . Genome-wide association studies (GWAS) identified variants in the GBA, SNCA, APOE, and MAPT loci influencing the individual risk for DLB, suggesting that it has shared genetic risk features with PD and AD [32, 155], while the APOE4 haplotype may be an indication of PDD . However, to date, the genetic differences between both entities have not been studied in detail ; further studies will increase our understanding of the pathophysiology of these diseases .
Mutations are most prevalent risk factors for sporadic DLB [271, 272]; associated with increased levels of AD pathology [183, 273].
Mutations associated with risk of PDD and agressive cognitive decline [274–283].
Associated with increased risk of DLB .
Strongly associated with dementia in PD [153, 275, 285–289].
APOE ε4 is overrepresented in DLB, and it is an increased risk for DLB [35, 290].
Mixed evidence for dementia risk in PD [291–297].
Rare multiplications and mutations are associated with dementia in monogenic PD [292, 300], but show phenotypic variations and clinical heterogeneity [301–306].
No evidence for dementia risk [287, 288, 307–309], but polymorphisms may contribute to cognitive deficits in PD .
No association with cognitive impairment [311, 312].
Not essential for DLB .
No association with PDD [314–322].
Not related with DLB .
The development of broadly applicable CSF and other biomarkers for both DLB and PDD remains elusive, with only few biomarker candidates having been shown to specifically reflect the underlying disease process [159–161] (Table 2). A CSF AD profile is more common in DLB , while cortical atrophy in PDD is associated with increased total CSF αSyn and t-tau . However, cognitive impairment in GBA-associated PD does not seem to be associated with Aβ and tau profiles in CSF . The elevated tau/Aβ42 index in the order PD < PDD < DLB < AD may be related to an increased AD pathology . Further, levels of αSyn oligomers in CSF are increased in PDD but not in DLB [165–167]. Although many CSF and some plasma markers have been identified in both disorders, very few studies have examined samples from both disorders simultaneously, and only a minority have been confirmed by post mortem studies [167, 168].
The pathological substrates of DLB and PDD have been extensively investigated [9, 27, 29, 30, 35–37, 41, 169–181]. The most difficult problem in defining DLB and PDD at autopsy is their relationship with AD. DLB is, in part, conceived as a variant of AD ('Lewy body variant of AD')  and significant AD pathology is a consistent but not universal finding in both disorders . Cerebral neurofibrillary tangle burden, along with αSyn and Aβ plaque pathology, are the strongest predictors of a shorter interval between motor and dementia symptom onset and shorter survival .
The pathological substrate of PDD includes (1) Lewy/αSyn pathology in cortical, limbic, and brainstem structures, (2) AD-related pathologies, and (3) a combination of these lesions that has been shown to most robustly correlate with the severity of cognitive impairment [41, 169, 173, 174]. Approximately 50% of PDD patients showed Braak LB stages 4–6 plus severe AD-type pathology [92, 174], which may act synergistically [9, 27, 35, 172–174, 184, 185], influencing clinical features including a shorter duration or a more malignant course [169, 172]. AD neuropathology seems to be a more specific correlate of dementia than cortical αSyn pathology [169, 173]. Substantia nigra cell loss is more severe in PDD than in DLB , consistent with more advanced parkinsonism.
Multiple neurotransmitter deficits occur in PDD [29, 172], including loss of limbic and cortically projecting dopaminergic neurons in the mesocortical limbic system  and involvement of the cholinergic system with loss of neurons in the nucleus basalis of Meynert leading to cortical cholinergic denervation [9, 171, 186]. Severe pathology also involves the noradrenergic locus coeruleus, causing dysfunction of the related circuitry . Pedunculopontine cholinergic cell loss occurs in hallucinating PDD patients but not in DLB, which may indicate a different pattern of degeneration of cholinergic input structures .
DLB is featured by the co-occurrence of Lewy/αSyn pathology involving cortical and limbic areas (Braak LB stages 3–6) and AD-related pathologies. While some authors suggest that high cortical LB burden is the only independent predictor of dementia in DLB , others consider AD-related pathology to be more important ; however, studies have shown a strong correlation between both cortical pathologies [169, 173].
The DLB clinical syndrome is positively correlated to the extent of LB pathology (LBP) and negatively to the severity of neuritic AD pathology, while Aβ load has no effect . A subgroup with the clinical picture of DLB was shown to have minimal cerebral amyloid deposition . The higher cortical LB load in the temporal and parietal regions, which seems to be a distinguishing feature of DLB, may account for the shorter latency to dementia and could be accelerated by the APOE ε4 allele . Further, αSyn is an important predictor of disease duration both independently and synergistically with tau and Aβ load .
Other co-occurring pathologies (cerebrovascular lesions, cerebral amyloid angiopathy, hippocampal sclerosis, argyrophilic grain disease, and TDP-43 deposits) in PDD (19%) and DLB-AD (31.3%) brains appear to be of minor importance [35, 172, 192–194], although they may influence the development of dementia . Cerebrovascular lesions in DLB are relatively mild, showing an inverse relationship with the severity of LBP [196–198]. Cerebral microbleeds are more frequent in DLB than in PDD , with highest densities in the occipital lobe , but they appear to be independent of cerebral amyloid angiopathy .
Both PDD and DLB may show similar neuropathological features, with a variable mixture of αSyn/LB and AD-related pathologies (Table 4). A common pathophysiological factor is synaptic dysfunction due to the initial aggregation of αSyn in the presynapses causing functional disconnection  due to interference with axonal transport and neurotransmitter deprivation [178, 180, 203, 204]. The relationship between phosphorylated αSyn and tau accumulation to Aβ deposition in the cerebral cortex [205, 206] suggests that there is an overlap in the pathology between AD and DLB, and that Aβ promotes the accumulation of both αSyn and tau [35–37]. Thus, cognitive decline and related symptoms are not a consequence of αSyn-induced neurodegeneration alone since Aβ and tau pathologies also contribute to the overall deficits [33, 35–37, 207].
