Long non-coding RNA LINC00858 promotes cells proliferation and invasion through the miR-153-3p/Rabl3 axis in hepatocellular carcinoma.

OBJECTIVE: Long non-coding RNA (lncRNA) LINC00858 is a cancer-associated lncRNA frequently dysregulated in many types of human cancers. In the current study, we aimed to explore the role of LINC00858 in hepatocellular carcinoma (HCC). PATIENTS AND METHODS: The relative expression levels of LINC00858 in HCC samples and adjacent non-tumor samples were determined by qRT-PCR. Loss-of-function assay was performed to examine the function of LINC00858 in HCC in vitro. Bioinformatic analysis and the following Luciferase activity reporter assay were utilized to explore the downstream molecules of LINC00858. CCK-8 assay was performed to detect cell proliferation of HCC cells. Transwell assay was performed to evaluate the invasive ability of HCC cells. RESULTS: Our results showed that LINC00858 was highly expressed in both HCC tissues and cell lines. Knockdown of LINC00858 inhibited the proliferation and invasion of HCC cells. Moreover, LINC00858 was found to act as a sponge of miR-153-3p, which directly bound to Rabl3 and regulated the Rabl3 expression. Furthermore, inhibition of miR-153-3p counteracted the effects of LINC00858 knockdown on proliferation and invasion of HCC cells. In addition, the overexpression of Rabl3 rescued the effects of miR-153-3p on cell proliferation and invasion of HCC cells. CONCLUSIONS: In summary, these findings showed that LINC00858 exerted an ontogenetic role in HCC via regulating miR-153-3p/Rabl3 axis. Thus, LINC00858 might be utilized as a therapeutic target for the treatment of HCC.

[Therapeutic effect of different surgical methods for congenital small intestine atresia].

Objective: To compare and analyze the curative effect of three surgical methods in the treatment of small intestine atresia, and to provide evidence for individualized surgical treatment of children with small intestine atresia. Methods: The clinical diagnosis and treatment of 168 children with small intestine Ⅱ, Ⅲ, Ⅳ type atresia in our hospital from January 2008 to September 2017 were retrospectively analyzed and they were divided into different types according to the operation. The three groups were end-to-end anastomosis group (EEA, n=58), end oblique anastomosis group (EOA, n=68), and proximal end-end anastomosis group (PEA, n=42). The EEA group and the EOA group were further divided into group a (EEA-a/EOA-a) with a proximal intestinal tube diameter greater than 4.0 times the distal end and a group b ((EEA-b/EOA-b) with a diameter less than or equal to 4.0 times the distal intestinal tube diameter. The gender, gestational age, birth weight, type of atresia, and postoperative defecation time, postoperative feeding time, postoperative hospital stay and postoperative follow-up complications were compared. Results: There was no significant difference in gender, gestational age and birth weight between the groups (P>0.05). The PEA group was better than EEA-a group and EOA-a group in postoperative defecation time, postoperative feeding time, postoperative hospital stay and complications (P<0.05). The postoperative defecation time, postoperative feeding time, postoperative hospital stay and complications of the EOA-a group were better than those of the EEA-a group (P<0.05). There was no statistically significant difference in postoperative defecation time, postoperative feeding time, and complications between the EEA-b group and the EOA-b group (P>0.05), but the postoperative hospital stay in the EEA-b group was longer than that in the EOA-b group (P<0.05). Conclusion: PEA is recommended for children with a proximal intestinal canal diameter greater than 4.0 times greater than the distal end because of the rapid recovery and fewer complications; EOA is recommended for children with a proximal intestinal canal diameter of 4.0 or less because of its advantage of shorter hospital stay than EEA surgery. Congenital intestinal atresia has a better effect according to the specific conditions of the child.

Study of expression levels and clinical significance of miR-503 and miR-375 in patients with esophageal squamous cell carcinoma.

