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Articles by S Reuter
Total Records ( 6 ) for S Reuter
  S Reuter , S Prasad , K Phromnoi , J Ravindran , B Sung , V. R Yadav , R Kannappan , M. M Chaturvedi and B. B. Aggarwal

The discovery of new uses for older, clinically approved drugs is one way to expedite drug development for cancer. Thiocolchicoside, a semisynthetic colchicoside from the plant Gloriosa superba, is a muscle relaxant and used to treat rheumatologic and orthopedic disorders because of its analgesic and anti-inflammatory mechanisms. Given that activation of the transcription factor NF-B plays a major role in inflammation and tumorigenesis, we postulated that thiocolchicoside would inhibit NF-B and exhibit anticancer effects through the modulation of NF-B–regulated proteins. We show that thiocolchicoside inhibited proliferation of leukemia, myeloma, squamous cell carcinoma, breast, colon, and kidney cancer cells. Formation of tumor colonies was also suppressed by thiocolchicoside. The colchicoside induced apoptosis, as indicated by caspase-3 and poly(ADP-ribose) polymerase cleavage, and suppressed the expression of cell survival [e.g., Bcl-2, X-linked inhibitor of apoptosis (XIAP), MCL-1, bcl-xL, cIAP-1, cIAP-2, and cFLIP] proteins. Cell proliferation biomarkers such as c-MYC and phosphorylation of phosphoinositide 3-kinase and glycogen synthase kinase 3β were also blocked by thiocolchicoside. Because most cell survival and proliferation gene products are regulated by NF-B, we studied the effect of thiocolchicoside on this transcription factor and found that thiocolchicoside inhibited NF-B activation, degradation of inhibitory B (IB), IB ubiquitination, and phosphorylation, abolished the activation of IB kinase, and suppressed p65 nuclear translocation. This effect of thiocolchicoside on the NF-B pathway led to inhibition of NF-B reporter activity and cyclooxygenase-2 promoter activity. Our results indicate that thiocolchicoside exhibits anticancer activity through inhibition of NF-B and NF-B–regulated gene products, which provides novel insight into a half-century old drug. Cancer Prev Res; 3(11); 1462–72. ©2010 AACR.

  P Bordachar , P Defaye , E Peyrouse , S Boveda , B Mokrani , C Marquie , L Barandon , E. M Fossaert , S Garrigue , S Reuter , J Laborderie , E Marijon , J. C Deharo , P Jacon , S Kacet , S Ploux , A Deplagne , M Haissaguerre , J Clementy , P Ritter and D. Klug

Some operators routinely extract chronically implanted transvenous leads from a femoral, whereas others prefer a superior approach. This prospective study compared the safety and effectiveness of laser sheaths versus femoral snare extractions.

Methods and Results—

The single-center study comprised 101 patients referred for unequivocal indications to extract ≥1 transvenous lead(s). Patients were >4 years of age and were randomly assigned to extractions with a laser sheath (group 1: n=50) versus a snare via femoral approach (group 2: n=51). The multicenter study comprised 358 patients who underwent extraction of old transvenous leads using laser sheaths (n=218, group 3) in 3 centers and from a femoral approach (n=138, group 4) in 3 other centers. In the single-center study, the success and complications rates were similar in groups 1 and 2. No patient died of a periprocedural complication. The procedural duration (51±22 versus 86±51 minutes) and duration of total fluoroscopic exposure (7±7 versus 21±17 minutes) were significantly shorter (each P<0.01) in group I than in group 2. In the multicenter study, we observed 2 procedure-associated deaths in group 3 versus 1 in group 4. Major procedural complications were observed in 3% of patients in group 3, versus 3% in group 4 (P=NS). The rates of complete, partial, and unsuccessful extractions were similar in groups 3 and 4.


Old transvenous leads were extracted with similar success and complication rates by the femoral and laser approaches. However, the femoral approach was associated with longer procedures and a longer duration of fluoroscopic exposure.

  N Sichtig , S Sierra , R Kaiser , M Daumer , S Reuter , E Schulter , A Altmann , G Fatkenheuer , U Dittmer , H Pfister and S. Esser

We investigated the prevalence of raltegravir resistance-associated mutations at baseline and their evolution during raltegravir therapy in patients infected with different HIV-1 subtypes.


