Best Core Stabilization for Anticipatory Postural Adjustment and Falls in Hemiparetic Stroke

Objectives

To compare the effects of conventional core stabilization and dynamic neuromuscular stabilization (DNS) on anticipatory postural adjustment (APA) time, balance performance, and fear of falls in chronic hemiparetic stroke.

Dendritic arborization and axon trajectory of neurons in the hypothalamic arcuate nucleus of the rat--updated

Neurons in the hypothalamic arcuate nucleus (arcuate neurons) were traced on Golgi-impregnated sections. Dendrites of arcuate neurons showed characteristic orientation patterns. Dendrites along the lateral side follow the convex border of the nucleus by running parallel to the tanycyte processes. Neurons located in the ventrolateral portion of the nucleus have dendrites running parallel to the basal surface of the hypothalamus. Fine, beaded axons of arcuate neurons project mostly ventrally, and less frequently dorsally and dorsolaterally. Ventrally projecting axons converge towards the tuberoinfundibular sulcus which emerges into the ventral portion of the arcuate nucleus from below.     

电针对实验性类风湿性关节炎大鼠海马中C—fos表达的影响

以 Freund氏完全佐剂复制的实验性类风湿性关节炎 (RA) ,选用悬钟、昆仑穴 ,采用免疫组织化学等方法 ,观察电针 (EA)对实验性 RA海马中 c-fos表达的影响及其痛阈的变化 ,进一步探讨EA抗炎镇痛的中枢作用机制。结果显示电针对实验性 RA有确切的抗炎镇痛效应 ,可以抑制炎症痛模型的 FL I阳性细胞的表达。对探讨针刺对 RA的抗炎镇痛中枢作用机制具有一定的参考价值。     

Experimental Oncology Differential expression of TIS21 and TIS1 genes in the various organs of Balb/c mice,thymic carcinoma tissues and human cancer cell lines

As a part of a series of investigations on the functions of TIS21 and TIS1 genes, we measuredin vivo 12-O-tetradecanoylphorbol-13-acetate (TPA) inducibility of primary response genes (TIS21, TIS8 and TIS1) in the Balb/c mice and the changes of TIS gene expression in thymic carcinoma tissues and A549 and NCIH69 human lung cancer cell lines.In vivo induction of the TIS genes (TIS21, –8 and –1) by intraperitoneal injection of TPA was dramatic only at the needle contact site,i.e. in the abdominal muscle, not in the thigh muscle. Expression of TIS21 and TIS1 in the Balb/c mice thymus, lung, stomach and spleen was very strong (Lim IK et al. 1994a), regardless of TPA injection. Thymic carcinoma tissues developed in SV40-T-antigen-containing transgenic mice did not express TIS21 and TIS1, and expressed TIS8 weakly. Interestingly, induction of TIS21 expression was obliterated in the human lung cancer cells; A549 cells completely lost the ability to express TIS21 after a combined treatment of TPA and cycloheximide. We also measured the induction of TIS genes by TPA and/or cycloheximide in Raw264.7 mouse macrophage cells and U937 human histiocytic lymphoma cells. However, the induction profile was quite different; repressed and deregulated expression in the U937 cells as compared to rapid and transient induction of TIS genes in the Raw264.7 cells. These data may suggest a repressed expression of TIS21 and TIS1 in the cancer tissue and cells derived from the organs that constitutively express TIS21 in mice and in human cancer cells.Abbreviations TPA 12-O-tetradecanoylphorbol-13-acetate - PBS phosphate-buffered saline - FBS fetal bovine serum     

Induction of growth inhibition of 293 cells by downregulation of the cyclin E and cyclin-dependent kinase 4 proteins due to overexpression of TIS21

