Lonicera flos and Cnicus japonicus extracts improved egg quality partly by modulating antioxidant status, inflammatory-related cytokines and shell matrix protein expression of oviduct in laying hens.

This study was conducted to investigate the effects of Lonicera flos and Cnicus japonicus extracts (LCE) on the laying performance, egg quality, morphology, antioxidant status, inflammatory-related cytokines, and shell matrix protein expression of oviduct in laying hens. A total of 1,728 Roman Pink laying hens aged 73-wk-old were randomly assigned into 4 groups (18 replicates/group, 24 layers/replicate) fed basal diets supplemented with 0, 300, 500, and 1,000 mg of LCE per kg of diet, respectively. The trial lasted for 11 wk, including 2-wk adjustment period and 9-wk testing period. The results indicated that laying hens fed diets supplemented with LCE linearly increased egg weight, yolk color and shell thickness at wk 78 and albumen height, Haugh unit and shell thickness at wk 83 (P < 0.05). At wk 78, LCE groups linearly affected the hydrogen peroxide content in magnum (P < 0.05) and 300 mg/kg LCE groups had the highest catalase activity in isthmus (P < 0.05). At wk 83, LCE groups linearly reduced (P < 0.05) hydrogen peroxide content in the magnum and isthmus and malondialdehyde content in the uterus whereas increased catalase activity in isthmus (P < 0.05). Furthermore, LCE levels quadratically affected glutathione peroxidase activity in isthmus at wk 83 (P < 0.05). At wk 78, the mRNA expressions of inducible nitric oxide synthase and interferon-γ in isthmus and ovalbumin and ovocleidin-116 in uterus had linear effects in response to LCE levels (P < 0.05) and 1,000 mg/kg LCE group had the lowest mRNA expression of interleukin-6 in magnum (P < 0.05). At wk 83, LCE supplementation linearly decreased the mRNA expression of interleukin-1ß, interferon-γ and tumor necrosis factor-α in magnum and tumor necrosis factor-α and inducible nitric oxide synthase in uterus (P < 0.05). It is concluded that LCE improved egg quality partly by modulating antioxidant status, inflammatory-related cytokines and shell matrix protein expression of oviduct in laying hens.

Retraction Note: LINC01296 promotes the proliferation and invasion by regulating microRNA-760 expression and predicts poor prognosis of hepatocellular carcinoma.

The article "LINC01296 promotes the proliferation and invasion by regulating microRNA-760 expression and predicts poor prognosis of hepatocellular carcinoma", by Z.-C. Wang, S. Yang, M.-Q. Chen, S.-S. Wu, H.-H. Lv, W.-X. Jin, published in Eur Rev Med Pharmacol Sci 2019; 23 (22): 9848-9856-DOI: 10.26355/eurrev_201911_19548- PMID: 31799652 has been retracted by the author for the following reasons: After the publication of this article, the authors reviewed the process of the experiment and found there were mistakes in the methodology search. Not all the carcinoma specimens used in the experiment were from hepatocellular carcinoma. The prognosis and clinical features the rate of lymph node metastasis and the treatment and prognosis between these types of cancers are different. For example, intrahepatic cholangiocarcinoma tends to involve a high frequency of lymph node metastasis, and the prognosis is worse than hepatocellular carcinoma; hepatocellular carcinoma seldom involves lymph node metastasis but often involves intrahepatic metastasis; colorectal cancer liver metastasis is far more sensitive to chemotherapy and has a relatively long survival, and neuroendocrine carcinoma is sometimes sensitive to hormone therapy and generally has better survival than hepatocellular carcinoma. As a result, the clinical results and gene test results mentioned in this article were incorrect. After that the authors found that there was a mistake, they subsequently carried out supplementary experiments and found that they could not confirm that there was an increase in the expression of the LICO01296 gene in hepatocellular carcinoma, so they could not link some clinical results with the results of the basic research results mentioned in this article. Therefore, from the perspective of academic rigor, they requested to withdraw the article. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/19548.

[Evaluation of root resorption after surgical orthodontic treatment of skeletal Class â ¢ malocclusion by three-dimensional volumetric measurement with cone-beam CT].

