Periodic vacuum and particles in two dimensions

Different dynamical symmetry breaking patterns are explored for the two dimensional phi4 model with higher order derivative terms. The one-loop saddle point expansion predicts a rather involved phase structure and a new Gaussian critical line. This vacuum structure is corroborated by the Monte Carlo method, as well. Analogies with the structure of solids, the density wave phases and the effects of the quenched impurities are mentioned. The unitarity of the time evolution operator in real time is established by means of the reflection positivity.Comment: Final version, additional references and the proof of reflection positivity added, 41 pages, 16 figure

A genetically modified minipig model for Alzheimer's disease with SORL1 haploinsufficiency

The established causal genes in Alzheimer’s disease (AD), APP, PSEN1, and PSEN2, are functionally characterized using biomarkers, capturing an in vivo profile reflecting the disease’s initial preclinical phase. Mutations in SORL1, encoding the endosome recycling receptor SORLA, are found in 2%–3% of individuals with early-onset AD, and SORL1 haploinsufficiency appears to be causal for AD. To test whether SORL1 can function as an AD causal gene, we use CRISPR-Cas9-based gene editing to develop a model of SORL1 haploinsufficiency in Göttingen minipigs, taking advantage of porcine models for biomarker investigations. SORL1 haploinsufficiency in young adult minipigs is found to phenocopy the preclinical in vivo profile of AD observed with APP, PSEN1, and PSEN2, resulting in elevated levels of β-amyloid (Aβ) and tau preceding amyloid plaque formation and neurodegeneration, as observed in humans. Our study provides functional support for the theory that SORL1 haploinsufficiency leads to endosome cytopathology with biofluid hallmarks of autosomal dominant AD

Sequestration and Tissue Accumulation of Human Malaria Parasites: Can We Learn Anything from Rodent Models of Malaria?

The sequestration of Plasmodium falciparum–infected red blood cells (irbcs) in the microvasculature of organs is associated with severe disease; correspondingly, the molecular basis of irbc adherence is an active area of study. In contrast to P. falciparum, much less is known about sequestration in other Plasmodium parasites, including those species that are used as models to study severe malaria. Here, we review the cytoadherence properties of irbcs of the rodent parasite Plasmodium berghei ANKA, where schizonts demonstrate a clear sequestration phenotype. Real-time in vivo imaging of transgenic P. berghei parasites in rodents has revealed a CD36-dependent sequestration in lungs and adipose tissue. In the absence of direct orthologs of the P. falciparum proteins that mediate binding to human CD36, the P. berghei proteins and/or mechanisms of rodent CD36 binding are as yet unknown. In addition to CD36-dependent schizont sequestration, irbcs accumulate during severe disease in different tissues, including the brain. The role of sequestration is discussed in the context of disease as are the general (dis)similarities of P. berghei and P. falciparum sequestration

Marianne Landau Collection 1886-1966

Correspondence, legal and official documents, books and pamphletsThe bulk of the correspondence generated through the post-war years until her death in 1964 consists of restitution claims conducted by her lawyers and bank statements, while her illustrious father's career receives attention only on the occassion of the 100th anniversary of his birth.The following individuals are mentioned in this collection: Schueching, Susanne von; Landua, Johanna; Landau, Matthias; Heuss, Theodor; Marquardt, Martha; Schmidt-Polek, Hans W.; I. G. Farben Hoechst; Berliner Handelsbank; Schueching, Heinz von; Schueching, Sylvia von; Schoenberg, Iso (Isaak); Landau, Edmund; Lehmann, Trude; Pinkus, Felix; Pinkus, Hermann; Kaskell, Joseph; Herzfeld, Karl; Waltzog, Alfons; Hahn, Kurt 1886-1976; Landau, Marianne 1886-1964See inventory listMarianne Landau, born in Berlin, 1886, was the daughter of Paul Ehrlich, the 1908 Nobel Prize laureate for work in chemo- and immunotherapy and developer of the drug Salvasan, instrumental in treating veneral disease. The Landau family escaped Nazi Germany and formed new homes in the U.S. and England, where they pursued academic careers. A very energetic and somewhat opinionated lady, Mrs. Landau never tired in keeping alive her father's memory and legacy, as well as to promote the research work of the Paul Ehrlich Institute in Frankfurt am Main. Beyond that, she doggedly pursued her legal claims against Germany for lost property (her mother-in-law's) and financial compensation (her own and her late husband's, Edmund, a well-known mathematician), constantly changing her lawyers and creating dissension in her own family. Marianne Landau died in Zurich in 1964.Inventory list in filedigitize

