Pronounced Increase (pronounced + increase)

Distribution by Scientific Domains


Selected Abstracts


N -methyl- d -aspartate, hyperpolarization-activated cation current (Ih) and ,-aminobutyric acid conductances govern the risk of epileptogenesis following febrile seizures in rat hippocampus

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 7 2010
Mohamed Ouardouz
Abstract Febrile seizures are the most common types of seizure in children, and are generally considered to be benign. However, febrile seizures in children with dysgenesis have been associated with the development of temporal lobe epilepsy. We have previously shown in a rat model of dysgenesis (cortical freeze lesion) and hyperthermia-induced seizures that 86% of these animals developed recurrent seizures in adulthood. The cellular changes underlying the increased risk of epileptogenesis in this model are not known. Using whole cell patch-clamp recordings from CA1 hippocampal pyramidal cells, we found a more pronounced increase in excitability in rats with both hyperthermic seizures and dysgenesis than in rats with hyperthermic seizures alone or dysgenesis alone. The change was found to be secondary to an increase in N -methyl- d -aspartate (NMDA) receptor-mediated excitatory postsynaptic currents (EPSCs). Inversely, hyperpolarization-activated cation current was more pronounced in naïve rats with hyperthermic seizures than in rats with dysgenesis and hyperthermic seizures or with dysgenesis alone. The increase in GABAA -mediated inhibition observed was comparable in rats with or without dysgenesis after hyperthermic seizures, whereas no changes were observed in rats with dysgenesis alone. Our work indicates that in this two-hit model, changes in NMDA receptor-mediated EPSCs may facilitate epileptogenesis following febrile seizures. Changes in the hyperpolarization-activated cation currents may represent a protective reaction and act by damping the NMDA receptor-mediated hyperexcitability, rather than converting inhibition into excitation. These findings provide a new hypothesis of cellular changes following hyperthermic seizures in predisposed individuals, and may help in the design of therapeutic strategies to prevent epileptogenesis following prolonged febrile seizures. [source]


Assessment of methane and nitrous oxide flux from mangroves along Eastern coast of India

GEOFLUIDS (ELECTRONIC), Issue 4 2008
R. CHAUHAN
Abstract Mangroves are considered to be a minor source of greenhouse gases (CH4 and N2O) in pristine environmental condition. However, estimates of efflux suggest that anthropogenic activities have led to a pronounced increase in greenhouse gas emission. Along the east coast of India, mangroves vary substantially in area, physiography and freshwater input, which ultimately modify the biogeochemical processes operating within this ecosystem. An attempt has here been made to elucidate the existing variation and role of climatic variability on the emission of greenhouse gases from mangroves. The flux estimates of CH4 and N2O have been quantified from Bhitarkanika mangrove accounting for spatial and temporal (seasonal) variation. The annual rates were estimated to be 0.096 × 10 9 g CH4 year,1 and 5.8 × 103g N2O year,1 for the whole mangrove area of the east coast of India. Upscaling these estimates yield an annual emission of 1.95 × 10 12 g CH4 year,1 and 1.1 × 10 11 g N2O year,1 from worldwide mangrove areas. The influence of elevated nutrient inputs through anthropogenic influence enhances the emission of greenhouse gas. The present article shows the need to develop an inventory on greenhouse gas flux from mangrove ecosystem. [source]


Sustained BMP Signaling in Osteoblasts Stimulates Bone Formation by Promoting Angiogenesis and Osteoblast Differentiation,,

JOURNAL OF BONE AND MINERAL RESEARCH, Issue 7 2009
Fengjie Zhang
Abstract Angiogenesis and bone formation are tightly coupled during the formation of the skeleton. Bone morphogenetic protein (BMP) signaling is required for both bone development and angiogenesis. We recently identified endosome-associated FYVE-domain protein (endofin) as a Smad anchor for BMP receptor activation. Endofin contains a protein-phosphatase pp1c binding domain, which negatively modulates BMP signals through dephosphorylation of the BMP type I receptor. A single point mutation of endofin (F872A) disrupts interaction between the catalytic subunit pp1c and sensitizes BMP signaling in vitro. To study the functional impact of this mutation in vivo, we targeted expression of an endofin (F872A) transgene to osteoblasts. Mice expressing this mutant transgene had increased levels of phosphorylated Smad1 in osteoblasts and showed increased bone formation. Trabecular bone volume was significantly increased in the transgenic mice compared with the wildtype littermates with corresponding increases in trabecular bone thickness and number. Interestingly, the transgenic mice also had a pronounced increase in the density of the bone vasculature measured using contrast-enhanced ,CT imaging of Microfil-perfused bones. The vessel surface and volume were both increased in association with elevated levels of vascular endothelial growth factor (VEGF) in osteoblasts. Endothelial sprouting from the endofin (F872A) mutant embryonic metatarsals cultured ex vivo was increased compared with controls and was abolished by an addition of a VEGF neutralizing antibody. In conclusion, osteoblast targeted expression of a mutant endofin protein lacking the pp1c binding activity results in sustained signaling of the BMP type I receptor, which increases bone formation and skeletal angiogenesis. [source]


