Research on fault diagnosis method of planetary gearbox based on dynamic simulation and deep transfer learning.

To address the issue of not having enough labeled fault data for planetary gearboxes in actual production, this research develops a simulation data-driven deep transfer learning fault diagnosis method that applies fault diagnosis knowledge from a dynamic simulation model to an actual planetary gearbox. Massive amounts of different fault simulation data are collected by creating a dynamic simulation model of a planetary gearbox. A fresh deep transfer learning network model is built by fusing one-dimensional convolutional neural networks, attention mechanisms, and domain adaptation methods. The network model is used to learn domain invariant features from simulated data, thereby enabling fault diagnosis on real data. The fault diagnosis experiment is verified by using the Drivetrain Diagnostics Simulator test bench. The validity of the proposed means is evaluated by comparing the diagnostic accuracy of various means on various diagnostic tasks.

Pachymic Acid Ameliorates Pulmonary Hypertension by Regulating Nrf2-Keap1-ARE Pathway.

OBJECTIVE: Pulmonary hypertension (PH) is a severe pulmonary vascular disease that eventually leads to right ventricular failure and death. The purpose of this study was to investigate the mechanism by which pachymic acid (PA) pretreatment affects PH and pulmonary vascular remodeling in rats. METHODS: PH was induced via hypoxia exposure and administration of PA (5 mg/kg per day) in male Sprague-Dawley rats. Hemodynamic parameters were measured using a right ventricular floating catheter and pulmonary vascular morphometry was measured by hematoxylin-eosin (HE), α-SMA and Masson staining. MTT assays and EdU staining were used to detect cell proliferation, and apoptosis was analyzed by TUNEL staining. Western blotting and immunohistochemistry were used to detect the expression of proteins related to the Nrf2-Keap1-ARE pathway. RESULTS: PA significantly alleviated hypoxic PH and reversed right ventricular hypertrophy and pulmonary vascular remodeling. In addition, PA effectively inhibited proliferation and promoted apoptosis in hypoxia-induced pulmonary artery smooth muscle cells (PASMCs). Moreover, PA pretreatment inhibited the expression of peroxy-related factor (MDA) and promoted the expression of antioxidant-related factors (GSH-PX and SOD). Furthermore, hypoxia inhibited the Nrf2-Keap1-ARE signaling pathway, while PA effectively activated this pathway. Most importantly, addition of the Nrf2 inhibitor ML385 reversed the inhibitory effects of PA on ROS generation, proliferation, and apoptosis tolerance in hypoxia-induced PASMCs. CONCLUSION: Our study suggests that PA may reverse PH by regulating the Nrf2-Keap1-ARE signaling pathway.

Leukemia Inhibitory Factor Decreases Neurogenesis and Angiogenesis in a Rat Model of Intracerebral Hemorrhage.

Neurogenesis and angiogenesis can improve the neurologic function after intracerebral hemorrhage (ICH). Leukemia inhibitory factor (LIF) plays an important role in neurogenesis and angiogenesis. In this study, a rat model of autologous blood-induced ICH was used to evaluate the effect of LIF on the neurogenesis and angiogenesis following ICH. After ICH, LIF-positive neurons and dilated vessels were detected in the peri-hematomal region. It was found that LIF levels increased significantly and peaked 14 days after ICH induction. Double immunofluorescence confirmed that LIF was expressed in neurons and endothelial cells. ICH also led to increases of doublecortin (DCX)- and von Willebrand factor (vWF)-positive cells as well as proliferation of cell nuclear antigen (PCNA)+/DCX+ and PCNA+/vWF+ nuclei. All these ICH-induced increases were significantly attenuated by exogenous LIF infusion. These data suggested that LIF was a negative regulator of neurogenesis and angiogenesis after ICH.

Buyang Huanwu Decoction () Attenuates Glial Scar by Downregulating the Expression of Leukemia Inhibitory Factor in Intracerebral Hemorrhagic Rats.

