Definitions of targeted movement task parameters (error, deviation, toe-height).

The continuous line shows the trajectory of the big toe of the moving leg.</p

The big toe trajectory of the ipsilateral leg targeted movement tasks of a representative control (blue lines) and stroke (red lines) participant.

Circle: starting position; triangle: target location; continuous line: trajectory of the big toe; dotted line: direct line between the starting position and target in the sagittal plane.</p

Results of correlation and regression analysis.

Background and purposeMotor deficits of the ipsilateral lower limb could occur after stroke and may be associated with walking performance. This study aimed to determine whether the accuracy and movement path of targeted movement in the ipsilateral lower limb would be impaired in the chronic stage of stroke and whether this impairment would contribution to gait.MethodsTwenty adults with chronic stroke and 20 age-matched controls went through Mini Mental Status Examination (MMSE), and a series of sensorimotor tests. The targeted movement tasks were to place the big toe ipsilateral to the lesion at an external visual target (EXT) or a proprioceptive target (PRO, contralateral big toe) with eyes open (EO) or closed (EC) in a seated position. A motion analysis system was used to obtain the data for the calculation of error distance, deviation from a straight path, and peak toe-height during the targeted movement tasks and gait velocity, step length, step width and step length symmetry of the lower limb ipsilateral to the brain lesion during walking.ResultsThe stroke group had significantly lower MMSE and poorer visual acuity on the ipsilateral side, but did not differ in age or other sensorimotor functions when compared to the controls. For the targeted movement performance, only the deviation in PRO-EC showed significant between-group differences (p = 0.02). Toe-height in both EXT-EO and in PRO-EO was a significant predictor of step length (R2 = 0.294, p = 0.026) and step length symmetry (R2 = 0.359, p = 0.014), respectively.Discussion and conclusionsThe performance of ipsilateral lower limb targeted movement could be impaired after stroke and was associated with step length and its symmetry. The training of ipsilateral targeted movement with unseen proprioceptive target may be considered in stroke rehabilitation.</div

Basic characteristics, targeted movement performance and gait.

Ipsilateral and contralateral side refers to the side Ipsilateral and contralateral to the stroke, respectively.</p

Correlations among metabolic syndrome, <i>H</i>. <i>pylori</i> status and other factors.

<p>† data expressed as coefficient (<i>p</i> value)</p><p>Correlations among metabolic syndrome, <i>H</i>. <i>pylori</i> status and other factors.</p

Characteristics of metabolic syndrome status between different age groups.

<p>† data expressed as No (%)</p><p>Characteristics of metabolic syndrome status between different age groups.</p

<i>H</i>. <i>pylori</i> antibody status, proportion of metabolic syndrome and HOMA-IR in subjects greater or less than 50 years of age.

<p>† MS: metabolic syndrome</p><p>‡ <i>p</i>-value of Cochran-Mantel-Haenszel test for the independence of age and <i>H</i>. <i>pylori</i> antibody controlling for the factor of metabolic syndrome.</p><p><i>H</i>. <i>pylori</i> antibody status, proportion of metabolic syndrome and HOMA-IR in subjects greater or less than 50 years of age.</p

Predictors of metabolic syndrome by multivariate logistic regression analysis.

<p>†95% CI: 95% confidence interval</p><p>Predictors of metabolic syndrome by multivariate logistic regression analysis.</p

Characteristics of Study Subjects.

<p>*: mean±standard deviation (SD)</p><p><i>H</i>. <i>pylori</i> Ab: <i>Helicobacter pylori</i> antibody</p><p>HOMA-IR: Homeostasis model assessment of insulin resistance</p><p>BMI: body mass index</p><p>SBP: systolic blood pressure</p><p>DBP: diastolic blood pressure</p><p>TG: triglyceride</p><p>HDL: high density lipoprotein</p><p>LDL: low density lipoprotein</p><p>VLDL: very low density lipoprotein</p><p>TCHOL: total cholesterol</p><p>FBG: fasting blood glucose</p><p>HbA1c: glycosylated hemoglobin</p><p>AG: average glucose</p><p>AST: aspartate aminotransferase</p><p>ALT: alanine aminotransferase</p><p>HS-CRP: high sensitivity C-reactive protein</p><p>TNF-α: tumor necrosis factor α</p><p>Characteristics of Study Subjects.</p

Activation of JNK Contributes to Evodiamine-Induced Apoptosis and G₂/M Arrest in Human Colorectal Carcinoma Cells: A Structure-Activity Study of Evodiamine

<div><p>Evodiamine (EVO; 8,13,13b,14-tetrahydro-14-methylindolo[2′3′-3,4]pyrido[2,1-b]quinazolin-5-[7H]-one derived from the traditional herbal medicine <i>Evodia rutaecarpa</i> was reported to possess anticancer activity; however, the anticancer mechanism is still unclear. In this study, we investigated the anticancer effects of EVO on human colon COLO205 and HT-29 cells and their potential mechanisms. MTT and lactate dehydrogenase (LDH) release assays showed that the viability of COLOL205 and HT-29 cells was inhibited by EVO at various concentrations in accordance with increases in the percentage of apoptotic cells and cleavage of caspase-3 and poly(ADP ribose) polymerase (PARP) proteins. Disruption of the mitochondrial membrane potential by EVO was accompanied by increased Bax, caspase-9 protein cleavage, and cytochrome (Cyt) c protein translocation in COLO205 and HT-29 cells. Application of the antioxidant N-acetyl-L-cysteine (NAC) inhibited H₂O₂-induced reactive oxygen species (ROS) production and apoptosis, but did not affect EVO-induced apoptosis of COLO205 or HT-29 cells. Significant increases in the G₂/M ratio and cyclinB1/cdc25c protein expression by EVO were respectively identified in colon carcinoma cells via a flow cytometric analysis and Western blotting. Induction of extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) protein phosphorylation was detected in EVO-treated cells, and the JNK inhibitor, SP600125, but not the ERK inhibitor, U0126, inhibited EVO-induced phosphorylated JNK protein expression, apoptosis, and G₂/M arrest of colon carcinoma cells. Data of the structure-activity analysis showed that EVO-related chemicals containing an alkyl group at position 14 were able to induce apoptosis, G₂/M arrest associated with increased DNA ladder formation, cleavage of caspase-3 and PARP, and elevated cycB1 and cdc25c protein expressions in COLO205 and HT-29 cells. Evidence supporting JNK activation leading to EVO-induced apoptosis and G₂/M arrest in colon carcinoma cells is provided, and alkylation at position 14 of EVO is a critical substitution for treatment of colonic cancer.</p></div