Despite many similarities, several morphological differences have been demonstrated, including higher Aβ load in striatum [34, 208], cortex, and claustrum [33, 177, 197, 209–211] and in the entorhinal cortex, amygdala, and putamen in DLB . The presence of Aβ in DLB and less so in PDD, along with its great sensitivity to differentiate between the disorders, have been extensively investigated [33, 34, 177, 209], with a hierarchy PD < PDD < DLB in both Aβ and tau burden  (Table 4).
Further differences include a more severe αSyn load in hippocampal subarea C2 in DLB  and in amygdala in DLB compared to in PDD (78.7% vs. 36% and 92% vs. 30%, respectively) , whereas αSyn loads in PD are highest in the cingulate cortex . Other deviations include the severity and distribution pattern of lesions in substantia nigra pars compacta (predominant neuronal loss in the ventrolateral parts in PDD versus more severe damage in the dorsolateral parts in DLB) and less marked nigral neuronal loss causing less severe postsynaptic dopaminergic upregulation [209, 213]. Additionally, significantly higher 5-HT1A receptor binding density in the cortex was seen in DLB compared to PDD . The heterogeneous neurochemistry of both DLB and PDD, which depends on differences in pathology, suggests that these αSyn-related disorders and AD share a common, underlying molecular pathogenesis; however, this needs further elucidation.
The clinicopathological features of DLB, PDD, and other synucleinopathies are highly variable and heterogeneous [9, 29, 215–217], although the spread of LBP was originally suggested to be uniformly ordered according to the Braak scheme [218, 219]. There are three current major staging systems in use for LB disorders, including one for PD [218, 219], one for DLB , and revised guidelines for LB disease [2, 220, 221]. Based on semiquantitative assessment of LBs in large autopsy series, a staging of the chronological spread of LBP was proposed to designate its predictable caudo-rostral sequence in the CNS, which, however, is not identical with the spreading and location of αSyn pathology [222, 223]. Cases with severe LBP (Braak 'neocortical' stages 5 and 6) that show overlap or transition between PD and DLB are frequently associated with cognitive impairment, which increases with progressing neuropathological changes .
The validity of the Braak staging scheme, which corresponds roughly to the classification of LB disorders as either a (1) predominantly brainstem pathology, (2) limbic system (limbic/transitional type) pathology, or (3) diffuse neocortical pathology , has gained wide support as a standard for assessment of LBDs [98, 225, 226], but has also been a matter of vigorous debate [216, 227–231]. The Braak staging scheme often, but not consistently, shows acceptable correlations between morphological findings and clinical data, mainly in a subgroup with early onset and prolonged disease duration , whereas a new unified staging system allows the classification of all cases of LBDs, including PD, PDD, DLB, incidental LBD, and DLB-AD .
According to the Braak scheme, αSyn aggregates, forming the major components of LBs, and Lewy neurites appear first in the olfactory structures and enteric nervous system and then progressively spread into the brain, moving from cell to cell (neuron to neuron) and through neuronal circuits in a 'prion-like' manner, thus contributing to synaptic failure  due to impaired axonal transport and accounting for the progression of LBP [234–236]. More recently, it has been hypothesized that αSyn itself may be a critical factor in mediating transmission of disease pathology by such a 'prion-like' process, which appears essential for the pathogenesis of both PDD and DLB . It remains to be seen if the species of aggregates of αSyn responsible for propagation and neurodegeneration are different and whether the various strains of αSyn fibrils underlie the differences in cellular and regional distribution of lesions in different synucleinopathies, as has been observed following the injection of αSyn aggregates in animal models [238, 239].
An essential problem in distinguishing between DLB and PDD is the impact of AD-related pathology and its co-occurrence with LBP, although both types of lesion have been shown to be strongly correlated with one another [169, 173]. However, recent clinicopathological studies showed that the clinical features of DLB are the consequence of multiple regional pathologies that are less pronounced in PDD [9, 27, 30, 73]. Nevertheless, the genetic and molecular mechanisms responsible for the, at least partially, different pathogenetic factors of both disorders await further elucidation.
Currently, there are no disease-modifying therapies for LBDs available (however, see ), although robust evidence supports the use of cholinesterase inhibitors (ChEIs) to treat these disorders [241, 242], related to the reduction of cholinergic markers in both PDD and DLB [243, 244]. Meta-analyses have indicated beneficial effects of both donepezil and rivastigmine for cognitive and psychiatric symptoms in both disorders [245–248], while only one study found an effect of memantine in PDD . The efficacy of memantine in DLB is thus less clear, but may have benefits either as monotherapy or as adjunctive to a ChEI ; further, it induced longer survival in patients with DLB and PDD . Although the effects were relatively small, ChEIs gave a better response of cognitive impairment in DLB and PDD than in AD , and may produce reduction in apathy, visual hallucinations, and delusions . The use of antipsychotics should be avoided given the risk of serious reactions in DLB [2, 253]. When atypical antipsychotic agents are needed, quetiapine, and particularly clozapine, are less likely exacerbate parkinsonism . Levodopa is generally well tolerated, but produces significantly less motor response in DLB than in PD and may be associated with an increased risk of psychosis [242, 254, 255]. Additionally, strategies to decrease the level of αSyn, to prevent cell-to-cell transmission of misfolded αSyn, and deep brain stimulation of the cholinergic nucleus basalis of Meynert have been discussed [39, 256]. Future therapeutic strategies should include disease-modifying strategies, possibly based on recent vaccination trials against αSyn, Aβ, and tau proteins [257, 258]. Preliminary results of anti-αSyn-immunotherapy in a combined model of synucleinopathy  may open the way to potential new treatments. A recent review of non-pharmacological interactions for DLB gave no definite results , while bilateral deep brain stimulation of the NBM for PDD showed potential improvement of neuropsychiatric symptoms .
