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  • 1
    Publication Date: 2018-11-28
    Description: How cells maintain their size has been extensively studied under constant conditions. In the wild, however, cells rarely experience constant environments. Here, we examine how the 24-h circadian clock and environmental cycles modulate cell size control and division timings in the cyanobacterium Synechococcus elongatus using single-cell time-lapse microscopy. Under constant...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 2
    ISSN: 1615-6722
    Keywords: Schlüsselwörter Sarkoidose ; Morbus Boeck ; Herzinsuffizienz ; Myokardbeteiligung ; Medikamentöse Therapie ; Key words Sarcoidosis ; Boeck's disease ; Congestive heart failure ; Myocardial manifestation ; Drug therapy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Abstract Background: Sarcoidosis is a multisystemic disorder that may involve every organ. A symptomatic manifestation of the myocardium is possible, in these cases arrhythmias are the most common symtpoms. Case Report: This case report presents a 26-year-old female with the recurrence of Boeck's sarcoid. Fever, chill and a severe reduction in stress tolerance were the first symtoms. At the time of admission she complained of Grade III dyspnea according to the NYHA classification. The echocardiogram showed a severe impairment of the global and left ventricular function. The left ventricular ejection fraction was reduced to 30% and the Tei index was elevated to 1,0. A specimen taken from a mediastinal tumor confirmed the hypothesis of the recurrence of the sarcoidosis. Myocardial perfusion scintigraphy showed typical leasions for myocardial sarcoidosis. There were signs of an old anteroseptal infarction in the resting ECG without evidence of myocardial ischemia during a stress test. Repeated Holter-ECGs were without signs of severe arrhythmias whereas ventricular late potentials were positive. After the combined therapy with steroids, digitalis and an angiotensin-1 receptor antagonist, mediastinal mass and Tei index were reduced and the ejection fraction moved to 56%. Dyspnoe was classified with Grade II according to the NYHA classification. Conclusion: Treatment of asymptomatic sarcoidosis is still controversial, whereas the treatment of life-threatening sarcoidosis, eye involvement of severe hypercalcemia is accepted. This case report presents the successful treatment of severe heart failure with predinisone, glycosides and an angiotensin-1 receptor antagonist. With this combined therapy an improvement of subjective and objective parameters was possible.
    Notes: Zusammenfassung Hintergrund: Bei der Sarkoidose handelt es sich um eine Multisystemerkrankung, bei der grundsätzlich alle Organe betroffen sein können. Eine symptomatische Herzbeteiligung ist möglich und äußert sich meist in Form von Herzrhythmusstörungen. Fallbeschreibung: Wir berichten über eine 26jährige Patientin, bei der es zu einem Rezidiv eines Morbus Boeck mit ausgeprägter kardialer Symptomatik kam. Neben Fieber und Schüttelfrost bestand bei der Patientin eine massive Beeinträchtigung der körperlichen Leistungsfähigkeit. Bei stationärer Aufnahme litt sie unter einer Dyspnoe im NYHA-Stadium III. Die Echokardiographie zeigte mit einer Ejektionsfraktion von 30% und einem Tei-Index von 1,0 eine massive Einschränkung der linksventrikulären und globalen Funktion. Bei gleichzeitiger mediastinaler Raumforderung konnte das Rezidiv der Sarkoidose bioptisch gesichert werden. Die Thalliummyokardzintigraphie zeigte typische Veränderungen für eine myokardiale Beteiligung. Bei Hinweisen auf einen stattgehabten Anteroseptalinfarkt im EKG fanden sich positive Spätpotentiale im signalgemittelten EKG ohne einen Hinweis auf eine belastungsabhängige Ischämie in der Ergometrie oder Herzrhythmusstörungen im Holter-EKG. Angesichts des schweren Krankheitsbildes begannen wir eine immunsuppressive Therapie mit Prednison sowie eine Herzinsuffizienztherapie mit einem Digitalisglykosid und einem Angiotensin-1-Rezeptor-Antagonisten. Nach Abschluß der Therapie hatte sich die mediastinale Raumforderung zurückgebildet, der Tei-Index betrug nur noch 0,6, und die linksventrikuläre Ejektionsfraktion war auf 