Microplastic abundance and distribution in a Central Asian desert.

Microplastic pollution is widespread, affecting even the remotest places on Earth. However, observational data on microplastic deposition in deserts, which comprise 21% of the total land area, are relatively rare. The current study aims to address the knowledge gap in terms of microplastic distribution in Asian deserts. The Badain Jaran Desert in Central Asia is the second largest desert in China. We investigated microplastic distribution and deposition on dunes and lakes of this desert. Microplastics were extracted from surface sediments to determine their characteristics and polymer types by microscopic inspection and µ-FTIR. The abundance of microplastics (detection limit is approximately 40 µm) in the uninhabited area ranged from 0.7 ± 1.5 to 11.7 ± 15.5 items/kg, with an average of 6.0 ± 15.4 items/kg. Fragments and fibers accounted for 77% and 23% of the total microplastics, respectively. Epoxy resin (28%), polyethylene terephthalate (25%), phenoxy resin (25%), and polyamide (9%) were the main polymer components, whose sizes were concentrated at 50-200 µm. Back-trajectory modeling was then performed to explore the possible source direction of the microplastics. The results showed that the microplastics mainly originated from the populated areas southeast of the desert, indicating long-distance atmospheric transport and deposition in deserts. The desert-edge zone with some tourism activity contained more microplastics (8.2 ± 17.9 items/kg) than the non-tourism zone (0.9 ± 1.6 items/kg), indicating a potential contribution from tourism. The abundance in the non-tourism zone (0.9 items/kg) can be used as a reference for microplastic background values in the Central Asian deserts, as this value is critical for simulating and predicting global microplastic yields.

Expression and prognostic significance of epithelial tissue-specific transcription factor ESE3 in hepatocellular carcinoma.

BACKGROUND: Epithelium-specific ETS 3 (ESE3) is down-regulated frequently in several malignancies and involved in carcinogenesis and progression. However, ESE3 expression pattern and its relationship with clinical features and prognosis in hepatocellular carcinoma (HCC) are still largely unknown. METHODS: ESE3 expression was analyzed by quantitative real-time PCR and western blotting in HCC cell lines, and then, it was analyzed by immunohistochemistry in HCC tissues and peritumoral normal tissues from total 94 HCC patients. The relationship between ESE3 expression and clinical features was investigated to illustrate the potential prognostic value in HCC. ESE3 roles on HCC progression were evaluated in vitro and vivo by MTT assay and mice tumor model, respectively. RESULTS: ESE3, mainly located in the cytoplasm, was remarkably down-regulated in HCC tissues and cell lines. Low ESE3 expression was positively associated with tumor progression and metastasis features. Kaplan-Meier analysis demonstrated that low ESE3 expression contributed to poor recurrence-free survival (RFS) and overall survival (OS) (both p < 0.01) of patients, and maintained its prognostic value in predicting poor RFS and OS of "Early-stage" HCC patients regardless of clinical features being studied. Multivariate survival analysis was also identified ESE3 as an independent prognostic factor for RFS (p = 0.05 for marginal significance) and OS (p = 0.031). ESE3 expression restoration in cells led to a significant inhibition in HepG2 cell proliferation in vitro and vivo (both p < 0.001). CONCLUSIONS: Down-regulated ESE3 expression in HCC tissues could serve as a potential therapeutic target against HCC and appears to be as a poor prognostic indicator for prognosis, especially in "Early-stage" HCC patients.

A Modified Suture Technique in Hepaticojejunostomy.

