DPDH-CapNet: A Novel Lightweight Capsule Network with Non-routing for COVID-19 Diagnosis Using X-ray Images.

COVID-19 has claimed millions of lives since its outbreak in December 2019, and the damage continues, so it is urgent to develop new technologies to aid its diagnosis. However, the state-of-the-art deep learning methods often rely on large-scale labeled data, limiting their clinical application in COVID-19 identification. Recently, capsule networks have achieved highly competitive performance for COVID-19 detection, but they require expensive routing computation or traditional matrix multiplication to deal with the capsule dimensional entanglement. A more lightweight capsule network is developed to effectively address these problems, namely DPDH-CapNet, which aims to enhance the technology of automated diagnosis for COVID-19 chest X-ray images. It adopts depthwise convolution (D), point convolution (P), and dilated convolution (D) to construct a new feature extractor, thus successfully capturing the local and global dependencies of COVID-19 pathological features. Simultaneously, it constructs the classification layer by homogeneous (H) vector capsules with an adaptive, non-iterative, and non-routing mechanism. We conduct experiments on two publicly available combined datasets, including normal, pneumonia, and COVID-19 images. With a limited number of samples, the parameters of the proposed model are reduced by 9x compared to the state-of-the-art capsule network. Moreover, our model has faster convergence speed and better generalization, and its accuracy, precision, recall, and F-measure are improved to 97.99%, 98.05%, 98.02%, and 98.03%, respectively. In addition, experimental results demonstrate that, contrary to the transfer learning method, the proposed model does not require pre-training and a large number of training samples.

SRXN1 stimulates hepatocellular carcinoma tumorigenesis and metastasis through modulating ROS/p65/BTG2 signalling.

Sulfiredoxin 1 (SRXN1) is a pivotal regulator of the antioxidant response in eukaryotic cells. However, the role of SRXN1 in hepatocellular carcinoma (HCC) is far from clear. The present study aims to elucidate whether SRXN1 participates in tumorigenesis and metastasis of HCC and to determine the molecular mechanisms. We found that SRXN1 expression was up-regulated in HCC tissue samples and correlated with poor prognosis in HCC patients. We also observed that SRXN1 knockdown by transient siRNA transfection inhibited HCC cell proliferation, migration and invasion. Overexpression of SRXN1 increased HCC cell migration and invasion. B-cell translocation gene 2 (BTG2) was identified as a downstream target of SRXN1. Mechanistic studies revealed that SRXN1-depleted reactive oxygen species (ROS) modulated migration and invasion of HCC cells. In addition, the ROS/p65/BTG2 signalling hub was found to regulate the epithelial-mesenchymal transition (EMT), which mediates the pro-metastasis role of SRXN1 in HCC cells. In vivo experiments showed SRXN1 promotes HCC tumour growth and metastasis in mouse subcutaneous xenograft and metastasis models. Collectively, our results revealed a novel pro-tumorigenic and pro-metastatic function of SRXN1 in HCC. These findings demonstrate a rationale to exploit SRXN1 as a therapeutic target effectively preventing metastasis of HCC.

Alterations in ACE and ABCG2 expression levels in the testes of rats subjected to atropine-induced toxicity.

Atropine-induced damage is associated with enzyme and protein alterations. The aim of the present study was to investigate atropine­induced alterations in testicular expression levels of angiotensin­converting enzyme (ACE) and adenosine 5'-triphosphate binding cassette sub­family G member 2 (ABCG2) following atropine treatment. Male Wistar rats received 15 mg/kg/day atropine for 7 days; control rats received an identical volume of saline, Following treatment, the testes were harvested for immunohistochemistry and in situ hybridization to examine the protein and gene expression levels of ACE and ABCG2 by digital image analysis. ACE gene and protein expression levels were significantly reduced in the testes of atropine­treated rats, compared with control rats (P=0.0001 and P<0.001, respectively). In addition, ABCG2 gene and protein expression levels were significantly increased in the testes of atropine­treated rats, compared with control rats (P=0.0017 and P<0.001, respectively). Thus, the results of the present study demonstrate that testicular protein and gene expression levels of ACE and ABCG2 were altered as a result of atropine­induced toxicity in the rats. These alterations may result in abnormal testicular function, and the proteins and genes identified in the present study may be useful to elucidate the mechanisms underlying atropine­induced toxicity and provide a direction for further studies.

Emodin affects biofilm formation and expression of virulence factors in Streptococcus suis ATCC700794.

