Objective: To study the expression of miR-142-5p in lung adenocarcinoma tissues, and to explore its effect on proliferation, invasion, migration and epithelieal-mesenchymal transition (EMT) of H1650 cells and the potential mechanisms. Methods:Atotal of 107 pairs of lung adenocarcinoma tissues and corresponding para-cancerous tissues from patients, who underwent tumor resection and were pathologically confirmed at the Department of Thoracic Surgery, the Fourth Hospital of Hebei Medical University between Jan. 2014 and Jan. 2015, were collected for this study; in addition, human lung adenocarcinoma cell lines (H1650, HCC827, A549, H1975, PC9) and human bronchial epithelial BEAS-2B cells were also used in this study. qPCR was used to detect the expression of miR-142-5p in lung adenocarcinoma tissues and cell lines. The correlation between expression of miR-142-5p and clinical features was analyzed.After transfection with miR-142-5p mimics or miR-negative control (miR-NC) plasmid, the proliferation, invasion and migration of H1650 cells were detected with CCK-8, Transwell invasion assay and Wound healing assay, respectively. The bioinforamtics tool was used to predict the target genes of miR-142-5p, and Luciferase reporter gene assay was performed to validate the regulation of miR-142-5p on target gene. Western blotting (WB) was used to detect the expressions of cyclin-dependent kinase 5 (CDK5) and EMTrelated protein. Results: Compared to Para-cancerous tissues and BEAS-2B cells, the expression of miR-142-5p was lower in lung adenocarcinoma tissues and cell lines (all P<0.01). Of the 107 cases of lung adenocarcinoma tissues, 61 cases (57.01%) showed decreased miR-142-5 expression, which was correlated with the TNM stage and lymph node metastasis (both P<0.01). Transfection of miR-142-5p mimics significantly up-regulated the expression of miR-142-5p and decreased the proliferation, invasion and migration of H1650 cells (all P<0.05 or P<0.01). Bioinformatics showed that CDK5 was a target gene of miR-142-5p. Luciferase reporter gene assay and WB validated that miR-142-5p could significantly down-regulate CDK5 expression in H1650 cells, up-regulate the expression of E-cadherin and down-regulate the expressions of N-cadherin, Twist and Snail in H1650 cells (all P<0.01). Conclusion: miR-142-5p is low expressed in lung adenocarcinoma tissues and cell lines; it suppresses the EMT process to inhibit, invasion and migration of H1650 cells via down-regulating the expression of CDK5.

<b>Objectiveb> To explore the efficacy of the resolving depression and tranquilizing herbal sachets in alleviating sleep disorders of soldiers in naval vessels. <b>Methodsb> Fifty-nine soldiers with sleep disorders (PSQI scale score ≥8 and SAS scale score ≥50) were selected before training at sea, and were randomly divided into sachet treatment group, mindfulness meditation group and control group. During the training period, the sachet treatment group was given traditional Chinese medicine sachet treatment, the mindfulness meditation group was trained in mindfulness meditation, and the control group was not given any intervention. <b>Resultsb> Compared with the control group, the PSQI and SAS scores of soldiers in both the experimental sachet treatment group and the positive meditation group were significantly improved; compared with the pre-intervention data, the PSQI and SAS scores of both the positive meditation group and the sachet treatment group were significantly decreased, and the degree of decrease was comparable. <b>Conclusionb> The homemade improving depression and tranquilizing TCM sachets have the effect of alleviating the sleep disorders of naval troops served on vessels, which is equivalent to mindfulness meditation. It is easy to use and operate, which is suitable for promotion in the military.

