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Background: Operating room nurses experience verbal abuse, high levels of job stress, and burnout that may increase turnover intention. Purpose: This study was designed to investigate and identify factors influencing turnover intention among operating room nurses in South Korea. Methods: This study used a cross-sectional descriptive design. The sample included 193 nurses, all of whom had over 3 months of work experience at operating rooms in hospitals in Seoul, South Korea. Measures used included the Verbal Abuse Experience Scale, Job Stress Scale, Burnout Scale, and Turnover Intention Scale. Results: Burnout was found to have the greatest influence on turnover intention (β =.34, p <.001), followed by verbal abuse (β = −.23, p =.004), job stress (β =.22, p =.001), age (β = −20, p =.032), and job satisfaction (β = −.14, p =.020). Conclusions/Implications for Practice: The findings support burnout and verbal abuse, respectively, as the most significant and second most significant predictors of turnover intention among operating room nurses in South Korea. These factors should be proactively and effectively addressed to reduce turnover intention in this important group of healthcare professionals. [ABSTRACT FROM AUTHOR]

A sufficient β-cell mass is crucial for preventing diabetes, and perinatal β-cell proliferation is important in determining the adult β-cell mass. However, it is not yet known how perinatal β-cell proliferation is regulated. Here, we report that serotonin regulates β-cell proliferation through serotonin receptor 2B (HTR2B) in an autocrine/paracrine manner during the perinatal period. In β-cell-specific Tph1 knockout (Tph1 βKO) mice, perinatal β-cell proliferation was reduced along with the loss of serotonin production in β-cells. Adult Tph1 βKO mice exhibited glucose intolerance with decreased β-cell mass. Disruption of Htr2b in β-cells also resulted in decreased perinatal β-cell proliferation and glucose intolerance in adulthood. Growth hormone (GH) was found to induce serotonin production in β-cells through activation of STAT5 during the perinatal period. Thus, our results indicate that GH-GH receptor-STAT5-serotonin-HTR2B signaling plays a critical role in determining the β-cell mass by regulating perinatal β-cell proliferation, and defects in this pathway affect metabolic phenotypes in adults. [ABSTRACT FROM AUTHOR]

Purpose: In recent years, there has been an increasing interest in peri-articular injections (PAI) to control post-operative pain after total knee arthroplasty (TKA). Previous studies have evaluated the effect of PAI using multimodal analgaesic protocols, but the concomitant use of patient-controlled analgesia (PCA) may has masked the genuine effects of PAI. We investigated the efficacy of PAI compared with PCA and determined whether conventional PCA can be effectively replaced with PAI after TKA.Methods: Eighty patients undergoing unilateral TKA were randomised into two groups. The PCA group consisted of patients who used PCA after surgery, while the PAI group included patients who did not use PCA post-operatively but were given PAI during surgery. We measured changes in visual analogue scale (VAS) scores, straight leg raising (SLR), range of motion (ROM) and consumption of antiemetics or analgaesics.Results: Pain levels in the PAI group were significantly lower than in the PCA group during two weeks post-operatively (p < 0.05).; functional recovery in the SLR test showed no difference between groups (p > 0.05).; mean ROM showed no difference; (p > 0.05) and there was no difference in the number of patients who needed additional analgaesics. However, antiemetic use was significantly lower for the PAI group (p < 0.05).Conclusions: PAI offered improved pain control and minimal side effects compared with PCA. Thus, PAI can replace conventional PCA for controlling post-operative pain after TKA. [ABSTRACT FROM AUTHOR]

ABSTRACT Retinal degeneration is caused by neovascularization and persistent inflammation in the retinal pigment epithelium (RPE) and choroid, and causes serious eye disease including age-related macular degeneration (AMD). Thus, inhibiting inflammation and neovascularization may be a primary approach to protect the retina from degeneration. The purpose of this study was to determine whether substance P (SP), which can suppress inflammation and mobilize stem cells, can protect the RPE from degeneration. The effect of SP was evaluated by analyzing systemic inflammation, cell survival, and neovascularization within the argon laser-injured retina of mice. At 1 week postinjury, the SP-treated group had lower tumor necrosis factor-alpha and higher interleukin-10 serum concentrations, and a more intact retinal structure compared to the vehicle-treated group. In mice administered SP repeatedly for 4 weeks, the retinal structure appeared normal and showed sparse neovascularization, whereas the vehicle-treated group showed severe retinal destruction and dense neovascularization. Moreover, the efficacy of SP was identical to that of mesenchymal stem cells that were transplanted into the vitreous after retinal injury. This study highlights the potential for the endogenous neuropeptide SP as a treatment for retinal damage to prevent conditions such as AMD. [ABSTRACT FROM AUTHOR]

