A Long-Term Video Tracking Method for Group-Housed Pigs.

Pig tracking provides strong support for refined management in pig farms. However, long and continuous multi-pig tracking is still extremely challenging due to occlusion, distortion, and motion blurring in real farming scenarios. This study proposes a long-term video tracking method for group-housed pigs based on improved StrongSORT, which can significantly improve the performance of pig tracking in production scenarios. In addition, this research constructs a 24 h pig tracking video dataset, providing a basis for exploring the effectiveness of long-term tracking algorithms. For object detection, a lightweight pig detection network, YOLO v7-tiny_Pig, improved based on YOLO v7-tiny, is proposed to reduce model parameters and improve detection speed. To address the target association problem, the trajectory management method of StrongSORT is optimized according to the characteristics of the pig tracking task to reduce the tracking identity (ID) switching and improve the stability of the algorithm. The experimental results show that YOLO v7-tiny_Pig ensures detection applicability while reducing parameters by 36.7% compared to YOLO v7-tiny and achieving an average video detection speed of 435 frames per second. In terms of pig tracking, Higher-Order Tracking Accuracy (HOTA), Multi-Object Tracking Accuracy (MOTP), and Identification F1 (IDF1) scores reach 83.16%, 97.6%, and 91.42%, respectively. Compared with the original StrongSORT algorithm, HOTA and IDF1 are improved by 6.19% and 10.89%, respectively, and Identity Switch (IDSW) is reduced by 69%. Our algorithm can achieve the continuous tracking of pigs in real scenarios for up to 24 h. This method provides technical support for non-contact pig automatic monitoring.

α-Synuclein aggregation causes muscle atrophy through neuromuscular junction degeneration.

BACKGROUND: Sarcopenia is common in patients with Parkinson's disease (PD), showing mitochondrial oxidative stress in skeletal muscle. The aggregation of α-synuclein (α-Syn) to induce oxidative stress is a key pathogenic process of PD; nevertheless, we know little about its potential role in regulating peripheral nerves and the function of the muscles they innervate. METHODS: To investigate the role of α-Syn aggregation on neuromuscular system, we used the Thy1 promoter to overexpress human α-Syn transgenic mice (mThy1-hSNCA). hα-Syn expression was evaluated by western blot, and its localization was determined by confocal microscopy. The impact of α-Syn aggregation on the structure and function of skeletal muscle mitochondria and neuromuscular junctions (NMJs), as well as muscle mass and function were characterized by flow cytometry, transmission electron microscopy, Seahorse XF24 metabolic assay, and AAV9 in vivo injection. We assessed the regenerative effect of mitochondrial-targeted superoxide dismutase (Mito-TEMPO) after skeletal muscle injury in mThy1-hSNCA mice. RESULTS: Overexpressed hα-Syn protein localized in motor neuron axons and NMJs in muscle and formed aggregates. α-Syn aggregation increased the number of abnormal mitochondrial in the intramuscular axons and NMJs by over 60% (P < 0.01), which inhibited the release of acetylcholine (ACh) from presynaptic vesicles in NMJs (P < 0.05). The expression of genes associated with NMJ activity, neurotransmission and regulation of reactive oxygen species (ROS) metabolic process were significantly decreased in mThy1-hSNCA mice, resulting in ROS production elevated by ~220% (P < 0.05), thereby exacerbating oxidative stress. Such process altered mitochondrial spatial relationships to sarcomeric structures, decreased Z-line spacing by 36% (P < 0.05) and increased myofibre apoptosis by ~10% (P < 0.05). Overexpression of α-Syn altered the metabolic profile of muscle satellite cells (MuSCs), including basal respiratory capacity (~170% reduction) and glycolytic capacity (~150% reduction) (P < 0.05) and decreased cell migration and fusion during muscle regeneration (~60% and ~40%, respectively) (P < 0.05). We demonstrated that Mito-TEMPO treatment could restore the oxidative stress status (the complex I/V protein and enzyme activities increased ~200% and ~150%, respectively), which caused by α-Syn aggregation, and improve the ability of muscle regeneration after injury. In addition, the NMJ receptor fragmentation and ACh secretion were also improved. CONCLUSIONS: These results reveal that the α-synuclein aggregation plays an important role in regulating acetylcholine release from neuromuscular junctions and induces intramuscular mitochondrial oxidative stress, which can provide new insights into the aetiology of muscle atrophy in patients with Parkinson's disease.

Bergaptol Alleviates LPS-Induced Neuroinflammation, Neurological Damage and Cognitive Impairment via Regulating the JAK2/STAT3/p65 Pathway.

