Number Of Tangles Research Articles

Deformation mechanisms of additively manufactured Hf10Nb12Ti40V38 refractory high-entropy alloy: Dislocation channels and kink bands

To date, the reported refractory high-entropy alloys (RHEAs) with strength and ductility synergy all have up to 1 GPa strain hardening rate (SHR). Keeping the SHR of more than 1 GPa in the RHEAs can postpone the point of plastic instability, thus prolonging the uniform tensile ductility (UTD). In this paper, Hf10Nb12Ti40V38 RHEA with high strength and ductility is successfully manufactured by laser-directed energy deposition (L-DED). The yield strength of the alloy is about 1011 MPa with the tensile ductility of ∼12.6 %. Interestingly, the SHR of the alloy is very low, far below 1 GPa. The stress-strain curve of the alloy does not only show no premature dropout, but also exhibits a flat plateau-type curve. For this interesting phenomenon, the deformation mechanisms of Hf10Nb12Ti40V38 alloy are systematically investigated by investigating the deformation microstructures. The results indicate that the dislocation modes are diversifying, but the limited number of tangles generated by the intersection of dislocation channels are the main source of SHR. Various dislocation configurations such as single dislocation channel and cross-slip are stimulated sequentially, and although they have no positive effect on the SHR of the alloy, they allow alloy to accommodate plastic deformation. Combined with the kink bands as a strain softening mechanism, it improves the ductility while decreasing the SHR. Multiple dislocation channels interactions and kink bands are clearly identified as the two deformation mechanisms governing strain hardening and strain softening. The competition between two mechanisms generates the phenomenon mentioned above. This study does not only shed new insights on the unique deformation behavior of Hf10Nb12Ti40V38 RHEA but also complement the current general perception about the relationship between SHR and ductility of RHEAs.

Tangle number of virtual rational tangles

We extend the classical coloring rule to compute the tangle (fraction) number of a virtual rational tangle. We use the contemporary argument used by Kauffman [Virtual knot theory, Eur. J. Comb. 20(7) (1999) 662–690] and show that tangle (fraction) number is a complete invariant. The main purpose of this paper is to provide an alternate yet elementary proof of John Conway’s classification theorem for the virtual rational tangles.

Enumeration of planar Tangles

A planar Tangle is a smooth simple closed curve piecewise defined by quadrants of circles with constant curvature. We can enumerate Tangles by counting their dual graphs, which consist of a certain family of polysticks. The number of Tangles with a given length or area grows exponentially, and we show the existence of their growth constants by comparing Tangles to two families of polyominoes.

Author response: Late-life blood pressure association with cerebrovascular and Alzheimer disease pathology.

We appreciate the interest in our study on late-life blood pressure (BP) and postmortem neuropathology in nearly 1,300 community-dwelling, autopsied persons.1 While we chose to separately examine longitudinal systolic BP (SBP) and diastolic BP (DBP) data, and indeed found more robust associations of a higher mean and more rapidly declining SBP with neuropathology, we agree that examining other BP variables provides additional insight into this area of research. Using the same datasets and a similar analytic approach of adjusted ordinal regression analyses, we found consistent results using additional BP variables. Increased variability in SBP over the years ( p = 0.002), but not variability in DBP ( p = 0.945), was associated with increased odds of brain infarcts, and increased mean pulse pressure over the years increased the odds of infarcts by 24% ( p 0.574), and there was a borderline association of increased mean pulse pressure with a higher number of tangles ( p = 0.084). Ongoing research will further elucidate the complex relationship of cardiovascular disease with brain dysfunction,2,3 including whether specific neuropathologies mediate the relation of BP to dementia in aging.

Late-life blood pressure association with cerebrovascular and Alzheimer disease pathology.

