Schizandrol A: a lignan from Schisandra chinensis

The title compound (systematic name: 1,2,3,10,11,12-hexa­meth­oxy-6,7-dimethyl-5,6,7,8-tetra­hydro­dibenzo[a,c]cyclo­oc­ten-6-ol), C24H32O7, has a dibenzocyclo­octa­diene skeleton. There are three mol­ecules in the asymmetric unit, which are related by a pseudo-translation in the direction of the c axis. Nevertheless, the three mol­ecules differ in the torsion angle of one of the meth­oxy groups. The dihedral angles between the two aromatic rings are 62.39 (10), 62.65 (10) and 61.84 (10)° for the three mol­ecules. The crystal packing is stabilized by a series of O—H⋯O and C—H⋯O hydrogen bonds, as well as C—H⋯π inter­actions

The Statistical Analysis of a Certain Kind of Sales Diffusion Model

The essay works out MLE (Maximum Likelihood Estimation) of probability model parameter about the third sales diffusion curve given by ZHENG Zukang and researches the existence of the estimation. Besides, this essay inspects the accuracy of the estimation via Monte Carlo simulation and throws light on methods of essay by simulated data.Key words: Sales diffusion model; Maximum Likelihood Estimation; Monte Carlo simulatio

Activated Protein C Induces Endoplasmic Reticulum Stress and Attenuates Lipopolysaccharide-Induced Apoptosis Mediated by Glycogen Synthase Kinase-3β

This study investigated the relationship between antiapoptotic activities induced by activated protein C and endoplasmic reticulum stress. In this study, it was observed that activated protein C elicited a rise in glucose-regulated protein 78 and glycogen synthase kinase-3β and inhibited apoptosis in human umbilical vein endothelial cells induced by lipopolysaccharide. Calcium inhibition did not alter the antiapoptotic effect of activated protein C. The antiapoptotic efficiency of activated protein C was reduced in human umbilical vein endothelial cells following treatment with glycogen synthase kinase-3β-siRNA. In summary, activated protein C induced endoplasmic reticulum stress and attenuated lipopolysaccharide-induced human umbilical vein endothelial cell apoptosis mediated by glycogen synthase kinase-3β

The Effect of Adoptive Immunotherapy after Percutaneous Microwave Ablation in Recurrent Hepatocellular Carcinoma Patients with Hepatitis B: A Preliminary Study

To observe the influence of adoptive immunotherapy combination with percutaneous microwave ablation (PMWA) on peripheral blood examination, hepatic function examination and serum alpha fetoprotein (AFP) in recurrent hepatocellular carcinoma (HCC) patients with hepatitis B. Fourteen recurrent HCC patients with 31 lesions (D≤6.0cm, fewer than four tumors) were treated with radical PMWA and continuous four courses of adoptive immunotherapy, which were administrated at 1, 2, 3 and 4 months after PMWA, respectively. Under sonographic guidance, tumor lysate-pulsed DCs (1ml) were injected into bilateral groin lymph nodes at 9th day, while CTL (25ml) were injected into the abdominal cavity at 11th day and CIK (100ml) was infused intravenously at 14th day after hemospasis in one course of treatment, respectively. Peripheral blood examination, serum AFP and hepatic function were reviewed 1, 3, 6 months after adoptive immunotherapy. The number of white blood cell (WBC), lymphocyte (LYM), serum albumin (ALB) and cholinesterase (CHE) were detected increase significantly at 3 and 6 months after therapy compared to pre-therapy (p0.05). Platelet (PLT) was detected increased significantly at 6 months after therapy (p0.05) compared to pre-therapy. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were detected decreased significantly at 1, 3 and 6 months after therapy (p0.05). As to serum AFP, it was detected decreased gradually, while there was no difference during the follow-up (6-16 months). No severe adverse effects were observed. Adoptive immunotherapy prescribed soon after PMWA was safe and ameliorated the laboratory examination and the immunity status of recurrent HCC patients, which may improve the prognosis

MATH5 controls the acquisition of multiple retinal cell fates

Math5-null mutation results in the loss of retinal ganglion cells (RGCs) and in a concurrent increase of amacrine and cone cells. However, it remains unclear whether there is a cell fate switch of Math5-lineage cells in the absence of Math5 and whether MATH5 cell-autonomously regulates the differentiation of the above retinal neurons. Here, we performed a lineage analysis of Math5-expressing cells in developing mouse retinas using a conditional GFP reporter (Z/EG) activated by a Math5-Cre knock-in allele. We show that during normal retinogenesis, Math5-lineage cells mostly develop into RGCs, horizontal cells, cone photoreceptors, rod photoreceptors, and amacrine cells. Interestingly, amacrine cells of Math5-lineage cells are predominately of GABAergic, cholinergic, and A2 subtypes, indicating that Math5 plays a role in amacrine subtype specification. In the absence of Math5, more Math5-lineage cells undergo cell fate conversion from RGCs to the above retinal cell subtypes, and occasionally to cone-bipolar cells and Müller cells. This change in cell fate choices is accompanied by an up-regulation of NEUROD1, RXRγ and BHLHB5, the transcription factors essential for the differentiation of retinal cells other than RGCs. Additionally, loss of Math5 causes the failure of early progenitors to exit cell cycle and leads to a significant increase of Math5-lineage cells remaining in cell cycle. Collectively, these data suggest that Math5 regulates the generation of multiple retinal cell types via different mechanisms during retinogenesis