Purpose: Neuroinflammation is considered a critical pathological process in various central nervous system (CNS) diseases and is closely related to neuronal death and dysfunction. Bergaptol is a natural 5-hydroxyfurocoumarin found in lemon, bergamot and other plants. Some studies have confirmed its anti-cancer, anti-inflammatory and anti-atherogenic functions, indicating that it may have significant medicinal value. In this study, we investigated the potential effect of Bergaptol in vitro and in vivo neuroinflammatory models. Methods: Mice were injected with LPS (40 µg/kg) into the hippocampal CA1 region and then injected intraperitoneally with Bergaptol (10, 20 and 40 mg/kg) once a day for two weeks. In addition, to verify the effect of Bergaptol on BV2 cells, Bergaptol with different concentrations (5, 10 and 20 µg/mL) was firstly incubated for 1 hour, then LPS with a concentration of 1 µg/mL was added and incubated for 23 hours. Results: Bergaptol treatment significantly improved the cognitive impairment induced by LPS. In addition, Bergaptol significantly inhibited the reduction of dendritic spines and the mRNA level of inflammatory factors (TNF-α, IL-6 and IL-1ß) in hippocampal induced by LPS. In vitro, Bergaptol inhibited the production of TNF-α, IL-6 and IL-1ß from LPS-treated BV-2 cells. In addition, Bergaptol treatment significantly reduced the phosphorylation levels of JAK2, STAT3 and p65 in LPS-stimulated BV-2 cells. Conclusion: In conclusion, our results suggest that Bergaptol alleviates LPS-induced neuroinflammation, neurological damage and cognitive impairment by regulating the JAK2/STAT3/P65 pathway, suggesting that Bergaptol is a promising neuroprotective agent.

Modeling Dynamic Recrystallization Behavior in a Novel HIPed P/M Superalloy during High-Temperature Deformation.

The dynamic recrystallization (DRX) features and the evolution of the microstructure of a new hot isostatic pressed (HIPed) powder metallurgy (P/M) superalloy are investigated by hot-compression tests. The sensitivity of grain dimension and DRX behavior to deformation parameters is analyzed. The results reveal that the DRX features and grain-growth behavior are significantly affected by deformation conditions. The DRX process is promoted with a raised temperature/true strain or a reduced strain rate. However, the grains grow up rapidly at relatively high temperatures. At strain rates of o.1 s-1 and 1 s-1, a uniform microstructure and small grains are obtained. Due to the obvious differences in the DRX rate at various temperatures, the piecewise DRX kinetics equations are proposed to predict the DRX behavior. At the same time, a mathematical model for predicting the grain dimension and the grain growth behavior is established. To further analyze the DRX behavior and the changes in grain dimension, the hot deformation process is simulated. The developed grain-growth equation as well as the piecewise DRX kinetics equations are integrated into DEFORM software. The simulated DRX features are consistent with the test results, indicating that the proposed DRX kinetics equations and the established grain-growth model can be well used for describing the microstructure evolution. So, they are very useful for the practical hot forming of P/M superalloy parts.

Skeletal Muscle Metabolic Alternation Develops Sarcopenia.

Sarcopenia is a new type of senile syndrome with progressive skeletal muscle mass loss with age, accompanied by decreased muscle strength and/or muscle function. Sarcopenia poses a serious threat to the health of the elderly and increases the burden of family and society. The underlying pathophysiological mechanisms of sarcopenia are still unclear. Recent studies have shown that changes of skeletal muscle metabolism are the risk factors for sarcopenia. Furthermore, the importance of the skeletal muscle metabolic microenvironment in regulating satellite cells (SCs) is gaining significant attention. Skeletal muscle metabolism has intrinsic relationship with the regulation of skeletal muscle mass and regeneration. This review is to discuss recent findings regarding skeletal muscle metabolic alternation and the development of sarcopenia, hoping to contribute better understanding and treatment of sarcopenia.

Tryptophan hydroxylase 1 drives glioma progression by modulating the serotonin/L1CAM/NF-κB signaling pathway.

