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1.
Pediatr Obes ; : e12628, 2020 Mar 06.
Artigo em Inglês | MEDLINE | ID: mdl-32141687

RESUMO

OBJECTIVES: To investigate the importance of time in pregnancy and neonatal sex on the association between maternal metabolic parameters and neonatal sum of skinfolds. METHODS: This was a longitudinal, secondary analysis of the vitamin D and lifestyle intervention for gestational diabetes mellitus study, conducted in nine European countries during 2012 to 2015. Pregnant women with a pre-pregnancy body mass index (BMI) of ≥29 kg/m2 were invited to participate. We measured 14 maternal metabolic parameters at three times during pregnancy: <20 weeks, 24 to 28 weeks, and 35 to 37 weeks of gestation. The sum of four skinfolds assessed within 2 days after birth was the measure of neonatal adiposity. RESULTS: In total, 458 mother-infant pairs (50.2% female infants) were included. Insulin resistance (fasting insulin and HOMA-index of insulin resistance) in early pregnancy was an important predictor for boys' sum of skinfolds, in addition to fasting glucose and maternal adiposity (leptin, BMI and neck circumference) throughout pregnancy. In girls, maternal lipids (triglycerides and fatty acids) in the first half of pregnancy were important predictors of sum of skinfolds, as well as fasting glucose in the second half of pregnancy. CONCLUSIONS: Associations between maternal metabolic parameters and neonatal adiposity vary between different periods during pregnancy. This time-dependency is different between sexes, suggesting different growth strategies.

2.
J Endocrinol ; 2020 Mar 01.
Artigo em Inglês | MEDLINE | ID: mdl-32171178

RESUMO

Gestational diabetes mellitus increases the risk of dysglycemia postpartum in part due to pancreatic ß-cell dysfunction. However, no histological evidence exists comparing endocrine pancreas after healthy and glucose intolerant pregnancies. This study sought to address this knowledge gap, in addition to exploring the contribution of an inflammatory environment to changes in endocrine pancreas after parturition. We used a previously established mouse model of gestational glucose intolerance induced by dietary low protein insult from conception until weaning. Pancreas and adipose samples were collected at 7, 30 and 90 days postpartum for histomorphometric and cytokine analyses, respectively. Glucose tolerance tests were performed prior to euthanasia and blood was collected via cardiac puncture. Pregnant female mice born to dams fed a low-protein diet previously shown to develop glucose intolerance at late gestation relative to controls continued to be glucose intolerant until 1 month postpartum. However, glucose tolerance normalized by 3 months postpartum. Glucose intolerance at 7 days postpartum was associated with lower beta- and alpha-cell fractional areas and higher adipose levels of proinflammatory cytokine, interleukin-6. By 3 months postpartum, a compensatory increase in the number of small islets and a higher insulin to glucagon ratio likely enabled euglycemia to be attained in the previously glucose intolerant mice. The results show that impairments in endocrine pancreas compensation in hyperglycemic pregnancy persist after parturition and contribute to prolonged glucose intolerance. These impairments may increase the susceptibility to development of future type 2 diabetes.

3.
IEEE Trans Cybern ; 2020 Jan 17.
Artigo em Inglês | MEDLINE | ID: mdl-31976924

RESUMO

In this article, we propose a learning-based fault diagnosis approach for a class of nonlinear sampled-data systems. First, the unmodeled sampled dynamics is acquired by the using deterministic learning method. The knowledge of the sampled dynamics of the normal and fault patterns is stored in the form of constant neural networks. Second, a fault detection scheme is designed in which memories of the learned knowledge can be recalled to give a rapid response to a fault. Third, analytical results concerning the fault detection condition and detection time are derived. It is shown that the mismatch function plays an important role in the performance properties of the diagnosis scheme. To analyze the effect of mismatch function on the residual, the concept of duty ratio is developed. Moreover, by comparing the constant neural networks of the normal and fault patterns, an extraction operator is designed to capture the feature of the mismatch function. By using this method, the performance of the diagnosis scheme can be improved. A simulation study is included to demonstrate the effectiveness of the approach.

