bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evaluation of the effect of topical application of lavender oil on autonomic nerve activity in dogs
Authors: Komiya Migiwa , Sugiyama Akihiko , Tanabe Kazuko , Uchino Tomiya , Takeuchi Takashi 
Published: June 2009

Abstract
Objective—To investigate the effect of topical application of undiluted lavender oil on sympathovagal activity in dogs.
Animals—5 healthy adult male Beagles.
Procedures—An ambulatory ECG monitor (Holter recorder) was placed on each dog (day0), and 48-hour ECGs were recorded, beginning at 8:00 the next day (day 1). Lavender oil (0.18 mL) or saline (0.9% NaCl) solution (0.18 mL) was topically applied to the inner pinnas of both ears of all dogs at 8:30, 12:00, 15:30, and 19:00 on day 2. Each trial was duplicated in each dog, with an interval of 3 to 4 days between trials. Spectral indices of heart rate variability, power in the high-frequency range, and the ratio of low-frequency to high-frequency power were calculated as an indirect estimate of autonomic nerve activity.
Results—When dogs were treated with lavender oil, the mean heart rate was significantly lower during the period of 19:00 to 22:30 on day 2, compared with the mean heart rate during the same period when dogs were treated with saline solution. On the other hand, high-frequency power during the period of 15:30 to 19:00 was significantly higher when dogs were treated with lavender oil, compared with the high-frequency power during the same period when dogs were treated with saline solution.
Conclusions and Clinical Relevance—The study revealed some evidence that topical application of lavender oil affected vagal activity in dogs. However, whether such an effect exists and whether lavender oil has a calming effect on dogs remains equivocal and requires additional investigation.
Leaf Flavonoid Aglycone Patterns, Ethnobotany and Conservation of <i>Schima wallichii</i>
Authors: Joshi Kunjani 
Published: June 2009

Schima wallichii (DC.) Korth (Chilaune) is widely distributed in the various habitats of Himalaya. Information regarding chemical constituents of this species is very limited. During the chemotaxonomic study of some angiosperms, falconoid aglycone : flavonal quercetin was isolated from the leaves of Schima Wallichii using standard procedures after seperation and purification by paper chromatography and TLC (thin layer chromatography) plates in several solvent system, but other falconoid were not detected. The ethno botanical study of Schima Wallichii was also carried out. Various parts and the products of this species are locally used for medicine, fuel and other domestic purposes. This indigenous knowledge can be integrated in the local plan that can help to the poverty alleviation and economic development of the villages. But at present, this plant is under serious threat due to habitat destruction and over-exploitation. A holistic approach is, therefore, essential for the sustainable conversation of this species. In this paper , strategies for conservation of the plant, its resources and habitatshave also been proposed.Key words: Flavonoids; quercetin; ethnobotany; consersation; holistic approachdoi: 10.3126/eco.v13i0.1622Ecoprint (An International Journal of Ecology) Vol. 13, No. 1, 2006 Page 9-13
Effect of Coal Smoke Pollution on the Biomass and Chlorophyll Pigments of <i>Brassica juncea</i>
Authors: Saquib Mohammad 
Published: June 2009

The effect of coal smoke pollution on the biomass and chlorophyll pigments of Brassica juncea were studied at 0.5, 2, 4, 6 and 20 km distance leeward from a thermal power plant complex. The root, shoot and total biomass and chlorophyll a, chlorophyll b and total chlorophyll were significantly reduced up to a distance of 4 km from the source of pollution. The data indicates that the degree of response increased with decreasing distance from the source of pollution in comparison to the reference site ‘c' situated at 20 km. Biomass and chlorophyll pigments showed a significant and positive relationship with the distance from the source. Key words: Air pollution, Brassica juncea, biomass, chlorophyll. doi: 10.3126/eco.v15i0.1935 ECOPRINT 15: 1-6, 2008
Seasonal Variation of Edaphic Features of Madhupur Sal Forest, Bangladesh
Authors: Hoque Ahmed Emdadul , Nazrul-Islam A K. M. , Imamul Huq S. M. 
Published: June 2009

