Characterization of the complete chloroplast genome of Barbella flagellifera (Cardot) Nog. 1938 (Bryidae, Meteoriaceae).

Whether Barbella flagellifera (Cardot) Nog. belongs to Neodicladiella has not yet been determined, and a study of the complete chloroplast (cp) genome of B. flagellifera would aid in determining its evolutionary position. In this study, we aimed to sequence the complete cp genome of B. flagellifera, an epiphytic species found in tropical and subtropical forests. The complete cp genome is 125,025 base pairs (bp) long and appears as a typical quadrilateral structure with a large single-copy (86,854 bp), a small single-copy (18,473 bp), and a pair of inverted repeats (19,698 bp). The overall GC content of the sequence is 41.0% and the genome encodes 127 genes, including 82 protein-coding genes, 37 tRNAs, and eight rRNAs. Phylogenetic analysis reveals that B. flagellifera clustered into a clade with other Hypnales groups with high bootstrap support. The complete cp genome presented here will provide helpful information for species identification of Barbella genus and Neodicladiella genus in Meteoriaceae.

IL-33 Can Promote the Process of Pulmonary Fibrosis by Inducing the Imbalance Between MMP-9 and TIMP-1.

IL-33 played an important role in inflammatory diseases as evidenced by their high levels of expression in diseased tissues. Previous studies showed that IL-33/ST2L signal transduction pathway participated in epithelial-mesenchymal transition (EMT) of A549 cells. Cytokine IL-1ß can increase the expression of MMPs by activating NF-kB. The excessive or inappropriate expression of MMP-9 may randomly and non-selectively destroy the extracellular matrix. TIMP-1 (tissue inhibitor of MMP-9) effects on ebb and flow of ECM by inhibiting activation of MMP-9. Therefore, IL-33 may take part in the process of pulmonary fibrosis by regulating expressions of MMP-9 and TIMP-1. To explore the acting mechanism of IL-33 in pulmonary fibrosis, proliferation of the human embryonic lung fibroblasts and expressions of related signal molecules was analyzed in vitro. We cultured HELF cells and stimulated HELF with rhIL-33 at different time points (24, 48, 72 h) and different concentrations respectively. The expression of the receptor ST2L was analyzed by RT-PCR and the proliferative rate of HELF was tested by MTT. The expressions of collagen IV, MMP-9, TIMP-1, and critical signal transducer TRAF-6 and NF-kappaB were tested by Western blotting. The rhIL-33 can promote proliferation of HELF and the concentration of 10 ng/ml was most significant at 72 h (P < 0.05). Hence, this experiment chose 10 ng/ml as stimulated concentration at following experiments. The expressions of collagen IV, MMP-9, TIMP-1, TRAF-6, and NF-kappaB increased and then reduced in protein levels at different time points (0, 6, 12, 24, 48, 72 h) (P < 0.05). IL-33 participates in the production of profibrotic cytokines and formation of mesenchymal substances in early inflammatory responses of pulmonary fibrosis. IL-33 can regulate deposition of ECM and promote the process of pulmonary fibrosis by inducing the imbalance between MMP-9 and TIMP-1.

The complete chloroplast genome of Atraphaxis jrtyschensis (polygonaceae), an endemic and endangered desert shrub to Xinjiang, China.

Atraphaxis jrtyschensis (Polygonacae) is an endangered desert shrub endemic to China in Xinjiang province with great ecological importance for sand fixation. However, its genomic resources are still very limited. Here, we generated the first chloroplast (cp) genome of A. jrtyschensis using genome skimming sequencing. The whole cp genome is 164,192 bp and comprises 130 genes, including 83 protein-coding genes, 37 tRNA genes, 8 rRNA genes, and 2 pseudogenes (rpl23). The overall GC content of A. jrtyschensis cp genome is 37.5%. The phylogenic analysis placed A. jrtyschensis at the base of Trib Rumiceae, which contained the genera Rheum and Oxyria. This study will be useful for future researches to investigate the conservation genetics and potential applications in sand fixation of the endangered desert shrub.

Comparison of gemcitabine combined with targeted agent therapy versus gemcitabine monotherapy in the management of advanced pancreatic cancer.