OBJECTIVE: To explore the method of measuring root volume with cone-beam computed tomography (CBCT) three-dimensional reconstruction technology, and to study root length and root volume of upper and lower central incisors in patients with skeletal Class Ⅲ malocclusion treated by surgical orthodontic treatment. METHODS: Twenty patients with skeletal Class Ⅲ malocclusion undergoing surgical orthodontic treatment were selected. CBCT data at three time points, before decompensation treatment (T0), after decompensation treatment (before orthognathic surgery, T1), and the end of post-operative orthodontic treatment (T2) were collected. Three-dimensional reconstruction technology was used to measure the root length and root volume of the upper and lower central incisors (including total root volume, cervical root and apical root), calculate the percentage of reduction volume, and measure the distance of tooth movement after orthodontic treatment. Data were statistically analyzed by SPSS 20.0 software. Least significant difference (LSD) method was used for pair comparison between the groups subject to normal distribution, and non-parametric test was used for comparison between the groups not subject to normal distribution. The differences of root length and root volume of upper and lower incisors were compared, and the characteristics of root absorption were analyzed. RESULTS: Root length and root volume of the upper and lower central incisors were reduced during the surgical orthodontic treatment (P < 0.05) in cases. Both the root volume of cervical root and apical root were significantly reduced (P < 0.05), the reduction of apical root was more significant. The percentage of root volume reduction of the upper central incisor was (30.51±23.23)%, and lower central incisor (23.24±11.96)%. Compared with the upper central incisor, the root volume reduction amount and percentage of the lower central incisor were smaller, and apical root volume reduction of the upper central incisor was greater than that of the lower central incisor, which was statistically significant (P < 0.05). During pre-surgical orthodontic treatment, maxillary central incisor palatal moving was in a controlled tipping manner, and the mandibular central incisor tipped labially. CONCLUSION: In patients with skeletal Class Ⅲ malocclusion, root length and total root volume of upper and lower central incisors decreased during surgical orthodontic treatment. Root volume measurement indicated that the cervical root also had root resorption. The difference in root resorption of the upper and lower central incisors might be related to the distance and direction of teeth movement. CBCT three-dimensional reconstruction will compensate for the limitation of root length measurement in evaluating root resorption.

Analysis of reporting quality of clinical practice guidelines/consensuses on metastatic colorectal cancer based on the RIGHT checklist.

OBJECTIVE: The current study aimed to assess the reporting quality of the clinical practice guidelines/consensuses on metastatic colorectal cancer based on the Reporting Items for Practice Guidelines in HealThcare (RIGHT) checklist. METHODS: We searched China National Knowledge Infrastructure, VIP database, Wanfang Data, Chinese Biological Literature Service System, PubMed, Web of Science, ScienceDirect, Elsevier clinicalkey, BMJ Database, EMBASE, Cochrane Library, World Health Organization Network and other websites. We collected clinical practice guidelines/consensuses on metastatic colorectal cancer with published between 1 January 2017 and 1 April 2021 after release of the RIGHT checklist. Two reviewers extracted the basic information independently and conducted a RIGHT evaluation. RESULTS: Eighteen guidelines/consensuses were included, 10 from China and 8 from other countries. The average reporting rate was 74.1%±11.2%. Thirteen items had 100% reporting rate, and the reporting rate for items No. 16 (11.1%), 17 (16.7%) and 18b (22.2%) was low. Basic information had the highest reporting rate (100%), whereas review and quality assurance had the lowest (13.9%). The average reporting rate of guidelines/consensuses published in other countries was higher than in China [p=0.005; odds ration (OR) 1.17, 95% confidence interval (CI) 1.07-1.28]. The average reporting rate of the guidelines was higher than that of the consensus statements (p<0.001; OR 1.20, 95% CI 1.10-1.31). The reporting rates of guidelines/consensuses focused on whole body (79.0%±12.7%) were higher than local organ (69.2%±7.3%) metastases (p=0.005; OR 1.14, 95% CI 1.04-1.25). CONCLUSIONS: The quality of reporting using the RIGHT checklist varied among the guidelines/consensuses on metastatic colorectal cancer. Low-quality items were external review and quality assurance. Developers of guidelines/consensuses should aim to improve the reporting quality in the future.

Delayed intracerebral hemorrhage after ventriculo-peritoneal shunt procedure: two case reports and a review of literature.

OBJECTIVE: Ventriculo-peritoneal shunt (VPS) is a commonly used procedure for treating hydrocephalus of various causes. Delayed intracerebral hemorrhage (DICH) is regarded as a very rare complication after VPS procedure, with mechanisms still indeterminate. We report two cases of this condition whereby we discuss the characteristics and potential explanations for it in a short review of literature. CASE REPORT: Two female patients, aged 49, 76 respectively, were admitted to our hospital for hydrocephalus in the year 2021 as ordinary participants among many other patients with the same diagnosis. Unforeseeably, what made them special was DICH situations occurred after regular VPS procedures. Luckily both of them responded well to subsequent conservative treatment with no deterioration and were discharged promisingly in the end. Surprisingly, both of the valve mechanisms in these two functioned properly so far even after the ominous DICH events. Quality of life also improved a lot for them, thus we could consider the VPS surgery successful as well as the later management of the unwanted hematomas, in other words, a full recovery from DICH. CONCLUSIONS: Only few cases or series of DICH were reported in the past decades and the mechanisms of it still lack a verdict. We intend to attribute physical vascular injury due to a closer contact between cerebral blood vessels and the VPS catheter for DICH in the younger patient, while degenerative changes of brain tissue might be the protagonist in the elder one. More discreetness should be expected in perioperative management of VPS patients, with still a long way to go to fully understand the mechanisms of DICH and prevent the complication in highest measure.

