Effects of a laughter programme with entrainment music on stress, depression, and health-related quality of life among gynaecological cancer patients.

OBJECTIVE: This study examined the effects of a laughter programme with entrainment music on stress, depression, and health-related quality of life (HRQoL) among gynaecological cancer patients. METHODS: This quasi-experimental study randomly assigned participants to either a laughter group (n = 17) or a control group (n = 19). The 8-week laughter programme included a weekly 60-min group session composed of laughter, deep breathing, stretching, meditation, and entrainment music-related activities (chorusing, body movement, and dancing). Values involving stress, depression, and HRQoL from before and after the programme were analysed using the Mann-Whitney U test and rank analysis of covariance. RESULTS: The laughter group exhibited improvements in relation with stress and depression, as well as improvement in the emotional and functional well-being of HRQoL domains. CONCLUSION: A laughter programme with entrainment music may be used as a stress-moderator and a positive emotion-enhancing strategy among gynaecological cancer patients.

Effects of rational emotive behavior therapy for senior nursing students on coping strategies and self-efficacy.

BACKGROUND: Senior nursing students are faced with various types of stressful events such as taking the national licensure exam or finding employment. Such stress can generate maladaptive behaviors as well as physical and psychological symptoms. There is evidence supporting the use of rational emotive behavior therapy (REBT) for reducing disruptive behaviors and negative emotions as well as improving self-efficacy and stress-coping strategies. OBJECTIVES: The purpose of this study is to examine the effects of rational emotive behavior therapy (REBT) on stress coping strategies and self-efficacy for senior nursing students. METHODS: Thirty-four senior nursing students in a nursing college were assigned randomly to an experimental group (n=18) and a control group (n=16). The REBT program consisted of 8 sessions, and it was implemented for a 4-week period. Outcome measures assessed stress-coping strategies and self-efficacy before and after intervention. RESULTS: After intervention with REBT, the mean difference scores for self-efficacy (p=.032) were significantly higher in the experimental group than in the control group. However, the mean difference scores for seeking social support (p=.166), problem solving (p=.126), and avoidance (p=.154) in stress-coping strategies were not significantly different between the two groups. CONCLUSION: The results imply that group counseling based on REBT enhances the self-efficacy among senior nursing students before graduation. As regards stress coping strategies, a longer intervention period is suggested.

Chronological changes of mechanical allodynia and spinal microglia activation by an intrathecal injection of MK-801.

The neuropathic pain that occurs after peripheral nerve injury may be related to abnormal central activity. The present experiments investigated the effects of MK-801 [N-methyl-D-aspartate (NMDA) receptor antagonist] on neuropathic pain behaviors and microglial activity in rats. Neuropathic pain was produced by L5 spinal nerve ligation of rats. MK-801 was injected to determine whether spinal microglial activation after nerve injury plays a crucial role in the development and/or maintenance of neuropathy through the NMDA receptor. Mechanical allodynia of the hind paw was examined with von Frey filaments postoperatively. Microglial activity was measured by observing changes in immunoreactivity with a microglia marker, OX-42. The MK-801, at a dose of 3 or 30 µg/5 µl, injection group showed higher neuropathic pain threshold and reduction of microglial activity. These results suggest that neuropathic pain behaviors following L5 spinal nerve ligation may be related to altered activity of the microglia involving the NMDA receptor, and chronological changes of microglial activation by MK-801 are related to maintenance of mechanical allodynia.

A novel rat forelimb model of neuropathic pain produced by partial injury of the median and ulnar nerves.

The vast majority of human peripheral nerve injuries occur in the upper limb, whereas the most animal studies have been conducted using the hindlimb models of neuropathic pain, involving damages of the sciatic or lumbar spinal nerve(s). We attempted to develop a rat forelimb model of peripheral neuropathy by partial injury of the median and ulnar nerves. The halves of each nerve were transected by microscissors at about 5mm proximal from the elbow joint and behavioral signs of neuropathic pain, such as mechanical and cold allodynia, and heat hyperalgesia, were monitored up to 126 days following nerve injury. Mechanical allodynia was assessed by measuring the forepaw withdrawal threshold to von Frey filaments, and cold allodynia was evaluated by measuring the time spent in lifting or licking the forepaw after applying acetone to it. Heat hyperalgesia was also monitored by investigating the forepaw withdrawal latencies using the Hargreaves' test. After the nerve injury, the experimental animals exhibited long-lasting clear neuropathic pain-like behaviors, such as reduced forepaw withdrawal threshold to von Frey filaments, the increased response duration of the forepaw to acetone application, and the decreased withdrawal latency to radiant heat stimulation. These behaviors were significantly alleviated by administration of gabapentin (5 or 50mg/kg, i.p.) in a dose-dependent manner. Therefore, these abnormal sensitivities are interpreted as the signs of neuropathic pain following injury of the median and ulnar nerves. Our rat forelimb model of neuropathic pain may be useful for studying human neuropathic pain and screening for valuable drug candidates.