Streptococcus suis (S. suis) is a swine pathogen and also a zoonotic agent. In this study, the effects of subinhibitory concentrations (sub-MICs) of emodin on biofilm formation by S. suis ATCC700794 were evaluated. As quantified by crystal violet staining, biofilm formation by S. suis ATCC700794 was dose-dependently decreased after growth with 1/2 MIC, 1/4 MIC, or 1/8 MIC of emodin. By scanning electron microscopy, the structural architecture of the S. suis ATCC700794 biofilms was examined following growth in culture medium supplemented with 1/2 MIC, 1/4 MIC, 1/8 MIC, or 1/16 MIC of emodin. Scanning electron microscopy analysis revealed the potential effect of emodin on biofilm formation by S. suis ATCC700794. The expression of luxS gene and virulence genes in S. suis ATCC700794 was investigated by quantitative RT-PCR. It was found that sub-MICs of emodin significantly decreased the expression of gapdh, sly, fbps, ef, and luxS. However, it was found that sub-MICs of emodin significantly increased the expression of cps2J, mrp, and gdh. These findings showed that sub-MICs of emodin could cause the difference in the expression level of the virulence genes.

Changes in FABP1 and gastrin receptor expression in the testes of rats that have undergone electrical injury.

Testicular trauma may occur due to accidental electrical injury. The aim of this study was to investigate alterations in the levels of fatty acid-binding protein 1 (FABP1) and gastrin receptor (gastrin R) in the testes following electrical injury. Sprague-Dawley rats were divided into control, fatal electrocution (220 V, 50 Hz, 60 sec) and electrical injury (220 V, 50 Hz, 60 sec) groups (n=8 per group). The animals in the fatal electrocution and electrical injury groups were deeply anesthetized with sodium pentobarbital prior to each treatment, in which the current was delivered via an anode connected to the left foreleg and a cathode to the right hindleg. The rats that survived were subsequently sacrificed by cervical dislocation. Control animals received cervical dislocation alone. Immunohistochemical analysis was performed to evaluate the protein expression of FABP1 and gastrin R in the testes. Sections were evaluated by digital image analysis. The expression levels of FABP1 and gastrin R were significantly increased following electrical injury, supported by an increase in the integrated optical density (IOD) when compared with that in the control group (P<0.05). However, no significant difference was found in FABP1 and gastrin R expression levels between the fatal electrocution and control groups. In summary, the protein expression levels of FABP1 and gastrin R were found to be significantly altered by electrical injury, suggesting that these two proteins may be important in underlying mechanisms of testicular injury during electrical injury. The findings indicate that such alterations would be reflected in abnormal testicular function.

Quantitative proteomic analysis of sub-MIC erythromycin inhibiting biofilm formation of S. suis in vitro.

Streptococcus suis (S. suis) is a swine pathogen and also a zoonotic agent. Biofilms of S. suis may cause persistent infections by the host immune system and antibiotics. Sub-minimal inhibitory concentration (sub-MIC) of erythromycin can inhibit biofilm formation in bacteria. Here, we performed comparative proteomic analyses of cells at two different conditions: sub-MIC erythromycin treated and nontreated cells. Using iTRAQ strategy, we found some novel proteins that involved in biofilm formation. 79 differentially expressed proteins were identified in sub-MIC erythromycin inhibiting planktonic cell when the protein had both a fold-change of more that a ratio >1.2 or <0.8 (p-value <0.05). Several cell surface proteins (such as Primosomal protein N', l-fucose isomerase, and ABC superfamily ATP binding cassette transporter, membrane protein), as well as those involved in Quorum-sensing, were found to be implicated in biofilm formation. Overall, our results indicated that cell surface proteins played an important role in biofilm formation. Quorum-sensing played a crucial role leading to biofilm formation. ABC superfamily ATP binding cassette transporter, membrane protein and comD might act as channels for erythromycin uptake in Quorum-sensing system. Thus, our data analyzed rough regulatory pathways of biofilm formation that might potentially be exploited to deal with biofilm infections of S. suis. This article is part of a Special Issue entitled: Microbial Proteomics. BIOLOGICAL SIGNIFICANCE: In this study, we identified many proteins involved in cell transport, biological regulation and signal transduction, stress responses and other metabolic processes that were not previously known to be associated with biofilm formation of S. suis and target spot of erythromycin. Therefore, our manuscript represents the most comprehensive analysis of protein profiles of biofilm formation of S. suis inhibited by sub-MIC erythromycin and provides new proteomic information about biofilm formation.

Electrocution-related mortality: a review of 71 deaths by low-voltage electrical current in Guangdong, China, 2001-2010.