BACKGROUND Hepaticojejunostomy is a common biliary reconstruction procedure in hepatobiliary surgery. The suture technique plays a key role in the procedure. The conventional suture technique is complex and time-consuming. To facilitate the procedure, we performed it with a modified suture technique. In the present study, we evaluated the efficacy and safety of the technique in hepaticojejunostomy. MATERIAL AND METHODS We enrolled 120 adult patients who underwent hepaticojejunostomy. The patients were divided into a conventional group and a modified suture group according to the suture technique used. Clinical data were collected for analysis. RESULTS No significant differences were found between the 2 groups in terms of demographic data. No significant differences were found between the 2 groups in terms of serum bilirubin, albumin, AST, ALT, or hemoglobin (p>0.05). There were no significant differences between the 2 groups in terms of bile hemorrhage, fever, or cholangitis (p>0.05). The incidences of stenosis and cholelithiasis were similar in the 2 groups (p>0.05). The incidence of bile leakage was lower in the modified suture group than in the conventional group (p=0.04). The average bile duct diameter was 25±6 mm in the modified continuous suture group and 29±7mm in the conventional group, but the difference was not statistically significant (p=0.5). The duration of the anastomosis procedure was 15.4±4.4 min in the modified continuous suture group, which was shorter than in the conventional group (p<0.05). CONCLUSIONS The modified continuous suture technique is efficient and safe for use in hepaticojejunostomy. It can facilitate the procedure and reduce the incidence of bile leakage after hepaticojejunostomy.

Overexpression of interleukin-32α promotes invasion by modulating VEGF in hepatocellular carcinoma.

Interleukin-32α (IL-32α) was reported to exhibit pluripotent pro-inflammatory properties. Recent studies indicate that it promotes the migration and invasion of cancers. We detected the expression of IL-32 in hepatocellular carcinoma (HCC) tissues and investigated its role in tumor angiogenesis and invasion. IL-32α expression in HCC was evaluated by real-time PCR, western blot analysis and immunohistochemical (IHC) staining. Secreted serum IL-32α and VEGF concentrations were detected using a custom-made sandwich ELISA. Furthermore, IL-32α was knocked down in HCC cell lines using siRNA and the cell migration and invasion abilities were assessed. IHC staining showed that IL32α-positive particles were mainly located in the cytoplasm of cancer cells, and it was significantly upregulated in the tumor tissues compared with that in peritumoral tissues. Notably, IL-32α was strongly expressed in perivascular areas. The mean serum concentration of IL-32α in HCC patients was significantly higher than that in the control group (571.45±102.28 vs. 144.60±51.172 pg/ml; P<0.01). Real-time RT-PCR showed that IL-32α mRNA was significantly overexpressed in HCC tumor tissues (IL-32/ß-actin, 15.59±7.8 vs. 3.37±0.47; P<0.01). The in vitro results indicated that IL-32α knockdown inhibited the activation of VEGF-STAT3 signaling in HCC tumor cell lines. IL-32α expression was correlated with clinical relevance in HCC tumor tissues. It is strongly suggested that IL-32α may be a potential predictor of anti-angiogenesis therapy and prognosis of HCC.

Modulation of IGF2BP1 by long non-coding RNA HCG11 suppresses apoptosis of hepatocellular carcinoma cells via MAPK signaling transduction.

Hepatocellular carcinoma (HCC) is a common malignancy of the liver. HCG11 is a member of long non­coding family, upregulation of which in HCC was proved by our previous study. In the present study, the role of HCG11 in the development of HCC was detected by focusing on the interaction between HCG11 and its target protein insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1). The expression status of HCG11 and IGF2BP1 was first investigated with clinical HCC samples. Then the expressions of HCG11 and IGF2BP1 were both inhibited in the human HCC cell line HepG2 and the cell viability, proliferation, apoptosis and metastasis potential of HepG2 cells were assessed. At molecular level, the expression levels of p-ERK, p-JNK, p-p38, p21 and cleaved caspase-3 were also determined to explain the pathways involved in the function of HCG11 in the progression of HCC. Expression of HCG11 and IGF2BP1 were significantly higher in HCC tissues than those in para-tumor tissues. Knockdown of both indicators led to decreased cell viability, proliferation, and migration ability in HepG2 cells while the cell apoptosis and G1 cell cycle arrest were induced after knockdown of HCG11 and IGF2BP1. In addition, suppressed activity of HCG11 and IGF2BP1 blocked the phosphorylation of anti-apoptosis factors, including ERK, JNK and p38 while the mitochondrial apoptosis in HCC cells was initiated by activation of p21 and cleaved caspase-3. HCG11 exerted its effect on HCC via interaction with IGF2BP1, leading to activation of MAPK signaling, which eventually promoted the progression of HCC.

