A search for high-mass resonances decaying to tau⁺ tau⁻ in pp collisions at sqrts=7 TeV with the ATLAS detector

This Letter presents a search for high-mass resonances decaying into tau(+)tau(-) final states using proton-proton collisions at root s = 7 TeV produced by the Large Hadron Collider. The data were recorded with the ATLAS detector and correspond to an integrated luminosity of 4.6 fb(-1). No statistically significant excess above the Standard Model expectation is observed; 95% credibility upper limits are set on the cross section times branching fraction of Z' resonances decaying into tau(+)tau(-) pairs as a function of the resonance mass. As a result, Z' bosons of the Sequential Standard Model with masses less than 1.40 TeV are excluded at 95% credibility.

Relationship between cobalamin-dependent metabolites and both serum albumin and alpha1 -proteinase inhibitor concentrations in hypocobalaminemic dogs of 7 different breeds.

BACKGROUND Increased serum concentrations of homocysteine (HCY) and methylmalonic acid (MMA), the 2 main cobalamin-dependent metabolites, as well as decreased serum albumin and canine alpha1 -proteinase inhibitor (cα1 -PI) concentrations have previously been described in hypocobalaminemic dogs with gastrointestinal disease. However, no studies have been conducted to evaluate potential relationships between these serum biomarkers. OBJECTIVE The aim of this study was to evaluate the relationship between HCY and MMA, 2 cobalamin-dependent metabolites, and both serum albumin and cα1 -PI concentrations in hypocobalaminemic dogs. METHODS Serum samples from 285 dogs including 7 different breeds (Beagle, Boxer, Cocker Spaniel, German Shepherd, Labrador Retriever, Chinese Shar-Pei, and Yorkshire Terrier) with hypocobalaminemia were used. Serum HCY, MMA, albumin, and cα1 -PI concentrations were determined. RESULTS There was a significant correlation between serum HCY and albumin concentrations, as well as serum HCY and cα1 -PI concentrations (ρ = 0.62 and ρ = 0.37, respectively; P < .0001). No correlations were observed between serum MMA and albumin concentrations, or cα1 -PI concentrations (ρ = 0.01 and ρ = 0.08, respectively; P > .05). In addition, significant breed-specific correlations were observed between serum MMA and albumin concentrations in German Shepherds, and serum HCY and MMA concentrations in Chinese Shar-Peis with hypocobalaminemia. CONCLUSIONS This study shows a correlation between serum albumin and cα1 -PI and HCY concentrations, but not with serum MMA concentration in dogs with hypocobalaminemia. In addition, significant breed-specific correlations were observed between serum MMA and albumin concentrations in German Shepherds, as well as serum HCY and MMA concentrations in Chinese Shar-Peis, emphasizing the unique metabolic interactions in those dog breeds affected by hypocobalaminemia.

Prognostic implications of coronary calcification in patients with obstructive coronary artery disease treated by percutaneous coronary intervention: a patient-level pooled analysis of 7 contemporary stent trials

OBJECTIVE To investigate the long-term prognostic implications of coronary calcification in patients undergoing percutaneous coronary intervention for obstructive coronary artery disease. METHODS Patient-level data from 6296 patients enrolled in seven clinical drug-eluting stents trials were analysed to identify in angiographic images the presence of severe coronary calcification by an independent academic research organisation (Cardialysis, Rotterdam, The Netherlands). Clinical outcomes at 3-years follow-up including all-cause mortality, death-myocardial infarction (MI), and the composite end-point of all-cause death-MI-any revascularisation were compared between patients with and without severe calcification. RESULTS Severe calcification was detected in 20% of the studied population. Patients with severe lesion calcification were less likely to have undergone complete revascularisation (48% vs 55.6%, p<0.001) and had an increased mortality compared with those without severely calcified arteries (10.8% vs 4.4%, p<0.001). The event rate was also high in patients with severely calcified lesions for the combined end-point death-MI (22.9% vs 10.9%; p<0.001) and death-MI- any revascularisation (31.8% vs 22.4%; p<0.001). On multivariate Cox regression analysis, including the Syntax score, the presence of severe coronary calcification was an independent predictor of poor prognosis (HR: 1.33 95% CI 1.00 to 1.77, p=0.047 for death; 1.23, 95% CI 1.02 to 1.49, p=0.031 for death-MI, and 1.18, 95% CI 1.01 to 1.39, p=0.042 for death-MI- any revascularisation), but it was not associated with an increased risk of stent thrombosis. CONCLUSIONS Patients with severely calcified lesions have worse clinical outcomes compared to those without severe coronary calcification. Severe coronary calcification appears as an independent predictor of worse prognosis, and should be considered as a marker of advanced atherosclerosis.