Ethnopharmacological relevance The roots of Angelica decursiva Fr. Et Sav (Umbelliferae) have been frequently used in traditional medicine as anti-inflammatory, antitussive, analgesic agents and expectorant, especially for treating cough, asthma, bronchitis and upper respiratory tract infections. To establish the scientific rationale for the clinical use of Angelica decursiva and to identify new agents for treating inflammatory lung disorders, pharmacological evaluation of the roots of Angelica decursiva and the isolated constituents was performed. Methods In vitro study was carried out using two lung cells, lung epithelial cells (A549) and alveolar macrophages (MH-S). The inflammatory markers such as IL-6 and nitric oxide (NO) for each cell line were examined. For in vivo study, a mouse model of lipopolysaccharide (LPS)-induced acute lung injury was used and the effects on lung inflammation were established by measuring the cell numbers in bronchoalveolar lavage fluid (BALF) and by histological observation. Results Water and 70% ethanol extracts of the roots of Angelica decursiva showed considerable inhibitory activity against LPS-induced lung inflammation in mice following oral administration at a dose of 400 mg/kg. Five coumarin derivatives including columbianadin, umbelliferone, umbelliferone 6-carboxylic acid, nodakenin and nodakenetin were isolated. Among the isolated compounds, columbianadin was found to possess strong inhibitory activity against the inflammatory response of IL-1β-treated A549 cells and LPS-treated MH-S cells. Columbianadin was found to inhibit NO production by down-regulation of inducible NO synthase. Moreover, columbianadin was also proved to possess significant inhibitory activity against LPS-induced lung inflammation following oral administration at a dose of 20–60 mg/kg. Conclusions The roots of Angelica decursiva were proved to be effective in the treatment of lung inflammation. Columbianadin can be a potential new agent for treating inflammatory lung disorders. [ABSTRACT FROM AUTHOR]

Abstract: Ethnopharmacological relevance: Artemisia capillaris has widespread traditional and pharmacological applications such as analgesic, anti-inflammatory, anti-pyretic, enhance immunity and anti-tumor activity properties. To evaluate the pharmacological activities of this plant, capillarisin, one of the potent constituent of Artemisia capillaris was studied based on anti-hyperalgesic and anti-allodynic effects with detailed mechanism. It can be assumed that measurement of anti-nociceptive effects of capillarisin is one of the parameter for the evaluation of this herb. Capillarisin has extensive pharmacological properties and has been considered to have promising ant-inflammatory and anti-nociceptive activities. The aim of the current study is to investigate the effect of capillarisin and underlying molecular mechanisms of action in preventing acute and subchronic inflammatory pain. Materials and methods: The inflammatory pain was induced after 40min or 1h of administration of vehicle, 70% EtOH extract of Artemisia capillaris (100mg/kg) or capillarisin (20 and 80mg/kg) by intraplantar (i.p.l.) injections of CFA and carrageenan in ICR mice, respectively. Mechanical hyperalgesia and allodynia were evaluated in both acute and subchronic models. Further analysis was performed in CFA-induced mice exploring various molecular and signaling pathways such as NF-κB, AP-1, and ERK-CREB involved in the persistent pain sensations. Results: In acute model, mechanical hyperalgesia and allodynia were evaluated after every 2h until 6h of CFA and after 4h of carrageenan injections. Whereas, in subchronic inflammatory pain model, mechanical hyperalgesia and paw edema were measured after 4h of CFA injection and every day after 4h of daily treatment until 5 days with interval of day four in order to assess the tolerance effect of capillarisin. Further analysis was performed in CFA-induced mice exploring various molecular and signaling pathways such as NF-κB, AP-1 and ERK-CREB involved in the persistent of pain sensations. Pre-treatment of capillarisin strongly inhibited NF-κB mediated genes (iNOS, COX-2), involved in pain. The plasma leading nitrite production was significantly reduced by capillarisin. Moreover, i.p. administration of capillarisin markedly suppressed the adenosine 5׳-triphosphate (ATP) in plasma and substance P in CFA-induced paw tissue. Conclusions: The present study indicates that capillarisin possessed promising anti-hyperalgesic and anti-allodynic effects through the inhibition of various inflammatory pain signaling, suggesting that capillarisin constitutes a significant component for the treatment of inflammatory pain. [Copyright &y& Elsevier]

