The impact of obesity-related single nucleotide polymorphisms on appetite and energy intake: a pilot study

An increasing number of studies have reported a heritable component for the regulation of energy intake and eating behaviour, although the individual polymorphisms and their ‘effect size’ are not fully elucidated. The aim of the present study was to examine the relationship between specific SNP and appetite responses and energy intake in overweight men. In a randomised cross-over trial, forty overweight men (age 32 (sd 09) years; BMI 27 (sd 2) kg/m2) attended four sessions 1 week apart and received three isoenergetic and isovolumetric servings of dairy snacks or water (control) in random order. Appetite ratings were determined using visual analogue scales and energy intake at an ad libitum lunch was assessed 90 min after the dairy snacks. Individuals were genotyped for SNP in the fat mass and obesity-associated (FTO), leptin (LEP), leptin receptor (LEPR) genes and a variant near the melanocortin-4 receptor (MC4R) locus. The postprandial fullness rating over the full experiment following intake of the different snacks was 17·2 % (P= 0·026) lower in A carriers compared with TT homozygotes for rs9939609 (FTO, dominant) and 18·6 % (P= 0·020) lower in G carriers compared with AA homozygotes for rs7799039 (LEP, dominant). These observations indicate that FTO and LEP polymorphisms are related to the variation in the feeling of fullness and may play a role in the regulation of food intake. Further studies are required to confirm these initial observations and investigate the ‘penetrance’ of these genotypes in additional population subgroups.

Impact of additional cytogenetic aberrations at diagnosis on prognosis of CML: long-term observation of 1151 patients from the randomized CML Study IV

The prognostic relevance of additional cytogenetic findings at diagnosis of chronic myeloid leukemia (CML) is unclear. The impact of additional cytogenetic findings at diagnosis on time to complete cytogenetic (CCR) and major molecular remission (MMR) and progression-free (PFS) and overall survival (OS) was analyzed using data from 1151 Philadelphia chromosome-positive (Ph(+)) CML patients randomized to the German CML Study IV. At diagnosis, 1003 of 1151 patients (87%) had standard t(9;22)(q34;q11) only, 69 patients (6.0%) had variant t(v;22), and 79 (6.9%) additional cytogenetic aberrations (ACAs). Of these, 38 patients (3.3%) lacked the Y chromosome (-Y) and 41 patients (3.6%) had ACAs except -Y; 16 of these (1.4%) were major route (second Philadelphia [Ph] chromosome, trisomy 8, isochromosome 17q, or trisomy 19) and 25 minor route (all other) ACAs. After a median observation time of 5.3 years for patients with t(9;22), t(v;22), -Y, minor- and major-route ACAs, the 5-year PFS was 90%, 81%, 88%, 96%, and 50%, and the 5-year OS was 92%, 87%, 91%, 96%, and 53%, respectively. In patients with major-route ACAs, the times to CCR and MMR were longer and PFS and OS were shorter (P < .001) than in patients with standard t(9;22). We conclude that major-route ACAs at diagnosis are associated with a negative impact on survival and signify progression to the accelerated phase and blast crisis.

Das Israelitische Vorschuss-Institut in Hamburg 186 - 1916

von N. M. Nathan

Ms. hebr. oct. 186 - Memorbuch de-ḳehilah ḳedoshah Offenbach

Vorbesitzer: Eljāqīm Carmoly

Comparison against 186 canid whole genome sequences reveals survival strategies of an ancient clonally transmissible canine tumor.

Canine transmissible venereal tumor (CTVT) is a parasitic cancer clone that has propagated for thousands of years via sexual transfer of malignant cells. Little is understood about the mechanisms that converted an ancient tumor into the world's oldest known continuously propagating somatic cell lineage. We created the largest existing catalog of canine genome-wide variation and compared it against two CTVT genome sequences, thereby separating alleles derived from the founder's genome from somatic drivers of clonal transmissibility. We show that CTVT has undergone continuous adaptation to its transmissible allograft niche, with overlapping mutations at every step of immunosurveillance, particularly self-antigen presentation and apoptosis. We also identified chronologically early somatic mutations in oncogenesis- and immune-related genes that may represent key initiators of clonal transmissibility. Thus, we provide the first insights into the specific genomic aberrations that underlie CTVT's dogged perseverance in canids around the world.

