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Rapid Induction (rapid + induction)
Selected AbstractsSurface Cooling for Rapid Induction of Mild Hypothermia After Cardiac Arrest: Design Determines EfficacyACADEMIC EMERGENCY MEDICINE, Issue 4 2010Thomas Uray MD Abstract Objectives:, Recently, a novel cooling pad was developed for rapid induction of mild hypothermia after cardiac arrest. The aim of this study was to evaluate the cooling efficacy of three different pad designs for in-hospital cooling. Methods:, Included in this prospective interventional study were patients with esophageal temperature (Tes) > 34°C on admission. The cooling pad consists of multiple cooling units, filled with a combination of graphite and water, which is precooled to ,18°C (design A) or to ,9°C (designs B and C) before use. The designs of the cooling pad differed in number, shape, and thickness of the cooling units, with weights of 9.7 kg (design A), 5.3 kg (design B), and 6.2 kg (design C). All three designs were tested in sequential order and were changed according to the results found in the previous trial. Cooling was started after admission until Tes = 34°C, when the cooling pad was removed. The target temperature of Tes = 32,34°C was maintained for 24 hours. Data are presented as medians and interquartile ranges (IQRs = 25%,75%) or proportions. Results:, Cooling rates were 3.4°C/hour (IQR = 2.5,3.7) with design A (n = 12), 2.8°C/hour (IQR = 1.6,3.3) with design B (n = 7), and 2.9°C/hour (IQR = 1.9,3.6) with design C (n = 10; p = 0.5). To reach 34°C, the cooling pad had to be exchanged with a new one due to melting and therefore depleting cooling capacity in three patients with design A, in five patients with design B, and in no patient with design C (p = 0.004). Conclusions:, With adequate design and storage temperature, the cooling pad proved to be efficient for rapid in-hospital cooling of patients resuscitated from cardiac arrest. ACADEMIC EMERGENCY MEDICINE 2010; 17:360,367 © 2010 by the Society for Academic Emergency Medicine [source] Rapid Induction of Apoptosis in Gastrulating Mouse Embryos by Ethanol and Its Prevention by HB-EGFALCOHOLISM, Issue 1 2006Brian A. Kilburn Background: Ethanol exposure during gastrulation and early neurulation induces apoptosis within certain embryonic cell populations, leading to craniofacial and neurological defects. There is currently little information about the initial kinetics of ethanol-induced apoptosis, and interest in the ability of endogenous survival factors to moderate apoptosis is growing. Ethanol alters intracellular signaling, leading to cell death in chick embryos, suggesting that apoptosis could occur rapidly and that signaling pathways activated by survival factors might reduce apoptosis. Methods: Pregnant mice were intubated with 1, 2, or 4 g/kg ethanol on day 7.5 of embryogenesis (E7.5) 1, 3, or 6, hours before harvesting gastrulation-stage embryos. Control animals received maltose/dextran. Blood alcohol concentrations (BAC) were determined by gas chromatography. E7.5 embryos isolated from untreated dams were cultured in vitro for 1 or 3 hr with 0 or 400 mg% ethanol and 0 or 5 nM heparin-binding epidermal growth factor (EGF)-like growth factor (HB-EGF). Apoptosis was quantified using fluorescence microscopy to detect annexin V binding and DNA fragmentation [terminal deoxynucleotidyl transferase-mediated dUTP-X nick end labeling (TUNEL)] in whole-mount or sectioned embryos. Results: Both annexin V binding and TUNEL were elevated (p<0.05) in embryos exposed in utero to 1 g/kg ethanol for 3 hours, increasing linearly with time and ethanol concentration. Apoptosis increased (p<0.05) in all germ cell layers. Mice treated with 4 g/kg sustained BAC of 400 mg% for nearly 3 hours, significantly increasing apoptosis within the first hour. Cultured embryos exposed to 400 mg% ethanol displayed 2- to 3-fold more TUNEL than vehicle-treated embryos (p<0.05); however, exogenous HB-EGF prevented apoptosis. Conclusions: Ethanol rapidly produced apoptosis in gastrulation-stage embryos, consistent with induction by intracellular signaling. The ethanol-induced apoptotic pathway was blocked by the endogenous survival factor, HB-EGF. Differences in the expression