Establishment of an immune-related gene prognostic model for head and neck tumors.

This study aimed to screen the key immune-related genes (IRGs) in head and neck squamous cell carcinoma (HNSC) and construct the IRGs-related prognostic model to predict the overall survival (OS) of patients with HNSC. The RNA-seq data and clinical data were downloaded from The Cancer Genome Atlas database, and IRGs were obtained from the Immunology Database and Analysis Portal. Differentially expressed genes (DEGs) between HNSC and normal samples were identified, followed by integration with IRGs to screen differentially expressed IRGs. After univariate and multivariate proportional hazard regression analyses, an IRG-based risk model was constructed. Meanwhile, data chip of GSE65858 as the validation set to assess the predicted performance of established model. Next, univariate and multivariate Cox regression analyses were performed to identify the independent prognostic factor of HNSC, and the Nomogram model was developed to predict patient outcome. Furthermore, the correlation between immune cell infiltration and risk score was analyzed. A total of 65 differently expressed IRGs associated with prognosis of HNSC were screened, and finally a 26-gene IRG signature was identified to construct a prognostic prediction model. The AUC of ROC curve was 0.750. Survival analysis showed that patients in the high-risk group had a worse prognosis. Independent prognostic analysis showed that risk score could be considered as an independent predictor for HNSC prognosis. Nomogram assessment showed that the model had high reliability for predicting the survival of patients with HNSC in 1, 2, 3 years. Ultimately, the abundance of B cells and CD4+ T cell infiltration in HNSC showed negative correlations with risk score. Our IRG-based prognostic risk model may be used to estimate the prognosis of HNSC patients.

Extracellular vesicles derived from bone marrow mesenchymal stem cells alleviate neuroinflammation after diabetic intracerebral hemorrhage via the miR-183-5p/PDCD4/NLRP3 pathway.

OBJECTIVES: Intracerebral hemorrhage (ICH) induced by diabetes results in further brain injury and nerve cell death. Bone marrow mesenchymal stem cell (BMSC) transplantation contributes to attenuating neurological deficits after ICH. This study investigated the mechanism of extracellular vesicles (EVs) derived from BMSCs in reducing neuroinflammation after diabetic ICH. METHODS: BMSC-EVs were isolated and identified. The rat model of db/db-ICH was established and the model rats were administered with EVs. miR-183-5p expression in brain tissues of db/db-ICH rats was detected. The brain injury of db/db-ICH rats was evaluated by measuring neurobehavioral score, brain water content and inflammatory factors. BV2 cells were cultured in vitro to establish high-glucose (HG)-Hemin-BV2 cell model. The levels of reactive oxygen species (ROS) and inflammatory factors in BV2 cells were measured, and BV2 cell viability and apoptosis were assessed. The targeting relationship between miR-183-5p and PDCD4 was predicted and verified. The activation of PDCD4/NLRP3 pathway in rat brain tissues and BV2 cells was detected. RESULTS: miR-183-5p expression was reduced in db/db-ICH rats brain tissues. BMSC-EVs ameliorated cranial nerve function, decreased brain water content and repressed inflammatory response by carrying miR-183-5p. BMSC-EVs mitigated HG-Hemin-BV2 cell injury, reduced ROS level and suppressed inflammatory response. miR-183-5p targeted PDCD4. PDCD4 promoted BV2 cell inflammation by activating the NLRP3 pathway. BMSC-EVs inhibited HG-Hemin-BV2 cell inflammation through the miR-183-5p/PDCD4/NLRP3 pathway, and inhibition of miR-183-5p reversed the protective effect of EVs. CONCLUSION: BMSC-EVs carried miR-183-5p into db/db-ICH rat brain tissues and repressed the NLRP3 pathway by targeting PDCD4, thus alleviating neuroinflammation after diabetic ICH.

Sevoflurane ameliorates adriamycin-induced myocardial injury in rats through the PI3K/Akt/GSK-3ß pathway.