To examine associations of average and change in late-life blood pressure (BP) with cerebrovascular and Alzheimer disease (AD) neuropathology in a large group of decedents followed longitudinally in vivo. This clinical-pathologic study was derived from prospective, community-based cohort studies of aging with similar design and data collection. Measurements of systolic BP (SBP) and diastolic BP (DBP) were obtained annually (mean follow-up 8 years, SD = 4.8). Postmortem neuropathologic evaluations documented diseases of aging. Using regression analyses, we examined associations of average and decline in late-life SBP, and separately in DBP, with neuropathology. In 1,288 persons (mean age at death = 88.6 years; 65% women), the mean standardized person-specific SBP across the study was 134 (SD = 13) and DBP was 71 (SD = 8) mm Hg. The odds of brain infarcts were increased for participants with a higher mean SBP. Specifically, a person with a 1 SD SBP above the mean (147 vs 134 mm Hg) would have a 46% increased odds of having one or more infarcts, and an increased odds of gross infarct (46%) and microinfarct (36%). Furthermore, a more rapidly declining SBP slope over time increased the odds of one or more infarcts. Mean DBP, not slope, was related to brain infarcts. AD pathology analyses showed an association of a higher mean SBP with higher number of tangles (p = 0.038) but not plaques or other pathology (all p > 0.06). Changes in BP were not significantly related to AD pathology. Higher average late-life SBP and DBP, and independently a faster decline in SBP, are associated with increasing number of brain infarcts, including gross and microinfarcts. We found some evidence for a relation of SBP with AD, specifically tangles. Both average and decline in BP are related to brain disease.

Zinc Exacerbates Tau Pathology in a Tau Mouse Model.

Hyperphosphorylated tau protein is a key pathology in Alzheimer's disease (AD), frontotemporal dementia, chronic traumatic encephalopathy, and Parkinson's disease. The essential trace element zinc exacerbates tauopathy in vitro as well as in a Drosophila model of AD. However, the interaction has never been assessed behaviorally or biochemically in mammals. Zinc supplementation is prevalent in society, finding use as a treatment for macular degeneration and cataracts, and is also taken as an immune system booster with high levels appearing in multivitamins marketed toward the elderly. Using a transgenic mouse model that contains the human gene for tau protein (P301L), we assessed the effects of excess chronic zinc supplementation on tau pathology. Behavioral tests included nest building, circadian rhythm, Morris Water Maze, fear conditioning, and open field. Biochemically, total tau and Ser396 phosphorylation were assessed using western blot. Number of tangles were assessed by Thioflavin-S and free zinc levels were assessed by Zinpyr-1. Tau mice demonstrated behavioral deficits compared to control mice. Zinc supplementation exacerbated tauopathic deficits in circadian rhythm, nesting behavior, and Morris Water Maze. Biochemically, zinc-supplemented tau mice showed increased phosphorylation at pSer396. Zinc supplementation in tau mice also increased tangle numbers in the hippocampus while decreasing free-zinc levels, demonstrating that tangles were sequestering zinc. These results show that zinc intensified the deficits in behavior and biochemistry caused by tau.

Parameters Tied to Treewidth

AbstractTreewidth is a graph parameter of fundamental importance to algorithmic and structural graph theory. This article surveys several graph parameters tied to treewidth, including separation number, tangle number, well‐linked number, and Cartesian tree product number. We review many results in the literature showing these parameters are tied to treewidth. In a number of cases we also improve known bounds, provide simpler proofs, and show that the inequalities presented are tight.

Pretzel knots with L-space surgeries

A rational homology sphere whose Heegaard Floer homology is the same as that of a lens space is called an L-space. We classify pretzel knots with any number of tangles which admit L-space surgeries. This rests on Gabai's classification of fibered pretzel links.

スリット型インターレーサの寸法がインターレース糸の生成挙動に及ぼす効果の高速度ビデオ画像による解析

In order to obtain knowledge of interlacers generating a high number of tangles, the yarn motion was observed in slit-type interlacers with various sizes with high-speed video cameras. Results obtained are as follows: (1) Interlaced yarn is generated by the iteration of closed, dispersion and twisting states of running yarn independent of size of interlacer. (2) Interlacers generating a high number of tangles are supposed to have the following characteristics: Yarn passage region, where the airflow velocity is low, is small. In addition, the twin vortex has high dynamic pressure, filaments disperse to the whole yarn passage, plural twists generate in a yarn cross-section by the twisting action of the twin vortex, and a series of entanglements with different twist types occurs in the direction of yarn axis. Hence, strong entanglements between filaments are formed.

