MicroRNA-141-3p promoted the progression of nasopharyngeal carcinoma through targeting DLC1.

OBJECTIVE: Previous studies have shown that the function of miR-141 has tissue specificity. However, the role of miR-141-3p has not been reported in nasopharyngeal carcinoma (NPC). Therefore, this study explored the function of miR-141-3p in NPC. PATIENTS AND METHODS: MiR-141-3p expression in NPC tissues was examined via quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) assay. Cell Counting Kit-8 (CCK-8) and transwell assays were used to explore the function of miR-141-3p. The relationship between miR-141-3p and DLC1 was verified by Dual-Luciferase assay. Protein expression was observed by immunocytochemical assay and Western blot analysis. RESULTS: Upregulation of miR-141-3p associated with poor prognosis was detected in NPC patients. Moreover, overexpression of miR-141-3p promoted cell proliferation, migration, and invasion in NPC cells. It was also found that miR-141-3p promoted EMT and activated the mTOR signaling pathway in NPC. Furthermore, DLC1 was indicated as a direct target of miR-141-3p and miR-141-3p negatively correlated with DLC1 expression in NPC. In particular, upregulation of DLC1 could impair the promoted effect of miR-141-3p in NPC. CONCLUSIONS: MiR-141-3p promotes the progression of NPC by targeting DLC1 and activating the mTOR pathway.

Maresins: anti-inflammatory pro-resolving mediators with therapeutic potential.

Although inflammation is protective of the body, uncontrolled acute inflammatory reactions may inflict tissue damage and lead to chronic inflammation. There is a fast-growing research interest in mechanisms that mediate regression of inflammation and actions of anti-inflammatory factors. Studies of inflammatory and anti-inflammatory mechanisms have uncovered roles for new lipid mediators, including lipoxins, resolvins, protectins, and maresins, collectively referred to as specialized pro-resolving mediators (SPM). Maresins have recently been discovered and are biosynthesized from docosahexaenoic acid (DHA) by macrophages and display strong anti-inflammatory and pro-resolving activities. Here, we summarize the actions and mechanisms of maresins in different diseases and suggest possible therapeutic uses.

TRIP13 promotes proliferation and invasion of epithelial ovarian cancer cells through Notch signaling pathway.

OBJECTIVE: Growing evidence supports the involvement of Thyroid hormone Receptor Interactor 13 (TRIP13) in the progression and metastasis of multiple cancers. However, the roles of TRIP13 in epithelial ovarian cancer (EOC) remains unknown. The present study aimed to investigate the expression pattern and biological function as well as the underlying molecular mechanism. PATIENTS AND METHODS: The expression patterns of genes in EOC tissues and normal ovarian tissues via microarray from GEO and TCGA datasets. The expression levels of TRIP13 in EOC cell lines were detected by Real Time-Polymerase Chain Reaction (RT-PCR). Next, we investigated the effect of TRIP13 on the proliferation, apoptosis, migration and invasion in the EOC cells. Western blot assay was used to explore the role of TRIP13 on the Notch signaling pathway proteins (Notch1, P21, Hes1). RESULTS: Bioinformatics analysis showed that TRIP13 was one of the most significantly upregulated in EOC. The results of RT-PCR also indicated that TRIP13 expression was markedly upregulated in EOC cell lines (SKOV-3, HEY and OVCAR-3) compared to normal ovarian cell lines. Functionally, our data revealed that silencing TRIP13 in EOC cells inhibits cell proliferation, decreases cell invasion and migration, and stimulates EOC cell apoptosis in vitro. Mechanistically, the knockdown of TRIP13 suppressed the Notch signaling pathway activation and subsequently inhibited EMT progression. CONCLUSIONS: The present study provided the first evidence that TRIP13 acted as an onco-promotive regulator in EOC development by modulating the Notch signaling pathway. Our findings enlarged our knowledge in the molecular pathology of TRIP13 tumorigenesis.

LncRNA HULC promotes non-small cell lung cancer cell proliferation and inhibits the apoptosis by up-regulating sphingosine kinase 1 (SPHK1) and its downstream PI3K/Akt pathway.

