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HYPERTENSION a ; Adequately controlled hypertension b ; Consistently elevated blood pressure levels properly taken measurements ; i ; systolic 140 to 159mmHg or diastolic 90 to 94mmHg ii ; systolic 160 or diastolic 95 mmHg c ; Vascular disease HISTORY OF HIGH BLOOD PRESSURE DURING PREGNANCY where current blood pressure is normal ; VENOUS THROMBO-EMBOLISM VTE ; includes deep vein thrombosis and pulmonary embolism ; a ; History of VTE b ; Current VTE on anticoagulants ; c ; Family history of VTE i ; First degree relative aged 45 years ii ; First degree relative aged 45 years d ; Major surgery i ; With prolonged immobilisation ii ; Without prolonged immobilisation e ; Minor surgery without immobilisation f ; Immobility unrelated to surgery ; e.g.- wheelchair use, debilitating illness KNOWN THROMBOGENIC MUTATIONS e.g. Factor V Leiden; Prothrombin mutation; Protein S, Protein C and Antithrombin deficiencies ; SUPERFICIAL VENOUS THROMBOSIS a ; Varicose veins b ; Superficial thrombophlebitis CURRENT AND HISTORY OF ISCHAEMIC HEART DISEASE STROKE history of cerebrovascular accident ; KNOWN HYPERLIPIDAEMIAS screening is NOT necessary for safe use of contraceptive methods ; VALVULAR AND CONGENITAL HEART DISEASE a ; Uncomplicated b ; Complicated eg. With pulmonary hypertension, atrial fibrillation, or a history of subacute bacterial endocarditis. Table 2. MFCs of EM-01D2 against yeast isolates MFC mg L ; Species C. albicans FLC susceptible C. albicans FLC resistant C. krusei C. parapsilosis C. glabrata C. tropicalis No. of isolates 24 28 23 Antifungal agent EM-01D2 FLC AMB EM-01D2 FLC AMB EM-01D2 FLC AMB EM-01D2 FLC AMB EM-01D2 FLC AMB EM-01D2 FLC AMB range 0.04 3.12 50 geometric meana 1.09 175 0.62 IC50 MFC50b 10 526.32 10.00.

The karyotypic abnormalities included 1 case each of trisomy 8, monosomy 7, t 3; 21 ; q27?; q22 ; figure 4 ; , del 20q ; , ider 20 ; q10 ; t 20; 21 ; q22; q22 ; , one multiaberrant karyotype including del 20q ; and t 7; 17 ; q11; q21 ; and two cases with loss of the Y chromosome. In all patients, archive material was analyzed to see if the abnormalities were detectable at any time prior to imatinib treatment. Patients #19 and #34 had achieved cytogenetic remission with IFN-alpha and after stem cell mobilization, respectively, and thus Ph-negative cells were available for study. However, the respective abnormalities were not detected in patient #34, a total of 900 interphases were analysed by FISH.