Biodegradable External Stents Inhibit Saphenous Vein Graft Thickening in the Pig

JOURNAL OF CARDIAC SURGERY, Issue 6 2002
P Gadsdon
Aim: External, non-restrictive, macro-porous stents prevent neointima formation in porcine vein grafts and have been proposed as a therapeutic approach to the prevention of late vein graft failure. Since these stents are non-biodegradable and therefore may elicit deleterious long-term, inflammatory, infective and mechanical complications the effect of external macro-porous biodegradable (polyglactin) stents on neointimal and medial thickening in porcine vein grafts was investigated. Methods: Bilateral vein saphenous vein-carotid artery interposition grafting was performed in Large White pigs (22,36 kg, n = 6) with external placement of 8 mm diameter polyglactin stents on one side, the contralateral side acting as a control. One month after surgery, graft wall dimensions were measured on histological sections using computer-aided planimetry and immunocytochemistry undertaken for selected parameters. Results: Polyglactin stents significantly reduced medial thickening compared to the All grafts were patent at explantation. Intimal thickness was significantly lower (p < 0.05) in the stented grafts (0.11 ± 0.01 mm) compared to the unstented controls (0.18 ± 0.01 mm). Similarly, medial thickness was significantly lower (p < 0.05) in the stented grafts (0.24 ± 0.03 mm) compared to the unstented controls (0.43 ± 0.04 mm) mm. Grafts externally supported with polyglactin had a pronounced increase in inflammatory cells (in particular, giant cells) around the biodegradable stent compared to both unstented controls and previously studied Dacron stented grafts. The space between graft and stent had become organised into a neo-adventitia with abundant microvessels which stained positively for VEGF and lectin (markers of micorvessels and endothelial cells). Conclusions: An over-size biodegradable stent reduces medial thickening, a component of late vein graft failure in experimental grafts. If subsequent studies confirm the preservation of this beneficial effect when the stent biodegrades completely, this form of stent may have an advantage over permanent stent material in the clinical use of external stenting to prevent vein graft thickening and failure. [source]


BNP-induced activation of cGMP in human cardiac fibroblasts: Interactions with fibronectin and natriuretic peptide receptors

JOURNAL OF CELLULAR PHYSIOLOGY, Issue 3 2006
Brenda K. Huntley
Cardiac remodeling involves the accumulation of extracellular matrix (ECM) proteins including fibronectin (FN). FN contains RGD motifs that bind integrins at DDX sequences allowing signaling from the ECM to the nucleus. We noted that the natriuretic peptide receptor A (NPR-A) sequence contains both RGD and DDX sequences. The goal of the current investigation was to determine potential interactions between FN and NPR-A on BNP induction of cGMP in cultured human cardiac fibroblasts (CFs). Further, we sought to determine whether a Mayo designed NPR-A specific RGD peptide could modify this interaction. Here we reconfirm the presence of all three natriuretic peptide receptors (NPR) in CFs. CFs plated on FN demonstrated a pronounced increase in cGMP production to BNP compared to non-coated plates. This production was also enhanced by the NPR-A specific RGD peptide, which further augmented FN associated cGMP production. Addition of HS-142-1, a NPR-A/B antagonist, abrogated the responses of BNP to both FN and the NPR-A specific RGD peptide. Finally, we defined a possible role for the NPR-C through non-cGMP mechanisms in mediating the anti-proliferative actions of BNP in CFs where the NPR-C antagonist cANF 4-28 but not HS-142-1 blocked BNP-mediated inhibition of proliferation of CFs. We conclude that NPR-A interacts with components of the ECM such as FN to enhance BNP activation of cGMP and that a small NPR-A specific RGD peptide augments this action of BNP with possible therapeutic implications. Lastly, the NPR-C may also have a role in mediating anti-proliferative actions of BNP in CFs. J. Cell. Physiol. 209: 943,949, 2006. © 2006 Wiley-Liss, Inc. [source]