BACKGROUND: Glioma is one of the main causes of cancer-related mortality worldwide and is associated with high heterogeneity. However, the key players determining the fate of glioma remain obscure. In the present study, we shed light on tumor metabolism and aimed to investigate the role of tryptophan hydroxylase 1 (TPH-1) in the advancement of glioma. METHOD: Herein, the levels of TPH-1 expression in glioma tissues were evaluated using The Cancer Genome Atlas (TCGA) database. Further, the proliferative characteristics and migration ability of TPH-1 overexpressing LN229/T98G cells were evaluated. Additionally, we performed a cytotoxicity analysis using temozolomide (TMZ) in these cells. We also examined the tumor growth and survival time in a mouse model of glioma treated with chemotherapeutic agents and a TPH-1 inhibitor. RESULTS: The results of both clinical and experimental data showed that excess TPH-1 expression resulted in sustained glioma progression and a dismal overall survival in these patients. Mechanistically, TPH-1 increased the production of serotonin in glioma cells. The elevated serotonin levels then augmented the NF-κB signaling pathway through the upregulation of the L1-cell adhesion molecule (L1CAM), thereby contributing to cellular proliferation, invasive migration, and drug resistance. In vivo experiments demonstrated potent antitumor effects, which benefited further from the synergistic combination of TMZ and LX-1031. CONCLUSION: Taken together, these data suggested that TPH-1 facilitated cellular proliferation, migration, and chemoresistance in glioma through the serotonin/L1CAM/NF-κB pathway. By demonstrating the link of amino acid metabolic enzymes with tumor development, our findings may provide a potentially viable target for therapeutic manipulation aimed at eradicating glioma.

Effects of Aging Treatment on Corrosion Behavior of a Tensile Deformed Al-Cu-Mn-Fe-Zr Alloy in 3.5% NaCl Solution.

In this paper, the effects of an aging treatment on the corrosion resistance/mechanism of a tensile deformed Al-Cu-Mn-Fe-Zr alloy are investigated. The impedance magnitude and polarization resistance increase, while the corrosion current decreases with the increased aging time and temperature. The discontinuously-distributed precipitates and precipitation-free zone, which can cut the corrosion channels, appear at grain boundaries when the temperature is relatively high and the aging time is relatively long. They can improve the corrosion resistance. Additionally, the intergranular and pitting corrosion are the main mechanisms. The intergranular corrosion is likely to occur in an under-aged alloy. This is because the potential difference between the grain boundaries and grains is high, due to the segregation of Cu atoms. When the aging degree is increased, the grain boundary precipitates reduce the potential difference, and the intragranular precipitates make the surrounding matrix prone to dissolution. As such, the pitting corrosion is likely to occur in the over-aged alloys.

Effect of Ultrasonic-Assisted Casting on Hot Deformation Mechanism and Microstructure of 35CrMo Steel Ingot.

Hot compression tests were performed with strain rates (0.01-10 s-1) and temperatures (850-1150 °C). The power law relationship between the critical stress and critical strain and Zener-Hollomon parameters was determined by θ-σ curves. Microstructure was investigated by electron backscattered diffraction. The results showed that the flow behavior and microstructure of 35CrMo steel was affected by ultrasonic-assisted casting. The activation energy of non-ultrasonic and ultrasonic-assisted 35CrMo steel were 410 ± 9.9 and 386 ± 9.4 kJ/mol, respectively, and the activation energy of ultrasonic-assisted specimens was reduced by 6%. In addition, the ultrasonic-assisted treatment refines the grains to some extent and makes the softening process of ultrasonic-assisted samples progress faster, which promoted the development of dynamic recrystallization and the production of Σ3 boundaries. The discontinuous dynamic recrystallization was the main DRX nucleation mechanism of the 35CrMo steel.

Regulation of myonuclear positioning and muscle function by the skeletal muscle-specific CIP protein.

The appropriate arrangement of myonuclei within skeletal muscle myofibers is of critical importance for normal muscle function, and improper myonuclear localization has been linked to a variety of skeletal muscle diseases, such as centronuclear myopathy and muscular dystrophies. However, the molecules that govern myonuclear positioning remain elusive. Here, we report that skeletal muscle-specific CIP (sk-CIP) is a regulator of nuclear positioning. Genetic deletion of sk-CIP in mice results in misalignment of myonuclei along the myofibers and at specialized structures such as neuromuscular junctions (NMJs) and myotendinous junctions (MTJs) in vivo, impairing myonuclear positioning after muscle regeneration, leading to severe muscle dystrophy in mdx mice, a mouse model of Duchenne muscular dystrophy. sk-CIP is localized to the centrosome in myoblasts and relocates to the outer nuclear envelope in myotubes upon differentiation. Mechanistically, we found that sk-CIP interacts with the Linker of Nucleoskeleton and Cytoskeleton (LINC) complex and the centriole Microtubule Organizing Center (MTOC) proteins to coordinately modulate myonuclear positioning and alignment. These findings indicate that sk-CIP may function as a muscle-specific anchoring protein to regulate nuclear position in multinucleated muscle cells.