OBJECTIVE: LncRNA HULC has been proved to have important functions in the pathogenesis of several types of cancers. While its involvement in non-small cell lung cancer (NSCLC), which is one of the most common malignancies, still hasn't been reported to date. Therefore, we aimed to investigate the role of HULC in NSCLC and to explore the possible mechanisms. PATIENTS AND METHODS: Tumor tissues and adjacent healthy tissues were collected from NSCLC patients, and blood samples were collected from both NSCLC patients and healthy controls. Expression of HULU in those tissues was detected by qRT-PCR. All patients were followed up for 5 years. Diagnostic and prognostic values of serum HULU for NSCLC were investigated by ROC curve analysis and survival curve analysis, respectively. HULC overexpression NSCLC cell lines were established and its effects on cell proliferation as well as apoptosis were investigated by CCK-8 assay and MTT assay, respectively. Effects of HULC overexpression on sphingosine kinase 1 (SPHK1) and its downstream PI3K/Akt pathway were investigated by Western blot. RESULTS: HULC expression level was increased in tumor tissues compared with adjacent healthy tissues in most patients. Serum level of HULC was higher in cancer patients than that in healthy control. Serum level of HULC was increased with the increased stage of primary tumor (T stage). Serum HULC can be used to accurately predict NSCLC and its prognosis. HULC overexpression promoted tumor cell proliferation, but inhibited cell apoptosis. HULC overexpression also increased expression level of SPHK1 and phosphorylation level of Akt in NSCLC cell, but showed on significant effects on Akt expression. Treatment with SPHK1 inhibitor and Akt reduced the effects of HULC overexpression on proliferation and apoptosis of NSCLC cells. But the treatment showed no significant effects on HULC expression. SPHK1 inhibitor treatment inhibited phosphorylation of Akt, while Akt inhibitor treatment showed no significant effects on SPHK1 expression. CONCLUSIONS: LncRNA HULC overexpression can promote NSCLC cell proliferation and inhibit cell apoptosis by up-regulating sphingosine kinase 1 (SPHK1) and further induce the activation of its downstream PI3K/Akt pathway.

Characterization of the novel HLA-C*07:613 allele by sequencing-based typing.

HLA-C*07:613 differs from HLA-C*07:01:01:01 by one nucleotide substitution at position 454.

Characterization of the novel HLA-C*03:02:17 allele by sequencing-based typing.

HLA-C*03:02:17 differs from HLA-C*03:02:02:01 by one nucleotide substitution at position 393.

Characterization of the novel HLA-B*40:01:51 allele by sequencing-based typing.

HLA-B*40:01:51 differs from HLA-B*40:01:01 by 2 nucleotide substitutions at position 72 and 126.

Characterization of the novel HLA-B*48:43 allele by sequencing-based typing.

HLA-B*48:43 differs from HLA-B*48:01:01:01 by two nucleotide substitutions at positions 981 and 986.

A novel HLA-DRB1*07 allele, HLA-DRB1*07:01:22, identified in a Chinese individual.

HLA-DRB1*07:01:22 differs from HLA-DRB1*07:01:01:01 at position 244 (C>T) in exon 2.

Characterization of the novel HLA-DQB1*05:155 allele by sequencing-based typing.

HLA-DQB1*05:155 differs from HLA-DQB1*05:01:01 by one nucleotide substitution at position 474 (G>C).

Characterization of the novel HLA-A*02:07:10 allele by sequencing-based typing.

HLA-A*02:07:10 differs from HLA-A*02:07:01 by one nucleotide substitution at position 117.

Characterization of the novel HLA-DRB1*13:241 allele by sequencing-based typing.

HLA-DRB1*13:241 differs from HLA-DRB1*13:02:01 by one nucleotide substitution at position 335.

Characterization of a novel HLA-C*04 allele, HLA-C*04:277.

HLA-C*04:277 has one nucleotide difference from HLA-C*04:01:01:01 at position 1034 (G>A).

Comparison of transvaginal surgery and methotrexate/mifepristone-combined transcervical resection in the treatment of cesarean scar pregnancy.