Heterogeneity of systemic inflammatory responses to periodontal therapy

JOURNAL OF CLINICAL PERIODONTOLOGY, Issue 4 2009
Jan H. Behle
Abstract Aims: We investigated the effect of comprehensive periodontal therapy on the levels of multiple systemic inflammatory biomarkers. Material and Methods: Thirty patients with severe periodontitis received comprehensive periodontal therapy within a 6-week period. Blood samples were obtained at: 1-week pre-therapy (T1), therapy initiation (T2), treatment completion (T3), and 4 weeks thereafter (T4). We assessed the plasma concentrations of 19 biomarkers using multiplex assays, and serum IgG antibodies to periodontal bacteria using checkerboard immunoblotting. At T2 and T4, dental plaque samples were analysed using checkerboard hybridizations. Results: At T3, PAI-1, sE-selectin, sVCAM-1, MMP-9, myeloperoxidase, and a composite summary inflammatory score (SIS) were significantly reduced. However, only sE-selectin, sICAM, and serum amyloid P sustained a reduction at T4. Responses were highly variable: analyses of SIS slopes between baseline and T4 showed that approximately 1/3 and 1/4 of the patients experienced a marked reduction and a pronounced increase in systemic inflammation, respectively, while the remainder were seemingly unchanged. Changes in inflammatory markers correlated poorly with clinical, microbiological and serological markers of periodontitis. Conclusions: Periodontal therapy resulted in an overall reduction of systemic inflammation, but the responses were inconsistent across subjects and largely not sustainable. The determinants of this substantial heterogeneity need to be explored further. [source]


Supersensitivity of P2X7 receptors in cerebrocortical cell cultures after in vitro ischemia

JOURNAL OF NEUROCHEMISTRY, Issue 5 2005
Kerstin Wirkner
Abstract Neuronally enriched primary cerebrocortical cultures were exposed to glucose-free medium saturated with argon (in vitro ischemia) instead of oxygen (normoxia). Ischemia did not alter P2X7 receptor mRNA, although serum deprivation clearly increased it. Accordingly, P2X7 receptor immunoreactivity (IR) of microtubuline-associated protein 2 (MAP2)-IR neurons or of glial fibrillary acidic protein (GFAP)-IR astrocytes was not affected; serum deprivation augmented the P2X7 receptor IR only in the astrocytic, but not the neuronal cell population. However, ischemia markedly increased the ATP- and 2,-3,- O -(4-benzoylbenzoyl)-adenosine 5,-triphosphate (BzATP)-induced release of previously incorporated [3H]GABA. Both Brilliant Blue G and oxidized ATP inhibited the release of [3H]GABA caused by ATP application; the Brilliant Blue G-sensitive, P2X7 receptor-mediated fraction, was much larger after ischemia than after normoxia. Whereas ischemic stimulation failed to alter the amplitude of ATP- and BzATP-induced small inward currents recorded from a subset of non-pyramidal neurons, BzATP caused a more pronounced increase in the frequency of miniature inhibitory postsynaptic currents (mIPSCs) after ischemia than after normoxia. Brilliant Blue G almost abolished the effect of BzATP in normoxic neurons. Since neither the amplitude of mIPSCs nor that of the muscimol-induced inward currents was affected by BzATP, it is assumed that BzATP acts at presynaptic P2X7 receptors. Finally, P2X7 receptors did not enhance the intracellular free Ca2+ concentration either in proximal dendrites or in astrocytes, irrespective of the normoxic or ischemic pre-incubation conditions. Hence, facilitatory P2X7 receptors may be situated at the axon terminals of GABAergic non-pyramidal neurons. When compared with normoxia, ischemia appears to markedly increase P2X7 receptor-mediated GABA release, which may limit the severity of the ischemic damage. At the same time we did not find an accompanying enhancement of P2X7 mRNA or protein expression, suggesting that receptors may become hypersensitive because of an increased efficiency of their transduction pathways. [source]