The aim of this study was to investigate the epidemiological characteristics of low-voltage electrocution deaths in Guangdong, China. Three thousand three hundred seventy autopsy reports from the Department of Forensic Pathology, Zhongshan School of Medicine, Sun Yat-Sen University, over a period of 10 years (2001-2010) were reviewed, of which 71 low-voltage electrocution cases were identified. The descriptive statistical analyses were carried out with the application of SPSS 19.0 software. Electrocution accounted for 2.11% of all autopsied cases. The age range was 3 to 57 years with a mean age of 31.77 ± 11.0 years. The average age of male victims was 33.08 ± 10.77 years, and that of female victims was 22.63 ± 11.06 years. The majority of the victims (87.33%) were male. Among the circumstances leading to electrocution, most of them occurred in factory and in the street. Considering the contact details, deaths were caused most frequently by touching electrical wires (n = 27, 38.02%), followed by touching charged machine (n = 20, 28.17%). There were no suicide and homicide cases. Of all electrocution cases, 50.70% occurred during the summer period from June through August. The upper extremity was the most frequently involved contact site (59.72%). No electrical burn marks were present in 14 cases (19.72%). Our results indicated that most deaths from electrocution occur more often in factories, in summer seasons, and to young male workers, which can help in the development of a differentiated strategy for the prevention of electrocution, while taking into consideration sex, age, occupation, and season of the year.

Connexin43 and angiotensin II alterations in hearts of rats having undergone an acute exposure to alcohol.

INTRODUCTION: Alcohol-induced heart damage is associated with enzyme and protein alterations. The purpose of this study was to investigate alcohol-induced alterations in cardiac connexin 43 (Cx43) and angiotensin II (Ang II) after acute alcohol administration. METHOD: Male Wistar rats were randomly divided into 2 groups: a control group and an ethanol group. The ethanol group intraperitoneally received 3.8 g/kg ethanol; the controls were given the same amount of saline via the same route. After the righting reflex disappeared, midsternotomy was performed in all animals. Immunohistochemical analysis was performed to evaluate protein expression of Cx43 and Ang II. Sections were analyzed by digital image analysis. RESULT: The expression of Cx43 was significantly reduced after acute ethanol treatment, with the integrated optical density lower when compared with control (P < 0.05). The expression of Ang II was significantly increased after acute ethanol treatment, supported by integrated optical density when compared with control (P < 0.05). CONCLUSIONS: In summary, cardiac protein expression of Cx43 and Ang II were found to be significantly altered after acute ethanol treatment, suggesting that these 2 proteins may be important underlying mechanisms of vulnerability to oxidative injury in the heart during acute ethanol. The present study indicated that acute ethanol toxicity caused different alterations in heart proteins that would be related to oxidative stress.

Elevated enolase and caveolin-1 in the heart of rats following dexamethasone-induced toxicity.

Dexamethasone (DEX)-induced heart damage is associated with enzyme and protein alterations. The purpose of this study was to investigate DEX-induced alterations in cardiac enolase and caveolin-1 (cav-1) following DEX administration. Male Wistar rats were randomly divided into two groups: a control and a DEX. The DEX group intraperitoneally received DEX at the single dose of 10 mg/kg for 7 consecutive days, and the control was given the same amount of saline via the same route. On day 8, the rats were anesthetized, and a thoracotomy was performed in all animals. Immunohistochemical analysis was performed to evaluate protein expression of enolase and cav-1. Sections were analyzed by digital image analysis. Our results demonstrated that cardiac protein expression of enolase and cav-1 was altered following DEX-induced toxicity in the rat. The expression of enolase and cav-1 was significantly increased after DEX treatment, supported by integrated optical density compared with the control (P<0.05). In conclusion, following DEX-induced toxicity, protein expression of enolase and cav-1 was significantly elevated. The current findings indicate that such alterations would be reflected in abnormal cardiac function, and the proteins identified in this study may be useful in revealing the mechanisms underlying DEX-induced toxicity and also in providing various clues for further research.

Reduction in Purkinje fiber number in rats undergone fatal electrocution.

