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  • 1
    Keywords: Germany ; DIAGNOSIS ; FOLLOW-UP ; imaging ; DISEASE ; PROTEIN ; PATIENT ; IMPACT ; CONTRAST ; MRI ; MAGNETIC-RESONANCE ; magnetic resonance imaging ; DIFFERENCE ; AGE ; STABILITY ; PROTEIN LEVELS ; DEMENTIA ; AD ; ATROPHY ; VASCULAR DEMENTIA ; CLINICAL-DIAGNOSIS ; DIFFERENTIAL-DIAGNOSIS ; A-BETA-1-42(43) ; APOLIPOPROTEIN-E GENOTYPE ; BIOCHEMICAL MARKER ; CSF-TAU ; dementia,differential diagnosis,CSF tau,volumetric MRI ; DIAGNOSTIC-ACCURACY ; E4 ALLELE ; TAU-PROTEIN
    Abstract: Increased tau levels are a well-established finding in Alzheimer's disease (AD). In contrast, the potential value of tau levels in the differential diagnosis of AD, vascular dementia (VD) and major depression warrants further investigation. The potential impact of psychotropic medication also needs to be established. We investigated cerebrospinal fluid (CSF) tau protein concentrations in 88 patients with AD, 23 patients with VD, 25 patients with major depression and 17 age-paralleled controls without cognitive impairment with respect to important clinical variables. type and dosage of psychotropic medication and cerebral changes as assessed by magnetic resonance imaging (MRI). The AD patients showed significantly elevated tau levels compared with patients with VD or major depression and controls. Tau levels obtained in the VD group were intermediate, with significant differences from both AD patients and patients with major depression and controls. Within the AD group, no significant correlation between tau levels, severity of dementia, age, duration of disease, type and dosage of psychotropic medication or MRI volumetric changes arose. A subgroup of AD patients without increased tau levels was characterized by a significantly larger percentage of patients with presenile onset. (C) 2003 Elsevier Science Ireland Ltd. All rights reserved
    Type of Publication: Journal article published
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  • 2
    Keywords: APOPTOSIS ; CELLS ; IN-VITRO ; BLOOD ; CELL ; Germany ; INHIBITION ; DISEASE ; HEART ; PATIENT ; MACROPHAGES ; SERA ; treatment ; ACID ; GLUTATHIONE ; PLASMA ; DECREASE ; cholesterol ; LDL ; LIPOPROTEIN ; PERIPHERAL-BLOOD ; OXIDATION ; cysteine ; arteriosclerosis,risk factors in hyperlipidemia,glutathione in atherosclerosis,redox status as a ris ; CORONARY-ARTERY DISEASE ; HEART-DISEASE ; N-ACETYL-CYSTEINE ; SERUM LEVELS
    Abstract: Treatment of hyperlipidemic patients with the thiol compound N-acetyleysteine (NAC) was previously shown to cause a significant dose-related increase in the high-density lipoprotein (HDL) -cholesterol serum level, suggesting the possibility that its disease-related decrease may result from a diminished thiol concentration and/or thiol/disulfide redox status (REDST) in the plasma. We therefore investigated plasma thiol levels and REDST in normo-/byperlipidemic subjects with and without coronary heart disease (CHD). The thiol level, REDST, and amino acid concentrations in the plasma and intracellular REDST of peripheral blood mononuclear cells (PBMC) have been determined in 62 normo- and hyperlipidemic subjects. Thirty-three of these subjects underwent coronary angiography, because of clinical symptoms of CHD. All groups of hyperlipidemic patients under test and those normolipidemic individuals with documented coronary stenoses showed a marked decrease in plasma thiol concentrations, plasma and intracellular REDST of PBMCs, and a marked increase in plasma taurine levels. Individual plasma thiol concentrations and plasma REDST were strongly negatively correlated with the serum LDL-cholesterol and positively correlated with the serum HDL-cholesterol level. Together with the earlier report about the effect of NAC on the HDL-cholesterol serum level, our findings suggest strongly that lower HDL-cholesterol serum levels may result from a decrease in plasma thiol level and/or REDST possibly through an excessive cysteine, catabolism into taurine. (C) 2003 Elsevier Inc