OBJECTIVE: The aim of this study was to explore the effects of sevoflurane (SEV) pretreatment on Adriamycin (ADR)-induced myocardial injury through the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/glycogen synthase kinase-3ß (GSK-3ß) pathway. MATERIALS AND METHODS: A total of 24 rats weighing 200-250 g were divided into four groups, including: control group (C group), ADR injection group (ADR group), SEV pretreatment group (ADR + SEV group) and inhibitor group (ADR + SEV + LY group). H9c2 cells were cultured in vitro and were divided into control group (C group), ADR treatment group (ADR group), and SEV pretreatment group (ADR + SEV group) and inhibitor group (ADR + SEV + LY group) as well. Next, the content of aspartate aminotransferase (AST), lactate dehydrogenase (LDH) and creatine kinase (CK) in the serum was detected via Enzyme-Linked Immunosorbent Assay (ELISA). Hematoxylin-eosin (HE) staining assay was performed to determine the severity of myocardial injury. Meanwhile, the apoptosis rate of cells was detected through terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) assay. Additionally, Western blotting (WB) was employed to measure the protein expression levels of phosphorylated (p)-GSK-3ß, p-PI3K, Akt and p-Akt. RESULTS: Compared with C group, ADR significantly increased the content of AST, LDH and CK in the serum (p<0.01), reduced protein expression levels of p-GSK-3ß, p-PI3K and p-Akt (p<0.01), increased apoptosis rate (p<0.01), and induced myocardial injury. SEV pretreatment significantly alleviated the effect of ADR, manifested as significantly lowered content of AST, LDH and CK in the serum (p<0.01), distinctly elevated protein expression levels of p-GSK-3ß, p-PI3K and p-Akt (p<0.01), notably reduced apoptosis rate (p<0.01), and relieved myocardial injury. LY294002 remarkably inhibited the protective effect of SEV against myocardial injury (p<0.01) CONCLUSIONS: SEV is able to prominently ameliorate ADR-induced myocardial injury by regulating the phosphorylation level of the PI3K/Akt/GSK-3ß signaling pathway.

Propofol alleviates intestinal ischemia/reperfusion injury in rats through p38 MAPK/NF-κB signaling pathway.

OBJECTIVE: The aim of this study was to investigate the influences of propofol on intestinal ischemia/reperfusion (I/R) injury in rats through the p38 mitogen-activated protein kinase (MAPK)/nuclear factor-kappa B (NF-κB) signaling pathway. MATERIALS AND METHODS: The models of intestinal I/R injury were first successfully established. All rats were randomly divided into 4 groups, namely, S group, I/R group, P group and P + S group. Pathological-morphological changes, injury score and wet-to-dry weight ratio of intestinal tissues as well as oxidative stress indexes in each group of rats were detected. Enzyme-linked immunosorbent assay (ELISA) was applied to measure the levels of inflammatory factors such as creatine kinase-MB (CK-MB), tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) in each group of rats. Furthermore, Western blotting (WB) assay was applied to determine the protein expression levels of p38 MAPK and NF-κB in different groups. RESULTS: Intestinal tissue injury was the severest in I/R group, with the infiltration of massive inflammatory cells and oozing of blood (Figure 1A, I/R). Compared with those in I/R group, the infiltration of inflammatory cells and damage to intestinal villi were notably relieved in P group and P + S group, revealing that the intestinal mucosal injury was remarkably repaired in P group and P + S group (Figure 1A, P). Moreover, the intestinal tissue injury score was evidently higher in I/R group, P group and P + S group than that in S group (p<0.05). However, it was markedly lower in P group and P + S group than that in I/R group (p<0.05). I/R group, P group and P + S group exhibited significantly increased wet-to-dry weight ratio of intestinal tissues in comparison with S group (p<0.05). However, P group and P + S group exhibited distinctly lower wet-to-dry weight ratio of intestinal tissues than I/R group (p<0.05). The content of malondialdehyde (MDA) was reduced prominently, while that of superoxide dismutase (SOD) was elevated significantly in P group and P + S group in contrast with those in I/R group (p<0.05). On the contrary, P + S group displayed remarkably lower MDA content and higher SOD content than P group (p<0.05). The levels of CK-MB, TNF-α and IL-6 in the blood rose markedly in I/R group compared with those in S group (p<0.05). However, they declined evidently in P group and P + S group in contrast with those in I/R group (p<0.05). Besides, the protein expression level of phosphorylated p38 MAPK was significantly higher in I/R group, P group and P + S group than that in S group (p<0.05). However, no significant difference was observed in the protein expression of total p38 MAPK among the four groups (p>0.05). However, the protein expression level of phosphorylated p38 MAPK was distinctly down-regulated in P group and P + S group in comparison with that in I/R group (p<0.05). Finally, I/R group, P group and P + S group had a prominently higher protein expression level of NF-κB than S group (p<0.05). However, P group and P + S group exerted a significantly lower protein expression level of NF-κB than I/R group (p<0.05). CONCLUSIONS: Propofol decreases the release of inflammatory factors and alleviates intestinal edema by inhibiting the p38 MAPK/NF-κB signaling pathway, thereby mitigating and treating the intestinal I/R injury in rats.

Traumatic fractures in China from 2012 to 2014: a National Survey of 512,187 individuals.

