Wedding portrait of Adolf Wolff and Eva Nathan with guests; Berlin, Germany.

Back row against wall, left to right: Josef Molling, Margaret Molling nee Benjamin, Werner Wolff, Miss Hermann (called "Ferna", Peter Molling's governess), " Selma" (partially hidden, Anna Marianne/Berthold Nathan's cook), "Lisbeth" (Anna Marianne/Berthold's maid), Ilse Joachim, Ernst Joachim, Annemarie Nathan (3rd wife of Julius Nathan), Julius Nathan (brother of Berthold Nathan), Ernst Kallmes (son of Ceilchen nee Wolff, Helene's sister). Very tall against the wall: Max Benjamin (son of Helene). Third row, left to right: Mathilde Kaufmann nee Benjamin, Adolf Molling, Paul Nathan (son of Anna Marianne/Berthold), Marianne Rasmussen (daughter of Waldemar), Hildegard Weinberger (friend of bride), Herta Albrecht (friend of bride), Dr. Franz Gruenberg (friend of groom), Leonie Wolff nee Simon (wife of Werner Wolff), Lina Molling nee Marx (wife of Richard), Waldemar Benjamin-Rasmussen (son of Helene/David), Luzi's Husband, Minka Bernard nee Nathan (sister of Berthold Nathan), Richard Molling (brother of Claerchen), Albert Wolff (brothter of Moritz Wolff). Second row, seated, left to right: Helene Benjamin nee Wolff, Berthold Nathan, Anna Marianne Nathan nee Benjamin, bride Eva Wolff nee Nathan, groom Adolf Wolff, Claerchen Wolff nee Molling, Moritz Wolff, standing Luzi Rasmussen nee Gruen (wife of Waldemar). Front row, children on floor, left to right: Peter Molling, Elizabeth Benjamin-Rasmussen mar. Engel, Louis Peter Wolff, Helmut Benjamin Rasmussen (became Henry)

Studio portrait of Adolf Rothschild and Sophie Rothschild nee Cohn.

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Studio portrait of unidentified Levy brother (most likely Arthur or Hermann) in military uniform; Nogent-Sur-Seine, France.

Photographer's imprint lower left corner

Lotte Schloss with her brother Helmut Schloss; Wolfenbüttel, Germany.

Verso: correspondence

Exterior view of the residence of brother-in-law Louis; Wolfenbuettel.

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Variation in BMPR1B, TGFRB1 and BMPR2 and control of dizygotic twinning

Genes in the TGF9 signaling pathway play important roles in the regulation of ovarian follicle growth and ovulation rate. Mutations in three genes in this pathway, growth differentiation factor 9 (GDF9), bone morphogenetic protein 15 (BMP15) and the bone morphogenetic protein receptor B 1 (BMPRB1), influence dizygotic (DZ) twinning rates in sheep. To date, only variants in GDF9 and BMP15, but not their receptors transforming growth factor ss receptor 1 (TGFBR1), bone morphogenetic protein receptor 2 (BMPR2) and BMPR1B, have been investigated with respect to their roles in human DZ twinning. We screened for rare and novel variants in TGFBR1, BMPR2 and BMPR1B in mothers of dizygotic twins (MODZT) from twin-dense families, and assessed association between genotyped and imputed variants and DZ twinning in another large sample of MODZT. Three novel variants were found: a deep intronic variant in BMPR2, and one intronic and one non-synonymous exonic variant in BMPRB1 which would result in the replacement of glutamine by glutamic acid at amino acid position 294 (p.Gln294Glu). None of these variants were predicted to have major impacts on gene function. However, the p.Gln294Glu variant changes the same amino acid as a sheep BMPR1B functional variant and may have functional consequences. Six BMPR1B variants were marginally associated with DZ twinning in the larger case-control sample, but these were no longer significant once multiple testing was taken into account. Our results suggest that variation in the TGF9 signaling pathway type II receptors has limited effects on DZ twinning rates in humans.