Behavioural and gene transcription alterations induced by spontaneous cannabinoid withdrawal in mice

JOURNAL OF NEUROCHEMISTRY, Issue 1 2003
José M. Oliva
Abstract This study examined behavioural signs that occur during tolerance development to cannabinoid treatment and hormonal and gene expression alterations induced by spontaneous cannabinoid withdrawal in mice. Tolerance to CP-55,940 treatment developed for hypothermia, ambulatory and exploratory locomotor activity. Cessation of cannabinoid treatment resulted in a behavioural withdrawal syndrome characterized by a pronounced increase in ambulatory activity and rearings. Corticosterone plasma concentrations dramatically increased 24 and 72 h after cessation of cannabinoid treatment. Similarly, an increase (40%) in cannabinoid [35S]GTP,S binding autoradiography was detected on days 1 and 3 of abstinence. Spontaneous cannabinoid withdrawal produced time-related significant alterations in gene transcription: (i) decreased (20%) tyrosine hydroxylase (TH) mRNA levels in the ventral tegmental area and increased (50%) in substantia nigra; (ii) increased proenkephalin (PENK) gene expression more than 100% in caudate-putamen, nucleus accumbens, olfactory tubercle and piriform cortex; (iii) increased (20,40%) pro-opiomelanocortin (POMC) gene expression in the arcuate nucleus of the hypothalamus. These results suggest that spontaneous cannabinoid withdrawal occur after cessation of CP-55,940 treatment. This ,syndrome' includes behavioural, hormonal and gene transcription alterations that seems to be part of the regulation of neuronal plasticity induced by spontaneous cannabinoid withdrawal. [source]


Morphology and Properties of Polyethylene/Clay Nanocomposite Drawn Fibers

MACROMOLECULAR MATERIALS & ENGINEERING, Issue 1 2008
Francesco Paolo La Mantia
Abstract The influence of an elongational flow on the morphology of PE/clay nanocomposite drawn fibers was studied. An increase of the elastic modulus and the tensile strength as well as a decrease of the elongation at break are observed with increasing draw ratio. The applied elongational gradient orients the polymer chains and the clay particles along the spinning direction. When the applied flow results in the formation and the orientation of exfoliated nanoparticles, a pronounced increase of the mechanical properties is observed. The dispersed clay particles can be broken and oriented by the extensional flow, which might indicate a flow-induced intercalated/exfoliated morphology transition. [source]


Progressive Renal Vascular Proliferation and Injury in Obese Zucker Rats

MICROCIRCULATION, Issue 4 2010
RADU ILIESCU
Microcirculation (2010) 17, 250,258. doi: 10.1111/j.1549-8719.2010.00020.x Abstract Objective:, Obesity, an independent risk factor for chronic kidney disease, may induce renal injury by promoting inflammation. Inflammatory cytokines can induce neovascularization in different organs, including the kidneys. However, whether obesity triggers renal neovascularization and, if so, its effect on renal function has never been investigated. Methods:, Blood pressure, proteinuria, and glomerular filtration rate (GFR) were measured in vivo. Renal microvascular (MV) architecture was studied by 3D micro-CT in lean and obese Zucker rats (LZR and OZR, n = 7/group) at 12, 22, and 32 weeks of age. Renal inflammation was assessed by quantifying interleukin (IL)-6, tumor necrosis factor (TNF)-alpha, and ED-1 expression, as renal fibrosis in trichrome-stained cross-sections. Results:, Mild inflammation and lower GFR was only observed in younger OZR, without renal fibrosis or changes in MV density. Interestingly, renal MV density increased in OZR at 32 weeks of age, accompanied by pronounced increase in renal IL-6 and TNF-alpha, ED-1+ cells, proteinuria, decreased GFR, and fibrosis. Conclusions:, This study shows increased renal cortical vascularization in experimental obesity, suggesting neovascularization as an evolving process as obesity progresses. Increased renal vascularization, possibly triggered by inflammation, may reflect an initially compensatory mechanism in obesity. However, increased inflammation and inflammatory-induced neovascularization may further promote renal injury as obesity advances. [source]


Cooperative inhibitory effect of ZD1839 (Iressa) in combination with 17-AAG on glioma cell growth,

