O «global player» Anselm Eckart SJ (1721–1809) e sua contribuição à História Natural e Etnografia da Amazônia no Século XVIII

Der aus einer vornehmen Mainzer Familie stammende Jesuit Anselm Eckart wirkte (neben anderen deutschsprachigen Ordenspriestern) zwischen 1753 und 1757 als Missionar in Amazonien, wo er insbesondere am Rio Abacaxis und in Trocano/Borba am Madeirafluss bedeutsame Forschungen auf dem Gebiet der Linguistik, Naturkunde und Zoologie durchführte – ein Gebiet, in dem auch der Co-Autor dieses Beitrags, Thomas Horst, rund 250 Jahre später am Rio Canumã ethnologisch tätig war. Eckart wurde nach seiner Ausweisung nach Portugal im Rahmen der rigorosen Kirchenpolitik des Marquês de Pombal im Jahr 1759 verhaftet und (wie viele seiner Mitbrüder, darunter Laurenz Wilhelm Kaulen SJ und Anton Meisterburg SJ) 18 Jahre lang eingekerkert, wovon seine später in Nürnberg zwischen 1779 und 1803 bei Christoph Gottlieb von Murr gedruckte Schrift «História Persecutionis Societatis Jesu in Lusitania» zeugt. Er verbrachte seinen Lebensabend im Jesuitenkolleg von Polazk (Połock, heute in Belarus) und verstarb im hohen Alter von 88 Jahren am 29. Juni 1809 in Dünaburg. Der vorliegende Beitrag gibt einen Überblick über die Rolle der deutschen Missionare in Amazonien und deren späteres trostloses Schicksal in den Kerkern von Portugal. Zudem werden die naturkundlichen bzw. zoologischen Beschreibungen Eckarts anhand eines im portugiesischen Nationalarchiv verwahrtem Manuskriptes (ANTT, MNEJ 59 n. 4) näher analysiert

Lowered Insulin Signalling Ameliorates Age-Related Sleep Fragmentation in <i>Drosophila</i>

<div><p>Sleep fragmentation, particularly reduced and interrupted night sleep, impairs the quality of life of older people. Strikingly similar declines in sleep quality are seen during ageing in laboratory animals, including the fruit fly <i>Drosophila</i>. We investigated whether reduced activity of the nutrient- and stress-sensing insulin/insulin-like growth factor (IIS)/TOR signalling network, which ameliorates ageing in diverse organisms, could rescue the sleep fragmentation of ageing <i>Drosophila</i>. Lowered IIS/TOR network activity improved sleep quality, with increased night sleep and day activity and reduced sleep fragmentation. Reduced TOR activity, even when started for the first time late in life, improved sleep quality. The effects of reduced IIS/TOR network activity on day and night phenotypes were mediated through distinct mechanisms: Day activity was induced by adipokinetic hormone, dFOXO, and enhanced octopaminergic signalling. In contrast, night sleep duration and consolidation were dependent on reduced S6K and dopaminergic signalling. Our findings highlight the importance of different IIS/TOR components as potential therapeutic targets for pharmacological treatment of age-related sleep fragmentation in humans.</p></div

Reduced IIS causes day hyperactivity through increased octopaminergic signalling.

<p>(A) Two days feeding with mianserin hydrochloride (0.2 mg/ml) reverted the day activity phenotype of <i>dilp2-3,5</i> mutants (age 10 d), but not night activity, sleep, sleep bouts, and sleep bouts length (<i>w^Dah n = </i>17/24, <i>dilp2-3,5 n</i> = 17/27 +/− mianserin). GLM was used to determine significance of treatment by genotype interactions in sleep and activity behaviours on treatment with mianserin in controls and IIS mutants. Significant differences were seen in day activity (<i>p</i> = 0.0031), in day sleep (<i>p</i> = 0.0148), and day bout number (<i>p</i> = 0.002), but not in night behaviours (activity <i>p</i> = 0.31, sleep <i>p</i> = 0.49, bout number <i>p</i> = 0.72, night bout length <i>p</i> = 0.15). (B) Average activity count data (30 min bins) under 12∶12 h LD. (A) Kruskal Wallis test with Dunn's multiple comparison of selected pairs. ***<i>p</i><0.001, **<i>p</i><0.01, and *<i>p</i><0.05. Error bars represent s.e.m.</p

Day hyperactivity of IIS mutants is dependent on the <i>AkhR</i>.

