Skeleton-of-Thought: Large Language Models Can Do Parallel Decoding

This work aims at decreasing the end-to-end generation latency of large language models (LLMs). One of the major causes of the high generation latency is the sequential decoding approach adopted by almost all state-of-the-art LLMs. In this work, motivated by the thinking and writing process of humans, we propose "Skeleton-of-Thought" (SoT), which guides LLMs to first generate the skeleton of the answer, and then conducts parallel API calls or batched decoding to complete the contents of each skeleton point in parallel. Not only does SoT provide considerable speed-up (up to 2.39x across 11 different LLMs), but it can also potentially improve the answer quality on several question categories in terms of diversity and relevance. SoT is an initial attempt at data-centric optimization for efficiency, and reveal the potential of pushing LLMs to think more like a human for answer quality.Comment: Technical report, work in progres

Switchable multi-wavelength mode-locked Yb-doped fiber laser using a polarization maintaining 45°-tilted fiber gratings based Lyot filter

We demonstrate a multi-wavelength mode-locked Yb-doped fiber laser by incorporating a pair of polarization maintaining 45° tilted fiber gratings (PM-45°TFG) based Lyot filter. Thanks to the functions of the polarizer and the comb filtering introduced by the Lyot filter, dissipative soliton (DS) pulses centered at 1035.26 nm, 1044.93 nm, 1055.62 nm, 1066.11 nm and 1076.63 nm can be generated respectively by finely tuning the intracavity polarization controllers (PCs). Moreover, the laser also can operate in a multi-wavelength regime via appropriately adjusting the pump power and polarization orientation. The high nonlinearity induced by the long cavity length leads to the generation of h-shaped mode-locked pulse with a repetition rate of 566.27 kHz. In the absence of any disturbance, the laser can operate steadily, that can potentially be used in various fields including wavelength division multiplexing systems etc

Micro-CT imaging reveals<i> Mekk3 </i>heterozygosity prevents cerebral cavernous malformations in <i>Ccm2</i>-deficient mice

Mutations in CCM1 (aka KRIT1), CCM2, or CCM3 (aka PDCD10) gene cause cerebral cavernous malformation in humans. Mouse models of CCM disease have been established by deleting Ccm genes in postnatal animals. These mouse models provide invaluable tools to investigate molecular mechanism and therapeutic approaches for CCM disease. However, the full value of these animal models is limited by the lack of an accurate and quantitative method to assess lesion burden and progression. In the present study we have established a refined and detailed contrast enhanced X-ray micro-CT method to measure CCM lesion burden in mouse brains. As this study utilized a voxel dimension of 9.5μm (leading to a minimum feature size of approximately 25μm), it is therefore sufficient to measure CCM lesion volume and number globally and accurately, and provide high-resolution 3-D mapping of CCM lesions in mouse brains. Using this method, we found loss of Ccm1 or Ccm2 in neonatal endothelium confers CCM lesions in the mouse hindbrain with similar total volume and number. This quantitative approach also demonstrated a rescue of CCM lesions with simultaneous deletion of one allele of Mekk3. This method would enhance the value of the established mouse models to study the molecular basis and potential therapies for CCM and other cerebrovascular diseases

Pump-controlled wavelength switchable dissipative soliton mode-locked Yb-doped fiber laser using a 45° tilted fiber grating

We demonstrate a pump-controlled wavelength switchable Yb-doped fiber laser (YDFL) by nonlinear polarization rotation (NPR) for the first time. The polarizer replaced by a 45° tilted fiber grating (45°-TFG) combines with a section of polarization maintaining fiber (PMF) to form a fiber-based birefringent filter. Stable dissipative soliton (DS) with center wavelength of 1068.39 nm is generated under the mode-locked threshold of 277 mW. The operating wavelength switching between 1046.51 nm and 1067.90 nm can be realized via increasing the pump power simply while keeping the polarization controllers (PCs) in a fixed state. The laser maintains stable mode-locking operation at each wavelength, which can be regarded as a type of multi-wavelength ultrafast light source with precise control and integration potential

Schizophrenia-associated somatic copy-number variants from 12,834 cases reveal recurrent NRXN1 and ABCB11 disruptions

While germline copy-number variants (CNVs) contribute to schizophrenia (SCZ) risk, the contribution of somatic CNVs (sCNVs)—present in some but not all cells—remains unknown. We identified sCNVs using blood-derived genotype arrays from 12,834 SCZ cases and 11,648 controls, filtering sCNVs at loci recurrently mutated in clonal blood disorders. Likely early-developmental sCNVs were more common in cases (0.91%) than controls (0.51%, p = 2.68e−4), with recurrent somatic deletions of exons 1–5 of the NRXN1 gene in five SCZ cases. Hi-C maps revealed ectopic, allele-specific loops forming between a potential cryptic promoter and non-coding cis-regulatory elements upon 5′ deletions in NRXN1. We also observed recurrent intragenic deletions of ABCB11, encoding a transporter implicated in anti-psychotic response, in five treatment-resistant SCZ cases and showed that ABCB11 is specifically enriched in neurons forming mesocortical and mesolimbic dopaminergic projections. Our results indicate potential roles of sCNVs in SCZ risk