MOLECULAR CARCINOGENESIS, Issue 5 2006
Daniel R. Premkumar
Abstract ZD1839 ("Iressa") is an orally active, selective epidermal growth factor (EGF) receptor-tyrosine kinase inhibitor. We evaluated the antitumor activity of ZD1839 in combination with HSP90 antagonist, 17-AAG in malignant human glioma cell lines. ZD1839 independently produced a dose-dependent inhibition of cellular proliferation in glioma cells grown in culture with time- and dose-dependent accumulation of cells in G1 phase of the cell cycle on flow cytometric analysis, although the concentrations required for optimal efficacy were at or above the limits of clinically achievable levels. Because the heat shock protein (HSP) is involved in the conformational maturation of a number of signaling proteins critical to the proliferation of malignant glioma cells, we hypothesized that the HSP90 inhibitor 17-AAG would potentiate ZD 1839-mediated glioma cytotoxicity by decreasing the activation status of EGF receptor, as well as downregulating the levels of other relevant signaling effectors. We, therefore, examined the effects of ZD1839 and 17-AAG, alone and in combination, on signal transduction and apoptosis in a series of malignant glioma cell lines. Simultaneous exposure to these inhibitors significantly induced cell death and quantitative analysis revealed that interaction between ZD1839 and 17-AAG-induced cytotoxicity was synergistic, leading to a pronounced increase in active caspase-3 and PARP cleavage. No significant growth inhibition or caspase activation was seen in control cells. The enhanced cytotoxicity of this combination was associated with diminished Akt activation and a significant downregulation of EGFR receptor, Raf-1 and mitogen activated protein kinase (MAPK). Cells exposed to 17-AAG and ZD1839 displayed a significant reduction in cell cycle regulatory proteins, such as CDK4 and CDK6. Taken together, these findings suggest that ZD1839, an EGF receptor tyrosine kinase inhibitor, plays a critical role in regulating the apoptotic response to 17-AAG and that multi-site targeting of growth signaling and cell survival pathways could provide a potent strategy to treat patients with malignant gliomas. © 2006 Wiley-Liss, Inc. [source]


Establishing a missing link: warm summers and winter snow cover promote shrub expansion into alpine tundra in Scandinavia

NEW PHYTOLOGIST, Issue 4 2010
Martin Hallinger
Summary ,Shrub expansion in alpine and arctic areas is a process with possibly profound implications for ecosystem functioning. The recent shrub expansion has been mainly documented by remote sensing techniques, but the drivers for this process largely remain hypotheses. ,Here, we outline a dendrochronological method, adapted to shrubs, to address these hypotheses and then present a mechanism for the current shrub expansion by linking recent climate change to shrub growth performance in northern Sweden. ,A pronounced increase in radial and vertical growth during recent decades along an elevational gradient from treeline to shrubline indicates an ongoing shrub expansion. Age distribution of the shrub population indicates the new colonization of shrubs at high elevations. ,Shrub growth is correlated with warm summers and winter snow cover and suggests the potential for large-scale ecosystem changes if climate change continues as projected. [source]


Morphology and Anatomy of Shoot, Root, and Propagation Systems in Hoffmannseggia glauca

PLANT BIOLOGY, Issue 6 2007
T. A. Kraus
Abstract: Hoffmannseggia glauca is a perennial weed that has tubers and root-borne buds. Some authors only consider root tubers without mentioning root-borne buds, while others consider that more anatomic studies become necessary to determine the origin of these structures and to interpret their behaviour. The objectives are: to study the growth form of the plant in order to analyze the ontogeny of its propagation organs, and to study its shoot and root anatomical characters that affect water conductivity. Hoffmannseggia glauca was collected in Argentina. Development of its shoot and root systems was observed. Shoots and roots were processed to obtain histological slides. Macerations were prepared to study vessel members. Primary and lateral roots originate buds that develop shoots at the end of the first year. In winter, aerial parts die and only latent buds at soil surface level and subterranean organs remain. In the following spring, they develop innovation shoots. Roots show localized swellings (tuberous roots), due to a pronounced increase of ray thickness and parenchymatous proliferation in the root center. Root vessel members are wider than those of aerial and subterranean shoots. Early development of an extensive root system, presence of root borne buds, anatomic and physiological specialization of innovation shoots, capability of parenchymatous rays to originate buds and tuberous roots, and high water transport efficiency in subterranean organs lead Hoffmannseggia glauca to display higher colonization potential than other species. [source]


