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The transport of intensity equation (TIE) is a non-interferometric phase retrieval method that originates from the imaginary part of the Helmholtz equation and is equivalent to the law of conservation of energy. From the real part of the Helmholtz equation, the transport of phase equation (TPE), which represents the Eikonal equation in the presence of diffraction, can be derived. The amplitude and phase for an arbitrary optical field should satisfy these coupled equations simultaneously during propagation. In this work, the coupling between the TIE and TPE is exploited to improve the phase retrieval solutions from the TIE. Specifically, a non-recursive fast Fourier transform (FFT)-based phase retrieval method using both the TIE and TPE is demonstrated. Based on the FFT-based TIE solution, a correction factor calculated by the TPE is introduced to improve the phase retrieval results.
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A simple non-interferometric incoherent light ray propagation model is introduced to perform three-dimensional profiling of transparent objects with typical thicknesses of the order of mm to cm by analyzing the distorted captured image behind the object. A two-dimensional cosine fringe is used as the incident reference image, whose periodicity is markedly altered by the shape of the object. By monitoring the local change in the period, the surface profile is simulated and optimized to achieve minimal error with experimental data and thus determine the final morphology. Our proposed method is simple, robust, straightforward, and single-shot, and can be used with coherent or incoherent illumination. Its feasibility for more complex applications is verified experimentally through rigorous error calculation. Moreover, the application of this technique for arbitrary transparent objects is theoretically attainable and promising.
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BACKGROUND: Astrocytic glycogen works as an essential energy reserve for surrounding neurons and is reported to accumulate excessively during cerebral ischemia/reperfusion (I/R) injury. Our previous study found that accumulated glycogen mobilization exhibits a neuroprotective effect against I/R damage. In addition, ischemia could transform astrocytes into A1-like (toxic) and A2-like (protective) subtypes. However, the underlying mechanism behind accumulated glycogen mobilization-mediated neuroprotection in cerebral reperfusion injury and its relationship with the astrocytic A1/A2 paradigm is unknown. METHODS: Astrocytic glycogen phosphorylase, the rate-limiting enzyme in glycogen mobilization, was specifically overexpressed and knocked down in mice and in cultured astrocytes. The I/R injury was imitated using a middle cerebral artery occlusion/reperfusion model in mice and an oxygen-glucose deprivation/reoxygenation model in cultured cells. Alterations in A1-like and A2-like astrocytes and the expression of phosphorylated nuclear transcription factor-κB (NF-κB) and phosphorylated signal transducer and activator of transcription 3 (STAT3) were determined by RNA sequencing, immunofluorescence and immunoblotting. Metabolites, including glycogen, NADPH, glutathione and reactive oxygen species (ROS), were analyzed by biochemical analysis. RESULTS: Here, we observed that astrocytic glycogen mobilization inhibited A1-like astrocytes and enhanced A2-like astrocytes after reperfusion in an experimental ischemic stroke model in vivo and in vitro. In addition, glycogen mobilization could enhance the production of NADPH and glutathione by the pentose phosphate pathway (PPP) and reduce ROS levels during reperfusion. NF-κB inhibition and STAT3 activation caused by a decrease in ROS levels were responsible for glycogen mobilization-induced A1-like and A2-like astrocyte transformation after I/R. The astrocytic A1/A2 paradigm is closely correlated with glycogen mobilization-mediated neuroprotection in cerebral reperfusion injury. CONCLUSIONS: Our data suggest that ROS-mediated NF-κB inhibition and STAT3 activation are the key pathways for glycogen mobilization-induced neuroprotection and provide a promising metabolic target for brain reperfusion injury in ischemic stroke.