56% angestiegen, Dyspnoe bestand nur noch bei stärkerer körperlicher Belastung (NYHA II). Schlußfolgerung: Die Behandlung einer asymptomatischen Verlaufsform der Sarkoidose ist umstritten. Es besteht jedoch Konsens darüber, daß bei vitaler Gefährdung, Augenbeteiligung oder massiver Hyperkalzämie eine immunsuppressive Therapie indiziert ist. Der vorliegende Fallbericht schildert die erfolgreiche Therapie einer symptomatischen, schweren Herzinsuffizienz mittels immunsuppressiver Therapie mit Prednison in Verbindung mit einem Digitalisglykosid und einem Angiotensin-1-Rezeptor-Antagonisten. Mit dieser Kombinationstherapie konnte die Beeinträchtigung der Patientin durch die schwere Herzinsuffizienz nach subjektiven und objektiven Parametern deutlich vermindert werden.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1573-7241
    Keywords: orthostatic hypotension ; Bradbury Eggleston Syndrome ; norepinephrine infusion therapy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-2277
    Keywords: Key words Chronic rejection ; lymphocytes ; Lymphocytes ; migration ; chronic rejection
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Histological analyses have identified lymphocytes and macrophages as the predominant leukocyte populations that infiltrate organs undergoing chronic rejection. In order to define the time frame of this infiltration, we investigated the in vivo migration pattern of lymphocytes in a well-established rat model of chronic kidney allograft rejection. F344 kidneys were orthotopically transplanted into bilaterally nephrectomized Lewis rats. Recipients were treated with cyclosporin A (1.5 mg/kg/per day) for the first 10 days. After anti-CD18 or vehicle pretreatment, peripheral blood lymphocytes obtained from naive Lewis rats and labeled with 3H-uridine were injected into transplanted rats 12 and 16 weeks after transplantation. Organs were harvested 4, 8, and 12 h thereafter. After 12 weeks, proteinuria developed, accompanied by all signs of chronic rejection including glomerular sclerosis. Labeled lymphocytes rapidly infiltrated grafted kidneys 4 h after injection. Even more lymphocytes had accumulated in the grafts 12 h after injection. After 16 weeks, few lymphocytes had emigrated into the graft at 4 h, while infiltration was most pronounced by 12 h. Pretreatment with anti-CD18 inhibited the influx of lymphocytes. There was no difference between the patterns of lymphocytes derived from naive and transplanted rats. Our results emphasize the importance of endothelial cells in chronically rejecting kidneys for the control of leukocyte influx. β2-integrins may play a central role in determining the transendothelial migration during this process.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-2277
    Keywords: Rescue therapy, tacrolismus, kidney/pancreas transplantation ; Tacrolimus, kidney/pancreas transplantation ; Kidney/pancreas transplantation, rescue therapy ; Pancreas/kidney transplantation, tacrolismus, rescue therapy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Tacrolimus has been effective both in primary and rescue therapy following steroid and OKT3-resistant acute rejection in liver and kidney transplantation. Due to the effects of tacrolimus on glucose metabolism, there has been concern about its use in simultaneous pancreas/kidney transplantation. We report on the results of six patients (three female, three male, age 35.2 ± 7.3 years) converted from cyclosporin A to tacrolimus following simultaneous pancreas/kidney transplantation in steroid-resistant acute rejection. Tacrolimus was induced 2.8 ± 1.7 months (range 1–4.8 months) after transplantation; follow-up was 3–18 months. Following conversion, creatinine levels declined in all patients [3.5 ± 1.2 mg/dl before conversion, 3.0 ± 1.9 mg/dl (n = 6) at three months, 1.4 ± 0.1 mg/dl at 1 year (n = 3)]. Before conversion, fasting blood glucose levels averaged 154 ± 33 mg/dl, with three patients receiving insulin. Three months later no patient required insulin, the mean glucose level being 107 ± 23 mg/dl (n = 6); at 1 year it was 92 ± 9 mg/dl (n = 3). One patient lost his pancreatic graft after 4 months due to a mycotic aneurysm. We conclude that conversion to tacrolimus is a safe and effective treatment in cases of steroid-resistant rejections following pancreas/kidney transplantation.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-2277
