Photonic implementation of the input and reservoir layers for a reservoir computing system based on a single VCSEL with two Mach-Zehnder modulators.

Hardware implementation of reservoir computing (RC), which could reduce the power consumption of machine learning and significantly enhance data processing speed, holds the potential to develop the next generation of machine learning hardware devices and chips. Due to the existing solution only implementing reservoir layers, the information processing speed of photonics RC system are limited. In this paper, a photonic implementation of a VMM-RC system based on single Vertical Cavity Surface Emitting Laser (VCSEL) with two Mach Zehnder modulators (MZMs) has been proposed. Unlike previous work, both the input and reservoir layers are realized in the optical domain. Additionally, the impact of various mask signals, such as Two-level mask, Six-level mask, and chaos mask signal, employed in system, has been investigated. The system's performance improves with the use of more complex mask(t). The minimum Normalized mean square error (NMSE) can reach 0.0020 (0.0456) for Santa-Fe chaotic time series prediction in simulation (experiment), while the minimum Word Error Rate (WER) can 0.0677 for handwritten digits recognition numerically. The VMM-RC proposed is instrumental in advancing the development of photonic RC by overcoming the long-standing limitations of photonic RC systems in reservoir implementation. Linear matrix computing units (the input layer) and nonlinear computing units (the reservoir layer) are simultaneously implemented in the optical domain, significantly enhancing the information processing speed of photonic RC systems.

Characterizing the aggregated encoding method utilizing bursts activated by a VCSEL-neuron with a feedback structure.

The rapid advancement of photonic technologies has facilitated the development of photonic neurons that emulate neuronal functionalities akin to those observed in the human brain. Neuronal bursts frequently occur in behaviors where information is encoded and transmitted. Here, we present the demonstration of the bursting response activated by an artificial photonic neuron. This neuron utilizes a single vertical-cavity surface-emitting laser (VCSEL) and encodes multiple stimuli effectively by varying the spike count during a burst based on the polarization competition in the VCSEL. By virtue of the modulated optical injection in the VCSEL employed to trigger the spiking response, we activate bursts output in the VCSEL with a feedback structure in this scheme. The bursting response activated by the VCSEL-neuron exhibits neural signal characteristics, promising an excitation threshold and the refractory period. Significantly, this marks the inaugural implementation of a controllable integrated encoding scheme predicated on bursts within photonic neurons. There are two remarkable merits; on the one hand, the interspike interval of bursts is distinctly diminished, amounting to merely one twenty-fourth compared to that observed in optoelectronic oscillators. Moreover, the interspike period of bursts is about 70.8% shorter than the period of spikes activated by a VCSEL neuron without optical feedback. Our results may shed light on the analogy between optical and biological neurons and open the door to fast burst encoding-based optical systems with a speed several orders of magnitude faster than their biological counterparts.

Noisy image segmentation based on synchronous dynamics of coupled photonic spiking neurons.

The collective dynamics in neural networks is essential for information processing and has attracted much interest on the application in artificial intelligence. Synchronization is one of the most dominant phenomenon in the collective dynamics of neural network. Here, we propose to use the spiking dynamics and collective synchronization of coupled photonic spiking neurons for noisy image segmentation. Based on the synchronization mechanism and synchronization control, the noised pattern segmentation is demonstrated numerically. This work provides insight into the possible application based on the collective dynamics of large-scale photonic networks and opens a way for ultra-high speed image processing.

Hybrid photonic deep convolutional residual spiking neural networks for text classification.