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Astrócitos/metabolismo , Isquemia Encefálica/metabolismo , Glicogênio/metabolismo , AVC Isquêmico/metabolismo , Neuroproteção/fisiologia , Traumatismo por Reperfusão/metabolismo , Animais , Animais Recém-Nascidos , Astrócitos/patologia , Isquemia Encefálica/patologia , Isquemia Encefálica/prevenção & controle , Técnicas de Cocultura , Feminino , AVC Isquêmico/patologia , AVC Isquêmico/prevenção & controle , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Espécies Reativas de Oxigênio/metabolismo , Traumatismo por Reperfusão/patologia , Traumatismo por Reperfusão/prevenção & controleRESUMO
A simple and robust technique of Moiré topography with single-image capture and incorporating digital filtering along with a four-step digitally implemented phase-shifting method is introduced for three-dimensional (3D) surface mapping. Feature details in the order of tens to hundreds of microns can be achieved using interferometrically generated structured light to illuminate the object surface. Compared to the traditional optical phase-shifting method, a digital phase-shifting method based on Fourier processing is implemented with computer-generated sinusoidal patterns derived from the recorded deformed fringes. This enables a single capture of the image that can be used to reconstruct the 3D topography of the surface. Single-shot imaging is simple to implement experimentally and avoids errors in introducing the correct phase shifts. The feasibility of this technique is verified experimentally, and applications to metallic surfaces are demonstrated.
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Cerebral glycogen is principally localized in astrocytes rather than in neurons. Glycogen metabolism has been implicated in higher brain functions, including learning and memory, yet the distribution patterns of glycogen in different types of astrocytes have not been fully described. Here, we applied a method based on the incorporation of 2-NBDG, a D-glucose fluorescent derivative that can trace glycogen, to investigate glycogen's distribution in the brain. We identified two types of astrocytes, namely, 2-NBDGI (glycogen-deficient) and 2-NBDGII (glycogen-rich) cells. Whole-cell patch-clamp and fluorescence-activated cell sorting (FACS) were used to separate 2-NBDGII astrocytes from 2-NBDGI astrocytes. The expression levels of glycogen metabolic enzymes were analyzed in 2-NBDGI and 2-NBDGII astrocytes. We found unique glycogen metabolic patterns between 2-NBDGI and 2-NBDGII astrocytes. We also observed that 2-NBDGII astrocytes were mainly identified as fibrous astrocytes but not protoplasmic astrocytes. Our data reveal cell type-dependent glycogen distribution and metabolism patterns, suggesting diverse functions of these different astrocytes.
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Astrócitos/metabolismo , Glicogênio/metabolismo , Análise de Célula Única/métodos , 4-Cloro-7-nitrobenzofurazano/análogos & derivados , 4-Cloro-7-nitrobenzofurazano/química , Animais , Astrócitos/química , Células Cultivadas , Córtex Cerebral/metabolismo , Desoxiglucose/análogos & derivados , Desoxiglucose/química , Glucose , Glicogênio/análise , Glicogênio/deficiência , Camundongos , Camundongos Endogâmicos C57BL , Neurônios/metabolismoRESUMO
BACKGROUND: The steroid hormone estrogen (17-ß-estradiol, E2) provides neuroprotection against cerebral ischemic injury by activating estrogen receptors. The novel estrogen receptor G protein-coupled receptor 30 (GPR30) is highly expressed in the brain and provides acute neuroprotection against stroke. However, the underlying mechanisms remain unclear. METHODS: In this study, ovariectomized female mice were subjected to middle cerebral artery occlusion (MCAO), and E2, G1, and ICI182780 were administered immediately upon reperfusion. The infarction volume, neurological scores, and neuronal injuries were examined. Primary microglial cells were subjected to oxygen-glucose deprivation (OGD), and the drugs were administered immediately upon reintroduction. The pro-inflammatory cytokines TNF-α, IL-1ß, and IL-6 in penumbra and microglia were assessed by ELISA. The cell viability and lactose dehydrogenase (LDH) release of neurons co-cultured with microglia were analyzed using cell counting kit-8 (CCK8) and LDH release assays. Microglial activation as well as GPR30, Iba1, and Toll-like receptor 4 (TLR4) protein expression and TLR4 mRNA expression were detected. Additionally, NF-κB activity was detected in lipopolysaccharide (LPS)-activated microglia after the activation of GPR30. RESULTS: GPR30 was highly expressed in microglia and significantly increased after ischemic injury. The activation of GPR30 significantly reduced the infarction volume, improved the neurological deficit, and alleviated neuronal injuries. Moreover, GPR30 activation significantly reduced the release of TNF-α, IL-1ß, and IL-6 from ischemic penumbra and microglia subjected to OGD and alleviated neuronal injury as assessed using the CCK8 and LDH assays. Finally, the activation of GPR30 relieved microglial activation, reduced Iba1 and TLR4 protein expression and TLR4 mRNA levels, and inhibited NF-κB activity. CONCLUSIONS: Microglial GPR30 exerts acute neuroprotective effects by inhibiting TLR4-mediated microglial inflammation, which indicates that GPR30 may be a potential target for the treatment of ischemic stroke.
