Impaired Indole Acetic Acid and Reduced Indole-Producing Bacteria Contribute to Swainsonine-Induced Liver Inflammation.

Liver inflammation could be elicited by swainsonine in livestock, affecting the development of agriculture and animal husbandry. Our previous study showed an important role of bile acids (BAs) in swainsonine-induced hepatic inflammation. However, its pathogenesis, particularly the roles of a comprehensive profile of liver and serum metabolites and microbial-derived indole metabolites, has not been clarified. This study aimed to demonstrate the mechanisms linking the indole-producing bacteria and indole metabolites to swainsonine-induced hepatic inflammation by combining Targeted 500 metabolomics and quantitative analysis of indole metabolites. Swainsonine significantly disturbed the liver and serum metabolomes in mice. Genus Akkermansia alleviating inflammation and genus Lactobacillus producing indole metabolites were significantly declined. Indole acetic acid (IAA) was the only reduced aryl hydrocarbon receptor (AHR) ligand in this study. Analogously, some bacteria causing liver damage markedly increased. These findings suggested that indole-producing bacteria and indole metabolites may be potential triggers of swainsonine-induced hepatic inflammation.

Extracellular Vesicles Obtained From Lung Adenocarcinoma Cells Cultured Under Intermittent Hypoxia Induce M2 Macrophage Polarization via miR-20a-5p Delivery.

Conclusion: These findings indicate that EVs obtained from lung adenocarcinoma cells cultured under IH deliver miR-20a-5p to promote M2 macrophage polarization by targeting PTEN.

New tricks for old drugs- praziquantel ameliorates bleomycin-induced pulmonary fibrosis in mice.

BACKGROUND: Pulmonary fibrosis is a chronic progressive disease with complex pathogenesis, short median survival time, and high mortality. There are few effective drugs approved for pulmonary fibrosis treatment. This study aimed to evaluate the effect of praziquantel (PZQ) on bleomycin (BLM)-induced pulmonary fibrosis. METHODS: In this study, we investigated the role and mechanisms of PZQ in pulmonary fibrosis in a murine model induced by BLM. Parameters investigated included survival rate, lung histopathology, pulmonary collagen deposition, mRNA expression of key genes involved in pulmonary fibrosis pathogenesis, the activity of fibroblast, and M2/M1 macrophage ratio. RESULTS: We found that PZQ improved the survival rate of mice and reduced the body weight loss induced by BLM. Histological examination showed that PZQ significantly inhibited the infiltration of inflammatory cells, collagen deposition, and hydroxyproline content in BLM-induced mice. Besides, PZQ reduced the expression of TGF-ß and MMP-12 in vivo and inhibited the proliferation of fibroblast induced by TGF-ß in vitro. Furthermore, PZQ affected the balance of M2/M1 macrophages. CONCLUSIONS: Our study demonstrated that PZQ could ameliorate BLM-induced pulmonary fibrosis in mice by affecting the balance of M2/M1 macrophages and suppressing the expression of TGF-ß and MMP-12. These findings suggest that PZQ may act as an effective anti-fibrotic agent for preventing the progression of pulmonary fibrosis.

Klotho inhibits the activation of NLRP3 inflammasome to alleviate lipopolysaccharide-induced inflammatory injury in A549 cells and restore mitochondrial function through SIRT1/Nrf2 signaling pathway.

Acute lung injury is a severe clinical condition constituting a major cause of mortality in intensive care units. This study aimed to investigate the role of klotho in alleviating lipopolysaccharide (LPS)-induced acute lung injury. LPS-induced acute lung injury was used to simulate the acute lung injury caused by severe pneumonia in vitro. The viability and apoptosis of A549 cells were detected by cell counting kit-8 assay and flow cytometry. The inflammatory response, oxidative stress, and mitochondrial function in A549 cells were analyzed by commercial assay kits and 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethyl-benzimidazolyl carbocyanine iodide (JC-1) staining. The expression of apoptosis-related proteins, Sirtuin 1 (SIRT1)/nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway-related proteins, and NOD-like receptor family pyrin domain containing 3 (NLRP3) expression in A549 cells was detected by western blot. The mtDNA synthase level in A549 cells was analyzed by reverse transcription-quantitative polymerase chain reaction. The results showed that, klotho had no cytotoxic effect on A549 cells. The viability and mitochondrial function were inhibited and apoptosis, inflammatory response, and oxidative stress were aggravated in LPS-induced A549 cells, which were all reversed by klotho. Klotho activated the SIRT1/Nrf2 signaling pathway to inhibit the LPS-induced NLRP3 inflammasome activation in A549 cells. However, EX527, a SIRT1 inhibitor, attenuated the klotho effect to suppress viability and mitochondrial function and promoted apoptosis, inflammatory response, and oxidative stress of A549 cells. In conclusion, klotho inhibited the activation of NLRP3 inflammasome to alleviate LPS-induced inflammatory injury of A549 cells and restore mitochondrial function through activating the SIRT1/Nrf2 signaling pathway.