DE-loop mutations affect ,2 microglobulin stability, oligomerization, and the low-pH unfolded form

PROTEIN SCIENCE, Issue 7 2010
Carlo Santambrogio
Abstract ,2 microglobulin (,2m) is the light chain of class-I major histocompatibility complex (MHC-I). Its accumulation in the blood of patients affected by kidney failure leads to amyloid deposition around skeletal joints and bones, a severe condition known as Dialysis Related Amyloidosis (DRA). In an effort to dissect the structural determinants of ,2m aggregation, several ,2m mutants have been previously studied. Among these, three single-residue mutations in the loop connecting strands D and E (W60G, W60V, D59P) have been shown to affect ,2m amyloidogenic properties, and are here considered. To investigate the biochemical and biophysical properties of wild-type (w.t.) ,2m and the three mutants, we explored thermal unfolding by Trp fluorescence and circular dichroism (CD). The W60G mutant reveals a pronounced increase in conformational stability. Protein oligomerization and reduction kinetics were investigated by electrospray-ionization mass spectrometry (ESI-MS). All the mutations analyzed here reduce the protein propensity to form soluble oligomers, suggesting a role for the DE-loop in intermolecular interactions. A partially folded intermediate, which may be involved in protein aggregation induced by acids, accumulates for all the tested proteins at pH 2.5 under oxidizing conditions. Moreover, the kinetics of disulfide reduction reveals specific differences among the tested mutants. Thus, ,2m DE-loop mutations display long-range effects, affecting stability and structural properties of the native protein and its low-pH intermediate. The evidence presented here hints to a crucial role played by the DE-loop in determining the overall properties of native and partially folded ,2m. [source]


Mechanisms of ultrasound foam interactions

ASIA-PACIFIC JOURNAL OF CHEMICAL ENGINEERING, Issue 2 2009
J. B. Winterburn
Abstract An experimental investigation into the effects of two frequencies of low-power ultrasound on detergent (Teepol) stabilised air-water foams is presented. Foam was subjected to ultrasound at 28 and 40 kHz with a power-to-foam volume ratio of approximately 3 W l,1 with particular consideration being given to the acoustic impedance discontinuity between air and water. The foam height, liquid drainage and collapse behaviour were compared to experiments conducted without ultrasound. In the case of 40 kHz ultrasound, an increased liquid drainage rate was observed and a pronounced increase and subsequent peak in mean liquid hold-up, which occurred at 4 min, was observed. These results appear to be independent of the initial liquid hold-up of the foam. Liquid drainage and mean liquid hold-up results were related to foam collapse mechanisms of homogeneous rupture (HR) and rupture front breakage (FR), concluding that rupture front breakage dominates the collapse of foam under the influence of 40 kHz ultrasound. Copyright © 2009 Curtin University of Technology and John Wiley & Sons, Ltd. [source]


Multilineage differentiation of dental follicle cells and the roles of Runx2 over-expression in enhancing osteoblast/cementoblast-related gene expression in dental follicle cells

CELL PROLIFERATION, Issue 3 2010
K. Pan
Objectives:, Dental follicle cells (DFCs) provide the origin of periodontal tissues, and Runx2 is essential for bone formation and tooth development. In this study, pluripotency of DFCs was evaluated and effects of Runx2 on them were investigated. Materials and methods:, The DFCs were induced to differentiate towards osteoblasts, adipocytes or chondrocytes, and alizarin red staining, oil red O staining or alcian blue staining was performed to reveal the differentiated states. Bone marrow stromal cells (BMSCs) and primary mouse fibroblasts served as controls. DFCs were also infected with recombinant retroviruses encoding either full-length Runx2 or mutant Runx2 without the VWRPY motif. Western blot analysis, real-time real time RT-PCR and in vitro mineralization assay were performed to evaluate the effects of full-length Runx2 or mutant Runx2 on osteogenic/cementogenic differentiation of the cells. Results:, The above-mentioned staining methods demonstrated that DFCs were successfully induced to differentiate towards osteoblasts, adipocytes or chondrocytes respectively, confirming the existence of pluripotent mesenchymal stem cells in dental follicle tissues. However, staining intensity in DFC cultures was weaker than in BMSC cultures. Real-time PCR analysis indicated that mutant Runx2 induced a more pronounced increase in expression levels of OC, OPN, Col I and CP23 than full-length Runx2. Mineralization assay also showed that mutant Runx2 increased mineralization nodule formation more prominently than full-length Runx2. Conclusions:, Multipotent DFCs can be induced to differentiate towards osteoblasts, adipocytes or chondrocytes in vitro. Runx2 over-expression up-regulated expression levels of osteoblast/cementoblast-related genes and in vitro enhanced osteogenic differentiation of DFCs. In addition, mutant Runx2-induced changes in DFCs were more prominent than those induced by full-length Runx2. [source]