OBJECTIVE: To evaluate the effect of Buyang Huanwu Decoction (, BYHWD) on glial scar after intracerebral hemorrhage (ICH) and investigate the underlying mechanism. METHODS: Collagenase type VII (0.5 U) was injected stereotaxically into right globus pallidus to induce ICH model. One hundred and twenty Sprague-Dawley rats were randomly divided into 3 groups according to a random number table, including normal group (n=40), ICH model group (n=40) and BYHWD group (n=40), respectively. After ICH, the rats in the BYHWD group were intragastrically administered with BYHWD (4.36 g/kg) once a day for 21 days, while the rats in ICH group were administered with equal volume of distilled water for 21 days, respectively. Double immunolabeling was performed for proliferating cell nuclear antigen (PCNA)+/glial fibrillary acidic protein (GFAP)+ nuclei. The expression of GFAP and leukemia inhibitory factor (LIF) was evaluated by immunohistochemistry and quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: The astrocytes with hypertrophied morphology around the hematoma was observed on day 3 after ICH. The number of GFAP positive cells and GFAP mRNA levels increased notably on day 3 and reached the peak on day 14 post-ICH (P<0.01). PCNA+/GFAP+ nuclei were observed around the hematoma and reached the peak on day 14 post-ICH (P<0.01). In addition, LIF-positive astrocytes and LIF mRNA level in the hemorrhagic region increased significantly till day 14 post-ICH (P<0.01). However, BYHWD not only reduced the number of PCNA+/GFAP+ nuclei, but also decreased GFAP and LIF levels (P<0.05). CONCLUSIONS: BYHWD could attenuate ICH-induced glial scar by downregulating the expression of LIF in the rats.

2-Methoxyestradiol Inhibits Intracerebral Hemorrhage- Induced Angiogenesis in Rats.

AIM: Angiogenesis occurs after intracerebral hemorrhage (ICH). Hypoxia-inducible factor-1? (HIF-1?) is a critical regulator of angiogenesis. However, its role in the central nervous system remains controversial. 2-Methoxyestradiol (2ME2), a natural metabolite of estrogen, is known to inhibit HIF-1?. In the present study, we investigated the effect of 2ME2 in a rat model of ICH-induced angiogenesis. MATERIAL AND METHODS: Sprague-Dawley male rats (n=50) were randomly divided into 5 groups: Sham operated group; ICH; ICH+2ME2; and ICH+Vehicle groups. ICH model was induced by stereotactic injection of collagenase type VII into the right globus pallidus. 2ME2 or vehicle (10% dimethyl sulfoxide) was administered intraperitoneally 10 min after ICH. Angiogenesis and expression of HIF-1? was evaluated by immunohistochemistry, quantitative real time-reverse transcription polymerase chain reaction and western blot, respectively. RESULTS: Proliferating cell nuclear antigen (PCNA)-labeled nuclei were detected in cerebral endothelial cells (ECs) around the hematoma. The labeling peaked at 14 days post-ICH. HIF-1?-immunoreactive microvessels with dilated outline were detected in the perihematomal tissues. The vessels extended into the clot from the surrounding tissues from day 7 onwards. HIF-1? protein levels increased, while no change was observed in HIF-1? mRNA expression after ICH. 2ME2 decreased the PCNA-labeled nuclei in cerebral ECs and down-regulated the expression of HIF-1? protein as well, while it had little effect on the mRNA expression of HIF-1?. CONCLUSION: HIF-1? inhibitor, 2ME2, inhibited post-ICH angiogenesis by suppressing HIF-1? expression, thus exerting detrimental effects in ICH.

Activation of the Notch-1 signaling pathway may be involved in intracerebral hemorrhage-induced reactive astrogliosis in rats.

OBJECTIVE Reactive astrogliosis, a key feature that is characterized by glial proliferation, has been observed in rat brains after intracerebral hemorrhage (ICH). However, the mechanisms that control reactive astrogliosis formation remain unknown. Notch-1 signaling plays a critical role in modulating reactive astrogliosis. The purpose of this paper was to establish whether Notch-1 signaling is involved in reactive astrogliosis after ICH. METHODS ICH was induced in adult male Sprague-Dawley rats via stereotactic injection of autologous blood into the right globus pallidus. N-[ N-(3,5-difluorophenacetyl)-l-alanyl]- S-phenylglycine t-butyl ester (DAPT) was injected into the lateral ventricle to block Notch-1 signaling. The rats' brains were perfused to identify proliferating cell nuclear antigen (PCNA)-positive/GFAP-positive nuclei. The expression of GFAP, Notch-1, and the activated form of Notch-1 (Notch intracellular domain [NICD]) and its ligand Jagged-1 was assessed using immunohistochemical and Western blot analyses, respectively. RESULTS Notch-1 signaling was upregulated and activated after ICH as confirmed by an increase in the expression of Notch-1 and NICD and its ligand Jagged-1. Remarkably, blockade of Notch-1 signaling with the specific inhibitor DAPT suppressed astrocytic proliferation and GFAP levels caused by ICH. In addition, DAPT improved neurological outcome after ICH. CONCLUSIONS Notch-1 signaling is a critical regulator of ICH-induced reactive astrogliosis, and its blockage may be a potential therapeutic strategy for hemorrhagic injury.