    Type of Publication: Journal article published
    PubMed ID: 14607527
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  • 3
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  33. Kongress der Deutschsprachigen Gesellschaft für Intraokularlinsen-Implantation, Interventionelle und Refraktive Chirurgie (DGII); 20190214-20190216; Berlin; DOC19dgii077 /20190301/
    Publication Date: 2019-03-07
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 4
    ISSN: 1432-5233
    Keywords: Key words Experimental diabetes ; Albuminuria ; Glomerular metabolism ; ACE inhibitors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Clinical studies indicate a nephro-protective effect in conjunction with the use of ACE inhibitors. This study's aim was to determine whether ACE inhibitors influence the metabolism of glomerular cells in addition to their known hemodynamic effects. Streptozotocin diabetic rats were treated with lisinopril (DLis 1.5 mg/l water), or hydralazine (Dhyd, 50 mg/l water) over 4 weeks. Untreated diabetic rats (DC) and non-diabetic rats (C) served as controls. After four weeks of treatment, urinary excretion of albumin, blood pressure and metabolic control (Glyc-Hb) were measured. After treatment glomeruli were isolated and homogenized, and β-NAG and total proteolytic activity against azocasein were measured. Glycated hemoglobin levels were similar in all diabetic groups (DC, 12%, Dhyd, 10%; DLis 11%). Blood pressure of DLis rats (79 ± 3 mmHg) and DHyd rats (46 ± 2 mmHg) was lower than that of DC rats (111 ± 3 mmHg). Urinary albumin excretion of diabetic groups was lowest in DLis. Diabetic rats showed a decrease in glomerular β-NAG (10 vs. 60.5 U/g protein) and total proteolytic activity against azocasein (148 vs. 170 U/mg protein hour) compared to non-diabetic rats. Lisinopril increased β-NAG (30 vs. 14 U/g protein) and total proteolytic activity (160.5 vs. 141.5 U/mg protein hour) compared with hydralazine. Our study confirms that the nephro-protective effect of ACE inhibitors is partially due to modulatory effects on the metabolism of basement membrane proteins.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Research in experimental medicine 161 (1973), S. 89-100 
    ISSN: 1433-8580
    Keywords: Tissue injury ; Plasma kininogen ; Suprarenal glands ; Urinary kinin excretion ; Gewebsschädigung ; Plasmakininogen ; Nebennierenfunktion ; Kininausscheidung im Urin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Nach experimentell gesetzten Gewebsschädigungen kommt es bei Ratten zu einer Vermehrung der Kininogene im Plasma. Präkallikreingehalt und Kininaseaktivität des Plasmas sind nicht signifikant verändert. Dauer und Ausmaß der Kininogenzunahme sind der Größe der Gewebsläsion proportional. Der Anstieg des Plasmakininogenspiegels korreliert signifikant mit derα-Globulin-Vermehrung und der Albuminabnahme, eine signifikante Beziehung zum Fibrinogengehalt des Plasmas besteht nicht. Phorbolderivate mit entzündlicher und cocarcinogener Wirkung verursachen, in Mikrogramm-Mengen intramuskulär verabreicht, einen größeren Kininogenanstieg im Plasma als äquimolare Mengen von Phorbolderivaten mit nur entzündlicher Wirkung. Die erhöhte Kininogenkonzentration im Plasma führt wahrscheinlich zu einem gesteigerten Kininogenumsatz in der Niere; die Ausscheidung pharmakologisch wirksamer Kinine mit dem Urin ist nach Gewebsschädigung stark vermehrt. Antiphlogistica vermindern nach Gewebsschädigung Fibrinogen- undα-Globulin-Vermehrung, nicht den Kininogenanstieg. Die Zunahme des Kallikreinsubstrates verläuft im Plasma unabhängig von der Nebennierenfunktion; TSH und Gonadotropin beeinflussen den Kininogenspiegel nicht. Es ist denkbar, daß noch unbekannte Vorgänge am Ort der Gewebsläsion eine vermehrte Kininogensynthese in der Leber auslösen.