DLB and PDD are major neurocognitive disorders with LBD, sharing many clinical, genetic, pathophysiological, imaging, and morphological features. Thus far, a clear and objective distinction between the two entities, other than the arbitrary timing of the appearance of cognitive and motor impairments (1-year rule), has not been established [5, 10, 15, 220], while others maintain that the two entities may merge  or may become the same disease . The revised Movement Disorder Society clinical definition of PD, considering DLB with presence of parkinsonism a 'DLB subtype of PD' [18, 31], was criticized since it would confuse rather than clarify the distinction between both entities . However, the 1-year time period may not be the optimal method for diagnostic distinction between both disorders  since cognitive decline has been reported to start as early as 6 years prior to PD diagnosis . Yet, it appears questionable whether this and other recent clinical studies on impaired cognition years before manifestation of parkinsonism  may blur the distinction between PD and DLB, which has been supported by recent neuroimaging and postmortem studies indicating that, in addition to predominant LB/αSyn pathology, AD-related lesions may contribute to the timing of dementia onset relative to motor signs .
The clinical pictures of both phenotypes, characterized by recent diagnostic criteria (for DLB  and for PDD [24, 72, 84]), despite individual variability, show many overlapping and distinguishing features [3, 8, 126, 265] (Table 1).
Several genetic markers have been shown to be risk factors for DLB and/or PDD, with some differences among them (Table 3). However, it appears premature to recommend genetic testing for clinical diagnosis and differentiation between DLB and PDD. A number of indicative and supportive biomarkers may contribute to the clinical diagnosis of probable DLB and PDD (Table 2).
Despite considerable overlap between DLB and PDD, recent neuroimaging and postmortem studies have demonstrated differences in the quantity and distribution pattern of LB/αSyn and AD-related pathologies between these two entities (Table 4). A correlation between these lesions suggests (1) a synergistic/additive or triggering effect between these protein pathologies , with increasing levels of AD pathology inducing an increasing burden of αSyn pathology; (2) an overlap in the pathology between DLB and AD; and (3) that the cognitive decline and related symptoms are not a consequence of αSyn-induced neurodegeneration alone, but of mixed pathologies contributing to the overall deficits [30, 35, 37, 183, 207, 266].
A possible interpretation of the available data would be that PDD and DLB are sub/phenotypes or two ends of the LBD spectrum , in which DLB may reside at the more severe side next to AD, while incidental LBD would be on the other (initiating) end . The suggested spectrum is as follows: incidental LBD > PD/non-demented > PDD > DLB > DLB/AD nearing AD. Recent GWAS studies suggested, as another possibility, that DLB and PDD would be distinct diseases with shared genetic risk features with PD and AD . Although some genetic factors that predispose to the development of dementia may differ in PDD and DLB, further extensive GWAS studies in autopsy-confirmed cohorts are warranted.
DLB and PDD are clinically similar illnesses, distinguished on the basis of the relative timing of dementia and parkinsonism (the 1-year rule). In view of the heterogeneity of the clinical course and symptomatology of both disorders that share the same pathophysiology , the question of whether this is a biologically valid distinction, or whether they are merely subtypes in a continuum of LBDs remains to be elucidated based on the results of combined biomarkers, new molecular imaging tracers [268, 269], and multimodal imaging . Their distinction would be useful for further diagnostics and, in particular, new and disease-specific preventive and curative measurements.
At present, neuropathological (differential) diagnosis of DLB and PDD with no or insufficient clinical data would be difficult . However, according to the preliminary criteria proposed in Table 5 (which need further validation and reproducibility), this may be possible. In view of the recent data on the clinical diagnostic criteria for DLB , their accuracy remains limited, while, to the best of our knowledge, no comparable studies are available for PDD. In order to support the notion that DLB and PDD are separate diseases, a unique pathogenic process should be identified for either one or the other. Therefore, at present, they cannot be strictly separated as distinct, whereas clinical, imaging, and morphological parameters can distinguish DLB from AD and frontotemporal dementia. The solution of this problem – if at all possible – warrants extensive multidisciplinary studies designed to shed further light on the relationship between PDD and DLB, including identifying genetic and environmental risk factors, and improving our understanding of the biological mechanisms responsible for their pathogenesis such that preventative or curative management can be developed .
Nevertheless, the wide acceptance of the term DLB is evidence of its clinical utility, which is likely to result in the maintenance of the term; it is useful in the differential diagnosis of cases presenting with cognitive decline. Whether such patients are likely to develop extrapyramidal symptoms (DLB) or not (AD, etc.) has prognostic value and indicates the type of therapy (e.g., typical or atypical neuroleptics) and is thus of clinical importance. Although we favor the concept of a continuum between DLB and PDD, it must be recognized that biological factors must exist that determine whether the synucleinopathy will present earlier with cognitive decline or with extrapyramidal features. Identifying such factors is important scientifically and may lead to the development of disease-modifying therapies.
The authors thank Mr. E. Mitter-Ferstl, PhD, for secretarial and editorial work.
The study was partially funded by the Society for the Promotion of Research in Experimental Neurology, Vienna, Austria.
KAJ and ADK contributed to the conception of the manuscript; KAJ contributed literature research, drafted the manuscript, prepared tables and figure. Both authors contributed to the final editing of the manuscript and prepared it.
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Creese B, Bell E, Johar I, Francis P, Ballard C, Aarsland D. Glucocerebrosidase mutations and neuropsychiatric phenotypes in Parkinson's disease and Lewy body dementias: review and meta-analyses. Am J Med Genet B Neuropsychiatr Genet. 2017; https://doi.org/10.1002/ajmg.b.32549.