Seven stands were selected in different areas of the Madhupur Sal (Shorea robusta) forest to study the seasonal variation of available nutrients in soils. Soil samples were collected after every two months at two depths (top soil 0-10 cm and 10-20 cm) and their physicochemical properties were determined. The percentage of soil moisture was found to vary in different stands and pH values of soil ranged from 4.60 to 6.28. Seasonal fluctuation of electrical conductivity was observed. An increasing trend of sodium accumulation was found in both top and sub-soil layers at all the stands. The concentration of potassium also showed a decreasing tendency in both layers. The exchangeable calcium and magnesium contents did not show significant (pH 0.05) seasonal variation. The high values of manganese and iron were confined to top soil and values decreased down the profile. Key words: Shorea robusta, soil, physico-chemical characteristics, seasonal variation. doi: 10.3126/eco.v15i0.1936 ECOPRINT 15: 7-14, 2008
Species Richness and Biomass Relationship in Burned Sites of <i>Imperata-Saccharum</i> Grassland in Suklaphanta Wildlife Reserve, Nepal
Authors: Pant Pitamber , Lekhak Hari Datt 
Published: June 2009

Present study was conducted in the Suklaphanta Wildlife Reserve, Kanchanpur district, far western Nepal during June-July, 2005. A total of 150 quadrats (1m x 1m) were sampled in three differentially treated sites (unburned, early burned and late burned). Plant community composition and above ground biomass at different sites were quantified. The relationship between species richness and biomass was detected in the Imperata-Saccharum grassland. Altogether 100 plant species were recorded in the grassland. The highest number of species (62) was recorded in early burned site, whereas lowest (54) species were recorded from unburned site. Among all species recorded, 23 were common to all sites. The highest species richness (13 species/m²) was recorded in the early burned plot. The above ground biomass was highest (583.93 g/m²) in unburned plot. Mean above ground biomass of all the three sites of the grassland was 249.72 g/m². These results indicate that the burning has significant impact on both species richness and biomass. Maximum species richness was found in the biomass interval between ca. 100-300 g/m² when all the sites were combined. A hump shaped pattern was observed in the grassland when all the data were combined. Key words: Species richness, biomass, generalized linear model, fire. doi: 10.3126/eco.v15i0.1938 ECOPRINT 15: 23-27, 2008
Effect of some Essential Oils on Seed Germination and Seedling Length of <i>Parthenium hysterophorous</i> L.
Authors: Paudel V. R. , Gupta V.N. P. 
Published: June 2009

Effect of plant essential oils on seed germination and seedling growth of Parthenium hysterophorus was examined. Essential oils of Eucalyptus, Camphor, and Lemongrass were used in the experiments at different concentrations (0 to 20 ml.l-1). Water imbibed (36 h) seeds were germinated at 25°C ± 1 in petriplates containing 3 layers of filter papers soaked in distilled water and added with 1.5 ml of a given essential oil of particular concentration. Experiments were carried out taking three replicas. Observations were made at an interval of 24 h from the 4th day of incubation till 20th. All essential oils significantly (P < 0.05) reduced seed germination irrespective of their sources. Effects of plant sources were, however, not significant (P>0.05). Key words: Noxious weed, terpenes, sesquiterpenes, essential oil. doi: 10.3126/eco.v15i0.1945 ECOPRINT 15: 69-73, 2008
Critical roles of decompression in functional recovery of ex vivo spinal cord white matter
Authors: Ouyang Hui , Galle Beth , Li Jianming , Nauman Eric , Shi Riyi 
Published: June 2009

Object
The correlations between functional deficits, the magnitude of compression, and the role of sustained compression during traumatic spinal cord injury remain largely unknown. Thus, the functional outcome of this type of injury with or without surgical intervention is rather unpredictable. To elucidate how severity and duration of compression affect cord function, the authors have developed a method to study electrophysiological characteristics and axonal membrane damage in white matter from guinea pig spinal cord.

Methods
Ventral white matter strips isolated from adult guinea pigs were compressed by a compression rod at a level of either 60 or 80% and held briefly, for 30 minutes, or for 60 minutes. In half the experimental groups, a decompression phase consisting of probe withdrawal and 30 minutes of recovery was also applied. For all cord samples, functional response was continuously monitored through compound action potential (CAP) recording. In addition, axonal membrane damage was assessed by a horseradish peroxidase (HRP) exclusion assay.

Results
After 30 minutes of sustained compression at levels of 60 or 80%, a spinal cord decompression procedure caused a significant CAP recovery, with specimens reaching 97.5 ± 6.84% (p < 0.05) and 56.2 ± 6.14% (p < 0.05) of preinjury amplitude, respectively. After 60 minutes of compression, the amount of CAP recovery following the decompression stage was only 65.5 ± 9.33% for 60% compression (p < 0.05) and 29.8 ± 6.31% for 80% compression (p < 0.05). Unlike the CAP response, HRP uptake did not increase during sustained compression, and the data showed that HRP staining was primarily time dependent.