Spiking neural networks (SNNs) offer powerful computation capability due to its event-driven nature and temporal processing. However, it is still limited to shallow structure and simple tasks due to the training difficulty. In this work, we propose a deep convolutional residual spiking neural network (DCRSNN) for text classification tasks. In the DCRSNN, the feature extraction is achieved via a convolution SNN with residual connection, using the surrogate gradient direct training technique. Classification is performed by a fully-connected network. We also suggest a hybrid photonic DCRSNN, in which photonic SNNs are used for classification with a converted training method. The accuracy of hard and soft reset methods, as well as three different surrogate functions, were evaluated and compared across four different datasets. Results indicated a maximum accuracy of 76.36% for MR, 91.03% for AG News, 88.06% for IMDB and 93.99% for Yelp review polarity. Soft reset methods used in the deep convolutional SNN yielded slightly better accuracy than their hard reset counterparts. We also considered the effects of different pooling methods and observation time windows and found that the convergence accuracy achieved by convolutional SNNs was comparable to that of convolutional neural networks under the same conditions. Moreover, the hybrid photonic DCRSNN also shows comparable testing accuracy. This work provides new insights into extending the SNN applications in the field of text classification and natural language processing, which is interesting for the resources-restrained scenarios.

BP-based supervised learning algorithm for multilayer photonic spiking neural network and hardware implementation.

We introduce a supervised learning algorithm for photonic spiking neural network (SNN) based on back propagation. For the supervised learning algorithm, the information is encoded into spike trains with different strength, and the SNN is trained according to different patterns composed of different spike numbers of the output neurons. Furthermore, the classification task is performed numerically and experimentally based on the supervised learning algorithm in the SNN. The SNN is composed of photonic spiking neuron based on vertical-cavity surface-emitting laser which is functionally similar to leaky-integrate and fire neuron. The results prove the demonstration of the algorithm implementation on hardware. To seek ultra-low power consumption and ultra-low delay, it is great significance to design and implement a hardware-friendly learning algorithm of photonic neural networks and realize hardware-algorithm collaborative computing.

Cigarette smoke extract-induced inflammatory response via inhibition of the TFEB-mediated autophagy in NR8383 cells.

Objective: Chronic pulmonary inflammation caused by long-term smoking is the core pathology of COPD. Alveolar macrophages (AMs) are involved in the pulmonary inflammation of COPD. The accumulation of damaged materials caused by impaired autophagy triggers inflammatory response in macrophages. As a key transcription regulator, transcription factor EB (TFEB) activates the transcription of target genes related autophagy and lysosome by binding to promoters, whereas it is unclarified for the relationship between inflammatory response induced by cigarette smoke extract (CSE) and TFEB-mediated autophagy. Thus, we investigated the role of TFEB-mediated autophagy in inflammatory response induced by CSE in NR8383 cells, and to explore its potential mechanism. Methods: Based on cell viability and autophagy, cells treated with 20% concentration of CSE for 24 h were selected for further studies. Cells were divided into control group, chloroquine (CQ, the autophagy inhibitor) group, CSE group, CSE + rapamycin (the autophagy inducer) group and CSE + fisetin (the TFEB inducer) group. The levels of tumor necrosis factor α (TNF-α), interleukin 1ß (IL-1ß), and IL-6 in supernatant were detected by ELISA kits. The protein expressions were tested by western blot. The intensity of fluorescence of Lysosome-associated membrane protein 1 (LAMP1) and TFEB was detected by immunofluorescence. Lyso-Tracker Red staining was applied to detect the lysosome environment. Results: CSE inhibited the cell viability, increased the contents of TNF-α, IL-1ß, IL-6, the ratio of LC3II/I, and the level of P62 protein. Besides, CSE decreased the fluorescence intensity of LAMP1 protein and Lyso-Tracker Red staining, as well as the ratio of nucleus/cytosol of TFEB protein. Activating autophagy with rapamycin alleviated CSE-induced inflammatory response. The activation of TFEB via fisetin alleviated CSE-induced autophagy impairment and lysosomal dysfunction, thus alleviated inflammatory response in NR8383 cells. Conclusion: CSE-induced inflammatory response in NR8383 cells, which may be related to the inhibition of TFEB-mediated autophagy.

Neuromorphic convolution with a spiking DFB-SA laser neuron based on rate coding.