Share your love of the ocean with charms! Seashell Charm features a textured metal shell shape and is perfect for adding to charm bracelets, necklaces, earrings, anklets, key chains, and more. Let your jewelry speak for itself and accessorize yourself with style.


Write a 950 word paper in which you analyze the relationship between ethics and professional behavior in the administration of criminal justice. Explain the role of critical thinking with regard to the relationship of ethics and professional behavior. Include in your paper a proposal for a seminar in ethics training for law enforcement officers. In your proposal choose five areas of ethical conduct and that will be stressed in the seminar. Explain why you chose those areas and what the expected benefits of the training will be for both officers and the community.


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text:
August 2013 Issue 85
What price would you pay for security?
B2B Editor 7 August 2013
In previous editions of B2B, elringtons have written about the relatively new Personal Property Security Act ("PPSA"), and its farreaching effects on businesses and commercial interests.
Since the PPSA's inception in January 2012, the legal community has been waiting for a court decision to assist in interpreting its operation, especially transitional provisions and migrated security interests. The NSW Supreme Court handed down a PPSA decision in June 2013.
The Maiden Civil case – the Facts
Before the PPSA commenced operation, Queensland Excavation Service Pty Limited ("QES") purchased 3 Caterpillar civil construction vehicles ("Caterpillars") under finance. QES then gave possession of the Caterpillars to Maiden Civil (P&E) Pty Ltd ("Maiden"), and by agreement Maiden reimbursed QES for the deposits it had paid. Periodically from then on, Maiden paid QES the finance repayments plus 10 per cent.
Neither QES nor its financiers registered their interests in the Caterpillars on the Northern Territory register of motor vehicles, and after January 2012 they also did not register on the PPSA register ("the PPSR").In March 2012 Maiden sought finance from Fast Financial Solutions ("Fast") and the Caterpillars were included in the assets provided as security for this loan. Fast registered its security on the PPSR.
In July 2012, Maiden defaulted. Fast appointed a receiver and Maiden went into administration. The courts now had to decide – who gets the Caterpillars?
The Competing Claims
QES argued that it was the true owner of the Caterpillars and that the PPSA gave it a protected "transitional interest". That is, QES argued priority over the later Fast registration because the QES interest already existed at the time the new PPSA came in.
The receivers (acting in the interests of Fast) claimed that the Caterpillars belonged to Maiden and were only financed by QES.
Fast claimed as a secured creditor under the administration because it had a perfected security interest on the PPSR.
The Court found that the competing security interests must be resolved according to the system of priorities in the PPSA, regardless of whether QES is the "true owner". Brenton J ruled that although QES and Fast both had security interests in the Caterpillars (and QES actually owned two of them that had not been paid out), Fast had priority because Fast had correctly used the PPSR to perfect its interest whereas QES had not. QES had not registered its interest on the NT register that existed before the PPSA so it was not a perfected "transitional interest".
The lesson is clear – ownership itself is no longer the winning card. If you supply goods (by sale or lease) for which you are not paid and you want security over those goods, you must get advice about the PPSA.
Craig Painter
Contact Elringtons T: (02) 6206 1300,
Level 7, 221 London Circuit, Canberra City
visit: elringtons.com.au
Contact Elringtons T: (02) 6206 1300, Level 7, 221 London Circuit, Canberra City visit: elringtons.com.au
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Landlords and the PPSR – are you protected?
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PPSR – PPS huh?
It has now been over four years since the Personal Properties Securities Act 2009 (Cth) (PPSA) took substantive effect on...
Is your business PPSA compliant?
Personal Properties Securities Act 2009 (PPSA) which came into force on 31 January 2014 fundamentally changes the way security interests...