Effect of Combined Systemic and Local Morpholino Treatment on the Spinal Muscular Atrophy Δ7 Mouse Model Phenotype

BACKGROUND: Spinal muscular atrophy (SMA) is a fatal motor neuron disease of childhood that is caused by mutations in the SMN1 gene. Currently, no effective treatment is available. One possible therapeutic approach is the use of antisense oligos (ASOs) to redirect the splicing of the paralogous gene SMN2, thus increasing functional SMN protein production. Various ASOs with different chemical properties are suitable for these applications, including a morpholino oligomer (MO) variant with a particularly excellent safety and efficacy profile. OBJECTIVE: We investigated a 25-nt MO sequence targeting the negative intronic splicing silencer (ISS-N1) 10 to 34 region. METHODS: We administered a 25-nt MO sequence against the ISS-N1 region of SMN2 (HSMN2Ex7D[-10-34]) in the SMAΔ7 mouse model and evaluated the effect and neuropathologic phenotype. We tested different concentrations (from 2 to 24 nM) and delivery protocols (intracerebroventricular injection, systemic injection, or both). We evaluated the treatment efficacy regarding SMN levels, survival, neuromuscular phenotype, and neuropathologic features. RESULTS: We found that a 25-nt MO sequence against the ISS-N1 region of SMN2 (HSMN2Ex7D[-10-34]) exhibited superior efficacy in transgenic SMAΔ7 mice compared with previously described sequences. In our experiments, the combination of local and systemic administration of MO (bare or conjugated to octaguanidine) was the most effective approach for increasing full-length SMN expression, leading to robust improvement in neuropathologic features and survival. Moreover, we found that several small nuclear RNAs were deregulated in SMA mice and that their levels were restored by MO treatment. CONCLUSION: These results indicate that MO-mediated SMA therapy is efficacious and can result in phenotypic rescue, providing important insights for further development of ASO-based therapeutic strategies in SMA patients.

Oxypurinol directly and immediately activates the drug-specific T cells via the preferential use of HLA-B*58:01

Allopurinol (ALP) hypersensitivity is a major cause of severe cutaneous adverse reactions and is strongly associated with the HLA-B*58:01 allele. However, it can occur in the absence of this allele with identical clinical manifestations. The immune mechanism of ALP-induced severe cutaneous adverse reactions is poorly understood, and the T cell-reactivity pattern in patients with or without the HLA-B*58:01 allele is not known. To understand the interactions among the drug, HLA, and TCR, we generated T cell lines that react to ALP or its metabolite oxypurinol (OXP) from HLA-B*58:01(+) and HLA-B*58:01(-) donors and assessed their reactivity. ALP/OXP-specific T cells reacted immediately to the addition of the drugs and bypassed intracellular Ag processing, which is consistent with the "pharmacological interaction with immune receptors" (p-i) concept. This direct activation occurred regardless of HLA-B*58:01 status. Although most OXP-specific T cells from HLA-B*58:01(+) donors were restricted by the HLA-B*58:01 molecule for drug recognition, ALP-specific T cells also were restricted to other MHC class I molecules. This can be explained by in silico docking data that suggest that OXP binds to the peptide-binding groove of HLA-B*58:01 with higher affinity. The ensuing T cell responses elicited by ALP or OXP were not limited to particular TCR Vβ repertoires. We conclude that the drug-specific T cells are activated by OXP bound to HLA-B*58:01 through the p-i mechanism.

Measurement of Higgs boson production in the diphoton decay channel in pp collisions at center-of-mass energies of 7 and 8 TeV with the ATLAS detector

A measurement of the production processes of the recently discovered Higgs boson is performed in the two-photon final state using 4.5  fb −1 of proton-proton collisions data at s √ =7  TeV and 20.3  fb −1 at s √ =8  TeV collected by the ATLAS detector at the Large Hadron Collider. The number of observed Higgs boson decays to diphotons divided by the corresponding Standard Model prediction, called the signal strength, is found to be μ=1.17±0.27 at the value of the Higgs boson mass measured by ATLAS, m H =125.4  GeV . The analysis is optimized to measure the signal strengths for individual Higgs boson production processes at this value of m H . They are found to be μ ggF =1.32±0.38 , μ VBF =0.8±0.7 , μ WH =1.0±1.6 , μ ZH =0.1 +3.7 −0.1 , and μ tt ¯ H =1.6 +2.7 −1.8 , for Higgs boson production through gluon fusion, vector-boson fusion, and in association with a W or Z boson or a top-quark pair, respectively. Compared with the previously published ATLAS analysis, the results reported here also benefit from a new energy calibration procedure for photons and the subsequent reduction of the systematic uncertainty on the diphoton mass resolution. No significant deviations from the predictions of the Standard Model are found.