<p>(A) Loss of <i>AkhR</i> abrogated the day activity phenotype of <i>dilp2-3,5</i> mutants (age 15 d, <i>w^Dah n</i> = 18, <i>dilp2-3,5 n</i> = 15, <i>AkhR n</i> = 18, <i>AkhR dilp-3,5 n</i> = 17). GLM was used to determine significance of genotype by genotype interactions in sleep and activity behaviours on loss of <i>AkhR</i> in controls and <i>dilp2-3,5</i> mutants. Significant differences were seen in day activity (<i>p</i> = 0.0057) and day bout number (<i>p</i> = 0.044) but not in day sleep (<i>p</i> = 0.14) or night behaviours (activity <i>p</i> = 0.09, sleep <i>p</i> = 0.63, bout number <i>p</i> = 0.22, night bout length <i>p</i> = 0.067). Corresponding nighttime behaviours are shown in <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.1001824#pbio.1001824.s004" target="_blank">Figure S4A</a>. (B) Two-day tolbutamide (1.35 mg/ml) treatment increased day activity of <i>w^Dah</i> flies. Lack of <i>dfoxo</i>, <i>AkhR</i>, or <i>dilp2-3,5</i> blocked the tolbutamide effect on day activity (nighttime behaviour shown in <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.1001824#pbio.1001824.s004" target="_blank">Figure S4B</a>) (age 15 d, <i>w^Dah n</i> = 51/47, <i>AkhR n</i> = 30/34, <i>dfoxo^Δ94 n</i> = 36/34, <i>dilp2-3,5 n</i> = 22/18, +/− tolbutamide). Analysis of genotype by treatment interactions (GLM) in sleep and activity behaviours on tolbutamide treatment in <i>IIS</i>, <i>AkhR</i>, and <i>dfoxo</i> mutants compared to controls showed day activity (<i>p</i> = 0.049), day sleep (<i>p</i> = <0.0001), and bout number (<i>p</i> = 0.008) were significantly different. However, no differences were seen in night behaviours (activity <i>p</i> = 0.58, sleep <i>p</i> = 0.89, bout number <i>p</i> = 0.28). (C) Mass spectrometry measurement of octopamine levels in head extracts (age 10 d, <i>w^Dah n</i> = 7, <i>dilp2-3,5 n</i> = 6, <i>AkhR n</i> = 6, <i>AkhR,dilp2-3,5 n</i> = 6). (A and B) Kruskal Wallis test with Dunn's multiple comparison test (selected pairs). (C) Mann–Whitney test. (C) One-way ANOVA with Bonferroni's multiple comparison test. ***<i>p</i><0.001, **<i>p</i><0.01, and *<i>p</i><0.05. Error bars represent s.e.m.</p

Reduced IIS affected activity and sleep and ameliorated age-related sleep fragmentation.

<p>(A) Locomotor activity over 9 d of <i>w^Dah</i> control and <i>dilp2-3,5</i> mutant flies under 12∶12 h LD and constant darkness 12∶12 h DD (<i>n = </i>12, age 20 d). Mean free running period (τ) in DD ± s.e.m. (B) Average activity count data (30 min bins) under 12∶12 h LD conditions (25 d <i>w^Dah n = </i>48, <i>dilp2-3,5 n = </i>31). (C) <i>dilp2-3,5</i> mutants were more active during the day and less active during the night compared to controls. (D) There was no significant difference in wakefulness (average activity per waking minute). (E) <i>dilp2-3,5</i> mutants slept more at night and less during the day than controls. (F) Minutes of sleep per 30 min (25 d <i>w^Dah n = </i>48, <i>dilp2-3,5 n = </i>31). (G) Day and night sleep of <i>dilp2-3,5</i> mutants were interrupted by fewer waking periods compared to controls. (H) <i>dilp2-3,5</i> flies had longer sleep bouts during the night. (I) Longer sleep bouts were more prevalent in <i>dilp2-3,5</i> mutants (age 25 d). (J) <i>w^Dah</i> control flies, but not <i>dilp2-3,5</i> mutants, show a significant age-related increase in night sleep bouts (age 10 d, 25 d, 45 d, 55 d, and 65 d). (B–F) <i>w^Dah</i> , <i>n</i> = 31, 43, 46, 26, and 31 for ages 10 d, 25 d, 45 d, 55 d, and 65 d, respectively; <i>dilp2-3,5</i>, <i>n</i> = 31, 31, 32, 29, and 43 for ages 10 d, 25 d, 45 d, 55 d, and 65 d, respectively. Kruskal Wallis test with Dunn's multiple comparison (selected pairs). ***<i>p</i><0.001, **<i>p</i><0.01, and *<i>p</i><0.05. Error bars represent s.e.m.</p