Association between ORMDL3, IL1RL1 and a deletion on chromosome 17q21 with asthma risk in Australia

Genome-wide association studies followed by replication provide a powerful approach to map genetic risk factors for asthma. We sought to search for new variants associated with asthma and attempt to replicate the association with four loci reported previously (ORMDL3, PDE4D, DENND1B and IL1RL1). Genome-wide association analyses of individual single nucleotide polymorphisms (SNPs), rare copy number variants (CNVs) and overall CNV burden were carried out in 986 asthma cases and 1846 asthma-free controls from Australia. The most-associated locus in the SNP analysis was ORMDL3 (rs6503525, P = 4.8 x 10(-)(7)). Five other loci were associated with P < 10(-)(5), most notably the chemokine CXC motif ligand 14 (CXCL14) gene (rs31263, P = 7.8 x 10(-)(6)). We found no evidence for association with the specific risk variants reported recently for PDE4D, DENND1B and ILR1L1. However, a variant in IL1RL1 that is in low linkage disequilibrium with that reported previously was associated with asthma risk after accounting for all variants tested (rs10197862, gene wide P = 0.01). This association replicated convincingly in an independent cohort (P = 2.4 x 10(-)(4)). A 300-kb deletion on chromosome 17q21 was associated with asthma risk, but this did not reach experiment-wide significance. Asthma cases and controls had comparable CNV rates, length and number of genes affected by deletions or duplications. In conclusion, we confirm the association between asthma risk and variants in ORMDL3 and identify a novel risk variant in IL1RL1. Follow-up of the 17q21 deletion in larger cohorts is warranted.

Margot Molling with her brother Adolf Molling; Laughlin, Nevada Portraits Family

Temperature: 117 F

Brother of Lola Gruenthal in Nice, France Portraits Men

Brother of Lola Gruenthal

Portrait of Ruth Augusta Beatrice Goldschmidt with her brother Henry H. Goldschmidt Gould Portraits Family

Henry, born July 15, 1914, died August 6, 1978; Ruth, born 1923?

Studio portraits of the brother of Max Rieser; Krakow Portraits Men

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Recent insights into microbial triggers of interleukin-10 production in the host and the impact on infectious disease pathogenesis

Since its initial description as a Th2-cytokine antagonistic to interferon-alpha and granulocyte-macrophage colony-stimulating factor, many studies have shown various anti-inflammatory actions of interleukin-10 (IL-10), and its role in infection as a key regulator of innate immunity. Studies have shown that IL-10 induced in response to microorganisms and their products plays a central role in shaping pathogenesis. IL-10 appears to function as both sword and shield in the response to varied groups of microorganisms in its capacity to mediate protective immunity against some organisms but increase susceptibility to other infections. The nature of IL-10 as a pleiotropic modulator of host responses to microorganisms is explained, in part, by its potent and varied effects on different immune effector cells which influence antimicrobial activity. A new understanding of how microorganisms trigger IL-10 responses is emerging, along with recent discoveries of how IL-10 produced during disease might be harnessed for better protective or therapeutic strategies. In this review, we summarize studies from the past 5 years that have reported the induction of IL-10 by different classes of pathogenic microorganisms, including protozoa, nematodes, fungi, viruses and bacteria and discuss the impact of this induction on the persistence and/or clearance of microorganisms in the host.