Achievements and Prospects of Tef Improvement - Proceedings of the Second International Workshop, November 7-9, 2011, Debre Zeit, Ethiopia

These proceedings on ‘Achievements and Prospects of tef Improvement’ is the outcome of the Second International Tef Workshop held at Debre Zeit (Ethiopia), the location which represents the major tef growing areas in the country as well as the oldest and biggest center on tef research. As an indigenous crop, the bulk of tef research is carried out in the country by scientists based at various higher-learning and research institutions. Hence, unlike major crops of the world such as wheat and rice, research on tef benefited little from modern improvement techniques. However, in the recent years, there is an increasing interest by several researchers and funding organizations in developed nations to promote tef research and development through implementation of modern genetic and genomic tools. The recent efforts and progresses made on tef research and development were presented and discussed in detail at the workshop. The tef research and development in Ethiopia has recently shown tremendous improvement. This is witnessed by the decision of the Ethiopian government to award a Gold Medal in November 2012 to our Institute for the discovery and promotion of a very popular Quncho variety. At this juncture, I would like to congratulate all involved in research and development of tef as the achievement was obtained due to concerted efforts of the tef community. The editors of the proceedings did a wonderful job of undertaking the painstaking task of editing all 23 manuscripts presented at the workshop. In addition, the proceedings include a 44-point roadmap for future tef research and development which can be used as a guideline for researchers, development workers and policy makers. I would like to extend my thanks to sponsors of the workshop and the publication of the proceedings.

Transfer and effects of 1,2,3,5,7-pentachloronaphthalene in an experimental food chain.

Polychlorinated naphthalenes are environmentally relevant compounds that are measured in biota at concentrations in the μg/kg lipid range. Despite their widespread occurrence, literature data on the accumulation and effects of these compounds in aquatic ecosystems are sparsely available. The goal of this study was to gain insights into the biomagnification and effects of 1,2,3,5,7-pentachloronaphthalene (PeCN52) in an experimental food chain consisting of benthic worms and juvenile rainbow trout. Worms were contaminated with PeCN52 by passive dosing from polydimethylsiloxane silicone. The contaminated worms were then used to feed the juvenile rainbow trout at 0.12, 0.25 or 0.50 μg/g fish wet weight/day, and the resulting internal whole-body concentrations of the individual fish were linked to biological responses. A possible involvement of the cellular detoxification system was explored by measuring PeCN52-induced expression of the phase I biotransformation enzyme gene cyp1a1 and the ABC transporter gene abcb1a. At the end of the 28-day study, biomagnification factors were similar for all dietary intake levels with values between 0.5 and 0.7 kg lipid(fish)/kg lipid(worm). The average uptake efficiency of 60% indicated that a high amount of PeCN52 was transferred from the worms to the fish. Internal concentrations of up to 175 mg/kg fish lipid in the highest treatment level did not result in effects on survival, behavior, or growth of the juvenile trout, but were associated with the induction of phase I metabolism which was evident from the significant up-regulation of cyp1a1 expression in the liver. In contrast, no changes were seen in abcb1a transcript levels.

Cleavage and activation of calpain and its substrate caspase-7 in prostate cancer cells: Evidence for a role in apoptotic sensitization

