Formation Control for Unmanned Aerial Vehicles with Directed and Switching Topologies

Formation control problems for unmanned aerial vehicle (UAV) swarm systems with directed and switching topologies are investigated. A general formation control protocol is proposed firstly. Then, by variable transformation, the formation problem is transformed into a consensus problem, which can be solved by a novel matrix decomposition method. Sufficient conditions to achieve formation with directed and switching topologies are provided and an explicit expression of the formation reference function is given. Furthermore, an algorithm to design the gain matrices of the protocol is presented. Finally, numerical simulations are provided to illustrate the effectiveness of the theoretical results

Structural basis for the specificity of renin-mediated angiotensinogen cleavage.

The renin-angiotensin cascade is a hormone system that regulates blood pressure and fluid balance. Renin-mediated cleavage of the angiotensin I peptide from the N terminus of angiotensinogen (AGT) is the rate-limiting step of this cascade; however, the detailed molecular mechanism underlying this step is unclear. Here, we solved the crystal structures of glycosylated human AGT (2.30 Å resolution), its encounter complex with renin (2.55 Å), AGT cleaved in its reactive center loop (RCL; 2.97 Å), and spent AGT from which the N-terminal angiotensin peptide was removed (2.63 Å). These structures revealed that AGT undergoes profound conformational changes and binds renin through a tail-into-mouth allosteric mechanism that inserts the N terminus into a pocket equivalent to a hormone-binding site on other serpins. These changes fully extended the N-terminal tail, with the scissile bond for angiotensin release docked in renin's active site. Insertion of the N terminus into this pocket accompanied a complete unwinding of helix H of AGT, which, in turn, formed key interactions with renin in the complementary binding interface. Mutagenesis and kinetic analyses confirmed that renin-mediated production of angiotensin I is controlled by interactions of amino acid residues and glycan components outside renin's active-site cleft. Our findings indicate that AGT adapts unique serpin features for hormone delivery and binds renin through concerted movements in the N-terminal tail and in its main body to modulate angiotensin release. These insights provide a structural basis for the development of agents that attenuate angiotensin release by targeting AGT's hormone binding pocket

The advantage of point-of-care ultrasound in central venous catheterization and related pericardial effusion in infants in the NICU

BackgroundCentral venous catheterization (CVC) is broadly used in neonatal intensive care units (NICUs) for efficient vascular access; however, its establishment and maintenance are associated with numerous risks and complications. Here, we focus on investigating the value of point-of-care ultrasound (POCUS) in the early diagnosis and treatment of pericardial effusion associated with CVC and compare the differences in ultrasound and radiography in CVC localization and monitoring in the NICU.MethodsTwenty-five infants with CVC-associated pericardial effusion (PCE) who were hospitalized in the NICU of Peking University Third Hospital between January 2013 and March 2023 were retrospectively selected for the study. Data concerning their catheterization characteristics, CVC tip position, clinical and imaging manifestations of PCE, treatments, and prognoses were analyzed.ResultsThe mean gestational age of our cohort was 29.3 ± 3.1 weeks, and the mean birth weight was 1,211 ± 237 g. The incidence of CVC-associated PCE was 0.65%, and 80% of PCE cases occurred within 4 days of CVC. After PCE, the most common symptoms were tachypnea (44%) and tachycardia (64%). Chest radiographs revealed cardiothoracic enlargement, and only 2 cases (9.10%) showed a “flask heart”. Cardiac ultrasound showed that the catheter tip extended deep into the heart in 72% of infants with PCE. Cardiac insufficiency was observed in 12 cases (48%). Overall, 8 infants (32%) had pericardial tamponade, 7 (87.5%) of whom underwent pericardiocentesis. Overall, 2 (8%) infants died, and the remaining 23 (92%) were cured.ConclusionCVC-associated PCE mostly occurs in the early post-catheterization stages (within 4 days) in infants. Some cases may have critical clinical manifestations and progress rapidly, with some even developing pericardial tamponade. A CVC tip being deep into the heart cavity is an important cause of PCE. Compared with chest radiography, point-of-care ultrasound is more accurate for CVC tip positioning and can detect PCE more quickly. Furthermore, it is more advantageous for locating and monitoring CVC-associated PCE. Early identification and diagnosis can effectively reduce fatality rates and improve the prognosis of infants with CVC-associated PCE

Unstructured regions in IRE1α specify BiP-mediated destabilisation of the luminal domain dimer and repression of the UPR

Funder: Medical Research Council; FundRef: http://dx.doi.org/10.13039/501100000265Funder: European Molecular Biology Organization; FundRef: http://dx.doi.org/10.13039/100004410Coupling of endoplasmic reticulum (ER) stress to dimerisation-dependent activation of the UPR transducer IRE1 is incompletely understood. Whilst the luminal co-chaperone ERdj4 promotes a complex between the Hsp70 BiP and IRE1’s stress-sensing luminal domain (IRE1LD) that favours the latter’s monomeric inactive state and loss of ERdj4 de-represses IRE1, evidence linking these cellular and in vitro observations is presently lacking. We report that enforced loading of endogenous BiP onto endogenous IRE1α repressed UPR signalling in CHO cells and deletions in the IRE1α locus that de-repressed the UPR in cells, encode flexible regions of IRE1LD that mediated BiP-induced monomerisation in vitro. Changes in the hydrogen exchange mass spectrometry profile of IRE1LD induced by ERdj4 and BiP confirmed monomerisation and were consistent with active destabilisation of the IRE1LD dimer. Together, these observations support a competition model whereby waning ER stress passively partitions ERdj4 and BiP to IRE1LD to initiate active repression of UPR signalling