Features of osteoporosis in male patients with bronchiectasis, a cross-sectional study.

Background: Osteoporosis increases the burden and disease related adverse events of comorbidities in some chronic disease. The relationships between osteoporosis and bronchiectasis are not fully understood. This cross-sectional study explores the features of osteoporosis in male patients with bronchiectasis. Methods: From January 2017 to December 2019, male patients (age >50 years) with stable bronchiectasis were included, as were normal subjects. Data on demographic characteristics and clinical features were collected. Results: Totally, 108 male patients with bronchiectasis and 56 controls were analyzed. Osteoporosis was observed in 31.5% (34/108) of patients with bronchiectasis and 17.9% (10/56) of controls (P=0.001). The T-score negatively correlated with age (R=-0.235, P=0.014) and bronchiectasis severity index score (BSI; R=-0.336, P<0.001). BSI score ≥9 was a major factor associated with osteoporosis [odd ratio (OR) =4.52; 95% confidence interval (CI): 1.57-12.96; P=0.005]. Other factors associated with osteoporosis included body-mass index (BMI) <18.5 kg/m2 (OR =3.44; 95% CI: 1.13-10.46; P=0.030), age ≥65 years (OR =2.87; 95% CI: 1.01-7.55; P=0.033), and a smoking history (OR =2.78; 95% CI: 1.04-7.47; P=0.042). Conclusions: The prevalence of osteoporosis was higher in male bronchiectasis patients than that in controls. Factors including age, BMI, smoking history, and BSI were associated with osteoporosis. Early diagnosis and treatment might be of great value in prevention and management of osteoporosis in patients with bronchiectasis.

Lipid metabolism changes in patients with severe COVID-19.

BACKGROUND: We investigated the dynamic changes in lipid profiles and their correlations with disease severity and clinical outcome in patients with severe COVID-19. METHODS: We retrospectively reviewed 519 severe COVID-19 patients with confirmed outcomes (discharged or deceased), admitted to the West Court of Union Hospital in Wuhan, China, between 29 January and 8 April 2020. RESULTS: Altogether, 424 severe COVID-19 patients, including 34 non-survivors and 390 survivors, were included in the final analyses. During hospitalization, low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C) and apolipoprotein A-I (apoA-I) showed an increasing trend in survivors, but showed a downward trend in non-survivors. The serum concentrations of HDL-C and apoA-I were inversely correlated with C-reactive protein (CRP), length of hospital stay of survivors, and disease severity scores. For in-hospital deaths, the areas under the receiver operating characteristic curves (AUCs) of the ratios of CRP/HDL-C and CRP/apoA-I at admission were 0.84 and 0.83, respectively. Moreover, patients with high ratios of CRP/HDL-C (＞77.39) or CRP/apoA-I (＞72.37) had higher mortality rates during hospitalization (log-rank p < 0.001). Logistic regression analysis demonstrated that hypertension, lactate dehydrogenase, SOFA score, and High CRP/HDL-C ratio were independent predictors of in-hospital mortality. CONCLUSIONS: During severe COVID-19, HDL-C and apoA-I concentrations are dramatically decreased in non-survivors. Moreover, High CRP/HDL-C ratio is significantly associated with an increase in mortality and a poor prognosis.

Thyroid dysfunction may be associated with poor outcomes in patients with COVID-19.