PURPOSE: Targeted therapy has brought great clinical benefits for patients with multiple solid tumors, but its effects in patients with locally advanced/metastatic pancreatic cancer (LA/MPC) are disputed. This systematic evaluation compared the efficacy and safety profiles of gemcitabine combined with targeted agents (GEM + TA) versus gemcitabine administered as monotherapy or combined with placebo (GEM ± PLC) in LA/MPC patients. METHODS: PubMed and EMBASE were searched for relevant randomized controlled trials published on or before April 30, 2013. The primary end points were overall survival (OS) and progression-free survival (PFS); the secondary end points were 1-year survival rate, objective response rate (ORR), and toxicity rates (TRs), defined as the prevalence of grade 3/4 adverse events. The systematic evaluation was performed by using Review Manager version 5.1.7. FINDINGS: A total of 10 randomized controlled trials involving 3899 patients (2195 males; mean age, 63.6 years) were included in the systematic evaluation. The results reported that there was no significant difference in OS (hazard ratio [HR] = 0.97 [P = 0.85]), PFS (HR = 0.95 [P = 0.14]), or ORR (odds ratio [OR] = 0.95 [P = 0.69]) between GEM + TA and GEM ± PLC. However, a marginal difference in 1-year survival rate (OR = 0.80 [P = 0.05]) between the 2 groups was observed. The grade 3/4 TRs of anemia, diarrhea, nausea, neutropenia, thrombocytopenia, and vomiting were not significantly different between the 2 groups. However, the prevalence of grade 3/4 rash was significantly greater in the GEM + TA group (OR = 8.31 [P < 0.01]). IMPLICATIONS: Based on the results from this analysis, the addition of targeted agents to a regimen of gemcitabine treatment does not bring survival benefits except 1-year survival rate to patients with LA/MPC.

Association between LMP2/LMP7 genetic variability and the metastasis risk of ovarian cancer in Chinese women in Beijing.

LMP2/LMP7 gene (LMP, low molecular mass protein) perform a critical role in the foreign antigen processing via the major histocompatibility complex-I (MHC-I) complex CD8(+) cytotoxic T lymphocytes (CTL) pathway. This study was designed to investigate whether the sequence variants in LMP2/LMP7 gene would increase the risk of ovarian cancer in the Chinese population. Total of 235 patients with ovarian cancer and 338 normal controls were recruited. Two polymorphisms of LMP2-60 (Arg→His) and LMP7-145 (Gln→Lys) were identified by PCR-RFLP (RFLP, restriction fragment length polymorphism) method. The association of LMP2/LMP7 gene variations with ovarian cancer was assessed by logistic regression analysis. The results revealed that LMP7-145 Gln/Lys and Lys/Lys alleles were associated with the risk of ovarian cancer (P=0.002, OR=2.47; P<0.001, OR=3.23). Meanwhile, the relationship between the LMP7-145 polymorphism and the lymph node metastasis and tumor distant metastasis were also found. No statistical correlation between any of the LMP2-60 polymorphic genotypes and the ovarian cancer clinicopathological characteristics were observed (P>0.05). These results suggested that LMP7 genetic variant could increase the susceptibility to ovarian cancer development; especially increase the risk of lymph node and tumor distant metastasis.

The function of human epidermal growth factor receptor-3 and its role in tumors (Review).

Human epidermal growth factor receptor-3 (HER-3) is the third member of the HER family. It was previously considered not to contain tyrosine kinase activity and catalytic activity and the intracellular region of HER-3 could not bind ATP and be auto-phosphorylated. Thus, the clinical value of HER-3 was ignored. Currently, biochemical analysis has confirmed that the kinase domain of HER-3 is a specific allosteric activator; it acts as a functional activator to activate the recipient kinase (HER-1, HER-2, HER-4). With the in-depth knowledge of its structure and function, studies on the relationship of HER-3 and human tumors are rapidly increasing. HER-3 is closely related to tumorigenesis, progression and metastasis. HER-3 is involved in resistance to targeted therapy, and may serve as a new therapeutic target. The expression of HER-3 helps to predict prognosis and treatment efficacy. HER-3 has become a focus of concern in the HER family and has gained significant attention in the search for cancer treatment.

Lack of association between the unique LMP2 gene polymorphism and the outcome of lung cancer in a population of Chinese Han nationality.

Lung cancer is characterized by a widely ranging incidence variation; it is the most common cancer in China. In this study we will assess the association of low-molecular-mass protease 2 (LMP2) gene codon 60 polymorphism with the risk of lung cancer. Genomic DNA of peripheral blood mononuclear cells was isolated from 207 patients with lung cancer and 264 healthy controls. DNA direct sequencing and polymerase chain reaction-restriction fragment length polymorphism were performed to scrutinize LMP2 gene codon 60 polymorphism. The risk of LMP2 gene polymorphism in lung cancer was assessed using an unconditional logistic regression model adjusted by the confounding factors. As a result of DNA direct sequencing, the LMP2 codon 60 polymorphic substitution of the nucleotide was CGC → TGC in Chinese individuals, not CGC → CAC as reported in other ethnic populations. In histology-specific analysis and TNM stages, there was no apparent association between this LMP2 gene polymorphism and any of the histologic types or TNM stages of lung cancer using the Arg/Arg genotypes as the reference group (all p values > 0.05). These results suggest that the polymorphic site is unique in the Chinese population of Han nationality at the LMP2 codon 60 loci (Arg60Cys), but a lack of association with lung cancer exists.