Abstract: Ethnopharmacological relevance: Ginseng and ginsenosides are frequently used in the treatment of chronic inflammatory diseases. Recently, 20-O-β- d-glucopyranosyl-20(S)-protopanaxadiol (GPD), the main metabolite of ginsenosides, was reported to have both anti-allergic and anti-pruritic effects. The immunomodulatory effects of GPD-fortified ginseng extract (GFGE) on atopic dermatitis (AD)-like symptoms in mice were investigated. This study was designed to investigate the preventive effect of GFGE on AD-like symptoms. Materials and methods: The effects of orally administered GFGE on Dermatophagoides farinae body extract (DFE)-induced AD-like symptoms in NC/Nga mice were assessed by analyzing dermatitis score, ear thickness, scratching time, skin histological changes, and serum level of macrophage-derived chemokine (MDC). In addition, splenocytes were isolated from the mice and stimulated with anti-CD3 and anti-CD28 monoclonal antibodies to produce cytokines. Results: Oral administration of GFGE significantly attenuated DFE-induced increases in dermatitis score, ear thickness, scratching time, and severity of skin lesions in NC/Nga mice. GFGE treatment also reduced level of MDC in serum, infiltration of eosinophils and mast cells in skin, and production of cytokines in splenocytes. Conclusions: These results suggest that GFGE might ameliorate DFE-induced AD-like symptoms and be an alternative therapeutic agent for the prevention of AD. [ABSTRACT FROM AUTHOR]

Abstract: Ethnopharmacological relevance: Geniposidic acid (GA) is an iridoid glucoside isolated from Gardeniae jasminoides Ellis (Rubiaceae) that has long been used to treat inflammation, jaundice and hepatic disorders. Aims of the study: This study examined the cytoprotective properties of GA against d-galactosamine (GalN)/lipopolysaccharide (LPS)-induced fulminant hepatic failure. Materials and methods: Mice were given an intraperitoneal injection of GA (12.5, 25, 50mg/kg) 1h before receiving GalN (800mg/kg)/LPS (40μg/kg). Liver and blood samples were collected 1 and 8h after GalN/LPS injection. Results: The survival rate of the GA group was significantly higher than the control. GalN/LPS increased serum aminotransferase activity, serum tumor necrosis factor-α level and hepatic lipid peroxidation and decreased hepatic glutathione content. These changes were attenuated by GA. GA augmented increases in serum interleukin-6 level, heme oxygenase-1 and NF-E2-related factor 2 protein expression. Mice treated with GA decreased cleaved caspase-8 and caspase-3 protein expression and showed significantly fewer apoptotic cells. GA increased Bcl-xL protein expression and decreased Bax protein expression. Moreover, GA treatment enhanced phosphorylation of signal transducer and activator of transcription 3. Conclusion: Our findings suggest that geniposidic acid alleviates GalN/LPS-induced liver injury by enhancing antioxidative defense system and reducing apoptotic signaling pathways. [Copyright &y& Elsevier]