Leukemia Inhibitory Factor Contributes to Reactive Astrogliosis via Activation of Signal Transducer and Activator of Transcription 3 Signaling after Intracerebral Hemorrhage in Rats.

Reactive astrogliosis has occurred after intracerebral hemorrhage (ICH). Leukemia inhibitory factor (LIF) can act as a modulator for glial gene expression. Signal transducer and activator of transcription 3 (STAT3) is a critical regulator of reactive astrogliosis. The present study tested whether endogenous LIF acted on ICH-induced reactive astrogliosis via the STAT3 signaling pathway. Rats were divided into three experimental groups: 1) Rats received either an ICH or a needle insertion (sham), 2) Rats received 100 ng LIF or an equal volume of phosphate-buffered saline (PBS) by direct infusion into the lateral ventricle (LV) after ICH, and 3) AG490 (0.25 mg/kg) was injected into the LV to block STAT3 signaling. Brains were perfused to identify proliferating cell nuclear antigen (PCNA)+/glial fibrillary acidic protein (GFAP)+nuclei. The expression of GFAP, LIF, LIF receptor (LIFR), glycoprotein 130 (gp130), and phospho-STAT3 (p-STAT3) was evaluated by immunohistochemistry and Western blot, respectively. After ICH, the number of the PCNA+/GFAP+ nuclei and the expression of GFAP, LIF, LIFR, gp130, and p-STAT3 were increased. Moreover, LIF increased the number of PCNA+/GFAP+ nuclei and the expression of GFAP, LIFR, gp130, and p-STAT3. The number of PCNA+/ GFAP+ nuclei and GFAP protein levels were attenuated markedly after inhibition of p-STAT3. Together, these data suggest that LIF contributes to ICH-related reactive astrogliosis via activation of STAT3 signaling.

Simultaneous-Fault Diagnosis of Gearboxes Using Probabilistic Committee Machine.

This study combines signal de-noising, feature extraction, two pairwise-coupled relevance vector machines (PCRVMs) and particle swarm optimization (PSO) for parameter optimization to form an intelligent diagnostic framework for gearbox fault detection. Firstly, the noises of sensor signals are de-noised by using the wavelet threshold method to lower the noise level. Then, the Hilbert-Huang transform (HHT) and energy pattern calculation are applied to extract the fault features from de-noised signals. After that, an eleven-dimension vector, which consists of the energies of nine intrinsic mode functions (IMFs), maximum value of HHT marginal spectrum and its corresponding frequency component, is obtained to represent the features of each gearbox fault. The two PCRVMs serve as two different fault detection committee members, and they are trained by using vibration and sound signals, respectively. The individual diagnostic result from each committee member is then combined by applying a new probabilistic ensemble method, which can improve the overall diagnostic accuracy and increase the number of detectable faults as compared to individual classifiers acting alone. The effectiveness of the proposed framework is experimentally verified by using test cases. The experimental results show the proposed framework is superior to existing single classifiers in terms of diagnostic accuracies for both single- and simultaneous-faults in the gearbox.

Electroacupuncture improves recovery after hemorrhagic brain injury by inducing the expression of angiopoietin-1 and -2 in rats.

BACKGROUND: Angiopoietin (Ang) is one of the major effectors of angiogenesis, playing a critical role in neurovascular remodeling after stroke. Acupuncture has been widely used for treating stroke in China for a long time. Recently, we have demonstrated that electroacupuncture (EA) can accelerate intracerebral hemorrhage (ICH)-induced angiogenesis in rats. In the present study, we investigated the effect of EA on the expression of Ang-1 and Ang-2 in the brain after ICH. METHODS: ICH was induced by stereotactic injection of collagenase type VII into the right globus pallidus. Adult male Sprague-Dawley rats were randomized into the following four groups: sham-operation (SHAM), stroke-no electroacupuncture (SNE), stroke-EA at the Zusanli acupoint (SEZ), and stroke-EA at a nonacupoint (SEN). EA was applied to the bilateral Zusanli (ST36) acupoint in the SEZ group and a nonacupoint in the SEN group. The expression of Ang-1 and Ang-2 was evaluated by immunohistochemistry and quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: Some Ang-1 and Ang-2 immunoreactive microvessels with a dilated outline were detected in the perihematomal tissues after ICH, and the vessels extended into the clot from the surrounding area since day 7. The expression of Ang-1 increased notably as long as 2 weeks after ICH, while Ang-2 immunoreactivity declined at about 7 days following a striking upregulation at 3 days. EA at the Zusanli (ST36) acupoint upregulated the expression of Ang-1 and Ang-2 at both the protein and mRNA levels. However, EA at a nonacupoint had little effect on the expression of Ang-1 and Ang-2. CONCLUSIONS: Our data suggest that EA at the Zusanli (ST36) acupoint exerts neuroprotective effects on hemorrhagic stroke by upregulation of Ang-1 and Ang-2.