OBJECTIVE: This study aims to investigate the expression levels and clinical significance of miR-503 and miR-375 in patients with esophageal squamous cell carcinoma. PATIENTS AND METHODS: 40 cases of cancer tissues and adjacent tissues in patients with esophageal squamous cell carcinoma were collected from March 2017 to September 2017 in the Department of Gastroenterology in the First Affiliated Hospital of Henan Polytechnic University. qRT-PCR was used to analyze the expressions of miR-503 and miR-375 in cancer tissues and adjacent normal tissues. The association between their expressions and the gender, age, degree of tumor differentiation, TNM staging, presence or absence of lymph node metastasis, and other clinicopathological characteristics of patients with esophageal squamous cell carcinoma was analyzed. RESULTS: The results showed that the expression level of miR-503 in esophageal squamous cell carcinoma tissues (6.83±2.14) was significantly higher than that in adjacent tissues (2.45±1.13). The expression level of miR-375 in esophageal squamous cell carcinoma tissues (3.75±1.06) was significantly lower than that in adjacent tissues (7.45±1.13). The expression levels of miR-503 and miR-375 in esophageal squamous cell carcinoma were related to the existence of lymph node metastasis, degree of differentiation of esophageal squamous cell carcinoma and TNM staging (p<0.001). There was no correlation between the expressions of miR-503 and miR-375 and the age, gender and tumor size of patients (p>0.05). CONCLUSIONS: miR-503 was highly expressed in esophageal squamous cell carcinoma and miR-375 was lowly expressed in esophageal squamous cell carcinoma. miR-503 and miR-375 were closely related to the lymphatic metastasis, degree of differentiation and TNM staging of the tumor.

Upregulated serum sclerostin level in the T2DM patients with femur fracture inhibits the expression of bone formation/remodeling-associated biomarkers via antagonizing Wnt signaling.

OBJECTIVE: Bone formation/remodeling-associated biomarkers, such as osteocalcin, amino pro-peptide of type 1 collagen (P1NP) and CrossLaps (CTX) have been deregulated in type 2 diabetes mellitus (T2DM) patients. In particular, the T2DM-associated sclerostin markedly inhibits the bone formation, suppresses the osteoblast activity and downregulates the bone turnover. PATIENTS AND METHODS: In the present study, we examined the serum levels of sclerostin, osteocalcin, P1NP and CTX in the T2DM patients. We evaluated the regulation on osteocalcin, P1NP and CTX by sclerostin treatment in osteoblast hFOB 1.19 cells. Finally, we determined the mediation of Wnt signaling in the regulation by sclerostin on osteocalcin, P1NP and CTX in human osteoblast hFOB 1.19 cells. RESULTS: It was demonstrated that osteocalcin, P1NP and CTX were downregulated in the femur fracture of patients with T2DM, whereas the serum level of the sclerostin was markedly higher in the femur fracture of patients with T2DM. Moreover, the downregulated osteocalcin, P1NP or CTX was negatively associated with the upregulated sclerostin. In vitro results confirmed that sclerostin downregulated the expression of osteocalcin, P1NP and CTX in hFOB 1.19 cells. Also, our results demonstrated that Wnt/ß-catenin inhibition was associated with the sclerostin-mediated inhibition of osteocalcin, P1NP and CTX in hFOB 1.19 cells. The Wnt/ß-catenin level was markedly inhibited by sclerostin treatment, and the siRNA-mediated downregulation of ß-catenin reduced the levels of osteocalcin, P1NP and CTX. CONCLUSIONS: Our study demonstrated that the upregulated serum sclerostin level in the T2DM patients with fracture inhibited the expression of the bone formation/remodeling-associated biomarkers via antagonizing Wnt signaling. It suggests that sclerostin might be an effective target for T2DM-associated bone fracture and delayed fracture healing.

[Application of three-dimensional visualization technology in surgical treatment for patients with hepatic alveolar echinococcosis].

OBJECTIVE: To determine the clinical value of three-dimensional(3D) visualization technology in pre-operative assessment and surgical planning for patients with hepatic alveolar echinococcosis. METHODS: Eighty-five hepatic alveolar echinococcosis patients received surgical treatment in the First Affiliated Hospital of Xinjiang Medical University between May 2011 and May 2015.3D reconstruction and virtual surgeries were performed on diseased livers using a 3D visualization reconstruction system for liver, which based on the data set of 64-slice CT from those patients and indicated the feasibility and safety of liver resection. The pre-operative measurement results were compared with intra-operative conditions to verify the accuracy of pre-operative evaluation. RESULTS: All surgical strategies of patients underwent surgical treatment(59 of 85 received traditional liver resection and 26 of 85 received liver auto-transplantation)were consistent with pre-operative surgical planning in 3D reconstruction. Furthermore, the pre-operative resection liver volume((751±510)cm(3)) estimated by 3D calculation method was positively correlated with the actual weight((777±567)g) after the surgery(r=0.990), and the error rate was 4.7%; the pre-operative remaining liver volume((829±157)cm(3)) estimated by 3D calculation method was positively correlated with the actual weight((770±206) g) after the surgery(r=0.978). Patients were followed for 6-46 months after the surgery, and 3 post-operative death and 2 recurrence (one case received secondary surgery and one case received drug therapy) were reported during the follow-up period. CONCLUSIONS: A liver 3D visualization technology has application value in the pre-assessment and surgical planning.When it combined with ultrasound, CT and MRI, traditional examinations, the liver 3D visualization technology can effectively improve the success rate of operation, reduce the risks of surgery.