redpajama_set_name: RedPajamaCommonCrawl


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  .hero .hero-inner {
    max-width: 68em;
    margin-left: auto;
    margin-right: auto;
    color: white;
    margin: auto;
    padding: 3.5em;
    text-align: center; }
    .hero .hero-inner::after {
      clear: both;
      content: "";
      display: table; }
    .hero .hero-inner::after {
      clear: both;
      content: "";
      display: table; }
    .hero .hero-inner .hero-copy {
      text-align: center; }
      .hero .hero-inner .hero-copy h1 {
        font-size: 1.6em;
        margin-bottom: 0.5em; }
        @media screen and (min-width: 53.75em) {
          .hero .hero-inner .hero-copy h1 {
            font-size: 1.8em; } }
      .hero .hero-inner .hero-copy p {
        font-weight: 200;
        line-height: 1.4em;
        margin: 0 auto 3em auto; }
        @media screen and (min-width: 53.75em) {
          .hero .hero-inner .hero-copy p {
            font-size: 1.1em;
            max-width: 40%; } }
    .hero .hero-inner button {
      background-color: #477DCA;
      border-radius: 3px;
      border: none;
      color: white;
      display: inline-block;
      font-size: inherit;
      font-weight: bold;
      padding: 7px 18px;
      text-decoration: none;
      background-clip: padding-box;
      padding: 0.7em 1em; }
      .hero .hero-inner button:hover:not(:disabled) {
        background-color: #578ad4;
        cursor: pointer; }
      .hero .hero-inner button:active:not(:disabled), .hero .hero-inner button:focus:not(:disabled) {
        background-color: #3c71bb;
        cursor: pointer; }
      .hero .hero-inner button:disabled {
        opacity: 0.5;
        cursor: not-allowed; }

/*# sourceMappingURL=neat.css.map */

redpajama_set_name: RedPajamaGithub


text:
#!/usr/bin/env node
(function () {
  "use strict";

  var args = require('./argparse').parse()
    , findBrowser = require('../has-browser').findBrowser
    , findPackage = require('../has-package').findPackage
    , pakmanager
    , cwd
    ;

  function isReady(env) {
    console.log('Targeted Environment:', env);
    args.env = env;
    args.environment = env;

    pakmanager = require('../lib').create({ packageRoot: cwd });

    function doAction() {
      var action = args.subcommand_name
        ;

      console.log('[[[' + action + ']]]');
      if (pakmanager[action]) {
        pakmanager[action](function () {
          if ('build' === action) {
            console.log('wrote pakmanaged.js');
          } else {
            console.log('pakmanager', arguments);
          }
        }, args);
      }
    }

    return doAction();
    //tryPackageJson();
  }

  /*
  console.log('parsed args:');
  console.log(typeof args);
  console.dir(args);
  */
  /*
    {
        environment: 'guess',
        change_dir: '/path/to/dir',
        subcommand_name: 'build',
        env: null
    }
  */

  // TODO try to find root by rwalk
  cwd = args.change_dir || process.cwd();
  args.packageRoot = cwd;
  console.log(cwd);

  if (-1 !== ['browser', 'node'].indexOf(args.environment)) {
    isReady(args.environment);
    return;
  }

  findBrowser(function (type) {
    if ('guess' !== type) {
      isReady(type);
      return;
    }

  //"browserDependencies": {},
    // TODO don't default so heavily to browser
    findPackage(function (type1) {
      if ('guess' !== type1) {
        isReady(type1);
      } else {
        console.warn('\n\n======================= WARNING =======================');
        console.warn('Assuming browser mode by default is deprecated.');
        console.warn('  Include browserDependencies in your package.json');
        console.warn('  -- OR --');
        console.warn('  pakmanager -e browser build');
        console.warn('\nIn the next release of pakmanager, the node environment will be assumed as default');
        console.warn('=======================================================\n\n');
        isReady('browser');
      }
    }, cwd);
  }, cwd);
}());


Jennifer Itzkowitz joined the Seton Hall faculty in 2009 after earning a Ph.D. in Finance from the University of Florida. Her research examines contemporary problems in corporate finance, banking, and behavioral finance. Professor Itzkowitz's work has been published in the Journal of Corporate Finance, the Review of Finance, the Journal of Behavioral Finance, and The Research Handbook on International Banking and Governance.
Jennifer's research has also been presented at a number of conferences including the annual meetings of the Financial Management Association, Western Finance Association, Midwest Finance Association, European Financial Management Association, and the INFINITI Conference on International Finance. Her work has been written about and discussed by Time.com, Money.CNN.com, TheStreet.com, NJTV, and NPR. At Seton Hall, she is responsible for the coordination and teaching of the core finance course and teaches a seminar dealing with advanced corporate finance topics.


Caravan Tea Towel and Hand Towel gift set for anyone who loves a caravanning holiday.
Caravan Tea Towel and Hand Towel gift set for anyone who loves a caravanning holiday. A embroidered caravan design and personalised name(s) on a white cotton tea towel and a white cotton bathroom hand towel. Both items personalised in your choice of text and text thread colour and font style.
Caravan Tea Towel and Hand Towel gift set for anyone who loves a caravanning holiday. A embroidered caravan design and personalised name(s) on a white cotton tea towel and a white cotton bathroom hand towel. Both items personalised in your choice of text and text thread colour and font style. Tea Towel measures approx. 42x73cm Hand Towel measures approx. 49 x 90cm Useful hand and tea towel gift set perfect for all caravan club members!


Reducing sedation for pediatric body MRI using accelerated and abbreviated imaging protocols.
Magnetic resonance imaging (MRI) is an established diagnostic imaging tool for investigating pediatric disease. MRI allows assessment of structure, function, and morphology in cardiovascular imaging, as well as tissue characterization in body imaging, without the use of ionizing radiation. For MRI in children, sedation and general anesthesia (GA) are often utilized to suppress patient motion, which can otherwise compromise image quality and diagnostic efficacy. However, evidence is emerging that use of sedation and GA in children might have long-term neurocognitive side effects, in addition to the short-term procedure-related risks. These concerns make risk-benefit assessment of sedation and GA more challenging. Therefore, reducing or eliminating the need for sedation and GA is an important goal of imaging innovation and research in pediatric MRI. In this review, the authors focus on technical and clinical approaches to reducing and eliminating the use of sedation in the pediatric population based on image acquisition acceleration and imaging protocols abbreviation. This paper covers important physiological and technical considerations for pediatric body MR imaging and discusses MRI techniques that offer the potential of recovering diagnostic-quality images from accelerated scans. In this review, the authors also introduce the concept of reporting elements for important indications for pediatric body MRI and use this as a basis for abbreviating the MR protocols. By employing appropriate accelerated and abbreviated approaches based on an understanding of the imaging needs and reporting elements for a given clinical indication, it is possible to reduce sedation and GA for pediatric chest, cardiovascular and abdominal MRI.


