Central Compartment Atopic Disease and Its Surgical Outcomes: Olfactory Changes and Technical Notes.

Background: Central compartment atopic disease (CCAD) is a recent, novel phenotype of chronic rhinosinusitis. Only a few studies have assessed olfactory function in patients with CCAD. Objectives: We aimed to investigate olfactory function changes after functional endoscopic sinus surgery (FESS) in patients with CCAD and proposed some surgical techniques to enhance the postoperative olfactory outcomes in such patients. Design: A retrospective cohort study. Methods: We collected data from 23 patients (8 men and 15 women) with CCAD who underwent FESS performed by a surgeon in Taiwan, between June 2018 and December 2021. The demographic data, olfactory function, and serum and tissue eosinophil percentages of the included patients were analyzed. The Top International Biotech Smell Identification Test (TIBSIT; Top International Biotech, Taipei, Taiwan) was used to assess olfactory function. Results: Of the 23 patients, most (95%) showed a positive reaction to aeroallergens, and 2 patients (8.7%) had asthma. Ten patients (43.5%) had peripheral eosinophilia, and 9 (39%) had eosinophilic nasal polyps. Moreover, the patients presented with variable olfactory dysfunction; the mean preoperative TIBSIT (pr-TIBSIT) score was 12.8 ± 2.3 (range: 0-43), whereas the mean postoperative TIBSIT (po-TIBSIT) score was 29.2 ± 1.9 (range: 16-44). The po-TIBSIT score was significantly better than the pre-TIBSIT score (paired t test, P < .0001). The improvement in olfactory function was not significantly correlated with the patients' age, serum eosinophil percentages, and nasal polyp eosinophil counts. Conclusion: Our findings indicate that CCAD is significantly associated with olfactory dysfunction and that FESS can effectively improve olfactory function. To optimize postoperative olfactory outcomes, precise removal of polyps from the olfactory cleft without damaging the neuroepithelium is recommended. Our study provides valuable insights into the management of CCAD patients undergoing FESS and can guide surgical decision-making to achieve optimal olfactory function outcomes.

Cross-Scale Fusion Transformer for Histopathological Image Classification.

Histopathological images provide the medical evidences to help the disease diagnosis. However, pathologists are not always available or are overloaded by work. Moreover, the variations of pathological images with respect to different organs, cell sizes and magnification factors lead to the difficulty of developing a general method to solve the histopathological image classification problems. To address these issues, we propose a novel cross-scale fusion (CSF) transformer which consists of the multiple field-of-view patch embedding module, the transformer encoders and the cross-fusion modules. Based on the proposed modules, the CSF transformer can effectively integrate patch embeddings of different field-of-views to learn cross-scale contextual correlations, which represent tissues and cells of different sizes and magnification factors, with less memory usage and computation compared with the state-of-the-art transformers. To verify the generalization ability of the CSF transformer, experiments are performed on four public datasets of different organs and magnification factors. The CSF transformer outperforms the state-of-the-art task specific methods, convolutional neural network-based methods and transformer-based methods. The source code will be available in our GitHub https://github.com/nchucvml/CSFT.

Severinia buxifolia-isolated acridones inhibit lung cancer invasion and decrease HIFα protein synthesis involving 5'UTR-mediated translation inhibition.

