Experimental tests on the lifetime Asymmetry

The experimental test problem of the left-right polarization-dependent lifetime asymmetry is discussed. It shows that the existing experiments cannot demonstrate the lifetime asymmetry to be right or wrong after analyzing the measurements on the neutron, the muon and the tau lifetime, as well as the $g-2$ experiment. However, It is pointed out emphatically that the SLD and the E158 experiments, the measurements of the left-right integrated cross section asymmetry in $Z$ boson production by $e^+e^-$ collisions and by electron-electron M{\o}ller scattering, can indirectly demonstrate the lifetime asymmetry. In order to directly demonstrate the lifetime asymmetry, we propose some possible experiments on the decays of polarized muons. The precise measurement of the lifetime asymmetry could have important significance for building a muon collider, also in cosmology and astrophysics. It would provide a sensitive test of the standard model in particle physics and allow for exploration of the possible $V+A$ interactions.Comment: 11 pages, 1 figur

Hypocalcemia-Induced Seizure: Demystifying the Calcium Paradox

Calcium is essential for both neurotransmitter release and muscle contraction. Given these important physiological processes, it seems reasonable to assume that hypocalcemia may lead to reduced neuromuscular excitability. Counterintuitively, however, clinical observation has frequently documented hypocalcemia€™s role in induction of seizures and general excitability processes such as tetany, Chvostek€™s sign, and bronchospasm. The mechanism of this calcium paradox remains elusive, and very few pathophysiological studies have addressed this conundrum. Nevertheless, several studies primarily addressing other biophysical issues have provided some clues. In this review, we analyze the data of these studies and propose an integrative model to explain this hypocalcemic paradox

Ketones Improves Apolipoprotein E4-Related Memory Deficiency Via Sirtuin 3

Background: Apolipoprotein E4 (ApoE4) is the major genetic risk factor of Alzheimer\u27s disease (AD). ApoE4 carriers have cerebral hypometabolism which is thought as a harbinger of AD. Our previous studies indicated ketones improved mitochondria energy metabolism via sirtuin 3 (Sirt3). However, it is unclear whether ketones upregulate Sirt3 and improve ApoE4-related learning and memory deficits. Results: Ketones improved learning and memory abilities of ApoE4 mice but not ApoE3 mice. Sirt3, synaptic proteins, the NAD+/ NADH ratio, and ATP production were significantly increased in the hippocampus and the cortex from ketone treatment. Methods: Human ApoE3 and ApoE4 transgenic mice (9-month-old) were treated with either ketones or normal saline by daily subcutaneous injections for 3 months (ketones, beta-hydroxybutyrate (BHB): 600 mg/kg/day; acetoacetate (ACA): 150 mg/kg/day). Learning and memory ability of these mice were assessed. Sirt3 protein, synaptic proteins (PSD95, Synaptophysin), the NAD+/ NADH ratio, and ATP levels were measured in the hippocampus and the cortex. Conclusion: Our current studies suggest that ketones improve learning and memory abilities of ApoE4 transgenic mice. Sirt3 may mediate the neuroprotection of ketones by increasing neuronal energy metabolism in ApoE4 transgenic mice. This provides the foundation for Sirt3\u27s potential role in the prevention and treatment of AD

Increasing Precision of Clinical Diagnosis of Alzheimer\u27s Disease Using a Combined Algorithm Incorporating Clinical and Novel Biomarker Data

Establishing the in vivo diagnosis of Alzheimer€™s disease (AD) or other dementias relies on clinical criteria; however, the accuracy of these criteria can be limited. The diagnostic accuracy is 77% for a clinical diagnosis of AD, even among experts. We performed a review through PubMed of articles related to specific diagnostic modalities, including APOE genotyping, cerebrospinal fluid (CSF) testing, fludeoxyglucose F 18 positron emission tomography (PET), amyloid PET, tau PET, computed tomography (CT), single-photon emission CT, magnetic resonance imaging (MRI), and B12 and thyroid-stimulating hormone screening, to determine the specificity and sensitivity of each test used in the clinical diagnosis of AD. We added a novel immunomagnetic reduction assay that provides ultrasensitivity for analyzing the levels of plasma tau and beta amyloid 42 (Aβ42). The sensitivity and specificity of the current diagnostic approach (structural CT or MRI with screening labs) remain low for clinical detection of AD and are primarily used to exclude other conditions. Because of limited diagnostic capabilities, physicians do not feel comfortable or skilled in rendering a clinical diagnosis of AD. Compounding this problem is the fact that inexpensive, minimally invasive diagnostic tests do not yet exist. Biomarkers (obtained through CSF testing or PET imaging), which are not routinely incorporated in clinical practice, correlate well with pathologic changes. While PET is particularly costly and difficult to assess, CSF measures of tau and beta amyloid are not costly, and these tests may be worthwhile when the tiered approach proposed here warrants further testing. There is a need for developing bloodborne biomarkers that can aid in the clinical diagnosis of AD. Here we present a streamlined questionnaire-enriched, biomarker-enriched approach that is more cost-effective than the current diagnosis of exclusion and is designed to increase clinical confidence for a diagnosis of dementia due to AD

Sirtuin 3 Attenuates Amyloid-Beta Induced Neuronal Hypometabolism

Alzheimer\u27s disease (AD) is manifested by regional cerebral hypometabolism. Sirtuin 3 (Sirt3) is localized in mitochondria and regulates cellular metabolism, but the role of Sirt3 in AD-related hypometabolism remains elusive. We used expression profiling and weighted gene co-expression network analysis (WGCNA) to analyze cortical neurons from a transgenic mouse model of AD (APPSwInd). Based on WGCNA results, we measured NAD+ level, NAD+/ NADH ratio, Sirt3 protein level and its deacetylation activity, and ATP production across both in vivo and in vitro models. To investigate the effect of Sirt3 on amyloid-β (Aβ)-induced mitochondria damage, we knocked down and over-expressed Sirt3 in hippocampal cells. WGCNA revealed Sirt3 as a key player in Aβ-related hypometabolism. In APP mice, the NAD+ level, NAD+/ NADH ratio, Sirt3 protein level and activity, and ATP production were all reduced compared to the control. As a result, learning and memory performance were impaired in 9-month-old APP mice compared to wild type controls. Using hippocampal HT22 cells model, Sirt3 overexpression increased Sirt3 deacetylation activity, rescued mitochondria function, and salvaged ATP production, which were damaged by Aβ. Sirt3 plays an important role in regulating Aβ-induced cerebral hypometabolism. This study suggests a potential direction for AD therapy

Improved language identification using deep bottleneck network

Effective representation plays an important role in automatic spoken language identification (LID). Recently, several representations that employ a pre-trained deep neural network (DNN) as the front-end feature extractor, have achieved state-of-the-art performance. However the performance is still far from satisfactory for dialect and short-duration utterance identification tasks, due to the deficiency of existing representations. To address this issue, this paper proposes the improved representations to exploit the information extracted from different layers of the DNN structure. This is conceptually motivated by regarding the DNN as a bridge between low-level acoustic input and high-level phonetic output features. Specifically, we employ deep bottleneck network (DBN), a DNN with an internal bottleneck layer acting as a feature extractor. We extract representations from two layers of this single network, i.e. DBN-TopLayer and DBN-MidLayer. Evaluations on the NIST LRE2009 dataset, as well as the more specific dialect recognition task, show that each representation can achieve an incremental performance gain. Furthermore, a simple fusion of the representations is shown to exceed current state-of-the-art performance