Alteration of thrombospondin-1 and -2 in rat brains following experimental intracerebral hemorrhage. Laboratory investigation.

OBJECT: Spontaneous intracerebral hemorrhage (ICH) is among the most intractable forms of stroke. Angiogenesis, an orchestrated balance between proangiogenic and antiangiogenic factors, is a fundamental process to brain development and repair by new blood vessel formation from preexisting ones and can be induced by ICH. Thrombospondin (TSP)­1 and TSP-2 are naturally occurring antiangiogenic factors. The aim of this study was to observe their expression in rat brains with ICH. METHODS: Intracerebral hemorrhage was induced in adult male Sprague-Dawley rats by stereotactic injection of collagenase VII or autologous blood into the right globus pallidus. The expression of TSP-1 and -2 was evaluated by immunohistochemistry and quantitative real-time reverse transcription­polymerase chain reaction analysis. RESULTS: After the induction of ICH, some TSP1- or TSP2-immunoreactive microvessels resided around the hematoma for ~ 7 days and extended into a clot thereafter. Cerebral endothelial cells expressed the TSPs. The expression of TSP-1 and TSP-2 mRNA peaked at 4 and 14 days after collagenase-induced ICH, respectively. CONCLUSIONS: Findings in this study suggest that ICH can alter the expression of TSP-1 and TSP-2, which may be involved in modulating angiogenesis in brains following ICH.

[Effect of buyang huanwu decoction on expressions of angiopoietin-1 and its receptor mRNA in brain of rat after intracerebral hemorrhage].

OBJECTIVE: To investigate the mechanisms of Buyang Huanwu Decoction (BYHWD) by observing its effects on expressions of angiopoietin-1 (Ang-1) and the endothelial-specific receptor tyrosine kinase (Tie-2) mRNA in damaged region of rats' brain after intracerebral hemorrhage (ICH). METHODS: One hundred and sixty Sprague-Dawley rats were randomly divided into four groups, 10 in the normal control group, 60 in the sham-operative group, 60 in the ICH model group, and 30 in the BYHWD-treated group. The ICH model was established by injecting collagenase type VII 0.5 U stereotaxically into right globus pallidus. Animals in the BYHWD-treated group were administered orally with BYHWD, while animals in the sham-operative group and the ICH model group were administered orally with equal volume distilled water, and those in the normal control group drank water freely. The positional variations of the expression of Ang-1 and Tie-2 in the sham-operative group and the model group were assayed by immunohistochemistry on dayl, 4, 7, 14, 21 and 28 after modeling, in the meantime, the dynamic changes of Ang-1 and Tie-2 mRNA expressions in all groups were assayed by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: No significant expression of Ang-1 and Tie-2 in brain of rats in the normal or the sham-operative group was found during the experiment. In the model group, the Ang-1 and Tie-2 positive micrangio-segments appeared at the edge of clot on day 1 to day 4, they gradually penetrated to hematoma area from day 7; with Ang-1 and Tie-2 mRNA expressed from day 1, but very weak until day 4, showing no significant difference to that on day 1; thereafter, they increased gradually, and reached the peak on day 28 (P <0.05). While the two expressions in the BYHWD treated group reached the peak on day 21, and from day 7 to day 28, they were all significantly higher than those in ICH model group at the corresponding time points (P <0.01). CONCLUSION: BYHWD can promote the up-regulation of Ang-1 and Tie-2mRNA expressions in brain of intracerebral hemorrhagic rats, which might accelerate the angiogenesis in the reconstruction of microvascular network in the damaged zone, and thus facilitating the repairing of damaged tissue.

Synthesis and investigation of novel branched PEG-based soluble polymer supports.

The efficient synthesis of a number of novel poly(ethylene glycol)-based branched soluble polymer supports with high loading capacities has been developed. These compounds are characterized and tested for their loading levels utilizing a number of coupling reactions.

Photochemistry on soluble polymer supports: synthesis of nucleosides.

[reaction: see text] A new soluble polymer support synthesis of nucleosides is described. The photochemical ring expansion of cyclobutanones in the presence of poly(ethylene glycol) (PEG) results in polymer-supported ribosides. These photoadducts can be cleaved from the polymer under Vorbrüggen coupling conditions with TMS-protected purines and pyrimidines to give ribonucleosides. The method has been extended to include modified PEGs with dendritic end-groups in order to improve the loading levels for these coupling reactions.