We earlier reported that TIS21 mRNA expression was markedly decreased in A549 and NCIH69 human lung cancer cells and in thymic carcinoma tissues obtained from transgenic mice containing simian virus 40 large T antigen (J Cancer Res Clin Oncol 121:279–284, 1995). To determine how TIS21 inhibits growth, we made 293 cells that constitutively expressed TIS21 protein. The constitutive TIS21 expresser lines C9 and C11 grew to a lower saturation density than did those in the vector-transfected clones (V7 and V10) and antisense-transfected clones (AS1 and AS4), and the size of the C9 and C11 cells increased significantly after transfection with TIS21 cDNA. The serum-stimulated cell cycle was analyzed by fluorescence-activated cell sorting after double thymidine treatment; V10 progressed normally through the cell division cycle, but C9 and C11 cells accumulated continuously in G₁ phase until 36 h after treatment. On the other hand, the progression of cells that had already entered to S or G₂/M phase was not inhibited. When cell-cycle regulatory proteins were measured, C9 and C11 cells showed significantly reduced synthesis of cyclin E and cyclin-dependent kinase (cdk) 4 as well as a decrease in cyclin E–associated cdk activity. These observations led us to conclude that TIS21 overexpression in G₁ phase decreased the amounts of cyclin E and cdk4, thereby decreasing the activity of cdks at the G₁-S transition. Mol. Carcinog. 23:25–35, 1998. © 1998 Wiley-Liss, Inc.     

Regulation of prostaglandin synthase-1 and prostaglandin synthase-2

It has been assumed that the rate-limiting step in the ligand-induced synthesis of prostaglandins is the release of arachidonic acid from membrane phospholipid stores as a result of the activation of phospholipase. The assumption has been that the arachidonic acid is converted to PGH₂ by the constitutive prostaglandin synthase/cyclooxygenase EC1.14.99.1 (PGS-1) enzyme present in cells. In this model, PGS-1 is proposed to be present in excess, and the production of arachidonic acid is thought to be rate limiting. However, a second prostaglandin synthase gene, PGS-2 has recently been described. The PGS-2 gene is induced by a variety of ligands, in cells as diverse as fibroblasts, monocytes, macrophages, smooth muscle cells, ovarian granulosa cells, epithelial cells, endothelial cells, and neurons. Moreover, PGS-2 induction is inhibited in nearly all contexts by glucocorticoids. It seems likely, therefore, that the regulation of PGS-2 expression plays a critical role in the production of prostanoids, both in normal physiological processes and in pathophysiological processes involving these paracrine mediators. In this review, we consider the regulation of the two genes, PGS-1 and PGS-2, that encode the isoforms of prostaglandin synthase.     

Pharmacodynamics of curcumin as DNA hypomethylation agent in restoring the expression of Nrf2 via promoter CpGs demethylation

Prostate cancer (PCa) is one of the most deadly malignancies among men in the United States. Although localized prostate cancer can be effectively treated via surgery or radiation, metastatic disease is usually lethal. Recent evidence suggests that the development and progression of human prostate cancer involves complex interplay between epigenetic alterations and genetic defects. We have recently demonstrated that Nrf2, a master regulator of cellular antioxidant defense systems, was epigenetically silenced during the progression of prostate tumorigenesis in TRAMP mice. The aim of this study is to investigate the potential of curcumin (CUR), a dietary compound that we have reported to be able to prevent the development of prostate cancer in TRAMP mice, as a DNA hypomethylation agent. Using bisulfite genomic sequencing (BGS), treatment of TRAMP C1 cells we showed that CUR reversed the methylation status of the first 5 CpGs in the promoter region of the Nrf2 gene. Methylation DNA immunoprecipitation (MeDIP) analysis revealed that CUR significantly reduced the anti-mecyt antibody binding to the first 5 CpGs of the Nrf2 promoter, corroborated the BGS results. Demethylation of Nrf2 was found to be associated with the re-expression of Nrf2 and one of its downstream target gene, NQO-1, one of the major anti-oxidative stress enzymes, both at the mRNA and protein levels. Taken together, our current study suggests that CUR can elicit its prostate cancer chemopreventive effect, potentially at least in part, through epigenetic modification of the Nrf2 gene with its subsequent induction of the Nrf2-mediated anti-oxidative stress cellular defense pathway.