BACKGROUND: Lung cancer is one of the most common cancers worldwide and is by far the leading cause of cancer death attributed to its rapid metastasis and poor prognosis. Given that hypoxia-inducible factors (HIFs) are associated with cancer metastasis, discovering agents to inhibit HIF-mediated invasive cancer is highly desired. PURPOSE: This study aimed to investigate the natural acridone compounds isolated from Severinia buxifolia for the potential to delay hypoxia-induced lung cancer invasiveness by HIF inhibition. METHODS: Using a hypoxia-responsive element (HRE) luciferase reporter, cell migration and invasion assays, real-time PCR, Western blot, and DNA recombinant clones, compound effect on HIF activity, cancer metastasis, HIF-1α mRNA transcription, HIFs protein stability, and HIF-1α translation were observed under hypoxia conditions. RESULTS: Atalaphyllidine (Sbs-A) and atalaphyllinine (Sbs-B) were found to show the most potent effects on HIF transcriptional activity and HIF-1α protein expression in NSCLC cell line A549, although Sbs-A and Sbs-B might not attribute decreasing HIF-1α mRNA expression to potent inhibition of HIF activity. HIF-1α protein stability was not affected by Sbs-A; also, prolyl hydroxylase and proteasome inhibitors could not reverse the inhibitory effect from compounds. Furthermore, 3 - 10 µM low concentrations of Sbs-A inhibited HIF target gene expression, gelatin zymography activity, and A549 cancer invasion. Ultimately, Sbs-A inhibited HIF-1α 5'UTR-mediated translation independent of oxygen concentration, underlying the mechanism of compounds inhibiting HIF-1α protein expression. CONCLUSION: Our study proposed Severinia buxifolia-isolated acridone compounds inhibited 5'-mRNA HIFA-mediated translation and provided evidence supporting the ability of acridone compounds in targeting HIFα for delayed lung cancer metastasis.

L1CAM expression in either metastatic brain lesion or peripheral blood is correlated with peripheral platelet count in patients with brain metastases from lung cancer.

Background: Systemic immune-inflammation states across the heterogeneous population of brain metastases from lung cancer are very important, especially in the context of complex brain-immune bidirectional communication. Previous studies from our team and others have shown that the L1 cell adhesion molecule (L1CAM) is deeply involved in the aggressive phenotype, immunosuppressive tumor microenvironment (TME), and metastasis during multiple malignancies, which may lead to an unfavorable outcome. However, little is known about the relationship between the L1CAM expression and the systemic immune-inflammation macroenvironment beyond the TME in brain metastases from lung cancer. Methods: Two cohorts of patients with brain metastases from lung cancer admitted to the National Cancer Center, Cancer Hospital of Chinese Academy of Medical Sciences, were studied in the present research. The L1CAM expression in cranial metastatic lesions by immunohistochemistry was explored in patients treated with neurosurgical resection, whereas the L1CAM expression in peripheral blood by ELISA was tested in patients treated with non-surgical antitumor management. Furthermore, based on peripheral blood cell counts in the CBC test, six systemic immune-inflammation biomarkers [neutrophil count, lymphocyte count, platelet count, systemic immune-inflammation index (SII), neutrophil-to-lymphocyte ratio (NLR), and platelet-to-lymphocyte ratio] were calculated. Then, the relationship between the L1CAM expression and these systemic immune-inflammation biomarkers was analyzed. In addition, these systemic immune-inflammation biomarkers were also used to compare the systemic immune-inflammation states in two cohorts of patients with brain metastases from lung cancer. Results: Positive L1CAM expressions in the metastatic brain lesions were accompanied with significantly increased peripheral platelet counts in patients treated with neurosurgical tumor resection (P < 0.05). Similarly, in patients treated with non-surgical antitumor management, L1CAM expressions in the peripheral blood were positively correlated with peripheral platelet counts (P < 0.05). In addition, patients prepared for neurosurgical tumor resection were presented with poorer systemic immune-inflammation states in comparison with the one with non-surgical antitumor management, which was characterized by a significant increase in peripheral neutrophil counts (P < 0.01), SII (P < 0.05), and NLR (P < 0.05) levels. Conclusion: The L1CAM expression in either the metastatic brain lesion or peripheral blood is positively correlated with the peripheral platelet count in patients with brain metastases from lung cancer. In addition, brain metastases that are prepared for neurosurgical tumor resection show poor systemic immune-inflammation states.

CheXGAT: A disease correlation-aware network for thorax disease diagnosis from chest X-ray images.

