996 resultados para 205-1255


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The Pilot Club International was a service oriented club for women, however men are now allowed to join. The South Carolina District was founded in the 1930s for “the promotion of social welfare through the performance of civil and beneficial service of the character generally accomplished by civic organizations, rendering aid and assistance to local Pilot Clubs and implementing at the district level the programs and policies of Pilot Club International.” The Pilot Club International South Carolina District Records consist of a certificate of incorporation, minutes, annual reports, correspondence, resolutions and lists of standing rules.

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Ovarian stimulation and cryopreservation of fertilized oocytes before cancer therapy is the best established and efficient fertility preservation technique and should still be considered before chemotherapy. Within a short time frame of 2 weeks, between 8.6 (18-25 y) and 5.1 (36-40 y) fertilized oocytes can be cryopreserved.

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Background and purpose Intra-arterial treatment (IAT) is effective when performed within 6 h of symptom onset in selected stroke patients (‘T < 6H’). Its safety and efficacy is unclear when the patient has had symptoms for more than 6 h (‘T > 6H’) or for an unknown time (unclear-onset stroke, UOS), or woke up with a stroke (wake-up stroke, WUS). In this study we compared the safety of IAT in these four patient groups. Methods Eight-hundred and fifty-nine patients treated with IAT were enrolled. The main outcome parameters were clinical outcome [excellent: modified Rankin Scale (mRS) 0 or 1; or favorable: mRS 0–2] or mortality 3 months after treatment. Further outcome parameters were the rates of vessel recanalization, and cerebral and systemic hemorrhage. Results Six-hundred and fifty-four patients were treated before (T < 6H) and 205 after 6 h or an unknown time (128 T > 6H, 55 WUS and 22 UOS). NIHSS scores were higher in UOS patients than in T < 6H patients, vertebrobasilar occlusion was more common in T > 6H and UOS patients, and middle cerebral artery occlusions less common in T > 6H than in T < 6H patients. Other baseline characteristics were similar. There was no significant difference in clinical outcome and the rate of hemorrhage in multivariable regression analysis. Conclusions Clinical outcome of our four groups of patients was similar with no increase of hemorrhage rates in patients treated after awakening, after an unknown time or more than 6 h. Our preliminary data suggest that treatment of such patients may be performed safely. If confirmed in randomized trials, this would have major clinical implications.

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The treatment of high-risk prostate cancer (HRPCa) is a tremendous challenge for uro-oncologists. The identification of predictive moleculobiological markers allowing risk assessment of lymph node metastasis and systemic progression is essential in establishing effective treatment. In the current study, we investigate the prognostic potential of miR-205 in HRPCa study and validation cohorts, setting defined clinical endpoints for both. We demonstrate miR-205 to be significantly down-regulated in over 70% of the HRPCa samples analysed and that reconstitution of miR-205 causes inhibition of proliferation and invasiveness in prostate cancer (PCa) cell lines. Additionally, miR-205 is increasingly down-regulated in lymph node metastases compared to the primary tumour indicating that miR-205 plays a role in migration of PCa cells from the original location into extraprostatic tissue. Nevertheless, down-regulation of miR-205 in primary PCa was not correlated to the synchronous presence of metastasis and failed to predict the outcome for HRPCa patients. Moreover, we found a tendency for miR-205 up-regulation to correlate with an adverse outcome of PCa patients suggesting a pivotal role of miR-205 in tumourigenesis. Overall, we showed that miR-205 is involved in the development and metastasis of PCa, but failed to work as a useful clinical biomarker in HRPCa. These findings might have implications for the use of miR-205 as a prognostic or therapeutic target in HRPCa.

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Postprimary tuberculosis occurs in immunocompetent people infected with Mycobacterium tuberculosis. It is restricted to the lung and accounts for 80% of cases and nearly 100% of transmission. Little is known about the immunopathology of postprimary tuberculosis due to limited availability of specimens. Tissues from 30 autopsy cases of pulmonary tuberculosis were located. Sections of characteristic lesions of caseating granulomas, lipid pneumonia, and cavitary stages of postprimary disease were selected for immunohistochemical studies of macrophages, lymphocytes, endothelial cells, and mycobacterial antigens. A higher percentage of cells in lipid pneumonia (36.1%) and cavitary lesions (27.8%) were positive for the dendritic cell marker DEC-205, compared to granulomas (9.0%, P < .05). Cavities contained significantly more T-regulatory cells (14.8%) than found in lipid pneumonia (5.2%) or granulomas (4.8%). Distribution of the immune cell types may contribute to the inability of the immune system to eradicate tuberculosis.

