Cutoff Point of Mini-Balance Evaluation Systems Test Scores for Elderly Estimated by Center of Pressure Measurements by Linear Regression and Decision Tree Classification.

BACKGROUND: Understanding balance ability and assessing the risk of possible falls are very important for elderly rehabilitation. The Mini-Balanced Evaluation System Test (Mini-BESTest) is an important survey for older adults to evaluate subject balance, but it is not easy to complete due to various limitations of physical activities, including occasional fear of injury. A center of pressure (CoP) signal can be extracted from a force pressure plate with a short recording time, and it is relatively achievable to ask subjects to stand on a force pressure plate in a clinical environment. The goal of this study is to estimate the cutoff score of Mini-BESTest scores from CoP data. METHODS: CoP signals from a human balance evaluation database with data from 75 people were used. Time domain, frequency domain, and nonlinear domain parameters of 60 s CoP signals were extracted to classify different cutoff point scores for both linear regression and a decision tree algorithm. Classification performances were evaluated by accuracy and area under a receiver operating characteristic curve. RESULTS: The correlation coefficient between real and estimated Mini-BESTest scores by linear regression is 0.16. Instead of linear regression, binary classification accuracy above or below a cutoff point score was developed to examine the CoP classification performance for Mini-BESTest scores. The decision tree algorithm is superior to regression analysis among scores from 16 to 20. The highest area under the curve is 0.76 at a cutoff point score of 21 for the CoP measurement condition of eyes opened on the foam, and the corresponding classification accuracy is 76.15%. CONCLUSIONS: CoP measurement is a potential tool to estimate corresponding balance and fall survey scores for elderly rehabilitation and is useful for clinical users.

Efficacy of Acupoints Dual-Frequency Low-Level Laser Therapy on Knee Osteoarthritis.

BACKGROUND: Knee osteoarthritis (OA) presented with knee pain and limitation of mobility is common, and it may become a chronic problem resulting in major loss of function, with related impaired activity of daily living. Current traditional therapy for knee OA includes pharmacological treatment and physiotherapy, but the efficacies are limited. An alternative noninvasive treatment low-level laser therapy (LLLT) applied to acupoints is still contradictory and the efficacy needs to be assessed. METHODS AND MATERIALS: We conduct the randomized double-blind control study to investigate the efficacy of a dual-frequency LLLT (combines red light (780 nm) and near-infrared light (830 nm)) in patients suffering knee OA. Participates were randomly assigned into active laser therapy (ALT) and placebo laser therapy (PLT) groups. Subjects in the ALT group were separately treated by laser apparatus at the three acupoints (SP9, SP10, and EX-LE2) on their knee joints under continuous radiation for 15 min at the maximum intensity, three times per week for four weeks. The PLT group used laser apparatus of the same model according to similar procedures without laser light emission. Outcome Measurements including visual analog scale (VAS), pain pressure threshold (PPT), and Lequesne index were used. RESULTS: A total of 30 subjects with two-sided knee OA in both groups completed the experiment. Statistically significant decreases were observed in the Lequesne index (5.27 ± 3.26 vs. 10.83 ± 3.83), conscious VAS 4 weeks after treatment (moving: 2.87 ± 1.13 vs. 5.67 ± 1.72; resting: 0.33 ± 0.62 vs. 2.67 ± 1.29), and the increase was noted in PPT (21.23 ± 1.82 kg vs. 13.02 ± 1.46 kg) in the ALT group compared with the PLT group. CONCLUSION: It appears that the knee OA pain and disability can be decreased after a dual-frequency LLLT applied to acupoints (SP9, SP10, and EX-LE2). The clinical efficacy of LLLT is highly related to the therapeutic settings of the laser apparatus; hence, more clinical trials with diffident parameter settings are needed to be further clarified.

Neuroprotective Effect of Paeonol Mediates Anti-Inflammation via Suppressing Toll-Like Receptor 2 and Toll-Like Receptor 4 Signaling Pathways in Cerebral Ischemia-Reperfusion Injured Rats.