Tunnel number of tangles and knots

We study bridge number and tunnel number of tangles and knots, and also study their behavior under tangle decomposition of knots.

Effect of Geometry on Performance of Interlacer

Abstract Interlacer is the key part of interlacing technology that is adopted to improve the cohesion between loose multifilaments. Aimed at finding the interlacers with better performance, the present research designed five interlacers that can be classified into round type and cornered type. These five interlacers are different in cross-sectional shapes of yarn channel but are the same in the cross-sectional area. The evaluation of the performance of the interlacer includes the number and the strength of the tangles of the interlaced yarn it produces. Experiments are carried out at various supplied air pressures, yarn speeds and feed ratios. It was found that the interlacer with round cross-sectional shape of yarn channel is capable of producing an interlaced yarn with a large number of tangles and the cornered cross-sectional shape is effective in improving the strength of tangles. Among these five interlacers, the interlacer with an elliptical or an inverse-triangular shape has the best processing performance

Olfactory bulbectomy as a putative model for Alzheimer’: The protective role of essential fatty acids

While the removal of the rat's olfactory bulb is considered a valid animal model of depression, recently studies found that those rats exhibited an increase in the hyperphosphorylation of brain Tau proteins and in the number of tangles. The present study investigated the possibility of using rat's olfactory bulbectomy as a putative model for Alzheimer's disease. Olfactory bulbectomy indeed mimics a complex of Alzheimer's symptoms. We evaluated the effect of pretreatment with a specific mixture of omega-3/omega-6 fatty acids: After olfactory bulbectomy, the rats were cognitive impaired, hyperactive, anorectic, and hyperthermic and expressed increased levels of homocysteine and pro-inflammatory cytokines, including IL-17A. Pretreatment with a specific mixture of omega-3/omega-6 fatty acids blocked these adverse effects. We recommend using this model to scan potential new anti-Alzheimer's drugs and to investigate the role of fatty acids in Alzheimer's disease.

Clinically concordant variations of Alzheimer pathology in aphasic versus amnestic dementia

Primary progressive aphasia is a neurodegenerative syndrome characterized by gradual dissolution of language but relative sparing of other cognitive domains, especially memory. It is associated with asymmetric atrophy in the language-dominant hemisphere (usually left), and differs from typical Alzheimer-type dementia where amnesia is the primary deficit. Various pathologies have been reported, including the tangles and plaques of Alzheimer's disease. Identification of Alzheimer pathology in these aphasic patients is puzzling since tangles and related neuronal loss in Alzheimer's disease typically emerge in memory-related structures such as entorhinal cortex and spread to language-related neocortex later in the disease. Furthermore, Alzheimer pathology is typically symmetric. How can a predominantly limbic and symmetric pathology cause the primary progressive aphasia phenotype, characterized by relative preservation of memory and asymmetric predilection for the language-dominant hemisphere? Initial investigations into the possibility that Alzheimer pathology displays an atypical distribution in primary progressive aphasia yielded inconclusive results. The current study was based on larger groups of patients with either primary progressive aphasia or a typical amnestic dementia. Alzheimer pathology was the principal diagnosis in all cases. The goal was to determine whether Alzheimer pathology had clinically-concordant, and hence different distributions in these two phenotypes. Stereological counts of tangles and plaques revealed greater leftward asymmetry for tangles in primary progressive aphasia but not in the amnestic Alzheimer-type dementia (P < 0.05). Five of seven aphasics had more leftward tangle asymmetry in all four neocortical regions analysed, whereas this pattern was not seen in any of the predominantly amnestic cases. One aphasic case displayed higher right-hemisphere tangle density despite greater left-hemisphere hypoperfusion and atrophy during life. Although there were more tangles in the memory-related entorhinal cortex than in language-related neocortical areas in both phenotypes (P < 0.0001), the ratio of neocortical-to-entorhinal tangles was significantly higher in the aphasic cases (P = 0.034). Additionally, overall numbers of tangles and plaques were greater in the aphasic than amnestic cases (P < 0.05), especially in neocortical areas. No significant hemispheric asymmetry was found in plaque distribution, reinforcing the conclusion that tangles have greater clinical concordance than plaques in the spectrum of Alzheimer pathologies. The presence of left-sided tangle predominance and higher neocortical-to-entorhinal tangle ratio in primary progressive aphasia establishes clinical concordance of Alzheimer pathology with the aphasic phenotype. The one case with reversed asymmetry, however, suggests that these concordant clinicopathological relationships are not universal and that individual primary progressive aphasia cases with Alzheimer pathology exist where distributions of plaques and tangles do not account for the observed phenotype.