BACKGROUND: Coronavirus disease (COVID-19) has resulted in considerable morbidity and mortality worldwide. Thyroid hormones play a key role in modulating metabolism and the immune system. However, the prevalence of thyroid dysfunction (TD) and its association with the prognosis of COVID-19 have not yet been elucidated. In this study, we seek to address this gap and understand the link between TD and COVID-19. METHODS: Herein, we enrolled patients who were hospitalized with COVID-19 and had normal or abnormal thyroid function test results at the West Court of Union Hospital in Wuhan, China, between 29 January and February 26, 2020. We carried out follow up examinations until April 26, 2020. Data on clinical features, treatment strategies, and prognosis were collected and analyzed. TD was defined as an abnormal thyroid function test result, including overt thyrotoxicosis, overt hypothyroidism, subclinical hypothyroidism, subclinical hyperthyroidism, and euthyroid sick syndrome. RESULTS: A total of 25 and 46 COVID-19 patients with and without TD, respectively, were included in the study. COVID-19 patients with TD had significantly higher neutrophil counts and higher levels of C-reactive protein, procalcitonin, lactate dehydrogenase, serum creatine kinase, aspartate transaminase, and high-sensitive troponin I and a longer activated partial thromboplastin time but lower lymphocyte, platelet, and eosinophil counts. A longitudinal analysis of serum biomarkers showed that patients with TD presented persistently high levels of biomarkers for inflammatory response and cardiac injury. COVID-19 patients with TD were more likely to develop a critical subtype of the disease. Patients with TD had a significantly higher fatality rate than did those without TD during hospitalization (20% vs 0%, P = 0.002). Patients with TD were more likely to stay in the hospital for more than 28 days than were those without TD (80% vs 56.52%, P = 0.048). CONCLUSIONS: Our preliminary findings suggest that TD is associated with poor outcomes in patients with COVID-19.

Canagliflozin alleviates LPS-induced acute lung injury by modulating alveolar macrophage polarization.

BACKGROUND: Canagliflozin (CANA), a sodium-glucose cotransporter 2 inhibitor, is a novel therapeutic agent that exhibits multiple actions in type 2 diabetes. CANA can regulate intracellular glucose metabolism and exert anti-inflammatory effects in immune cells. Alveolar macrophage polarization balance is often associated with lower inflammation in acute lung injury (ALI). However, little is known about the anti-inflammatory effect of CANA on ALI. METHODS: This study aimed to determine the effect of CANA on ALI as well as its potential ability to modulate alveolar macrophage polarization in ALI mouse models and bone marrow-derived macrophages (BMDMs). RESULTS: The histopathological changes indicated that CANA alleviated lung injury in lipopolysaccharide-induced ALI mice models and exerted anti-inflammatory effects in the presence of lower levels of tumor necrosis factor-ɑ, interleukin-6, and interleukin-1ß in bronchoalveolar lavage fluid (BALF) and serum. Moreover, flow cytometry analysis of mouse BALF cells and BMDMs demonstrated that CANA can modulate and reconstitute M1 and M2 macrophage balance, inhibiting macrophages with the M1 phenotype while promoting macrophages to shift to the M2 phenotype. Immunohistochemistry and reverse transcription polymerase chain reaction were also performed. CONCLUSIONS: These findings indicate that CANA alleviates lung injury and exerts anti-inflammatory effects by modulating alveolar macrophage polarization balance, suggesting that CANA might act as a novel anti-inflammatory drug for treating ALI.

Para-aortic lymph node tracing and dissection in advanced gastric cancer: Effectiveness of carbon nanoparticles injection through the no. 12b lymph node.