We propose a neuromorphic convolution system using a photonic integrated distributed feedback laser with a saturable absorber (DFB-SA) as a photonic spiking neuron. The experiments reveal that the DFB-SA laser can encode different stimulus intensities at different frequencies, similar to biological neurons. Based on this property, optical inputs are encoded into rectangular pulses of varying intensities and injected into the DFB-SA laser, enabling the convolution results to be represented by the firing rate of the photonic spiking neuron. Both experimental and numerical results show that the binary convolution is successfully achieved based on the rate-encoding properties of a single DFB-SA laser neuron. Furthermore, we numerically predict 4-channel quadratic convolution and accomplish MNIST handwritten digit classification using a spiking DFB-SA laser neuron model with rate coding. This work provides a novel approach for convolution computation, indicating the potential of integrating DFB-SA laser into future photonics spiking neural networks.

Experimental implementation of spike-based neuromorphic XOR operation based on polarization-mode competition in a single VCSOA.

We experimentally and numerically propose an approach for implementing spike-based neuromorphic exclusive OR (XOR) operation using a single vertical-cavity semiconductor optical amplifier (VCSOA). XOR operation is realized based on the neuron-like inhibitory dynamics of the VCSOA subject to dual-polarized pulsed optical injections. The inhibitory dynamics based on the polarization-mode competition effect are analyzed, and the inhibitory response can be obtained in a suitable range of wavelength detuning. Here, all input and output bits are represented by spikes that are compatible with the photonic spiking neural network. The experimental and numerical results show that XOR operation can be realized in two polarization modes by adjusting the time offset in the inhibitory window and setting defined reference thresholds. In addition, the influences of delay time and input intensity ratio on XOR operation are studied experimentally. This scheme is energy efficient because VCSOA neuromorphic photonics computing and information processing.

[Electroacupuncture preconditioning improves pulmonary function via inhibiting inflammatory response and up-regulating expression of ACE2 and Ang (1-7) in lipopolysaccharide-induced acute lung injury rats].

OBJECTIVE: To observe the effect of electroacupuncture (EA) at "Zusanli"(ST36) pretreatment on lung functions, inflammatory response, and levels of angiotensin-converting enzyme 2 (ACE2) and angiotensin (1-7) ï¼»Ang (1-7)ï¼½ in rats with sepsis-induced acute lung injury (ALI), so as to explore its mechanisms underlying improvement of ALI. METHODS: Thirty male SD rats were randomly divided into normal, model and EA groups (n=10 in each group). The sepsis-related ALI model was established by intraperitoneal injection of lipopolysaccharide (LPS, 5 mg/kg). Rats of the EA group received EA (4 Hz/20 Hz, 1-3 mA) stimulation at bilateral ST36 for 30 min, once each day, for 7 days before modeling. The lung functions including forced vital capacity (FVC), forced expiratory volume at 0.1 second (FEV0.1) and FEV0.3 were detected using a respiratory function detector for small animals at 3 h after modeling. The bronchoalveolar lavage fluid (BALF) was collected for assaying the contents of Ang (1-7), tumor necrosis factor-α (TNF-α) and interleukin-1 ß (IL-1ß) using ELISA. The lung wet/dry weight (W/D) ratio, FEV0.1/FVC, and FEV0.3/FVC were calculated. The histopathological changes of lung tissues were displayed by hematoxylin-eosin (H.E.) staining. The expression of ACE2 and mitochondrial assembly receptor (MasR) mRNAs and proteins in the lung tissue was detected by fluorescence quantitative real-time PCR and Western blot, separately. RESULTS: Following modeling, the levels of FVC, FEV0.1, FEV0.3, ratio of FEV0.1/FVC and FEV0.3/FVC, content of Ang (1-7) in the BALF, and the expression levels of ACE2 and MasR mRNAs and proteins in the lung tissue were significantly decreased (P<0.01), while the level of W/D ratio and TNF-α and IL-1ß contents in the BALF significantly increased (P<0.01) in the model group relevant to the normal group. In comparison with the model group, the levels of FVC, FEV0.1, FEV0.3, ratio of FEV0.1/FVC and FEV0.3/FVC, content of Ang (1-7) in the BALF, and expression levels of ACE2 and MasR mRNAs and proteins in the lung tissue were significantly increased (P<0.05, P<0.01), whereas the level of W/D ratio, and TNF-α and IL-1ß contents in the BALF were significantly decreased (P<0.05, P<0.01) in the EA group. H.E. staining showed pulmonary interstitial edema and alveolar septum thickening with severe inflammatory cell infiltration in the model group, which was relatively milder in the EA group. CONCLUSION: EA preconditioning at ST36 can improve pulmonary function in sepsis-related ALI rats, which may be related to its effects in inhibiting inflammatory response and up-regulating ACE2 and MasR expression and Ang (1-7) content in the lung tissue.