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Infarto da Artéria Cerebral Média/metabolismo , Inflamação/patologia , Microglia/patologia , Receptores de Estrogênio/metabolismo , Receptores Acoplados a Proteínas G/metabolismo , Receptor 4 Toll-Like/metabolismo , Animais , Animais Recém-Nascidos , Hipóxia Celular/efeitos dos fármacos , Células Cultivadas , Técnicas de Cocultura , Modelos Animais de Doenças , Estradiol/farmacologia , Antagonistas do Receptor de Estrogênio/farmacologia , Feminino , Fulvestranto/farmacologia , Glucose/deficiência , Infarto da Artéria Cerebral Média/complicações , Infarto da Artéria Cerebral Média/tratamento farmacológico , Inflamação/etiologia , Lipopolissacarídeos/farmacologia , Camundongos , Camundongos Endogâmicos C57BL , Microglia/efeitos dos fármacos , Neurônios/efeitos dos fármacos , OvariectomiaRESUMO
Post-operative cognitive dysfunction (POCD) has been widely reported, especially in elderly patients. An association between POCD and inhalational anesthetics, such as isoflurane, has been suggested. The TWIK-related K+ channel-1 (TREK-1) controls several major cellular responses involved in memory formation and is believed to participate in the development of depression, cerebral ischemia and blood-brain barrier dysfunction. However, the specific role of TREK-1 in mediating anesthesia-induced POCD remains unknown. In the current study, we determined that exposure to isoflurane affected memory in middle-aged mice and altered TREK-1 expression. In addition, TREK-1 over-expression exacerbated isoflurane-induced memory impairment, while TREK-1 silence attenuated the impairment. Taken together, our data demonstrate that inhibition of TREK-1 protects mice from cognitive impairment induced by anesthesia and TREK-1 is a potential therapeutic target against memory impairment induced by volatile anesthetics.
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Hipocampo/metabolismo , Isoflurano/administração & dosagem , Memória/efeitos dos fármacos , Canais de Potássio de Domínios Poros em Tandem/metabolismo , Animais , Masculino , Aprendizagem em Labirinto/efeitos dos fármacos , Memória/fisiologia , Transtornos da Memória/induzido quimicamente , Camundongos Endogâmicos C57BL , Transdução de SinaisRESUMO
BACKGROUND: There are growing concerns that anaesthetic exposure can cause extensive apoptotic degeneration of neurons and the impairment of normal synaptic development and remodelling. However, little attention has been paid to exploring the possible cytotoxicity of inhalation anaesthetics, such as isoflurane, in astrocytes. In this research, we determined that prolonged exposure to an inhalation anaesthetic caused cytotoxicity in astrocytes, and we identified the underlying molecular mechanism responsible for this process. METHODS: Astrocytes were exposed to isoflurane, and astrocytic survival was then measured via LDH release assays, MTT assays, and TUNEL staining. TWIK-related potassium (K+) channel-1 (TREK-1) over-expression and knockdown models were also created using lentiviruses. The levels of TREK-1 and brain-derived neurotrophic factor (BDNF) were measured via Western blot and qRT-PCR. RESULTS: Prolonged exposure to isoflurane decreased primary astrocytic viability in a dose- and time-dependent manner. Moreover, with prolonged exposure to isoflurane, the TREK-1 level increased, and the BDNF level was reduced. TREK-1 knockdown promoted the survival of astrocytes and increased BDNF expression following isoflurane exposure. CONCLUSIONS: Overdoses of and prolonged exposure to isoflurane induce cytotoxicity in primary astrocytes. TREK-1 plays an important role in isoflurane-induced cultured astrocytic cytotoxicity by down-regulating the expression of BDNF.