BACKGROUND AND OBJECTIVES: The relative effectiveness of tracers in guiding para-aortic lymph node dissection (PAND) in advanced gastric cancer is undefined. In this single-center, prospective study, we aimed to discuss the effectiveness of such tracers. MATERIALS AND METHODS: Between January 2015 and January 2016, 90 consecutive patients with stage T4a gastric cancer were evenly assigned to receive 0.2 mL of carbon nanoparticles (a), methylene blue (b), or no tracer (c) injection through no. 12b lymph nodes before PAND. RESULTS: There was no difference in the baseline characteristics between the three groups. Group A vs. B or C had a higher number of dissected lymph nodes (34.1 ± 9.8, 25.5 ± 5.5, and 22.6 ± 3.7; P < 0.001; B vs. C: P =0.321) and no. 16a2/b1 para-aortic lymph nodes (PANs; 11.8 ± 4.8, 7.0 ± 1.2, and 5.5 ± 1.2; P < 0.001; B vs. C: P =0.178) and similar rates of lymph node metastasis (20.9 ± 17.5%, 19.1 ± 15.1%, and 23.6 ± 19.7%; P = 0.511), positive dissected PAN (23.3% [7/30], 16.7% [5/30], and 16.7% [5/30]), surgery duration (252.9 + 35.4, 244.4 ± 29.0, and 250.3 + 29.9 min; P = 0.421), and blood loss (266.7 ± 115.5, 270.0 ± 82.6, and 260.0 ± 116.3 mL, P = 0.933). There was no common bile duct damage by tracer injection, and one case of duodenal stump fistula, one abdominal infection, and two anastomotic leakages in Groups A-C, respectively, were treated successfully. CONCLUSIONS: In advanced gastric cancer treatment, carbon nanoparticle injection into no. 12b nodes appears to better trace no. 16a2/b1 PAN.

Association of diabetes mellitus with disease severity and prognosis in COVID-19: A retrospective cohort study.

AIMS: The 2019 novel coronavirus disease (COVID-19) emerged in Wuhan, China, and was characterized as a pandemic by the World Health Organization. Diabetes is an established risk associated with poor clinical outcomes, but the association of diabetes with COVID-19 has not been reported yet. METHODS: In this cohort study, we retrospectively reviewed 258 consecutive hospitalized COVID-19 patients with or without diabetes at the West Court of Union Hospital in Wuhan, China, recruited from January 29 to February 12, 2020. The clinical features, treatment strategies and prognosis data were collected and analyzed. Prognosis was followed up until March 12, 2020. RESULTS: Of the 258 hospitalized patients (63 with diabetes) with COVID-19, the median age was 64 years (range 23-91), and 138 (53.5%) were male. Common symptoms included fever (82.2%), dry cough (67.1%), polypnea (48.1%), and fatigue (38%). Patients with diabetes had significantly higher leucocyte and neutrophil counts, and higher levels of fasting blood glucose, serum creatinine, urea nitrogen and creatine kinase isoenzyme MB at admission compared with those without diabetes. COVID-19 patients with diabetes were more likely to develop severe or critical disease conditions with more complications, and had higher incidence rates of antibiotic therapy, non-invasive and invasive mechanical ventilation, and death (11.1% vs. 4.1%). Cox proportional hazard model showed that diabetes (adjusted hazard ratio [aHR] = 3.64; 95% confidence interval [CI]: 1.09, 12.21) and fasting blood glucose (aHR = 1.19; 95% CI: 1.08, 1.31) were associated with the fatality due to COVID-19, adjusting for potential confounders. CONCLUSIONS: Diabetes mellitus is associated with increased disease severity and a higher risk of mortality in patients with COVID-19.

PKR suppress NLRP3-pyroptosis pathway in lipopolysaccharide-induced acute lung injury model of mice.

To explore the effect of double-stranded RNA-dependent kinase (PKR) in acute lung injury (ALI) and resultant acute respiratory distress syndrome (ARDS). A mouse model of lipopolysaccharide (LPS)-induced ALI was used to evaluate the levels of phosphorylated (p)-PKR and NLRP3 in lung tissue, and the protective effects of a PKR inhibitor on lung injury. And in vitro, macrophages were incubated with LPS, with or without PKR inhibitor pre-treatment. It was observed that the levels of p-PKR protein and NLRP3 protein were significantly increased compared with those in control tissues after LPS administration. Meanwhile, treatment with PKR inhibitor decreased inflammation, injury score, wet/dry weight ratio, bronchoalveolar lavage fluid (BALF) protein levels, neutrophil count in BALF, myeloperoxidase activity and expression of high-mobility group box1(HMGB1) and interleukin(IL)-1ß in the lungs of LPS-challenged mice. In vitro, we demonstrated that the levels of p-PKR and NLRP3, and cell mortality rate were increased in macrophages which were incubated with LPS compared with those without LPS administration, and PKR inhibitor significantly suppressed the level of NLRP3, caspase-1, HMGB1 and IL-1ß. These results indicate that PKR plays a key role in ALI through NLRP3-pyrotosis pathway and pharmacological inhibition of PKR may have potential therapeutic effects in the treatment of patients with ALI and ARDS.