Purkinje fibers in cardiac conduction tissue during fatal electrocution. A total of 16 Sprague Dawley rats were divided into 2 groups as follows: the electrocution group and the control group.Animals were deeply anesthetized with sodium pentobarbital and, in the electrocution group, all 8 rats underwent a fatal electrical shock (220 v,50 Hz) followed by cervical dislocation. In the control group, all 8 rats underwent execution by cervical dislocation. Following death, hearts were rapidly excised and perfused with 1% paraformaldehyde before tissues of the left ventricular anterior wall (LVAW) were isolated. The microscopic structure of the Purkinje fibers were subsequently analyzed using conventional hematoxylin and eosin staining. A majority of the Purkinje fibers were located in groups among the cardiac muscle of the LVAW. A significant reduction in Purkinje fiber expression was displayed in the electrocution group compared with the control group (P G 0.05).The mean total number of Purkinje fibers for the electrocution and control groups were 59 T 11 and 3287 T 19 cells, respectively (P G 0.05).The estimated number of Purkinje fibers in the LVAW of the control group was significantly greater than observed in the electrocution group(41.09 T 0.24 vs. 0.7375 T 0.14, P G 0.05). The findings of the current study suggest that such a reduction would be reflected in abnormal cardiac conduction and a possible cause of sudden death.

Endothelin-1 and type III collagen alterations in the heart of rats following cisplatin-induced toxicity.

Cisplatin-induced heart damage is associated with enzymes and protein alterations. The purpose of this study was to investigate cisplatin-induced alterations in cardiac endothelin (ET)-1 and type III collagen following administration of cisplatin. Male Wistar rats were randomly divided into two groups: a control and a cisplatin group. The cisplatin group received cisplatin intraperitoneally (i.p.) at a single dose of 7 mg/kg on day 6, while the controls were given the same amount of saline via the same route. On day 11, the rats were anesthetized and a thoracotomy was performed on all animals. Immunohistochemical analysis was performed to evaluate the protein expression of ET-1 and type III collagen. Sections were analyzed by digital image analysis. Results showed that the cardiac protein expression of ET-1 and type III collagen was altered following cisplatin-induced toxicity in rats. The expression of ET-1 and type III collagen was significantly increased after cisplatin treatment, supported by integrated optical density, when compared to the control group (P<0.05). The present findings indicate that such alterations may be reflected in abnormal cardiac function. Additionally, the proteins identified in this study may benefit investigations into the mechanisms underlying cisplatin-induced toxicity, thereby providing the necessary evidence for further research.

Connexin 43, angiotensin II, endothelin 1, and type III collagen alterations in heart of rats having undergone fatal electrocution.

Death due to accidental electrocution occurs frequently. The aim of this study was to investigate alterations in cardiac connexin 43 (Cx43), angiotensin II (Ang II), endothelin 1 (ET-1), and type III collagen associated with fatal electrocution.Twenty-four Sprague-Dawley rats were divided into control, fatal electrocution (220 V, 50 Hz, 60 seconds), and electrical injury (220 V, 50 Hz, 60 seconds) groups. Animals were deeply anesthetized with sodium pentobarbital before each treatment, with the anode connected to the left foreleg and the cathode to the right hindleg, followed by cervical dislocation. Control animals received cervical dislocation alone. Immunohistochemical analysis was performed to evaluate the cardiac protein expression of Cx43, Ang II, ET-1, and type III collagen. Sections were analyzed by digital image analysis.The expression of Cx43 was significantly reduced after fatal electrocution, with the integrated optical density also lower when compared with control (P < 0.05). Expression of both Ang II and ET-1 was significantly increased after fatal electrocution, supported by integrated optical density when compared with control (P < 0.05). But no significant difference was found in type III collagen expression between the fatal electrocution group and the control group.In summary, cardiac protein expression of Cx43, Ang II, and ET-1 was found to be significantly altered with fatal electrocution, suggesting that these 3 proteins may be important underlying mechanisms of death during fatal electrocution. The current findings indicate that such alterations would be reflected in abnormal cardiac function and a possible cause of sudden death.

α-Enolase and caveolin alterations in the heart of rats having undergone gentamicin-induced toxicity.

Gentamicin (GM)-induced heart damage is associated with alterations in expression levels of various enzymes and proteins. The aim of the present study was to investigate GM-induced alterations in cardiac α-enolase and caveolin after GM administration. Male Wistar rats were randomly divided into two groups: a control group and a GM group. The GM group intraperitoneally received GM at a single dose of 7 mg/kg for 8 days, while the controls were given the same amount of saline via the same route. On Day 9, the rats were anesthetized and a thoracotomy was performed in all animals. Immunohistochemical analysis was performed to evaluate protein expression of α-enolase and caveolin. Sections were analyzed by digital image analysis. Our results revealed that cardiac protein expression of α-enolase and caveolin was altered after GM-induced toxicity in the rat. The expression of α-enolase and caveolin was significantly increased after GM-induced toxicity, as determined by integrated optical density analysis, when compared with the control (P<0.05). The current findings indicate that such changes in protein expression may be reflected in abnormal cardiac function, and the proteins identified in this study may be useful for elucidating the mechanisms underlying GM-induced toxicity and may also provide various clues for further investigations.