The China National Fracture Study has been conducted to provide a national dataset of traumatic fractures across China. A national representative sample of 512,187 individuals was selected. The population-weighted incidence rates, distribution, injury mechanisms, and risk factors for traumatic fractures were identified for various groups of individuals. INTRODUCTION: The China National Fracture Study (CNFS) has been conducted to provide a comprehensive and up-to-date national dataset of traumatic fractures across China. This study aims to report the national incidences and distributions of traumatic fractures that occurred in 2012, 2013, and 2014 and to analyze the risk factors. METHODS: A national representative sample of individuals was selected from 24 rural counties and 24 urban cities of 8 provinces using stratified random sampling and the probability proportional to size (PPS) methodology. Participants were interviewed to identify whether they sustained traumatic fractures of the trunk and/or four extremities that had occurred in 2012, 2013, and 2014. The main risk factors associated with traumatic fractures were analyzed by multiple logistic regression models. RESULTS: A total of 512,187 individuals, including 259,649 males and 252,538 females, participated in the CNFS. The population-weighted incidence rates of traumatic fractures in China were calculated to be 2.5 (95% CI, 2.2-2.8) per 1000 population in 2012, 2.8 (95% CI, 2.5-3.3) in 2013, and 3.2% (95% CI, 2.8-3.6) in 2014. The population-weighted incidence rates of fragility fractures among participants aged 65 years and older were calculated to be 27.4 (95% CI, 21.4-33.4) per 1000 population in 2012, 36.0 (95% CI, 28.6-43.5) in 2013, and 42.4 (95% CI, 34.9-49.9) in 2014. The most common cause of fracture was low-energy injuries, followed by traffic accidents. For all age groups, sleeping less than 7 h was a risk factor for traumatic fractures. Alcohol consumption and previous fracture history were identified as risk factors for adults aged 15 years and over. Cigarette smoking was found to be a risk factor for males aged 15-64 years old. For individuals aged 15-64 years old, underweight incurred a risk effect for males and overweight for females. Alcohol consumption, sleeping less than 7 h per day, living in the central and eastern regions, a body mass index less of than 18.5, and having a previous fracture history were identified as strong risk factors for fragility fractures. CONCLUSION: The national incidence, distribution, and injury mechanisms for traumatic fractures were revealed in the CNFS. Risk factors were identified for various groups of individuals.

Downregulation of nuclear protein-1 induces cell cycle arrest in G0/G1 phase in glioma cells in vivo and in vitro via P27.

Nuclear protein-1 (NUPR1), also named as p8 or Com1, has been since found overexpressed in several human malignant tumor cells, such as glioma. NUPR1 also regulates cell cycle progression, however, the role of NUPR1 in regulating glioma cell cycle remains poorly understood. Knockdown efficiency of U87 and U251 cells infected with the lentiviral vector was detected by quantitative real-time PCR and western blot in vitro and in vivo. Flow cytometry and western blot were used to explore a mechanism by which NUPR1 modulates cell cycle in U87 and U251 cells. Immunohistochemistry was applied to detect expression levels of P27, CDK2, and cyclin E in human glioma tissues with NUPR1 positive expression and tumorigenesis in nude mice. We confirmed that the downregulation of NUPR1 arrested the cell cycle in the G0/G1 phase in U87 and U251 cells in vitro. Furthermore, the expression level of P27 was increased, and CDK2 and cyclin E were decreased upon silencing NUPR1 expression in vitro and in vivo. In conclusion, the knockdown of NUPR1 induces cell cycle arrest in the G0/G1 phase in glioma cells via P27.

LncRNA TRERNA1 promotes malignant progression of NSCLC through targeting FOXL1.

OBJECTIVE: Previous studies have shown the carcinogenic role of long-chain non-coding RNAs (lncRNA) TRERNA1. However, the role of TRERNA1 in non-small cell lung cancer (NSCLC) has not been reported. This research aims to explore the regulatory effect of TRERNA1/FOXL1 axis on the malignant progression of NSCLC. PATIENTS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to examine the expression levels of TRERNA1 and FOXL1 in 39 pairs of tumor tissues and paracancerous ones collected from NSCLC patients. The potential relation between TRERNA1 expression and clinical indicators of NSCLC patients was analyzed. Meanwhile, expression levels of TRERNA1 and FOXL1 in NSCLC cell lines were also detected by qRT-PCR. In addition, TRERNA1 knockdown model was constructed in H358 and SPC-A1 cells. Cell counting kit-8 (CCK-8), cell colony formation assay, and flow cytometry were applied to analyze the influence of TRERNA1 on NSCLC cell biological functions. Finally, Dual-Luciferase reporter gene assay and cell reverse recovery experiments were performed to figure out the underlying mechanisms of TRERNA1 in regulating NSCLC progression. RESULTS: QRT-PCR results indicated that the expression level of lncRNA TRERNA1 in tumor tissue samples of NSCLC patients was remarkably higher than that in adjacent tissues. Compared with NSCLC patients with low expression of TRERNA1, patients with high TRERNA1 expression had a worse pathological stage and overall survival. Similarly, compared with cells in sh-NC group, the proliferation ability of cells in sh-TRERNA1 group was remarkably attenuated. In addition, cell ratio in the G1 phase increased after knockdown of TRERNA1, suggesting the arrested G1/S cell cycle. Subsequently, FOXL1 was downregulated in NSCLC cell lines and tumor tissues. Meanwhile, FOXL1 level was verified to be negatively correlated with TRERNA1 level. Additionally, the binding between TRERNA1 and FOXL1 was confirmed by Dual-Luciferase reporter gene assay. Cell reverse investigation indicated the involvement of FOXL1 in TRERNA1-regulated malignant progression of NSCLC. CONCLUSIONS: LncRNA TRERNA1 was up-regulated both in NSCLC tissues and cell lines. Its level was associated with pathological stage and poor prognosis in NSCLC. In addition, lncRNA TRERNA1 could promote the malignant progression of NSCLC via modulating FOXL1.

