Julius Briske Family Collection 1879-1985

Typescript about Julius and Paula (née Hirsch) Briske and their three children, Hans, Elisabeth, and Julius. Also included are Judge Briske’s letters of appointment.

Simson Wolf Oppenheimer Family.

Translation of part of family history about the family of Simon Wolf Oppenheimer from Frankfurt am Main

Dornhelm Family Collection.

Six photographs of members of the Dornhelm family in Austrian army during WW I

Seligmann Family Collection 1877-1938

Materials pertaining to Julius Seligmann (born 1903 in Werden) and to his parents (?), Sigmund Seligmann (b. 1871) and Minna, née Oppenheimer (b. 1873)

Wolf family chronicle.

A chronicle of the Wolf family of Schluechtern in Hesse (Germany), reacing back to 1680

Eva Stroh Family Collection 1860-2005 Bulk: 1912-1950

The Eva Stroh Family Collection provides material on the lives and family history of members of the Sondheimer and Stroh families. The collection consists of numerous photos and several photo albums, family trees, official documents, correspondence, published articles and clippings and some notes, a notebook documenting cultural activities and some daily calendars.

Ephrussi Family Collection 1792-1958

Family tree, explanation

Erlanger Family Collection, Frankfurt a.M.

Family tree of the descendents of Ludwog Erlanger (1780-1857) with explanations

Bronne Family Collection 1981-1990

Family trees reaching back to the 1700s and other materials pertaining to the extended Bronne family. Also included is a typescript about the Bronne Shirt Company in Glens Falls, New York.

Family-based interventions in preventing children and adolescents from using tobacco: A systematic review and meta-analysis

- Background Tobacco is the main preventable cause of death and disease worldwide. Adolescent smoking is increasing in many countries with poorer countries following the earlier experiences of affluent countries. Preventing adolescents starting smoking is crucial to decreasing tobacco-related illness. - Objective To assess effectiveness of family-based interventions alone and combined with school-based interventions to prevent children and adolescents from initiating tobacco use. - Data Sources 14 bibliographic databases and the Internet, journals hand-searched, experts consulted. - Study Eligibility Criteria, Participants, and Interventions Randomised controlled trials (RCTs) with children or adolescents and families, interventions to prevent starting tobacco use, follow-up ≥ 6 months. - Study Appraisal/Synthesis methods Abstracts/titles independently assessed and data independently entered by two authors. Risk-of-bias assessed with the Cochrane Risk-of-Bias tool. - Results Twenty-seven RCTs were included. Nine trials of never-smokers compared to a control provided data for meta-analysis. Family intervention trials had significantly fewer students who started smoking. Meta-analysis of twoRCTs of combined family and school interventions compared to school only, showed additional significant benefit. The common feature of effective high intensity interventions was encouraging authoritative parenting. - Limitations Only 14 RCTs provided data for meta-analysis (about 1/3 of participants). Of the 13 RCTs which did not provide data for meta-analysis eight compared a family intervention to no intervention and one found significant effects, and five compared a family + school intervention to a school intervention and none found additional significant effects. - Conclusions and Implications of Key Findings There is moderate quality evidence that family-based interventions prevent children and adolescents starting to smoke.

Pairing technology and meals: A contextual enquiry in the family household

Recent research about technology during mealtime has been mostly concerned with developing technology rather than creating a deeper understanding of the context of family mealtimes and associated practices. In this paper, we present a two-phase study discussing how the temporal, social, and food related features are intertwined with technology use during mealtimes. Our findings show how people differentiate technology usage during weekday meals, weekend meals, and among different meals of the day. We identify and analyse prototypical situations ranging from the use of arbitrary technologies while eating solitary, to idiosyncratic family norms and practices associated with shared technologies. We discuss the use of mealtime technology to create appropriate ambience for meals with guests and demonstrate how technology can be used to complement food in everyday meals and special occasions. Our findings make recommendation about the need for HCI research to recognize the contextual nature of technology usage during family mealtimes and to adopt appropriate design strategies.

A new family of low-power CT/SUP 2/L circuits

A new family of low-power logic circuits, employing a multiemitter transistor input circuit and a modified complementary p-n-p n-p-n output stage, having almost the same performance as standard TTL circuits and suitable for IC use, is reported in this correspondence.

Enzymes with radical tendencies: the PFL family

The first glycyl radical in an enzyme was described 20 years ago and since then the family of glycyl radical enzymes (GREs) has expanded to include enzymes catalysing five chemically distinct reactions. The type enzymes of the family, anaerobic ribonucleotide reductase (RNRIII) and pyruvate formate lyase (PFL) had been studied long before it was known that they are GREs. Spectroscopic measurements on the radical and an observation that exposure to oxygen irreversibly inactivates the enzymes by cleavage of the protein proved that the radical is located on a particular glycine residue, close to the C-terminus of the protein. Both anaerobic RNRIII and PFL, are important for many anaerobic and facultative anaerobic bacteria as RNRIII is responsible for the synthesis of DNA precursors and PFL catalyses a key metabolic reaction in glycolysis. The crystal structures of both were solved in 1999 and they revealed that, although the enzymes do not share significant sequence identity, they share a similar structure - the radical site and residues necessary for catalysis are buried inside a ten stranded $\ualpha $/$\ubeta $-barrel. GREs are synthesised in an inactive form and are post-translationally activated by an activating enzyme which uses S-adenosyl methionine and an iron-sulphur cluster to generate the radical. One of the goals of this thesis work was to crystallise the activating enzyme of PFL. This task is challenging as, like GREs, the activating component is inactivated by oxygen. The experiments were therefore carried out in an oxygen free atmosphere. This is the first report of a crystalline GRE activating enzyme. Recently several new GREs have been characterised, all sharing sequence similarity to PFL but not to RNRIII. Also, the genome sequencing projects have identified many PFL-like GREs of unknown function, usually annotated as PFLs. In the present thesis I describe the grouping of these PFL family enzymes based on the sequence similarity and analyse the conservation patterns when compared to the structure of E. coli PFL. Based on this information an activation route is proposed. I also report a crystal structure of one of the PFL-like enzymes with unknown function, PFL2 from Archaeoglobus fulgidus. As A. fulgidus is a hyperthermophilic organism, possible mechanisms stabilising the structure are discussed. The organisation of an active site of PFL2 suggests that the enzyme may be a dehydratase. Keywords: glycyl radical, enzyme, pyruvate formate lyase, x-ray crystallography, bioinformatics