4.
Clin Nutr ; 39(3): 976-984, 2020 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-31053513

RESUMO

BACKGROUND & AIMS: As vitamin D deficiency is associated with an increased risk of gestational diabetes mellitus (GDM), we aimed to test vitamin D supplementation as a strategy to reduce GDM risk (evaluated after fasting plasma glucose (FPG), insulin resistance and weight gain) in pregnant overweight/obese women. METHODS: The DALI vitamin D multicenter study enrolled women with prepregnancy body mass index (BMI) ≥ 29 kg/m2, ≤19 + 6 weeks of gestation and without GDM. Participants were randomized to receive 1600 IU/day vitamin D3 or placebo (each with or without lifestyle intervention) on top of (multi)vitamins supplements. Women were assessed for vitamin D status (sufficiency defined as serum 25-hydroxyvitamin D (25(OH)D) ≥ 50 nmol/l), FPG, insulin resistance and weight at baseline, 24-28 and 35-37 weeks. Linear or logistic regression analyses were performed to assess intervention effects. RESULTS: Average baseline serum 25(OH)D was ≥50 nmol/l across all study sites. In the vitamin D intervention arm (n = 79), 97% of participants achieved target serum vitamin 25(OH)D (≥50 nmol/l) at 24-28 weeks and 98% at 35-37 weeks vs 74% and 78% respectively in the placebo arm (n = 75, p < 0.001). A small but significantly lower FPG (-0.14 mmol/l; CI95 -0.28, -0.00) was observed at 35-37 weeks with the vitamin D intervention without any additional difference in metabolic status, perinatal outcomes or adverse event rates. CONCLUSION: In the DALI vitamin D trial, supplementation with 1600 IU vitamin D3/day achieved vitamin D sufficiency in virtually all pregnant women and a small effect in FPG at 35-37 weeks. The potential of vitamin D supplementation for GDM prevention in vitamin D sufficient populations appears to be limited. TRIAL REGISTRATION NUMBER: ISRCTN70595832.

5.
J Comp Neurol ; 528(1): 48-60, 2020 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-31265125

RESUMO

Large cerebral infarctions are major predictors of death and severe disability from stroke. Conversely, data concerning these types of infarctions and the affected adjacent brain circuits are scarce. It remains to be determined if the co-morbid concurrence of large infarct and ß-amyloid (Aß) toxicity can precipitate the early development of dementia. Here, we described a dose-dependent effect of a unilateral striatal injection of vasoconstrictive endothelin-1 (ET-1) along with Aß toxicity on CNS pathogenesis; driven by the anatomical and functional networks within a brain circuit. After 21 days of treatment, a high dose (60 pmol) of ET-1 (E60) alone caused the greatest increase in neuroinflammation, mainly in the ipsilateral striatum and distant regions with synaptic links to the striatal lesion such as white matter (subcortical white matter, corpus callosum, internal capsule, anterior commissure), gray matter (globus pallidus, thalamus), and cortices (cingulate, motor, somatosensory, entorhinal). The combined E60 + Aß treatment also extended perturbation in the contralateral hemisphere of these rats, such as increased deposition of amyloid precursor protein fragments associated with the appearance of degenerating cells and the leakage of laminin from the basement membrane across a compromised blood-brain barrier. However, the cerebral damage induced by the 6 pmol ET-1 (E6), Aß and E6 + Aß rats was not detrimental enough to injure the complete network. The appreciation of the causal interactions among distinct anatomical units in the brain after ischemia and Aß toxicity will help in the design of effective and alternative therapeutics that may disassociate the synergistic or additive association between the infarcts and Aß toxicity.

