Attenuation of skeletal muscle atrophy via acupuncture, electro-acupuncture, and electrical stimulation.

Background: Accelerated skeletal muscle wasting is a shared trait among many pathologies and aging. Acupuncture has been used as a therapeutic intervention to control pain; however, little is known about its effects on skeletal muscle atrophy and function. The study's purpose was to compare the effects of acupuncture, electro-acupuncture, and electrical stimulation on cast-induced skeletal muscle atrophy. Methods: Forty female Sprague Dawley rats were randomly divided into groups: Control, casted (CAST), CAST+Acupuncture (CAST-A), 4) CAST+Electro-acupuncture (CAST-EA), and CAST+Electrical stimulation (CAST-ES) (n = 8). Plaster casting material was wrapped around the left hind limb. Acupuncture and electro-acupuncture (10 Hz, 6.4 mA) treatments were applied by needling acupoints (stomach-36 and gallbladder-34). Electrical stimulation (10 Hz, 6.4 mA) was conducted by needling the lateral and medial gastrocnemius muscles. Treatments were conducted for 15 min, three times/week for 14 days. Muscle atrophy F-box (MAFbx), muscle RING finger 1 (MuRF1), and contractile properties were assessed. Results: Fourteen days of cast-immobilization decreased muscle fiber CSA by 56% in the CAST group (p = 0.00); whereas, all treatment groups demonstrated greater muscle fiber CSA than the CAST group (p = 0.00). Cast-immobilization increased MAFbx and MuRF1 protein expression in the CAST group (p<0.01) while the CAST-A, CAST-EA, and CAST-ES groups demonstrated lower levels of MAFbx and MuRF1 protein expression (p<0.02) compared to the CAST group. Following fourteen days of cast-immobilization, peak twitch tension did not differ between the CAST-A and CON groups (p = 0.12). Conclusion: Skeletal muscle atrophy, induced by 14 days of cast-immobilization, was significantly attenuated by acupuncture, electro-acupuncture, or electrical stimulation.

Development of a heat labile antibiotic eluting 3D printed scaffold for the treatment of osteomyelitis.

In general, osteomyelitis is treated with antibiotics, and in severe cases, the inflammatory bone tissue is removed and substituted with poly (methyl methacrylate) (PMMA) beads containing antibiotics. However, this treatment necessitates re-surgery to remove the inserted PMMA beads. Moreover, rifampicin, a primary heat-sensitive antibiotic used for osteomyelitis, is deemed unsuitable in this strategy. Three-dimensional (3D) printing technology has gained popularity, as it facilitates the production of a patient-customized implantable structure using various biodegradable biomaterials as well as controlling printing temperature. Therefore, in this study, we developed a rifampicin-loaded 3D scaffold for the treatment of osteomyelitis using 3D printing and polycaprolactone (PCL), a biodegradable polymer that can be printed at low temperatures. We successfully fabricated rifampicin-loaded PCL 3D scaffolds connected with all pores using computer-aided design and manufacturing (CAD/CAM) and printed them at a temperature of 60 °C to prevent the loss of the antibacterial activity of rifampicin. The growth inhibitory activity against Escherichia coli (E. coli) and Staphylococcus aureus (S. aureus), the representative causative organisms of osteomyelitis, was confirmed. In addition, we optimized the rifampicin-loading capacity that causes no damage to the normal bone tissues in 3D scaffold with toxicity evaluation using human osteoblasts. The rifampicin-releasing 3D scaffold developed herein opens new possibilities of the patient-customized treatment of osteomyelitis.

Longan (Dimocarpus longan Lour.) Fruit Extract Stimulates Osteoblast Differentiation via Erk1/2-Dependent RUNX2 Activation.

Longan (Dimocarpus longan Lour.) has been used as a traditional oriental medicine and possesses a number of physiological activities. In this study, we used cell-based herbal extract screening to identify longan fruit extract (LFE) as an activator of osteoblast differentiation. LFE up-regulated alkaline phosphatase (ALP) activity, induced mineralization, and activated Runx2 gene expression in MC3T3-E1 cells. Furthermore, treatment of MC3T3-E1 cells with LFE promoted the phosphorylation of extracellular signal-regulated kinase1/2 (Erk1/2); however, abrogation of Erk1/2 activation with PD98059 resulted in down-regulation of the phospho- SMAD1/5/8 and Runx2 levels, which in turn reduced the ALP activity. Our findings suggest that LFE exerts its osteogenic activity through activation of the ERK signaling pathway and may have potential as an herbal therapeutic or a preventive agent for the treatment of osteoporosis.

Gastroprotective effect of Cochinchina momordica seed extract in nonsteroidal anti-inflammatory drug-induced acute gastric damage in a rat model.