Can Fish We Eat Compromise Our Body Defenses?
Traditionally, we tend to consider seafood as a highly beneficial nourishment for our bodies. Its enhanced digestibility and intake of unsaturated, fatty omega-3, is vitally useful for cardiovascular health.
This reality may be changing rapidly, due to the alarming and rising rate of environmental pollution. Our oceans and seas are becoming a global sink of persistent pollutants in which fish, humans, and animals are exposed collectively.
A new study warns us that we may lose the benefits of consuming fish in general. Hence, the consumption of seafood may be jeopardizing our body's capability to cope with the new found pollutants because the toxins in our fish have now the potential to harm our bodies badly.
This new study warns that the environmental pollutants (ocean polluters) found in fish can hamper the human body's natural defense system. In other words, it can impede our immune system to flush out these harmful toxins. The study finding makes it more urgent to know how the pollutants act, especially as they are often found in combination.
Although it is known that these pollutants are potentially hazardous to human health and the environment, their real impact is not entirely understood. One of these is the pesticide DDT, which was banned by an international treaty in 2001. Others include chemicals used as industrial flame retardants.
The pollution grows exponentially and of course also affects all of us at a global level, even reaching fisheries and fish farms from around the world, amplifying the risk of experiencing adverse effects of contaminated fish.
The research, conducted by the Scripps Institution of Oceanography at the University of California, San Diego, noted ten pollutants persistent organic (POPs–persistent organic pollutants), in the yellowfin tuna from the Gulf of Mexico (sometimes at relatively high levels).
The residues are believed to be derived from environmental disasters, also took place thousands of kilometers away. All of these pollutants have the effect of reducing the effectiveness of an essential protein in humans and animals, the P-gp, which identifies and eliminates the toxic and harmful substances in the human body.


We work really hard for our Five Star Reviews on Google and Ten Star Reviews on Homestars. Alternatively, we are well recognized on Facebook and other sites too. Dang Good is so excited to share some of our Reviews with you – see below. If you are looking for one of the Best Cleaning Services Company out there yet still trying to keep costs down, look no further than Dang Good Carpet and Furnace Cleaning.
When things go wrong, (and unfortunately we are only human, so just occasionally they do), you'll likely find us to be way more upset about it than you! As a result, we will go out of our way to put the situation right where we believe we are at fault. We are for sure, humble enough to admit our mistakes when they happen.
Of course, you would need to tell us about it. Just click the Unhappy Icon above. On the contrary, if we have done a good cleaning job, we would love your vote of confidence. You can express that by clicking the Happy Icon above and following the instructions there. Your feedback is really appreciated.
From the first call to Dang Good I was impressed. The person that answered the phone was able to answer... read more all my questions and get me booked in that same week!
Mark called and gave me a heads up he was on the way. Showed up on time and did an AMAZING job! My carpets look new again.
He was knowledgable and very friendly, got the job done fast and didn't miss a spot!
Will definitely book again, great prices too!!
Just had my carpets done this morning and couldn't be more pleased! Not only was the young man who... read more entered my home kind and well mannered, he was efficient and professional. My carpets which were heavily stained now look and smell like new! I am so pleased to have stumbled across your company while I was google searching. I will definitely recommend your company and would have you come into my home again!
I had actually booked a different company for my Saturday carpet clean. They then cancelled due to weather the morning... read more of the job.
I found Dang Good online and called at 8am on Saturday morning, Mark booked me in and quoted me a fair price and was here within hours. My home was being listed and I needed it done urgently so he came out himself to ensure I got the service right away in minus 25 and laughed about the other company canceling because it was "too cold to work".
Super friendly, efficient and superb customer service. Highly recommend this company. Their pricing is AMAZING in comparison to other companies and the quality is unbeatable. I will absolutely be using this company again and will recommending them at every chance I get.