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Anestésicos Inalatórios/toxicidade , Astrócitos/efeitos dos fármacos , Astrócitos/metabolismo , Citotoxinas/toxicidade , Isoflurano/toxicidade , Canais de Potássio de Domínios Poros em Tandem/fisiologia , Animais , Animais Recém-Nascidos , Astrócitos/patologia , Sobrevivência Celular/efeitos dos fármacos , Sobrevivência Celular/fisiologia , Células Cultivadas , Relação Dose-Resposta a Droga , Camundongos , Camundongos Endogâmicos C57BL , Neurônios/efeitos dos fármacos , Neurônios/metabolismo , Neurônios/patologiaRESUMO
ABSTRACT: Although antipsychotics that act via monoaminergic neurotransmitter modulation have considerable therapeutic effect, they cannot completely relieve clinical symptoms in patients suffering from psychiatric disorders. This may be attributed to the limited range of neurotransmitters that are regulated by psychotropic drugs. Recent findings indicate the need for investigation of psychotropic medications that target less-studied neurotransmitters. Among these candidate neurotransmitters, lactate is developing from being a waste metabolite to a glial-neuronal signaling molecule in recent years. Previous studies have suggested that cerebral lactate levels change considerably in numerous psychiatric illnesses; animal experiments have also shown that the supply of exogenous lactate exerts an antidepressant effect. In this review, we have described how medications targeting newer neurotransmitters offer promise in psychiatric diseases; we have also summarized the advances in the use of lactate (and its corresponding signaling pathways) as a signaling molecule. In addition, we have described the alterations in brain lactate levels in depression, anxiety, bipolar disorder, and schizophrenia and have indicated the challenges that need to be overcome before brain lactate can be used as a therapeutic target in psychopharmacology.
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Folate was enriched during quinoa germination, while molecular mechanisms were not well understood. In this study, three quinoa varieties were selected for germination, and changes in substrate content and enzyme activity of the folate biosynthesis pathway were monitored. 5-Methyltetrahydrofolate (5-CH3-THF) and 5-formyltetrahydrofolate (5-CHO-THF) were significantly enriched in quinoa sprouts. Among the selected varieties, QL-2 exhibited the lowest content of the oxidation product MeFox and the highest total folate content. Based on transcriptome analysis, the p-ABA branch was found to be crucial for folate accumulation, while the pterin branch served as a key control point for the one carbon pool by folate pathway, which limited further folate biosynthesis. In the one carbon pool by folate pathway, genes CqMTHFR and CqAMT significantly contributed to the enrichment of 5-CH3-THF and 5-CHO-THF. Findings gained here would facilitate the potential application of quinoa sprouts as an alternative strategy for folate supplementation.
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Chenopodium quinoa , Chenopodium quinoa/genética , Chenopodium quinoa/química , Ácido Fólico , Sementes/genética , Sementes/química , Perfilação da Expressão Gênica , Carbono/análiseRESUMO
Post-stroke depression (PSD) is a significant complication in stroke patients, increases long-term mortality, and exaggerates ischemia-induced brain injury. However, the underlying molecular mechanisms and effective therapeutic targets related to PSD have remained elusive. Here, we employed an animal behavioral model of PSD by combining the use of middle cerebral artery occlusion (MCAO) followed by spatial restraint stress to study the molecular underpinnings and potential therapies of PSD. Interestingly, we found that sub-chronic application of gastrodin (Gas), a traditional Chinese medicinal herb Gastrodia elata extraction, relieved depression-related behavioral deficits, increased the impaired expression of synaptic transmission-associated proteins, and restored the altered spine density in hippocampal CA1 of PSD animals. Furthermore, our results indicated that the anti-PSD effect of Gas was dependent on membrane cannabinoid-1 receptor (CB1R) expression. The contents of phosphorated protein kinase A (p-PKA) and phosphorated Ras homolog gene family member A (p(ser188)-RhoA) were decreased in the hippocampus of PSD-mice, which was reversed by Gas treatment, and CB1R depletion caused a diminished efficacy of Gas on p-PKA and p-RhoA expression. In addition, the anti-PSD effect of Gas was partially blocked by PKA inhibition or RhoA activation, indicating that the anti-PSD effect of Gas is associated with the CB1R-mediated PKA/RhoA signaling pathway. Together, our findings revealed that Gas treatment possesses protective effects against the post-stroke depressive-like state; the CB1R-involved PKA/RhoA signaling pathway is critical in mediating Gas's anti-PSD potency, suggesting that Gas application may be beneficial in the prevention and adjunctive treatment of PSD.