LINC01296 promotes the proliferation and invasion by regulating microRNA-760 expression and predicts poor prognosis of hepatocellular carcinoma.

OBJECTIVE: The aim of this study was to investigate the role of LINC01296 in the progression of liver cancer (LCa) and to explore its possible molecular mechanisms. PATIENTS AND METHODS: TCGA database was used for information mining to verify the expression of LINC01296 in liver tumor tissues and normal tissues. The levels of LINC01296 in 40 pairs of LCa and adjacent tissues, as well as normal liver cell lines and liver cancer cell lines, were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The Chi-square test was performed to analyze the clinical characteristics of tumor samples and LINC01296 expression. Meanwhile, the Chi-square test was used to explore the relationship between different clinical indicators and the expression of LINC01296. The liver cancer cell lines were screened and transfected with siRNA-LINC01296 and microRNA-760 inhibitor, as well as corresponding negative controls, respectively. Cell counting kit-8 (CCK-8) and Transwell assays were used to determine the effects of LINC01296 on the proliferative and invasive capacities of cells. Furthermore, the regulatory association between LINC01296 and microRNA-760 was verified by the Dual-Luciferase reporter assay. RESULTS: LINC01296 expression was remarkably higher in LCa tissues than that of normal liver tissues. Meanwhile, LINC01296 expression was associated with poor prognosis of LCa. Patients with high LINC01296 expression were more likely to have lymph node metastasis. In vitro experiments showed that the knockdown of LINC01296 significantly inhibited the proliferation and migration of HCC cells. Meanwhile, microRNA-760 was remarkably lowly expressed in LCa tissues and cells. Subsequent experiments indicated that LINC01296 was regulated by miR760 in LCa tissues, and high expression of linc0129 could limit microRNA-760 expression. Furthermore, the inhibition of microRNA-760 in HCC cells reversed the effect of LINC01296 knockdown on cell proliferation and invasion. CONCLUSIONS: LINC01296 could promote the proliferative ability and invasiveness of hepatoma cells by inhibiting the expression of microRNA-760. Moreover, its expression was closely related to lymph node metastasis and poor prognosis of LCa.

MicroRNA-507 represses the malignant behaviors of non-small cell lung cancer via targeting zinc finger E-box binding homeobox 2.

OBJECTIVE: Non-small cell lung cancer (NSCLC) is one of the most common malignancies around the world and effective therapeutic method is yet to be excavated for advance NSCLC. MicroRNA-507 (miR-507) was found to be aberrantly expressed and affected cancer cell behaviors in some types of cancers. However, the role of miR-507 in NSCLC is largely unknown. The expression, biological role, and the underlying mechanism of miR-507 in NSCLC were explored in this study. PATIENTS AND METHODS: Quantitative real-time PCR (qRT-PCR) assay was applied for the detection of miR-507 in NSCLC tissues and cell lines. Cell Counting Kit-8 (CCK-8) and colony formation assays were carried out to assess the proliferative abilities of NSCLC cells. Cell invasive capabilities were determined by transwell assays. We used Dual-Luciferase reporter assays to verify the binding between miR-507 and zinc finger E-box binding homeobox 2 (ZEB2). RESULTS: MiR-507 was found to be downregulated in NSCLC tissues and cell lines. Low expression of miR-507 was correlated with poor prognosis of NSCLC. Overexpression of miR-507 repressed NSCLC cell invasion and proliferation. ZEB2 was predicted to be a direct downstream molecular of miR-507 and their direct binding was verified by Dual-Luciferase reporter assays. Up-regulation of ZEB2 could significantly rescue the suppressive effects of miR-507 on NSCLC cells' invasion and proliferation. CONCLUSIONS: MiR-507 was noticeably downregulated in NSCLC and correlated with poor prognosis of NSCLC patients. MiR-507 represses the invasion and proliferation of NSCLC via targeting ZEB2. This study indicated that miR-507 might serve as a potential therapeutic target for NSCLC.

Up-regulation of miR-765 predicts a poor prognosis in patients with esophageal squamous cell carcinoma.