NETs promote ALI/ARDS inflammation by regulating alveolar macrophage polarization.

Neutrophils activated during acute lung injury (ALI) form neutrophil extracellular traps (NETs) to capture pathogens. However, excessive NETs can cause severe inflammatory reactions. Macrophages are classified as M1 macrophages with proinflammatory effects or M2 macrophages with anti-inflammatory effects. During ALI, alveolar macrophages (AMs) polarize to the M1 phenotype. This study tested the hypothesis that NETs may aggravate ALI or acute respiratory distress syndrome (ARDS) inflammation by promoting alveolar macrophage polarization to the M1 type. Our research was carried out in three aspects: clinical research, animal experiments and in vitro experiments. We determined that NET levels in ARDS patients were positively correlated with M1-like macrophage polarization. NET formation was detected in murine ALI tissue and associated with increased M1 markers and decreased M2 markers in BALF and lung tissue. Treatment with NET inhibitors significantly inhibitor NETs generation, downregulated M1 markers and upregulated M2 markers. Regardless of LPS pre-stimulation, significant secretion of proinflammatory cytokines and upregulated M1 markers were detected from bone marrow-derived macrophages (M0 and M2) cocultured with high concentrations of NETs; conversely, M2 markers were downregulated. In conclusion, NETs promote ARDS inflammation during the acute phase by promoting macrophage polarization to the M1 phenotype. We propose that NETs play an important role in the interaction between neutrophils and macrophages during the early acute phase of ALI.

Relationship between celiac artery variation and number of lymph nodes dissection in gastric cancer surgery.

BACKGROUND: Radical D2 lymphadenectomy for advanced gastric cancer as a standard procedure has gained global consensus. Mounting studies have shown that the number of lymph nodes dissection directly affects the prognosis and recurrence of gastric cancer. Our previous study showed that there was no obvious lymph node around the abnormal hepatic artery derived from the superior mesenteric artery. AIM: To investigate the relationship between celiac artery variation and the number of lymph nodes dissection in gastric cancer surgery. METHODS: The clinicopathological data of 421 patients treated with radical D2 lymphadenectomy were analyzed retrospectively. The difference of the number of lymph nodes dissection between the celiac artery variation group and the normal vessels group and the relationship with prognosis were analyzed. RESULTS: Celiac artery variation was found in 110 patients, with a variation rate of 26.13%. Celiac artery variation, tumor staging, and Borrmann typing were factors that affected lymph node clearance in gastric cancer, and the number of lymph nodes dissection in patients with celiac artery variation was significantly less than that of non-variant groups (P < 0.05). Univariate analysis showed that there was no significant difference in survival time between the two groups (P > 0.05). Univariate and multiple Cox regression analysis showed that celiac artery variation was not a prognostic factor for gastric cancer (P > 0.05). Tumor staging, intraoperative bleeding, and positive lymph node ratio were prognostic factors for gastric cancer patients (all P < 0.05). CONCLUSION: The number of lymph nodes dissection in patients with celiac artery variation was reduced, but there was no obvious effect on prognosis. Therefore, lymph nodes around the abnormal hepatic artery may not need to be dissected in radical D2 lymphadenectomy.

Robust and energy-efficient expression recognition based on improved deep ResNets.

To improve the robustness and to reduce the energy consumption of facial expression recognition, this study proposed a facial expression recognition method based on improved deep residual networks (ResNets). Residual learning has solved the degradation problem of deep Convolutional Neural Networks (CNNs); therefore, in theory, a ResNet can consist of infinite number of neural layers. On the one hand, ResNets benefit from better performance on artificial intelligence (AI) tasks, thanks to its deeper network structure; meanwhile, on the other hand, it faces a severe problem of energy consumption, especially on mobile devices. Hence, this study employs a novel activation function, the Noisy Softplus (NSP), to replace rectified linear units (ReLU) to get improved ResNets. NSP is a biologically plausible activation function, which was first proposed in training Spiking Neural Networks (SNNs); thus, NSP-trained models can be directly implemented on ultra-low-power neuromorphic hardware. We built an 18-layered ResNet using NSP to perform facial expression recognition across datasets Cohn-Kanade (CK+), Karolinska Directed Emotional Faces (KDEF) and GENKI-4K. The results achieved better anti-noise ability than ResNet using the activation function ReLU and showed low energy consumption running on neuromorphic hardware. This study not only contributes a solution for robust facial expression recognition, but also consolidates the low energy cost of their implementation on neuromorphic devices, which could pave the way for high-performance, noise-robust and energy-efficient vision applications on mobile hardware.