[Effect of electroacupuncture on pulmonary neuroendocrine cells and secretion of neuroactive substances in lung of COPD rats].

OBJECTIVE: To observe the effect of electroacupuncture (EA) at "Zusanli" (ST36) and "Feishu" (BL13) on the activation and secretion of calcitonin gene-related peptide (CGRP) and 5-hydroxytryptamine (5-HT) of pulmonary neuroendocrine cells (PNECs) and inflammatory response in rats with chronic obstructive pulmonary disease (COPD), so as to explore its underlying mechanisms in treating COPD. METHODS: Male SD rats were randomly divided into normal control, COPD model and EA groups, with 7 rats in each group. The COPD model was established by forced inhale of cigarette smoke for 1 h in a self-made box (1 m×1 m×1 m in volume), twice daily for 12 weeks. EA (4 Hz/20 Hz, 1-3 mA) was applied at bilateral ST36 and BL13 acupoints for 30 min, once a day for 14 consecutive days. The pulmonary function including the forced vital capacity (FVC), forced expiratory volume at 0.1 second (FEV0.1), FEV0.3, FEV0.1/FVC and FEV0.3/FVC was detected using a lung function analyzer for small animals. The lung tissue was sampled for observing histopathological changes by using H.E. staining, for observing expression and distribution of PNECs by Grimelius silver staining, and for detecting the immunoactivity (integrated optical density) of CGRP and 5-HT by using immunohistochemistry. The contents of CGRP, 5-HT, tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß) and transforming growth factor-ß1 (TGF-ß1) in the bronchoalveolar lavage fluid (BALF) and lung tissue were detected by ELISA, and the correlations between TNF-α and CGRP, IL-1ß and CGRP, TNF-α and 5-HT, and IL-1ß and 5-HT levels were analyzed. The mRNA and protein expression levels of nerve fiber markers of CGRP and purinergic receptor P2X ligand gated ion channel 3 (P2X3) which dominate PNECs in the lung tissue were detected by real-time fluorescence quantitative PCR and Western blot, respectively. RESULTS: Compared with the normal control group, the levels of FVC, FEV0.1, FEV0.3, and the ratios of FEV0.1/FVC and FEV0.3/FVC were significantly decreased (P<0.05, P<0.01), while the immunoactivity of PNECs, CGRP and 5-HT, the contents of CGRP, 5-HT, TNF-α, IL-1ß and TGF-ß1 in the BALF and lung tissue, and the expression levels of CGRP and P2X3 mRNAs and proteins in the lung tissue significantly increased in the COPD model group (P<0.01, P<0.05). Following EA intervention, both the increased and decreased levels of all the indexes mentioned above were reversed (P<0.05, P<0.01) except FEV0.3. H.E. staining showed severe deformed bronchial lumen with thickened wall and alveolar septum, and obvious inflammatory cell infiltration and reduced number of alveolar lumen fusion in the COPD model group, which was mild in the EA group. A positive correlation was found between TNF-α and CGRP, IL-1ß and CGRP, TNF-α and 5-HT,IL-1ß and 5-HT levels in both BALF and lung tissues (P<0.01). CONCLUSION: EA at ST36 and BL13 can improve lung function and reduce inflammatory response in COPD rats, which may be related to its function in inhibiting the activation of PNECs and release of neuroactive substances.

Hydrogen regulates the M1/M2 polarization of alveolar macrophages in a rat model of chronic obstructive pulmonary disease.