    Notes: Summary In rats tissue injuries are followed by an increase of plasma kininogens. Prekallikrein content and kininase activity of the plasma do not change significantly. The period and the amount of kininogen increase are proportional to the extent of tissue damage. There are significant correlations between the rise of plasma kininogen content with both the increase of plasmaα-globulins and the decrease of plasma albumins. Plasma fibrinogen content does not correlate with kininogen content. Derivatives of phorbol having inflammatory and cocarcinogenic properties are more effective in increasing the plasma kininogen level than aequimolar amounts of phorbol derivatives with only inflammatory qualities. An elevated plasma kininogen concentration probably leads to an increased turnover of kininogen in the kidney; the urinary excretion of pharmacologically active kinins is augmented significantly after tissue injury. After tissue damage fibrinogen andα-globulin increase are lowered by antiphlogistic agents but not kininogen enrichment. The increase of the kallikrein substrate kininogen in plasma is independent of the function of adrenals; TSH or gonadotropine do not change the plasma kininogen level. Probably an augmented kininogen synthesis in the liver is caused by still unknown substances liberated at the site of tissue damage.
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  • 6
    ISSN: 1432-0584
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary 1. The proteinase-inhibitor of beef-liver was isolated out of extracts over deproteinising by perchloric acid, cationexchange-chromatography, and the trypsin-inhibitor-complex (0,277 μg protein/ImU). 2. The identity of the functional groups of both proteinase-inhibitors was demonstrated by the following results: there are no differences in the proportion of the inhibition of trypsin, and kallikrein; both inhibitors do not inhibit kallikrein of dogs, and rats; pancreas trypsin cannot displace the kallikrein from the liver-inhibitor-compound in one hour; the same is true for the complexes with Trasylol. 3. In the blood-coagulation-test with normal blood, hemophilia A- and hemophilia B-blood Trasylol, and liver-inhibitor retard the coagulation to the same degree. 4. The inhibitors inhibit the coagulation of hemophilia B-blood much more than that of hemophilia A-blood. 5. The rough extracts of bovine liver retard the coagulation of blood more than Trasylol does, they also have a small inhibiting affect against pepsin. 6. In pig-liver extracts won in the same manner an inhibiting effect against the mentioned proteinases, and blood coagulation was not to be demonstrated.
    Notes: Zusammenfassung 1. Der Proteinasen-Inhibitor aus Rinderleber wurde über Enteiweißung mit Perchlorsäure, Kationenaustausch-Chromatographie und den Trypsin-Inhibitor-Komplex rein dargestellt (0,277 μg Protein/ImE) und mit Trasylol verglichen. 2. Die Identität der funktionellen Gruppen beider Inhibitoren wurde an Hand folgender Ergebnisse erwiesen: Im Hemmungsverhältnis für Trypsin und Kallikrein bestehen keine Unterschiede; beide Inhibitoren hemmen Pankreas-Kallikrein von Hund und Ratte nicht; Trypsin kann Kallikrein innerhalb 1 Std. aus der Bindung mit Leber-Inhibitor nicht verdrängen; Kallikrein kann Trypsin aus der Bindung mit Leber-Inhibitor nicht verdrängen; das entsprechende gilt für die Trasylol-Komplexe. 3. Im Nativ-Venenblut-Gerinnungs-Test mit Normalblut, Hämophilie-A-Blut und Hämophilie-B-Blut verzögern Trasylol und gereinigter Leber-Inhibitor die Blutgerinnung gleich stark. 4. Die Inhibitoren verzögern die Gerinnung von Hämophilie-B-Blut erheblich stärker als die von Hämophilie-A-Blut. 5. Ungereinigte Rinderleberextrakte verzögern die Blutgerinnungszeit stärker als Trasylol; sie haben auch eine geringe Hemmwirkung für Pepsin. 6. In gleichartig gewonnenen Schweineleberextrakten war eine Hemmwirkung gegen die untersuchten Proteinasen und die Blutgerinnung nicht nachweibar.