BACKGROUND: The pancreas is surrounded by soft tissue known as the peripancreatic space (PPS). Pathologic lesions of the PPS are infrequent and have only rarely been reported in the cytopathology literature. METHODS: A retrospective review of cytopathology files at two large institutions revealed 42 cases of PPS lesions obtained by transabdominal fine needle aspiration (FNA) or endoscopic ultrasound-guided FNA over a 16-year period. Clinicoradiologic findings and follow-up information were also reviewed. RESULTS: Patients ranged in age from 23-83 years (mean, 60 years) with an equal gender distribution. The major clinical presentations included pain, jaundice, nausea/vomiting, and abnormal liver enzymes. Radiographic characteristics included lymphadenopathy and cystic/solid soft tissue masses with a size range of 1.5 to 8 cm. Cytologically, 4 (9.5%) cases were nondiagnostic, 9 (21.5%) were diagnosed as benign, 4 (9.5%) were atypical or suspicious for cancer, and 25 (59.5%) were malignant. Six of 25 (24%) patients had metastasis of a prior known malignancy. CONCLUSIONS: FNA of PPS masses is a rare occurrence. The majority of lesions are metastatic carcinomas from a variety of primary sites. Flow cytometry and immunoperoxidase studies are useful adjuncts to determine the tumor origin. The sensitivity of PPS aspiration for a malignant diagnosis is 90% with a positive predictive value of 100%.
Adenocarcinoma ; Biopsy, Fine-Needle ; Flow Cytometry ; Follow-Up Studies ; Humans ; Jaundice ; Liver ; Lymphatic Diseases ; Neoplasm Metastasis ; Pancreas ; Retrospective Studies

[Abstract] Objective: To investigate the effect of metformin on the senescence-associated secretory phenotype (SASP) of doxorubicin-induced gastric cancer BGC823 cells. Methods: Human gastric cancer BGC823 cells were cultured in vitro and treated with doxorubicin at gradient concentrations (50, 100, 150 and 200 nmol/L). Cell senescence was detected by SA-β-gal staining, and SASP factor expression was detected by ELISA. The effects of metformin on cell senescence and SASP factor secretion induced by doxorubicin (100 nmol/L) were observed by adding gradient concentrations of metformin (0, 5, 10 and 20 mmol/L). Results: With the increase of doxorubicin concentration and treatment time, the senescence rate of gastric cancer BGC823 cells increased first and then decreased. At 96 h after 100 nmol/L doxorubicin treatment, the peak aging rate reached 68.7%, accompanied with significantly increased expressions of SASP factors IL-1a, IL-6, IL-8 and CXCL1. The proportion of senescent cells was (55.2±1.9)%, (48.7±2.2)% and (40.8±2.3)% respectively under the effects of 5, 10 and 20 mmol/L metformin, which was significantly lower than that in the non-metformin treatment group (P< 0.01). At the same time, with the increase of metformin concentration, the production of SASP factors IL-1α, IL-6, IL-8 and CXCL1 showed a gradient decline. Compared with the non-metformin treatment group, IL-6 and IL-8 decreased significantly under the effect of metformin above 10 mmol/L (P<0.05 or P<0.01), while IL-1α and CXCL1 decreased significantly under the effect of 20 mmol/L metformin (all P<0.05). Conclusion: Metformin can inhibit the senescence and SASP production of gastric cancer cells induced by doxorubicin.

Bavachinin is a dihydroflavone isolated from dried ripe fruits of Psoralea corylifolia L.，which has various pharmacological activities, such as anti-tumor, anti-virus, anti-diabetes, anti-inflammatory and neuroprotective, and good potential in clinical applications. With the increasing concern about the safety of P. corylifolia applications in clinical, the bavachinin has been found to be one of the main components causing liver injury. In this paper, the pharmacological activities and hepatotoxicity of bavachinin in the recent 20 years were reviewed, in order to provide reference for the further study and clinical application.