Roles of CCM-MEKK3 signaling in cardiac development and CCM disease

Cerebral cavernous malformations are relatively common vascular malformations. This disease is caused by loss-of-function mutations of KRIT1 (CCM1), CCM2 and PDCD10 (CCM3), which encode the three CCM proteins. These three CCM proteins form an intracellular adaptor protein complex and are required by endothelial cells for vascular development during embryogenesis and preventing the formation of CCM lesions after birth. However, roles of CCM signaling in the developing heart and the molecular mechanism underneath the pathogenesis of CCMs are not known. By applying a combination of mutant zebrafish and mouse models, morpholino gene knockdown in zebrafish, and cell culture, we determined roles of CCM signaling in both cardiac development and CCM formation. Our experiments reveal that loss of CCM signaling in endocardial cells results in mid-gestation heart failure due to premature degradation of cardiac jelly. Loss of CCM signaling dramatically increases endocardial expression of Klf2 and Klf4 transcription factors and the Adamts4 and Adamts5 metalloproteinases that degrade cardiac jelly. These changes in gene expression result from increased activity of MEKK3, a mitogen-activated protein kinase that binds CCM2 in endothelial cells. MEKK3 is both necessary and sufficient for expression of these genes, and partial loss of MEKK3 rescues cardiac defects in CCM-deficient embryos. These findings reveal that CCM signaling controls endothelial gene expression by repressing MEKK3 activity during cardiovascular development. Using a neonatal mouse model of CCM disease, we show that expression of the MEKK3 target genes Klf2 and Klf4, as well as Rho and ADAMTS protease activity, are increased in the endothelial cells of early CCM lesions. Endothelial-specific loss of Map3k3 (also known as Mekk3), Klf2 or Klf4 markedly prevents lesion formation, reverses the increase in Rho activity, and rescues lethality. Consistent with these findings in mice, we show that endothelial expression of KLF2 and KLF4 is increased in human familial and sporadic CCM lesions, and that a disease-causing human CCM2 mutation abrogates the MEKK3 interaction without affecting CCM complex formation. These studies identify gain of MEKK3 signaling and KLF2/4 function as causal mechanisms for CCM pathogenesis that may be targeted to develop new CCM therapeutics

Roles of CCM-MEKK3 signaling in cardiac development and CCM disease

Cerebral cavernous malformations are relatively common vascular malformations. This disease is caused by loss-of-function mutations of KRIT1 (CCM1), CCM2 and PDCD10 (CCM3), which encode the three CCM proteins. These three CCM proteins form an intracellular adaptor protein complex and are required by endothelial cells for vascular development during embryogenesis and preventing the formation of CCM lesions after birth. However, roles of CCM signaling in the developing heart and the molecular mechanism underneath the pathogenesis of CCMs are not known. By applying a combination of mutant zebrafish and mouse models, morpholino gene knockdown in zebrafish, and cell culture, we determined roles of CCM signaling in both cardiac development and CCM formation. Our experiments reveal that loss of CCM signaling in endocardial cells results in mid-gestation heart failure due to premature degradation of cardiac jelly. Loss of CCM signaling dramatically increases endocardial expression of Klf2 and Klf4 transcription factors and the Adamts4 and Adamts5 metalloproteinases that degrade cardiac jelly. These changes in gene expression result from increased activity of MEKK3, a mitogen-activated protein kinase that binds CCM2 in endothelial cells. MEKK3 is both necessary and sufficient for expression of these genes, and partial loss of MEKK3 rescues cardiac defects in CCM-deficient embryos. These findings reveal that CCM signaling controls endothelial gene expression by repressing MEKK3 activity during cardiovascular development. Using a neonatal mouse model of CCM disease, we show that expression of the MEKK3 target genes Klf2 and Klf4, as well as Rho and ADAMTS protease activity, are increased in the endothelial cells of early CCM lesions. Endothelial-specific loss of Map3k3 (also known as Mekk3), Klf2 or Klf4 markedly prevents lesion formation, reverses the increase in Rho activity, and rescues lethality. Consistent with these findings in mice, we show that endothelial expression of KLF2 and KLF4 is increased in human familial and sporadic CCM lesions, and that a disease-causing human CCM2 mutation abrogates the MEKK3 interaction without affecting CCM complex formation. These studies identify gain of MEKK3 signaling and KLF2/4 function as causal mechanisms for CCM pathogenesis that may be targeted to develop new CCM therapeutics