OBJECTIVE: Chronic obstructive pulmonary disease (COPD) is a respiratory disease with high morbidity and mortality worldwide, so far there is no ideal treatment method. Previous studies have shown that hydrogen (H2) is involved in the treatment of COPD as an antioxidant. In this study, the effect of H2 on M1/M2 polarization of alveolar macrophages in COPD rats was observed, and its anti-inflammatory mechanism was further elucidated. Methods: Twenty-four Sprague-Dawley rats were randomly divided into three groups including the control, COPD and H2 group. A rat model of COPD was established by cigarette exposure combined with lipopolysaccharide (LPS) induction. H2 therapy was administered 2 hours per day for 14 days. Lung function and pathology were assessed. The levels of interleukin (IL)-6, tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-ß1 and IL-10 in bronchoalveolar lavage fluid (BALF) and lung tissue were measured by enzyme-linked immunosorbent assay. The mRNA, protein expression and immunoreactivity of inducible nitric oxide synthase (iNOS) and arginase (Arg)-1 in lung were observed by quantitative real-time PCR, western blot and immunohistochemistry. Results: Compared with the control rats, there were a significant decline in lung function, a marked inflammatory infiltration and pulmonary parenchymal remodeling and the increases of IL-6, TNF-α and TGF-ß1 levels in BALF and lung tissue, but a lower expression of IL-10 in COPD rats. The iNOS mRNA and protein expression, as well as its optical density (OD), were increased significantly in lung tissue, while those of Arg-1 decreased significantly. H2 treatment improved the lung function and the parenchymal inflammation, reversed the increased levels of IL-6, TNF-α and TGF-ß1, and the lower IL-10. Meanwhile, H2 also down-regulated the expression of iNOS, but up-regulated expression of Arg-1 in lung tissue. Conclusion: H2 reduces inflammation in the lung of COPD, which may be related to its inhibition of M1 type polarization and activation of M2 type polarization of alveolar macrophage.

[Effect of electroacupuncture on the expression of autophagy related protein in lung tissue of rats with chronic obstructive pulmonary disease].

OBJECTIVE: To observe the effect of electroacupuncture (EA) at "Zusanli" (ST36) and "Feishu" (BL13) on the expression of autophagy related proteins in the lung tissue of rats with chronic obstructive pulmonary disease (COPD), so as to explore the mechanism of EA underlying improvement of COPD. METHODS: Thirty male SD rats were randomly divided into normal, model and EA groups (n=10 in each group). The COPD model was established by intratracheal infusion of Lipopolysaccharide (LPS, 1 mg/kg) and exposure in cigarette smoke. EA was applied to bilateral ST36 and BL13 for 30 min, once every other day for 2 weeks. The pulmonary function (forced vital capacity ï¼»FVCï¼½, forced expiratory volume in 0.1 s and 0.3 s ï¼»FEV0.1, FEV0.3ï¼½, FEV0.1/FVC and FEV0.3/FVC) was detected by animal pulmonary function analysis system. Histopathological changes of the airway and lung were displayed by H.E. staining. Autophagosomes in the airway and lung tissues were observed by electron microscope. The expression of AMP activated protein kinase (AMPK), mammalian target of rapamycin (mTOR), Unc-51 like autophagy activating kinase 1(ULK1), autophagy related protein ATG6(Beclin1)mRNAs in lung tissue were examined by quantitative real-time PCR. The expression of AMPK, mTOR, ULK1, Beclin1 and microtubule-associated protein 1 light chain 3 (LC3)proteins in lung tissue were examined by Western blot. The contents of tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6) in the broncho alveolar lavage fluid (BALF) were assayed by ELISA. RESULTS: Following modeling, the FVC, FEV0.1, FEV0.3, FEV0.1/FVC and FEV0.3/FVC levels were significantly decreased (P<0.01), the infiltration of inflammatory cells and the increase of autophagosomes were obvious in airway and lung tissue, the mRNA and protein expression of AMPK, ULK1, Beclin1 and the ratio of LC3Ⅱ/LC3Ⅰ were increased (P<0.01), while the mRNA and protein expression of mTOR were decreased (P<0.01), the contents of TNF-α and IL-6 in the BALF were increased in the model group compared with the normal group (P<0.01). After EA intervention, all the indexes mentioned above were completely reversed in the EA group relevant to the model group (P<0.01, P<0.05). CONCLUSION: EA at ST36 and BL13 can improve the lung function of COPD rats, which may be related to its effects in inhibiting the autophagy level and reducing the inflammation response in the lung.