OBJECTIVE: Up-regulation of miR-765 in esophageal squamous cell carcinoma (ESCC) has been reported in the previous study. The aim of the present study was to measure the levels of miR-765 expression in ESCC and evaluate its clinical significance in ESCC patients. PATIENTS AND METHODS: Quantitative Real-time PCR assays were performed to analyze the expression of miR-765 in human ESCC tissues and adjacent esophageal tissues. The relationships between miR-765 expression levels and the clinical factors were investigated by x2-test. Kaplan-Meier analysis was performed to evaluate the overall survival (OS) and disease-free survival (DFS) of ESCC patients with a different expression level of miR-765. The Cox proportional hazards regression model was used to assess the independent prognostic factors. RESULTS: The expression level of miR-765 in ESCC tissues was significantly higher than that in their corresponding normal tissues (p < 0.01). High miR-765 expression was significantly correlated with tumor stage (p = 0.001), lymph nodes metastasis (p = 0.005), clinical stage (p = 0.007). In addition, Kaplan-Meier analysis showed that patients with higher miR-765 expression had a significantly poorer OS (p = 0.0010) and DFS (p< 0.0001) than those with lower miR-765 expression. Multivariate analyses revealed that miR-765 expression served as an independent predictor for both OS (p = 0.001) and DFS (p = 0.001). CONCLUSIONS: Our findings provided the first evidence that miR-765 may serve as an indicator for prognosis of ESCC.

[Analysis of related factors of coins foreign bodies crossing the esophagus in 204 cases of children].

Objective:To explore the anti-tumor effect of Stat3 antisense oligodeoxynucleotide on human Hep-2 cell tumor-bearing BALB/c nude mouse, to study the therapeutic value of Stat3 antisense oligodeoxynucleotide on laryngeal cancer. Method:Hep-2 cells from human laryngeal carcinoma in logarithmic phase were inoculated subcutaneously into BALB/c mice to establish a model of human Hep-2 cell tumor-bearing BALB/c mice. They were divided into blank group, control group and different concentrations of AS3 groups(1 group, 2 group, 3 group, 4 group), and then intraperitoneally administered once a day for 4 weeks, measuring body weight twice a week, and the long and short diameters of the tumors were recorded. After 4 weeks, the mice in each group were weighted. The subcutaneous transplanted tumors were dissected, weighted, and inhibitory rate was obtained.Result:Stat3 antisense oligodeoxynucleotide can obviously inhibited the growth of human Hep-2 cell tumor-bearing BALB/c mice with the concentration of antisense oligodeoxynucleotide heightened. The IR in different concentration AS3 groups was obviously higher than that in the control group(P<0.01) .Conclusion:Stat3 antisense oligodeoxynucleotide can obviously inhibit the growth of subcutaneous transplanted tumors in human Hep-2 cell tumor-bearing BALB/c mice, and may have therapeutical effect on laryngeal cancer.

Hip fracture patients who experience a greater fluctuation in RDW during hospital course are at heightened risk for all-cause mortality: a prospective study with 2-year follow-up.

This study aims to detect whether there remains valuable prognostic information in fluctuation of red cell distribution width (RDW) in hip fracture patients. Results show that this readily available parameter may provide a more effective strategy for assessment of mortality risk, therefore providing a reference for clinical planning and decision-making. INTRODUCTION: Prognostic values have been found in the fluctuation of some hematologic parameters. The red cell distribution width (RDW) routinely reported with all complete blood cell counts (CBC) has proven to be associated with poor outcomes in various diseases. However, whether the fluctuation in RDW is predictive of long-term mortality in hip fracture patients treated with surgery remains unknown. METHODS: One thousand three hundred thirty hip fracture patients who underwent surgery from January 1, 2000 to November 18, 2012 were recruited in this prospective cohort study. Fluctuation in the RDW between admission and discharge was measured, and a Kaplan-Meier (KM) analysis and multivariable Cox regression model were applied to evaluate the relationship between this fluctuation and mortality. Risk factors for a larger fluctuation were detected by using Logistic regression analyses. RESULTS: In addition to the admission RDW, a high RDW level at the time of discharge was also associated with an increased risk of death, while no significant difference was found in the postoperative RDW. Fluctuation in the RDW between admission and discharge was an independent risk predictor for 2-year mortality (HR 1.45 95%CI 1.06-2.00, p = 0.022). Factors affecting the change in the RDW between admission and discharge included both the demographic characteristics of the patients and clinical interventions. CONCLUSION: Hip fracture patients who experience a greater fluctuation in RDW during the hospital course are at a heightened risk for 2-year all-cause mortality.

Multichannel continuous-wave fiber cavity ringdown gas sensing utilizing frequency-shifted interferometry.

