Sensing-Aided Scalable Peer-to-Peer Millimeter-Wave Communication

One of the bottlenecks of modern communication is to enable sensing and communication simultaneously with causing scheduling conflicts, and how sensing may be leveraged to help directional communication accuracy. To this end, we propose and implement a novel peer-to-peer mmWave communication system to achieve joint beamforming and sensing. A radar and IMU assisted tracking and beamforming algorithm is designed and tested and the results show robust tracking capacity with an overall higher throughtput obtained. The results demonstrated promising future extensions where with refinements the design and implementation can be deployed in a more scalable manner

Precheck Sequence Based False Base Station Detection During Handover: A Physical Layer Based Security Scheme

False Base Station (FBS) attack has been a severe security problem for the cellular network since 2G era. During handover, the user equipment (UE) periodically receives state information from surrounding base stations (BSs) and uploads it to the source BS. The source BS compares the uploaded signal power and shifts UE to another BS that can provide the strongest signal. An FBS can transmit signal with the proper power and attract UE to connect to it. In this paper, based on the 3GPP standard, a Precheck Sequence-based Detection (PSD) Scheme is proposed to secure the transition of legal base station (LBS) for UE. This scheme first analyzes the structure of received signals in blocks and symbols. Several additional symbols are added to the current signal sequence for verification. By designing a long table of symbol sequence, every UE which needs handover will be allocated a specific sequence from this table. The simulation results show that the performance of this PSD Scheme is better than that of any existing ones, even when a specific transmit power is designed for FBS

The poly(ADP-ribosyl)ation of BRD4 mediated by PARP1 promoted pathological cardiac hypertrophy

The bromodomain and extraterminal (BET) family member BRD4 is pivotal in the pathogenesis of cardiac hypertrophy. BRD4 induces hypertrophic gene expression by binding to the acetylated chromatin, facilitating the phosphorylation of RNA polymerases II (Pol II) and leading to transcription elongation. The present study identified a novel post-translational modification of BRD4: poly(ADP-ribosyl)ation (PARylation), that was mediated by poly(ADP-ribose)polymerase-1 (PARP1) in cardiac hypertrophy. BRD4 silencing or BET inhibitors JQ1 and MS417 prevented cardiac hypertrophic responses induced by isoproterenol (ISO), whereas overexpression of BRD4 promoted cardiac hypertrophy, confirming the critical role of BRD4 in pathological cardiac hypertrophy. PARP1 was activated in ISO-induced cardiac hypertrophy and facilitated the development of cardiac hypertrophy. BRD4 was involved in the prohypertrophic effect of PARP1, as implied by the observations that BRD4 inhibition or silencing reversed PARP1-induced hypertrophic responses, and that BRD4 overexpression suppressed the anti-hypertrophic effect of PARP1 inhibitors. Interactions of BRD4 and PARP1 were observed by co-immunoprecipitation and immunofluorescence. PARylation of BRD4 induced by PARP1 was investigated by PARylation assays. In response to hypertrophic stimuli like ISO, PARylation level of BRD4 was elevated, along with enhanced interactions between BRD4 and PARP1. By investigating the PARylation of truncation mutants of BRD4, the C-terminal domain (CTD) was identified as the PARylation modification sites of BRD4. PARylation of BRD4 facilitated its binding to the transcription start sites (TSS) of hypertrophic genes, resulting in enhanced phosphorylation of RNA Pol II and transcription activation of hypertrophic genes. The present findings suggest that strategies targeting inhibition of PARP1-BRD4 might have therapeutic potential for pathological cardiac hypertrophy

The treatment effect of posterior lumbar fusion surgery on patients suffering from lumbar disc herniation concurrent with peroneal nerve paralysis

PurposeThe purpose of this study is to investigate the clinical effect of posterior lumbar fusion surgery on patients who suffer from lumbar disc herniation concurrent with peroneal nerve paralysis.MethodsThe patients suffering from peroneal nerve paralysis and undergoing posterior lumbar fusion surgery between January 2012 and December 2019 were retrospectively reviewed. The data of the identified patients were then collected and processed. All patients were followed up post-operatively after discharge from the hospital. The data was analyzed in terms of Oswestry disability index (ODI), visual analogue scale (VAS) score, and relative lower-limb muscle strength.ResultsA total of 87 patients (52 males and 35 females) aged 54 ± 11 years met the inclusion criteria for this study. These patients stayed in hospital for 16 ± 6 days and were followed up for 81 ± 24 months. Data analysis showed that muscle strength of the tibialis anterior and extensor digitorum significantly recovered at the last follow-up with a grade of 3 (median), compared to grade 0 at admission (p < 0.001). Furthermore, the median VAS score decreased to 1 at the last follow-up from 6 at admission (p < 0.001), and the ODI greatly improved with 10% (median) at the last follow-up, while it was 58% at admission (p < 0.001). The ODI improvement rate was 60% on average at the last follow-up. Multivariate regression analysis regarding the ODI and muscle strength improvement rates showed that advanced age was a risk factor for postoperative recovery.ConclusionsMost of the patients suffering from lumbar disc herniation concurrent with peroneal nerve paralysis can improve after undergoing posterior lumbar fusion surgery, but few can reach full recovery. Advanced age might be a risk factor that affects the prognosis of these patients after surgery

Altered Synaptic Vesicle Release and Ca2+ Influx at Single Presynaptic Terminals of Cortical Neurons in a Knock-in Mouse Model of Huntington’s Disease