6.
Curr Diab Rep ; 19(12): 162, 2019 Dec 16.
Artigo em Inglês | MEDLINE | ID: mdl-31845115

RESUMO

PURPOSE OF REVIEW: The DALI (vitamin D and lifestyle intervention in the prevention of gestational diabetes mellitus (GDM)) study aimed to prevent GDM with lifestyle interventions or Vitamin D supplementation (1600 IU/day). This review summarizes the learnings from the DALI studies among pregnant women with a BMI ≥ 29 kg/m2. RECENT FINDINGS: Women diagnosed with GDM earlier in pregnancy had a worse metabolic profile than those diagnosed later. A combined physical activity (PA) and healthy eating (HE) lifestyle intervention improved both behaviours, limited gestational weight gain (GWG) and was cost-effective. Although GDM risk was unchanged, neonatal adiposity was reduced due to less sedentary time. Neither PA nor HE alone limited GWG or GDM risk. Fasting glucose was higher with HE only intervention, and lower with Vitamin D supplementation. Our combined intervention did not prevent GDM, but was cost-effective, limited GWG and reduced neonatal adiposity.

7.
Cell Mol Neurobiol ; 2019 Oct 10.
Artigo em Inglês | MEDLINE | ID: mdl-31599387

RESUMO

The original version of this article contained a random order of part labels for Fig. 4. The correct caption of Fig. 4 with correct order of part labels is given below.

8.
Saudi Pharm J ; 27(6): 756-766, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31516318

RESUMO

In the current work, two groups of chlorhexidine mucoadhesive buccal tablets were prepared, using either rod or irregularly-shaped spherical particles of hydroxypropyl methylcellulose and different ratios of poloxamer 407 (P407). The tablets were designed to release the drug over two hours. Their physicochemical properties and drug release profiles were investigated. The impact on dry granulation, the ex-vivo mucoadhesion, the swelling index, the morphology of swollen tablets and the drug release kinetic were investigated. Drug-polymers chemical interaction was studied using Fourier Transforms Infrared Spectroscopy (FTIR) and differential scanning calorimetry (DSC). Due to different particle shapes, the preparation of dry granules required a 40 KN force for rod-shaped particles compared to 10 KN for the irregularly-shaped spherical particles. All formulations showed at least two-hours residence time using ex-vivo mucoadhesion. Statistically, there was no significant difference in the swelling index, drug release nor its kinetic for both groups. However, the microscopical morphology of the swollen tablet and the size of the pores were affected by particle shape. Increasing the ratio of P407 to 62.5% resulted in a pronounced increase in drug release from around 60% to >90% after two hours. Following the FTIR and DSC analyses, no chemical interaction was noted apart from the steric hindrance effect of P407, which was observed even with the physical mixtures.

9.
Cell Mol Neurobiol ; 2019 Sep 14.
Artigo em Inglês | MEDLINE | ID: mdl-31522299

RESUMO

Besides other causes, ischemia and Alzheimer's disease pathology is also linked to decreased cerebral blood flow (CBF). There is little or no consensus about the role of neuroglial cells in maintaining CBF in various neuropathologies. This consensus becomes scarcer when it comes to clinical and experimental cases of comorbid Abeta-amyloid (Aß) toxicity and ischemia. Here, a comorbid rat model of Aß toxicity and endothelin-1 induced ischemia (ET1) not only demonstrated the appearance of axotomized phagocytosed pyknotic neurons (NeuN) immediately after the injury, but also showed a diversity of continuously changing neuroglia (MHC Class II/OX6, Iba1) and macrophage (Iba1/CD68) phenotypes with round, stout somas, and retracted processes. This is indicative of a response to a concomitant increase in large fluid-filled spaces due to the vascular leakage. Ironically 4 weeks after the injury despite a conclusive reduction in neurons, CBF restoration in ET1 rats was associated with a massive increase in neuroglial cell numbers, hypertrophy, ramification, and soma sizes bordering the continuously reducing lesion core and inflamed vasculature, possibly to shield their leaky phenotype. Astrocytes were also found to be releasing matrix metalloproteinase9 (MMP9), which stabilized matrix ligand ß-dystroglycan (ß-DG) in repaired or functional vessels. Changing neuroglia phenotypes, responses, motility, astrocytic recruitment of MMP9, and ß-DG stabilization implies the role of communication between neuroglia and endothelium in recovering CBF, in the absence of neurons, in ET1 rats compared to Aß+ET1 rats, which showed characteristics delayed neuroglial activation. Stimulation of timely neuroglial reactivity may serve as a viable strategy to compensate for the neuronal loss in restoring CBF in comorbid cases of ischemia and Aß toxicity.

