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Butterfly Conservation in Scotland The following three projects have been running in Scotland during 2005: 1. Butterflies and Moths mean Business This project started in September 2004 and runs until December 2005. Its main aim is to raise the profile of butterflies and moths in two areas; Lomond and Rural Stirling, and the Cairngorms. A programme of 15 free workshops were held to train volunteers and countryside staff to carry out surveys of both common and rarer species, they were attended by 146 people, occupying 182 places. In addition six workshops were provided for people who work in tourism e.g. B&B owners, hoteliers, visitor centre staff, countryside rangers etc. ; these gave basic information about local butterflies and where to see them that could readily be passed on to visitors. Other initiatives include producing local butterfly charts, promoting butterfly sites and helping local organisations to develop butterfly trails. The project is part-financed by the European Community through the Lomond and Rural Stirling, and Cairngorms LEADER + programmes, the Cairngorms National Park Authority and Scottish Natural Heritage SNH ; . Until September 2005 this project was managed by Julie Stoneman and subsequently by Hebe Carus. 2. Bringing Butterflies, Moths and People together in the Highlands In April Tom Prescott was appointed on a 2 year contract as Highland and Islands Project Officer to implement two new projects. This project comprises around 80% of the workload and is being part-funded by The European Community through the North Highland and WHELK Lochaber ; LEADER + Programmes, SNH and the Scottish Executive's Biodiversity Action Grants. The project aims to highlight the importance of butterflies and moths as a significant element of the biodiversity of the Highlands. The Highland region has the lowest human population density in the UK and consequently it is one of the most under-recorded areas for butterflies and moths, including common species. In its first year the project ran six volunteer workshops aimed at local communities often in remote and.
Men and women at least 50 years of age with systolic hypertension defined as seated clinic systolic BP of 150 to 165 mm Hg with a pulse pressure of 70 mm 165 to 200 mm Hg with a diastolic pressure of 95 mm were included in the trial. Patients were excluded from the trial if they had clinically significant heart, liver, or kidney disease or if the serum creatinine was 1.5 mmol L or 1.3 mmol L, for men and women, respectively, or if the serum potassium was 5.0 mmol L at baseline
1. How relevant were the objectives to the CE activity's purpose goals? The goal of this program is to provide oncology nurses with knowledge regarding dose-dense treatment regimens for non-Hodgkin's lymphoma, breast cancer, and lung cancer. 1 2.
A plateau at B ; : the MCV was unchanged a progressive decline. The MCV did not 79 fi ; until day 63 at C ; , approximately the iron. MRV The increased sequence.
Of animal models in which levels of Ang II were measured in blood or in kidney tissue isolated from anesthetized animals 4, 18 ; . However, we have clearly shown in our model of STZ-induced diabetes in intact, conscious animals that renal levels of Ang II are significantly increased at the target tissue level, where Ang II is believed to act primarily through the AT1 receptor. Valsartan, an Ang II receptor antagonist ARB ; , selectively blocks the AT1 receptor 19 ; , unlike ACE inhibitors that act nonspecifically to block an early enzymatic process in Ang II synthesis. Valsartan increases the tissue Ang II level through direct blockade of the AT1 short negative feedback loop, which, in turn, stimulates the increase in renin secretion. During blockade of the AT1 receptor, the excess Ang II may be renoprotective, because it is available to interact with the AT2 receptor 20 ; . The renoprotective effects of the AT2 receptor stem from its ability to increase generation of bradykinin, nitric oxide, and cGMP, as well as its antiproliferative and antifibrotic properties 8, 9, 14, ; . Diabetes is associated with increased levels of vasoconstrictors such as Ang II 19 ; , which can up-regulate the expression of inflammatory cytokines, including TNF- , as well as growth factors, adhesion molecules, and transcription factors 7 ; . TNF- may play a role in the development of diabetic nephropathy. Increased levels of the cytokines TNF- and IL-1 have been detected in isolated glomerular basement membranes from rats with STZ-induced diabetes 5 ; . In patients with coronary artery disease and increased levels of inflammatory molecules including TNF- , treatment with an ARB reduced