Abstract: Ethnopharmacological relevance: Artemisia capillaris Thunberg (Compositae) have been used as traditional medicine as a diuretic, liver protective agent, and for amelioration of inflammatory and analgesic disorders. The present study was carried out to establish the scientific rationale for treating inflammation and to find active principles from A. capillaris. The aim of the present study is to investigate the possible anti-inflammatory mechanism of the major component (capillarisin) isolated from A. capillaris via inhibition of MyD88/TIRAP inflammatory signaling both in vitro and in vivo models. Materials and methods: The nitrite, PGE2, and TNF-α productions were evaluated by Griess reagent and ELISA kits. The protein and mRNA expression levels were investigated by Western blot and RT-PCR. The NF-κB and AP-1 DNA-binding was performed by electrophoretic mobility shift assay. The CFA- and carrageenan-induced paw edema was performed in ICR mice in which 20 and 80mg/kg body weight of capillarisin was administered intraperitoneally (i.p.). Results: The results demonstrated that pretreatment with capillarisin effectively inhibited the LPS-induced activation of NF-κB, Akt, and MAP kinase-activated inflammatory genes, which is mediated by MyD88 and TIRAP. Treatment with capillarisin reduced the mRNA and protein levels of iNOS and COX-2 in RAW 264.7 cells as assessed by RT-PCR and Western blot. Capillarisin suppressed LPS-induced inhibitory kappa kinase (IKK) phosphorylation and the degradation of inhibitory kappa B (IκBα) and prevented the nuclear translocation of p65 and p50. Capillarisin also exhibited a promising inhibitory effect on the LPS-induced NF-κB and AP-1 DNA binding activity based on an electrophoretic mobility shift assay. The LPS-induced activation of p-JNK, p-p38, p-ERK, and p-Akt was significantly inhibited. In addition, the TNF-α level in the media was effectively reduced by capillarisin. In vivo experimental analysis revealed that capillarisin (20 and 80mg/kg, i.p.) inhibited complete Freund''s adjuvant (CFA)-and carrageenan-induced paw edema, nitrite production in plasma, and TNF-α, a pro-inflammatory cytokine production. Conclusion: The results presented here demonstrate that capillarisin has consistent anti-inflammatory properties and acts by inhibiting inflammatory mediators in in vitro and in vivo experimental models, and suggest its potential utility in the control of inflammatory disorders. [Copyright &y& Elsevier]

Abstract: Bone homeostasis is maintained by a balance between bone resorption by osteoclasts and bone formation by osteoblasts. Osteoporosis occurs when osteoclast activity surpasses osteoblast activity. Pro-inflammatory cytokines stimulate osteoclast differentiation and activity by increasing production of macrophage-colony stimulating factor and receptor activator of nuclear factor-κB ligand (RANKL). In this study, we investigated whether Magnoliae Flos (MF), one of the most commonly used Chinese medicinal herbs for managing rhinitis, sinusitis and headache, could effectively inhibit osteoporosis. In ovariectomized (OVX) mice compared to sham mice, the body weight increased and serum levels of alkaline phosphatase (ALP), tartrate resistant acid phosphatase 5b, calcium, and osteocalcin were significantly elevated. However, orally administrated MF extract substantially inhibited the increased body weight and serum levels of bone turnover markers, without any evidence of tissue toxicity. MF extract treatment significantly reversed the morphometric parameters of ovariectomy-induced bone loss, including trabecular bone volume, thickness, number, separation, and bone density, to almost the same levels of the sham mice. Furthermore, MF extract reduced the RANKL-mediated osteoclast differentiation and bone resorption by inhibiting the activities of matrix metalloproteinases (MMPs) and cathepsin K in mouse bone marrow macrophages. MF extract appeared to increase ALP activity in murine osteoblastic cells. Taken together, MF extract may be a beneficial supplement for the blockade of osteoporosis progression, particularly for the management of postmenopausal osteoporosis. [Copyright &y& Elsevier]

Abstract: Aims of the study: We recently reported the potential antioxidant and anti-inflammatory activities of umbelliferone 6-carboxylic acid (UMC) isolated from the whole plants of Angelica decursiva. In this study, we elucidated the anti-inflammatory mechanisms of UMC in vitro and in vivo. Methods: The inhibitory effects of UMC on the production of nitric oxide (NO), prostaglandin E2 (PGE2), and tumor necrosis factor-α (TNF-α), the expression of nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), the activation of nuclear factor kappa B (NF-κB) were evaluated using lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. The reactive oxygen species (ROS) generation inhibitory activity of UMC was evaluated using t-butyl hydroperoxide (t-BHP)-induced RAW 264.7 cells. Furthermore, the in vivo anti-inflammatory activity of UMC was evaluated using carrageenan induced mouse paw edema model. Results: UMC dose-dependently inhibited NO and PGE2 production by down-regulating iNOS and COX-2 protein expression in LPS-stimulated RAW 264.7 macrophages. UMC also suppressed the production of the proinflammatory cytokine TNF-α in LPS stimulated RAW 264.7 cells in a concentration dependent manner. In addition, UMC dose-dependently prevented LPS-induced nuclear translocation of NF-κB in RAW 264.7 macrophages. Furthermore, UMC exhibited the inhibitory activity against t-BHP-induced ROS generation in RAW 264.7 cells with an IC50 value of 705.1μg/ml. Moreover, UMC inhibited λ-carrageenan induced mouse paw edema by 70.40 and 60.20% at doses of 50 and 25mg/kg body weight, respectively. Conclusion: The combined results of this study indicate that UMC is an important anti-inflammatory constituent of A. decursiva and its anti-inflammatory effect was due to its ability to inhibit the production of inflammatory mediators via inhibition of NF-κB activation pathway. [Copyright &y& Elsevier]