Chest X-ray (CXR) imaging is one of the most common diagnostic imaging techniques in clinical diagnosis and is usually used for radiological examinations to screen for thorax diseases. In this paper, we propose a novel computer-aided diagnosis (CAD) system based on a hybrid deep learning model composed of a convolutional neural network (CNN) and a graph neural network (GNN). The system is intended to explore implicit correlations between thorax diseases to aid in the multilabel chest X-ray image classification task, which we term ‶CheXGAT‶. Specifically, the proposed CheXGAT framework comprises two main modules: an image representation learning (IRL) module and a graph representation learning (GRL) module. We employ the IRL module to learn high-level visual representation features from the CXR image. From the GRL module, the self-attention mechanism aggregates neighborhood features from the graphic structure to enhance the implicit correlation between thorax diseases. We adopted a data-driven method to create a disease correlation matrix that works on the message passing and aggregation process for the nodes in the GRL module. After end-to-end training, the GRL module enhances the correlation between thorax diseases to improve diagnosis performance. We performed experiments on the NIH Chest X-ray14 dataset, which contains 112,120 frontal-view radiographs; each image has multiple thorax disease labels. In the experimental results, the average AUC score of our proposed CheXGAT model reached 0.8266, and the AUC scores of Emphysema and Hernia reached 0.9447 and 0.9313, respectively. In addition, we visualized explanations via a gradient-based localization method in our proposed CheXGAT framework. Compared with previous studies, the experimental results show the competitive performance of our framework. Specifically, we propose a CAD system that uses a hybrid model to help radiologists identify CXR images from 14 chest diseases for clinical diagnosis.

Overexpression of LINC00673 Promotes the Proliferation of Cervical Cancer Cells.

OBJECTIVE: To study the expression of LINC00673 in cervical cancer and cervical intraepithelial neoplasia (CIN) and to explore the role of LINC00673 in the development of cervical cancer. METHODS: The expression of LINC00673 in serum from cervical cancer patients, CIN patients, and healthy participants was detected by RT-qPCR. The function of LINC00673 in cervical cancer cells was analyzed using in vitro and in vivo experiments. RESULTS: Our results revealed that serum LINC00673 levels were highest in cervical cancer patients, followed by patients with CIN and healthy controls. In vitro experiments demonstrated that overexpression of LINC00673 enhanced the proliferation and cell cycle progression of HeLa and SiHa cells. In vivo experiments showed that the tumor weight and volume of nude mice subcutaneously injected with LINC00673-overexpressing HeLa cells were larger than those of nude mice injected with control cells (P < 0.05). Western blotting showed that cell cycle-related proteins cyclin A2 and cyclin E and interstitial-associated proteins Snail and N-cadherin were upregulated and p53 signaling pathway-related proteins were downregulated in LINC00673-overexpressing HeLa and SiHa cells. CONCLUSION: LINC00673 plays an important role in the development of cervical cancer and may serve as a new therapeutic target for cervical cancer.

Investigation on reliability of red micro-light emitting diodes with atomic layer deposition passivation layers.

In this study, AlGaInP red light emitting diodes with sizes ranging from 5 to 50 micrometers were fabricated and characterized. The atomic layer deposition technology is applied to coat a layer of silicon dioxide for passivation and protection. The top emission area is covered by ITO layer to maximize the optical output. From the optical measurement, the linewidth and emission peaks shift very little among different current levels (from 30 to 150 A/cm2). High current level lifetests are performed and a 15 µm ALD device can last 27 hours of continuous operation at 100 A/cm2 before their diode junction failed. A much shorter lifetime of 5.32 hours was obtained when the driving current is raised to 400 A/cm2. When the same condition was applied to 15 µm PECVD devices, 25 hours and 4.33 hours are registered for 100 A/cm2 and 400 A/cm2 tests, respectively. The cross-sectional SEM reveals the voids, defects, and dark lines developed during the aging tests, and most of them are caused by top contact failure. The surface layers of ITO and SiO2 were melted and the dark lines which were originated from the top surface propagated through the device and led to the eventual failure of the diode. The optical intensity degradation slopes of different sizes of devices indicate a large device can last longer in this accelerated aging test. The efficiencies of the devices are also evaluated by the ABC model and the fitted bimolecular coefficient ranges from 1.35 to 3.40×10-10 cm3/s.

Therapeutic Role of Inducible Nitric Oxide Synthase Expressing Myeloid-Derived Suppressor Cells in Acetaminophen-Induced Murine Liver Failure.