BACKGROUND/AIMS: The major compounds of Cochinchina momordica seed extract (SK-MS10) include momordica saponins. We report that the gastroprotective effect of SK-MS10 in an ethanol-induced gastric damage rat model is mediated by suppressing proinflammatory cytokines and downregulating cytosolic phospholipase A2 (cPLA2), 5-lipoxygenase (5-LOX), and the activation of calcitonin gene-related peptide. In this study, we evaluated the gastroprotective effects of SK-MS10 in the nonsteroidal anti-inflammatory drug (NSAID)-induced gastric damage rat model. METHODS: The pretreatment effect of SK-MS10 was evaluated in the NSAID-induced gastric damage rat model using aspirin, indomethacin, and diclofenac in 7-week-old rats. Gastric damage was evaluated based on the gross ulcer index by gastroenterologists, and the damage area (%) was measured using the MetaMorph 7.0 video image analysis system. Myeloperoxidase (MPO) was measured by enzyme-linked immunosorbent assay, and Western blotting was used to analyze the levels of cyclooxygenase (COX)-1, COX-2, cPLA2, and 5-LOX. RESULTS: All NSAIDs induced gastric damage based on the gross ulcer index and damage area (p<0.05). Gastric damage was significantly attenuated by SK-MS10 pretreatment compared with NSAID treatment alone (p<0.05). The SK-MS10 pretreatment group exhibited lower MPO levels than the diclofenac group. The expression of cPLA2 and 5-LOX was decreased by SK-MS10 pretreatment in each of the three NSAID treatment groups. CONCLUSIONS: SK-MS10 exhibited a gastroprotective effect against NSAID-induced acute gastric damage in rats. However, its protective mechanism may be different across the three types of NSAID-induced gastric damage models in rats.

Subclinical Vitamin D Insufficiency in Korean School-aged Children.

PURPOSE: Recently, vitamin D insufficiency has increased and has been correlated to growth and puberty in children. This study was conducted to find the prevalence of subclinical vitamin D insufficiency and its influence on school-aged children in Korea. METHODS: The subjects of this study were 397 children aged 7 to 15 years who had been tested for 25-OH vitamin D3 among the outpatients of the Department of Pediatrics in Eulji General Hospital from March 2007 to February 2011. Data for age, sex, comorbidities, serum 25-OH vitamin D3, height, weight, body mass index (BMI), and sunlight exposure time were collected before and after 3 months of vitamin D administration, retrospectively. RESULTS: Vitamin D insufficiency was present in 343 (86%) of the subjects. In the vitamin D insufficient group, chronological age was 8.96±1.72 years, mean height (z-score [z]) was 0.51±1.26, mean BMI (z) was 0.81±2.20, and bone age was 10.26±1.75 years. In the vitamin D sufficient group, chronological age was 9.61±1.77 years, mean height (z) was-0.66±0.98, mean BMI (z) was-0.01±1.16, and bone age was 9.44±2.12 years. A paired t-test showed that three months after vitamin D administration, the mean 25-OH vitamin D3 level in the insufficient group increased to 24.38 ±10.03 ng/mL and mean BMI (z) decreased to 0.67±1.06. CONCLUSION: In Korean school-aged children, vitamin D insufficiency were relatively higher and may be closely related with higher BMI. Insufficient rise of the level of vitamin D after supplementation suggest the new supplementation guidelines, especially for Korean children.

Attenuation of cysteamine-induced duodenal ulcer with Cochinchina momordica seed extract through inhibiting cytoplasmic phospholipase A2/5-lipoxygenase and activating γ-glutamylcysteine synthetase.

BACKGROUND AND AIM: Cysteamine is a reducing aminothiol used for inducing duodenal ulcer through mechanisms of oxidative stress related to thiol-derived H(2)O(2) reaction. Cochinchina momordica saponins have been suggested to be protective against various gastric diseases based on their cytoprotective and anti-inflammatory mechanisms. This study was aimed to document the preventive effects of Cochinchina momordica seed extract against cysteamine-induced duodenal ulcer as well as the elucidation of its pharmacological mechanisms. METHODS: Cochinchina momordica seed extract (50, 100, 200 mg/kg) was administrated intragastrically before cysteamine administration, after which the incidence of the duodenal ulcer, ulcer size, serum gastrin level, and the ratio of reduced glutathione (GSH)/oxidized glutathione disulfide (GSSG) as well as biochemical and molecular measurements of cytoplasmic phospholipase A(2) (cPLA(2)), cyclooxygenase-2 (COX-2), 5-lipoxygenase and the expression of proinflammatory genes including IL-1ß, IL-6, COX-2 were measured in rat model. Additional experiments of electron spin resonance measurement and the changes of glutathione were performed. RESULTS: Cochinchina momordica seed extract effectively prevented cysteamine-induced duodenal ulcer in a dose-dependent manner as reflected with significant decreases in either duodenal ulcerogenesis or perforation accompanied with significantly decreased in serum gastrin in addition to inflammatory mediators including cPLA(2), COX-2, and 5-lipoxygenase. Cochinchina momordica seed extract induced the expression of γ-glutamylcysteine synthetase (γ-GCS)-related glutathione synthesis as well as significantly reduced the expression of cPLA(2). Cochinchina momordica seed extract preserved reduced glutathione through increased expressions of γ-GCS. CONCLUSION: Cochinchina momordica seed extracts exerted significantly protective effect against cysteamine-induced duodenal ulcer by either cPLA2 inhibition or glutathione preservation.

