This study aims to automatically diagnose thoracic diseases depicted on the chest x-ray (CXR) images using deep convolutional neural networks. The existing methods generally used the entire CXR images for training purposes, but this strategy may suffer from two drawbacks. First, potential misalignment or the existence of irrelevant objects in the entire CXR images may cause unnecessary noise and thus limit the network performance. Second, the relatively low image resolution caused by the resizing operation, which is a common preprocessing procedure for training neural networks, may lead to the loss of image details, making it difficult to detect pathologies with small lesion regions. To address these issues, we present a novel method termed as segmentation-based deep fusion network (SDFN), which leverages the higher-resolution information of local lung regions. Specifically, the local lung regions were identified and cropped by the Lung Region Generator (LRG). Two CNN-based classification models were then used as feature extractors to obtain the discriminative features of the entire CXR images and the cropped lung region images. Lastly, the obtained features were fused by the feature fusion module for disease classification. Evaluated by the NIH benchmark split on the Chest X-ray 14 Dataset, our experimental result demonstrated that the developed method achieved more accurate disease classification compared with the available approaches via the receiver operating characteristic (ROC) analyses. It was also found that the SDFN could localize the lesion regions more precisely as compared to the traditional method.

Background The novel coronavirus disease 2019 (COVID-19) is an emerging worldwide threat to public health. While chest computed tomography (CT) plays an indispensable role in its diagnosis, the quantification and localization of lesions cannot be accurately assessed manually. We employed deep learning-based software to aid in detection, localization and quantification of COVID-19 pneumonia. Methods A total of 2460 RT-PCR tested SARS-CoV-2-positive patients (1250 men and 1210 women; mean age, 57.7 ± 14.0 years (age range, 11-93 years) were retrospectively identified from Huoshenshan Hospital in Wuhan from February 11 to March 16, 2020. Basic clinical characteristics were reviewed. The uAI Intelligent Assistant Analysis System was used to assess the CT scans. Results CT scans of 2215 patients (90%) showed multiple lesions of which 36 (1%) and 50 patients (2%) had left and right lung infections, respectively (> 50% of each affected lung's volume), while 27 (1%) had total lung infection (> 50% of the total volume of both lungs). Overall, 298 (12%), 778 (32%) and 1300 (53%) patients exhibited pure ground glass opacities (GGOs), GGOs with sub-solid lesions and GGOs with both sub-solid and solid lesions, respectively. Moreover, 2305 (94%) and 71 (3%) patients presented primarily with GGOs and sub-solid lesions, respectively. Elderly patients (≥ 60 years) were more likely to exhibit sub-solid lesions. The generalized linear mixed model showed that the dorsal segment of the right lower lobe was the favoured site of COVID-19 pneumonia. Conclusion Chest CT combined with analysis by the uAI Intelligent Assistant Analysis System can accurately evaluate pneumonia in COVID-19 patients. Keywords 2019 novel coronavirus. Viral pneumonia. Artificial intelligence (AI). Computed tomography (CT). Ground glass opacity (GGO) Hai-tao Zhang, Jin-song Zhang and Hai-hua Zhang contributed equally to this work.

Smoke inhalation induced acute respiratory distress syndrome (ARDS) has become more and more common throughout the world and it is hard to improve the outcome. The present research was to investigate possible roles of angiotensin-converting enzyme (ACE) and ACE2 in lung injury resulted from smoke exposure. Rats were exposed to dense smoke to induce ARDS. Histological changes, blood gases, bronchoalveolar lavage fluids (BALF) and wet-to-dry weight were analyzed to evaluate lung injury after smoke inhalation; beside, we also measured the expression of ACE and ACE2 at different time points to explore the possible mechanism of those changes. The results showed that pH of arterial blood, partial blood oxygen (PaO₂) and blood oxygen saturation (SO₂) decreased after smoke inhalation at different time points (P<0.01); while, partial blood carbon dioxide (PaCO₂), wet-to-dry weight ratio, leukocytes count, protein concentration and inflammatory cytokines in BALF increased after smoke exposure (P<0.01). More importantly, both immunohistochemical staining and Western blot results showed that ACE and ACE2 expression in lungs from the experimental groups significantly increased compared with that of the control group (P<0.05). This study indicated that inflammation pulmonary edema and histological changes resulted from smoke inhalation induced lung injury were possibly attributed to abnormal expression of ACE and ACE2 related pathway.