these markers of inflammation in the circulation 21 ; . Antihypertensive therapy with both ACE inhibitors in type 1 diabetes ; and ARBs in type 2 diabetes ; has also had a beneficial effect in treating diabetic renal disease 19 ; . In patients with diabetic nephropathy, ACE inhibitors and ARBs have been shown in clinical trials to be renoprotective independent of their ability to lower blood pressure 2225 ; . In diabetic patients with advanced renal failure, levels of both TNF- and proteinuria were correlated. Treatment with pentoxifylline, an immune modulator with anti-TNF- activity, reduced proteinuria, possibly via its anticytokine activity 26 ; . The source of TNF- in RIF is not well established. Although TNF- can be produced by inflammatory cells, it can also be produced by the glomeruli, tubules, and blood vessels 2729 ; . The increase in RIF TNF- could reflect an increase in production or a decrease in degradation or clearance. In this study, we could not specifically distinguish between these possibilities. However, in our studies, there was a concomitant increase in urinary TNF- that suggests an increase in its production. The exact mechanism through which Ang II can stimulate TNF- production is not known. The increase in renal production of Ang II stimulates gene expression and, therefore, renal production of TNF- , as well as other proinflammatory mediators, including IL-1 and IL-6, possibly via activation of the transcription factor nuclear factor- B 27 ; , release of prostaglandin E2 29 ; , and reduction of intracellular cAMP 30 ; . This is consistent with our data showing reduction in RIF TNF- during AT1 receptor blockade. Insulin treatment over a 5-h time course lowered blood glucose levels to less than 100 mg dl. This was associated with reduced recovery of Ang II and TNF- in RIF. These results.
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1F5 Ab-SA, 1F5 scFv ; 4SA, B9E9 scFv ; 4SA, or CC49 scFv ; 4SA, and cleared from blood with 5.8 nM CA. Mice without tumors were used so that serial blood collections could be obtained without euthanizing mice because of xenograft growth. In addition, toxicities were evaluated after administration of 200 Ci 7.4 MBq ; of directly labeled 90Y-DOTA-1F5 Ab. Higher doses of directly labeled 90Y-DOTA-1F5 were not studied since they were lethal in 100% of mice.17 Weekly leukocyte, platelet, and hemoglobin values were obtained using blood sampled from the retro-orbital and multivitamin.
The ras family of proto-oncogenes comprises a group of Gproteins that have the ability to bind guanine nucleotides.1, 2 Ras is synthesized in the cytoplasm as a precursor protein that requires additional posttranslational modifications in order to attach to the inner surface of the plasma membrane, a prerequisite for Rasmediated signal transduction. These modifications are accomplished by a prenylation reaction involving the attachment of a 15-carbon farnesyl group to the C-terminal cysteine residue. This reaction is mediated by an enzyme called farnesyl protein transferase FPT ; .3, 4 Alternatively, prenylation may be accomplished by addition of a 20-carbon geranylgeranyl isoprenoid mediated by geranylgeranyl-protein transferase GGPT ; . Ras mutations and Ras protein activation are frequent features of malignant transformation. Approximately 30% of human cancers have been associated with ras mutations.5, 6 The frequency of ras mutations varies in hematologic malignancies, from 5% to 15% in acute lymphoblastic leukemia and up to 65% in chronic myelomonocytic leukemia.2, 5, 6 Ras activation may occur by mechanisms other than mutations. A prominent example is activation of Ras by the bcr abl chimeric gene.7, 8 Therefore, inhibition of Ras activation has been investigated as an antineoplastic therapy.9 One approach to Ras inhibition is inhibition of FPT.10-12 R115777 Zarnestra, Titusville, NJ ; is a potent nonpeptidomimetic FPT inhibitor FTI ; with significant antitumor effects in preclinical studies.13 In this study, we investigated the activity of R115777 in patients with Philadelphia chromosome Ph ; positive chronic myeloid leukemia CML ; , myelofibrosis MF ; , or multiple myeloma MM ; . Plasma concentrations of vascular endothelial growth factor VEGF ; have been found to be elevated in CML, 14, 15 and increased expression of VEGF correlates with poor prognosis.15 In addition, one of the proposed effects of FPT inhibition is suppression of angiogenesis with decreased expression of VEGF.16 Because of the clinical significance of VEGF in CML, we investigated whether R115777 has any in vivo effect on VEGF and other angiogenic factors to determine whether any clinical effect may be mediated through this mechanism.
