Charles M. Breder, Jr.: Atlantis Expedition, 1934

Dr. Charles M. Breder participated on the 1934 expedition of the Atlantis from Woods Hole, Massachusetts to Panama and back and kept a field diary of daily activities. The Atlantis expedition of 1934, led by Prof. A. E. Parr, was a milestone in the history of scientific discovery in the Sargasso Sea and the West Indies. Although naturalists had visited the Sargasso Sea for many years, the Atlantis voyage was the first attempt to investigate in detailed quantitative manner biological problems about this varying, intermittent ‘false’ bottom of living, floating plants and associated fauna. In addition to Dr. Breder, the party also consisted of Dr. Alexander Forbes, Harvard University and Trustee of the Woods Hole Oceanographic Institution (WHOI); T. S. Greenwood, WHOI hydrographer; M. D. Burkenroad, Yale University’s Bingham Laboratory, carcinology and Sargasso epizoa; M. Bishop, Peabody Museum of Natural History, Zoology Dept., collections and preparations and H. Sears, WHOI ichthyologist. The itinerary included the following waypoints: Woods Hole, the Bermudas, Turks Islands, Kingston, Colon, along the Mosquito Bank off of Nicaragua, off the north coast of Jamaica, along the south coast of Cuba, Bartlett Deep, to off the Isle of Pines, through the Yucatan Channel, off Havana, off Key West, to Miami, to New York City, and then the return to Woods Hole. During the expedition, Breder collected rare and little-known flying fish species and developed a method for hatching and growing flying fish larvae. (PDF contains 48 pages

Previous attentional set can induce an attentional blink with task-irrelevant initial targets

Identification of a second target is often impaired by the requirement to process a prior target in a rapid serial visual presentation (RSVP). This is termed the attentional blink. Even when the first target is task-irrelevant an attentional blink may occur providing this first target shares similar features with the second target (contingent capture). An RSVP experiment was undertaken to assess whether this first target can still cause an attentional blink when it did not require a response and did not share any features with the following target. The results revealed that such task-irrelevant targets can induce an attentional blink providing that they were task-relevant on a previous block of trials. This suggests that irrelevant focal stimuli can distract attention on the basis of a previous attentional set

Cardiomyocyte-specific estrogen receptor alpha increases angiogenesis, lymphangiogenesis and reduces fibrosis in the female mouse heart post-myocardial infarction

Experimental studies showed that 17{beta}-estradiol (E2) and activated Estrogen Receptors (ER) protect the heart from ischemic injury. However, the underlying molecular mechanisms are not well understood. To investigate the role of ER{alpha} in cardiomyocytes in the setting of myocardial ischemia, we generated transgenic mice with cardiomyocyte-specific overexpression of ER-{alpha} (ER{alpha}-OE) and subjected them to Myocardial Infarction (MI). At the basal level, female and male ER{alpha}-OE mice showed increased Left Ventricular (LV) mass, LV volume and cardiomyocyte length. Two weeks after MI, LV volume was significantly increased and LV wall thickness decreased in female and male WT-mice and male ER{alpha}-OE, but not in female ER{alpha}-OE mice. ER{alpha}-OE enhanced expression of angiogenesis and lymphangiogenesis markers (Vegf, Lyve-1), and neovascularization in the peri-infarct area in both sexes. However, attenuated level of fibrosis and higher phosphorylation of JNK signaling pathway could be detected only in female ER{alpha}-OE after MI. In conclusion, our study indicates that ER{alpha} protects female mouse cardiomyocytes from the sequelae of ischemia through induction of neovascularization in a paracrine fashion and impaired fibrosis, which together may contribute to the attenuation of cardiac remodelling

Clinical benefit of glasdegib plus low-dose cytarabine in patients with de novo and secondary acute myeloid leukemia: long-term analysis of a phase II randomized trial

This analysis from the phase II BRIGHT AML 1003 trial reports the long-term efficacy and safety of glasdegib + low-dose cytarabine (LDAC) in patients with acute myeloid leukemia ineligible for intensive chemotherapy. The multicenter, open-label study randomized (2:1) patients to receive glasdegib + LDAC (de novo, n = 38; secondary acute myeloid leukemia, n = 40) or LDAC alone (de novo, n = 18; secondary acute myeloid leukemia, n = 20). At the time of analysis, 90% of patients had died, with the longest follow-up since randomization 36 months. The combination of glasdegib and LDAC conferred superior overall survival (OS) versus LDAC alone; hazard ratio (HR) 0.495; (95% confidence interval [CI] 0.325–0.752); p = 0.0004; median OS was 8.3 versus 4.3 months. Improvement in OS was consistent across cytogenetic risk groups. In a post-hoc subgroup analysis, a survival trend with glasdegib + LDAC was observed in patients with de novo acute myeloid leukemia (HR 0.720; 95% CI 0.395– 1.312; p = 0.14; median OS 6.6 vs 4.3 months) and secondary acute myeloid leukemia (HR 0.287; 95% CI 0.151–0.548; p < 0.0001; median OS 9.1 vs 4.1 months). The incidence of adverse events in the glasdegib + LDAC arm decreased after 90 days’ therapy: 83.7% versus 98.7% during the first 90 days. Glasdegib + LDAC versus LDAC alone continued to demonstrate superior OS in patients with acute myeloid leukemia; the clinical benefit with glasdegib + LDAC was particularly prominent in patients with secondary acute myeloid leukemia. ClinicalTrials.gov identifier: NCT01546038

Metal site doping in the narrow-gap semiconductor FeGa₃

The effects and feasibility of metal site doping of the tetragonal diamagnetic insulator FeGa₃ by Fe/Co, Fe/Mn and Co/Ni substitution were investigated by X-ray, electron probe microanalysis, electrical resistivity, specific heat and magnetic susceptibility measurements. Substitution of Fe by Co in FeGa₃ does not change its structure type and preserves the structure of the binary parent compound (FeGa₃), whereas the solubility of Mn in the FeGa₃ structure type is limited to 3 at.% and a finite solubility of Ni in CoGa₃ is not detected.Методами рентгенівського, мікрорентгеноспектрального аналізу, дослідження електроопору, питомої теплоємності і магнетної сприйнятливості вивчено можливість та вплив легування Fe/Co, Fe/Mn і Co/Ni у положеннях атомів металу в тетрагональній структурі діамагнетного ізолятора FeGa₃. Заміщення атомів Fe на Co у сполуці FeGa₃ не змінює її кристалічну структуру. Розчинність Mn у FeGa₃ не перевищує 3 at.%, а розчинність Ni у CoGa₃ не виявлено.Методами рентгеновского, микрорентгеноспектрального анализа, исследования электросопротивления, удельной теплоемкости и магнитной восприимчивости исследована возможность и влияние легирования Fe/Co, Fe/Mn и Co/Ni в положениях атомов металла в тетрагональной структуре диамагнитного изолятора FeGa₃. Замещение атомов Fe на Co в соединении FeGa₃ не изменяет ее кристаллическую структуру. Растворимость Mn в FeGa₃ не превышает 3 at.%, а растворимость Ni в CoGa₃ не выявлено