Abstract: Background: Hyperechogenicity of substantia nigra (SN+) is a common finding in transcranial ultrasound studies of parkinsonian patients. However, this feature is also found in 13–16% of ET patients. The possible links between ET and PD are of special interest, particularly with the familial aggregated data supporting this association. However, few studies have been conducted regarding the factors associated with the emergence of PD in the ET population. In this study, we investigated the possible association between SN+ and putative premotor symptoms of PD in patients with ET. Methods: A total of 47 patients with PD and 64 patients with ET were enrolled in the study. All patients underwent TCS and completed a structured interview for putative premotor symptoms of PD. Results: As expected, there were significant differences observed in the frequency and size of SN+, and the prevalence of the putative premotor symptoms of PD. More interestingly, in the ET group a significant association between SN+ and each premotor symptom was observed and a trend was also found that ET cases with more putative premotor symptoms of PD had a greater size of SN+. In contrast, in the PD group, SN+ was not influenced by the cumulative effect of premotor symptoms. Conclusion: The results of this study suggest that SN+ in patients with ET is influenced by the putative premotor symptoms of PD. [Copyright &y& Elsevier]

Rehmanniae Radix Preparata, the steamed root of Rehmannia glutinosa Libosch, has been widely used for the treatment of inflammatory conditions in Oriental medicines. In this study we evaluated the effects of 2,5-dihydroxyacetophenone (DHAP) isolated from Rehmanniae Radix Preparata on inflammatory responses in lipopolysaccharide (LPS)-stimulated RAW264.7 mouse macrophages. LPS-stimulated RAW264.7 cells were used to investigate the anti-inflammatory activity of DHAP on the production of inflammatory mediators such as nitric oxide (NO), inducible NO synthase (iNOS), tumor necrosis factor-α (TNF-α), and interleukin (IL)-6. DHAP significantly inhibited NO production via the suppression of iNOS expression and significantly decreased levels of the pro-inflammatory cytokines TNF-α and IL-6 via the down-regulation of their mRNA expression in LPS-stimulated RAW264.7 cells. DHAP potently inhibited the phosphorylation of extracellular signal-related kinase (ERK) 1/2 and the nuclear translocation of nuclear factor-κB (NF-κB) p65 in LPS-stimulated cells. These results indicate that DHAP inhibits the production of inflammatory mediators in activated macrophages by blocking the ERK1/2 and NF-κB signaling pathways. Our results suggest that DHAP from Rehmanniae Radix Preparata has anti-inflammatory activity in activated macrophages, raising the possibility that this compound has a therapeutic potential for inflammatory conditions. [ABSTRACT FROM AUTHOR]

Abstract: Ethnopharmacological relevance: Cinnamomum cassia Blume has been used as a traditional Chinese herbal medicine for alleviation of fever, inflammation, chronic bronchitis, and to improve blood circulation. Aim of the study: We addressed whether 2-methoxycinnamaldehyde (2-MCA), one of active ingredients of Cinnamomum cassia, reduces vascular cell adhesion molecule-1 (VCAM-1) expression in tumor necrosis factor-alpha (TNF-α)-activated endothelial cells and protects ischemia/reperfusion (I/R)-injury due to heme oxygenase (HO)-1 induction. Materials and methods: Adult male rats were subjected to 30min of ischemia by occlusion of the left anterior descending coronary artery followed by 24h of reperfusion. Rats were randomized to receive vehicle or 2-MCA (i.v.) 10min before reperfusion. Results: Administration of 2-MCA significantly improved I/R-induced myocardial dysfunction by increasing the values of the first derivative (±dp/dt) of left ventricular pressure and decreased infarct size. In addition, 2-MCA reduced the expression of high mobility group box 1 (HMGB1), an activator of the inflammatory cascade when released into the extracellular space, and VCAM-1 in I/R myocardium along with increase of HO-1 induction. The reduced injury was accompanied by significantly reduction of neutrophils infiltration and increased SOD activity in ischemic tissues and reduced serum level of cardiac troponin I (cTnI). Furthermore, 2-MCA significantly increased HO-1 induction by translocation of Nrf-2 from cytosol to nucleus in endothelial cells. Inhibition of VCAM-1 expression by 2-MCA was reversed both by SnPPIX, a HO-1 inhibitor and siHO-1 RNA trasfection in TNF-α-activated cells. In addition, 2-MCA significantly inhibited NF-κB luciferase activity in TNF-α-activated endothelial cells. As expected, 2-MCA significantly inhibited monocyte (U937) adhesion to endothelial cells. Conclusion: We concluded that 2-MCA protects of myocardial I/R-injury due to antioxidant and anti-inflammatory action possibly by HO-1 induction which can be explained why Cinnamomum cassia has been used in inflammatory disorders. [Copyright &y& Elsevier]