Changes in the levels of intracellular calcium mediate multiple biological effects, including apoptosis, in some tumor cells. Early studies demonstrated that prostate cancer cells are highly sensitive to alterations in the levels of their intracellular calcium pools. Furthermore, it has been established that apoptosis in prostate cancer could be initiated through calcium-selective ionophores, or inhibitors of intracellular calcium pumps. High sensitivity to changes in intracellular calcium levels may therefore be exploited as a novel mechanism for controlling prostate cancer apoptotic thresholds; however, the mechanisms associated with this process are poorly understood. To investigate the role of calcium as a mediator of prostate cancer cell death and its effects on caspase activation, LNCaP and PC-3 cell response to the calcium ionophore A23187, were examined. LNCaP cells were highly sensitive to changes in intracellular calcium, and subtoxic concentrations of A23187 facilitated apoptosis initiated by cytokines (TNF or TRAIL). In contrast, PC-3 cell death was not affected by A23187 or cytokines. A23187 caused rapid and concentration-dependent activation of calpain in LNCaP (but not PC-3 cells) which correlated with cleavage of calpain substrates caspase-7 and PTP1B. Cleavage of PTP1B from a 50 kDa to 42 kDa protein correlated with its translocation from the endoplasmic reticulum to the cytosol and with inhibition of tyrosine phosphorylation. Caspase-7 was cleaved from a 35 kDa to 30 kDa protein in response to A23187 in LNCaP (but not PC-3) cells and correlated with activation of both upstream and downstream caspases. Extracts from A23187-treated LNCaP cells, or PC-3 cells transiently transfected with calpain, mediated similar processing of in vitro transcribed and translated (TNT) caspase-7. In vitro processing of caspase-7 correlated with its proteolytic activation, which was inhibited by calpain inhibitor (calpeptin) and to some degree, by caspase inhibitors (zVAD, DEVD). Together, these results suggest that calpain is directly involved in calcium-mediated apoptosis of prostate cancer cells through activation and cleavage of caspase-7 and other substrates. Loss of calpain activation may therefore play a critical role in apoptotic resistance of some prostate cancer cells. ^

An Inexpensive Alternative to CS Photoshop & Bridge: Archival Master Image Capture and Batch Derivative Creation in Canon Scan Gear & Adobe Photoshop Elements 7

This presentation was made at the Connecticut State Library Service Center, Willimantic, CT, April 14, 2009. It focused on digital capture workflows for both archival and derivative image creation using accepted current standards. Tools used were inexpensive by choice and focused towards the needs of small to mid-sized cultural heritage institutions who wish to begin digital capture in their own facilities.

Na 1 Nachlass Max Horkheimer, 7 - Korrespondenzen u.a. mit Familie Cahn (p. I 4, 1-297a)

1 Brief von Max Horkheimer an die Cadillac Motor Division, 05.06.1939; 148 Briefe zwischen Erwin Cahn, Lotte Cahn, Ilse Cahn, Max Cahn, Lilo Cahn, Lina Cahn und Max Horkheimer, 1938-1942; 10 Briefe zwischen dem Transmigration Bureau og the American Jewish Joint Distribution Committee und Friedrich Pollock, 1941-1942; 3 Briefe zwischen dem National Refugee Service und Max Horkheimer, 07.04.1941, 1941; 1 Brief von Julius S. Bach an die National City Bank of New York, 27.06.1940; 1 Brief von Julius S. Bach an den American Consul General Berlin, 15.04.1940; 1 Brief von Max Horkheimer an Julius S. Bach, 15.05.1940; 16 Briefe von Max Horkheimer an den American Consul General Stuttgart, 1938-1941; 2 Briefe zwischen der Auswandererstelle Marx und Max Horkheimer, 02.06.1941; 5 Briefe zwischen dem Reisebüro Anselm Stuttgart und Max Horkheimer, 1941; 9 Briefe zwischen der Sapt A.G und Max Horkheimer, 1940-1941; 3 Briefe zwischen Emanuel Green und Max Horkheimer, 26.09.1940, 1940; 3 Briefe zwischen der Zweigstelle Wüttemberg der Reichsvereinigung der Juden in Deutschland und Max Horkheimer, 1940, 19.09.1940; 2 Briefe zwischen der Auswandererstelle Adler und Max Horkheimer, 25.05.1940; 2 Briefe von Max Horkheimer an den American Consul General Berlin, 1939; 1 Brief von Max Horkheimer an S. Klein, 20.03.1939; 1 Brief von Max Horkheimer an den Collector of Customs, 27.02.1939; 1 Brief von Max Horkheimer an Ludwig Lewisohn,. 03.01.1939; 1 Brief von Friedlaender an Kahn, 15.12.1938; 1 Brief von Erwin Cahn an Max Horkheimer, 07.02.1935;

Na 1 Nachlass Max Horkheimer, 13 - Korrespondenzen u.a. mit Familie Eder (p. I 7, 1-223)