OBJECTIVE: To explore the safety and efficiency of transvaginal surgical treatment of cesarean scar pregnancy (CSP). PATIENTS AND METHODS: A retrospective analysis of 54 CSP patients that received treatment in our hospital from October 2011 to September 2015 was performed, dividing two groups: Group A (n=34) received transvaginal cesarean scar pregnancy focus clearance surgery while Group B (n=20) received transcervical resection following methotrexate/mifepristone-combined treatment. The basic clinical findings were collected and analyzed, along with the curative effects between the two groups. RESULTS: Differences in age (30.91 ± 4.59 years vs. 31.91 ± 5.53 years) for gravidity (2.97 ± 1.24 times vs. 2.75 ± 1.48 times), cesarean section (1.24 ± 0.43 vs. 1.20 ± 0.41), time interval from last cesarean section (56.53 ± 32.93 months vs. 58.70 ± 39.44 months), menelipsis (51.35 ± 10.90 days vs. 57.85 ± 16.62 days), pre-operative serum-hCG (27953.65 ± 37517.10 mIU/L vs. 17368.24 ± 35094.14 mIU/L), operation time (43.34 ± 12.38 min vs 40.07 ± 16.88 min), menstruation recovery time (1.23 ± 0.53 months vs. 1.55 ± 0.76 months) were not statistically significant (p > 0.05). The differences in the intraoperative blood loss (43.34 ± 12.38 ml vs. 40.07 ± 16.88 ml), average hospital stay (7.61 ± 2.47 days vs. 12.42 ± 3.64 days), time for ß-hCG to return to normal (18.50 ± 8.19 mIU/L vs. 29.00 ± 12.96 mIU/L) between the two groups were statistically significant (p < 0.05). Group A was significantly lower than Group B. CONCLUSIONS: Transvaginal surgery is an effective and relatively safe treatment option for CSP patients.

A new HLA-B*55 allele, B*55:83N with a stop codon in exon 4 generated by a point mutation, identified in a Chinese individual.

The new allele HLA-B*55:83N differs from HLA-B*55:02:01:01 by a single nucleotide.

Surgical treatment of Denis type B thoracolumbar burst fracture with neurological deficiency by paraspinal approach.

We aimed to describe the surgical technique and clinical outcomes of paraspinal-approach reduction and fixation (PARF) in a group of patients with Denis type B thoracolumbar burst fracture (TLBF) with neurological deficiencies. A total of 62 patients with Denis B TLBF with neurological deficiencies were included in this study between January 2009 and December 2011. Clinical evaluations including the Frankel scale, pain visual analog scale (VAS) and radiological assessment (CT scans for fragment reduction and X-ray for the Cobb angle, adjacent superior and inferior intervertebral disc height, and vertebral canal diameter) were performed preoperatively and at 3 days, 6 months, and 1 and 2 years postoperatively. All patients underwent successful PARF, and were followed-up for at least 2 years. Average surgical time, blood loss and incision length were recorded. The sagittal vertebral canal diameter was significantly enlarged. The canal stenosis index was also improved. Kyphosis was corrected and remained at 8.6±1.4o (P>0.05) 1 year postoperatively. Adjacent disc heights remained constant. Average Frankel grades were significantly improved at the end of follow-up. All 62 patients were neurologically assessed. Pain scores decreased at 6 months postoperatively, compared to before surgery (P<0.05). PARF provided excellent reduction for traumatic segmental kyphosis, and resulted in significant spinal canal clearance, which restored and maintained the vertebral body height of patients with Denis B TLBF with neurological deficits.

The effect of immunoglobulin treatment for hemolysis on the incidence of necrotizing enterocolitis - a meta-analysis.