Symptoms Signs: Incubation period is generally 1-6 days, although longer periods have been noted. Patients with inhalational anthrax would typically have fever, malaise, fatigue, dry cough and mild chest discomfort progressing to severe respiratory distress or dyspnea, diaphoresis, stridor, cyanosis, and shock. Death typically occurs within 24-36 hours after onset of severe symptoms. Other forms of anthrax include cutaneous papule progressing to dark-colored eschar or ulcer ; , and gastrointestinal nausea, vomiting, abdominal pain, bloody diarrhea; and including oropharyngeal anthrax with sore throat, dysphagia, and oral tonsillar lesions ; . Significant lymphadenopathy mediastinal in inhalational disease, regional in others ; is characteristic. Diagnosis: Physical findings are nonspecific. A widened mediastinum may be seen on CXR in later stages of illness. The organism is detectable by Gram stain of the blood and by blood culture late in the course of illness. Prophylaxis: Oral Ciprofloxacin or doxycycline for known or imminent exposure. An FDA-licensed vaccine is available. Soldiers going to areas of increased threat should already be vaccinated. Vaccine schedule is 0.5 mL SC at 0, 2, weeks, then 6, 12, and 18 months primary series ; , followed by annual boosters. Isolation and Decontamination: Standard precautions for HCWs. After an invasive procedure or autopsy is performed avoid if possible ; , the instruments and area used should be thoroughly disinfected with a sporicidal agent hypochlorite ; . Inhalation anthrax does not seem to be transmissible from person to person and murine.
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Mals were treated with collimated 1047-nm radiation at 125 J cm2. The mean tumor thickness in this group was 3.1 0.5 mm at the time of treatment. In marked contrast to treatment with focused irradiation at 125 J cm2, no tumor arrest was achieved in this group P .002 ; . Another 20 of 64 animals did not receive any laser treatment. All untreated tumors showed continuous growth beyond 12 mm in height. No lung or liver metastases were found in any of the treatment groups, although lung metastases were detected in 1 untreated animal. Tumors with complete regression after laser treatment showed a typical course. Upon application of focused 1047-nm irradiation, bleaching within 3 seconds after the start of laser treatment was noted. Occasionally, small retinal hemorrhages were observed during or within minutes after treatment. No initial changes were detected in the surrounding choroid. Maximum surrounding subretinal exudation was found several hours after treatment. Exudation decreased within 3 days after treatment, and all subretinal fluid was completely absorbed within 7 days after treatment. As the subretinal fluid resolved gradually, reductions of the tumor dimensions and vascular occlusion of the adjacent choroid were evident. Later, fibrotic pigmented chorioretinal scars evolved, surrounded by choroidal atrophy. No retinal traction or optic nerve atrophy was noted. A typical time course is given in Figure 1 and Figure 2. On fluorescein angiography, untreated tumors showed patchy hyperfluorescence increasing with time as a result of leaking intratumoral vessels. Fluorescein angiography performed 3 days after treatment indicated hypofluorescence of the tumor with some leakage at the margins Figure 1 and Figure 2 ; . Further follow-up revealed disap!
FIG. 5. Response of D2 activity to T4 in T1, GH4C1, and MSTO-211 cells. A, GH4C1 and MSTO-211 cells were kept in growth medium supplemented with 10 7 M Se, whereas T T1 were grown in growth medium. Cells were made hypothyroid by 24 h incubation in DMEM 10% charcoal-stripped FBS. Medium was replaced by DMEM 0.1% BSAcontaining vehicle or doses of free T4 FT4 ; , ranging from 0 to 8 hypothyroid hypo ; , 8 25 euthyroid Eu ; , and 25 400 hyperthyroid -hyper ; for 20 h. Cells were then processed for D2 activity * , P 0.001 vs. 0 of FT4 ; . B, T T1 cells were kept in growth medium until confluence and placed in hypothyroid medium for 24 h; medium was then replaced by 0.1% BSA-containing vehicle circle ; or 100 of free T4 square ; for 16 h. After that, vehicle open symbols ; or 100 M cycloheximide solid symbols ; was added to medium, and cells were harvested at 0, 0.5, 1, or 2 h * , P 0.05 vs. time 0 h ; . C, The data presented in B were normalized by the time point 0 h and plotted as fold difference n 2 6 and mycostatin.