Cytokine responses to allergens during the first 2 years of life in Estonian and Swedish children

CLINICAL & EXPERIMENTAL ALLERGY, Issue 5 2006
M. F. Böttcher
Summary Background The prevalence of atopic disease among children in the formerly socialist countries in Europe, with a life style similar to that prevailing in Western Europe 30,40 years ago, is low, whereas there has been a pronounced increase in industrialized countries over the last decades. The environment during infancy influences the risk of developing allergy for many years, perhaps even for life. Objective To investigate the development of allergen-specific cytokine responses during the first 2 years of life in two geographically adjacent countries with marked differences in living conditions and incidence of atopic diseases, i.e. Estonia and Sweden. Methods The development of immune responses to food (,-lactoglobulin (BLG) and ovalbumin (OVA)) and inhalant (cat and birch) allergens was studied from birth up to the age of 2 years in 30 Estonian and 76 Swedish infants. Clinical investigation and skin prick tests were performed and blood samples were obtained at birth and at 3, 6, 12 and 24 months. Results The levels of IL-5, IL-10 and IL-13 secreted by peripheral blood mononuclear cells stimulated with BLG, OVA and cat allergen in Estonian and Swedish infants declined during the first 3 months of life. All cytokines then progressively increased in the Swedish infants, indicating the replacement of non-specifically responding immature cord blood T cells with specific T memory cells, which are primed postnatally. The resurgence of allergen-specific responses in the Estonian infants was less marked. These differences were particularly notable for birch-specific T cell responses, which correlated with development of atopic disease in the Swedish children. Conclusions The development of specific T cell memory to food and inhalant allergens during the first 2 years of life differs between infants living in Sweden and Estonia, and mirrors the disparate patterns of expression of allergic disease which subsequently develops in the respective populations. [source]


Effects of a high-fat meal on resistance vessel reactivity and on indicators of oxidative stress in healthy volunteers

CLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 4 2001
Andreas Schinkovitz
High fat meals postprandially impair macrovascular endothelial function and a link to increased oxidative stress is suggested. Few information, on the other hand, exists on the effect of postprandial hyperlipidaemia on resistance vessel function. Under normal circumstances this vascular bed regulates tissue perfusion and, by controlling flow, impacts on macrovascular nitric oxide formation. The impact of a high fat meal (1200 kcal, 90 g fat, 46 g protein and 47 g carbohydrates) on postprandial resistance vessel reactivity and on indicators of oxidative stress was studied in 11 healthy subjects by venous-occlusion plethysmography using another six subjects as time control group. Ingestion of the test meal resulted in a pronounced increase of serum triglycerides from 1·05 ± 0·61 mmol l,1 in the fasting state to peak postprandial values of 1·94 ± 0·41 mmol l,1 (P < 0·001) reached after 4 h and a return to baseline after 8 h. Fasting peak reactive hyperaemia (RH) was 19·6 ± 2·4 ml min,1 (100 ml),1. Two hours after ingestion of the test meal peak RH was transiently reduced to 16·8 ± 2·2 ml min,1 (100 ml),1 (P < 0·05). No alteration of resting forearm perfusion was observed. The time course of peak RH suggested a potential biphasic effect of the test meal with an early impairment and a late increase of RH. Ingestion of a lipid rich test meal did not exert any influence on either total plasma antioxidant capacity given in trolox equivalents (513 ± 26 ,mol l,1 at baseline) or on plasma peroxides measured as H2O2 equivalents (469 ± 117 ,mol l,1). Our results suggest that ingestion of a meal containing 90 g of fat results in a transient impairment of reactive hyperaemia in healthy subjects but these vascular alterations are not accompanied by signs of systemically increased oxidative stress. [source]