[Living donor liver transplantation for the treatment complicated hepatic cystic echinococcosis: first case report from China].

OBJECTIVE: To report the first clinical experience of living donor liver transplantation(LDLT) in patient with complicated hepatic cystic echinococcosis in China. METHODS: First Affiliated Hospital of Xinjiang Medical University successfully implemented LDLT in the treatment of one patient with complicated hepatic cystic echinococcosis after four times liver surgery and secondary congestive cirrhosis on May 9, 2015. The clinical data of the patient has been retrospectively analyzed. RESULTS: LDLT procedure was successfully performed in a patient with four previous liver intervention due to his recurrence. The patient was lack of right lobe, while with significant hypertrophy in left lobe. The reoccurred lesion compressed the retrohepatic vena cava, left hepatic vein, portal vein, that led to the stricture of retrohepatic vena cava, left hepatic vein orifice. The phlebography displayed remarkable stricture in retrohepatic vena cava and rich collateral circulation by which the venous blood flow back to the right atrium via paravertebral vein. The orifice of left hepatic vein shaped as hair-like so that the stenting was impossibly. After the multi-disciplinary team discussion, the liver transplantation was proposed, while the autotransplantation was considered as first line option, and with the backup of living related donor. The laparotomy showed the hugely enlarged liver with nodular changes. The frozen section was tested twice and showed as spotty necrosis with pseudo-lobe formation. Although the enlarged left lobe about 2 000 g weight, the liver colored as grey with cotton-like texture, the plan for autotransplantation was abandoned regarding the high risk for post-operative liver failure. Therefore, LDLT was performed. The donor was her brother who donated right lobe with 685 g weight. The operation time was 1 005 min with anhepatic time 335 min. Total of 12 units red blood cell suspension was transfused. The coagulating function was back to normal in 3 days after operation. The patient was discharged at 30 days after operation, while the routine blood test and biochemical markers had back to normal levels. The patient had taken tacrolimus and methylprednisolone with normal life. The liver functions of transplanted liver were normal in 90 days after surgery. The patient was able to self-activity and regular outpatient follow-up. CONCLUSION: Hepatic CE is an infectious disease, and liver transplantation could be the last choice for complicated case, especially in combination with severe complications, like Budd-Chiari syndrome.

Ex Vivo Liver Resection and Autotransplantation for End-Stage Alveolar Echinococcosis: A Case Series.

The role of autotransplantation in end-stage hepatic alveolar echinococcosis (AE) is unclear. We aimed to present our 15-case experience and propose selection criteria for autotransplantation. All patients were considered to have unresectable hepatic AE by conventional resection due to critical invasion to retrohepatic vena cava, hepatocaval region along with three hepatic veins, and the tertiary portal and arterial branches. All patients successfully underwent ex vivo extended right hepatectomy and autotransplantation without intraoperative mortality. The median autograft weight was 706 g (380-1000 g); operative time was 15.5 hours (11.5-20.5 hours); and anhepatic time was 283.8 minutes (180-435 min). Postoperative hospital stay was 32.3 days (12-60 days). Postoperative complication Clavien-Dindo grade IIIa or higher occurred in three patients including one death that occurred 12 days after the surgery due to acute liver failure. One patient was lost to follow-up after the sixth month. Thirteen patients were followed for a median of 21.6 months with no relapse. This is the largest reported series of patients with end-stage hepatic AE treated with liver autotransplantation. The technique requires neither organ donor nor postoperative immunosuppressant. The early postoperative mortality was low with acceptable morbidity. Preoperative precise assessment and strict patient selection are of utmost importance.

Phylogeography of pink pineapple mealybugs, Dysmicoccus brevipes (Cockerell) reveals the history of pineapple introduction and cultivation in China.

The pink pineapple mealybug (PPM), Dysmicoccus brevipes (Cockerell) (Hemiptera: Pseudococcidae), is a widespread plant-sucking insect of considerable concern because it transmits the pineapple mealybug wilt-associated virus. Its distribution is closely linked with its host, the pineapple [Ananas comosus (L.) Merrill] because of its wingless and parthenogenetic characteristics. To investigate the history of D. brevipes introduction and the cultivation of pineapple in China, samples of D. brevipes were collected from the main pineapple production region in China, and from Thailand, and the mitochondrial cytochrome c oxidase subunit I (COI) gene was analyzed. Homologous sequences of D. brevipes COI from Brazil, Thailand, and Philippines that are deposited in GenBank were compared. Phylogenetic analyses suggest there are close genetic relationships between PPM populations from Hawaii, Brazil, the Philippines, and from Thailand and China, which probably originate from South America. It is suggested that most PPMs in China were introduced from South America by way of Southeast Asia, being accompanied by the pineapple seedling. Conversely, some PPMs represented by Haplotype-WN from Wanning of China, and Lampang of Thailand were found to differ greatly from populations in Hawaii, Brazil, the Philippines, Thailand, and China. It is possible that another route was used for the introduction and distribution of pineapple, or that pineapple might have originated in Southeast Asia.