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Brain glycogen, which is distinct from muscle glycogen and liver glycogen, has become a crucial node linking metabolism, epigenetics, and autophagy. Recent studies have suggested that brain glycogen governs multiple neurobehavioral processes, such as memory formation and consolidation. However, the changes in brain glycogen levels in mental diseases and the associations of these changes with the disease prognosis are unknown. Here, we review the psychological functions of brain glycogen and the different characteristics of astrocytic glycogen and neuronal glycogen. In addition, we summarize the alterations in brain glycogen levels in depression, schizophrenia and sleep disorders, highlighting that brain glycogen functions as an important metabolite responsible for the development of mental diseases. In summary, brain glycogen is a key to understanding the pathology of mental diseases and deserves more attention in future research.
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Glycophagy has evolved from an alternative glycogen degradation pathway into a multifaceted pivot to regulate cellular metabolic hemostasis in peripheral tissues. However, the pattern of glycophagy in the brain and its potential therapeutic impact on ischemic stroke remain unknown. Here, we observed that the dysfunction of astrocytic glycophagy was caused by the downregulation of the GABA type A receptor-associated protein like 1 (GABARAPL1) during reperfusion in ischemic stroke patients and mice. PI3K-Akt pathway activation is involved in driving GABARAPL1 downregulation during cerebral reperfusion. Moreover, glycophagy dysfunction-induced glucosamine deficiency suppresses the nuclear translocation of specificity protein 1 and TATA binding protein, the transcription factors for GABARAPL1, by decreasing their O-GlcNAcylation levels, and accordingly feedback inhibits GABARAPL1 in astrocytes during reperfusion. Restoring astrocytic glycophagy by overexpressing GABARAPL1 decreases DNA damage and oxidative injury in astrocytes and improves the survival of surrounding neurons during reperfusion. In addition, a hypocaloric diet in the acute phase after cerebral reperfusion can enhance astrocytic glycophagic flux and accelerate neurological recovery. In summary, glycophagy in the brain links autophagy, metabolism, and epigenetics together, and glycophagy dysfunction exacerbates reperfusion injury after ischemic stroke.
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Astrócitos , AVC Isquêmico , Traumatismo por Reperfusão , Astrócitos/metabolismo , Astrócitos/patologia , Animais , Traumatismo por Reperfusão/metabolismo , Traumatismo por Reperfusão/patologia , Camundongos , AVC Isquêmico/metabolismo , AVC Isquêmico/patologia , Humanos , Masculino , Glicogênio/metabolismo , Modelos Animais de Doenças , Proteínas Associadas aos Microtúbulos/metabolismo , Proteínas Associadas aos Microtúbulos/genética , Proteínas Proto-Oncogênicas c-akt/metabolismo , Fosfatidilinositol 3-Quinases/metabolismo , Proteínas Adaptadoras de Transdução de Sinal/metabolismo , Proteínas Adaptadoras de Transdução de Sinal/genética , Transdução de Sinais , AutofagiaRESUMO
BACKGROUND: Human immunodeficiency virus (HIV) infection has become a major contributor to the global burden of disease. Globally, the number of cases of HIV continues to increase. Electronic health (eHealth) interventions have emerged as promising tools to support disease self-management among people living with HIV. The purpose of this umbrella review is to systematically evaluate and summarize the evidence and results of published systematic reviews and meta-analyses on the effectiveness of eHealth interventions for HIV prevention, testing and management. METHODS: PubMed, Embase and the Cochrane Library were searched for reviews. The methodological quality of the included studies was assessed using AMSTAR-2. RESULTS: A total of 22 systematic reviews were included. The methodological quality of the reviews was low or critically low. EHealth interventions range from Internet, computer, or mobile interventions to websites, programs, applications, email, video, games, telemedicine, texting, and social media, or a combination of them. The majority of the reviews showed evidence of effectiveness (including increased participation in HIV management behaviours, successfully changed HIV testing behaviours, and reduced risk behaviours). EHealth interventions were effective in the short term. CONCLUSIONS: Ehealth interventions have the potential to improve HIV prevention, HIV testing and disease management. Due to the limitations of the low methodological quality of the currently available systematic reviews, more high-quality evidence is needed to develop clear and robust recommendations.