Background: Acetaminophen (APAP) overdose is one of the major etiologies of liver failure. Hepatocyte necrosis induced by toxic metabolites of APAP can activate proinflammatory responses, including elastase-expressing neutrophils, to exacerbate liver injury. Myeloid-derived suppressor cells (MDSCs) increased in inflammation can inhibit proinflammatory responses. Our aim is to investigate the role of MDSC in APAP-induced liver failure and the possible therapeutic application. Methods: BLAB/c mice were injected with a sublethal/lethal dose of APAP as the murine model of liver failure. MDSCs were defined as CD11b+Gr-1+ cells with the ability of T-cell suppression. Results: A sublethal challenge of APAP could increase the intrahepatic MDSC and protect mice against subsequent lethal challenge of APAP, lipopolysaccharide (LPS)/D-galatosamine or concanavalin A. This protection was lost if MDSCs were depleted and inducible nitric oxide synthase (iNOS) was the key molecule in this MDSC-mediated protection. Taking advantage of these observations, different bone marrow-derived MDSCs (BM-MDSCs) were generated. Among different cytokine-treated BM-MDSCs, tumor necrosis factor alpha/LPS-primed MDSCs (TNF-α/LPS MDSCs) had the strongest liver-protection ability after adoptive transfer. Further mechanistic explorations showed, iNOS-expressing TNF-α/LPS MDSCs induced the apoptosis of activated neutrophil and decreased the intrahepatic infiltration of elastase-expressing neutrophil. Moreover, we generated MDSCs from human peripheral blood mononuclear cells (PBMCs) with similar phenotype. Conclusion: We demonstrated the protective role of MDSCs and therapeutic effect of TNF-α/LPS MDSCs in APAP-induced liver failure. MDSC might protect against the APAP-induced liver failure by reducing the intrahepatic infiltration of activated neutrophil to limit inflammation. Therefore, a therapeutic role of MDSCs for APAP-induced liver failure was proposed.

A dedifferentiated solitary fibrous tumor of the parotid gland: a case report with Cytopathologic findings and review of the literature.

BACKGROUND: Solitary fibrous tumor (SFT) is a ubiquitous mesenchymal neoplasm but it rarely occurs in the parotid gland. The histological features are variable, with the majority having spindle cell morphology and non-specific branching (staghorn) ecstatic vascular pattern. SFT ranges from benign to overtly malignant. Dedifferentiation within SFTs represents an abrupt transition from a well-differentiated component to a high-grade area, the latter most often including poorly differentiated epithelioid/round cell or high-grade spindle cell morphology. To the best of our knowledge, dedifferentiated SFT in the parotid gland has not been previously reported. CASE PRESENTATION: A 33-year-old woman presented with a soft tissue tumor in the right parotid gland that had been present for 6 months. Fine needle aspiration (FNA) cytology indicated epithelioid morphology in the dedifferentiated component of the tumor, along with metachromatic myxoid matrix. The tumor was initially interpreted as a salivary gland neoplasm of uncertain malignant potential (SUMP).Right partial parotidectomy was performed, and microscopic examination of the resected specimen revealed a malignant spindle cell tumor with a central epithelioid/anaplastic component. The tumor cells were diffusely positive for CD34, STAT-6 and FLI-1, and negative for pan-cytokeratin, CAM5.2, p63, S100 protein, CD31, SMA, and calponin.ERG and Ki67 immunostaining showed an accentuated nuclear staining pattern in the central dedifferentiated area. There was no overexpression of p53 or p16. The patient is currently undergoing regular follow-up and is 11 months postresection with no evidence of recurrence or distant metastasis. CONCLUSIONS: Unlike the typical spindle cell morphology of conventional SFTs, malignant SFTs can show areas of dedifferentiation mimicking an epithelial neoplasm. FNA of dedifferentiated SFTs of the parotid gland may show, a combination of atypical epithelioid cells and metachromatic myxoid/collagenous matrix, which is a less emphasized cytological feature of SFT and may lead to misdiagnosis as a more common parotid gland epithelial neoplasm.

Induction of liver-specific intrahepatic myeloid cells aggregation expands CD8 T cell and inhibits growth of murine hepatoma.