7 Briefe zwischen Edward Mead Earle, American Committee for International Studies, Princeton N. J. und Max Horkheimer, 1940-1941; 3 Briefe zwischen Margaret Ebert und Margot von Mendelssohn, 1941, 28.08.1941; 6 Briefe zwischen C. C. Eckhardt und Max Horkheimer, 1940; 5 Briefe zwischen Kay Eckstein und Max Horkheimer, 1940; 2 Briefe zwischen George Eckstein und Max Horkheimer, 16.05.1939, 35.05.1939; 1 Brief von F. K. Eden an Max Horkheimer, 02.04.1944; 33 Briefe zwischen Leopold Eder, Frieda Eder, Ruth Eder und Max Horkheimer, 1937-1940; 2 Briefe zwischen Dale Edwards und Max Horkheimer, 16.07.1940; 1 Brief von Hedwig Ehrlich an Max Horkheimer; 1 Brief von Max Horkheimer an Albert Einstein, 20.02.1935; 1 Brief von Max Horkheimer an W. Eisemann, 02.11.1939; 1 Brief von Else Eisner an Max Horkheimer, 09.12.1935; 2 Briefe zwischen Edit Elbogen und Max Horkheimer, 24.03.1942, 26.03.1942; 1 Brief von Käte von Hirsch an Max Horkheimer, 03.08.1941; 2 Briefe von Emmy Elbogen an Margot von Mendelssohn, 1945; 2 Briefe zwischen Paul Elbogen und Max Horkheimer, 02.06.1944, 09.06.1944; 4 Briefe zwischen Norbert Elias und Max Horkheimer, 1934-1935; 1 Brief von Werner B. Ellinger an Max Horkheimer, 16.12.1937; 19 Briefe zwischen dem Emergency Committee in Aid of Displaced Foreign Scholars New York und Max Horkheimer, 1938-1944; 2 Briefe zwischen dem Emergency Rescue Committee New York und Max Horkheimer, 12.06.1941, 14.06.1941; 1 Brief von F.L. Neumann an Emhardt, 13.02.1939; 23 Briefe zwischen Alice Engel und Max Horkheimer, 1937-1941; 9 briefe zwischen Paul Doernberg, Sofie Doernberg und Max Horkheimer, 1940-1942; 3 Briefe zwischen der Hebrew Sheltering and Immigrant Aid Society New York und Max Horkheimer, 05.01.1942, 1942; 1 Brief von der Selfhelp of Emigres from Central Europe, New York an Max Horkheimer, 18.08.1941; 2 Briefe zwischen R. Weissmann und Max Horkheimer, 09.01.1941, 03.02.1941; 5 Briefe zwischen Ernst Engelberg und Max Horkheimer, 1939-1940, 07.06.1939; 1 Brief von Fritz Epstein an Max Horkheimer, 10.04.1937; 1 Brief von Erika Ermel an Max Horkheimer, 15.09.1948; 2 Briefe zwischen Max Ernst und Max Horkheimer, 23.01.1936; 4 Briefe zwischen Margot Esser und Max Horkheimer, 1935-1936; 16 Briefe zwischen Rene Etiemble und Max Horkheimer, 1936-1938; 4 Briefe zwischen L.M. Ettlinger und Max Horkheimer, 1937; 8 Briefe zwischen Walter Fabien und Max Horkheimer, 1937-1941; 1 Brief von Max Horkheimer an Henry Pratt Fairchild, 25.03.1941; 2 Briefe zwischen Marvin Farber und Max Horkheimer, 14.03.1940, 17.05.1940; 4 Briefe zwischen Walter Farley udn Max Horkheimer, 1935, 01.10.1935; 8 Briefe zwischen Alexander Farquharson und Max Horkheimer, 1935-1939;

Na 1 Nachlass Max Horkheimer, 14 - Korrespondenzen u.a. mit Hugo Fischer und Karl August Wittfogel (p. I 7, 224-429)

