Despite these advances, botanical gardens are still underutilized in climate change research. To address this, we review recent progress and describe promising future directions for research and public engagement at botanical gardens.Chrysotile, which is classified as a class I carcinogen by the International Agency for Research on Cancer (IARC), has extensive application in the industry and can lead to lung or other cancers. However, whether chrysotile causes malignant mesothelioma and its molecular mechanism remain debatable. Thus, this study aimed to demonstrate the mesothelioma-inducing potential of chrysotile at the mesothelial cellular level and the function of microRNA-28 in malignantly transformed mesothelial MeT-5A cells. MeT-5A cells malignantly transformed by a nontoxic dose of chrysotile were named Asb-T, and miR-28 expression was downregulated in Asb-T cells. Restoration of miR-28 expression inhibited the proliferation, migration and invasion of Asb-T cells. We verified that IMPDH is a putative target of miR-28. The expression of IMPDH was significantly higher in Asb-T MeT-5A cells than in control cells, whereas the opposite trend was observed with miR-28 overexpression. Additionally, inhibition of IMPDH had similar effects as miR-28 overexpression. After miR-28 was elevated or IMPDH was inhibited, Ras activation was reduced, and its downstream pathways (the Erk and Akt signalling pathways) were inhibited. Surprisingly, the content of miR-28 in the blood of mesothelioma patients was higher than that in control subjects. Overall, nontoxic doses of chrysotile can cause malignant transformation of MeT-5A cells. Moreover, miR-28 inhibits the proliferation, migration and invasion of Asb-T MeT-5A cells, negatively regulates the expression of IMPDH through the Ras signalling pathway and may be an important therapeutic target.
  To evaluate the impact of preemptive metformin on the level of glycosylated hemoglobin (HbA1c) at 36weeks of pregnancy in women with gestational diabetes mellitus controlled by diet change (GDMA1).
 
  A randomized, double-blind, placebo-controlled trial was performed in a university hospital. Women with GDMA1 were recruited at 16-30weeks of pregnancy and randomized to oral metformin 500mg twice daily or identical placebo tablets to delivery. Level of HbA1c was taken at recruitment and at 36weeks of pregnancy. The primary outcome was the change in level of HbA1c at recruitment and 36weeks of pregnancy.
 
  Data from 106 participants were analyzed. The level of HbA1c during pregnancy increased significantly with a mean increase of 0.20%±0.31% (P<0.001; metformin) versus 0.27%±0.31% (P<0.001; placebo). An increment of 0.07% across trial arms was not significant (P=0.310). Mean birth weight was significantly lower in the metformin group (2.81±0.41kg vs 2.98±0.37kg; P=0.030). Rates of macrosomia (≥3.5kg; 0/53 [0%] vs 4/53 [8%]; P=0.123) and low birth weight (<2.5kg; 11/53 [21%] vs 5/53 [9%]; P=0.102) were not significantly different.
 
  Preemptive metformin did not prevent the level of HbA1c at 36weeks of pregnancy from rising nor significantly reduce the increase of HbA1c. Mean birth weight was significantly lower in the metformin arm with a non-significant trend to low birth weight, which is concerning.
 
  ISRCTN10845466.
 ISRCTN10845466.CE has been demonstrated to be a useful and powerful separation method for the characterization of charged and neutral molecules. Since the end of the 1980s and the development of the first commercialized CE device, the use of this separation method has continued to grow for academic and industrial research involving inexorably increasing of the number of CE users.  https://www.selleckchem.com/products/FK-506-(Tacrolimus).html  Whatever the application domain, each CE user is daily confronted to the same problems often based on basic calculations of separation properties. In order to help the community of CE users to get quickly and easily a lot of information, and desiring to provide a tool running on mobile platforms, CEToolbox has been developed as a free Android application. Within few clicks, CEToolbox offers extensive injection information as injected volume, total capillary volume, proportion and amount of injected sample, rinsing time, and electrical field. Moreover, three additional tabs allow to obtain the calculation of the viscosity and the conductivity of BGE, and the separation flow rates. Finally, a last tab is dedicated to the calculation of electroosmotic mobility and effective mobilities for a maximum of 20 compounds. CEToolbox, which can be downloaded for free on Google and F-Droid application stores, was developed to simplify the daily of CE users regardless of the CE devices.Maduramicin frequently induces severe cardiotoxicity in target and nontarget animals in clinic. Apoptotic and non-apoptotic cell death mediate its cardiotoxicity; however, the underlying non-apoptotic cell death induced by maduramicin remains unclear. In current study, a recently described non-apoptotic cell death "methuosis" caused by maduramicin was defined in mammalian cells. Rat myocardial cell H9c2 was used as an in vitro model, showing excessively cytoplasmic vacuolization upon maduramicin (0.0625-5 μg/mL) exposure for 24 h. Maduramicin-induced reversible cytoplasmic vacuolization of H9c2 cells in a time- and concentration-dependent manner. The vacuoles induced by maduramicin were phase lucent with single membrane and were not derived from the swelling of organelles such as mitochondria, endoplasmic reticulum, lysosome, and Golgi apparatus. Furthermore, maduramicin-induced cytoplasmic vacuoles are generated from micropinocytosis, which was demonstrated by internalization of extracellular fluid-phase marker Dextran-Alexa Fluor 488 into H9c2 cells. Intriguingly, these cytoplasmic vacuoles acquired some characteristics of late endosomes and lysosomes rather than early endosomes and autophagosomes. Vacuolar H+ -ATPase inhibitor bafilomycin A1 efficiently prevented the generation of cytoplasmic vacuoles and decreased the cytotoxicity of H9c2 cells triggered by maduramicin. Mechanism studying indicated that maduramicin activated H-Ras-Rac1 signaling pathway at both mRNA and protein levels. However, the pharmacological inhibition and siRNA knockdown of Rac1 rescued maduramicin-induced cytotoxicity of H9c2 cells but did not alleviate cytoplasmic vacuolization. Based on these findings, maduramicin induces methuosis in H9c2 cells via Rac-1 signaling-independent seriously cytoplasmic vacuolization.