of survival factors within individual embryos could be partly responsible for variations in the teratogenic effects of ethanol among offspring exposed prenatally. [source] Rapid induction of apoptosis in B-cell lymphoma by functionally isolated human antibodiesINTERNATIONAL JOURNAL OF CANCER, Issue 2 2006Johan Fransson Abstract Novel panning and screening methodology was devised to isolate high affinity human recombinant scFv antibody fragments with functionally associated properties in B lymphoma cells. The approach was used to generate a panel of apoptosis-inducing antibodies specific for antigens differentially expressed in B lymphoma vs. T leukaemia cells. The selections resulted in an antibody pool with near perfect selectivity (>99%) for the B lymphoma target cells. Randomly picked clones (72) revealed 7 unique antibody genotypes. Six of these rapidly induced apoptosis in target cells. Following the conversion to full IgGs, the antibodies were shown to be specific for HLA-DR/DP, the B-cell receptor , chain and for CD54/ICAM-1. The latter receptor was not previously associated with apoptotic properties in B-cell lymphomas. Anti-ICAM-1 IgG induced apoptosis in a broad range of B lymphoma cell lines and were shown by immunohistochemistry to bind strongly to B lymphoma tissue obtained from 5 different B lymphoma patients. The recombinant IgG antibodies had affinities in the subnanomolar (0.3 nM) to nanomolar (3 nM) range. The described technology is generally applicable for the rapid isolation of high affinity human antibodies with specificity for differentially expressed cell surface receptors with intrinsic negative or positive signalling properties from naïve phage libraries. © 2006 Wiley-Liss, Inc. [source] Rapid induction of peroxisome proliferator,activated receptor , expression in human monocytes by monosodium urate monohydrate crystalsARTHRITIS & RHEUMATISM, Issue 1 2003Tohru Akahoshi Objective Peroxisome proliferator,activated receptor , (PPAR,) is a member of the nuclear hormone receptor superfamily and functions as a key regulator of lipid and glucose metabolism, atherosclerosis, and inflammatory responses. This study was undertaken to evaluate the biologic role of PPAR, in self-limiting episodes of acute gouty arthritis. To do this, we investigated PPAR, expression by monosodium urate monohydrate (MSU) crystal,stimulated monocytes, and we studied the effects of PPAR, ligands on crystal-induced acute inflammation. Methods PPAR, expression by MSU crystal,stimulated human peripheral blood mononuclear cells was determined by reverse transcription,polymerase chain reaction and immunostaining. Expression of CD36 on monocytes was detected by flow cytometric analysis. The effects of PPAR, ligands on in vitro crystal-induced cytokine production and on in vivo cellular infiltration during crystal-induced acute inflammation were also investigated. Results MSU crystals rapidly and selectively induced PPAR, expression by monocytes. Gene expression was detected as early as 2 hours, and maximum expression was observed at 4 hours after stimulation. The induced PPAR, was functional, since a PPAR, ligand was able to up-regulate CD36 expression on monocytes. A natural ligand of PPAR,, 15-deoxy-,12,14 -prostaglandin J2 (15deoxy-PGJ2), significantly reduced the crystal-induced production of cytokines by monocytes. Indomethacin inhibited cytokine production only at high concentrations, and an antidiabetic thiazolidinedione (troglitazone) failed to exert significant effects. Administration of troglitazone and 15deoxy-PGJ2 significantly prevented cellular accumulation in a mouse air-pouch model of MSU crystal,induced acute inflammation. Conclusion Rapid induction of PPAR, expression on monocytes by MSU crystals may contribute, at least in part, to the spontaneous resolution of acute attacks of gout. [source] Rapid induction of skin and mammary tumors in human c-Ha- ras proto-oncogene transgenic rats by treatment with 7,12-dimethylbenz[a]anthracene followed by 12- O -tetradecanoylphorbol 13-acetateCANCER SCIENCE, Issue 3 2004Cheol Beom Park We have established a transgenic rat line carrying 3 copies of the human c-Ha- ras proto-oncogene with its own promoter region (Jcl/SD-TgN(HrasGen)128Ncc) (Hras128 