Huntington’s disease (HD) is an inherited neurodegenerative disorder caused by the abnormal expansion of CAG repeats in the huntingtin (HTT) gene, which leads to progressive loss of neurons starting in the striatum and cortex. One possible mechanism for this selective loss of neurons in the early stage of HD is altered neurotransmission at synapses. Despite the recent finding that presynaptic terminals play an important role in HD, neurotransmitter release at synapses in HD remains poorly understood. Here, we measured synaptic vesicle release in real time at single presynaptic terminals during electrical field stimulation. We found the increase in synaptic vesicle release at presynaptic terminals in primary cortical neurons in a knock-in mouse model of HD (zQ175). We also found the increase in Ca2+ influx at presynaptic terminals in HD neurons during the electrical stimulation. Consistent with increased Ca2+-dependent neurotransmission in HD neurons, the increase in vesicle release and Ca2+ influx was rescued with Ca2+ chelators or by blocking N-type voltage-gated Ca2+ channels, suggesting N-type voltage-gated Ca2+ channels play an important role in HD. Taken together, our results suggest that the increased synaptic vesicles release due to increased Ca2+ influx at presynaptic terminals in cortical neurons contributes to the selective neurodegeneration of these neurons in early HD and provide a possible therapeutic target

FI-CEUS: a solution to improve the diagnostic accuracy in MRI LI-RADS-indeterminate (LR-3/4) FLLs at risk for HCC

ObjectiveTo evaluate the diagnostic accuracy of fusion imaging contrast-enhanced ultrasound (FI-CEUS) of magnetic resonance imaging (MRI) LI-RADS-indeterminate (LR-3/4) and conventional ultrasound undetected focal liver lesions (FLLs) in patients at risk for hepatocellular carcinoma (HCC).MethodsBetween February 2020 and July 2021, 71 FLLs in 63 patients were registered for diagnostic performance evaluation respectively for ultrasound-guided thermal ablation evaluation in this retrospective study. Diagnostic performance regarding FLLs was compared between FI-CEUS and contrast-enhanced MRI (CE-MRI).ResultsFor diagnostic performance evaluation, among 71 lesions in 63 patients, the diagnostic efficacy of FI-CEUS with LI-RADS was significantly higher than that of CE-MRI (P < 0.05) in both overall and hierarchical comparison (except for the group with lesion diameter ≥2 cm). For malignant lesions, the proportion of arterial phase hyperenhancement (APHE) and washout on FI-CEUS was higher than that on CE-MRI (P < 0.05).ConclusionFI-CEUS has a high value in the precise qualitative diagnosis of small FLLs (<2 cm) of MRI LI-RADS-indeterminate diagnosis (LR-3/4) that are undetected by conventional ultrasound in patients at risk for HCC and can be a good supplementary CE-MRI diagnostic method for thermal ablation evaluation

Altered Brain Structure and Functional Connectivity of Primary Visual Cortex in Optic Neuritis

Previous studies have revealed brain adaptations to injury that occurs in optic neuritis (ON); however, the mechanisms underlying the functional connectivity (FC) and gray matter volume (GMV) changes in ON have not been clarified. Here, 51 single attack ON patients and 45 recurrent attacks ON patients were examined using structural MRI and resting-state functional MRI (RS-fMRI), and compared to 49 age- and gender-matched healthy controls (HC). FC analysis with a seed in primary visual cortex (V1 area) was used to assess the differences among three groups. Whole brain GMV was assessed using voxel-based morphometry (VBM). Correlation analyses were performed between FC results, structural MRI and clinical variables. We found positive correlations between the Paced Auditory Serial Addition Test (PASAT) score and FC in V1 area with bilateral middle frontal gyrus. Disease duration is significantly negatively related to FC in V1 area with the left inferior parietal lobule. Compared to the HC, single attack ON patients were found to have decreased FC values in the frontal, temporal lobes, right inferior occipital gyrus, right insula, right inferior parietal lobule, and significant increased FC values in the left thalamus. Recurrent attacks ON patients had the same pattern with single attack ON. No significant differences were found in brain GMV among three groups. This study provides the imaging evidence that impairment and compensation of V1 area connectivity coexist in ON patients, and provides important insights into the underlying neural mechanisms of ON

Direct Gene Transfer with IP-10 Mutant Ameliorates Mouse CVB3-Induced Myocarditis by Blunting Th1 Immune Responses

Background: Myocarditis is an inflammation of the myocardium that often follows the enterovirus infections, with coxsackievirus B3 (CVB3) being the most dominant etiologic agent. We and other groups previously reported that chemokine IP-10 was significantly induced in the heart tissue of CVB3-infected mice and contributed to the migration of massive inflammatory cells into the myocardium, which represents one of the most important mechanisms of viral myocarditis. To evaluate the direct effect of IP-10 on the inflammatory responses in CVB3 myocarditis, herein an IP-10 mutant deprived of chemo-attractant function was introduced into mice to antagonize the endogenous IP-10 activity, and its therapeutic effect on CVB3-induced myocarditis was evaluated. Methodology/Principal Findings: The depletion mutant pIP-10-AT, with an additional methionine after removal of the 5 N-terminal amino acids, was genetically constructed and intramuscularly injected into BALB/c mice after CVB3 infection. Compared with vector or no treatment, pIP-10-AT treatment had significantly reduced heart/body weight ratio and serum CK-MB level, increased survival rate and improved heart histopathology, suggesting an ameliorated myocarditis. This therapeutic effect was not attributable to an enhanced viral clearance, but to a blunted Th1 immune response, as evidenced by significantly decreased splenic CD4 + /CD8 + IFN-c + T cell percentages and reduced myocardial Th1 cytokine levels. Conclusion/Significance: Our findings constitute the first preclinical data indicating that interfering in vivo IP-10 activit