1 Brief von Max Horkheimer an Rosel Favez, 03.12.1935; 5 Briefe zwischen Sidney B. Fay von der Bureau of International Search Cambridge, Massachusetts und Max Horkheimer, 1939-1941; 1 Brief von Max Horkheimer an James Feibleman, 02.03.1942; 5 Briefe von Hans Feibelmann an Max Horkheimer, 1936-1937; 2 Briefe zwischen Babette Feigenbaum und Max Horkheimer, 29.04.1941, 05.05.1941; 1 Brief von Arthur Feiler an Max Horkheimer, 15.10.1939; 1 Brief von Max Horkheimer an Adolf Feitler, 03.01.1935; 3 Briefe zwischen Frederick V. Filed von dem American Council Institute of Pacific Relations und Max Horkheimer, 1937, 05.04.1937; 9 Briefe zwischen Thea Field, Lowell Field und Max Horkheimer, 1935-1941; 1 Brief von Max Horkheimer an Finkelstein, 18.09.1941; 7 Briefe zwischen Harry Finkelstein und Max Horkheimer, 1936-1940; 1 Brief von Louis Finkelstein an Robert MacIver, 29.05.1940; 2 Briefe zwischen Louis Finkelstein und Max Horkheimer, 06.06.1940, 04.06.1940; 15 Briefe zwischen Hugo Fischer und Max Horkheimer, 1937-1938; 1 Brief von Hugo Fischer an P. Tillich; 1 Brief von Hugo Fischer an Karl A. Wittfogel, 17.06.1940; 2 Briefe von Max Horkheimer an Ernest Manheim, April 1942; 1 Brief von Alexander Farquharson an Max Horkheimer, 20.01.1940; 3 Briefe zwischen dem Institute of International Education, New York Edgar J. Fisher und Max Horkheimer, Oktober 1938, 18.10.1938; 10 Briefe zwischen Paul Fischer und Max Horkheimer, 1938-1940; 2 Briefe zwischen der Hessian Hills School New York und Max Horkheimer, 21.02.1938, 28.02.1938; 2 Briefe zwischen Dorothy Canfield Fisher und Max Horkheimer, 24.01.1939, 19.01.1939; 1 Brief von Ossip K. Flechtheim an Max Horkheimer, 04.01.1941; 2 Briefe zwischen der University of Minnesota, Minneapolis und Max Horkheimer, 02.08.1945, 15.09.1945; 3 Briefe zwischen Leo Löwenthal und Max Horkheimer, 1943-1945, 17.08.1945; 2 Briefe zwischen der University of Denver, Colorado und Max Horkheimer, 11.05.1943, 28.05.1943; 1 Brief von dem Institute Universitaire De Hautes Etudes Internationales Genf an Max Horkheimer, 25.01.1939; 1 Brief von Hans Kelsen an Max Horkheimer, 30.01.1939; Lebenslauf und 2 Empfehlungsschreiben von Max Fleischmann für Prof. Edwin Borchard; 1 Brief von der Columbia University in the City of New York an Franz Neumann, 17.04.1940; 3 Briefe zwischen Philipp Flesch und Max Horkheimer, 26.03.1940, 1939-1940; 17 Briefe zwischen Babette Fletcher, Theo Fletcher und Max Horkheimer, 1941-1950; 1 Brief von Max Horkheimer an Abraham Flexner, 07.06.1939; 1 Brief von Robert Fließ an Max Horkheimer, 24.10.1938; 1 Brief von der Foreign Policy Association New York an Max Horkheimer, 03.11.1934; 1 Brief von Max Horkheimer an Rudolf Forster, 10.01.1940; 2 Briefe von der Fortune Time & Life Building New York und Max Horkheimer, 1938-1940; 4 Briefe zwischen Siegmund H. Foulkes (Fuchs) und Max Horkheimer, 1936-1937, 31.12.1936; 5 Briefe zwischen Elsie M. Foulstone und Max Horkheimer, 1941; 1 Brief von Mary Fox an Max Horkheimer, 09.12.1938; 5 Briefe zwischen Ernst Fraenkel und Max Horkheimer, 1936-1938; 1 Heiratsanzeige Liesl Frank; 7 Briefe zwischen Philipp Frank und Max Horkheimer, 1937-1939; 6 Briefe zwischen Lothar G. Frank und Max Horkheimer, 1941; 7 Briefe zwischen Felix Frankfurter und Max Horkheimer, 1937-1941; 2 Briefe zwischen Joseph Freeman und Max Horkheimer, 22.11.1944; 1 Brief von der Free Synagogue New York an Max Horkheimer, 14.11.1938; 2 Briefe zwsichen Benjamin Freilichmann und Max Horkheimer, 07.01.1939, 23.01.1939; 2 Briefe zwischen dem Frenkel Travel Service New York und Max Horkheimer, 21.02.1936, 23.02.1936; 2 Briefe zwischen Hugo Freund und Max Horkheimer, 14.11.1938, 18.11.1938; 2 Briefe zwischen Julius A. Jr. Freynick und Max Horkheimer, 11.09.1939, 18.09.1939;