rat), expression being detectable in almost all organs. We have already demonstrated that the rat is highly sensitive to mammary, esophagus and bladder carcinogenesis. In the present study, male and female transgenic and wild-type littermates were topically treated with 2.5 mg of 7,12-dimethylbenz[a]anthracene (DMBA) dissolved in 1.0 ml of acetone on the back skin at 50 days after birth. Starting 1 week thereafter, they were again topically treated with 100 nmol of 12- O -tetradecanoylphorbol 13-acetate (TPA) dissolved in 0.5 ml of acetone 3 times weekly for the following 31 weeks. In males treated with DMBA and/or TPA, skin tumors, including both squamous cell papillomas (SCP) and carcinomas (SCC), were preferentially induced at the DMBA-TPA painting sites: DMBA-TPA, 15/15 (100%); DMBA, 6/8 (75%); TPA, 1/6 (16.7%). They were also, unexpectedly, induced on remote scrotal skin: DMBA-TPA, 13/15 (86.7%); DMBA, 5/8 (62.5%); TPA, 0/6 (0%). Lesions were thus more frequent in the DMBA-TPA group than with DMBA or TPA alone. In females, adenomas and adenocarcinomas of the mammary glands were preferentially induced: DMBA-TPA, 12/14 (85.7%); DMBA, 6/8 (75%); TPA, 3/6 (50%), with only a few small skin papillomas at painting sites. Incidences and numbers of the mammary and skin tumors were much greater in Hras128 rats than in their wild-type counterparts. PCR-RFLP analysis of the transgene indicated that the percentage of the cell populations harboring a mutation in codons 12 and/or 61 ranged from 2% to 60% in individual tumors; skin tumors showed more mutations in codon 61 in the DMBA-treated groups. In contrast, no mutations were detected in the endogenous rat c-Ha-ras gene. These results indicate that the Hras128 rat is highly susceptible to DMBA-TPA skin and mammary carcinogenesis, thus providing a unique painting model for skin as well as mammary gland carcinogenesis, that would be suitable for investigating the role of transgene mutations. [source] Phenotype and function of neonatal DCEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 1 2009Fabienne Willems Abstract Newborns face complex physical and immunological changes before and after birth. Although the uterus is a sterile environment for the fetus, it also contains non-self material from the mother. Birth involves the transition from the sterile intra-uterine environment to an environment rich in microbes and requires rapid induction of appropriate responses to control these microbes. In this review we focus on the similarities and differences of human and murine neonatal DC and their reaction to various stimuli. A better understanding of the newborn immune system , in particular, the DC,T-cell interaction , will be beneficial for the development of improved strategies to prevent or treat infections in this vulnerable population and prepare the immune system to cope with allergens and tumors later in life. [source] Role of the IGF-II receptor in mediating acute, non-genomic effects of retinoids and IGF-II on keratinocyte cell deathEXPERIMENTAL DERMATOLOGY, Issue 4 2003F. Louafi Abstract:, In this study, we have examined the effects of retinoic acid (RA) on the human immortalized keratinocyte cell line (HaCaT). A significant twofold (P < 0.01) increase in apoptotic cell death compared with the control was found within 24 h of treatment with 10,5 M of RA. Apoptosis was confirmed by flow cytometry. Cycloheximide did not inhibit this acute RA-induced apoptosis. Interestingly, insulin-like growth factor-II (IGF-II, 50 ng/ml) was able to significantly (67.3%; P < 0.05) reduce RA effects, whereas IGF-I (50 ng/ml) and insulin (75 ng/ml) were without effect. Furthermore, analogues of IGF-II [leu27 IGF-II and Des(1-6) IGF-II], with altered affinities for the IGF-I receptor and IGF-binding proteins (IGFBPs), but retained affinities for the IGF-II receptor, also completely inhibited (100%; P < 0.01) RA-induced apoptosis, while an IGF-I receptor antagonist did not reduce the survival effects of IGF-II. Insulin pretreatment negates the survival effect of IGF-II. In contrast, mannose 6 phosphate (M6P) did not alter RA or IGF-II actions. These results indicate that rapid induction of cell death by RA is independent of production or secretion