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par Isidore Loeb

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1 Brief von Max Horkheimer an Abel, 16.03.1936; 3 Briefe zwischen Hubert Abrahamsohn und Max Horkheimer, 1935-1936, 21.12.1936; 2 Briefe zwischen Emanuel Adler und Max Horkheimer, 12.04.1946, 26.04.1946; 2 Briefe zwischen Max Adler und Max Horkheimer, 16.03.1935, 29.03.1935; 1 Brief von Eva Ahamson an Max Horkheimer, 01.11.1944; 2 Briefe der Aircraft Warning Service Brentwood an Max Horkheimer, Mai 1942; 6 Briefe zwischen Librairie Félix Alcan und Max Horkheimer, 1935, 18.12.1935; 11 Briefe zwischen Franz Alexander und Max Horkheimer, 1938-1940; 2 Briefe zwischen der American Historical Review New York und Max Horkheimer, 01.04.1941, 07.04.1941; 1 Brief von Paul Reiwald an Max Horkheimer, 18.10.1940; 2 Briefe zwischen Helen Manice Alexander und Max Horkheimer, 1936; 2 Briefe zwischen Bernardine Allen und Max Horkheimer, 17.06.1938, 24.06.1938; 1 Brief der Alumni Federation of Columbia University an Max Horkheimer, 21.07.1942; 1 Brief der American Friends Service Comittee an Max Horkheimer, 10.12.1940; 3 Briefe zwischen der American Academy of Political and Social Science Philadelphia und Max Horkheimer, 1939,1940, 16.01.1939; 1 Brief der American Automobile Association Washington an Max Horkheimer, 22.03.1938; 1 Brief der American Association for the Advancement of Science Washington an Max Horkheimer, 16.08.1937; 2 Briefe von Max Horkheimer an den American Consulate General Berlin, 1939; 1 Brief von Max Horkheimer an den American Consulate General Havana, 03.03.1941; 4 Briefe von Max Horkheimer an den American Consul London, 1939-1941; 2 Briefe von Max Horkheimer an den American Consulate General Stuttgart, 1939-1941; 1 Brief von Max Horkheimer an den American Consul Zürich, 1939; 1 Brief von Friedrich Pollock an den American Council of Learned Society, Washington, 27.06.1941; 2 Briefe von Max Horkheimer an die American Friends of German Freedom New York, 1941; 4 Briefe der American Historical Association Washington an Max Horkheimer, 1937-1938; 1 Brief von Max Horkheimer an den American Red Cross Westwood Office, 21.06.1943; 18 Briefe zwschen der American Society for the Prevention of Cruelty to Animals New York und Max Horkheimer, 1936-1941; 1 Brief von Max Horkheimer an die American Women's Volunteer Service Pacific Palisades, 27.07.1942; 23 Briefe zwischen Eugene Anderson und Max Horkheimer, 1937-1941; 2 Briefe zwischen Norah Andreae und Max Horkheimer, 27.10.1944, 09.09.1946; 1 Brief von Rosa Nebel-Schenk, 04.03.1946; 1 Brief von der National Catholic Welfare Conference, 14.08.1944; 12 Briefe zwischen Werner Andreae und Max Horkheimer, 1945-1954; 1 Brief von Julius Marx an Werner Andreae, 10.05.1946, 11.05.1950; 2 Briefe von Josef Messinger an Werner Andreae, 23.10.1946, ohne Datum; 3 Briefe zwischen dem Advokatenbüro Hodler und Max Horkheimer, 1946, 09.05.1946;

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veröffentlicht in: Schopenhauer, Arthur : Arthur Schopenhauers sämtliche Werke - München : Piper - Bd. 14 : Der Briefwechsel Arthur Schopenhauers ; 1 (1799 - 1849), Nr. 270

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Frankfurter Latern, Devrient, Paris, Mathilde Heine, Anlage (nicht enthalten): Gedicht aus Heinrich Heines Nachlaß, "Brendelche Schnud", Dr. Heine, Dresden, Nizza

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Vorbesitzer: Michelangelo Gualandi

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p63, a p53 family member, is a transcription factor that has complex roles in cancer. This study focuses on the role of the ∆Np63α isoform in bladder cancer (BC). Epithelial – mesenchymal transition (EMT) is a physiological process that plays an important part in metastasis and drug resistance. At the molecular level, EMT is characterized by the loss of the epithelial marker E-cadherin, and the acquisition of the transcriptional repressors of E-cadherin (ZEB1, ZEB2, TWIST, SNAI1 and SNAI2). Recent publications highlight the role of microRNAs belonging to the miR-200 family and miR-205 in preventing EMT through suppression of ZEB1 and ZEB2. p53, the homologue of p63, is implicated in regulating EMT by modulating the expression of miR-200c; however, the mechanisms underlying miR-205 control remain unclear. Here we show that ∆Np63α regulates the transcription of miR-205 and controls EMT in human BC cells. We observed a strong correlation between the expression of ∆Np63α, miR-205 and E-cadherin in a panel of BC cell lines (n=28) and also in bladder primary tumors from a cohort of patients (n=98). A remarkably inverse correlation is observed between ∆Np63α and ZEB1/2 in cell lines. Stable knockdown (KD) ∆Np63α in UC6, an “epithelial” BC cell line, decreased the expression of miR-205 and induced ZEB1/2 expression, the effects that were reversed by expression of exogenous miR-205. Moreover, overexpressing ∆Np63α in UC3, a “messenchymal” BC cell line, brought about opposite results, an increase in miR-205 expression and a reduction in ZEB1/2 expression. Modulation of ∆Np63α expression resulted in a parallel change in the expression of miR-205 and miR-205 “host” gene (miR-205HG). Nuclear run-on and chromatin immunoprecipitation experiments demonstrated that ∆Np63α regulates the transcription of miR-205 through controlling the recruitment of RNA Polymerase II to the promoter of miR-205HG. Interestingly, high miR-205 expression correlated with poor clinical outcome in BC patients, consistent with our recent publication highlighting the enrichment of ∆Np63 in a lethal subset of muscle invasive BC. In summary, our data present the important roles of ∆Np63α in preventing EMT mediated by miR-205. Our study also identifies miR-205 as a potential molecular marker to predict clinical outcome in BC patients.

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http://lib.dr.iastate.edu/carver_narratives/1030/thumbnail.jpg