Na 1 Nachlass Max Horkheimer, 58 - Korrespondenzen u.a. mit Betty Drury (p. I 27, 186-333)

5 Briefe zwischen Konrad Wittwer und Max Horkheimer, 1936, 1938, 1939; 1 Brief von Max Horkheimer an Joseph Wohl, 18.08.1934; 1 Brief von Max Horkheimer an Hedwig Wollenberger, 25.02.1941; 2 Briefe zwischen Richard Wolf und Max Horkheimer, 22.10.1938, 07.11.1938; 2 Briefe zwischen Martha Wolfenstein und Max Horkheimer, 11.10.1937, 19.10.1937; 1 Brief von Clemy Wolff an Leo Löwenthal, 05.03.1941; 2 Briefe zwischen Ilse Wolff und Max Horkheimer, 29.08.1937, 03.09.1937; 1 Brief von Max Horkheimer an Howard Woolston, 25.03.1941; 1 Einladung von der Women's Conference, 1935; 1 Brief von Max Horkheimer an die Women's Conference, 15.03.1935; 1 Brief von der World Foundation an Max Horkheimer, 26.11.1937; 2 Briefe vom World Jewish Congress an Max Horkheimer, 1942, 1945; 1 Brief von Max Horkheimer an Francis Henry Russel, 28.09.1942; 1 Brief von Max Horkheimer an Dr. Opie, 28.09.1942; 1 Brief der Württembergische Hypothekenbank an Max Horkheimer, 24.12.1930; 12 Briefe zwischen Rösle Wuestholz und Max Horkheimer, 1935-1937, 1939; 1 Brief von Max Horkheimer an Frida Wunderlich, 22.11.1937; 1 Brief von Max Horkheimer an die Yale University Library, 22.12.1938; 2 Briefe zwischen Owen D. Young und Max Horkheimer, 22.04.1940, April 1940; 3 Briefe zwischen Hans Zeisel und Max Horkheimer, 21.07.1941, 1941, 1944; 2 Briefe zwischen der Zentrale Hilfsstelle für deutsche Flüchtlingskinder Prag und Max Horkheimer, 01.03.1938, 25.04.1938; 6 Briefe zwischen Gregory Zilboorg und Max Horkheimer, 1939; 16 Briefe und Beilage an Max Horkheimer und F. Pollock von Edgar Zilsel, 1939-1942; 1 Brief vom Social Science Research Counsil an Edgar Zilsel, 01.04.1940; 1 Brief von The Rockefeller Foundation an Edgar Zilsel, 20.06.1939; 9 Briefe und Beilage von Max Horkheimer und F. Pollock an Edgar Zilsel, 1939-1942 sowie Briefwechsel mit Betty Drury; 10 Briefe zwischen The Rockefeller Foundation und Max Horkheimer, 1939-1940; 1 Brief von Max Horkheimer an Edgar Zilsel, 20.06.1939; 12 Briefe zwischen Betty Drury und F. Pollock, 1939-1940; 7 Briefe zwischen Alexander Zinnemann und Max Horkheimer, 1936;

Na 50 Nachlass Arthur Schopenhauer - 'Schopenhauer-Archiv', 186 - Bitte um Anerkennung des Titels "Jünger des Schopenhauerschen Systems"

Abschrift liegt vor

Na 50 Nachlass Arthur Schopenhauer - 'Schopenhauer-Archiv', 1151 - Besorgnis um den Gesundheitszustand des Vaters und Angaben zum Verlauf des Studiums

z.H. Dr. Trinks; Theologie; Dogmatik; Religionsphilosophie; Professor Heinrich Wuttke;

Ms. Praed. 186 - Rosarium Bibliae

Vorbesitzer: Dominikanerkloster Frankfurt am Main

Ms.Ff.F.Stoltze 3. 186 - Brief von Alexander Linnemann an Friedrich Stoltze

Zu einem "komischen Oratorium"