of new proteins. The inhibition of RA action by IGF-II was independent of its ability to signal through the IGF-I receptor or to interact with IGFBPs. [source] 17, -Hydroxysteroid dehydrogenase type 11 is a major peroxisome proliferator-activated receptor ,-regulated gene in mouse intestineFEBS JOURNAL, Issue 20 2004Kiyoto Motojima In order to study the role of peroxisome proliferator-activated receptor , in mouse intestine, its agonist-induced proteins were identified by peptide mass fingerprinting followed by Northern blot analysis using their cDNAs. One of the most remarkably induced proteins was identified as 17,-hydroxysterol dehydrogenase type 11. Its very rapid induction by various agonists was most efficient in intestine and then in liver. These findings together with recently reported results showing the enzyme family's wide substrate spectrum, including not only glucocorticoids and sex steroids but also bile acids, fatty acids and branched chain amino acids, suggest new roles for both peroxisome proliferator-activated receptor , and 17,-hydroxysterol dehydrogenase type 11 in lipid metabolism and/or detoxification in the intestine. [source] Surface Cooling for Rapid Induction of Mild Hypothermia After Cardiac Arrest: Design Determines EfficacyACADEMIC EMERGENCY MEDICINE, Issue 4 2010Thomas Uray MD Abstract Objectives:, Recently, a novel cooling pad was developed for rapid induction of mild hypothermia after cardiac arrest. The aim of this study was to evaluate the cooling efficacy of three different pad designs for in-hospital cooling. Methods:, Included in this prospective interventional study were patients with esophageal temperature (Tes) > 34°C on admission. The cooling pad consists of multiple cooling units, filled with a combination of graphite and water, which is precooled to ,18°C (design A) or to ,9°C (designs B and C) before use. The designs of the cooling pad differed in number, shape, and thickness of the cooling units, with weights of 9.7 kg (design A), 5.3 kg (design B), and 6.2 kg (design C). All three designs were tested in sequential order and were changed according to the results found in the previous trial. Cooling was started after admission until Tes = 34°C, when the cooling pad was removed. The target temperature of Tes = 32,34°C was maintained for 24 hours. Data are presented as medians and interquartile ranges (IQRs = 25%,75%) or proportions. Results:, Cooling rates were 3.4°C/hour (IQR = 2.5,3.7) with design A (n = 12), 2.8°C/hour (IQR = 1.6,3.3) with design B (n = 7), and 2.9°C/hour (IQR = 1.9,3.6) with design C (n = 10; p = 0.5). To reach 34°C, the cooling pad had to be exchanged with a new one due to melting and therefore depleting cooling capacity in three patients with design A, in five patients with design B, and in no patient with design C (p = 0.004). Conclusions:, With adequate design and storage temperature, the cooling pad proved to be efficient for rapid in-hospital cooling of patients resuscitated from cardiac arrest. ACADEMIC EMERGENCY MEDICINE 2010; 17:360,367 © 2010 by the Society for Academic Emergency Medicine [source] Fas ligand-induced murine pulmonary inflammation is reduced by a stable decoy receptor 3 analogueIMMUNOLOGY, Issue 2 2003Mark A. Wortinger Summary Fas ligand (FasL)-induced lung inflammation has recently been suggested to play an important role in the pathogenesis of acute respiratory disease syndrome (ARDS). In order to further explore this connection, we established a FasL-induced murine model of pulmonary inflammation. Instillation of recombinant FasL (rFasL) into the lung induced neutrophil infiltration and increased pulmonary permeability, as evidenced by increased total protein in the airspace; both occur in patients with ARDS. These effects were accompanied with a rapid induction of proinflammatory mediators: cytokine granulocyte,macrophage colony-stimulating factor (GM-CSF) and the chemokines macrophage inflammatory protein-2 (MIP-2) and KC. Pretreatment with a FasL antagonist, a decoy receptor 3 analogue (DcR3 analogue), reduced neutrophil infiltration into the airspace and resulted in a highly significant reduction in the levels of GM-CSF, MIP-2 and KC in bronchoalveolar lavage (BAL) fluid. We postulate that