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Dr. Samuel K. Ludwin is one of Canada's leading researchers and world-renowned for his work on remyelination and demyelination related to multiple sclerosis. When he speaks, people listen. "We have reached a unique time of exciting opportunities in MS research. Now is the time for Canada to chart a new course towards a cure for multiple sclerosis, " said Dr. Ludwin, a researcher at Queen's University and Kingston General Hospital. Dr. Ludwin has agreed to lead a new project for the MS Society of Canada, one that will attract high quality researchers to work in Canada on a cure for MS. The project will also help to keep some of our brightest young scientific minds engaged in multiple sclerosis research here, building on the world-class success of researchers like Dr. Donald Paty, Dr. Jack Antel and Dr. Jock Murray. Dr. Ludwin also believes that success in the lab must ultimately reach the person with MS. "It is vitally important that research always be directed towards the individual, whether the research is about lab science trying to find the cause, cure and treatment of MS or whether it is clinical or health research aimed at improving the prognosis and quality of life for people with MS and their families and mysoline.
Neurotic state with depersonalization episode depersonalization associated with: anxiety 300.00-300.09 ; depression 300.4 ; manic-depressive disorder or psychosis 296.0-296.9 ; schizophrenia 295.0-295.9 ; Hypochondriasis Body dysmorphic disorder hypochondriasis in: hysteria 300.10-300.19 ; manic-depressive psychosis, depressed type 296.2-296.3 ; neurasthenia 300.5 ; obsessional disorder 300.3 ; schizophrenia 295.0-295.9 ; Other neurotic disorders 300.81 Somatization disorder Briquet's disorder Severe somatoform disorder Undifferentiated somatoform disorder Atypical somatoform disorder Somatoform disorder NOS Other Occupational neurosis, including writers' cramp Psychasthenia Psychasthenic neurosis.
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Productcenter » press releases - eeproductcenter : : press release : : mrv communications reports results mrv communications reports results prnewswire 02 05 2004 00 et ; prnewswire-firstcall - mrv communications, inc nasdaq: mrvc ; , a leading provider of scalable network infrastructure equipment and optical components for metro and fiber-to-the-premises solutions, today reported its results for the fourth quarter and annual periods ended december 31, 200 net loss for the fourth quarter of fiscal 2003 was $ 9 million, or $ 05 per share, compared to a net loss of 4 million, or $ 18 per share, for the fourth quarter of 2002 and a net loss of $ 9 million, or $ 06 per share, for the third quarter of 200 revenues for the fourth quarter of fiscal 2003 were 0 million compared to 7 million for the fourth quarter of last year, and 8 million for the third quarter 200 net loss for fiscal 2003 was 0 million, or $ 26 per share, compared with a net loss of 8 million, or $ 25 per share, for the year ended december 31, 200 revenues for the year ended december 31, 2003 were 8 million, compared with 5 million for the year ended december 31, 200 revenues for the year ended december 31, 2002 included million from the company's divested passive component division and mrv.
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In retrospect, it seems that war on the human scene is inevitable. If we do not war internally with our spiritual selves, in order to maintain our own integrity, then external war among individuals will become inevitable. Unfortunately, there can be no peace on earth. It is a question of whether it shall be an internal spiritual war or an external physical war. But external freedom, democracy, and peace seem predicated upon a spiritually warring citizenry. There is, as Shakespeare had said, "a divinity that shapes our ends, roughhew them as we will." This tide in the affairs of men seems to be blind, unheedful of human personalities, deaf to our arguments. Fate unkindly denied this nation the services of one of its potentially greatest presidents -Hubert H. Humphrey. As Vice-President he was and nafcillin.