First Report of Fusarium mangiferae Causing Mango Malformation in China.

Mango (Mangifera indica L.) malformation caused by Fusarium mangiferae has been reported in many mango-growing regions of the world (3). The disease was also observed in Yunnan and Sichuan provinces of China (1). Typical symptoms in seedlings included loss of apical dominance, hyperplasia and hypertrophy of vegetative buds, shortened internodes, and leaves that were more brittle than those of healthy plants. Inflorescences were abnormally branched and thickened, with panicles producing as much as two to five times the normal number of flowers. Flowers in the malformed inflorescence were much more enlarged and crowded than the generally hypertrophied axes of the panicle, thus producing no fruit or aborting early. To identify the pathogen, samples of malformed and healthy mango seedlings were collected from the affected plantings. For isolation, portions of stems were cut into 3- to 4-mm segments, surface disinfested, dried, and then plated on potato dextrose agar and incubated at 25°C. Within 5 days, white, fluffy, aerial mycelium developed. With the aid of an inverted microscope, single conidia were transferred to carnation leaf agar (CLA) medium. After 10 days of incubation, morphological characteristics were found to be identical to those of F. mangiferae (4). Aerial mycelium was white with no pigmentation observed on potato sucrose agar. Pigmentation on rice medium was pink. On CLA medium, conidia grew in branched conidiophores with false heads bearing monophialides or polyphialides. No conidiospores in chains were observed. Microconidia were ovate to long and oval, 0 to 1 septate, and 3.1 to 10.2 × 1.5 to 2.2 µm. Macroconidia are falculate, 3 to 5 septate, and 18 to 38 × 1.8 to 2.4 µm. Chlamydospores were not observed. Pathogenicity studies were conducted with 7-month-old asymptomatic mango seedlings. These seedlings, except for the controls, were inoculated by injection of the isolated fungus in the axillary or apical bud position. A 1-ml spore suspension (1 × 106 spores/ml) was injected slowly into the stems using a microsyringe with three buds per seedling, for a total of 10 seedlings. Typical malformation symptoms developed within 3 to 4 months, and none of the plants inoculated with sterile water resulted in malformation symptoms. Reisolations from the induced malformed shoots yielded the same fungus, and no fungal growth was observed to be growing from the control plants. To confirm identity of the causal fungus, the gene encoding translation elongation factor 1 alpha (EF-1α) was amplified and sequenced (2). The EF-1α sequence was 660 bp long. The sequence (GenBank Accession No. HM068871) was 99.68% similar to sequences of FD_01167 in the Fusarium ID database. On the basis of symptoms, fungal morphology, the EF-1α region sequence, and pathogenicity testing, this fungus was identified as F. mangiferae. To our knowledge, this is the first report of F. mangiferae causing mango malformation in China. This report will establish a foundation for further study of F. mangiferae and effectively addressing the disease. References: (1) X. H. Chen. Pract. Technol. (in Chinese) 6:5, 1992. (2) D. M. Geiser et al. Eur. J. Plant Pathol. 110:473, 2004. (3) J. Kumar et al. Annu. Rev. Phytopathol. 31:217, 1993. (4) J. F. Leslie and B. A. Summerell. The Fusarium Laboratory Manual. Blackwell Publishing, Ames, IA, 2006.

Ru(0001) model catalyst under oxidizing and reducing reaction conditions: in-situ high-pressure surface X-ray diffraction study.

With surface X-ray diffraction (SXRD) using a high-pressure reaction chamber we investigated in-situ the oxidation of the Ru(0001) model catalyst under various reaction conditions, starting from a strongly oxidizing environment to reaction conditions typical for CO oxidation. With a mixture of O(2) and CO (stoichiometry, 2:1) the partial pressure of oxygen has to be increased to 20 mbar to form the catalytically active RuO(2)(110) oxide film, while in pure oxygen environment a pressure of 10(-5) mbar is already sufficient to oxidize the Ru(0001) surface. For preparation temperatures in the range of 550-630 K a self-limiting RuO(2)(110) film is produced with a thickness of 1.6 nm. The RuO(2)(110) film grows self-acceleratedly after an induction period. The RuO(2) films on Ru(0001) can readily be reduced by H(2) and CO exposures at 415 K, without an induction period.