Are spinal GABAergic elements related to the manifestation of neuropathic pain in rat?

Impairment in spinal inhibition caused by quantitative alteration of GABAergic elements following peripheral nerve injury has been postulated to mediate neuropathic pain. In the present study, we tested whether neuropathic pain could be induced or reversed by pharmacologically modulating spinal GABAergic activity, and whether quantitative alteration of spinal GABAergic elements after peripheral nerve injury was related to the impairment of GABAergic inhibition or neuropathic pain. To these aims, we first analyzed the pain behaviors following the spinal administration of GABA antagonists (1 microg bicuculline/rat and 5 microg phaclofen/rat), agonists (1 microg muscimol/rat and 0.5 microg baclofen/rat) or GABA transporter (GAT) inhibitors (20 microg NNC-711/rat and 1 microg SNAP-5114/rat) into naïve or neuropathic animals. Then, using Western blotting, PCR or immunohistochemistry, we compared the quantities of spinal GABA, its synthesizing enzymes (GAD65, 67) and its receptors (GABA(A) and GABA(B)) and transporters (GAT-1, and -3) between two groups of rats with different severity of neuropathic pain following partial injury of tail-innervating nerves; the allodynic and non-allodynic groups. Intrathecal administration of GABA antagonists markedly lowered tail-withdrawal threshold in naïve animals, and GABA agonists or GAT inhibitors significantly attenuated neuropathic pain in nerve-injured animals. However, any quantitative changes in spinal GABAergic elements were not observed in both the allodynic and non-allodynic groups. These results suggest that although the impairment in spinal GABAergic inhibition may play a role in mediation of neuropathic pain, it is not accomplished by the quantitative change in spinal elements for GABAergic inhibition and therefore these elements are not related to the generation of neuropathic pain following peripheral nerve injury.

Randomized controlled trial of a cognitive-behavioral therapy for at-risk Korean male adolescents.

This study examined the effects of cognitive behavioral therapy (CBT) aimed at enhancing the resilience of high-risk adolescents with alcohol-dependent parents in Suwon, South Korea. The study used a randomized control group pretest and posttest design. The experimental group participated in 10 sessions of CBT, and the scores on resilience increased significantly after the intervention, whereas the scores of self-concept and depression did not change. In the control group, none of the scores of outcome variables changed significantly after the intervention period. The results indicate that the developed CBT program might be effective for improving the resilience of adolescents with alcohol-dependent parents.

The effects of a cognitive-behavioral therapy on career attitude maturity, decision making style, and self-esteem of nursing students in Korea.

The purpose of this study was to find out about the effectiveness of a cognitive-behavioral program for nursing student's career attitude maturity, decision making style, and self-esteem in Korea. The ultimate goal of this paper is to prepare career strategies so that they can improve career maturity development, on the basis of better understanding of one's self. The subjects were 40 nursing students from one college located in Gyeonggi Province; following the informed consent procedure, twenty participants were randomly assigned to an experimental group, and 20 were assigned to a control group. The cognitive-behavioral therapy consisted of 8-sessions and was implemented for 60 min during an 8 week period. Data were collected from May to June 2004, and analyzed χ(2)-test, Fisher's exact test and t-test were used in the analysis of the data. After treatment with cognitive-behavioral therapy, the experimental group significantly increased in the mean score for career attitude maturity, self-esteem compared to the control group, especially for confidence and independence. In conclusion, cognitive-behavioral therapy had a positive effect for increasing the career attitude maturity and self-esteem for nursing students in Korea. Therefore, cognitive-behavioral therapy for nursing student is recommended as a group counseling program on career maturity inventory.

Long-lasting neonatal inflammation enhances pain responses to subsequent inflammation, but not peripheral nerve injury in adult rats.

