Block Edit Errors with Transpositions: Deterministic Document Exchange Protocols and Almost Optimal Binary Codes

Document exchange and error correcting codes are two fundamental problems regarding communications. In the first problem, Alice and Bob each holds a string, and the goal is for Alice to send a short sketch to Bob, so that Bob can recover Alice\u27s string. In the second problem, Alice sends a message with some redundant information to Bob through a channel that can add adversarial errors, and the goal is for Bob to correctly recover the message despite the errors. In both problems, an upper bound is placed on the number of errors between the two strings or that the channel can add, and a major goal is to minimize the size of the sketch or the redundant information. In this paper we focus on deterministic document exchange protocols and binary error correcting codes. Both problems have been studied extensively. In the case of Hamming errors (i.e., bit substitutions) and bit erasures, we have explicit constructions with asymptotically optimal parameters. However, other error types are still rather poorly understood. In a recent work [Kuan Cheng et al., 2018], the authors constructed explicit deterministic document exchange protocols and binary error correcting codes for edit errors with almost optimal parameters. Unfortunately, the constructions in [Kuan Cheng et al., 2018] do not work for other common errors such as block transpositions. In this paper, we generalize the constructions in [Kuan Cheng et al., 2018] to handle a much larger class of errors. These include bursts of insertions and deletions, as well as block transpositions. Specifically, we consider document exchange and error correcting codes where the total number of block insertions, block deletions, and block transpositions is at most k <= alpha n/log n for some constant 0<alpha<1. In addition, the total number of bits inserted and deleted by the first two kinds of operations is at most t <= beta n for some constant 0<beta<1, where n is the length of Alice\u27s string or message. We construct explicit, deterministic document exchange protocols with sketch size O((k log n +t) log^2 n/{k log n + t}) and explicit binary error correcting code with O(k log n log log log n+t) redundant bits. As a comparison, the information-theoretic optimum for both problems is Theta(k log n+t). As far as we know, previously there are no known explicit deterministic document exchange protocols in this case, and the best known binary code needs Omega(n) redundant bits even to correct just one block transposition [L. J. Schulman and D. Zuckerman, 1999]

Sediment transport following water transfer from Yangtze River to Taihu Basin

AbstractTo meet the increasing need of fresh water and to improve the water quality of Taihu Lake, water transfer from the Yangtze River was initiated in 2002. This study was performed to investigate the sediment distribution along the river course following water transfer. A rainfall-runoff model was first built to calculate the runoff of the Taihu Basin in 2003. Then, the flow patterns of river networks were simulated using a one-dimensional river network hydrodynamic model. Based on the boundary conditions of the flow in tributaries of the Wangyu River and the water level in Taihu Lake, a one-dimensional hydrodynamic and sediment transport numerical model of the Wangyu River was built to analyze the influences of the inflow rate of the water transfer and the suspended sediment concentration (SSC) of inflow on the sediment transport. The results show that the water transfer inflow rate and SSC of inflow have significant effects on the sediment distribution. The higher the inflow rate or SSC of inflow is, the higher the SSC value is at certain cross-sections along the river course of water transfer. Higher inflow rate and SSC of inflow contribute to higher sediment deposition per kilometer and sediment thickness. It is also concluded that a sharp decrease of the inflow velocity at the entrance of the Wangyu River on the river course of water transfer induces intense sedimentation at the cross-section near the Changshu hydro-junction. With an increasing distance from the Changshu hydro-junction, the sediment deposition and sedimentation thickness decrease gradually along the river course

Modulating Microglia/Macrophage Activation by CDNF Promotes Transplantation of Fetal Ventral Mesencephalic Graft Survival and Function in a Hemiparkinsonian Rat Model

Parkinson's disease (PD) is characterized by the loss of dopaminergic neurons in substantia nigra pars compacta, which leads to the motor control deficits. Recently, cell transplantation is a cutting-edge technique for the therapy of PD. Nevertheless, one key bottleneck to realizing such potential is allogenic immune reaction of tissue grafts by recipients. Cerebral dopamine neurotrophic factor (CDNF) was shown to possess immune-modulatory properties that benefit neurodegenerative diseases. We hypothesized that co-administration of CDNF with fetal ventral mesencephalic (VM) tissue can improve the success of VM replacement therapies by attenuating immune responses. Hemiparkinsonian rats were generated by injecting 6-hydroxydopamine (6-OHDA) into the right medial forebrain bundle of Sprague Dawley (SD) rats. The rats were then intrastriatally transplanted with VM tissue from rats, with/without CDNF administration. Recovery of dopaminergic function and survival of the grafts were evaluated using the apomorphine-induced rotation test and smallanimal positron emission tomography (PET) coupled with [F-18] DOPA or [F-18] FE-PE2I, respectively. In addition, transplantation-related inflammatory response was determined by uptake of [F-18] FEPPA in the grafted side of striatum. Immunohistochemistry (IHC) examination was used to determine the survival of the grated dopaminergic neurons in the striatum and to investigate immune-modulatory effects of CDNF. The modulation of inflammatory responses caused by CDNF might involve enhancing M2 subset polarization and increasing fractal dimensions of 6-OHDA-treated BV2 microglial cell line. Analysis of CDNF-induced changes to gene expressions of 6-OHDA-stimulated BV2 cells implies that these alternations of the biomarkers and microglial morphology are implicated in the upregulation of protein kinase B signaling as well as regulation of catalytic, transferase, and protein serine/threonine kinase activity. The effects of CDNF on 6-OHDA-induced alternation of the canonical pathway in BV2 microglial cells is highly associated with PI3K-mediated phagosome formation. Our results are the first to show that CDNF administration enhances the survival of the grafted dopaminergic neurons and improves functional recovery in PD animal model. Modulation of the polarization, morphological characteristics, and transcriptional profiles of 6-OHDA-stimualted microglia by CDNF may possess these properties in transplantation-based regenerative therapies.Peer reviewe