10.
J Physiol ; 597(16): 4237-4250, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31206692

RESUMO

KEY POINTS: Pancreatic ß-cell dysfunction is hypothesized to be the significant determinant of gestational diabetes pathogenesis, however pancreatic samples from patients are scarce. This study reports a novel mouse model of gestational glucose intolerance in pregnancy, originating from previous nutrition restriction in utero, in which glucose intolerance was restricted to late gestation as is seen in human gestational diabetes. Glucose intolerance was attributed to reduced ß-cell proliferation, leading to impaired gestational ß-cell mass expansion in maternal endocrine pancreas, in addition to reduced glucose-stimulated insulin secretion. This model reproduces some of the features of gestational diabetes and is suitable for testing safe therapeutic interventions that increase ß-cell mass during pregnancy and prevent or reverse gestational glucose intolerance. ABSTRACT: Gestational diabetes mellitus (GDM) is an increasingly prevalent form of diabetes that appears during pregnancy. Pathological studies link a failure to adaptively increase maternal pancreatic ß-cell mass (BCM) in pregnancy to GDM. Due to the scarcity of pancreatic samples from GDM patients, we sought to develop a novel mouse model for impaired gestational glucose tolerance. Mature female C57Bl/6 mouse offspring (F1) born to dams fed either a control (C) or low-protein (LP) diet during gestation and lactation were randomly allocated into two subsequent study groups: pregnant (CP, LPP) or non-pregnant (CNP, LPNP). Glucose tolerance tests were performed at gestational day (GD) 9, 12 and 18. Subsequently, pancreata were removed for fluorescence immunohistochemistry to assess α-cell mass (ACM), BCM and ß-cell proliferation. An additional group of animals was used to measure insulin secretion from isolated islets at GD18. LPP females displayed glucose intolerance compared to CP females at GD18 (P < 0.001). BCM increased threefold at GD18 in CP females. However, LPP females had reduced BCM expansion (P < 0.01) concurrent with reduced ß-cell proliferation at GD12 (P < 0.05). LPP females also had reduced ACM expansion at GD18 (P < 0.01). LPP islets had impaired glucose-stimulated insulin secretion in vitro compared to CP islets (P < 0.01). Therefore, impaired glucose tolerance during pregnancy is associated with a failure to adequately adapt BCM, as a result of reduced ß-cell proliferation, in addition to lower glucose-stimulated insulin secretion. This model could be used to evaluate novel interventions during pregnancy to increase BCM or function as a strategy to prevent/reverse GDM.

11.
J Occup Environ Hyg ; 16(7): 507-518, 2019 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-31116671

RESUMO

In less than a decade since its identification in 2009, the emerging fungal pathogen Candida auris has become a major public health threat due to its multidrug resistant (MDR) phenotype, high transmissibility, and high mortality. Unlike other Candida species, C. auris has acquired high levels of resistance to an already limited arsenal of antifungals. As an emerging pathogen, there are currently a limited number of documented murine models of C. auris infection. These animal models use inoculums as high as 107-108 cells per mouse, and the environmental and occupational exposure of working with these models has not been clearly defined. Using real-time quantitative polymerase chain reaction (PCR) and culture, we monitored the animal holding room as well as the procedure room for up to 6 months while working with an intravenous model of C. auris infection. This study determined that shedding of the organism is dose-dependent, as detectable levels of C. auris were detected in the cage bedding when mice were infected with 107 and 108 cells, but not with doses of 105 and 106 cells. Autoclaving bedding in closed micro-isolator cages was found to be an effective way to minimize exposure for animal caretakers. We found that tissue necropsies of infected mice were also an important source of potential source exposure to C. auris. To mitigate these potential exposures, we implemented a rigorous "buddy system" workflow and a disinfection protocol that uses 10% bleach followed by 70% ethanol and can be used in any animal facility when using small animal models of C. auris infection.

