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BackgroundUlmus lamellosa(one of the ancient species ofUlmus) is an endemic and endangered plant that has undergone climatic oscillations and geographical changes. The elucidation of its demographic history and genetic differentiation is critical for understanding the evolutionary process and ecological adaption to forests in Northern China.ResultsPolymorphic haplotypes were detected in most populations ofU. lamellosavia DNA sequencing. All haplotypes were divided into three phylogeographic clades fundamentally corresponding to their geographical distribution, namely THM (Taihang Mountains), YM (Yinshan Mountains), and YSM (Yanshan Mountains) groups. The YSM group, which is regarded as ancestral, possessed higher genetic diversity and significant genetic variability in contrast to the YSM and YM groups. Meanwhile, the divergence time of intraspecies haplotypes occurred during the Miocene-Pliocene, which was associated with major Tertiary geological and/or climatic events. Different degrees of gene exchanges were identified between the three groups. During glaciation, the YSM and THM regions might have served as refugia forU. lamellosa. Based on ITS data, range expansion was not expected through evolutionary processes, except for the THM group. A series of mountain uplifts (e.g., Yanshan Mountains and Taihang Mountains) following the Miocene-Pliocene, and subsequently quaternary climatic oscillations in Northern China, further promoted divergence betweenU. lamellosapopulations.ConclusionsGeographical topology and climate change in Northern China played a critical role in establishing the current phylogeographic structural patterns ofU. lamellosa. These results provide important data and clues that facilitate the demographic study of tree species in Northern China.

Additional file 4: Figure S3. Correlation between geographic distance and pairwise FST/environmental distance for Ulmus lamellosa. (a), (b): relationship estimated by ITS and (c), (d): relationship estimated by Aat.

Additional file 2: Figure S1. The maximum likelihood tree of single-copy nuclear gene Aat haplotypes.

Additional file 3: Figure S2. Results of Bayesian clustering analysis conducted by STRUCTURE. The clustering patterns of ITS (a) and Aat (b) by three clusters (K = 3). The clustering patterns of Aat (c) by four clusters (K = 4).

Increasing evidence has accrued which indicates that mesenchymal stem cells (MSCs) have a potential clinical value in the treatment of certain diseases. Globally, nonalcoholic steatohepatitis (NASH) is a widespread disorder. In the present study, MSCs were isolated successfully from compact bone and a mouse model of NASH was established as achieved with use of a methionine-choline deficient (MCD) diet. Compact bone-derived MSCs transplantation reduced MCD diet-induced weight loss, hepatic lipid peroxidation, steatosis, ballooning, lobular inflammation and fibrogenesis. It was shown that MSCs treatment hampered MCD diet-induced proliferation of CD4+ IFN-γ+ and CD4+IL-6+ T spleen cells. In addition, CD4+IL-17+ lymphocytes that associated with anti-inflammation show little change in MCD as well as in MCD+MSCs splenocytes. We conclude that MSCs may have a potential clinical value upon NASH, through their capacity to suppress activation of CD4+ IFN-γ+ and CD4+IL-6+ lymphocytes.

Parthenolide, the principal sesquiterpene lactone present in medicinal plants such as feverfew, has anti-microbial, anti-inflammatory and anticancer activities. In the present study, we investigated the protective role of parthenolide against acute hepatitis in mice. Mice acute hepatitis were induced by Concanavalin A and treated by parthenolide in vivo. Results shown that parthenolide remarkably reduced the congestion and necroinflammation of the mice livers with Concanavalin A-induced acute hepatitis. Meanwhile, parthenolide treatment recover the liver function which indicated by decreased the serum alanine transaminase and alkaline phosphatase activities and promoted the expression of Ki67 in the livers of these mice. In addition, parthenolide administration suppressed the Concanavalin A-induced immune reaction, as indicated by the number of F4/80, CD49b and CD4 cells present in the liver. Furthermore, parthenolide also significantly reduced the expression of pro-inflammatory cytokines such as IFN-γ, TNF-α, IL-17A, IL-1β and IL-6 in lipopolysaccharide (LPS)-stimulated RAW264.7 cells in vitro. Moreover, parthenolide exposure decreased the phosphorylation of STAT3 and p38, and promoted the phosphorylation of p53 in RAW264.7 cells in vitro. In conclusion, parthenolide represents a drug candidate to protect the liver against Concanavalin A-induced acute hepatitis. The possible molecular mechanism involves the anti-inflammatory effects of parthenolide may by suppressing the STAT3/p38 signals and enhanced the p53 signals.