Conclusions
The degree of axonal membrane damage is not exacerbated during sustained compression. However, the electrical conductivity of the cord white matter weakens throughout the duration of compression. Therefore, decompression is a viable procedure for preservation of neurological function following compressive injury.
Small Interfering RNA against Transcription Factor STAT6 Inhibits Allergic Airway Inflammation and Hyperreactivity in Mice
Authors: Darcan-Nicolaisen Yasemin , Meinicke Holger , Fels Gabriele , Hegend Olga , Haberland Annekathrin , Kühl Anja , Loddenkemper Christoph , Witzenrath Martin , Kube Stefanie , Henke Wolfgang , Hamelmann Eckard 
Published: June 2009

Abstract
In the context of allergic immune responses, activation of STAT6 is pivotal for Th2-mediated IgE production and development of airway inflammation and hyperreactivity. We analyzed whether gene silencing of STAT6 expression by RNA interference was able to suppress allergen-induced immune and airway responses. Knockdown effectiveness of three different STAT6 siRNA molecules was analyzed in murine and human cell cultures. The most potent siRNA was used for further testing in a murine model of allergen-induced airway inflammation and airway hyperreactivity (AHR). BALB/c mice were sensitized with OVA/alum twice i.p. (days 1 and 14), and challenged via the airways with allergen (days 28–30). Intranasal application of STAT6 siRNA before and during airway allergen challenges reduced levels of infiltrating cells, especially of eosinophils, in the bronchoalveolar lavage fluid, compared with GFP siRNA-treated sensitized and challenged controls. Allergen-induced alterations in lung tissues (goblet cell hyperplasia, peribronchial inflammation with eosinophils and CD4 T cells) were significantly reduced after STAT6 siRNA treatment. Associated with decreased inflammation was a significant inhibition of the development of allergen-induced in vivo AHR after STAT6 siRNA treatment, compared with GFP siRNA-treated sensitized and challenged controls. Importantly, mRNA and protein expression levels of IL-4 and IL-13 in lung tissues of STAT6-siRNA treated mice were significantly diminished compared with sensitized and challenged controls. These data show that targeting the key transcription factor STAT6 by siRNA effectively blocks the development of cardinal features of allergic airway disease, like allergen-induced airway inflammation and AHR. It may thus be considered as putative approach for treatment of allergic airway diseases such as asthma.
Mechanism and Repertoire of ASC-Mediated Gene Expression
Authors: Hasegawa Mizuho , Imamura Ryu , Motani Kou , Nishiuchi Takumi , Matsumoto Norihiko , Kinoshita Takeshi , Suda Takashi 
Published: June 2009

Abstract
Apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) is an adaptor molecule that mediates inflammatory and apoptotic signals. Although the role of ASC in caspase-1-mediated IL-1β and IL-18 maturation is well known, ASC also induces NF-κB activation and cytokine gene expression in human cells. In this study, we investigated the molecular mechanism and repertoire of ASC-induced gene expression in human cells. We found that the specific activation of ASC induced AP-1 activity, which was required for optimal IL8 promoter activity. ASC activation also induced STAT3-, but not STAT1-, IFN-stimulated gene factor 3- or NF-AT-dependent reporter gene expression. The ASC-mediated AP-1 activation was NF-κB-independent and primarily cell-autonomous response, whereas the STAT3 activation required NF-κB activation and was mediated by a factor that can act in a paracrine manner. ASC-mediated AP-1 activation was inhibited by chemical or protein inhibitors for caspase-8, caspase-8-targeting small-interfering RNA, and p38 and JNK inhibitors, but not by a caspase-1 inhibitor, caspase-9 or Fas-associated death domain protein (FADD) dominant-negative mutants, FADD- or RICK-targeting small-interfering RNAs, or a MEK inhibitor, indicating that the ASC-induced AP-1 activation is mediated by caspase-8, p38, and JNK, but does not require caspase-1, caspase-9, FADD, RICK, or ERK. DNA microarray analyses identified 75 genes that were induced by ASC activation. A large proportion of them was related to transcription (23%), inflammation (21%), or cell death (16%), indicating that ASC is a potent inducer of inflammatory and cell death-related genes. This is the first report of ASC-mediated AP-1 activation and the repertoire of genes induced downstream of ASC activation.
Social Stress Enhances Allergen-Induced Airway Inflammation in Mice and Inhibits Corticosteroid Responsiveness of Cytokine Production
Authors: Bailey Michael T. , Kierstein Sonja , Sharma Satish , Spaits Matthew , Kinsey Steven G. , Tliba Omar , Sheridan John F. , Panettieri Reynold A. , Haczku Angela 
Published: June 2009