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Infecções por HIV , Telemedicina , Humanos , Infecções por HIV/prevenção & controle , Infecções por HIV/diagnóstico , Teste de HIVRESUMO
BACKGROUND: Problematic use of mobile phones (PMPU) has been described as a serious public health issue. METHODS: This study was a parallel three-arm randomized controlled trial and has completed registration (ClinicalTrials.gov Identifier: NCT05843591). Ninety college students with PMPU were randomly assigned to the aerobic exercise group (AE group, n = 30), the Tai Chi Chuan group (TCC group, n = 30), or the wait-list control group (WLC group, n = 30). At the end of the intervention, stool samples from the study participants were collected for biological analysis based on 16 S rDNA amplicon sequencing technology. The primary outcome was addiction symptoms assessed by the Smartphone Addiction Scale-Short Version (SAS-SV). The secondary outcomes are emotional symptoms, physical symptoms, and flora species. RESULTS: Compared with the WLC group, the AE and TCC groups showed reductions in PMPU levels, physical and mental fatigue, but there was no difference between the two groups. Moreover, the effect of increasing self-esteem embodied in the TCC group was not present in the AE group. Compared to the WLC group, the relative abundance of Bacteroidaceae and Bacteroides were lower in the AE group, while the relative abundance of Erysipelotrichaceae and Alistipes were lower in the TCC group. And the relative abundance of Bacteroidaceae, Bacteroides, and Alistipes were significantly and negatively correlated with the decline in PMPU scores. CONCLUSION: AE or TCC is an effective, safe and efficient intervention for college students with PMPU, providing some physiological and psychological benefits and having some impact on their intestinal flora.
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Uso do Telefone Celular , Microbioma Gastrointestinal , Tai Chi Chuan , Humanos , Exercício Físico , Estudantes/psicologiaRESUMO
Aligning human parts automatically is one of the most challenging problems for person re-identification (re-ID). Recently, the stripe-based methods, which equally partition the person images into the fixed stripes for aligned representation learning, have achieved great success. However, the stripes with fixed height and position cannot well handle the misalignment problems caused by inaccurate detection and occlusion and may introduce much background noise. In this article, we aim at learning adaptive stripes with foreground refinement to achieve pixel-level part alignment by only using person identity labels for person re-ID and make two contributions. 1) A semantics-consistent stripe learning method (SCS). Given an image, SCS partitions it into adaptive horizontal stripes and each stripe is corresponding to a specific semantic part. Specifically, SCS iterates between two processes: i) clustering the rows to human parts or background to generate the pseudo-part labels of rows and ii) learning a row classifier to partition a person image, which is supervised by the latest pseudo-labels. This iterative scheme guarantees the accuracy of the learned image partition. 2) A self-refinement method (SCS+) to remove the background noise in stripes. We employ the above row classifier to generate the probabilities of pixels belonging to human parts (foreground) or background, which is called the class activation map (CAM). Only the most confident areas from the CAM are assigned with foreground/background labels to guide the human part refinement. Finally, by intersecting the semantics-consistent stripes with the foreground areas, SCS+ locates the human parts at pixel-level, obtaining a more robust part-aligned representation. Extensive experiments validate that SCS+ sets the new state-of-the-art performance on three widely used datasets including Market-1501, DukeMTMC-reID, and CUHK03-NP.