The inhibition of H1N1 influenza induced apoptosis by sodium selenite through ROS-mediated signaling pathways.

The high variability of influenza viruses has made it more difficult for people to cope with influenza. When antigen transformation occurs, even new influenza without preventive vaccines may be produced, which poses a great threat to human health. Selenium is an essential trace element in humans and mammals, and has many biological activities. It has attracted people's research interest in recent years. In this study, MDCK cells were used as a model to observe the effect of sodium selenite on H1N1 influenza virus. Our research showed that sodium selenite (Na2SeO3) has an anti-influenza H1N1 virus effect, and the anti-viral effect of sodium selenite was further demonstrated by caspase-3, AKT, MAPK and p53 signaling pathways. The investigations of the mechanism revealed that the sodium selenite could block H1N1 influenza from infecting MDCK cells through inhibiting the production of ROS. The results demonstrate that selenium supplementation may provide a feasible approach to inhibit the infection of H1N1 influenza virus.

Effect of Hot Deformation Process Parameters on Microstructure and Corrosion Behavior of 35CrMoV Steel.

Hot deformation experiments of as-cast 35CrMoV steel, with strain rates of 0.01 s-1 and 10 s-1, deformation temperatures of 850, 950, and 1050 °C, and an extreme deformation reaching 50%, were carried out using a Gleeble-3810 thermal simulator. Electrochemical corrosion experiments were conducted on the deformed specimens. The microstructure was observed by optical microscope (OM), and the corrosion morphology and corrosion products of the specimens were investigated by scanning electron microscopy (SEM), energy disperse spectroscopy (EDS), confocal laser scanning microscopy (CLSM), and X-ray diffraction (XRD) techniques. The results show that the grain size increased gradually with an increase in the deformation temperature at the same strain rate, whereas the corrosion resistance deteriorated. At the same deformation temperature, the grain size becomes smaller as the strain rate increases, which enhances the corrosion resistance. This is mainly attributed to the fine grains, which can form more grain boundaries, increase the grain boundary area, and accelerate the formation of the inner rust layer at the beginning of corrosion. Moreover, fine grains can also refine the rust particles and enhance the bonding strength between the inner rust layer and the matrix. The denseness and stability of the inner rust layer increases as the corrosion process progresses, thereby improving corrosion resistance.

A wearable mixed-reality holographic computer for guiding external ventricular drain insertion at the bedside.

OBJECTIVE: The goal of this study was to explore the feasibility and accuracy of using a wearable mixed-reality holographic computer to guide external ventricular drain (EVD) insertion and thus improve on the accuracy of the classic freehand insertion method for EVD insertion. The authors also sought to provide a clinically applicable workflow demonstration. METHODS: Pre- and postoperative CT scanning were performed routinely by the authors for every patient who needed EVD insertion. Hologram-guided EVD placement was prospectively applied in 15 patients between August and November 2017. During surgical planning, model reconstruction and trajectory calculation for each patient were completed using preoperative CT. By wearing a Microsoft HoloLens, the neurosurgeon was able to visualize the preoperative CT-generated holograms of the surgical plan and perform EVD placement by keeping the catheter aligned with the holographic trajectory. Fifteen patients who had undergone classic freehand EVD insertion were retrospectively included as controls. The feasibility and accuracy of the hologram-guided technique were evaluated by comparing the time required, number of passes, and target deviation for hologram-guided EVD placement with those for classic freehand EVD insertion. RESULTS: Surgical planning and hologram visualization were performed in all 15 cases in which EVD insertion involved holographic guidance. No adverse events related to the hologram-guided procedures were observed. The mean ± SD additional time before the surgical part of the procedure began was 40.20 ± 10.74 minutes. The average number of passes was 1.07 ± 0.258 in the holographic guidance group, compared with 2.33 ± 0.98 in the control group (p < 0.01). The mean target deviation was 4.34 ± 1.63 mm in the holographic guidance group and 11.26 ± 4.83 mm in the control group (p < 0.01). CONCLUSIONS: This study demonstrates the use of a head-mounted mixed-reality holographic computer to successfully perform hologram-assisted bedside EVD insertion. A full set of clinically applicable workflow images is presented to show how medical imaging data can be used by the neurosurgeon to visualize patient-specific holograms that can intuitively guide hands-on operation. The authors also provide preliminary confirmation of the feasibility and accuracy of this hologram-guided EVD insertion technique.