Modulating Microglia/Macrophage Activation by CDNF Promotes Transplantation of Fetal Ventral Mesencephalic Graft Survival and Function in a Hemiparkinsonian Rat Model

Parkinson’s disease (PD) is characterized by the loss of dopaminergic neurons in substantia nigra pars compacta, which leads to the motor control deficits. Recently, cell transplantation is a cutting-edge technique for the therapy of PD. Nevertheless, one key bottleneck to realizing such potential is allogenic immune reaction of tissue grafts by recipients. Cerebral dopamine neurotrophic factor (CDNF) was shown to possess immune-modulatory properties that benefit neurodegenerative diseases. We hypothesized that co-administration of CDNF with fetal ventral mesencephalic (VM) tissue can improve the success of VM replacement therapies by attenuating immune responses. Hemiparkinsonian rats were generated by injecting 6-hydroxydopamine (6-OHDA) into the right medial forebrain bundle of Sprague Dawley (SD) rats. The rats were then intrastriatally transplanted with VM tissue from rats, with/without CDNF administration. Recovery of dopaminergic function and survival of the grafts were evaluated using the apomorphine-induced rotation test and small-animal positron emission tomography (PET) coupled with [18F] DOPA or [18F] FE-PE2I, respectively. In addition, transplantation-related inflammatory response was determined by uptake of [18F] FEPPA in the grafted side of striatum. Immunohistochemistry (IHC) examination was used to determine the survival of the grated dopaminergic neurons in the striatum and to investigate immune-modulatory effects of CDNF. The modulation of inflammatory responses caused by CDNF might involve enhancing M2 subset polarization and increasing fractal dimensions of 6-OHDA-treated BV2 microglial cell line. Analysis of CDNF-induced changes to gene expressions of 6-OHDA-stimulated BV2 cells implies that these alternations of the biomarkers and microglial morphology are implicated in the upregulation of protein kinase B signaling as well as regulation of catalytic, transferase, and protein serine/threonine kinase activity. The effects of CDNF on 6-OHDA-induced alternation of the canonical pathway in BV2 microglial cells is highly associated with PI3K-mediated phagosome formation. Our results are the first to show that CDNF administration enhances the survival of the grafted dopaminergic neurons and improves functional recovery in PD animal model. Modulation of the polarization, morphological characteristics, and transcriptional profiles of 6-OHDA-stimualted microglia by CDNF may possess these properties in transplantation-based regenerative therapies

Distributed Training Large-Scale Deep Architectures

Scale of data and scale of computation infrastructures together enable the current deep learning renaissance. However, training large-scale deep architectures demands both algorithmic improvement and careful system configuration. In this paper, we focus on employing the system approach to speed up large-scale training. Via lessons learned from our routine benchmarking effort, we first identify bottlenecks and overheads that hinter data parallelism. We then devise guidelines that help practitioners to configure an effective system and fine-tune parameters to achieve desired speedup. Specifically, we develop a procedure for setting minibatch size and choosing computation algorithms. We also derive lemmas for determining the quantity of key components such as the number of GPUs and parameter servers. Experiments and examples show that these guidelines help effectively speed up large-scale deep learning training

Promoter Polymorphism G-6A, which Modulates Angiotensinogen Gene Expression, Is Associated with Non-Familial Sick Sinus Syndrome

Background: It is well known that familial sick sinus syndrome (SSS) is caused by functional alterations of ion channels and gap junction. Limited information is available on the mechanism of age-related non-familial SSS. Although evidence shows a close link between arrhythmia and the renin-angiotensin system (RAS), it remains to be determined whether the RAS is involved in the pathogenesis of non-familial SSS. Methods: In this study, 113 patients with documented non-familial SSS and 125 controls were screened for angiotensinogen (AGT) and gap junction protein-connexin 40 (Cx40) promoter polymorphisms by gene sequencing, followed by an association study. A luciferase assay was used to determine the transcriptional activity of the promoter polymorphism. The interaction between nuclear factors and the promoter polymorphism was characterized by an electrophoretic mobility shift assay (EMSA). Results: Association study showed the Cx40 -44/+71 polymorphisms are not associated with non-familial SSS; however, it indicated that four polymorphic sites at positions -6, -20, -152, and -217 in the AGT promoter are linked to non-familial SSS. Compared to controls, SSS patients had a lower frequency of the G-6A AA genotype (OR 2.88, 95% CI 1.58–5.22, P = 0.001) and a higher frequency of the G allele at -6 position (OR 2.65, 95% CI 1.54–4.57, P = 0.0003). EMSA and luciferase assays confirmed that nucleotide G at position -6 modulates the binding affinity with nuclear factors and yields a lower transcriptional activity than nucleotide A (P,0.01). Conclusion: G-6A polymorphism, which modulates the transcriptional activity of the AGT promoter, may contribute to nonfamilial SSS susceptibility