Samuel and Eva Baeck nee Placzek with unidentified woman holding child in background Portraits; Family

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Preparation, structure, microwave absorption and other properties of the 125K superconductor Tl2Ca2Ba2Cu3O10+δ*1

It is shown that Tl2Ca2Ba2Cu3O10+δ (2223), the n=3 member of the Tl2O2. Can�1Ba2CunO2n+2 family shows a Tc (zero-resistance) of 125K (onset 140K) only when it is prepared by the sealed tube ceramic method starting from the 1313 composition. The structure is orthorhombic (Image compared to 30� of 2122), but electron diffraction patterns show two possible orthorhombic structures. Lattice images show the expected local structure and also the presence of dislocations and intergrowths. Both 2223 and 2122 oxides absorb microwaves (9.1GHz) intensely in the superconducting state, with some hysteresis. XPS measurements show Cu mainly in the 1+ state, suggesting the important role of oxygen holes.

The photographer Harry Polk outdoors with his daughter Grace Polk Portraits Family

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Portrait of Hugo Pollak with wife Thekla Lichtenstadt Pollak and their children Hans Pollak and Zdenka (Mimi) Pollak seated outdoors Portraits Family

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Unidentified family dressed in costume; Milan.

Handwritten caption: Mein Bruder Eduard links und Familie in Mailand Italien

Molecular Mechanisms of Androgen Receptor Interactions

The androgen receptor (AR) mediates the effects of the male sex-steroid hormones (androgens), testosterone and 5?-dihydrotestosterone. Androgens are critical in the development and maintenance of male sexual characteristics. AR is a member of the steroid receptor ligand-inducible transcription factor family. The steroid receptor family is a subgroup of the nuclear receptor superfamily that also includes receptors for the active forms of vitamin A, vitamin D3, and thyroid hormones. Like all nuclear receptors, AR has a conserved modular structure consisting of a non-conserved amino-terminal domain (NTD), containing the intrinsic activation function 1, a highly conserved DNA-binding domain, and a conserved ligand-binding domain (LBD) that harbors the activation function 2. Each of these domains plays an important role in receptor function and signaling, either via intra- and inter-receptor interactions, interactions with specific DNA sequences, termed hormone response elements, or via functional interactions with domain-specific proteins, termed coregulators (coactivators and corepressors). Upon binding androgens, AR acquires a new conformational state, translocates to the nucleus, binds to androgen response elements, homodimerizes and recruits sequence-specific coregulatory factors and the basal transcription machinery. This set of events is required to activate gene transcription (expression). Gene transcription is a strictly modulated process that governs cell growth, cell homeostasis, cell function and cell death. Disruptions of AR transcriptional activity caused by receptor mutations and/or altered coregulator interactions are linked to a wide spectrum of androgen insensitivity syndromes, and to the pathogenesis of prostate cancer (CaP). The treatment of CaP usually involves androgen depletion therapy (ADT). ADT achieves significant clinical responses during the early stages of the disease. However, under the selective pressure of androgen withdrawal, androgen-dependent CaP can progress to an androgen-independent CaP. Androgen-independent CaP is invariably a more aggressive and untreatable form of the disease. Advancing our understanding of the molecular mechanisms behind the switch in androgen-dependency would improve our success of treating CaP and other AR related illnesses. This study evaluates how clinically identified AR mutations affect the receptor s transcriptional activity. We reveal that a potential molecular abnormality in androgen insensitivity syndrome and CaP patients is caused by disruptions of the important intra-receptor NTD/LBD interaction. We demonstrate that the same AR LBD mutations can also disrupt the recruitment of the p160 coactivator protein GRIP1. Our investigations reveal that 30% of patients with advanced, untreated local CaP have somatic mutations that may lead to increases in AR activity. We report that somatic mutations that activate AR may lead to early relapse in ADT. Our results demonstrate that the types of ADT a CaP patient receives may cause a clustering of mutations to a particular region of the receptor. Furthermore, the mutations that arise before and during ADT do not always result in a receptor that is more active, indicating that coregulator interactions play a pivotal role in the progression of androgen-independent CaP. To improve CaP therapy, it is necessary to identify critical coregulators of AR. We screened a HeLa cell cDNA library and identified small carboxyl-terminal domain phosphatase 2 (SCP2). SCP2 is a protein phosphatase that directly interacts with the AR NTD and represses AR activity. We demonstrated that reducing the endogenous cellular levels of SCP2 causes more AR to load on to the prostate specific antigen (PSA) gene promoter and enhancer regions. Additionally, under the same conditions, more RNA polymerase II was recruited to the PSA promoter region and overall there was an increase in androgen-dependent transcription of the PSA gene, revealing that SCP2 could play a role in the pathogenesis of CaP.

Unidentified women and man Portraits Family

Handwritten on verso: Jetzt sind wir wieder vergnuegt und gluecklich zusammen. Herzlichst Deine (Illegible name Neni or Leni?)

Portrait of Hilde Rosenbaum with her father Julius Rosenbaum in military uniform Portraits Family

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Tombstone of the Benno Molling family on the Jewish cemetery; An der Strangriede, Hannover, Germany. Cemeteries Tombs

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Family and guests at Aenny Catzenstein nee Gottschalk's 80th birthday; London.

Front row l-r: Francine Durand, Beatrice Durand and Aenny Catzenstein, the boys are Ara-Serge Donabedian and Patrick Matthiesen and the adults are Susan Prior, Francis Matthiesen, Maren Matthiesen, Nino Fabri and Olga Matthiesen,

Portrait of the family of David Stern and Bernice Stern nee Propper.

Seated: David Stern, Bernice Stern, and Jessica Agosti; left to right: Doreen Stern, her husband Michael Stern, Carol Richardson, her husband Blake Richardson, John Agosti. The baby is Katherine Stern

Portrait of George Louis Wolff (Gerd Ludwig Wolff) holding a mouse in his genetics laboratory; Little Rock, Arkansas.

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Studio portrait of the Amram family; Buffalo, New York.

The Amrams are related to Hans Krakauer's maternal family the Mayer/Heumann's from Billigheim and Hoffenheim

Family portrait taken in a garden on the 75th birthday of Henriette Gottschalk nee Rothschild.

Front row, from left to right: Fritz Gottschalk, Walter Gottschalk, Kurt Gottschalk, Ursula Gottschalk, Hans Ludwig (Hal) Gottschalk, Rudolf Gottschalk, Elizabeth Gottschalk; babies, from left to right: Ilse Gottschalk, Freddy Gottschalk; adults, from left to right: Karl Gottschalk, Elisabeth Gottschalk nee Steinfeld, Ernst Gottschalk, Henriette Gottschalk nee Rothschild, Therese Gottschalk nee Molling, Fritz Joseph Gottschalk