Simulated coronary arterial hemodynamics of myocardial bridging.

The objective of this study was to explore the effects of myocardial bridge compression on blood flow, normal stress, circumferential stress and shear stress in mural coronary artery. An original mural coronary artery simulative device has been greatly improved and its measured hemodynamic parameters have been expanded from a single stress (normal stress) to multiple stresses to more fully and accurately simulate the true hemodynamic environment under normal stress, circumferential stress and shear stress. This device was used to more fully explore the relationship between hemodynamics and mural coronary atherosclerosis under the combined effects of multiple stresses. Results obtained from the mural coronary artery simulator showed stress abnormality to be mainly located in the proximal mural coronary artery where myocardial bridge compression was intensified and average and fluctuation values (maximum minus minimum) of proximal stress were significantly increased by 27.8% and 139%, respectively. It is concluded that myocardial bridge compression causes abnormalities in the proximal hemodynamics of the mural coronary artery. This is of great significance for understanding the hemodynamic mechanism of coronary atherosclerosis and has potential clinical value for the pathological effect and treatment of myocardial bridge.

The function and clinical relevance of lncRNA UBE2CP3-001 in human gliomas.

INTRODUCTION: Gliomas are the most frequent primary tumors in the human brain. Recent studies have identified a class of long noncoding RNAs, named lncRNAs, which were reported to participate in regulating the development of various diseases, including gliomas. In our previous studies, we found that lncRNA UBE2CP3-001 was overexpressed in gliomas but not in normal tissue. However, the molecular functions of UBE2CP3-001 in glioma are largely unknown. MATERIAL AND METHODS: The presence of UBE2CP3-001 in U87 cells, glioma tissues and normal brain tissues was detected by real-time RT-PCR. The ability of U87 cells to migrate was analyzed using a cellular wound healing assay after downregulation of UBE2CP3-001. The survival rate of U87 cells after UBE2CP3-001 knockdown was also analyzed using the CCK8 assay. In vivo tumor weights from xenograft tumors transfected with UBE2CP3-001 shRNA were further analyzed using in vivo animal experiments. The expression levels of MMP-9 and TRAF3IP2 were determined by Western blot. RESULTS: Our data showed that UBE2CP3-001 was overexpressed in most glioma tissues (p < 0.01). Downregulation of UBE2CP3-001 could inhibit cell migration (p < 0.01) and invasiveness (p < 0.01) of U87 cells. Downregulation of UBE2CP3-001 in U87 cells also suppressed the cell proliferation (p < 0.01) and promoted apoptosis (p < 0.01). Furthermore, in vivo studies confirmed that knockdown of UBE2CP3-001 could retard the growth of U87 xenograft tumors (p < 0.01). Western blot analysis showed that knockdown of UBE2CP3-001 could effectively inhibit the expression of MMP-9 (p < 0.01) and TRAF3IP2 (p < 0.01) in U87 glioma cells. CONCLUSIONS: These data suggest an important role of UBE2CP3-001 in glioma and indicate its potential application in anti-glioma therapy.

Differential effects of size-specific particulate matter on emergency department visits for respiratory and cardiovascular diseases in Guangzhou, China.