12.
IEEE Trans Cybern ; 2019 Mar 18.
Artigo em Inglês | MEDLINE | ID: mdl-30892257

RESUMO

In this paper, we investigate the consensus tracking control problem for networked multiagent systems (MASs) with unknown nonaffine dynamics. Our goal is to achieve asymptotic (rather than ultimately uniformly bounded) consensus tracking, which is quite challenging especially if nonvanishing/nonparametric uncertainties are involved and at the same time the control protocol is required to be fully distributed and continuous everywhere. Here, we present a conceptually new and structurally simple solution with distributed and continuous control action. The developed method is capable of ensuring zero-error tracking with a unique converging feature in that the consensus tracking error first converges to a small adjustable residual set around zero within a prescribed finite time, and then further shrinks to zero exponentially. The key technique lies in the utilization of a state transformation based on certain scaling function. Our method also prevents the restrictive requirement that all subsystems have access to the linearly parameterized information as imposed in most existing consensus tracking results for nonlinear MAS.

13.
Nutrients ; 11(3)2019 Mar 12.
Artigo em Inglês | MEDLINE | ID: mdl-30871106

RESUMO

Low birth weight is a risk factor for gestational and type 2 diabetes (T2D). Since mammalian target of rapamycin (mTOR) controls pancreatic ß-cell mass and hormone release, we hypothesized that nutritional insult in utero might permanently alter mTOR signaling. Mice were fed a low-protein (LP, 8%) or control (C, 20%) diet throughout pregnancy, and offspring examined until 130 days age. Mice receiving LP were born 12% smaller and ß-cell mass was significantly reduced throughout life. Islet mTOR levels were lower in LP-exposed mice and localized predominantly to α-rather than ß-cells. Incubation of isolated mouse islets with rapamycin significantly reduced cell proliferation while increasing apoptosis. mRNA levels for mTORC complex genes mTOR, Rictor and Raptor were elevated at 7 days in LP mice, as were the mTOR and Raptor proteins. Proglucagon gene expression was similarly increased, but not insulin or the immune/metabolic defense protein STING. In human and mouse pancreas STING was strongly associated with islet ß-cells. Results support long-term changes in islet mTOR signaling in response to nutritional insult in utero, with altered expression of glucagon and insulin and a reduced ß-cell mass. This may contribute to an increased risk of gestational or type 2 diabetes.


Assuntos
Dieta com Restrição de Proteínas , Proteínas na Dieta/administração & dosagem , Glucagon/metabolismo , Ilhotas Pancreáticas/efeitos dos fármacos , Fenômenos Fisiológicos da Nutrição Pré-Natal , Serina-Treonina Quinases TOR/metabolismo , Animais , Linhagem Celular , Feminino , Regulação da Expressão Gênica/efeitos dos fármacos , Glucagon/genética , Insulina/genética , Insulina/metabolismo , Ilhotas Pancreáticas/citologia , Ilhotas Pancreáticas/metabolismo , Camundongos , Camundongos Endogâmicos BALB C , Gravidez , Distribuição Aleatória , Serina-Treonina Quinases TOR/genética
14.
Diabetologia ; 62(5): 860-872, 2019 05.
Artigo em Inglês | MEDLINE | ID: mdl-30778623