Objective:To explore the characteristics of nosocomial infection in patients with spinal cord injury, and analyze the risk factors. Methods:From January, 2015 to June, 2017, 526 patients with spinal cord injury in our hospital were reviewed. The distribution of pathogens and the characteristics of drug resistance of strains were summarized, and the risk factors of nosocomial infection were analyzed. Results:There were 159 person-times with nosocomial infection, and most of the infections were found in urinary tract (60.4%) and lower in respiratory tract (28.9%). The main pathogenic germs were Escherichia coli (39.0%), Pseudomonas aeruginosa (15.7%), Klebsiella pneumoniae (11.3%) and Proteus mirabilis (9.4%). The main pathogens were resistant to second or third generation of cephalosporins and quinolones moderately or severely, but sensitive to compound preparations containing beta-lactamase inhibitors, carbapenems and aminoglycosides. The risk factors for the nosocomial infections in the spinal cord injury patients included the hospitalization time, severity of spinal cord injury, invasive operation history, nutritional risk and use of antibiotics (P < 0.05). Conclusion:Most of the nosocomial infections in patients with spinal cord injury are in urinary tract and respiratory tract. Gram-negative bacilli are the main pathogenic bacteria, which often show multiple drug resistance. It is necessary to take targeted interventions according to the risk factors of nosocomial infections in order to improve the quality of life of patients.

Objective:To evaluate the effect of threshold inspiratory muscle training (TIMT) on respiratory muscle strength and clinical outcomes for machinery ventilates patients. Methods:The Cochrane Library, PubMed, Embase, Web of Science, CBM, Wanfang Database, CNKI and VIP were searched for the randomized controlled trials (RCT) about the effect of TIMT on respiratory muscle strength and clinical outcomes from establishment to July 1st, 2018. Two researchers strictly evaluated literature quality and extracted information, and then a Meta-analysis was carried out. Results:A total of 14 literatures were included with 650 patients, 323 cases in the experimental group and 327 cases in the control group. Compared with the control group, the massive inspiratory pressure (MIP) increased (MD = -6.65, 95%CI -8.27~-5.03, P < 0.001), the respiratory muscle strength increased (MD = -5.04, 95%CI -7.68~-2.04, P = 0.0002), the weaning time reduced (MD = -1.01, 95%CI -1.65~-0.37, P = 0.002), the mechanical ventilation time shortened (MD= -2.24, 95%CI -4.33~-0.15, P = 0.04), as well as the intensive care unit (ICU) length of stay (MD= -3.41, 95%CI -6.06~-0.76, P= 0.01). There was no significant difference in maximum expiratory pressure (MEP) (MD= 1.22, 95%CI -6.55~9.00, P = 0.76), the rate of reintubation/tracheotomy (RR = 0.99, 95%CI 0.56~1.73, P = 0.96) and mortality (RR= 1.05, 95%CI 0.53~2.06, P = 0.89) between two groups. Conclusion:TIMP could improve MIP and respiratory muscle strength of patients with mechanical ventilation, shorten the weaning time, the mechanical ventilation time and the ICU length of stay, and then reduce the incidence of weaning failure.

<b>Objectiveb> To explore the role and potential mechanisms of all-trans retinoic acid （ATRA） on activation and oxidative stress of hepatic stellate cell （HSC）. <b>Methodsb> Platelet-derived growth factor （PDGF-bb, 10 ng/ml） was applied to induce the activation of HSCs, which was then treated with ATRA at a dosage of 5 μmol/L for 48 h. The effects of ATRA on HSC activation were evaluated by detecting changes in cell growth viability and phenotypic marker expression. The effects of ATRA on HSC oxidative stress were evaluated by detecting changes in intracellular reactive oxygen species （ROS）, reduced glutathione （GSH） and malondialdehyde （MDA）, and the expression of antioxidant genes. The effects of ATRA on HSC autophagic activity were evaluated by detecting changes in autophagy marker expression and autophagic flow. <b>Resultsb> Compared with the PDGF-bb group, the cell viability was significantly reduced in ATRA-treated HSCs （P<0.01）, as well as the expression of α-SMA and Collagen I. The intracellular levels of ROS and MDA were significantly reduced in ATRA-treated HSCs （P<0.01）, whereas the GSH level was significantly increased （P<0.01）. The expression levels of antioxidant genes （NRF2, HO-1, and ATF4）, were significantly higher in ATRA-treated HSCs than those in the normal ones under PDGF-bb condition （P<0.01）. Meanwhile, the expression of autophagy markers Beclin 1 and LC3 Ⅱ/I, and signal of autophagy flow in ATRA-treated HSCs were found to be significantly reduced （P<0.01）. <b>Conclusionb> ATRA significantly inhibited PDGF-bb-induced HSC activation and reduced the level of oxidative stress and autophagic activity of HSCs, which had potential applications in the prevention and treatment of liver fibrosis.