Unstructured regions in IRE1α specify BiP-mediated destabilisation of the luminal domain dimer and repression of the UPR

Coupling of endoplasmic reticulum stress to dimerisation‑dependent activation of the UPR transducer IRE1 is incompletely understood. Whilst the luminal co-chaperone ERdj4 promotes a complex between the Hsp70 BiP and IRE1's stress-sensing luminal domain (IRE1LD) that favours the latter's monomeric inactive state and loss of ERdj4 de-represses IRE1, evidence linking these cellular and in vitro observations is presently lacking. We report that enforced loading of endogenous BiP onto endogenous IRE1α repressed UPR signalling in CHO cells and deletions in the IRE1α locus that de-repressed the UPR in cells, encode flexible regions of IRE1LD that mediated BiP‑induced monomerisation in vitro. Changes in the hydrogen exchange mass spectrometry profile of IRE1LD induced by ERdj4 and BiP confirmed monomerisation and were consistent with active destabilisation of the IRE1LD dimer. Together, these observations support a competition model whereby waning ER stress passively partitions ERdj4 and BiP to IRE1LD to initiate active repression of UPR signalling

Aero-Engine Fault Diagnosis Using Improved Local Discriminant Bases and Support Vector Machine

This paper presents an effective approach for aero-engine fault diagnosis with focus on rub-impact, through combination of improved local discriminant bases (LDB) with support vector machine (SVM). The improved LDB algorithm, using both the normalized energy difference and the relative entropy as quantification measures, is applied to choose the optimal set of orthogonal subspaces for wavelet packet transform- (WPT-) based signal decomposition. Then two optimal sets of orthogonal subspaces have been obtained and the energy features extracted from those subspaces appearing in both sets will be selected as input to a SVM classifier to diagnose aero-engine faults. Experiment studies conducted on an aero-engine rub-impact test system have verified the effectiveness of the proposed approach for classifying working conditions of aero-engines

Nonstationary seismic response analysis of long-span structures by frequency domain method considering wave passage effect

In this paper, a frequency domain method is proposed for the nonstationary seismic analysis of long-span structures subjected to random ground motions considering the wave passage effect. Based on the correlation analysis theory and fast Fourier transform (FFT), a semi-analytical solution is derived for the evolutionary power spectral density of the random response of long-span structures in the frequency domain. The expression of this solution indicates that the evolutionary property of nonstationary random responses can be determined completely by the modulation function of random ground motions, and hence the solution has clear physical interpretations. For slowly varying modulation functions, the FFT can be implemented with a small sampling frequency, so the present method is very efficient within a given accuracy. In numerical examples, nonstationary random responses of a long-span cable stayed bridge to random ground motions with the wave passage effect are studied by the present method, and comparisons are made with those of the pseudo excitation method (PEM) to verify the present method. Then the accuracy and efficiency of the present method with different sampling frequencies are compared and discussed. Finally, the influences of the apparent velocity of the seismic waves on nonstationary random responses are investigated

Measurement of the total angiotensinogen and its reduced and oxidised forms in human plasma using targeted LC-MS/MS.

Angiotensinogen (AGT) is a critical protein in the renin-angiotensin-aldosterone system and may have an important role in the pathogenesis of pre-eclampsia. The disulphide linkage between cysteines 18 and 138 has a key role in the redox switch of AGT which modulates the release of angiotensin I with consequential effects on blood pressure. In this paper, we report a quantitative targeted LC-MS/MS method for the reliable measurement of the total AGT and its reduced and oxidised forms in human plasma. AGT was selectively enriched from human plasma using two-dimensional chromatography employing concanavalin A lectin affinity and reversed phase steps and then deglycosylated using PNGase F. A differential alkylation approach was coupled with targeted LC-MS/MS method to identify the two AGT forms in the plasma chymotryptic digest. An additional AGT proteolytic marker peptide was identified and used to measure total AGT levels. The developed MS workflow enabled the reproducible detection of total AGT and its two distinct forms in human plasma with analytical precision of ≤ 15%. The LC-MS/MS assay for total AGT in plasma showed a linear response (R2 = 0.992) with a limit of quantification in the low nanomolar range. The method gave suitable validation characteristics for biomedical application to the quantification of the oxidation level and the total level of AGT in plasma samples collected from normal and pre-eclamptic patients

MANF antagonizes nucleotide exchange by the endoplasmic reticulum chaperone BiP

Despite its known role as a secreted neuroprotectant, much of the mesencephalic astrocyte-derived neurotrophic factor (MANF) is retained in the endoplasmic reticulum (ER) of producer cells. There, by unknown mechanisms, MANF plays a role in protein folding homeostasis in complex with the ER-localized Hsp70 chaperone BiP. Here we report that the SAF-A/B, Acinus, and PIAS (SAP) domain of MANF selectively associates with the nucleotide binding domain (NBD) of ADP-bound BiP. In crystal structures the SAP domain engages the cleft between NBD subdomains Ia and IIa, stabilizing the ADP-bound conformation and clashing with the interdomain linker that occupies this site in ATP-bound BiP. MANF inhibits both ADP release from BiP and ATP rebinding to BiP, and thereby client release. Cells lacking MANF have fewer ER stress-induced BiP-containing high molecular weight complexes. These findings suggest that MANF contributes to protein folding homeostasis as a nucleotide exchange inhibitor that stabilizes certain BiP-client complexes.Wellcome Trust 200848/Z/16/