Abstract
Chronic psychosocial stress exacerbates asthma, but the underlying mechanisms remain poorly understood. We hypothesized that psychosocial stress aggravates allergic airway inflammation by altering innate immune cell function. The effects of stress on airway inflammation, lung function, and glucocorticoid responsiveness were studied in a novel in vivo murine model of combined social disruption stress and allergic sensitization. The effects of corticosterone were assessed on cytokine profile and glucocorticoid receptor activation in LPS-stimulated spleen cell cultures in vitro. Airway inflammation resolved 48 h after a single allergen provocation in sensitized control mice, but not in animals that were repeatedly exposed to stress before allergen challenge. The enhanced eosinophilic airway inflammation 48 h after allergen challenge in these mice was associated with increased levels of IL-5, GM-CSF, IgG1, thymus-activated and regulatory chemokine, TNF-α, and IL-6 in the airways and a diminished inhibition of these mediators by corticosterone in LPS-stimulated splenocyte cultures in vitro. Stress-induced reduction of the corticosteroid effects paralleled increased p65 expression and a decreased DNA-binding capability of the glucocorticoid receptor in vitro. Furthermore, glucocorticoid receptor mRNA and protein expression in the lungs of mice exposed to both stress and allergen was markedly reduced in comparison with that in either condition alone or in naive mice. Thus, exposure to repeated social stress before allergen inhalation enhances and prolongs airway inflammation and alters corticosterone responsiveness. We speculate that these effects were mediated at least in part by impaired glucocorticoid receptor expression and function.
Regulation of DNA Demethylation during Maturation of CD4+ Naive T Cells by the Conserved Noncoding Sequence 1
Authors: Aoki Kazuhisa , Sato Noriko , Yamaguchi Atsumi , Kaminuma Osamu , Hosozawa Takumi , Miyatake Shoichiro 
Published: June 2009

Abstract
Demethylation of transcriptional regulatory elements and gene coding regions is an important step in the epigenetic regulation of gene expression. Several noncoding conserved regions are required for the efficient transcription of cytokine genes. In this paper, we show that the deletion of one such sequence, conserved noncoding sequence 1 (CNS-1), interferes with the efficient demethylation of Th2 cytokine genes but has little effect on histone modifications in the area. Th2 cells derived from CD4 single-positive (SP) mature thymocytes exhibit more rapid demethylation of CNS-1 and Th2-specific cytokine genes and produce more Th2 cytokines than do Th2 cells derived from CD4-positive peripheral naive T cells. De-repression of the Th1 cytokine IFN-γ was also detected in Th2-primed CD4 SP thymocytes but not in naive T cells. Our results indicate that susceptibility to demethylation determines the efficiency and kinetics of cytokine gene transcription. The extrathymic maturation step undergone by naive T cells suppresses robust and rapid cytokine expression, whereas mature CD4 SP thymocytes maintain a rapid and less-specific cytokine expression profile. Finally, we detected the methyl cytosine binding protein MBD2 at CNS-1 in mature thymocytes, suggesting that this protein may regulate the demethylation of this region.
Steel Factor Enhances Supraoptimal Antigen-Induced IL-6 Production from Mast Cells via Activation of Protein Kinase C-β
Authors: Fehrenbach Kerstin , Lessmann Eva , Zorn Carolin N. , Kuhny Marcel , Grochowy Gordon , Krystal Gerald , Leitges Michael , Huber Michael 
Published: June 2009

Abstract
Ag-triggered mast cell (MC) activation follows a bell-shaped dose-response curve. Reduced activation in response to supraoptimal Ag concentrations is thought to be due to preferential engagement of inhibitory-acting proteins like SHIP1, Lyn, and protein kinase C (PKC)-δ. We show in this study that short-term prestimulation with Steel factor (SF) prevents supraoptimal Ag inhibition, resulting in synergistic MC degranulation and IL-6 secretion. These events are preceded by synergistic phosphorylation/activation of numerous signaling proteins, e.g., Erk, p38, and LAT. However, these effects of prestimulation with SF appear not to be due to reduced engagement of the attenuator SHIP1. Pharmacological analyses suggest that the activation of conventional PKCs is important for this synergy. Specifically, although we found that the conventional PKC inhibitor, Gö6976, likely has some PKC-independent targets in MCs, it led us to further studies that established SF plus Ag-induced IL-6 secretion was severely impaired in PKC-β−/− MCs, but not PKC-α−/− MCs. Thus, PKC-β joins PI3K and Btk as important players in this synergistic MC activation.
Ectodomain Shedding of FLT3 Ligand Is Mediated by TNF-α Converting Enzyme
Authors: Horiuchi Keisuke , Morioka Hideo , Takaishi Hironari , Akiyama Haruhiko , Blobel Carl P. , Toyama Yoshiaki 
Published: June 2009