BACKGROUND: Studies differentiating the cardiorespiratory morbidity effects of PM2.5, PM10, and PM2.5∼10 (i.e. coarse PM or PMc) are still limited and inconsistent. OBJECTIVE: To estimate the acute, cumulative, and harvesting effects of exposure to the three size-specific PM on cardiorespiratory morbidity, and their concentration-response relations. METHODS: A total of 6,727,439 emergency department (ED) visits were collected from 16 public teaching hospitals in Guangzhou, from January 1st 2012 to December 31st 2015, among which over 2.1 million were asthma, COPD, pneumonia, respiratory tract infection (RTI), hypertension, stroke, and coronary heart disease (CHD). Distributed lag non-linear models (DLNM) was used to estimate the associations between the three size-specific PM and ED visits for the cardiovascular diseases. Long-term trends, seasonality, influenza epidemics, meteorological factors, and other gas pollutants, including SO2, NO2, and O3, were adjusted. We stratified the analyses by gender and age. RESULTS: Elevated PM2.5 and PM10 were significantly associated with increased ED visits for pneumonia, RTI, and CHD at both lag0 and lag0-3. A 10 µg/m3 increment of PMc (at lag0-14) was estimated to increase ED visits for pneumonia by 6.32% (95% CI, 4.19, 8.49) and for RTI by 4.72% (95% CI, 3.81, 5.63), respectively. PMc showed stronger cumulative effects on asthma in children than elderly. We observed significant harvesting effects (i.e. morbidity displacements) of the three size-specific PM on respiratory but very little on cardiovascular ED visits. The concentration-response curves suggested non-linear relations between exposures to the three different sizes of PM and respiratory morbidity. CONCLUSIONS: Overall, the three size-specific PM demonstrated distinct acute and cumulative effects on the cardiorespiratory diseases. PM2.5 and PMc would have significant effects on pneumonia and RTI. Strategies should be considered to further reduce levels of ambient PM2.5 and PMc.

Four case reports on pelvic tumors with deep venous thromboses as main symptoms and literature review.

To probe into the reasons for misdiagnoses of pelvic tumor as deep venous thromboses as well as the diagnostic methods and effective treatments on pelvic tumor. Four case reports on misdiagnosing pelvic tumor as deep venous thromboses and further analysis on the causes of misdiagnosis, diagnosis, and treatment with the literature study. The four cases were misdiagnosed as pelvic tumor, which actually were fibroneuroma, myxo.fluidity liposarcoma, moderately differentiated squamous cell carcinoma, and synovial sarcoma, respectively. The tumor in first case was completely removed, and the tumor in other three cases, which were malignant tumors, were resected when the tumors shrank with clear boundary and less blood supply after applied with 3. cycles of intra.arterial chemotherapy via an implanted pumpies. Pelvic tumor usually show up or is misdiagnosed as deep venous thromboses for its untypical clinical manifestation, so it should be on the alert for pelvic tumor when deep venous thromboses occurs. Tumor resection is preferred for benign tumor, and intra.arterial intervention chemotherapy should be applied first for malignant tumor followed by surgery.

ITIH4: Effective Serum Marker, Early Warning and Diagnosis, Hepatocellular Carcinoma.

Hepatocellular carcinoma (HCC) is a highly lethal malignant tumor evolved from cirrhosis. It is quite significant to seek accurate, easy markers for early warning and diagnosis of HCC. Through prospective cohort follow-up study and mass spectrometry, we discovered and verified a serum marker valuable for early warning and diagnosis. Follow-up observation was performed on cirrhosis patients. Matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS) was adopted to detect the serums of patients, and the serum polypeptides with a potential value in early HCC warning and diagnosis were screened. Electrospray ionization quadrupole time-of-flight tandem mass spectrometry (ESI-Q-TOF-MS/MS) was exploited to identify these screened polypeptides. Moreover, the serum marker concentration was determined by ELISA to validate the clinical value of the serum marker. Among 109 cirrhosis patients followed up for two years, 29 patients (26.6%) finally progressed into HCC. MALDI-TOF MS shows that the concentration of a 3155.66Da polypeptide was significantly different between the patients that progressed into HCC and those not. Through MS/MS identification, it is confirmed that the polypeptide is inter-alpha-trypsin inhibitor heavy chain 4 (ITIH4). The serum ITIH4 concentrations in two groups were measured with ELISA and compared with Alpha-fetoprotein (AFP). Results show that serum ITIH4 and AFP concentrations were negatively correlated (r=-0.263, p=0.0006), and the ITIH4 concentration had a significant intergroup difference (p=0.000). Receiver operating characteristic (ROC) curve indicates that its predictive value (area under the curve, AUC) is 0.667, superior to AFP. For the patients progressing into HCC, serum samples were separately collected when they were recruited and diagnosed as cirrhosis. Measurement on these samples reveals that ITIH4 was declining during the progression of HCC (p=0.006). By virtue of mass spectrometry, we discovered and identified a biomarker valuable for early HCC warning and diagnosis. This marker overperforms the commonly used AFP, demonstrating a bright prospect.