    Keywords: Key words Cystatin C ; Diagnostic test ; Glomerular filtration rate ; Kidney transplantation ; ROC curve ; Sensitivity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The performance of serum cystatin C as a screening marker of reduced creatinine clearance in renal transplantation was evaluated and compared to serum creatinine. In addition we studied whether cystatin C accurately reflects creatinine clearance over the entire range of transplant function. Serum cystatin C, serum creatinine, and creatinine clearance were measured in 110 adult renal transplant recipients. Cystatin C detected reduced creatinine clearance with the high sensitivity of 95 %. Serum cystatin C and serum creatinine did not differ regarding 90 and 95 % sensitivity, derived from the receiver-operating characteristics plot. We demonstrated a strong correlation and linear association between 1/cystatin C and creatinine clearance over the entire range of transplant function, equivalent to that of 1/creatinine. In summary, serum cystatin C accurately reflects creatinine clearance over the entire range of transplant function and is as efficacious as serum creatinine to detect reduced creatinine clearance in renal transplant recipients.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-2277
    Keywords: Kidney transplantation, chronic rejection, rat ; Kidney transplantation, lipopolysaccaride rat ; Rejection, chronic lipopolysaccharide, rat kidney
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The etiology of chronic rejection is unknown, although acute rejection, viral infection, and initial graft ischemia have been implicated. To test the effects of infections on the process of chronic rejection, we simulated bacterial infection by the administration of the endotoxin lipopolysaccharide (LPS), a potent activator of various cell types in an established rat model of chronic rejection. Lewis recipients of Fisher 344 kidneys were treated with a single dose of LPS or vehicle 8 weeks following transplantation and grafts were examined at various time points. In the chronically rejecting controls leukocytic infiltration and the expression of cytokines peaked at 16 weeks. In LPS-treated hosts, leukocyte infiltration and cytokine expression peaked at 12 weeks. By 16 weeks, glomeruli in LPS-treated recipients had become far more sclerotic than those in controls, mimicking the changes observed in controls at 24 weeks. We conclude that infections may play an important role in the development of chronic rejection.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-1912
    Keywords: Key words:α1A-adrenoceptors, α1B-adrenoceptors – Rat kidney – Inositol phosphates – G protein – Calcium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. We have compared the coupling mechanisms of rat renal α1A- and α1B-like adrenoceptors to inositol phosphate formation. The experiments were performed in parallel in native renal tissue preparations and in those where α1B-adrenoceptors had been inactivated by treatment with 10 μmol/l chloroethylclonidine for 30 min at 37°C; renal slices were used in most experiments but isolated renal cells were also used in some cases. The Ca2+ chelating agent, EGTA (5 mmol/l), reduced noradrenaline-stimulated inositol phosphate formation in native but enhanced it in chloroethylclonidine-treated renal slices. The inhibitory effect of EGTA was not mimicked by 100 nmol/l nifedipine. Inactivation of 87% of cellular Gi by 16–20 h treatment with 500 ng/ml pertussis toxin did not significantly affect noradrenaline-stimulated inositol phosphate formation in isolated renal cells but abolished the inhibitory effect of chloroethylclonidine. The adenylate cyclase activator, forskolin (20 μmol/l), inhibited noradrenaline-stimulated inositol phosphate formation in native and chloroethylclonidine-treated slices, and the inhibitory effects of chloroethylclonidine treatment and forskolin were additive. We conclude that in rat kidney inositol phosphate formation via α1B-like adrenoceptors may involve the influx of extracellular Ca2+ and a pertussis toxin-sensitive G-protein but is insensitive to inhibition by forskolin. In contrast α1A-like adrenoceptor-mediated inositol phosphate formation does not require the presence of extracellular Ca2+ or of Gi and is sensitive to inhibition by forskolin. In comparison to published data from other model systems we further conclude that the signaling mechanisms of α1-adrenoceptor subtypes may depend on their cellular environment.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-1912