Zac1/GPR39 phosphorylating CaMK-II contributes to the distinct roles of Pax3 and Pax7 in myogenic progression.

Both Pax3 and Pax7 can activate a large panel of genes involved in muscle stem cell function. Despite a significant overlap in their transcriptional network, functional difference between them is observed. After overexpressing Pax3 or Pax7 in C2C12, we find both Zac1 and GPR39 are upregulated by Pax7 but not Pax3. Further studies suggest Zac1 interacts directly with Pax7, which can regulate GPR39 expression by activating Zac1. In addition, the effect of Zac1/GPR39 system on myogenic progression has been illuminated: Zac1/GPR39 can promote myogenic differentiation and produce type-II muscle fibers. Gait analysis verifies that transplanting GFP-labeled Pax7 RV/siZac1 transfected cells into mdx mice with muscle injury would delay muscle function repair. Molecular mechanism studies reveal the Zac1/GPR39 system is associated with different myogenic functions of Pax3 and Pax7: Pax7 activates Zac1/GPR39, which mediates the phosphorylation of CaMK-II, resulting in p-ERK1/2 dephosphorylation and ß-catenin inhibition, that promotes the formation of type-II muscle fibers; cells lacking Zac1/GPR39 system tend to remain stemness and form type-I muscle fibers after induced differentiation. This study will help the better understanding of the molecular mechanism of Pax3 and Pax7 in the regulation of myogenic progression and muscle fiber types, laying the providing suitable targets for the treatment of muscle diseases.

Chloride-accelerated Cu-Fenton chemistry for biofilm removal.

Biofilms present challenges to numerous industries. Herein, a simple approach was developed based on chloride-accelerated Fenton chemistry, where copper oxide nanoparticles facilitate efficient generation of reactive chlorine species for biofilm removal.

Poly(C)-binding protein 1 (Pcbp1) regulates skeletal muscle differentiation by modulating microRNA processing in myoblasts.

Regulation of gene expression during muscle development and disease remains incompletely understood. microRNAs are a class of small non-coding RNAs that regulate gene expression and function post-transcriptionally. The poly(C)-binding protein1 (Pcbp1, hnRNP-E1, or αCP-1) is an RNA-binding protein that has been reported to bind the 3'-UTRs of target genes to regulate mRNA stability and protein translation. However, Pcbp1's biological function and the general mechanism of action remain largely undetermined. Here, we report that Pcbp1 is a component of the miRNA-processing pathway that regulates miRNA biogenesis. siRNA-based inhibition of Pcbp1 in mouse skeletal muscle myoblasts led to dysregulated cellular proliferation and differentiation. We also found that Pcbp1 null mutant mice exhibit early embryonic lethality, indicating that Pcbp1 is indispensable for embryonic development. Interestingly, hypomorphic Pcbp1 mutant mice displayed defects in muscle growth due to defects in the proliferation and differentiation of myoblasts and muscle satellite cells, in addition to a slow to fast myofibril switch. Moreover, Pcbp1 modulated the processing of muscle-enriched miR-1, miR-133, and miR-206 by physically interacting with argonaute 2 (AGO2) and other miRNA pathway components. Our study, therefore, uncovers the important function of Pcbp1 in skeletal muscle and the microRNA pathway, signifying its potential as a therapeutic target for muscle disease.

PAX3+ skeletal muscle satellite cells retain long-term self-renewal and proliferation.

INTRODUCTION: Different populations of satellite cells (SCs) have been identified, but their functional difference remains unclear. METHODS: We used cell-surface markers and paired box transcription factor 3 (Pax3)/paired box transcription factor 7 (Pax7) expression to separate SC populations. In addition, self-renewal, proliferation, and differentiation abilities of each population were analyzed. RESULTS: Pax3+ /Pax7- SCs exhibited higher proliferation ability characterized by forming clusters of myogenic colonies with more self-renewing cells after several passages, while Pax3- /Pax7+ SCs had faster differentiation. The myotubes derived from Pax3+ /Pax7- SCs tended to express slow-myosin heavy chain and exhibited rhythmic contraction, while myotubes originating from Pax3- /Pax7+ SCs primarily formed fast-myosin heavy chains characterized by transitory contraction. CONCLUSIONS: Pax3+ /Pax7- SCs exhibited the ability of long-term self-renewal and proliferation, whereas Pax3- /Pax7+ SCs demonstrated faster differentiation. Muscle Nerve 54: 943-951, 2016.