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Wire-bonding technology is the most commonly used chip interconnection technology in microelectronic packaging. Metal bonding wire is the key material for wire bonding and plays an important role in the reliability of electronic devices. In recent years, palladium-plated copper (PdCu) bonding wire has been widely used because of its low cost, good electrical and thermal conductivity, the fact that it is not easy to oxidize, and its high reliability. Therefore, it is necessary to review its research progress. In this paper, the preparation and application of palladium-plated copper bonding wire are reviewed. Firstly, the preparation methods of electroplating, electroless plating, and direct plating are introduced. Secondly, the factors affecting the distribution of Pd in free air balls and bonding interfaces, the effect of Pd on the formation and growth of intermetallic compounds in PdCu wire, stitch bond, and reliability of PdCu wire are summarized and analyzed in the application process. Finally, its development prospect is prospected. Hopefully, this review can help readers to have a comprehensive understanding of the preparation and application of palladium-plated copper bonding wires, and can accelerate the promotion of its application in more fields in the future.
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In person re-identification (re-ID), extracting part-level features from person images has been verified to be crucial to offer fine-grained information. Most of the existing CNN-based methods only locate the human parts coarsely, or rely on pretrained human parsing models and fail in locating the identifiable nonhuman parts (e.g., knapsack). In this article, we introduce an alignment scheme in transformer architecture for the first time and propose the auto-aligned transformer (AAformer) to automatically locate both the human parts and nonhuman ones at patch level. We introduce the "Part tokens (PARTs)", which are learnable vectors, to extract part features in the transformer. A PART only interacts with a local subset of patches in self-attention and learns to be the part representation. To adaptively group the image patches into different subsets, we design the auto-alignment. Auto-alignment employs a fast variant of optimal transport (OT) algorithm to online cluster the patch embeddings into several groups with the PARTs as their prototypes. AAformer integrates the part alignment into the self-attention and the output PARTs can be directly used as part features for retrieval. Extensive experiments validate the effectiveness of PARTs and the superiority of AAformer over various state-of-the-art methods.
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Diffraction-limited optical imaging through scattering media has the potential to transform many applications such as airborne and space-based imaging (through the atmosphere), bioimaging (through skin and human tissue), and fiber-based imaging (through fiber bundles). Existing wavefront shaping methods can image through scattering media and other obscurants by optically correcting wavefront aberrations using high-resolution spatial light modulators-but these methods generally require (i) guidestars, (ii) controlled illumination, (iii) point scanning, and/or (iv) statics scenes and aberrations. We propose neural wavefront shaping (NeuWS), a scanning-free wavefront shaping technique that integrates maximum likelihood estimation, measurement modulation, and neural signal representations to reconstruct diffraction-limited images through strong static and dynamic scattering media without guidestars, sparse targets, controlled illumination, nor specialized image sensors. We experimentally demonstrate guidestar-free, wide field-of-view, high-resolution, diffraction-limited imaging of extended, nonsparse, and static/dynamic scenes captured through static/dynamic aberrations.
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Background: Smartphone addiction (SA) is associated with adverse consequences, especially for freshmen. Evidence indicates that SA is associated with depression, and it is necessary to conduct a longitudinal study to explore the association further. Methods: SA (measured by the Smartphone Addiction Scale-Short Version) and depression (measured by the Zung's Self-Rating Depression Scale) among 1,186 freshmen were surveyed at baseline and a respective 12-month follow-up for each participant. The application of a cross-lagged panel model approach (CLPM) revealed an association between SA and depression after adjusting for demographic variables. Results: The CLPM results showed a significant path from baseline SA to follow-up depression (ß = 0.08, P < 0.001) and a significant path from baseline depression to follow-up SA (ß = 0.08, P < 0.001). Compared with the overall cross-lagged model, the cross-lagged coefficient of the path from baseline SA to follow-up depression increased in the female group (ß = 0.10, P = 0.015), and the cross-lagged coefficient of the path from baseline depression to follow-up SA also increased significantly (ß = 0.15, P < 0.001). In contrast, the cross-lagged model in the male group showed no predictive effect between SA and depression (P > 0.05). Conclusions: The current study showed a significant bidirectional association between smartphone addiction and depression among freshmen, but only in the female population.