E-cadherin and caveolin-1 alterations in the heart of rats having undergone chlorpromazine-induced toxicity.

Heart damage induced by chlorpromazine (CPZ) toxicity is associated with changes in the expression of various enzymes and proteins. This study aimed to investigate CPZ­induced alterations in cardiac E-cadherin and caveolin-1 (cav-1) after CPZ administration. Male Wistar rats were randomly divided into two groups: a control group and a CPZ group. The CPZ group was administered CPZ intraperitoneally at a single dose of 10 mg/kg for 21 days; the controls were given the same amount of saline via the same route. On Day 22, the rats were anesthetized, and a thoracotomy was performed in all animals. Immunohistochemical analysis was performed to evaluate protein expression of E-cadherin and cav-1. Sections were analyzed by digital image analysis. Results of the present study revealed that cardiac protein expression of E-cadherin and cav-1 was altered after CPZ-induced toxicity in the rat. The expression of E-cadherin was significantly reduced, while expression of cav-1 was significantly increased after CPZ treatment, as supported by integrated optical density analysis, compared with the control (P<0.05). The current findings indicate that such changes in the expression of E-cadherin and cav-1 may be reflected in abnormal cardiac function, and these proteins may be useful in revealing the mechanisms underlying CPZ-induced toxicity and may also provide additional insight for further research.

E-cadherin and 5-HT alterations in the heart of rats having undergone atropine-induced toxicity.

Atropine-induced heart damage is associated with changes in the expression of various enzymes and proteins. The purpose of this study was to investigate atropine-induced alterations in cardiac E-cadherin and 5-hydroxytryptamine (5-HT) after atropine administration. Male Wistar rats were randomly divided into two groups: a control group and an atropine group. The atropine group intraperitoneally received atropine at a single dose of 15 mg/kg for 7 days; the controls received the same amount of saline via the same route. On Day 8, the rats were anesthetized, and a thoracotomy was performed in all animals. Immunohistochemical analysis was performed to evaluate protein expression of E-cadherin and 5-HT. Sections were analyzed by digital image analysis. Cardiac protein expression of E-cadherin and 5-HT was altered after atropine­induced toxicity in the rat. The expression levels of E-cadherin and 5-HT were significantly decreased after atropine treatment, supported by IOD analysis, when compared with the control (P<0.05). The current findings indicate that such changes would be reflected in abnormal cardiac function, and these proteins may be useful for revealing the mechanisms underlying atropine-induced toxicity and may also provide various clues for further research.

Chronic ingestion of alcohol modulates expression of ubiquitin editing enzyme A20 in lung macrophages.

BACKGROUND: Alcohol abuse is involved in the pathogenesis of multiple organ disorders; the underlying mechanism is incompletely understood. The ubiquitin editing enzyme A20 is involved in regulating activities in the cell. Suppression of A20 is suggested as one factor in the initiation of inflammation. This study investigates the mechanism by which chronic alcohol consumption modulates the levels of ubiquitin editing enzyme A20 in macrophages and further contributes to induce endothelial barrier dysfunction in the lung. METHODS: Mice were gavage-fed with 40% alcohol daily for 0-3 weeks. Airway macrophages were collected by lung lavage. Expression of ubiquitin editing enzyme A20 in isolated macrophages was assessed at both mRNA and protein levels. The endothelial barrier function of the lung was evaluated by the Evans blue method. RESULTS: Mice treated with alcohol for 3 weeks showed an increase in cell infiltration in the lung in response to exposure to peptidoglycan; over 80% of the infiltrated cells were macrophages. Furthermore, we observed that A20 level was suppressed in macrophages of mice treated with alcohol; the levels of tumor necrosis factor, interleukin-6 and nuclear factor kappa B in macrophage were increased. In addition, the endothelial barrier function of the lung was compromised, showing excessive infiltration of Evans blue in the lung indicating lung edema. Pretreatment with synthesized A20 inhibited alcohol-induced lung endothelial barrier dysfunction. CONCLUSIONS: We conclude that chronic alcohol ingestion disturbs the endothelial barrier function in the lung by modulating macrophage properties. Increase in A20 in the cell may have potential for the treatment of inflammatory disorders.