New Diagnostic Criteria for Alzheimer‘s Disease

More than 100 years ago, Alois Alzheimer described the clinical presentation and neu‐ ropathological changes, including neuronal loss, extracellular plaques and intraneuronal tangles, in a single patient with the disease that now bears his name [1]. Over the years, it became clear that the pathological character‐ istics of Alzheimer’s disease (AD) were com‐ mon in individuals who died demented. The finding of a correlation between plaque counts and dementia severity put great focus on the involvement of plaques in the disease process [2]. Similar but even stronger correlations were later seen between dementia severity and the number of tangles in the cerebral cortex [3]. However, it took almost 80 years from Alzheimer’s case presentation to reveal the molecular compo‐ sition of plaques and tangles (i.e., aggregated amyloid‐b [Ab] [4,5] and hyperphosphorylated tau proteins [6,7]).

Substrate-specific reduction of PP2A activity exaggerates tau pathology

Phosphorylation of the microtubule-associated protein tau is regulated by the balanced interplay of kinases and phosphatases. Disturbance of this balance causes hyperphosphorylation of tau and neurofibrillary tangle formation in Alzheimer’s disease brain. Here, we crossed Dom5 mice that express a substrate-specific dominant negative mutant form, L309A Cα, of protein phosphatase 2A (PP2A) with neurofibrillary-tangle-forming P301L mutant tau transgenic pR5 mice. This exacerbated the tau pathology of pR5 mice significantly. Double-transgenic Dom5/pR5 mice showed 7-fold increased numbers of hippocampal neurons that specifically phosphorylated the pathological S422 epitope of tau. They showed 8-fold increased numbers of tangles compared to pR5 mice, in agreement with our previous finding that tangle formation is correlated with and preceded by phosphorylation of tau at the S422 epitope. This suggests that, in addition to kinases, PP2A and its regulatory subunits may be a therapeutic target for Alzheimer’s disease.

Effects of Cross-Sectional Shape of Yarn Duct of Interlacer on the Properties of Interlaced Yarn

This study deals with the effect of cross-sectional shape of yarn duct of interlacer on the performance of interlaced yarn and aims at finding the interlacers with better performance. The performance of the interlaced yarn is evaluated by the number and strength of tangles. Seven interlacers with different shapes of yarn duct were designed. Each of them has the same cross-sectional area of yarn duct. Experiments were carried out at various supplied air pressures, yarn speeds and feed ratios. We have found that the interlacer with round cross-sectional shape of yarn duct is capable of producing an interlaced yarn with a large number of tangles and the cornered cross-sectional shape is effective in improving the strength of tangles. Among these seven interlacers, the interlacer with an elliptical or an inverse-triangular shape has the best processing performance. And the interlacer with a square cross-sectional shape has the worst processing performance.

Down‐regulation of vesicular glutamate transporters precedes cell loss and pathology in Alzheimer's disease

Alzheimer's disease (AD) is characterized pathologically by plaques, tangles, and cell and synapse loss. As glutamate is the principle excitatory neurotransmitter of the CNS, the glutamatergic system may play an important role in AD. An essential step in glutamate neurotransmission is the concentration of glutamate into synaptic vesicles before release from the presynaptic terminal. Recently a group of proteins responsible for uptake has been identified - the vesicular glutamate transporters (VGLUTs). The generation of antibodies has facilitated the study of glutamatergic neurones. Here, we used antibodies to the VGLUTs together with immunohistochemistry and western blotting to investigate the status of glutamatergic neurones in temporal, parietal and occipital cortices of patients with AD; these regions were chosen to represent severely, moderately and mildly affected regions at the end stage of the disease. There was no change in expression of the synaptic markers in relation to total protein in the temporal cortex, but a significant reduction in synaptophysin and VGLUT1 was found in both the parietal and occipital cortices. These changes were found to relate to the number of tangles in the temporal cortex. There were no correlations with either mental test score or behaviour syndromes, with the exception of depression.