At pre-treatment screening, the integrase gene from plasma samples from patients infected with subtype B and non-B viruses was analysed. Raltegravir resistance evolution was further evaluated in 10 heavily pre-treated patients.


Two hundred and nine plasma samples from 94 subtype B and 115 non-B patients were sequenced. No signature/primary raltegravir resistance mutations were detected at baseline. The secondary mutations L74M, T97A, V151I and G163R were observed with a frequency of <4%. The primary mutations N155H, Q148R/H or Q143R were observed during raltegravir therapy. The Q148R/H was detected only in subtype B. A switch of the primary mutation during raltegravir treatment was not restricted to the subtype B viruses. The prevalence of each primary mutation varied depending on the length of the raltegravir therapy. The Q148R/H was mostly detected after short exposure to raltegravir, while the Y143R was observed only after prolonged raltegravir exposure. We detected an association between the presence of the T206S in the baseline genotype and the absence of the primary Q148R/H mutation or any secondary mutation accompanying the N155H following raltegravir failure.


A number of secondary and additional mutations were found in baseline genotypes. During therapy, when the virus was not optimally suppressed, resistance mutations developed, which were dependent on subtype and time on raltegravir.

  M Siekierka Harreis , K Ivens , O Adams , S Reuter and L. C. Rump

The pandemic new influenza A (H1N1/09) virus may be especially threatening for immunosuppressed renal transplant patients as they are at increased risk for complications, prolonged infection and mortality. This is the first case report of renal transplant patients with PCR-confirmed H1N1 respiratory tract infection. They showed a surprisingly mild clinical course despite respiratory fungal or viral co-infections in two cases. Treatment with oseltamivir in standard dosage was immediately started after diagnosis and proved to be rapidly beneficial with respect to clinical outcome and virus shedding without deteriorating renal transplant function.

  K. L Ang , L. T Shenje , S Reuter , M. H Soonpaa , M Rubart , L. J Field and M. Galinanes

Accurate nuclear identification is crucial for distinguishing the role of cardiac myocytes in intrinsic and experimentally induced regenerative growth of the myocardium. Conventional histologic analysis of myocyte nuclei relies on the optical sectioning capabilities of confocal microscopy in conjunction with immunofluorescent labeling of cytoplasmic proteins such as troponin T, and dyes that bind to double-strand DNA to identify nuclei. Using heart sections from transgenic mice in which the cardiomyocyte-restricted -cardiac myosin heavy chain promoter targeted the expression of nuclear localized β-galactosidase reporter in >99% of myocytes, we systematically compared the fidelity of conventional myocyte nuclear identification using confocal microscopy, with and without the aid of a membrane marker. The values obtained with these assays were then compared with those obtained with anti-β-galactosidase immune reactivity in the same samples. In addition, we also studied the accuracy of anti-GATA4 immunoreactivity for myocyte nuclear identification. Our results demonstrate that, although these strategies are capable of identifying myocyte nuclei, the level of interobserver agreement and margin of error can compromise accurate identification of rare events, such as cardiomyocyte apoptosis and proliferation. Thus these data indicate that morphometric approaches based on segmentation are justified only if the margin of error for measuring the event in question has been predetermined and deemed to be small and uniform. We also illustrate the value of a transgene-based approach to overcome these intrinsic limitations of identifying myocyte nuclei. This latter approach should prove quite useful when measuring rare events.

  J Nolting , C Daniel , S Reuter , C Stuelten , P Li , H Sucov , B. G Kim , J. J Letterio , K Kretschmer , H. J Kim and H. von Boehmer

It has been reported that retinoic acid (RA) enhances regulatory T (T reg) cell conversion by inhibiting the secretion of cytokines that interfere with conversion. This report shows that these conclusions provide a partial explanation at best. First, RA not only interfered with cytokine secretion but also with the ability of these cytokines to inhibit T reg cell conversion of naive T cells. Furthermore, RA enhanced conversion even in the absence of inhibitory cytokines. The latter effect depended on the RA receptor (RAR) but did not require Smad3, despite the fact that RA enhanced Smad3 expression. The RAR1 isoform was not essential for RA-dependent enhancement of transforming growth factor β–driven conversion, suggesting that conversion can also be mediated by RAR2. Interleukin (IL)-6 strongly reduced RAR expression levels such that a deficiency of the predominant RAR1 isoform leaves too little RAR2 for RA to inhibit the generation of Th17 cells in the presence of IL-6.

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