[Electroacupuncture improves lung function by suppressing mucin-5AC mediated EGFR-p38MAPK signaling and inflammation reaction in chronic obstructive pulmonary disease rats].

OBJECTIVE: To observe the effect of electroacupuncture (EA) at "Zusanli"(ST36) on the expression of epidermal growth factor receptor (EGFR), tumor necrosis factor α(TNF-α) transfer growth factor α(TGF-α), interleukin-8(IL-8), p38 mitogen-activated protein kinases (p38MAPK), mucin-5AC (MUC5AC) and other related factors in chronic obstructive pulmonary disease (COPD) rats, so as to reveal its underlying mechanisms in improving COPD. METHODS: A total of thirty male SD rats were randomly divided into normal control, model and EA groups, with 10 rats in each group. The COPD model was replicated using a combined method of tracheal infusion of lipopolysaccharide (LPS) and forced smoke-inhaling. EA (1-3 mA, 4 Hz/20 Hz) was applied to bilateral ST36 for 30 min, once daily for two consecutive weeks. The lung ventilation activities including the forced vital capacity (FVC) and forced expiratory volume (FEV) at 0.1 and 0.3 s (FEV0.1, FEV0.3) were detected. Histopathological changes of the middle lobe and bronchus of the right lung were observed after H.E. staining. The contents of TGF-α, TNF-α and IL-8 in the serum, bronchoalveolar lavage fluid (BALF) and superior lobe of the right lung were assayed by using ELISA, and the expression levels of EGFR, p38MAPK and MUC5AC proteins (inferior lobe of the left lung) and mRNAs (inferior lobe of the right lung) detected using Western blot, immunohistochemistry (strept avidin-biotin complex, SABC method) and real-time quantitative PCR, respectively. RESULTS: Compared with the normal group, the FVC, FEV0.1, FEV0.3, FEV0.1/FVC and FEV0.3/FVC levels were significantly decreased (P<0.01), while the contents of TNF-α, TGF-α and IL-8 in the serum, BALF and lung tissues, expression levels of EGFR, p38MAPK and MUC5AC mRNAs and proteins, and the immunoactivity of EGFR, p38MAPK and MUC5AC in the lung tissues were significantly increased in the model group (P<0.01). After EA intervention, the decreased levels of the FVC, FEV0.1, FEV0.3, FEV0.1/FVC and FEV0.3/FVC, and the increased levels of the abovementioned genes and proteins were all reversed in the EA group (P<0.01, P<0.05). After modeling, the bronchial walls were thickened, with enlarged alveolar cavities, fractured alveolar walls, obvious inflammatory cell infiltration, and rich mucus secretion in the lumen, which was relatively milder in the EA group. CONCLUSION: EA of ST36 can improve the ventilation function in COPD rats, which may be associated with its function in down-regulating the levels of TNF-α, TGF-α, IL-8, EGFR, p38MAPK and MUC5AC mRNAs and proteins in the lung tissues, inhibiting EGFR-p38MAPK signaling mediated expression of MUC5AC.

Electroacupuncture inhibits IL-17/IL-17R and post-receptor MAPK signaling pathways in a rat model of chronic obstructive pulmonary disease.