The early postnatal period has been suggested to be the vulnerable time for structural and functional reorganization of sensory systems, and painful stimuli at this time may alter neuronal circuits, thereby leading to changes in an individual's response to pain later in life. In the present study, we examined whether inflammatory experience in the early life can affect pain responses to subsequent noxious insults later in life. The two groups of neonatal rats, treated with an inflammatory irritant and untreated, were subjected to inflammation and peripheral nerve injury in adulthood. Neonatal inflammation was induced by injection of complete Freund's adjuvant (CFA, 25 microl) into the hindpaw or tail of newborn rat pups. Adult rats which had suffered from neonatal paw inflammation at P0 were subjected to re-injection of CFA into the paw neonatally exposed to CFA or L5 spinal nerve ligation. Paw thickness and histology of inflamed paw were examined to assess the neonatal inflammation. Adult animals whose tail had been subjected to CFA injection on P3 received tail-innervating nerve injury. The results showed that the neonatal CFA-treated rats suffered from chronic inflammation, confirmed by persistent increase of paw thickness and histological result of inflamed paw. These animals showed enhanced pain responses to re-inflammatory challenge by injection of CFA (200 microl) into the neonatally inflamed paw 8 weeks after birth compared with the neonatally untreated animals. However, neuropathic pain on the hindpaw and the tail which had been induced by peripheral nerve injury in the neonatal CFA-treated group were not different from those of the untreated group. The present data suggest that early neonatal long-lasting inflammation differentially affects pain responses later in life, depending on the types of subsequent noxious insults.

Developmental characteristics of neuropathic pain induced by peripheral nerve injury of rats during neonatal period.

To gain an insight into the developmental characteristics of neuropathic pain induced by peripheral nerve injury during neonatal period, we employed three groups of rats suffering from peripheral nerve injury at different postnatal times, and compared the onset time, severity and persistency of neuropathic pain behaviors, such as mechanical and cold allodynia. The first group (P0 group) was subjected to partial injury of tail-innervating nerves within 24 h after birth, the second group (P10 group) underwent nerve injury at postnatal day (P) 10, and the third group (P60 group) was subjected to injury at P60. Although mechanical allodynia was readily detectable in the P60 group even 1 day after nerve injury, the signs of neuropathic pain were observed from 6 or 8 weeks after nerve injury in the P0 or P10 groups, respectively. Compared with the P60 group, the P0 group showed more robust mechanical and cold allodynia, whereas the P10 group exhibited rather milder pains. In addition, while the P0 and P60 groups showed long-lasting signs of mechanical allodynia, the P10 group exhibited shorter persistency. These results indicate that peripheral nerve injury during neonatal period leads to neuropathic pain with distinct developmental characteristics later in life.

A critical role of toll-like receptor 2 in nerve injury-induced spinal cord glial cell activation and pain hypersensitivity.

The activation of spinal cord glial cells has been implicated in the development of neuropathic pain upon peripheral nerve injury. The molecular mechanisms underlying glial cell activation, however, have not been clearly elucidated. In this study, we found that damaged sensory neurons induce the expression of tumor necrosis factor-alpha, interleukin-1beta, interleukin-6, and inducible nitric-oxide synthase genes in spinal cord glial cells, which is implicated in the development of neuropathic pain. Studies using primary glial cells isolated from toll-like receptor 2 knock-out mice indicate that damaged sensory neurons activate glial cells via toll-like receptor 2. In addition, behavioral studies using toll-like receptor 2 knock-out mice demonstrate that the expression of toll-like receptor 2 is required for the induction of mechanical allodynia and thermal hyperalgesia due to spinal nerve axotomy. The nerve injury-induced spinal cord microglia and astrocyte activation is reduced in the toll-like receptor 2 knock-out mice. Similarly, the nerve injury-induced pro-inflammatory gene expression in the spinal cord is also reduced in the toll-like receptor 2 knock-out mice. These data demonstrate that toll-like receptor 2 contributes to the nerve injury-induced spinal cord glial cell activation and subsequent pain hypersensitivity.

Induction of total insensitivity to capsaicin and hypersensitivity to garlic extract in human by decreased expression of TRPV1.

TRPV1 is a cation channel which is activated by temperature (> or =42 degrees C) and capsaicin. In the present study, we found a person with total insensitivity to capsaicin and attempted to unravel its causes. The expression levels of TRPV1 protein and mRNA in the cells of the person's buccal mucosa were less than half of those in a normal subject. Sequential analysis of mRNA and genomic DNA revealed several point mutations mostly in the second intron of the person's TRPV1. Interestingly, the subject showed hypersensitivity to garlic extract, but TRPA1 (allicin receptor) level was normal. These results suggest that the decreased expression of TRPV1 may be related to a functional knock out in capsaicin sensation and hypersensitivity to allicin in humans.