Descriptions of Leptolaimus sinensis sp. nov. and Perspiria brevicaudata sp. nov. (Nematoda) from the Yellow Sea, China.

Two new free-living marine nematodes which were collected at silt beach of Rizhao along the Yellow Sea are identified here as Leptolaimus sinensis sp. nov. and Perspiria brevicaudata sp. nov. Leptolaimus sinensis sp. nov. is characterized by annulated cuticle with lateral alae, 2 µm in width; buccal cavity cylindrical; cephalic setae 2 µm long; amphidial fovea unispiral, circular in outline; six to seven evenly spaced tubular precloacal supplements and 23-29 continuous alveolar supplements extending from cloaca to level of the base of buccal cavity; spicules slender, slightly arcuate; gubernaculum with dorso-caudal apophysis; tail conico-cylindrical, about 6 times cloacal body diameter in males and elongated in females, about 9 times anal body diameter in length. Perspiria brevicaudata sp. nov. is characterized by having four cephalic setae and four cervical setae; small buccal cavity with dorsal tooth and minute ventral tooth; amphidial fovea unispiral, looking like double circle in outline, surrounded partially by cuticle striations; spicules arcuate with ventral velum, handle-like proximally and tapered distally; gubernaculum plate-shaped, without apophysis; twelve winged precloacal supplements present. Updated identification keys for group of Leptolaimus species characterized by the presence of both alveolar and tubular precloacal supplements and for species of Perspiria are also given.

Cyclic peptide *CRRETAWAC* attenuates fibronectin-induced cytokine secretion of human airway smooth muscle cells by inhibiting FAK and p38 MAPK.

α5ß1 integrin is highly expressed in airway smooth muscle cells and mediate the adhesion of airway smooth muscle cells to fibronectin to regulate airway remodelling in asthma. This study aimed to investigate the effects of synthetic cyclic peptide *CRRETAWAC* on fibronectin-induced cytokine secretion of airway smooth muscle cells and the underlying mechanism. Human airway smooth muscle cells were isolated and treated with fibronectin, IL-13, *CRRETAWAC* peptide, α5ß1 integrin-blocking antibody, FAK inhibitor or p38 MAPK inhibitor. The transcription and secretion of eotaxin-1 and RANTES were detected by real-time PCR and ELISA, respectively. The phosphorylation of FAK and MAPKs including p38, ERK1/2 and JNK1/2 was detected by Western blot analysis. The transcription and secretion of eotaxin-1 and RANTES increased in airway smooth muscle cells cultured in fibronectin-coated plates. However, α5ß1 integrin-blocking antibody, *CRRETAWAC* peptide, FAK inhibitor or p38 MAPK inhibitor significantly reduced mRNA levels and the secretion of eotaxin-1 and RANTES in airway smooth muscle cells cultured in fibronectin-coated plates. In addition, the phosphorylation of FAK and p38 MAPK was significantly increased in airway smooth muscle cells cultured in fibronectin-coated plates compared to the cells cultured in uncoated plates and was significantly reduced in airway smooth muscle cells treated with *CRRETAWAC* peptide. Fibronectin induces cytokine synthesis and secretion of airway smooth muscle cells. Peptide *CRRETAWAC* antagonizes fibronectin-induced cytokine synthesis and secretion of airway smooth muscle cells via the inhibition of FAK and p38 MAPK, and is a potential agent for the therapy of asthma.

A special subtype of POEMS syndrome: IgG4 subtype.

Both POEMS syndrome and IgG4 related diseases are uncommon and clinical manifestations have been multifarious and nonspecific. There is still no literature describing the relationships between these two diseases. This study describes a case of a 33-year-old woman with POEMS syndrome, who had high serum IgG4 concentration and monoclonal IgG4 positive plasmacyte tissue infiltration. This is the first available report of the IgG4 subtype of POEMS syndrome. It is found that the best treatment is to find a novel therapy that targets the plasma cells directly.

CXCL12 G801A polymorphism and cancer risk: An updated meta-analysis.

Many studies have reported the relationship between CXCL12 G801A polymorphism and cancer risk, with conflicting results. In this study, we tried to clarify the possibility that this polymorphism may increase cancer risk by conducting an updated meta-analysis. PubMed and EMbase were searched for case-control studies regarding the association of the gene polymorphism and cancer risk. Data were extracted and odds ratios (ORs) with 95% confidence intervals (95% CIs) were used to assess the strength of the association. Heterogeneity among articles and publication bias was also assessed. Significantly increased risk for cancer was found (A vs. G: OR=1.26, 95% CI=1.13-1.40, P<0.01; AA+AG vs. GG: OR=1.33, 95% CI=1.16-1.52, P<0.01). In subgroup analysis, statistically elevated cancer risk was found in both Asian and Caucasian populations (for Asian, AA+AG vs. GG: OR=1.74, 95% CI=1.22-2.47, P<0.01; for Caucasian, AA+AG vs. GG: OR=1.24, 95% CI=1.09-1.42, P<0.01). Our result indicated that CXCL12 G801A polymorphism is a risk factor for cancer. To validate the finding, further large-size case-control studies are warranted.