Abstract: Ethnopharmacological relevance: Cyperus rotundus, a well-known oriental traditional medicine, has been reported to exhibit wide spectrum activity in biological systems including the circulatory system, however, little information is available on its antiplatelet activity. This study was undertaken to investigate the antiplatelet effects of Cyperus rotundus EtOH extract (CRE) and its constituent compounds. Materials and methods: The antiplatelet activities of CRE and its eight constituent compounds were evaluated by examining their effects on rat platelet aggregations in vitro and ex vivo, and on mice tail bleeding times. Results: During the in vitro platelet aggregation study, CRE showed significant and concentration-dependent inhibitory effects on collagen-, thrombin-, and/or AA-induced platelet aggregation. Of its eight components, (+)-nootkatone was found to have the most potent inhibitory effect on collagen-, thrombin-, and AA-induced platelet aggregation. In addition, CRE- and (+)-nootkatone-treated mice exhibited significantly prolonged bleeding times. Furthermore, (+)-nootkatone had a significant inhibitory effect on rat platelet aggregation ex vivo. Conclusions: This study demonstrates the antiplatelet effects of CRE and its active component (+)-nootkatone, and suggests that these agents might be of therapeutic benefit for the prevention of platelet-associated cardiovascular diseases. [Copyright &y& Elsevier]

Abstract: Ethnopharmacological relevance: The methanol extract of Cimicifugae Rhizome has been traditionally used in various disorders including inflammation. Aim of the study: The aim of the study is to explore whether anti-inflammatory action of 3 active compounds, two triterpenoid glycosides (cimiside E, 23-O-actylshengmanol-3-xyloside) and one furanocoumarin (isoimperatorin), isolated from Cimicifugae Rhizome is related with peroxisome proliferator-activated receptor-γ (PPAR-γ) expression in human umbilical endothelial cell line, EA.hy926 cells. Materials and methods: Cell viability and production of reactive oxygen species were performed. In addition, adhesion of monocyte into endothelial cells and western blot for expression of adhesion molecules and signal proteins were investigated in tumor necrosis factor-α (TNF-α)-activated cells. Results: Pretreatment of test compounds significantly reduced reactive oxygen species (ROS) production and expression of vascular cell adhesion molecule-1 (VCAM-1), but not intercellular cell adhesion molecule-1 (ICAM-1). Three compounds all dose-dependently increased not only PPAR-γ expression in EA.hy926 cells but inhibited TNF-α-induced phosphorylation of Akt, extracelullar-signal-regulated kinase (ERK) and protein kinase C (PKC) with different specificity. Finally, they prevented TNF-α-induced adhesion of U937 monocytic cells to EA.hy926 cells. Conclusions: The present results show that cimiside E, 23-O-actylshengmanol-3-xyloside, isoimperatorin isolated from Cimicifugae Rhizome selectively inhibits TNF-α-induced expression of VCAM-1 at least by upregulation of PPAR-γ, and signals for ERK1/2, PI3K, and PKC are involved in this effect. [Copyright &y& Elsevier]

The purpose of our study was to prospectively evaluate cardiac [(123)I]metaiodobenzylguanidine (MIBG) uptake in patients with cerebrovascular disease (CVD) who develop clinical symptoms of vascular Parkinsonism (VP). A total of 19 consecutive patients who developed Parkinsonism during the course of their CVD were enrolled in the study; 16 age-matched subjects, and 30 patients with Parkinson's disease (PD) were also evaluated with cardiac MIBG uptake. MIBG uptake was assessed using the ratio of the heart to the upper mediastinum (H/M) according to planar scintigraphic data. The mean H/M ratio was significantly higher in patients with VP than in those with PD (2.28 +/- 0.41 vs. 1.27 +/- 0.13; P < 0.001). MIBG uptake did not differ between VP and controls (2.46 +/- 0.33; P > 0.05). Our findings suggest that myocardial postganglionic sympathetic dysfunction found in PD is absent in most patients with VP. MIBG single photon emission computed tomography imaging may be useful to help distinguish between PD and VP patients in clinical practice. [ABSTRACT FROM AUTHOR]