RESUMO

AIMS/HYPOTHESIS: The role of non-cardiomyocytes in diabetic cardiomyopathy has not been fully addressed. This study investigated whether endothelial cell calpain plays a role in myocardial endothelial injury and microvascular rarefaction in diabetes, thereby contributing to diabetic cardiomyopathy. METHODS: Endothelial cell-specific Capns1-knockout (KO) mice were generated. Conditions mimicking prediabetes and type 1 and type 2 diabetes were induced in these KO mice and their wild-type littermates. Myocardial function and coronary flow reserve were assessed by echocardiography. Histological analyses were performed to determine capillary density, cardiomyocyte size and fibrosis in the heart. Isolated aortas were assayed for neovascularisation. Cultured cardiac microvascular endothelial cells were stimulated with high palmitate. Angiogenesis and apoptosis were analysed. RESULTS: Endothelial cell-specific deletion of Capns1 disrupted calpain 1 and calpain 2 in endothelial cells, reduced cardiac fibrosis and hypertrophy, and alleviated myocardial dysfunction in mouse models of diabetes without significantly affecting systemic metabolic variables. These protective effects of calpain disruption in endothelial cells were associated with an increase in myocardial capillary density (wild-type vs Capns1-KO 3646.14 ± 423.51 vs 4708.7 ± 417.93 capillary number/high-power field in prediabetes, 2999.36 ± 854.77 vs 4579.22 ± 672.56 capillary number/high-power field in type 2 diabetes and 2364.87 ± 249.57 vs 3014.63 ± 215.46 capillary number/high-power field in type 1 diabetes) and coronary flow reserve. Ex vivo analysis of neovascularisation revealed more endothelial cell sprouts from aortic rings of prediabetic and diabetic Capns1-KO mice compared with their wild-type littermates. In cultured cardiac microvascular endothelial cells, inhibition of calpain improved angiogenesis and prevented apoptosis under metabolic stress. Mechanistically, deletion of Capns1 elevated the protein levels of ß-catenin in endothelial cells of Capns1-KO mice and constitutive activity of calpain 2 suppressed ß-catenin protein expression in cultured endothelial cells. Upregulation of ß-catenin promoted angiogenesis and inhibited apoptosis whereas knockdown of ß-catenin offset the protective effects of calpain inhibition in endothelial cells under metabolic stress. CONCLUSIONS/INTERPRETATION: These results delineate a primary role of calpain in inducing cardiac endothelial cell injury and impairing neovascularisation via suppression of ß-catenin, thereby promoting diabetic cardiomyopathy, and indicate that calpain is a promising therapeutic target to prevent diabetic cardiac complications.


Assuntos
Calpaína/genética , Calpaína/fisiologia , Cardiomiopatias Diabéticas/metabolismo , Cardiomiopatias Diabéticas/terapia , Células Endoteliais/enzimologia , Neovascularização Patológica , Neovascularização Fisiológica , Animais , Apoptose , Diabetes Mellitus Tipo 2/metabolismo , Fibroblastos/metabolismo , Deleção de Genes , Macrófagos/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Miocárdio/metabolismo , Miócitos Cardíacos/citologia , Miócitos Cardíacos/metabolismo , Transdução de Sinais , beta Catenina/metabolismo
15.
Mol Neurobiol ; 56(4): 2714-2727, 2019 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-30054859