Abschlussbericht des Projekts der Kommission der Europaeischen Gemeinschaft zur vorbereitenden Fortbildung italienischer Lehrer in der Bundesrepublik Deutschland 1981

UuStB Koeln(38)-8306349 / FIZ - Fachinformationszzentrum Karlsruhe / TIB - Technische InformationsbibliothekSIGLEDEGerman

Long-Term Results from the IDEAL-CRT Phase 1/2 Trial of Isotoxically Dose-Escalated Radiation Therapy and Concurrent Chemotherapy for Stage II/III Non-small Cell Lung Cancer

Purpose: The IDEAL-CRT phase 1/2 multicenter trial of isotoxically dose-escalated concurrent chemoradiation for stage II/III non-small cell lung cancer investigated two 30-fraction schedules of 5 and 6 weeks' duration. We report toxicity, tumor response, progression-free survival (PFS), and overall survival (OS) for both schedules, with long-term follow-up for the 6-week schedule. Methods and Materials: Patients received isotoxically individualized tumor radiation doses of 63 to 71 Gy in 5 weeks or 63 to 73 Gy in 6 weeks, delivered concurrently with 2 cycles of cisplatin and vinorelbine. Eligibility criteria were the same for both schedules. Results: One-hundred twenty patients (6% stage IIB, 68% IIIA, 26% IIIB, 1% IV) were recruited from 9 UK centers, 118 starting treatment. Median prescribed doses were 64.5 and 67.6 Gy for the 36 and 82 patients treated using the 5- and 6-week schedules. Grade >= 3 pneumonitis and early esophagitis rates were 3.4% and 5.9% overall and similar for each schedule individually. Late grade 2 esophageal toxicity occurred in 11.1% and 17.1% of 5- and 6-week patients. Grade >= 4 adverse events occurred in 17 (20.7%) 6-week patients but no 5-week patients. Four adverse events were grade 5, with 2 considered radiation therapy related. After median follow-up of 51.8 and 26.4 months for the 6- and 5-week schedules, median OS was 41.2 and 22.1 months, respectively, and median PFS was 21.1 and 8.0 months. In exploratory analyses, OS was significantly associated with schedule (hazard ratio [HR], 0.56; 95% confidence interval [CI], 0.32-0.98; P = .04) and fractional clinical/internal target volume receiving >= 95% of the prescribed dose (HR, 0.88; 95% CI, 0.77-1.00; P = .05). PFS was also significantly associated with schedule (HR, 0.53; 95% CI, 0.33-0.86; P = .01). Conclusions: Toxicity in IDEAL-CRT was acceptable. Survival was promising for 6-week patients and significantly longer than for 5-week patients. Survival might be further lengthened by following the 6-week schedule with an immune agent, motivating further study of such combined optimized treatments

A genetically modified minipig model for Alzheimer's disease with SORL1 haploinsufficiency

The established causal genes in Alzheimer's disease (AD), APP, PSEN1, and PSEN2, are functionally characterized using biomarkers, capturing an in vivo profile reflecting the disease's initial preclinical phase. Mutations in SORL1, encoding the endosome recycling receptor SORLA, are found in 2%–3% of individuals with early-onset AD, and SORL1 haploinsufficiency appears to be causal for AD. To test whether SORL1 can function as an AD causal gene, we use CRISPR-Cas9-based gene editing to develop a model of SORL1 haploinsufficiency in Göttingen minipigs, taking advantage of porcine models for biomarker investigations. SORL1 haploinsufficiency in young adult minipigs is found to phenocopy the preclinical in vivo profile of AD observed with APP, PSEN1, and PSEN2, resulting in elevated levels of β-amyloid (Aβ) and tau preceding amyloid plaque formation and neurodegeneration, as observed in humans. Our study provides functional support for the theory that SORL1 haploinsufficiency leads to endosome cytopathology with biofluid hallmarks of autosomal dominant AD