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Abstract. Non-small cell lung cancer (NSCLC) accounts for 80-85% of all lung cancer cases and the prognosis of NSCLC patients is unsatisfactory since 5-year survival rate of NSCLC is still as low as 11%. Natural compounds derived from plants with few or no side effects have been recognized as alternative or auxiliary cure for cancer patients. Phloretin is such an agent possessing various pharmacological activities; however, there is scarce information on its anticancer effects on NSCLC. It was evaluated and confirmed, in the present study, that phloretin inhibited proliferation and induced apoptosis in A549, Calu-1, H838 and H520 cells in a dosedependent manner, phloretin also suppressed the invasion and migration of NSCLC cells. We further confirmed that phloretin dose-dependently suppressed the expression of Bcl-2, increased the protein expression of cleaved-caspase-3 and -9, and deregulated the expression of matrix metalloproteinases (MMP)-2 and -9 on gene and protein levels. Besides, evaluations revealed that phloretin enhanced the anticancer effects of cisplatin on inhibition of proliferation and induction of apoptosis in NSCLC cells. Moreover, phloretin facilitated the effects of cisplatin on deregulation of Bcl-2, MMP-2 and -9, and upregulation of cleaved-caspase-3 and -9. In conclusion, the present study demonstrated that phloretin possessed anticancer effects and enhanced the anticancer effects of cisplatin on NSCLC cell lines by suppressing proliferation, inducing apoptosis and inhibiting invasion and migration of the cells through regulating apoptotic pathways and MMPs. IntroductionLung cancer is the most frequent reason for cancer related death and non-small cell lung cancer (NSCLC) accounts for ~80-85% of all lung cancer cases (1). Although there has been notable progression in combination chemotherapy and surgical techniques, the prognosis of NSCLC patients is still unsatisfactory since 5-year survival rate of NSCLC with all stages and histological types is as low as 11% (2). Besides the prolonged life time, the survival quality of NSCLC patients should also be taken care of, while the high toxicity of anticancer drugs adopted in clinical first line to normal tissues and cells is an impassable barrier for cancer therapy and a heavy burden for patients to bear. It would be better if there were some methods that could improve the clinical therapy effects and relieve the pain of the patients.Agents derived from various plants with few or no side effects have been recognized as potential alternative or auxiliary cure for cancer patients. Flavonoids, one major class of polyphenols, are well known for their antioxidant activity by eliminating reactive oxygen species (3) and chelating metal atoms (4,5). There is also substantial research suggesting that flavonoids have anticancer effects (6). Phloretin [3-(4-hydroxyphenyl)-1-(2,4,5-trihydroxyphenyl)] is one of the major phenolic flavonoid glucosides (structure showed in Fig. 1) found in apples and other plants, such as Pieris japonica, Hoveniae Lignum and...

Resveratrol is a plant-derived natural compound which possesses potential anticancer properties. However, there are scarce reports on its anticancer effects in non-small cell lung cancer and its auxiliary function on the anticancer effects of cisplatin. In the present study, we investigated the effects of resveratrol on the cell viability and apoptosis in human non-small cell lung cancer H838 and H520 cell lines. It has been found that resveratrol inhibited the proliferation of H838 and H520 cells in a dose- and time-dependent manner, and apoptosis was increased in cells treated with resveratrol which was associated with the depolarization of mitochondrial membrane potential, release of cytochrome c from mitochondria to cytosol, and abnormal expression of Bcl-2 and Bax proteins. Above all, resveratrol enhanced the effects of cisplatin on inhibition of cancer cell proliferation, induction of cell apoptosis, depolarization of mitochondrial membrane potential, release of cytochrome c and regulation on expression of Bcl-2 and Bax. Results from the present study demonstrated that resveratrol exhibited its anticancer effects on non-small cell lung cancer H838 and H520 cell lines, and enhanced the antitumor effects of cisplatin by regulating the mitochondrial apoptotic pathway. These results have put forward the rationale for further basic research and preclinical investigation on the anticancer effects of resveratrol against human non-small cell lung cancer.

In drowning victims, acute respiratory failure and hypoxia are very common, 1) and hypoxia-induced organ damage due to pulmonary edema caused by aspiration of water has been recognized as a major cause of death in near-drowning victims. [2][3][4] But the exact mechanisms remain unclear. Previous clinical studies have shown that white blood cell and neutrophils apparently increased in most acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) drowning patients' plasma with bilateral diffuse or localized alveolar infiltrates on chest X-ray obtained shortly after arrival. 5) In seawater aspiration-induced ALI rabbits model, the infiltration of inflammatory cells are increased in alveolar spaces with evidence of increasing of myeloperoxidase (MPO) activity and tumor necrosis factor-a (TNF-a) concentration in lung tissue. 6) These results may provide a potential mechanism that inflammation could partly explain the lung injury following seawater aspiration.Danshen, a traditional medical ingredient herbal drug deriving from dried roots of Salvia miltiorrhiza BUNGE, has been widely used in the treatment of acute or chronic diseases as circulatory, cerebrovascular disorders. 7) Tanshinone IIA (TIIA), one of the major active components of Danshen, has been reported to protect against lipopolysaccharide (LPS)-induced lung injury in mice.8) It is also shown that TIIA has an anti-inflammatory effect through the inhibition of nuclear factor-kB (NF-kB) activity 9) and the expression of inflammatory mediators such as nitric oxide, TNF-a, interleukin-1 (IL-1) and interleukin-6 (IL-6) in macrophage cells.10) Whether TIIA plays a protective effect on lung injury following seawater aspiration is unknown.Macrophage migration inhibitory factor (MIF) is recognized as a proinflammatory cytokine which derived from many cell types including macrophages and T lymphocytes.11) It is reported that serum MIF levels are significantly increased in ALI patients or animal model compared to healthy controls, as revealed MIF is a putative biomarker in ALI.12) Additionally, after activating NF-kB, MIF can induce the production of subsequent cytokines.13) The selective inhibition of inflammatory cytokine activities may remain an important goal for the effective treatment of acute lung injury.In the present study, we reported that TIIA treatment significantly attenuated seawater aspiration-induced lung injury. It was probably associated with downregulation of MIF and the subsequent inhibition of NF-kB activity as well as expression of IL-6 and TNF-a. MATERIALS AND METHODSChemicals Tanshinone IIA (sulfonate, purity is 99%) was purchased from the National Institute for the Control of Pharmaceutical and Biological Products (NICPBP, Beijing, China). The kits for determination of myeloperoxidase activity were obtained from Jiancheng Bioengineering Institute (Nanjing, China). Anti-phospho-NF-kB p65 and anti-b-actin monoclonal antibodies were obtained from Santa Cruz Biotechnology Inc. (Santa Cruz, CA, U.S.A.). Anti-MIF monoclonal antibody was g...

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