So what if tangles precede plaques?

As proposed by Hardy and Higgins in 1992 [8], the amyloid hypothesis had two tenets. First, that deposition of -amyloid (A ) is the causative agent of Alzheimer’s disease (AD) pathology, and secondly that other lesions (tangles, dystrophic neurites, synaptic and cell loss, vascular degeneration) follow directly from this deposition. In their paper analyzing early formation of amyloid plaques and neurofibrillary tangles, Schonheit et al. aim to refute the second tenet, arguing that tangles form without or prior to the presence of plaques, and therefore that A cannot be the causative agent for neurofibrillary lesions. As discussed below, their argument is consistent with earlier observations that at least the initial formation of tangles is independent of A . On the other hand, the first tenet of the amyloid hypothesis is now supported so strongly by several lines of evidence that it is difficult to refute it. The challenge is how to reconcile these seemingly contradictory conclusions. Probably, the most compelling evidence that A is the causative agent of AD comes from observations on genetic mutations or other conditions that cause familial forms of AD, all of which produce an elevation in A or its more toxic form, A 1–42 [21,22]. These mutations occur directly in the gene for amyloid precursor protein (APP), and produce excess A , or occur in the genes for the Presenilin proteins, which form an important part of the -secretase complex that cuts APP to liberate A . Down’s Syndrome, with triplication of chromosome 21, also results almost invariably in AD, beginning at ages at which AD is extremely rare. Because the gene for APP is on the chromosome 21, an excess amount of A is generated. Amyloid plaques develop in Down’s Syndrome brains at about the age of 20–30 years, and large numbers of tangles appear in these cases during the third to fifth decades of life [9,11,12,26]. Although these genetic conditions account for only a small fraction of the total number of AD cases, the associated pattern of

Oxidative Modifications and Down-regulation of Ubiquitin Carboxyl-terminal Hydrolase L1 Associated with Idiopathic Parkinson's and Alzheimer's Diseases

Alzheimer's disease (AD) and Parkinson's disease (PD) are the two most common neurodegenerative diseases that occur either in relatively rare, familial forms or in common, sporadic forms. The genetic defects underlying several monogenic familial forms of AD and PD have recently been identified, however, the causes of other AD and PD cases, particularly sporadic cases, remain unclear. To gain insights into the pathogenic mechanisms involved in AD and PD, we used a proteomic approach to identify proteins with altered expression levels and/or oxidative modifications in idiopathic AD and PD brains. Here, we report that the protein level of ubiquitin carboxyl-terminal hydrolase L1 (UCH-L1), a neuronal de-ubiquitinating enzyme whose mutation has been linked to an early-onset familial PD, is down-regulated in idiopathic PD as well as AD brains. By using a combination of two-dimensional gel electrophoresis and mass spectrometry, we have identified three human brain UCH-L1 isoforms, a full-length form and two amino-terminally truncated forms. Our proteomic analyses reveal that the full-length UCH-L1 is a major target of oxidative damage in AD and PD brains, which is extensively modified by carbonyl formation, methionine oxidation, and cysteine oxidation. Furthermore, immunohistochemical studies show that prominent UCH-L1 immunostaining is associated with neurofibrillary tangles and that the level of soluble UCH-L1 protein is inversely proportional to the number of tangles in AD brains. Together, these results provide evidence supporting a direct link between oxidative damage to the neuronal ubiquitination/de-ubiquitination machinery and the pathogenesis of sporadic AD and PD.

Frictional Strength of Entanglement of Interlaced Yarns

In order to explore the frictional strength of entanglement of interlaced yarns, interlaced yams were subjected to iterative frictional forces by reciprocating rubbers and afterward their number of tangles was measured. The frictional strength of entanglement was defined as the ratio of the number of residual tangles to that of original ones. The number of fractions, friction angle, static tension, friction speed, and kind of yarns were used as experimental factors. As a result, when the number of fractions, friction angle, static tension and friction speed are large, tangling parts are easily destroyed. The yarn with more filaments or larger fineness shows a larger frictional strength of entanglement.