[Abstract] Objective: To explore the relationship between cerebral endothelial cell adhesion molecule (CERCAM) and prognosis of colon cancer patients, so as to establish a nomogram with good prognostic value by using Cox model and verify its diagnostic value. Methods: The expression profile of CERCAM in colon cancer tissues and normal tissues as well as clinicopathologic data of colon cancer patients were downloaded from TCGA and GTEx databases. At the same time, colon cancer and paracancerous tissue samples collected from 4 colon cancer patients admitted to Nanjing First Hospital from Feburary 2013 to June 2019 were used for verification. Firstly, differential analysis, pathway enrichment analysis, and survival analysis were performed to investigate the tissue localization, functional and prognostic value of CERCAM expression. In addition, Cox regression analyses was conducted to screen the risk factors for the prognosis of colon cancer. A nomogram was established based on CERCAM and various risk factors, and was verified and evaluated by concordance indices, calibration curves, and time-dependent receiver operating characteristic (ROC) curves. In addition, the survival curves were plotted according to risk stratification. Results: The expression of CERCAM in colon cancer tissues was significantly lower than that in normal tissues (P<0.001). The overall survival (P=0.032) and survival status (P=0.002) of colon cancer patients with high CERCAM expression level was significantly inferior to those with low CERCAM expression level. CERCAM was correlated with the activation of proteoglycans in cancer and PI3K-Akt signaling pathway. Cox analysis showed that CERCAM expression level (HR=2.22, P=0.015), T stage (HR=5.65, P=0.015), M stage (HR=2.62, P=0.022) were independent risk factors for prognosis of colon cancer, while vascular infiltration (HR=2.30, P=0.089) was a risk factor as well. Based on the above factors, a nomogram was established. The concordance indices suggested good discrimination of the nomogram, and the training set was consistent with the test set. The calibration curves and ROC curves also indicated good predictive ability of the nomogram. Survival curves plotted according to risk stratification suggested that the high-risk group had lower survival rates (P<0.000 1). Conclusion: High level CERCAM expression is correlated with the poor prognosis of colon cancer patients, which is possibly associated with proteoglycans in cancer and PI3K-Akt signal pathway. The nomogram established based on CERCAM is superior to the traditional prediction model, which has certain clinical value in predicting survival prognosis of colon cancer patients. This practical model is helpful for the risk stratification and the optimization of treatment plan.

The discovery, sorting and identification methods as well as targeted drug delivery systems for cancer stem cells (CSCs) have been reviewed by consulting the recent research papers. CSCs have been believed to be responsible for the occurrence and development of chemo-resistance, leading to the failure of chemotherapy. Much progress has been made in the approaches for CSCs targeting drug delivery systems. The understanding and targeted drug delivery systems for CSCs are promising to provide an alternative for cancer therapy.
Animals ; Antineoplastic Agents ; pharmacology ; therapeutic use ; Apoptosis ; drug effects ; Drug Delivery Systems ; methods ; Drug Resistance, Neoplasm ; Flow Cytometry ; Humans ; Neoplasms ; drug therapy ; pathology ; Neoplastic Stem Cells ; drug effects ; pathology ; Signal Transduction ; drug effects ; Wnt Signaling Pathway ; drug effects