Effect of Guided Imagery Meditation During Laparoscopic Cholecystectomy on Reducing Anxiety: A Randomized Controlled Trial.

BACKGROUND: Up to 90% of patients still experience pain after abdominal surgery, which also affects their physical recovery and psychological anxiety. AIM: To evaluate the effects of guided imagery meditation on ameliorating anxiety, improving the quality of sleep, and relieving postoperative pain in patients after laparoscopic cholecystectomy surgery. METHOD: In the general surgical ward of a teaching hospital, patients were randomly assigned to usual care (n = 34) and guided imagery meditation intervention (n = 34) groups, using the method. The measuring outcomes included their anxiety score, quality of sleep, and pain control. RESULTS: In terms of the anxiety difference, the experimental group scored 0.42 (standard deviation [SD] = 0.97), while the control group scored 4.79 (SD = 7.56), which indicates a statistically significant difference (F = 8.04, p = .01, partial eta2 = 0.11). In terms of quality of sleep, the mean score of the experimental group was 2.67 (SD = 1.96), while the control group scored 7.55 (SD = 3.81), which indicates a significant difference (F = 39.99, p = .001, partial eta2 = 0.39). The mean of the degree of postoperative pain was 2.11 points (SD = 1.39), and the score of the control group was 4.00 points (SD = 1.62), which indicates a significant difference (p = .001). CONCLUSIONS: Guided imagery meditation is a simple, non-invasive, non-pharmacologic intervention measure. It can reduce anxiety and postoperative pain, and improve the quality of sleep. Thus, it should be promoted in clinical practice.

A new drug design targeting the adenosinergic system for Huntington's disease.

BACKGROUND: Huntington's disease (HD) is a neurodegenerative disease caused by a CAG trinucleotide expansion in the Huntingtin (Htt) gene. The expanded CAG repeats are translated into polyglutamine (polyQ), causing aberrant functions as well as aggregate formation of mutant Htt. Effective treatments for HD are yet to be developed. METHODOLOGY/PRINCIPAL FINDINGS: Here, we report a novel dual-function compound, N(6)-(4-hydroxybenzyl)adenine riboside (designated T1-11) which activates the A(2A)R and a major adenosine transporter (ENT1). T1-11 was originally isolated from a Chinese medicinal herb. Molecular modeling analyses showed that T1-11 binds to the adenosine pockets of the A(2A)R and ENT1. Introduction of T1-11 into the striatum significantly enhanced the level of striatal adenosine as determined by a microdialysis technique, demonstrating that T1-11 inhibited adenosine uptake in vivo. A single intraperitoneal injection of T1-11 in wildtype mice, but not in A(2A)R knockout mice, increased cAMP level in the brain. Thus, T1-11 enters the brain and elevates cAMP via activation of the A(2A)R in vivo. Most importantly, addition of T1-11 (0.05 mg/ml) to the drinking water of a transgenic mouse model of HD (R6/2) ameliorated the progressive deterioration in motor coordination, reduced the formation of striatal Htt aggregates, elevated proteasome activity, and increased the level of an important neurotrophic factor (brain derived neurotrophic factor) in the brain. These results demonstrate the therapeutic potential of T1-11 for treating HD. CONCLUSIONS/SIGNIFICANCE: The dual functions of T1-11 enable T1-11 to effectively activate the adenosinergic system and subsequently delay the progression of HD. This is a novel therapeutic strategy for HD. Similar dual-function drugs aimed at a particular neurotransmitter system as proposed herein may be applicable to other neurotransmitter systems (e.g., the dopamine receptor/dopamine transporter and the serotonin receptor/serotonin transporter) and may facilitate the development of new drugs for other neurodegenerative diseases.

Salvianolic acid B reverses the epithelial-to-mesenchymal transition of HK-2 cells that is induced by transforming growth factor-ß.

Salvianolic acid B (Sal B) is the most abundant bioactive molecule from Radix Salviae Miltiorrhizae, and has recently been used for treating renal fibrosis in traditional Chinese medicine. Here we investigated the ability reversal of Sal B to reverse the transdifferentiation of human kidney proximal tubular epithelial cells that was induced by transforming growth factor-beta 1 (TGF-ß1). The effects of Sal B on HK-2 cell morphology were observed by phase contrast microscopy, while alpha smooth muscle actin and E-cadherin were studied by immunocytochemistry and real-time reverse transcription polymerase chain reaction, respectively. Exposure of HK-2 cells to TGF-ß1 for 72 h induced a complete conversion of the epithelial cells to myofibroblasts. When HK-2 cells were co-incubated with Sal B and TGF-ß1 for a further 72 h, the morphology of myofibroblasts returned to that of proximal tubular epithelial cells, whereas the myofibroblast phenotype was maintained after exposure of cells to TGF-ß1 for 144 h. Sal B reduced alpha smooth muscle actin levels and increased E-cadherin levels compared with their epithelial-to-mesenchymal transition controls. The reversal effect of Sal B was dose-dependent. That Sal B reverses the epithelial-to-mesenchymal transition in vitro suggests that it could possibly facilitate the repair of tubular epithelial structures and the regression of renal fibrosis in injured kidneys.