Paeonol is a phenolic compound derived from Paeonia suffruticosa Andrews (MC) and P. lactiflora Pall (PL). Paeonol can reduce cerebral infarction volume and improve neurological deficits through antioxidative and anti-inflammatory effects. However, the anti-inflammatory pathway of paeonol remains unclear. This study investigated the relationship between anti-inflammatory responses of paeonol and signaling pathways of TLR2 and TLR4 in cerebral infarct. We established the cerebral ischemia-reperfusion model in Sprague Dawley rats by occluding right middle cerebral artery for 60 min, followed by reperfusion for 24 h. The neurological deficit score was examined, and the brains of the rats were removed for cerebral infarction volume and immunohistochemistry (IHC) analysis. The infarction volume and neurological deficits were lower in the paeonol group (pretreatment with paeonol; 20 mg/kg i.p.) than in the control group (without paeonol treatment). The IHC analysis revealed that the number of TLR2-, TLR4-, Iba1-, NF-κB- (P50-), and IL-1ß-immunoreactive cells and TUNEL-positive cells was significantly lower in the paeonol group; however, the number of TNF-α-immunoreactive cells did not differ between the paeonol and control groups. The paeonol reveals some neuroprotective effects in the model of ischemia, which could be due to the reduction of many proinflammatory receptors/mediators, although the mechanisms are not clear.

Ellagic acid induces apoptosis in TSGH8301 human bladder cancer cells through the endoplasmic reticulum stress- and mitochondria-dependent signaling pathways.

To investigate the effects of ellagic acid on the growth inhibition of TSGH8301 human bladder cancer cells in vitro, cells were incubated with various doses of ellagic acid for different time periods. The phase-contrast microscope was used for examining and photographing the morphological changes in TSGH8301 cells. Flow cytometric assay was used to measure the percentage of viable cells, cell cycle distribution, apoptotic cells, ROS, mitochondrial membrane potential (ΔΨm), Ca(2+) , caspase-9 and -3 activities in TSGH8301 cells after exposure to ellagic acid. Western blotting was used to examine the changes of cell cycle and apoptosis associated proteins levels. Results indicated that ellagic acid induced morphological changes, decreased the percentage of viable cells through the induction of G0/G1 phase arrest and apoptosis, and also showed that ellagic acid promoted ROS and Ca(2+) productions and decreased the level of ΔΨm and promoted activities of caspase-9 and -3. The induction of apoptosis also confirmed by annexin V staining, comet assay, DAPI staining and DNA gel electrophoresis showed that ellagic acid induced apoptosis and DNA damage in TSGH8301 cells. Western blotting assay showed that ellagic acid promoted p21, p53 and decreased CDC2 and WEE1 for leading to G0/G1 phase arrest and promoting BAD expression, AIF and Endo G, cytochrome c, caspase-9 and -3 for leading to apoptosis in TSGH8301 cells. On the basis of these observations, we suggest that ellagic acid induced cytotoxic effects for causing a decrease in the percentage of viable cells via G0/G1 phase arrest and induction of apoptosis in TSGH8301 cells.

In vitro suppression of growth of murine WEHI-3 leukemia cells and in vivo promotion of phagocytosis in a leukemia mice model by indole-3-carbinol.

Indole-3-carbinol (I3C), a potential anticancer substance, can be found in cruciferous (cabbage family) vegetables, mainly cauliflower and Chinese cabbage. However, the bioactivity of I3C on the apoptotic effects of murine leukemia WEHI-3 cells and promotion of immune responses in leukemia mice model are unclear. In this study, we investigated the effect of I3C on cell-cycle arrest and apoptosis in vitro and immunomodulation in vivo. I3C decreased the viable WEHI-3 cells and caused morphological changes in a concentration- and time-dependent manner. I3C also led to G0/G1 phase arrest, decreased the levels of cyclin A, cyclin D, and CDK2, and increased the level of p21(WAF1/CIP1). Flow cytometric analyses further proved that I3C promoted ROS and intracellular Ca(2+) production and decreased the levels of ΔΨ(m) in WEHI-3 cells. Cells after exposure to I3C for 24 h showed DNA fragmentation and chromatin condensation. Comet assay also indicated that I3C induced DNA damage in examined cells. I3C increased the levels of cytochrome c, FADD, GADD153, GRP78, and caspase-12 as well as induced activities of caspase-3, -8, and -9. Moreover, I3C attenuated NF-κB DNA binding activity in I3C-treated WEHI-3 cells as shown by EMSA and Western blotting analyses. In the in vivo study, we examined the effects of I3C on WEHI-3 leukemia mice. Results showed that I3C increased the level of T cells and decreased the level of macrophages. I3C also reduced the weights of liver and spleen, and it promoted phagocytosis by macrophages as compared to the nontreated leukemia mice group. On the basis of our results, I3C affects murine leukemia WEHI-3 cells both in vitro and in vivo.