OBJECTIVE: The application of intravenous immune globulin (IVIG) has been recommended for treating hemolysis in neonates for several years. But in clinical work, more than one study reported that IVIG treatment maybe increased the risk of NEC in hemolytic patients. In light of this situation, we performed this meta-analysis. MATERIALS AND METHODS: We searched in PubMed, Embase, Cochrane databases for English references, and in Wanfang, VIP, Cnki databases for Chinese references (all last launched on 2015/12/18). Ultimately, 5 studies (Including 4 Chinese articles) were incorporated into this meta-analysis. Odds ratio (OR) and weighted mean difference (WMD) were calculated using a random-effects or fixed-effects model, depending on the data type and heterogeneity of the included studies. RESULTS: (1) Baseline data including gestational age, gender and TBil between IVIG and control groups were compared in hemolytic infants, and showed no significance. (2) With respect to possible inducement of NEC, SGA and formula feeding were found no significance between IVIG and control groups. In contrast, birth weight was found significantly different between the two groups (WMD = 33.35; 95% CI, 20.70-46.01; p < 0.00001). (3) Regarding the incidence of NEC and mortality, the result showed that there was a significant difference between the IVIG and the control groups in the risk of NEC (OR: 4.53; 95% CI, 2.34-8.79; p < 0.00001). CONCLUSIONS: Our results indicate that IVIG treatment for hemolysis may increase the risk of NEC in infants. But it does not increase the risk of final mortality.

A new HLA-C*07 allele, C*07:02:70, identified in a Chinese individual.

A novel allele HLA-C*07:02:70 differs from HLA-C*07:02:01:01 by a single nucleotide at position 987 (C>T).

Effect of procyanidine on VEGFR-2 expression and transduction pathway in rat endothelial progenitor cells under high glucose conditions.

The protective effect of procyanidine and its oligomers against high glucose-mediated oxidative stress injury in endothelial progenitor cells (EPCs), and effect of procyanidin on vascular endothelial growth factor receptor-2 (VEGFR-2) expression and downstream signal pathway were analyzed in vitro. Rat bone marrow mononuclear cells were isolated, cultured under normal and high glucose (HG) conditions, and the changes in cell morphology observed. The EPCs were identified, and the oxidative stress products produced by EPCs (under normal and HG conditions) were quantified. Subsequently, an appropriate number of EPCs were cultured with and without procyanidin (OPC), and the MDA concentration and relative expression of VEGFR-2, AKT, IκB-α, and nuclear factor (NF)-κB were detected 1, 3, 5, and 7 days post-culture. We observed minor (round, translucent, gradually adhering) and significant (fusiform morphology/pebble distribution) cell morphological changes 3 and 7 days post-culture, respectively. Apoptosis and oxidative stress product release in EPCs cultured with HG increased significantly compared to the control group (P < 0.05). The oxidative stress product generation and relative expression of VEGFR-2, AKT, IkB-α, and NF-κB were not significantly affected by OPC addition in normal glucose conditions (P > 0.05); alternately, products generated as a result of oxidative stress were significantly reduced, the relative expression of VEGFR-2, AKT, and NF-κB protein was upregulated, and that of IκB-α was downregulated (P < 0.05) in HG + OPC EPCs. Therefore, procyanidin may promote cell proliferation by alleviating oxidative damage to EPCs under HG conditions, and upregulating VEGFR-2 expression and its downstream signal pathway.

Surgical treatment of Denis type B thoracolumbar burst fracture with neurological deficiency by paraspinal approach

We aimed to describe the surgical technique and clinical outcomes of paraspinal-approach reduction and fixation (PARF) in a group of patients with Denis type B thoracolumbar burst fracture (TLBF) with neurological deficiencies. A total of 62 patients with Denis B TLBF with neurological deficiencies were included in this study between January 2009 and December 2011. Clinical evaluations including the Frankel scale, pain visual analog scale (VAS) and radiological assessment (CT scans for fragment reduction and X-ray for the Cobb angle, adjacent superior and inferior intervertebral disc height, and vertebral canal diameter) were performed preoperatively and at 3 days, 6 months, and 1 and 2 years postoperatively. All patients underwent successful PARF, and were followed-up for at least 2 years. Average surgical time, blood loss and incision length were recorded. The sagittal vertebral canal diameter was significantly enlarged. The canal stenosis index was also improved. Kyphosis was corrected and remained at 8.6±1.4o (P>0.05) 1 year postoperatively. Adjacent disc heights remained constant. Average Frankel grades were significantly improved at the end of follow-up. All 62 patients were neurologically assessed. Pain scores decreased at 6 months postoperatively, compared to before surgery (P<0.05). PARF provided excellent reduction for traumatic segmental kyphosis, and resulted in significant spinal canal clearance, which restored and maintained the vertebral body height of patients with Denis B TLBF with neurological deficits.