We present a multichannel continuous-wave (CW) fiber cavity ringdown (FCRD) gas sensing method based on frequency-shifted interferometry (FSI). This scheme detects gas concentration by measuring the intensity decay rates of continuous light from different ringdown cavities in the spatial domain, unlike conventional FCRD techniques, which measure the decay rates of pulse light in the time domain. This method shares one CW light source, one slow detector, and one slow data collector. In order to illustrate the theory, acetylene gas concentration measurement in a two-channel FSI-FCRD system was experimentally conducted in the range of 0%-1%. A linear relation was established between concentration and absorption loss, which is proportional to the intensity decay rate, and the measurement resolutions of 3.871%/dB and 3.658%/dB were achieved, respectively. The results reveal that the proposed system has the advantages of low cost, high sensitivity, high precision, and good stability in multichannel gas detection.

[Magnetic resonance imaging of dystrophinopathy that mimics adductor enthesopathy].

OBJECTIVE: To report thigh muscle magnetic resonance imaging (MRI) tests of four Chinese patients with dystrophinopathy with edema changes in adductor longus muscles that mimics adductor enthesopathy. METHODS: Four boys, who were from four unrelated families and aged from 5 to 11 years, were investigated because of the clinical manifestations including myalgia or muscle weakness or the incidental findings of elevated serum creatine kinase levels, and were diagnosed with dystrophinopathy by gene test of Duchenne muscular dystrophy (DMD). Their creatine kinase levels were increased from 4 087 IU/L to 32 700 IU/L (Normal range: 75-175 IU/L). The muscle biopsy of three patients all demonstrated a dystrophic pattern including necrosis, regeneration, hypertrophy, atrophy and connective tissue proliferation, with different proportions of dystrophin-negative muscle fibers. The gene test of DMD showed an out-frame deletion of exons in three of the four patients, involving either exons 45 or exons 49-52 deletion or exon 62 duplication, and c.2665 C>T with nonsense mutation in the other one. Muscle MRI tests of the bilateral thighs were performed with T1 weighed sequence and slow tau inversion recovery sequence. The degree of fatty infiltration changes was scored. RESULTS: MRI of the thigh muscles showed mild to severe fatty infiltration changes in T1 weighed sequence with the total scores from 2 to 13.The most severe fatty infiltration changes were in the long head of biceps femoris and adductor magnus. Obvious hyperintensities appeared mainly in the adductor longus muscles on slow tau inversion recovery (STIR) images in all the patients without any abnormal signals in the attachment of the ligament, indicating edema changes of the adductor longus muscles which mimiced adductor enthesopathy. Two of the four patients presented with edema changes in the bilateral adductor longus muscles, while the other two were with only unilateral changes. Furthermore, other thigh muscles, including adductor magnus, semitendinosus, sartorius and rectus femoris muscles, could also have mild edema changes in two of the four patients. CONCLUSION: Dystrophinopathy can manifest as edema changes in the adductor longus muscles in thigh muscle MRI tests, which is a typical lesion in adductor enthesopathy. The adductor longus muscles in the dystrophinopathy patients may be easy to be impaired due to traction injury during sports.

Clinical characteristics and risk factors of postoperative pneumonia after hip fracture surgery: a prospective cohort study.

UNLABELLED: In this study, we attempt to determine the clinical characteristic and risk factors of postoperative pneumonia (POP) after hip fracture surgery in a well-defined hip fracture cohort. We find that intrinsic factors as well as major clinical interventions were all important risk factors of POP. INTRODUCTION: Postoperative pneumonia (POP) is one of the major complications following hip fractures surgery. However, the risk factors of POP are not well studied in hip fracture cohorts. We attempt to determine the clinical characteristic and risk factors of POP after hip fracture surgery in a well-defined hip fracture cohort. METHODS: Datasets from a prospective hip fracture cohort study with a 2-year follow-up period, from 2000 to 2011, were reanalyzed for characteristics of POP. Multivariate Cox proportional regression was used to evaluate the association between the incidence of POP and all-cause mortality. Multivariate logistic regression was used to screen for potential risk factors of POP by analyzing demographic factors, comorbidities, major clinical interventions, and hematological parameters. RESULTS: In 1429 patients who underwent hip surgery, the incidence of POP was 4.9 % (n = 70). All-cause mortality of patients with POP was significantly higher than that of patients without POP at 30 days (hazard ratio (HR) 3.05, 95 % confidence intervals (CI) 1.88-4.94), 1 year (HR 1.87, 95 % CI 1.41-2.48), and 2 years (HR 1.57, 95 % CI 1.23-1.99) postoperatively. Multivariate logistic regression showed that intrinsic factors (advanced age, anemia, diabetes, prior stroke, number of comorbidities, ASA score ≥III, and some laboratory biomarkers) as well as major clinical interventions were all significant risk factors for POP. CONCLUSION: Intrinsic factors and major clinical interventions were all important risk factors of POP in patients after hip fracture surgery. Targeted preventive measures to mitigate the above risk factors may help in reducing the incidence of POP.