Toll-Like Receptor 9 (TLR9) stimulation selectively triggers the formation of a cell cluster termed intrahepatic myeloid aggregation for T cell expansion" (iMATE) in a mouse chronic viral hepatitis model. iMATE expands cytotoxic T cells and controls viral hepatitis infection. The liver-specific immune response prompted this investigation of whether the effect could control tumor growth in the murine hepatic tumor model. Murine hepatic BNL cells were used to establish an orthotropic liver tumor model. We found that intravenous infusion of TLR 9 agonist, CpG oligodeoxynucleotide (ODN) induced iMATE formation in non-tumor parts of liver and suppressed the murine BNL tumor growth. The ratio of intra-tumor CD8+ T cells have increased after CpG ODN. These cells expressed higher levels of effector and checkpoint molecules, and produce more Th1 cytokine upon ex vivo stimulation. The CD11b+Ly6ChiLy6G - subset of CD11b+ myeloid cells in the tumor microenvironment has increased. Both CD11b+Ly6ChiLy6G - and CD11b+Ly6CloLy6G+ subsets expressed higher level of interferon-gamma post CpG ODN treatment, although still presented a suppressive phenotype. Their suppressive ability was decreased, instead, the targeted CD8+ T cell proliferation was promoted at a higher dose of CD11b+Ly6ChiLy6G- cells. The phenomenon was further proven in DEN induced liver tumor model. In conclusion, systemic CpG ODN treatment induced iMATE formation that expanded effector CD8+ T cells to control tumor growth in the mouse hepatic tumor model. This novel strategy provides a new rationale for liver-specific tumor immunotherapy.

A Panel of Serum Noncoding RNAs for the Diagnosis and Monitoring of Response to Therapy in Patients with Breast Cancer.

BACKGROUND The aim of this study was to identify a panel of serum noncoding RNAs (ncRNAs) as potential diagnostic and prognostic biomarkers for breast cancer. MATERIAL AND METHODS Patients with breast cancer (n=30), and normal controls (n=30) were included in the 'training set.' A 'validation set' included cases of breast cancer (n=128) and controls (n=77). All cases provided blood samples for serum analysis. All cases of breast cancer were confirmed histologically and were staged. Quantitative reverse transcription polymerase chain reaction (RT-qPCR) was used to detect the expression of 11 candidate ncRNAs, including long noncoding RNAs (lncRNAs) and microRNAs (miRNAs), in the serum. The expression of the panel of ncRNAs was further analyzed following surgery or chemotherapy. RESULTS The four ncRNAs identified in the serum of patients with breast cancer included let-7a, miR-155, miR-574-5p, and metastasis-associated lung adenocarcinoma transcript 1 (MALAT1). Analysis based on the risk score showed that the panel of these four ncRNAs could effectively distinguish between patients with breast cancer and the control group. For the training set and the validation set, analysis of the receiver-operating characteristic (ROC) curve showed that the areas under the curve (AUCs) were 0.960 and 0.968, respectively. Also, the serum expression levels of the four ncRNAs differed in the pre-treatment and the post-treatment patients with breast cancer, with levels of miR-155 showing a significant decrease following chemotherapy. CONCLUSIONS A panel of serum ncRNAs, including let-7a, miR-155, miR-574-5p, and MALAT1, was shown to be present in patients with breast cancer.

Tissue Factor-bearing MPs and the risk of venous thrombosis in cancer patients: A meta-analysis.

Cancer patients with Tissue Factor (TF)-bearing MPs have been presented association with increased risk of venous thromboembolism (VTE), but results of these studies have not been consistent. We aimed to conduct a meta-analysis to assess the relationship between TF-bearing MPs and risk of VTE in patients with cancer. PubMed, Web of Science and EMBASE Databases were systematically retrieved up to1th June 2017. Two case-control studies and four cohort studies met the entry requirements in this analysis. The summary odd ratio (OR) were estimated by a random effect model. The overall OR was 1.76 (95% CI: 1.21-2.56, I2 = 62.0%). The OR of case-control studies was 3.41 (95% CI: 1.45-8.02, I2 = 0.0%) and that of cohort studies was1.53 (95% CI: 1.05-2.24, I2 = 66.1%). The association between TF-bearing MPs and the risk of VTE in cancer patients was found in this meta-analysis. Publication bias testing and sensitivity subgroup analysis suggested that results of this meta-analysis were robustness. In conclusion, TF-bearing MPs were associated with increased risk of VTE in patients with cancer. Whereas, more well-designed studies and more comprehensive adjustments for confounders in further studies are warranted to affirm the association.