text:
Soldier Song: A True Story of the Civil War
In 1862, after the fearsome Battle of Fredericksburg, the Union and Confederate armies went into camp on opposite sides of the Rappahannock River. Soon a new battle emerged, as soldiers volleyed competing songs back and forth across the water: "The Battle Cry of Freedom" from the North. "God Save the South" from the Confederates. "Yankee Doodle." "Dixie." "The Battle Hymn of the Republic." "The Bonnie Blue Flag."
As winter set in, however, the men and boys on both sides found themselves longing for the same thing, and thinking of the same song. As the notes of "Home, Sweet Home" rose up over the river, enemies were united in song. For one night, they found common ground.
Interwoven with soldiers' letters and journal entries, this true story shows the power of music–and the possibility of seeing the humanity even in one's enemy, even in those with whom we are locked in conflict.
Disney-Hyperion
Ages 8 up
IndieBound | Amazon | Barnes & Noble
Soldier Song Educator Guide
*Publishers Weekly Best Books of 2017*
*Bank Street College Best Books 2018 Edition
*Huffington Post Best Picture Books of 2017*
*Notable Social Studies Trade Book 2018 (National Council for the Social Studies and Children's Book Council)
*Capitol Choices Noteworthy Books 2018
*2018 Texas Topaz Nonfiction Reading List*
*Society of Illustrators Original Art 2017 Silver Medal for Gilbert Ford's Illustrations*
* "An arresting, soulful tribute to the power of music and the shared humanity that underlies conflict."
–Booklist (starred review)
* "Through insightful narration and vibrant silhouettes and cartooning, Levy (I Dissent) and Ford (The Marvelous Thing That Came from a Spring) vividly bring to life a chapter in the U.S. Civil War and the integral role music played during the conflict."
—Publishers Weekly (starred review)
"A moving tale of ordinary soldiers in a great conflict who find solace in music."
" . . . a sophisticated picture book . . . . Levy and Ford leave readers satisfied."
This organization is dedicated to the preservation of Civil War battlefields, and its website is a fount of information about that war. The web pages under its "Education" tab are excellent–I recommend starting with "Civil War Facts."
Listen to "Home, Sweet Home"
As President Lincoln heard it: Soldier Song relates a story about how President Lincoln and his wife, Mary, asked an Italian singer named Adelina Patti to sing "Home, Sweet Home" when she visited the White House. This occurred in 1862 (the same year as the Battle of Fredericksburg), so of course there is no recording of this private concert. However, Adelina was only 19 years old at that time, and she lived until 1919–by which time the phonograph had been invented. Forty-three years later, when she was in her 60s, Adelina made a recording of the song for the newfangled record-player–and we can listen to it today. Just think: we're hearing the voice the Lincolns heard when, mourning the recent death of their son Willie, they asked Adelina to sing "Home, Sweet Home" to help ease their pain. Listen here.
As played by a brass band: The Federal City Brass Band plays "Taps" and then "Home, Sweet Home" in 2012 in this video, much as the Union and Confederate musicians would have played these tunes in the time of Soldier Song.
Soldier Song in the Classroom
The American Association of School Librarians has published librarian Tom Bober's guide to using Soldier Song and primary sources in the classroom. You'll find this excellent resource here.
Interviews and Blog Posts About the Book
Matthew Winner's "All The Wonders" podcast
The Children's Book Review
Here are some vintage pictures I examined in researching Soldier Song (hover mouse over thumbnail for caption; click for larger image):
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This kit has all you need to get the ReThink911 message out in duplicate! Work as a team with your matching t-shirts and baseball caps while handing out the fact-filled Street Brochure, and putting the oval stickers in highly visible areas where allowed. The hand sign can also be use as a lawn sign, while the vinyl banner is ideal for either street action or overpass hanging.
If you are an AE911TRUTH petition signer, you can also download the art for each item and make your own. If you aren't yet a signer, then please sign the petition.
T-shirt is available in both men's and women's style – women's front and men's back shown above.
Vinyl Banner is available in plain (shown) or detailed with pictures of WTC 7 – see enlarged image.


Please comment below to be added. Thanks.
My one and only brother, the youngest of us 5, turned 1 today!
Well, I'm back. I've been back since Sunday afternoon, actually, but I fell asleep immediately after getting home, despite having tons of things to do for school.
I MAY HAVE TO CUT MY HAIR.
I also really hope I don't get stuck sleeping on the streets, like my formator said. 'Cause then, I really won't know what to do with my stuff.
I shouldn't have looked at Leeke's winter event!
AS WELL AS A RELEASE OF THE HONEY HEAD WITH RE-FACEUP!
AND IT WAS A 9:30AM CLASS.
I just found my old Wild Arms 1 CD!
In general, do you find yourself more attracted to people with similar or different interests, life experiences, political beliefs, and religious backgrounds? Do you think having some common interests/goals is essential for a successful relationship?
I believe that, even if they don't have the same interests on the surface, if a group of people have the same core values as each other, only then can they have a successful relationship. It won't work otherwise.
Haha, all that aside though, it's pretty nice. Just wish that Masashi guy could've made it a little more different, so as not to seem like a Magician-version of One Piece.


The STM32 Nucleo pack is designed for USB Type-C™ and Power Delivery specifications.
Used with the embedded X-CUBE-USBPD certified software, the P-NUCLEO-USB002 represents a development tool enabling fast prototyping of USBPD applications leveraging ready-to-use ST componentry and software.
The P-NUCLEO-USB002 kit is designed to exploit the performance of the STM32F072 32-bit microcontroller based on ARM® Cortex®-M0 and two STUSB1602 USB Type-C™ port controllers, to develop applications managing up to two USB Type-C™ ports.
The STUSB1602 is a Type-C™ controller designed with 20-V technology that integrates a fully-featured USB Type-C state machine and a USBPD PHY + BMC driver. This analog front end features: Type-C™ attach and cable orientation detection; source / sink / DRP power role configuration; integrated VCONN power switch; integrated VBUS and VCONN discharge path; high voltage protection (including CC pins); VBUS switch gate drivers.
The P-NUCLEO-USB002 is fully configurable and ready to support different power roles such as: provider, consumer or DRP.
The X-CUBE-USBPD is compliant with the USB Type-C™ 1.3 and USB Power Delivery 2.0 and 3.0 specifications.