1. Tumor necrosis factor (TNF)-alpha is known to induce the expression of CCL11 and CCR3 via the activation of NF-kappaB. CCL11 (eotaxin), the C-C chemokine, is a potent chemoattractant for eosinophils and Th2 lymphocytes, and CCR3 is the receptor for CCL11. 2. In order to determine the effects of rosmarinic acid on the TNF-alpha-induced upregulation of CCL11 and CCR3 in human dermal fibroblasts, we performed an enzyme-linked immunosorbent assay for CCL11 and a Western blot assay for CCR3. The TNF-alpha-induced expression of CCL11 and CCR3 genes was attenuated by rosmarinic acid. 3. In our NF-kappaB luciferase reporter system, TNF-alpha-induced NF-kappaB activation was observed to be reduced by rosmarinic acid. In accordance with this result, rosmarinic acid also inhibited TNF-alpha-induced phosphorylation and degradation of IkappaB-alpha, as well as nuclear translocation of NF-kappaB heterodimer induced by TNF-alpha. This suggests that rosmarinic acid downregulates the expression of CCL11 and CCR3 via the inhibition of NF-kappaB activation signaling. 4. Using the NF-kappaB luciferase reporter system, Western blot analysis, and IKK-beta activity assay, we determined that rosmarinic acid inhibits IKK-beta activity in NF-kappaB signaling, which upregulates the expression of CCL11 and CCR3. Additionally, TNF-alpha-induced secretion of soluble intercellular adhesion molecule-1 and soluble vascular cell adhesion molecule-1 molecules was found to be attenuated by rosmarinic acid. 5. Our results show that rosmarinic acid inhibits the expression of CCL11 and CCR3 by suppressing the IKK-beta activity in NF-kappaB activation signaling. Further, these results suggest that rosmarinic acid might inhibit the expression of NF-kappaB promoter-related genes. [ABSTRACT FROM AUTHOR]

1. The effects of acharan sulphate, a glycosaminoglycan isolated from the giant African snail Achatina fulica, on angiogenesis in the granulation tissue were analysed using an air pouch-type carrageenin-induced inflammation model in rats and a cotton thread-induced inflammation model in mice. 2. In the carrageenin-induced inflammation model in rats, intra-pouch injections of acharan sulphate (5 and 50 micro g) inhibited the pouch fluid accumulation and the granulation tissue formation as well as the angiogenesis in the granulation tissue at day 6 in a dose-dependent manner. 3. The inhibitory effects of acharan sulphate at 50 micro g on the pouch fluid accumulation and the leucocyte infiltration into the pouch fluid was not so effective as that of the cyclo-oxygenase inhibitor indomethacin at 100 micro g, but the inhibitory effects of acharan sulphate at 50 micro g on the granulation tissue formation and angiogenesis in the granulation tissue were almost the same as those of indomethacin at 100 micro g. 4. Acharan sulphate did not affect levels of vascular endothelial growth factor (VEGF) in the granulation tissue and in the pouch fluid at day 6, but indomethacin significantly lowered them. 5. In the cotton thread-induced inflammation model in mice, injections of acharan sulphate (10 micro g) at the site of the cotton thread implantation inhibited the granulation tissue formation and angiogenesis as indomethacin (20 micro g) did. Acharan sulphate (10 micro g) did not affect levels of VEGF in the cotton thread-induced granulation tissue at day 5, but indomethacin (20 micro g) significantly lowered them. 6. In culture of human vascular endothelial cells, acharan sulphate at 10 and 100 micro g ml(-1) inhibited VEGF-induced capillary tube formation. 7. These findings suggest that the inhibitory effect of acharan sulphate on angiogenesis in carrageenin- and cotton thread-induced granulation tissues is not due to the inhibition of VEGF protein induction, but is due to the inhibition of VEGF-induced vascular tube formation. [ABSTRACT FROM AUTHOR]