Bacillus cereus spores and cereulide in food-borne illness

B. cereus is a gram-positive bacterium that possesses two different forms of life:the large, rod-shaped cells (ca. 0.002 mm by 0.004 mm) that are able to propagate and the small (0.001 mm), oval shaped spores. The spores can survive in almost any environment for up to centuries without nourishment or water. They are insensitive towards most agents that normally kill bacteria: heating up to several hours at 90 ºC, radiation, disinfectants and extreme alkaline (≥ pH 13) and acid (≤ pH 1) environment. The spores are highly hydrophobic and therefore make them tend to stick to all kinds of surfaces, steel, plastics and live cells. In favorable conditions the spores of B. cereus may germinate into vegetative cells capable of producing food poisoning toxins. The toxins can be heat-labile protein formed after ingestion of the contaminated food, inside the gastrointestinal tract (diarrhoeal toxins), or heat stable peptides formed in the food (emesis causing toxin, cereulide). Cereulide cannot be inactivated in foods by cooking or any other procedure applicable on food. Cereulide in consumed food causes serious illness in human, even fatalities. In this thesis, B. cereus strains originating from different kinds of foods and environments and 8 different countries were inspected for their capability of forming cereulide. Of the 1041 isolates from soil, animal feed, water, air, used bedding, grass, dung and equipment only 1.2 % were capable of producing cereulide, whereas of the 144 isolates originating from foods 24 % were cereulide producers. Cereulide was detected by two methods: by its toxicity towards mammalian cells (sperm assay) and by its peculiar chemical structure using liquid-chromatograph-mass spectrometry equipment. B. cereus is known as one of the most frequent bacteria occurring in food. Most foods contain more than one kind of B. cereus. When randomly selected 100 isolates of B. cereus from commercial infant foods (dry formulas) were tested, 11% of these produced cereulide. Considering a frequent content of 103 to 104 cfu (colony forming units) of B. cereus per gram of infant food formula (dry), it appears likely that most servings (200 ml, 30 g of the powder reconstituted with water) may contain cereulide producers. When a reconstituted infant formula was inoculated with >105 cfu of cereulide producing B. cereus per ml and left at room temperature, cereulide accumulated to food poisoning levels (> 0.1 mg of cereulide per serving) within 24 hours. Paradoxically, the amount of cereulide (per g of food) increased 10 to 50 fold when the food was diluted 4 - 15 fold with water. The amount of the produced cereulide strongly depended on the composition of the formula: most toxin was formed in formulas with cereals mixed with milk, and least toxin in formulas based on milk only. In spite of the aggressive cleaning practices executed by the modern dairy industry, certain genotypes of B. cereus appear to colonise the silos tanks. In this thesis four strategies to explain their survival of their spores in dairy silos were identified. First, high survival (log 15 min kill ≤ 1.5) in the hot alkaline (pH >13) wash liquid, used at the dairies for cleaning-in-place. Second, efficient adherence of the spores to stainless steel from cold water. Third, a cereulide producing group with spores characterized by slow germination in rich medium and well preserved viability when exposed to heating at 90 ºC. Fourth, spores capable of germinating at 8 ºC and possessing the psychrotolerance gene, cspA. There were indications that spores highly resistant to hot 1% sodium hydroxide may be effectively inactivated by hot 0.9% nitric acid. Eight out of the 14 dairy silo tank isolates possessing hot alkali resistant spores were capable of germinating and forming biofilm in whole milk, not previously reported for B. cereus. In this thesis it was shown that cereulide producing B. cereus was capable of inhibiting the growth of cereulide non-producing B. cereus occurring in the same food. This phenomenon, called antagonism, has long been known to exist between B. cereus and other microbial species, e.g. various species of Bacillus, gram-negative bacteria and plant pathogenic fungi. In this thesis intra-species antagonism of B. cereus was shown for the first time. This brother-killing did not depend on the cereulide molecule, also some of the cereulide non-producers were potent antagonists. Interestingly, the antagonistic clades were most frequently found in isolates from food implicated with human illness. The antagonistic property was therefore proposed in this thesis as a novel virulence factor that increases the human morbidity of the species B. cereus, in particular of the cereulide producers.

Memoirs of an immigrant and his ashtray

The memoirs were written in 1999. Childhood memories in a small town in Lower Austria. Passion for playing football (soccer). Recollections of daily life with rituals of coffeehouse visits and family dinners in the countryside. First experiences of antisemitism in the mid 1930s. Rising Nazi movement and illegal meetings in the local community. Annexation of Austria in 1938. First encounters with anti-Jewish regulations and discrimination by neighbors and acquaintances. Walter experienced severe difficulties at school and was frequently insulted and beaten up. Decision to leave school. The family was forced to leave Eggenburg soon thereafter, and the town declared itself "Judenfrei" (free of Jews). Move to Vienna, where they stayed with relatives. Walter, who had been brought up as a Catholic, suddenly saw himself confronted with orthodox Jewish people of different customs. Increasing restrictions for Jews. Walter was enrolled in a program at the Vienna Jewish community to learn carpentry. Recollections of the terror of Kristallnacht. Walter and his brother Ludwig were signed up for a children transport to England by the Quaker organization and left Vienna in December 1938. Difficult feeling to depart from their parents. Arrival in Harwige. They were taken to a camp in Lowestoft. Cultural differences. Walter and his brother were sent to a training farm in Parbold. Simple living conditions and difficult circumstances. Farm work and school lessons. Outbreak of the war. Scarce news of their parents, who tried to leave for Argentina. Walter's older brother Ludwig was sent to an internment camp in Adelaide, Australia. After two years he volunteered in the Pioneer Corps and returned to England. In 1941 their parents finally managed to emigrate to Argentina. Walter decided to join them, and in 1943 he left for Buenos Aires. During the passage on the Atlantic the ship was sunk by a German submarine. Rescue by the US Army. Continuation of his trip via New York.