A multi-band centroid contrastive reconstruction fusion network for motor imagery electroencephalogram signal decoding

Motor imagery (MI) brain-computer interface (BCI) assist users in establishing direct communication between their brain and external devices by decoding the movement intention of human electroencephalogram (EEG) signals. However, cerebral cortical potentials are highly rhythmic and sub-band features, different experimental situations and subjects have different categories of semantic information in specific sample target spaces. Feature fusion can lead to more discriminative features, but simple fusion of features from different embedding spaces leading to the model global loss is not easily convergent and ignores the complementarity of features. Considering the similarity and category contribution of different sub-band features, we propose a multi-band centroid contrastive reconstruction fusion network (MB-CCRF). We obtain multi-band spatio-temporal features by frequency division, preserving the task-related rhythmic features of different EEG signals; use a multi-stream cross-layer connected convolutional network to perform a deep feature representation for each sub-band separately; propose a centroid contrastive reconstruction fusion module, which maps different sub-band and category features into the same shared embedding space by comparing with category prototypes, reconstructing the feature semantic structure to ensure that the global loss of the fused features converges more easily. Finally, we use a learning mechanism to model the similarity between channel features and use it as the weight of fused sub-band features, thus enhancing the more discriminative features, suppressing the useless features. The experimental accuracy is 79.96% in the BCI competition Ⅳ-Ⅱa dataset. Moreover, the classification effect of sub-band features of different subjects is verified by comparison tests, the category propensity of different sub-band features is verified by confusion matrix tests and the distribution in different classes of each sub-band feature and fused feature are showed by visual analysis, revealing the importance of different sub-band features for the EEG-based MI classification task

Effect of Vertical Metal Plate on Transfer Efficiency of the Wireless Power Transfer System

Power transfer efficiency is an important issue in wireless power transfer (WPT). In actual applications, the WPT system may be exposed to a complex electromagnetic environment. The metal which is inevitably or accidentally close to the system will impact the power transfer efficiency. Most previous research has aimed at the effect of the metallic sheet paralleled to the resonant coil. This paper focuses on the effect of the metallic plate perpendicular to the resonant coils. Firstly, based on the theoretical analysis, a simulation model is setup using COMSOL Multiphysics. The efficiencies of the double-coils magnetic resonant WPT system with the presence of the parallel and vertical aluminum plate are studied comparatively. Efficiency improvement is observed with the vertical plate while the reduction appeared with the presence of the parallel plate. The vertical metallic plate has shown a magnetic field shielding effect according to the magnetic field distribution. It can reduce the radial magnetic field and enhance the axial magnetic field. Then, the effects of the position and size of the vertical plate are studied. It is found that the transfer efficiency has a preferable improvement when the vertical aluminum plate with a larger size is placed between the resonant coils and near outer edge of the windings. Finally, the experiment is carried out to verify the effect of the vertical aluminum plate on the WPT system

China nationwide landscape of 16 types inherited metabolic disorders: a retrospective analysis on 372,255 clinical cases

Abstract Background Inherited metabolic disorders (IMDs) usually occurs at young age and hence it severely threatening the health and life of young people. While so far there lacks a comprehensive study which can reveals China’s nationwide landscape of IMDs. This study aimed to evaluate IMDs incidence and regional distributions in China at a national and province level to guide clinicians and policy makers. Methods The retrospective study conducted from January 2012 to March 2021, we analyzed and characterized 372255 cases’ clinical test information and diagnostic data from KingMed Diagnostics Laboratory. The samples were from 32 provincial regions of China, the urine organic acids were detected by gas chromatography-mass spectrometry (GC–MS), amino acids and acylcarnitines in dried blood spots were detected by liquid chromatography-tandem mass spectrometry (LC–MS/MS). We did a statistical analysis of the distribution of the 16 most common IMDs in amino acid disorders and organic acidemias, and then paid special attention to analyze the age and regional distributions of different IMDs. The statistical analyses and visualization analysis were performed with the programming language R (version 4.2.1). Results There were 4911 positive cases diagnosed, which was 1.32% of the total sample during the ten-year study period. Most diseases tended to occur at ages younger than 18 year-old. The Ornithine Transcarbamylase Deficiency tended to progress on male infants who were less than 28 days old. While the peak of the positive case number of Citrin Deficiency disease (CD) was at 1–6 months. Different IMDs’ had different distribution patterns in China’s provinces. Methylmalonic Acidemias and Hyperphenylalaninemia had an imbalanced distribution pattern in China and its positive rate was significantly higher in North China than South China. Conversely, the positive rate of CD was significantly higher in South China than North China. Conclusions Results of this work, such as the differences in distribution pattern of different diseases in terms of age, region, etc. provide important insights and references for clinicians, researchers and healthcare policy makers. The policy makers could optimize the better health screening programs for covering children and infants in specific ages and regions based on our findings