RESUMO

The hippocampus, a brain region vital for memory and learning, is sensitive to the damage caused by ischemic/hypoxic stroke and is one of the main regions affected by Alzheimer's disease. The pathological changes that might occur in the hippocampus and its connections, because of cerebral injury in a distant brain region, such as the striatum, have not been examined. Therefore, in the present study, we evaluated the combined effects of endothelin-1-induced ischemia (ET1) in the striatum and ß-amyloid (Aß) toxicity on hippocampal pathogenesis, dictated by the anatomical and functional intra- and inter-regional hippocampal connections to the striatum. The hippocampal pathogenesis induced by Aß or ET1 alone was not severe enough to significantly affect the entire circuit of the hippocampal network. However, the combination of the two pathological states (ET1 + Aß) led to an exacerbated increase in neuroinflammation, deposition of the amyloid precursor protein (APP) fragments with the associated appearance of degenerating cells, and blood-brain-barrier disruption. This was observed mainly in the hippocampal formation (CA2 and CA3 regions), the dentate gyrus as well as distinct regions with synaptic links to the hippocampus such as entorhinal cortex, thalamus, and basal forebrain. In addition, ET1 + Aß-treated rats also demonstrated protracted loss of AQP4 depolarization, dissolution of ß-dystroglycan, and basement membrane laminin with associated IgG and dysferlin leakage. Spatial dynamics of hippocampal injury in ET1 + Aß rats may provide a valuable model to study new targets for clinical therapeutic applications, specifically when areas remotely connected to hippocampus are damaged.


Assuntos
Peptídeos beta-Amiloides/toxicidade , Corpo Estriado/patologia , Hipocampo/irrigação sanguínea , Hipocampo/lesões , Hipocampo/patologia , Animais , Corpo Estriado/efeitos dos fármacos , Hipocampo/metabolismo , Masculino , Ratos Wistar
16.
IEEE Trans Cybern ; 49(4): 1138-1147, 2019 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-29994574

RESUMO

In this paper, we present a new prescribed-time distributed control method for consensus and containment of networked multiple systems. Different from both regular finite-time control (where the finite settling time is not uniform in initial conditions) and the fixed-time control (where the settling time cannot be preassigned arbitrarily), the proposed one is built upon a novel scaling function, resulting in prespecifiable convergence time (the settling time can be preassigned as needed within any physically allowable range). Furthermore, the developed control scheme not only ensures that all the agents reach the average consensus in prescribed finite time under undirected connected topology, but also ensures that all the agents reach a prescribed-time consensus with the root's state being the group decision value under the directed topology containing a spanning tree with the root as the leader. In addition, we extend the result to prescribed-time containment control involving multiple leaders under directed communication topology. Numerical examples are provided to verify the effectiveness and the superiority of the proposed control.

17.
IEEE Trans Cybern ; 49(3): 897-906, 2019 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-29994593

RESUMO

In this paper, based on the deterministic learning (DL) theory, an approach for detection for small faults in a class of nonlinear closed-loop systems is proposed. First, the DL-based neural control approach and identification approach are employed to extract the knowledge of the control effort that compensates the fault dynamics (change of the control effort) and the fault dynamics (the change of system dynamics due to fault). Second, two types of residuals are constructed. One is to measure the change of system dynamics, another one is to measure change of the control effort. By combining these residuals, an enhanced residual is generated, in which the fault dynamics and the control effort are combined to diagnose the fault. It is shown that the major fault information is compensated by the control, and the major fault information is double in the enhanced residual. Therefore, the fault information in the diagnosis residual is enhanced. Finally, an analysis of the fault detectability condition of the diagnosis scheme is given. Simulation studies are included to demonstrate the effectiveness of the approach.

18.
ACS Appl Mater Interfaces ; 10(50): 44183-44189, 2018 Dec 19.
Artigo em Inglês | MEDLINE | ID: mdl-30460845

RESUMO

Nanoscale materials are frequently coated with surface stabilization layers during growth that prevent flocculation in solution and facilitate processing technologies such as ink-jet device printing. Here, we show that few-nanometer-thick stabilization layers typically used swell in the presence of certain solvents and impart significant stresses to the nanomaterial that remains even after the solvent has evaporated. Solvent swelling of the surface layer dramatically enhances nanomaterial-substrate adhesion via the collapse of the stabilization layer during solvent evaporation, preventing stress relaxation. We demonstrate the stress modulation of Ag, Au, and Si nanowires functionalised with surface polymers and surfactant layers and detect strain levels between 0.1 and 0.6% using atomic force microscopy mechanical measurement and Raman spectroscopy. Dry-transferred nanowires exhibit poor adhesion and show no evidence of incorporated stress but become stressed immediately following solvent exposure. Strain engineering is demonstrated by coating nanowires with few-nanometer-thick solvent-responsive polymer layers.