The long noncoding RNAs PVT1 and uc002mbe.2 in sera provide a new supplementary method for hepatocellular carcinoma diagnosis.

Hepatocellular carcinoma (HCC) is the most common primary malignancy of the liver in adults worldwide. Several studies have demonstrated that long noncoding RNAs (lncRNAs) are involved in the development of various types of cancer, including HCC. These findings prompted us to examine the detectability of lncRNAs in blood samples from patients with HCC. In this study, we explored the expression levels of 31 cancer-related lncRNAs in sera from 71 HCC patients and 64 healthy individuals by reverse transcription and quantitative polymerase chain reaction (RT-qPCR). We found that 25 lncRNAs could be detected in the serum and that 7 had significantly different expression levels. A 2-lncRNA signature (PVT1 and uc002mbe.2) identified by stepwise regression showed potential as a diagnostic marker for HCC. The area under the receiver operating characteristic (ROC) curve was 0.764 (95% CI: 0.684-0.833). The sensitivity and specificity values of this serum 2-lncRNA signature for distinguishing HCC patients from the healthy group were 60.56% and 90.62%, respectively. The diagnostic ability of the combination of the serum 2-lncRNA signature with alpha-fetoprotein (AFP) was much greater than that of AFP alone. The expression levels of the 2 lncRNAs were associated with clinical parameters including tumor size, Barcelona Clinic Liver Cancer (BCLC) stage, and serum bilirubin.

Feasibility and safety of sorafenib treatment in hepatocellular carcinoma patients with spontaneous rupture.

AIM: To report the outcome of patients with ruptured hepatocellular carcinoma (HCC) treated at a single center during a 5-year period. METHODS: We retrospectively analyzed 32 patients who presented with ruptured HCC at Shandong Provincial Hospital Affiliated to Shandong University between 2008 and 2013. RESULTS: The mean age of the patients was 53 years (range 39-71 years). Of these patients, 22 received surgical management, 10 underwent transarterial embolization (TAE) or transarterial chemoembolization (TACE), and 12 received sorafenib after surgery, TAE or TACE. Cumulative survival rates at 4, 8 and 12 mo were 72.9%, 50.0% and 33.3%, respectively, in the surgery only group and were 90.0%, 80.6% and 64.1%, respectively, in the surgery plus sorafenib group. Cumulative survival rates at 4, 8 and 12 mo were 68.4%, 43.6% and 19.4%, respectively, in the surgery only or TAE/TACE only groups, and were 91.7%, 75.0% and 60.2%, respectively, in the sorafenib combination groups (P = 0.04). No unexpected side effects due to sorafenib were observed. The most common side effect was hand-foot skin reaction. To date, 5 patients have died. Median follow-up from the start of sorafenib therapy for the remaining 7 patients is 12.7 mo (range 5.8-32.2 mo). CONCLUSION: Sorafenib can be used in patients with ruptured HCC as it has interesting activity and is well tolerated; dose adjustment is generally not required. However, a larger prospective study is necessary to determine the efficacy of sorafenib in this group of patients.

Possible benefit of splenectomy in liver transplantation for autoimmune hepatitis.

Liver transplantation for autoimmune hepatitis (AIH) is usually successful with excellent long-term outcomes, but primary disease may recur. The recurrence of AIH is a significant cause of graft loss. This study was to analyze the effect of splenectomy in preventing AIH relapse. The clinical courses of 12 patients who had transplantation for AIH were analyzed retrospectively. All patients were subjected to transplantation for end-stage liver disease caused by chronic AIH. Based on the duration of immunosuppressive treatment before liver transplantation, simultaneous splenectomy was performed in ten patients. Two patients underwent liver transplantation without splenectomy, one of them developed recurrent AIH and died from graft failure caused by AIH relapse. However, no episode of AIH recurrence was observed in patients who had undergone simultaneous splenectomy. Splenectomy might be an option to prevent AIH relapse in some patients with high risk factors.