    Keywords: α1A-adrenoceptors ; α1B-adrenoceptors ; Rat kidney ; Inositol phosphates ; G protein ; Calcium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We have compared the coupling mechanisms of rat renal α1A- and α1B-like adrenoceptors to inositol phosphate formation. The experiments were performed in parallel in native renal tissue preparations and in those where α1B-adrenoceptors had been inactivated by treatment with 10 μmol/l chloroethylclonidine for 30 min at 37°C; renal slices were used in most experiments but isolated renal cells were also used in some cases. The Ca2+ chelating agent, EGTA (5 mmol/l), reduced noradrenaline-stimulated inositol phosphate formation in native but enhanced it in chloroethylclonidine-treated renal slices. The inhibitory effect of EGTA was not mimicked by 100 nmol/l nifedipine. Inactivation of 87% of cellular Gi by 16–20 h treatment with 500 ng/ml pertussis toxin did not significantly affect noradrenaline-stimulated inositol phosphate formation in isolated renal cells but abolished the inhibitory effect of chloroethylclonidine. The adenylate cyclase activator, forskolin (20 μmol/l), inhibited noradrenaline-stimulated inositol phosphate formation in native and chloroethylclonidine-treated slices, and the inhibitory effects of chloroethylclonidine treatment and forskolin were additive. We conclude that in rat kidney inositol phosphate formation via α1B-like adrenoceptors may involve the influx of extracellular Ca2+ and a pertussis toxin-sensitive G-protein but is insensitive to inhibition by forskolin. In contrast α1A-like adrenoceptor-mediated inositol phosphate formation does not require the presence of extracellular Ca2+ or of Gi and is sensitive to inhibition by forskolin. In comparison to published data from other model systems we further conclude that the signaling mechanisms of α1-adrenoceptor subtypes may depend on their cellular environment.
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  • 10
    ISSN: 1432-1912
    Keywords: Key words Noradrenaline ; Neuropeptide Y ; α1A-adrenoceptor ; Y1 NPY receptor ; Microvessel
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  We have studied the contractile effects of the sympathetic transmitter noradrenaline and its cotransmitter neuropeptide Y (NPY) given alone and in combination on isolated rat mesenteric resistance vessels (200–300 μm diameter). Noradrenaline and NPY each concentration-dependently contracted rat mesenteric microvessels (EC50≈800 nM and 10 nM, respectively), but noradrenaline caused considerably greater maximal effects than NPY (14.3 mN vs. 3.5 mN). A low antagonistic potency of yohimbine indicated that the response to noradrenaline did not involve α2-adrenoceptors, and the subtype-selective antagonists 5-methylurapidil, tamsulosin and chloroethylclonidine indicated mediation via an α1A-adrenoceptor. Shallow Schild regressions for prazosin and 5-methylurapidil indicated that an α1-adrenoceptor subtype with relatively low prazosin affinity might additionally be involved. Studies with the NPY analogues PYY, [Leu31, Pro34]NPY and NPY18-36 demonstrated that NPY acted via a Y1 NPY receptor. In addition to its direct vasoconstricting effects NPY also lowered the noradrenaline EC50 but did not appreciably affect maximal noradrenaline responses indicating possible potentiation. The potentiating NPY response occured with similar agonist potency as the direct contractile NPY effects and also via a Y1 NPY receptor. The Ca2+ entry blocker nitrendipine (300 nM) reduced direct contractile responses to noradrenaline and NPY but did not affect the potentiation response to NPY.
    Type of Medium: Electronic Resource
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