Bands I've played with in the last decade, including the Matt Skinner Band, Halden Wofford & the Hi*Beams, Hwy 287, Whiskey Trip, Open Road and more.
I'm not sure why you would want to sound like me, but if you do, here's how.
A gallery of (mostly) show posters. I've either played the show or designed the poster for most of them.
Places I've played in Colorado, New Mexico, Utah, Wyoming, Texas, Montana, New York, California, Oregon.


text:
if it's halaal, it's gotta be good!
HalaalBuzz
Banking, Finance & Takaful
Toiletries & Cosmetics
Japan to increase halal food export
by hq©
Japan plans to increase its export of halal food as demand for Japanese food grows in Muslim countries in the Middle-East and Asia. Prime Minister Shinzo Abe has announced plans to double exports by 2020 in a move that will bring an extra $10.3 billion to the country.
The Kuwait News Agency reported that the Japanese government is prepared to pay for half of the costs involved in upgrading processing facilities to make them compliant to halal standards.
The Japanese government hopes to increase beef exports in particular. At the moment Hong Kong and Thailand are the main customers of Japanese beef, but there is also a high demand for it in the UAE. They also aim to expand the market to Saudi Arabia, Indonesia and Malaysia.
Source: World Bulletin
TagsJapan • Japan halal food • Middle East
0 comments on "Japan to increase halal food export"
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If it's halaal, it's gotta be good!
Your daily fix for the latest news, analysis and much more on what's happening in the Halaal industry!
HQ Office
1st Floor Block 2330 | Century Square
Jalan Usahawan
| 63000 Cyberjaya
Email: ahlan@halaalquest.com


text:
Portugal govt official quits, is 10th to leave in a year
LISBON, Portugal (AP) — The Portuguese government's chief official in charge of transportation, including the fate of the troubled national airline and a long-postponed plan for high-speed train lines, has resigned.
Infrastructure and Housing Minister Pedro Nuno Santos quit late Wednesday amid an outcry over a 500,000-euro ($532,000) compensation payment made to a board member of state-owned flag carrier TAP Air Portugal while many other people face hardship due to a cost-of-living crisis.
The junior minister for infrastructure also quit, making a total of 10 senior government officials who have left their jobs since the center-left Socialist Party won a general election in a landslide last January. The departures have brought accusations from opposition parties that the administration is unsteady.
The TAP Air Portugal board member left the company earlier this year, half-way through her four-year term, after disagreements with the airline's CEO. She was deemed to be entitled to the payout for the loss of projected earnings.
Santos, a minister in Socialist governments for the past seven years, said he wasn't directly involved in the matter but was leaving his post due to the outcry.
"Given the public perception and the general sentiment created by this case, (the minister) feels that, in this context, he should accept political responsibility and has tendered his resignation," a statement issued after midnight said.


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Not only do we give you great yoga at a great price, you can earn rewards with us for simply doing the things you do. Each reward point translates into credit with the studio.
Join our referral program. Your friends will get their first class half price and you'll earn 500 reward points (£5) for every new person who attends the studio. To sign up, just follow this link. Pop in the email address you use to book your classes with us, the email addresses of up to 25 of your friends and family and away you go. They'll get an email via the system with a promotion code to book their first class at 50% discount (make sure they check their junk if the email doesn't come through) and each time someone new attends the studio, you'll receive £5 in account credit.
We're passionate about getting people away from their desks and onto a mat. Bad backs and stress and anxiety account for 80% of all work-related illnesses, all of which could be avoided with a regular yoga class. So, if you'd like to see yoga form part of your company's, wellness activities, introduce us to your HR team. We'll say a big "thank you" with a whopping 1,000 reward points (£10). Just send the information to info@sweatstudios.co.uk. Here's how we've helped other businesses.
Follow this link and key in your usual email address and password.
To see what rewards you have, click on the 'Account' link under 'My Info', scroll to the very bottom of the page and your rewards balance will be shown.
To spend your rewards, you can select the 'Classes' tab to book a class and then choose to use your rewards at the checkout. Alternatively, select the 'Online Store' tab and decide which product you'd like to buy and again you'll have the option to pay with rewards.
Please note that rewards can only spent online in this way, they are not available via the app or the timetable and booking system accessible on this website.
To make a purchase with us in the studio, simply tell the reception team you'd like to use your rewards and they'll do the rest. Rewards cannot be redeemed against items which are already discounted and must be spent up within a year of you earning them.
New to yoga? We're here to help!


text:
const Commands = require('./commands');
const Protocol = require('../protocol');

function Dispatcher (client, onMessage) {
    var state = {
        credentials: {
            id: 0,
            key: ''
        }
    };

    this.dispatch = (command) => {
        switch (command.type) {

        case Commands.SEND_BROADCAST_REQUEST:
            client.write(JSON.stringify({
                credentials: state.credentials,
                message: command.message,
                type: Protocol.BROADCAST_REQUEST
            }));
            break;

        case Commands.SEND_CREATE_SESSION_REQUEST:
            client.write(JSON.stringify({
                credentials: state.credentials,
                type: Protocol.CREATE_SESSION_REQUEST
            }));
            break;

        case Commands.SEND_CREDENTIALS_REQUEST:
            client.write(JSON.stringify({
                type: Protocol.CREDENTIALS_REQUEST
            }));
            break;

        case Protocol.BROADCAST_RESPONSE:
            onMessage(command.message);
            break;

        case Protocol.CREDENTIALS_RESPONSE:
            state = Object.assign({}, state, {
                credentials: command.credentials
            });
            break;

        default:
            break;
        };
    };
};

module.exports = Dispatcher;