The diagnosis of fronto-temporal dementia will be made using Manchester Lund criteria The diagnosis of Lewy Body Dementia will be made using Newcastle criteria When participants meet criteria for more than one type of dementia, up to three dementia diagnoses may be recorded, noting which is believed to be the primary cause of the difficulties The case should be referred to the Diagnostic Review Committee for review. Prior to a Diagnostic Review Committee meeting, the CO will request copies of the results of the dementia evaluation battery, laboratory testing, and neuroimaging. In addition, the field site will be asked to provide a comprehensive but succinct approximately 1.5 pages ; narrative of the participant's history. No statistical difference was observed between the 2 study groups concerning the number of patients who had at least one presyncope during follow-up and the total number of presyncopal episodes. On repeated head-up tilt testing performed 3 to 6 days after the start of treatment, etilefrine did not appear superior to placebo in preventing tilt-induced syncope negative response 52% in etilefrine group versus 45% in placebo group and kytril. Renal artery stenosis STENOSIS, RENAL ARTERY BUERGERS BERGERS ; DISEASE Polyarteritis POLYARTERITIS, RENAL * CODE IN ERROR: ASSUMED TO BE 4462. Vasculitis and its derivatives ANTI-GLOMERULOBASEMENT MEMBRANE GLOMER. GOODPASTURES Wegeners granulomatosis GRANULOMATOSIS WEGENERS GRANULOMATOSIS WEGENERS SY THROMBOTIC THROMBOCYTOPENIC PURPURA Hepatorenal syndrome HEPATORENAL SYNDROME Post infectious GN, SBE GLOMERULONEPHRITIS, ACUTE Rapidly progressive GN GLOMERULONEPHRITIS, ACUTE WITH LESION OF RAPIDLY PROGR Acute interstitial nephritis ACUTE INTERSTITIAL NEPHRITIS ACUTE GLOMERULONEPHRITIS WITH UNSPECIFIED PATHOLOGICAL FOCAL GLOMERULONEPHRITIS FOCAL GLOMERULOSCLEROSIS WI FOCAL GLOMERULOSCLEROSIS WITH NEPHROTIC SYNDROME NEPHROTIC SYNDROME NEPHROSIS Other proliferative GN * UNRECONCILABLE CODE * Focal glomerulosclerosis, focal sclerosing GN FOCAL GLOMERULOSCLEROSIS CHRONIC INTERSTITIAL NEPHRITIS HEREDITARY INTERSTITI Glomerulonephritis GN ; CHRONIC GLOMERULONEPHRITIS, INCLUDING WITH UNSPECIFIED Radiation nephritis PROLIFERATIVE GLOMERULONEPHRITIS RADIATION NEPHRITIS Membranous nephropathy MEMBRANOUS GLOMERULONEPHRITIS Membranoproliferative GN type 1, diffuse MPGN Dense deposit disease, MPGN type 2 MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS MESANGIOCAP Goodpastures Syndrome ANTI-GBN GLOMERULONEPHRITIS Tubular necrosis no recovery ; * UNRECONCILABLE CODE * NEPHRITIS OR NEPHROPATHY WITH RENAL MEDULLARY LESION IgA nephropathy, Bergers disease IgM nephropathy NEPHRITIS AND NEPHROPATHY, NOT SPECIFIED AS ACUTE OR C Chronic interstitial nephritis ANALGESIC NEPHROPATHY OTHER INTERST NEPHRITIS INTE Secondary GN, other Nephropathy due to heroin abuse and related drugs Drash syndrome, mesangial sclerosis GLOMERULON. NEPHRITIS NEPHROPATHY BRIGHTS DISEAS NEPHROTOXINS VARIOUS ; TOXIC NEPHROPATHY SPECIFY ; CHRONIC RENAL FAILURE CHRONIC UREMIA HEROIN ABUSE RENAL FAILURE, UNSPECIFIED UREMIA, NOT OTHERWISE SPE GLOMERULOSCLEROSIS UNILATERAL SMALL KIDNEY BILATERAL SMALL KIDNEY SMALL KIDNEY, UNSPECIFIED SMALL KIDNEY OF UNKNOWN CAUSE CHRONIC PYELONEPHRITIS WITHOUT LESION OF RENAL MEDULLA PYELONEPHRITIS, CHRONIC WITH LESION OF RENAL MEDULLARY Chronic pyelonephritis, reflux nephropathy CHRONIC PYELONEPHRITIS PYELONEPHRITIS, UNSPECIFIED NECROSIS, RENAL GANGREN Nephropathy caused by other agents INFECTIONS OF KIDNEY HYDRONEPHROSIS Nephrolithiasis CALCULI RENAL ; NEPHROLITHIASIS STAGHORN CALCULUS Urolithiasis URINARY CALCULUS, UNSPECIFIED Renal artery occlusion Cholesterol emboli, renal emboli THROMBOSIS RENAL ARTERY KIDNEY ARTERY EMBOLISM OCC Other renal disorders OBSTRUCTIVE KIDNEY OBSTRUCTIVE NEPHROPATHY RENAL INSUFFICIENCY URINARY TRACT INFECTION, SITE NOT SPECIFIED Acquired obstuctive uropathy URINARY OBSTRUCTION, UNSPECIFIED OBSTRUCTIVE UROPATH OBSTRUCTIVE UROPATHY, ACQUIRED URINARY OBSTRUCTION HYPERPLASIA OF PROSTATE CHRONIC UREMIA UREMIA * PMMIS DOC. ERROR--SHOULD Post partum renal failure RENAL FAILURE IN PREGNANCY, CHILDBIRTH, PUERPERIUM ; RENAL FAILURE IN PREGNANCY, CHILDBIRTH, PUERPERIUM ; LUPUS ERYTHEMATOSUS Lupus erythematosus, SLE nephritis ; SYSTEMIC LUPUS ERYTHEMATOSUS LUPUS NEPHRITIS Scleroderma SCLERODERMA RHEUMATOID ARTHRITIS RAMBDOMYOLYSIS.

Occurred diffusely throughout the cytoplasm and was associated with the basolateral membrane of relatively large cells Fig. 5 ; , presumably mitochondrion-rich see Wilson et al., 1997 ; . It was expected that the V-H + -ATPase would be localized to the apical cell membrane of pavement cells and or Na + -ATPase-rich cells as it has been described in freshwater teleost species Lin et al., 1994; Sullivan et al., 1995; Wilson et al., 2000 ; . Basolateral localization of V-H + ATPase is relatively rare in vertebrates and to date has only been described in -type intercalated cells of the mammalian collecting duct and turtle urinary bladder Stetson and Steinmetz, 1985; Brown et al., 1988a; Brown et al., 1988b; Verlander et al., 1992; Brown and Breton, 1996 ; . If the V-H + ATPase-rich cells of freshwater stingray gills are analogous in function to -type intercalated cells then they would be involved with HCO3- excretion and Cl- uptake via an apical Cl- HCO3- exchanger Weiner and Hamm, 1990 ; . This would be in contrast to freshwater teleost fishes in which Cl- HCO3- exchange is thought to occur in Na + -ATPase-rich chloride cells Sullivan et al., 1996; Wilson et al., 2000 ; . In the seawater-acclimated and seawater stingray gills, there appeared to be qualitative differences in the V-H + -ATPase labeling, such as stronger staining in the cytoplasm and less distinct staining along the basolateral membrane, relative to freshwater individuals Fig. 5 ; . Although ultrastructural studies would be required to quantify these qualitative differences, our findings are consistent with V-H + -ATPase regulation in other vertebrate tissues, in which recycling of the transporter between a cytoplasmic pool of vesicles and the plasma membrane has been demonstrated Dixon et al., 1986; Stetson and Steinmetz, 1986; Verlander et al., 1992; Verlander et al., 1994; Brown and Breton, 2000 ; . Therefore, the qualitative staining differences may indicate that seawateracclimated and seawater stingrays have more V-H + -ATPase stored in cytoplasmic vesicles, and less transporter on the basolateral membrane, relative to freshwater stingrays. If the V-H + -ATPase-rich cells are functionally analogous to intercalated cells see above ; , then this trend would be expected, because Cl- HCO3- exchange in marine stingrays could be driven by the favorable gradient for Cl- to enter the cells from sea water, rather than the active generation of a gradient by a V-H + -ATPase. In seawater stingrays, V-H + -ATPase-rich cells were only.

708. DNA-Microarray Analysis of Brain Cancer: Molecular Classification For Therapy and lenalidomide.

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