OBJECTIVE: Interleukin (IL)-17, as a T-helper 17 cell (Th17) cytokine, plays a key role in chronic obstructive pulmonary disease (COPD) pathophysiology including chronic inflammation and airway obstruction, which lead to decreased pulmonary function. The aim of this study was to investigate the effect of acupuncture on IL-17, its receptor (IL-17R) and the mitogen-activated protein kinase (MAPK) signaling pathway, in a rat model of COPD. METHODS: The COPD model was induced in Sprague Dawley rats by exposure to cigarette smoke for 12 weeks. The model rats were treated with electroacupuncture (EA) at BL13 and ST36. The lung function and histology of the rats were observed. IL-17, tumor necrosis factor (TNF)-α, and IL-10 were detected by enzyme-linked immunosorbent assay (ELISA) in bronchoalveolar lavage fluid (BALF) and in plasma. The leukocytes and macrophages in the BALF were counted. The expression levels of IL-17R were assayed in lung tissue by real-time polymerase chain reaction (PCR), western blotting, and immunohistochemistry. MAPK signaling pathway molecules including c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK)1/2 and p38, and their phosphorylated forms, were observed in the lung by western blotting. RESULTS: Compared with the control group rats, lung function decreased and there was a severe inflammatory infiltration of the pulmonary parenchyma in the COPD rats. EA effectively improved lung function and alleviated the inflammatory infiltration in the lungs of COPD rats. EA also reversed the elevated total leukocyte and macrophage counts, the high levels of IL-17 and TNF-α, and the low IL-10 content in COPD rats. Meanwhile, EA downregulated the increased mRNA and protein expression of IL-17R, and significantly inhibited the elevated levels of phosphorylated JNK, ERK1/2, and p38 in the lungs of COPD rats. CONCLUSION: Our results suggest that the protective effects of acupuncture therapy on the lungs of COPD rats are likely related to inhibition of IL-17/IL-17R and the post-receptor MAPK signaling pathways.

Computing Primitive of Fully VCSEL-Based All-Optical Spiking Neural Network for Supervised Learning and Pattern Classification.

We propose computing primitive for an all-optical spiking neural network (SNN) based on vertical-cavity surface-emitting lasers (VCSELs) for supervised learning by using biologically plausible mechanisms. The spike-timing-dependent plasticity (STDP) model was established based on the dynamics of the vertical-cavity semiconductor optical amplifier (VCSOA) subject to dual-optical pulse injection. The neuron-synapse self-consistent unified model of the all-optical SNN was developed, which enables reproducing the essential neuron-like dynamics and STDP function. Optical character numbers are trained and tested by the proposed fully VCSEL-based all-optical SNN. Simulation results show that the proposed all-optical SNN is capable of recognizing ten numbers by a supervised learning algorithm, in which the input and output patterns as well as the teacher signals of the all-optical SNN are represented by spatiotemporal fashions. Moreover, the lateral inhibition is not required in our proposed architecture, which is friendly to the hardware implementation. The system-level unified model enables architecture-algorithm codesigns and optimization of all-optical SNN. To the best of our knowledge, the computing primitive of an all-optical SNN based on VCSELs for supervised learning has not yet been reported, which paves the way toward fully VCSEL-based large-scale photonic neuromorphic systems with low power consumption.

Image edge detection with a photonic spiking VCSEL-neuron.

We report both experimentally and in theory on the detection of edge features in digital images with an artificial optical spiking neuron based on a vertical-cavity surface-emitting laser (VCSEL). The latter delivers fast (< 100 ps) neuron-like optical spikes in response to optical inputs pre-processed using convolution techniques; hence representing image feature information with a spiking data output directly in the optical domain. The proposed technique is able to detect target edges of different directionalities in digital images by applying individual kernel operators and can achieve complete image edge detection using gradient magnitude. Importantly, the neuromorphic (brain-like) spiking edge detection of this work uses commercially sourced VCSELs exhibiting responses at sub-nanosecond rates (many orders of magnitude faster than biological neurons) and operating at the important telecom wavelength of 1300 nm; hence making our approach compatible with optical communication and data-centre technologies.

Experimental investigation of the time-delay signature of chaotic output and dual-channel physical random bit generation in 1550 nm mutually coupled VCSELs with common FBG filtered feedback.