rFasL may be responsible for induction of proinflammatory chemokines and cytokines in the lung, which in turn attract neutrophil infiltration into the airspace. This proinflammatory process and the associated pulmonary permeability may, in part, explain the association of FasL with severe pulmonary inflammation, such as ARDS, and shed new light on FasL and its role in lung injury. [source] Studies on the mechanism of rapid activation of protein tyrosine phosphorylation activities, particularly c-Src kinase, by TCDD in MCF10AJOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, Issue 6 2005Olga Mazina Abstract While the process of the Ah receptor activation leading to cytochrome P450 induction has been well studied, the mechanism and the process through which the Ah receptor activates tyrosine kinases, within a few minutes of its ligand binding, is not known. Previously, it was reported by Tannheimer et al. (Carcinogenesis 1998; 19:1291,1297) that TCDD causes rapid induction of tyrosine phosphorylation activities in the MCF10A human mammary epithelial cell line. To study the mechanistic aspect of this phenomenon, particularly that occurs within a few minutes after administration, we first studied the effect of insulin on MCF10A under serum free conditions with added EGF. The addition of insulin induced a rapid (5 min) tyrosine phosphorylation on several 160,190 kDa proteins which was followed by significant dephosphorylation activities on these proteins by 15 min. TCDD increased the rate of tyrosine phosphorylation on those proteins but at 15 min, the level of phosphorylation was still high. When insulin and TCDD were added together, the ability of insulin to induce de-phosphorylation by 15 min disappeared. Such an action of TCDD was accompanied by an increase in the titer of the activated form of Src kinase (i.e. c-Src protein with 418 tyrosine phosphorylation), and a concomitant decrease in the level of 529 tyrosine phosphorylated form (an inactivated form). The TCDD-induced activation of c-Src could be blocked by pretreated MCF10A cells with antisense oligonucleotides against c-src or with a specific inhibitor of Src kinase, PP-2. These results support the conclusion that c-Src kinase is at least one of the earliest and the most upstream components of toxic signaling of the Ah-receptor activated by TCDD through the post-transcriptional process. © 2005 Wiley Periodicals, Inc. J Biochem Mol Toxicol 18:313,321, 2004; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20041 [source] Mask induction of anaesthesia with isoflurane or sevoflurane in premedicated catsJOURNAL OF SMALL ANIMAL PRACTICE, Issue 1 2002P. Lerche A comparison was made of the time to and quality of induction of anaesthesia when sevoflurane (n=14) or isoflurane (n=14) was delivered by mask in premedicated healthy adult cats presented for elective surgery. Times to induction and intubation were significantly shorter with sevoflurane (210 ±57 seconds and 236 ±60 seconds, respectively) than with isoflurane (264 ±75 seconds and 292 ±73 seconds). The quality of induction was similar for both agents. Two cats in each group developed opisthotonus of less than 45 seconds'duration. Both sevoflurane and isoflurane produced mask induction of anaesthesia of a similar quality in this species. Sevoflurane provided more rapid induction of anaesthesia and establishment of a controlled airway than isoflurane. [source] Meta-analysis: the efficacy and safety of certolizumab pegol in Crohn's diseaseALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 6 2009L.-M. SHAO Summary Background, Certolizumab pegol is the third anti-TNF-, agent approved by the Food and Drug Administration of the United States. Aim, To provide a comprehensive up-to-date review of the efficacy and safety of certolizumab in Crohn's disease (CD). Methods, Electronic databases, including PubMed, EMBASE, the Cochrane library and the Science Citation Index, were searched to retrieve relevant trials. In addition, meeting abstracts and the reference lists of retrieved articles were reviewed for further relevant studies. Results, Three trials, enrolling a total of 1040 patients, are included in the meta-analysis to evaluate the short-term efficacy of certolizumab, which