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  • 7
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
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  • 8
    ISSN: 1432-0584
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
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  • 9
    ISSN: 1432-0584
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary The Kallikrein inhibitor of liver (Werle andAppel), the effect of which on trypsin and chymotrypsin was previously known, was compared with Kallikrein inhibitor from the parotid in respect of its effect on fibrinolysis and clotting of human blood. A variety of techniques was employed. In whole blood, the inhibitory preparation of liver inhibited clotting by an effect on the pre-phase. Its effect on the value mε in the DCF (depression of thrombus consistency) was stronger than that of the almost inert inhibitor from the parotid. Further, its power of inducing pseudo-fibrinolysis (thrombus-antiadhesion effect) is also greater. In differential treatment the hepatic inhibitor should be determined when a powerful anti-proteinase action (e.g., in pancreatitis and concurrent thrombophlebitis) together with an anti-coagulation effect causing thrombostasis is medically indicated. This may also be true in some cases of varicose thrombosis in which thrombosis with good effect on haemodynamics associated with obliteration of the veins may desirable when a general tendency to thrombosis if to be avoided.
    Notes: Zusammenfassung Ein Kallikreininhibitor aus Leber (Werle undAppel), dessen Wirkung auf Trypsin und Chymotrypsin bereits bekannt war, wurde vergleichend mit Parotis-Kallikreininhibitor hinsichtlich seiner Wirkung auf die extravasale Fibrinolyse und Gerinnung von Humanblut mit verschiedenen Methoden näher untersucht. Im Gesamtblut erwies sich das Leberinhibitorpräparat gerinnungshemmend durch Beeinflussung der Vorphase der Gerinnung. Sein Einfluß auf den Meßwert mε im TEG (Thrombusfestigkeitsdepression) war stärker als der des fast gerinnungsneutralen Parotisinhibitors, ebenso seine Pseudofibrinolyse induzierende Fähigkeit (Thrombus- Antiadhäsionswirkung). Differentialtherapeutisch erscheint der Leberinhibitor allenfalls dann prüfenswert, wenn eine starke Antiproteinaseaktivität z. B. bei Pankreatitis und Begleitthrombophlebitis zugleich mit einer Antikoagulationswirkung zur Thrombostase ärztlich erwünscht ist. Dies könnte auch bei manchen Varizenthrombosen der Fall sein, bei denen die Thrombosierung mit hämodynamisch günstiger, nachfolgender Venenverödung unter gleichzeitiger Vermeidung einer Generalisierungstendenz der Thromboseneigung erwünscht ist.
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  • 10
    ISSN: 1432-0584
    Keywords: Key words Heavy-chain disease ; Direct antiglobulin test ; Coombs test ; Hyperglobulinemia ; Anemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  We report here for the first time a patient with μ heavy-chain disease (HCD), hyperimmunoglobulinemia, and a positive direct antiglobulin test (DAT, Coombs test). The heavy-chain diseases involve the proliferation of lymphoplasma cells of B cell origin and are characterized by the production of incomplete heavy chains devoid of light chains. The association of μ heavy-chain disease with either hyperglobulinemia or a positive DAT has not been reported in the literature to date. In this patient, immunofixation of serum proteins with monospecific antisera to α-, γ-, μ,- or δ-chains and to κ- and λ-chains revealed a precipitation band with antibody to IgM, but not with κ and λ light-chain antibodies, indicating μ heavy-chain disease. Hyperglobulinemia was present, which is very uncommon for HCD. A DAT of the patient's red blood cells (RBC) was found to be strongly positive for anti-IgG but negative for anti-IgM, -IgA, -C3c, and -C3d. However, when the eluate from the patient's red blood cells was investigated with nephelometry, it was found to contain antigens reactive with anti-γ as well with anti-μ-antiserum. When a DAT was performed with a randomly chosen test cell incubated with the eluate, the antibody-containing eluate was shown to react with anti-IgG as well as with anti-IgM-antiserum. In summary, the eluate from the patient's RBCs contained IgG and an immunoglobulin structure reactive with anti-IgM in an RBC agglutination assay as well as with anti-μ antiserum in a nephelometric investigation. Whether this IgM on the patient's erythrocytes is penta- or oligomeric, complete IgM, or the heavy chain cannot be concluded from these observations.
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