Date: September 2427, 2000 Location: University of Saarland, Saarbrcken, Germany Chairperson: M. Pfreundschuh, Chairman, Department of Internal Medicine I Further information: Kontaktstelle fr Wissens-und Technologietransfer-KWT der Universitt des Saarlandes, Frau U. Merkle, Im Stadtwald, Geb. 5, 66123 Saarbrcken, Germany E-mail: info kongresse-kwt : kongresse-kwt lymphoma2000
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15 Reynolds PC, Antoine JA, Bettencourt J, Starck TW. Regional hypothermia affects somatosensory evoked potentials. Anesth Analg 1991; 73: 6536 Nuwer MR. Basic electrophysiology: evoked potentials and signal processing. In: Nuwer MR, ed. Evoked Potential Monitoring in the Operating Room. New York: Raven Press, 1986; 548 17 Stohr M. Somatosensory evoked potentials. In: Maurer K, Lowitzsch K, Stohr M, eds. Evoked Potentials. Toronto: Decker, 1989; 12975 18 Vauzelle C, Stagnara P, Jouvinroux P. Functional monitoring of spinal cord activity during spinal surgery. Clin Orthop 1973; 93: 1738 Nuwer MR, Daube J, Fischer C, Schramm J, Yingling CD. Neuromonitoring during surgery. Report of an IFCN committee. Electroencephalogr Clin Neurophysiol 1993; 87: 26376 Tsuji S, Luders H, Lesser RP, Dinner DS, Klem G. Subcortical and cortical somatosensory potentials evoked by posterior tibial nerve stimulation: normative values. Electroencephalogr Clin Neurophysiol 1984; 59: 21428 Dawson EG, Sherman JE, Kanim LEA, Nuwer MR. Spinal Cord Monitoring: Results of the Scoliosis Research Society and the European Spinal Deformity Society survey. Spine 1991; 16: S3614 22 Haghighi SS, Oro JJ. Effects of hypovolemic hypotensive shock on somatosensory and motor evoked potentials. Neurosurgery 1989; 24: 24652 Haghighi SS, Oro JJ, Gibbs SR, McFadden M. Effect of graded hypoxia on cortical and spinal somatosensory evoked potentials. Surg Neurol 1992; 37: 3505 Russ W, Sticher J, Scheld H, Hempelmann G. Effects of hypothermia on somatosensory evoked responses in man. Br J Anaesth 1987; 59: 148491 Van Rheineck Leyssius AT, Kalkman CJ, Bovill JG. Influence of moderate hypothermia on posterior tibial nerve somatosensory evoked potentials. Anesth Analg 1986; 65: 47580 Browning JL, Heizer ML, Baskin DS. Variations in corticomotor and somatosensory evoked potentials: effects of temperature, halothane anesthesia, and arterial partial pressure of CO2. Anesth Analg 1992; 74: 6438 Schubert A, Drummond JC. The effect of acute hypocapnia on human median nerve somatosensory evoked responses. Anesth Analg 1986; 65: 2404 Sloan TB. Nondepolarizing neuromuscular blockade does not alter sensory evoked potentials. J Clin Monit 1994; 10: 410 Lam AM, Sharar SR, Mayberg TS, Eng CC. Isoflurane compared with nitrous oxide anaesthesia for intra-operative monitoring of somatosensory-evoked potentials. Can J Anaesth 1994; 41: 295300 Schubert A, Licina MG, Lineberry PJ. The effect of ketamine on human somatosensory evoked potentials and its modification by nitrous oxide. Anesthesiology 1990; 72: 339 Freye E, Hartung E, Schenk GK. Somatosensory-evoked potentials during block of surgical stimulation with propofol. Br J Anaesth 1989; 63: 3579 Maurette P, Simeon F, Castagnera L, Esposito J, Macouillard G, Heraut LA. Propofol anaesthesia alters somatosensory evoked cortical potentials. Anaesthesia 1988; 43 Suppl. ; : 445 33 Sebel PS, Lowdon JD. Propofol: A new intravenous anesthetic. Anesthesiology 1989; 71: 26077 and multivitamin.
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