Neuroplastic changes within the brains of manganese-exposed welders: recruiting additional neural resources for successful motor performance.

BACKGROUND: In a previous study, regional delivery of manganese (Mn)ions within the brain revealed that the metal accumulates in the basal ganglia, where it induces degeneration of the globus pallidus. Degeneration of the basal ganglia impairs motor ability by compromising an important neural circuit involved in the regulation of motor control. Therefore, much research has been devoted to identifying a sensitive and non-invasive imaging marker to evaluate the functional correlates of Mn-related brain dysfunction. METHODS: We performed the first-ever sequential finger-tapping functional MRI (fMRI) experiment to investigate the behavioural significance of additionally recruited brain regions in welders with chronic Mn exposure. RESULTS: During the finger tapping task, activation of the bilateral primary sensorimotor cortex (SM1), bilateral supplementary motor area (SMA), bilateral dorsolateral premotor cortex, bilateral superior parietal cortex and ipsilateral dentate nucleus was higher in the welding group (42 welders) than in the control group (26 controls). The pallidal index correlated with the activation observed in the contralateral SM1 for the finger tapping task of the left hand. The fMRI variables correlated with motor behaviour. Grooved Pegboard performances (right hand) correlated with activation, as seen in the ipsilateral and contralateral SMAs obtained during the finger tapping task of the right hand. CONCLUSION: Our findings suggest that increased brain activation results from the compensational activation of ancillary cortical pathways, which ensures adequate motor function.

The prognostic significance of ERCC1, BRCA1, XRCC1, and betaIII-tubulin expression in patients with non-small cell lung cancer treated by platinum- and taxane-based neoadjuvant chemotherapy and surgical resection.

OBJECTIVES: The DNA repair pathway and isotype composition of beta-tubulin are known to be associated with resistance to platinum- and taxane-based chemotherapy, respectively. The aim of this study was to identify the clinical significance of excision repair cross-complementation 1 (ERCC1), breast cancer susceptibility gene 1 (BRCA1), X-ray repair cross-complementation 1 (XRCC1) and betaIII-tubulin on the chemotherapy response and overall survival in patients with non-small cell lung cancer (NSCLC) who received neoadjuvant chemotherapy. METHODS: Protein expression profiles were evaluated by immunohistochemistry on surgical specimens of 82 NSCLC patients who underwent platinum- and taxane-based neoadjuvant chemotherapy. The expression levels of proteins were measured semi-quantitatively and the correlation with tumor responses, pathologic cell death rate and survival were evaluated. RESULTS: There were 73 (89.0%) clinical stage III patients. Lobectomy, bilobectomy, and pneumonectomy were performed in 54 (65.0%), 11 (13.4%), and 17 (20.7%) patients, respectively. There was no correlation between clinical response and protein expression. The expression levels of ERCC1, BRCA1, and XRCC1 increased proportionally to the cell death rate (p<0.05); however, betaIII-tubulin expression did not correlate with cell viability. Multivariate analysis demonstrated that early pathologic stage, adjuvant chemotherapy, high ERCC1 and low betaIII-tubulin expression were good prognostic factors for overall survival (p<0.05). CONCLUSIONS: The inverse correlation between DNA repair proteins and cell viability suggests that these protein expression levels can be markers for chemotherapy responsiveness. However, only ERCC1 and betaIII-tubulin were prognostic factors after platinum- and taxane-based neoadjuvant chemotherapy following surgical resection.

[The experiences of recovery from disease in patients doing meditation].

PURPOSE: The purpose of this study was to explore the experiences of recovery from disease in the patients doing a kind of Buddhist meditation, and to develop a grounded theory about meditation. METHOD: Data was collected by an in-depth interview using tape-recordings from sixteen participants doing meditation. The data was analyzed using the grounded theory method proposed by Strauss and Corbin(1998). RESULT: The core category was discovering the true self. The participants began to do meditation because of their disease. They experienced obstacles due to incomplete religious acceptance. However, their faith grew gradually based on religious experiences that were indescribable. Finally, they entirely trusted the inner healer, which is emphasized in meditation. The strategies that they used were self reflection and seeking help for accepting deep meditation. They were stabilized in physical, psychological and social daily living. The processes of discovering the true self were identified as entering religious discipline, embodying religious discipline, self-accomplishing religious faith, and recovering mind-body health. CONCLUSION: This study provided the understanding of mind-body integration. Empirical research may be needed to prove scientifically the effects of meditation.