GDNF family receptors in peripheral target innervation and hormone production

Glial cell line-derived neurotrophic factor (GDNF) family ligands: GDNF, neurturin, persephin and artemin, signal through a receptor tyrosine kinase Ret by binding first to a co-receptor (GFRα1-4) that is attached to the plasma membrane. The GDNF family factors can support the survival of various peripheral and central neuronal populations and have important functions also outside the nervous system, especially in kidney development. Activating mutations in the RET gene cause tumours in neuroendocrine cells, whereas inactivating mutations in RET are found in patients with Hirschsprung s disease (HSCR) characterized by loss of ganglionic cells along the intestine. The aim of this study was to examine the in vivo functions of neurturin receptor GFRα2 and persephin receptor GFRα4 using knockout (KO) mice. Mice lacking GFRα2 grow poorly after weaning and have deficits in parasympathetic and enteric innervation. This study shows that impaired secretion of the salivary glands and exocrine pancreas contribute to growth retardation in GFRα2-KO mice. These mice have a reduced number of intrapancreatic neurons and decreased cholinergic innervation of the exocrine pancreas as well as reduced excitatory fibres in the myenteric plexus of the small intestine. This study also demonstrates that GFRα2-mediated Ret signalling is required for target innervation and maintenance of soma size of sympathetic cholinergic neurons and sensory nociceptive IB4-binding neurons. Furthermore, lack of GFRα2 in mice results in deficient perception of temperatures above and below thermoneutrality and in attenuated inflammatory pain response. GFRα4 is co-expressed with Ret predominantly in calcitonin-producing thyroid C-cells in the mouse. In this study GFRα4-deficient mice were generated. The mice show no gross developmental deficits and have a normal number of C-cells. However, young but not adult mice lacking GFRα4 have a lower production of calcitonin in thyroid tissue and consequently, an increased bone formation rate. Thus, GFRα4/Ret signalling may regulate calcitonin production. In conclusion, this study reveals that GFRα2/Ret signalling is crucial for the development and function of specific components of the peripheral nervous system and that GFRα4-mediated Ret signalling is required for controlling transmitter synthesis in thyroid C-cells.

Structure-Function Studies of GDNF Family Ligand-RET signalling

Glial cell line-derived neurotrophic factor (GDNF) and its family members neurturin (NRTN), artemin (ARTN) and persephin (PSPN) are growth factors, which are involved in the development, differentiation and maintenance of many neuron types. In addition, they function outside of the nervous system, e.g. in the development of kidney, testis and liver. GDNF family ligand (GFL) signalling happens through a tetrameric receptor complex, which includes two glycosylphosphatidylinositol (GPI)-anchored GDNF family receptor (GFRα) molecules and two RET (rearranged during transfection) receptor tyrosine kinases. Each of the ligands binds preferentially one of the four GFRα receptors: GDNF binds to GFRα1, NRTN to GFRα2, ARTN to GFRα3 and PSPN to GFRα4. The signal is then delivered by RET, which cannot bind the GFLs on its own, but can bind the GFL-GFRα complex. Under normal cellular conditions, RET is only phosphorylated on the cell surface after ligand binding. At least the GDNF-GFRα1 complex is believed to recruit RET to lipid rafts, where downstream signalling occurs. In general, GFRαs consist of three cysteine-rich domains, but all GFRα4s except for chicken GFRα4 lack domain 1 (D1). We characterised the biochemical and cell biological properties of mouse PSPN receptor GFRα4 and showed that it has a significantly weaker capacity than GFRα1 to recruit RET to the lipid rafts. In spite of that, it can phosphorylate RET in the presence of PSPN and contribute to neuronal differentiation and survival. Therefore, the recruitment of RET to the lipid rafts does not seem to be crucial for the biological activity of all GFRα receptors. Secondly, we demonstrated that GFRα1 D1 stabilises the GDNF-GFRα1 complex and thus affects the phosphorylation of RET and contributes to the biological activity. This may be important in physiological conditions, where the concentration of the ligand or the soluble GFRα1 receptor is low. Our results also suggest a role for D1 in heparin binding and, consequently, in the biodistribution of released GFRα1 or in the formation of the GFL-GFRα-RET complex. We also presented the crystallographic structure of GDNF in the complex with GFRα1 domains 2 and 3. The structure differs from the previously published ARTN-GFRα3 structure in three significant ways. The biochemical data verify the structure and reveal residues participating in the interactions between GFRα1 and GDNF, and preliminarily also between GFRα1 and RET and heparin. Finally, we showed that, the precursor of the oncogenic MEN 2B (multiple endocrine neoplasia type 2) form of RET gets phosphorylated already during its synthesis in the endoplasmic reticulum (ER). We also demonstrated that it associates with Src homology 2 domain-containing protein (SHC) and growth factor receptor-bound protein (GRB2) in the ER, and has the capacity to activate several downstream signalling molecules.