is effective for rapid induction and long-term maintenance of clinical response or remission and can improve quality of life in patients with Crohn's disease. Certolizumab is also effective for patients who have lost response to infliximab. However, its efficacy in infliximab-exposed patients is probably less than in infliximab-naive patients. Re-induction with certolizumab in patients who have flared on maintenance therapy can rescue a significant proportion of patients. There is no significant association between the efficacy of certolizumab and the baseline C-reactive protein level. In comparison with placebo, certolizumab does not increase the risk of serious adverse events. Conclusions, Certolizumab is effective and safe in treating Crohn's disease. Further studies are still required to assess its full safety profile. [source] The chloroplast protein RPH1 plays a role in the immune response of Arabidopsis to Phytophthora brassicaeTHE PLANT JOURNAL, Issue 2 2009Khaoula Belhaj Summary Plant immune responses to pathogens are often associated with enhanced production of reactive oxygen species (ROS), known as the oxidative burst, and with rapid hypersensitive host cell death (the hypersensitive response, HR) at sites of attempted infection. It is generally accepted that the oxidative burst acts as a promotive signal for HR, and that HR is highly correlated with efficient disease resistance. We have identified the Arabidopsis mutant rph1 (resistance to Phytophthora 1), which is susceptible to the oomycete pathogen Phytophthora brassicae despite rapid induction of HR. The susceptibility of rph1 was specific for P. brassicae and coincided with a reduced oxidative burst, a runaway cell-death response, and failure to properly activate the expression of defence-related genes. From these results, we conclude that, in the immune response to P. brassicae, (i) HR is not sufficient to stop the pathogen, (ii) HR initiation can occur in the absence of a major oxidative burst, (iii) the oxidative burst plays a role in limiting the spread of cell death, and (iv) RPH1 is a positive regulator of the P. brassicae -induced oxidative burst and enhanced expression of defence-related genes. Surprisingly, RPH1 encodes an evolutionary highly conserved chloroplast protein, indicating a function of this organelle in activation of a subset of immune reactions in response to P. brassicae. The disease resistance-related role of RPH1 was not limited to the Arabidopsis model system. Silencing of the potato homolog StRPH1 in a resistant potato cultivar caused susceptibility to the late blight pathogen Phytophthora infestans. [source] Red jungle fowl (Gallus gallus) as a model for studying the molecular mechanism of seasonal reproductionANIMAL SCIENCE JOURNAL, Issue 3 2009Hiroko ONO ABSTRACT Photoperiodism is an adaptation mechanism that enables animals to predict seasonal changes in the environment. Japanese quail is the best model organism for studying photoperiodism. Although the recent availability of chicken genome sequences has permitted the expansion from single gene to genome-wide transcriptional analysis in this organism, the photoperiodic response of the domestic chicken is less robust than that of the quail. Therefore, in the present study, we examined the photoperiodic response of the red jungle fowl (Gallus gallus), a predecessor of the domestic chicken, to test whether this animal could be developed as an ideal model for studying the molecular mechanisms of seasonal reproduction. When red jungle fowls were transferred from short-day- to long-day conditions, gonadal development and an increase in plasma LH concentration were observed. Furthermore, rapid induction of thyrotropin beta subunit, a master regulator of photoperiodism, was observed at 16 h after dawn on the first long day. In addition, the long-day condition induced the expression of type 2 deiodinase, the key output gene of photoperiodism. These results were consistent with the results obtained in quail and suggest that the red jungle fowl could be an ideal model animal for the genome-wide transcriptional analysis of photoperiodism. [source] Induction of triggering receptor expressed on myeloid cells 1 in murine resident peritoneal