Abstract
FLT3 ligand (FLT3L) has diverse roles in the hematopoietic system, which include stimulating proliferation of hematopoietic precursors and development of NK cells and dendritic cells. FLT3L is initially synthesized as a membrane-bound protein, which must be cleaved to become a soluble growth factor. However, little is known about the enzyme involved in the proteolytic release of FLT3L. In the current study, we show that shedding of FLT3L is metalloprotease-dependent, and that this proteolytic activity was abolished in fibroblasts lacking TNF-α converting enzyme (TACE) and could be rescued by reintroducing wild-type TACE in these cells. Moreover, we found that cells derived from the thymus of conditional TACE-deficient mice produce less FLT3L, and that serum FLT3L levels in these TACE mutant mice are significantly lower, both after LPS treatment and in the absence of such a challenge, further corroborating the relevance of TACE as FLT3L sheddase in vivo. Considering the involvements of FLT3 and FLT3L in hematopoietic malignancies and stem cell mobilization, the identification of the enzyme involved in FLT3L shedding may have important clinical implications.
Altered Expression of 15-Hydroxyprostaglandin Dehydrogenase in Tumor-Infiltrated CD11b Myeloid Cells: A Mechanism for Immune Evasion in Cancer
Authors: Eruslanov Evgeniy , Kaliberov Sergei , Daurkin Irina , Kaliberova Lyudmila , Buchsbaum Donald , Vieweg Johannes , Kusmartsev Sergei 
Published: June 2009

Abstract
Many cancers are known to produce high amounts of PGE2, which is involved in both tumor progression and tumor-induced immune dysfunction. The key enzyme responsible for the biological inactivation of PGE2 in tissue is NAD+-dependent 15-hydroxyprostaglandin dehydrogenase (15-PGDH). It is well established that cancer cells frequently show down-regulated expression of 15-PGDH, which plays a major role in catabolism of the PGE2. Here we demonstrate that tumor-infiltrated CD11b cells are also deficient for the 15-PGDH gene. Targeted adenovirus-mediated delivery of 15-PGDH gene resulted in substantial inhibition of tumor growth in mice with implanted CT-26 colon carcinomas. PGDH-mediated antitumor effect was associated with attenuated tumor-induced immune suppression and substantially reduced secretion of immunosuppressive mediators and cytokines such as PGE2, IL-10, IL-13, and IL-6 by intratumoral CD11b cells. We show also that introduction of 15-PGDH gene in tumor tissue is sufficient to redirect the differentiation of intratumoral CD11b cells from immunosuppressive M2-oriented F4/80+ tumor-associated macrophages (TAM) into M1-oriented CD11c+ MHC class II-positive myeloid APCs. Notably, the administration of the 15-PGDH gene alone demonstrated a significant therapeutic effect promoting tumor eradication and long-term survival in 70% of mice with preestablished tumors. Surviving mice acquired antitumor T cell-mediated immune response. This study for the first time demonstrates an important role of the 15-PGDH in regulation of local antitumor immune response and highlights the potential to be implemented to enhance the efficacy of cancer therapy and immunotherapy.
The Bcl-2 Family Antagonist ABT-737 Significantly Inhibits Multiple Animal Models of Autoimmunity
Authors: Bardwell Philip D. , Gu Jijie , McCarthy Donna , Wallace Craig , Bryant Shaughn , Goess Christian , Mathieu Suzanne , Grinnell Chris , Erickson Jamie , Rosenberg Saul H. , Schwartz Annette J. , Hugunin Margaret , Tarcsa Edit , Elmore Steven W. , McRae Bradford , Murtaza Anwar , Wang Li Chun , Ghayur Tariq 
Published: June 2009

Abstract
The Bcl-2 family of proteins plays a critical role in controlling immune responses by regulating the expansion and contraction of activated lymphocyte clones by apoptosis. ABT-737, which was originally developed for oncology, is a potent inhibitor of Bcl-2, Bcl-xL, and Bcl-w protein function. There is evidence that Bcl-2–associated dysregulation of lymphocyte apoptosis may contribute to the pathogenesis of autoimmunity and lead to the development of autoimmune diseases. In this study, we report that ABT-737 treatment resulted in potent inhibition of lymphocyte proliferation as measured by in vitro mitogenic or ex vivo Ag-specific stimulation. More importantly, ABT-737 significantly reduced disease severity in tissue-specific and systemic animal models of autoimmunity. Bcl-2 family antagonism by ABT-737 was efficacious in treating animal models of arthritis and lupus. Our results suggest that treatment with a Bcl-2 family antagonist represents a novel and potentially attractive therapeutic approach for the clinical treatment of autoimmunity.