19.
ACS Nano ; 12(10): 10554-10563, 2018 Oct 23.
Artigo em Inglês | MEDLINE | ID: mdl-30235417

RESUMO

Nanowires (NWs) with axial p-i-n junctions have been widely explored as microscopic diodes for optoelectronic and solar energy applications, and their performance is strongly influenced by charge recombination at the surface. We delineate how the photovoltaic performance of these diodes is dictated not only by the surface but also by the complex and seemingly counterintuitive interplay of diode geometry, that is, radius ( R) and intrinsic length ( Li), with the surface recombination velocity ( S). An analytical model to describe these relationships is developed and compared to finite-element simulations, which verify the accuracy and limitations of the model. The dependence of the dark saturation current ( I0), internal quantum efficiency (IQE), short-circuit current ( ISC), and open-circuit voltage ( VOC) on both geometric and recombination parameters demonstrates that no single set of parameters produces optimal performance; instead, various trade-offs in performance are observed. For instance, longer Li might be expected to produce higher ISC, yet at high values of S the ISC declines because of decreases in IQE. Moreover, longer Li produces a concurrent decline in VOC regardless of S due to increases in I0. We also find that ISC and VOC trends are radius independent, yet I0 is directly proportional to R, causing NWs with smaller R to display higher turn-on voltages. The analysis regarding the interplay of these parameters, verified by experimental measurements with various p-i-n geometries and surface treatments, provides clear guidance for the rational design of performance metrics for photodiode and photovoltaic devices.

20.
Islets ; 10(4): 137-150, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30110202

RESUMO

Both bone marrow-derived hematopoietic stem cells (HSC) and mesenchymal stem cells (MSC) improve glycemic control in diabetic mice, but their kinetics and associated changes in pancreatic morphology have not been directly compared. Our goal was to examine the time course of improvements in glucose tolerance and associated changes in ß-cell mass and proliferation following transplantation of equivalent numbers of HSC or MSC from the same bone marrow into diabetic non-obese diabetic severe combined immune deficiency (NOD.SCID) mice. We used transgenic mice with a targeted expression of yellow fluorescent protein (YFP) driven by the Vav1 gene promoter to genetically tag HSC and progeny. HSC were separated from bone marrow by fluorescence-activated cell sorting and MSC following cell culture. Equivalent numbers of isolated HSC or MSC were transplanted directly into the pancreas of NOD.SCID mice previously made diabetic with streptozotocin. Glucose tolerance, serum insulin, ß-cell mass and ß-cell proliferation were examined up to 28 days following transplant. Transplantation with MSC improved glucose tolerance within 7 days and serum insulin levels increased, but with no increase in ß-cell mass. Mice transplanted with HSC showed improved glucose tolerance only after 3 weeks associated with increased ß-cell proliferation and mass. We conclude that single injections of either MSC or HSC transiently improved glycemic control in diabetic NOD.SCID mice, but with different time courses. However, only HSC infiltrated the islets and were associated with an expanded ß-cell mass. This suggests that MSC and HSC have differing mechanisms of action.


Assuntos
Células-Tronco Hematopoéticas/fisiologia , Hiperglicemia/terapia , Insulina/sangue , Células-Tronco Mesenquimais/fisiologia , Transplante de Células-Tronco/métodos , Animais , Glicemia/metabolismo , Medula Óssea , Modelos Animais de Doenças , Teste de Tolerância a Glucose/métodos , Células Secretoras de Insulina/patologia , Células Secretoras de Insulina/fisiologia , Camundongos , Camundongos Endogâmicos NOD , Camundongos SCID , Fatores de Tempo , Resultado do Tratamento
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