Here we propose and experimentally demonstrate mutually coupled 1550 nm vertical-cavity surface-emitting lasers (VCSELs), subject to common fiber Bragg grating (FBG) feedback (FMC-VCSELs), to conceal the time-delay signature (TDS) of chaotic outputs. The autocorrelation function and delayed mutual information are used to quantitatively identify the TDS of chaotic output. For comparison, the evolution of the TDS of chaotic output in mutually coupled VCSELs (MC-VCSELs) is also presented. The effects of injection power, frequency detuning between two VCSELs, and frequency detuning between FBG and VCSELs on the TDS concealment are experimentally measured. Experimental results show that FMC-VCSELs have a better TDS suppression performance than MC-VCSELs for varying injection power. In addition, for the FMC-VCSELs system, the TDS can be suppressed to below 0.1 when the VCSELs x-polarization component is located at the edge of the main FBG lobe. Furthermore, dual-channel physical random numbers with verified randomness at a rate of 800 Gbps (2×5LSBs×80GHz) are achieved by utilizing the chaotic outputs with a low TDS from two VCSELs in the FMC-VCSELs system.

Time-delay signature concealment of chaos and ultrafast decision making in mutually coupled semiconductor lasers with a phase-modulated Sagnac loop.

We propose and experimentally demonstrate the generation of dual-channels chaos with time delay signature (TDS) concealment by introducing a phase-modulated Sagnac loop in mutually coupled semiconductor lasers (MCSL). Furthermore, we demonstrate the utilization of the dual-channels chaos to solve multi-armed bandit (MAB) problem in reinforcement learning. The experimental results agree well with the numerical simulations. For the purpose of comparison, the MCSL with a conventional Sagnac loop is also considered. It is found that the TDS of dual-channels chaotic signals can be better concealed in our proposed system. Besides, the proposed system allows for a better decision making performance in MAB problem. Moreover, compared with the one-channel chaotic system, the proposed dual-channels chaotic system achieves ultrafast decision making in parallel, and thus, is highly valuable for further improving the security of communication systems and the performance of photonic intelligence.

All-optical neuromorphic XOR operation with inhibitory dynamics of a single photonic spiking neuron based on a VCSEL-SA.

We propose a simple hardware architecture for solving exclusive OR (XOR) tasks in a single step by using a single photonic spiking neuron based on vertical-cavity surface-emitting lasers with an embedded saturable absorber (VCSEL-SA) subject to dual-polarized pulsed optical injection. We model the inhibitory photonic spiking neuron by extending the Yamada model and spin-flip model to incorporate the two polarization-resolved modes and the saturable absorber. It is shown that, by carefully adjusting the temporal difference according to the inhibitory window, the XOR operation can be realized in a single photonic spiking neuron, which is interesting and valuable for the photonic neuromorphic computing and information processing.

Andrographolide attenuates oxidative stress injury in cigarette smoke extract exposed macrophages through inhibiting SIRT1/ERK signaling.

Andrographolide (AG), an ingredient extracted from traditional Chinese herbal medicine Andrographis paniculata, has been demonstrated to have potent anti-inflammatory and anti-oxidative stress properties. The purpose of this study was to investigate whether and how AG attenuated CSE-induced mitochondrial dysfunction, inflammation and oxidative stress in RAW 264.7 cells (a mouse macrophages line). The results showed that AG significantly reduced CSE-induced upregulation of pro-inflammatory cytokines (i.e., TNF-α and IL-1ß) in the RAW 264.7 cells. AG inhibited CSE-induced production of reactive oxygen species (ROS) and prevented the reduction of superoxide dismutase (SOD) and glutathione/oxidized glutathione (GSH/GSSG) ratio, indicating the anti-oxidative stress effects of AG in macrophages. AG also improved mitochondrial function and mitochondrial membrane potential. In addition, AG inhibited CSE-induced increase of heme oxygenase (HO)-1, matrix metalloproteinase (MMP)-9 and MMP-12. Moreover, AG increased SIRT1 transcription and expression, suggesting AG inhibits mitochondrial dysfunction, inflammation and oxidative stress via a SIRT1 dependent signaling. We also demonstrated that AG inhibited CSE-induced ERK phosphorylation, and treatment with PD980589, a ERK inhibitor, reversed CSE-induced inflammation and oxidative stress. These results indicated that AG may prevent COPD via the inhibition of SIRT1/ERK signaling pathway, and subsequently inhibition of mitochondrial dysfunction, inflammation, and oxidative stress in macrophages.