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Sporulation and inoculation methods were studied to determine the pathogenicity of Ustilaginoidea albicans S Wang and JK Bai, the cause of white rice false smut, isolated in China. High sporulation was obtained using solid culture, liquid fermentation and double layer incubation system. In liquid culture, the culture media composition contributed to observed differences in sporulation. Potato sucrose broth was the optimal media to promote conidia production, increasing the concentration to up to 4.8 · 10 8 spores⁄ml. Inoculation by injection and spraying resulted in disease development, demonstrating that conidia of white rice false smut are virulent to rice plants, despite apparent differences in disease incidence. Estimates of mean disease severity were higher for injection than for spraying as assessed by percent infected panicles. The two methods resulted in disease severity ranging from 12.0 to 28.7% and 8.2 to 20.7%, respectively. Low temperature exposure after inoculation had a strong stimulatory effect on disease development.

European Journal of Rheumatology (Eur J Rheumatol) is an international, open access peer reviewed journal committed to promoting the highest standards of scientific exchange and education. The journal is published quarterly on January, April, July and October. The aim of the European Journal of Rheumatology is to cover various aspects of rheumatology for its readers, encompassing the spectrum of diseases with arthritis, musculoskeletal conditions, autoinflammatory diseases, connective tissue disorders, osteoporosis, translational research, the latest therapies and treatment programs. European Journal of Rheumatology publishes original articles, invited reviews, case based reviews, letters to the editor and images in rheumatology. The publication language of the journal is English. Accepted manuscripts are copy-edited for grammar, punctuation, and format. Once the publication process of a manuscript is completed, it is published online on the journal's webpage as an aheadof-print publication before it is included in its scheduled issue. A PDF proof of the accepted manuscript is sent to the corresponding author and their publication approval is requested within 2 days of their receipt of the proof.

Inadequate oxygen supply is probably one of the most important pathophysiological mechanisms of cardiomyocyte damage in ischemic heart disease. Tetramethylpyrazine (TMP, also known as ligustrazine) is the main active ingredient isolated from the rhizome of Ligusticum chuanxiong Hort. A previous study reported that the TMP could exert cardioprotective activity. This study aimed to explore the molecular mechanism of the protective effects of TMP on cardiomyocyte damage caused by hypoxia. The viability and apoptosis of cardiomyocytes H9c2 were detected using cell counting kit‐8 assay and annexin V‐FITC/PI staining, respectively. Quantitative reverse transcription polymerase chain reaction was conducted to measure the expression level of microRNA‐449a (miR‐449a). Cell transfection was performed to upregulate the expression level of miR‐449a or downregulate the expression level of sirtuin 1 (Sirt1). The protein expression levels of Sirt1 and key factors involved in cell apoptosis and phosphatidylinositol 3‐kinase/protein kinase 3 (PI3K/AKT) pathway were evaluated using western blot analysis. We found that the hypoxia incubation inhibited H9c2 viability, induced cell apoptosis, and inactivated the PI3K/AKT pathway. TMP treatment partially relieved the hypoxia‐caused H9c2 cell viability loss and apoptosis, as well as reversed the hypoxia‐caused inactivation of the PI3K/AKT pathway. Moreover, TMP partially alleviated the upregulation of miR‐449a in H9c2 cells caused by hypoxia. Overexpression of miR‐449a weakened the effects of TMP on hypoxia‐treated H9c2 cells. Furthermore, Sirt1 was a target gene of miR‐449a. Knockdown of Sirt1 also weakened the effects of TMP on hypoxia‐treated H9c2 cells. In conclusion, TMP partially relieved hypoxia‐caused cardiomyocytes H9c2 viability loss and apoptosis at least through downregulating miR‐499a, upregulating Sirt1, and then activating the PI3K/AKT pathway.