<i>dfoxo</i> affected daytime activity and sleep phenotypes of <i>INR^DN</i> flies.

<p>Loss of <i>dfoxo</i> in <i>da-Gal4/UAS-INR^DN</i> flies but not in wild-type flies (age 20 d) decreased day activity but had no effect on night activity, had no significant effect on wakefulness (average activity per waking minute), increased day sleep duration but had no effect on night sleep duration, and reverted the low sleep bout phenotype of <i>da-Gal4/UAS-INR^DN</i> flies by day but not at night and increased night sleep bout duration. <i>dfoxo</i> indicates the <i>dfoxo^Δ94</i>allele (<i>n = </i>35 for all genotypes). Kruskal Wallis test with Dunn's multiple comparison test (selected pairs). ***<i>p</i><0.001, **<i>p</i><0.01, and *<i>p</i><0.05. Error bars represent s.e.m. Independent experiments verifying activity and sleep phenotypes of <i>INR^DN;dfoxo</i> double mutants are shown in <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.1001824#pbio.1001824.s003" target="_blank">Figure S3</a>.</p

Rapamycin rescued age-related night sleep fragmentation in an S6K-dependent manner.

<p>(A) Rapamycin treatment (9 d) did not significantly affect day/night activity or wakefulness, but significantly increased night sleep duration, reduced night sleep fragmentation, and increased the length of night sleep periods (<i>w^Dah</i>, age 10 d, <i>n</i> = 21/20 control/rapamycin). (B) Average activity count data (30 min bins) under 12∶12 h LD. (C) Acute rapamycin treatment of 45-d-old flies for 3 d did not significantly affect day/night activity or wakefulness, but significantly increased night sleep duration, reduced night sleep fragmentation, and increased the length of night sleep periods (<i>w^Dah</i>, <i>n</i> = 64/64). Rapamycin-mediated night sleep, bout number, and bout length were independent of (D) 4E-BP (<i>n</i> = 19/19) and (E) reduced autophagy (a = <i>da-Gal4/UAS-ATG5-RNAi</i>, <i>n</i> = 20/17 or genetic controls c1 = <i>da-Gal4/+</i>, <i>n = </i>20/21 and c2 = <i>UAS-ATG5-RNAi/+</i>, <i>n</i> = 23/19). Flies with reduced autophagy responded to rapamycin as controls in sleep (<i>p</i> = 0.81), bout number (<i>p</i> = 0.82), and night bout length (<i>p</i> = 0.42) (GLM). (F) Ubiquitous expression of constitutively active S6K blocked the rescue of night sleep fragmentation by rapamycin (c1 = <i>da-Gal4/+</i>, <i>n = </i>20/21, and c2 = <i>UAS-S6K^STDETE/+</i>, <i>n = </i>20/18, <i>S6K = da-Gal4/UAS-S6K^STDETE</i>, <i>n = </i>20/17). Flies expressing a constitutively active form of S6K significantly differed from controls in the response to rapamycin (sleep <i>p</i> = 0.01, bout number <i>p</i> = 0.03, night bout length <i>p</i> = <0.0001, GLM). Kruskal Wallis test with Dunn's multiple comparisons of selected pairs. ***<i>p</i><0.001, **<i>p</i><0.01, and *<i>p</i><0.05. Error bars represent s.e.m. Day behaviours of (D–F) are shown in <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.1001824#pbio.1001824.s006" target="_blank">Figure S6B–D</a>.</p