macrophages by monosodium urate monohydrate crystalsARTHRITIS & RHEUMATISM, Issue 2 2006Yousuke Murakami Objective Triggering receptor expressed on myeloid cells 1 (TREM-1) is a cell surface molecule that was recently identified on monocytes and neutrophils. TREM-1 has been implicated in the early inflammatory responses induced by microbes, but its pathophysiologic role in nonmicrobial inflammation remains unknown. In the present study, we investigated the role of TREM-1 in acute inflammation induced by monosodium urate monohydrate (MSU) crystals. Induction of TREM-1 expression by MSU crystal,stimulated murine resident peritoneal macrophages and infiltrating leukocytes in a murine air-pouch model of crystal-induced acute inflammation was determined. The biologic role of TREM-1 in crystal-induced cytokine production by resident peritoneal macrophages was also investigated. Methods TREM-1 expression by resident peritoneal macrophages and infiltrating leukocytes in a murine air-pouch model was determined by quantitative real-time polymerase chain reaction, Western blot analysis, and flow cytometry. Cytokine production by resident peritoneal macrophages after incubation with MSU crystals in the presence or absence of an anti,TREM-1 agonist antibody was determined by enzyme-linked immunosorbent assay. Results TREM-1 expression by resident peritoneal macrophages was significantly induced after stimulation with the crystals. Maximum expression of TREM-1 transcripts and protein occurred at 1 and 4 hours after exposure to the crystals, respectively. Costimulation of resident peritoneal macrophages with MSU crystals and an anti,TREM-1 agonist antibody synergistically increased the production of both interleukin-1, and monocyte chemotactic protein 1 compared with stimulation with the crystals alone. MSU crystals also induced TREM-1 expression in infiltrating leukocytes in a murine air-pouch model of crystal-induced acute inflammation. Conclusion These findings suggest that rapid induction of TREM-1 expression on resident peritoneal macrophages and neutrophils by MSU crystals may contribute to the development of acute gout through enhancement of inflammatory responses. [source] Speed of induction of anaesthesia in dogs administered halothane, isoflurane, sevoflurane or propofol in a clinical settingAUSTRALIAN VETERINARY JOURNAL, Issue 1-2 2008RG Pottie Objective To compare the speed and quality of induction of general anaesthesia using three different inhalant agents and one intravenous agent, in healthy dogs undergoing desexing surgery. Materials and methods Less excitable dogs were not premedicated; others were premedicated with intramuscular acepromazine and morphine. Anaesthesia induction protocol was randomly assigned, with halothane, isoflurane or sevoflurane delivered by mask, or propofol delivered intravenously. Maximum vaporiser settings were used for inhalant inductions. Induction of anaesthesia was considered complete at the time of endotracheal intubation. Quality of induction was scored by the administering veterinarian. Results Seventy-one dogs were enrolled. Twenty-four received no premedication and 47 received premedication. Isoflurane inductions were significantly faster than halothane inductions (2.86 ± 0.25 vs 3.71 ± 0.22 min; mean ± SE, P = 0.013). Sevoflurane inductions (3.29 ± 0.24 min) were not significantly different from either halothane (3.71 ± 0.22 min, P = 0.202) or isoflurane inductions (2.86 ± 0.25 min, P = 0.217). Induction with propofol (1.43 ± 0.13 min) was significantly faster than inhalant induction (P < 0.001 in each case). Premedication decreased the dose requirement and time to induction for dogs induced with propofol, but did not significantly change the time to intubation for inhalant inductions. Dogs administered propofol and/or premedication were significantly more likely to have an excellent quality of induction, but there was no difference between inhalant agents in terms of induction quality. Conclusion Sevoflurane possesses chemical properties that should produce a more rapid induction of anaesthesia in comparison to halothane or isoflurane. However, in clinical practice patient related factors outweigh this improvement. [source] | |||||||||||||||||||||||||