A circulating non-coding RNA panel as an early detection predictor of non-small cell lung cancer.

AIMS: Early non-small cell lung cancer (NSCLC) diagnosis is generally poor due to the lack of convenient and noninvasive tools. MicroRNAs (miRNAs) and the long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) are non-coding RNAs, that have attracted increased attention for their use as NSCLC tumor diagnostic markers. MAIN METHODS: We constructed a serum miRNA and MALAT1 non-coding RNA panel and tested its diagnostic performance as an NSCLC biomarker. We tested the expression of 11 candidate miRNAs and MALAT1 in a training set (36 NSCLCs vs. 36 controls) by quantitative reverse transcription polymerase chain reactions. The serum non-coding RNA panel's diagnostic efficiency was tested and validated in a second validation sample set (120 NSCLCs and 71 controls) by receiver operating characteristic (ROC) curve analyses. KEY FINDINGS: In the training set, the expression of the four non-coding RNAs (miR-1254, miR-485-5p, miR-574-5p, and MALAT1) was obviously different between the NSCLC patients and healthy controls. Risk score analysis revealed that the four non-coding RNA panel can distinguish NSCLC patient samples from controls. The ROC curve results revealed areas under the curves (AUCs) of 0.861 (95% confidence interval (CI) 0.771-0.952) and 0.844 (95% CI0.778-0.910) for the training set and validation set, respectively. SIGNIFICANCE: The four non-coding RNA risk scores were also associated with NSCLC progression, and its diagnostic efficiency was relatively high for stages I/II/III. In conclusion, these data indicate that the four non-coding RNA panel can serve as a convenient tool for early NSCLC diagnosis.

The de-ubiquitinase UCHL1 promotes gastric cancer metastasis via the Akt and Erk1/2 pathways.

Ubiquitin C-terminal hydrolase-L1 (UCHL1) is a de-ubiquitinating enzyme, which enzymatic activity relies on the C90 site. The function of UCHL1 is controversial in different types of cancer, and its role in gastric cancer progression remains unclear. In this study, immunohistochemistry staining was applied to detect the expression of UCHL1 in primary gastric cancer and liver metastases from gastric cancer. MKN45 and BGC823 cell lines with stable expression of de-ubiquitinase active UCHL1 or inactive UCHL1-variant C90S were established by lentiviral infection. The effect of UCHL1 on cell proliferation was evaluated by MTT and colony formation assays. The abilities of cell migration and invasion were determined by transwell assay. Protein expression levels were determined by Western blot. The results indicated that UCHL1 had a significantly higher positive expression rate in liver metastases from gastric cancer compared with primary gastric cancer. Overexpression of UCHL1 in MKN45 and BGC823 cells promoted cell proliferation, migration, and invasion depending on its de-ubiquitinase activity. UCHL1 activated Akt and Erk1/2, which process also required enzymatic activity and was necessary for mediating cell migration and invasion. These findings demonstrated that UCHL1 promoted cell proliferation, migration, and invasion depending on its de-ubiquitinase activity by activating Akt and Erk1/2, which may account for its higher positive expression rate in liver metastases from gastric cancer. UCHL1 could be a candidate biomarker and a therapeutic target for gastric cancer metastasis.

NAIF1 inhibits gastric cancer cells migration and invasion via the MAPK pathways.

PURPOSE: Nuclear apoptosis-inducing factor 1 (NAIF1) could induce apoptosis in gastric cancer cells. Previously, we have reported that the expression of NAIF1 protein is down-regulated in gastric cancer tissues compared with the adjacent normal tissues. However, the role of NAIF1 in gastric cancer cells is not fully understood. METHODS: The effects of NAIF1 on cell viability were evaluated by MTT and colony formation assays. The ability of cellular migration and invasion were analyzed by transwell assays. The expression levels of targeted proteins were determined by western blot. The relative RNA expression levels were analyzed using quantitative polymerase chain reaction assays. Xenograft experiment was employed to determine the anti-tumor ability of NAIF1 in vivo. RESULTS: The study demonstrates that transient transfection of NAIF1 in gastric cancer cells BGC823 and MKN45 could inhibit the cell proliferation, migration, and invasion of the two gastric cancer cell lines. The tumor size is smaller in NAIF1-overexpressed MKN45 cell xenograft mice than in unexpressed group. Further in-depth analysis reveals that NAIF1 reduces the expression of MMP2 as well as MMP9, and inhibits the activation of FAK, all of which are key molecules involved in regulating cell migration and invasion. In addition, NAIF1 inhibits the expression of c-Jun N-terminal kinase (JNK) by accelerating its degradation through ubiquitin-proteasome pathway. Meanwhile, NAIF1 reduces the mRNA and protein expression of ERK1/2. CONCLUSIONS: Our study revealed that NAIF1 plays a role in regulating cellular migration and invasion through the MAPK pathways. It could be a therapeutic target for gastric cancer.

Identification of a circulating microRNA signature for colorectal cancer detection.

Prognosis of patients with colorectal cancer (CRC) is generally poor because of the lack of simple, convenient, and noninvasive tools for CRC detection at the early stage. The discovery of microRNAs (miRNAs) and their different expression profiles among different kinds of diseases has opened a new avenue for tumor diagnosis. We built a serum microRNA expression profile signature and tested its specificity and sensitivity as a biomarker in the diagnosis of CRC. We also studied its possible role in monitoring the progression of CRC. We conducted a two phase case-control test to identify serum miRNAs as biomarkers for CRC diagnosis. Using quantitative reverse transcription polymerase chain reactions, we tested ten candidate miRNAs in a training set (30 CRCs vs 30 controls). Risk score analysis was used to evaluate the diagnostic value of the serum miRNA profiling system. Other independent samples, including 83 CRCs and 59 controls, were used to validate the diagnostic model. In the training set, six serum miRNAs (miR-21, let-7g, miR-31, miR-92a, miR-181b, and miR-203) had significantly different expression levels between the CRCs and healthy controls. Risk score analysis demonstrated that the six-miRNA-based biomarker signature had high sensitivity and specificity for distinguishing the CRC samples from cancer-free controls. The areas under the receiver operating characteristic (ROC) curve of the six-miRNA signature profiles were 0.900 and 0.923 for the two sets of serum samples, respectively. However, for the same serum samples, the areas under the ROC curve used by the tumor markers carcinoembryonic antigen (CEA) and carbohydrate antigen 19-9 (CA19-9) were only 0.649 and 0.598, respectively. The expression levels of the six serum miRNAs were also correlated with CRC progression. Thus, the identified six-miRNA signature can be used as a noninvasive biomarker for the diagnosis of CRC, with relatively high sensitivity and specificity.

A study on radiation technological degradation of organic chloride wastewater--exemplified by TCE and PCE.

This paper describes the potential of using gamma radiation technology to degrade trichloroethylene (TCE) and perchloroethylene (PCE) wastewater. The experimental method is divided into two parts: (1) using the gamma-ray to irradiate the TCE and PCE solution, the dose-rate is 10Gy/minute, the irradiation dosage is 0-2.5kGy and (2) self-making the UV irradiation system, the tube specification is 254nm and 6W, and turning on 8 tubes at the same time to make the irradiation. The efficiency of degradation ratio for gamma-ray is better than UV in the range of 0.1-250ppm; for example, as for the concentration of 0.1ppm, when TCE is degraded to D(90) and T(90), the gamma-ray only needed 46.7Gy and took about 4.67 minutes, but UV needed to take about 28.1 minutes. The dose-concentration equations of TCE and PCE are: TCE: y=44.58+8.832x, R(2)=0.999; and PCE: y=81.33+12.81x, R(2)=0.997. We verified that the radiation technology is able to effectively degrade the organic chlorine wastewater without yielding the secondary pollution, and the TCE and PCE that degraded by using gamma-ray will be reached US-EPA and Taiwan Effluent Standard (5ppb).