Danbury’s Fire Bug of the 1880s and 1890s

The Connecticut State Firemen’s Association, which was formed in 1885, reported that incendiarism was an increasing problem around Connecticut, but Danbury’s fire bug of the 1880s and 1990s was extraordinary. The fire bug caused the modern equivalent of tens of millions of dollars in damage around Danbury and many of the fires were in such close proximity that there was an area dubbed to be the Firebug District. The fire bug was elusive to Danbury’s police, and by 1891, with three years yielding no real suspect, authorities hired an operative from Pinkerton\u27s National Detective Agency. The Pinkerton operative’s investigation ultimately led to no arrests, though after his investigation there were significantly fewer incendiary fires reported and, except for a couple of fires in 1893, none in the press attributed to a fire bug. While there was no single culprit or group that was indicted for Danbury’s rash of fires during this period, the fire bug episode was the byproduct and confluence of the political, labor, and ethnic unrest that was playing out on a local and national level. Moreover, the episode punctuated Danbury’s difficult transition both in name and nature to becoming a city. In the middle of these fiery expressions was Morris Meyers, the first Chief of the City of Danbury’s paid fire department; Meyers was a successful Democrat and a German Jewish immigrant whose important place in the new city government was the embodiment of a shift in the composition of the electorate

Further Expansion of the Archivists\u27 Toolkit into the ATReference

The open-sourced Archivists\u27 Toolkit developed to streamline archival work-flows has seen the development of a patron registration module. This added development is called the ATReference and it is now available to archives from its developers at the Rockefeller Archive Center

An Optical-based Aggregate Approach to Measuring Condensation Heat Transfer

Condensation heat transfer is significant in many applications such as such as desalination, energy conversion [1], atmospheric water harvesting [2, 3], electronics cooling, and other high heat flux applications [4]. However, condensate on the surface adds a thermal resistance that limits condensation rates. The rate of condensation heat transfer is inversely proportional to the diameter of the condensate drops [5]. In industrial condensing systems, the resistance is minimized by removing the condensate via gravity or a vapor shear, but the minimum size of droplet removal is typically on the order of the capillary length of the condensate, about 2.7 mm for water

Micropatterned Cell–Cell Interactions Enable Functional Encapsulation of Primary Hepatocytes in Hydrogel Microtissues

Drug-induced liver injury is a major cause of drug development failures and postmarket withdrawals. In vitro models that incorporate primary hepatocytes have been shown to be more predictive than model systems which rely on liver microsomes or hepatocellular carcinoma cell lines. Methods to phenotypically stabilize primary hepatocytes ex vivo often rely on mimicry of hepatic microenvironmental cues such as cell–cell interactions and cell–matrix interactions. In this work, we sought to incorporate phenotypically stable hepatocytes into three-dimensional (3D) microtissues, which, in turn, could be deployed in drug-screening platforms such as multiwell plates and diverse organ-on-a-chip devices. We first utilize micropatterning on collagen I to specify cell–cell interactions in two-dimensions, followed by collagenase digestion to produce well-controlled aggregates for 3D encapsulation in polyethylene glycol (PEG) diacrylate. Using this approach, we examined the influence of homotypic hepatocyte interactions and composition of the encapsulating hydrogel, and achieved the maintenance of liver-specific function for over 50 days. Optimally preaggregated structures were subsequently encapsulated using a microfluidic droplet-generator to produce 3D microtissues. Interactions of engineered hepatic microtissues with drugs was characterized by flow cytometry, and yielded both induction of P450 enzymes in response to prototypic small molecules and drug–drug interactions that give rise to hepatotoxicity. Collectively, this study establishes a pipeline for the manufacturing of 3D hepatic microtissues that exhibit stabilized liver-specific functions and can be incorporated into a wide array of emerging drug development platforms.National Institutes of Health (U.S.) (Grant UH2 EB017103)National Institutes of Health (U.S.) (Grant R01 EB008396)National Institutes of Health (U.S.) (Grant R01 DK85713)National Cancer Institute (U.S.) (Koch Institute Support (Core) Grant P30-CA14051)American Gastroenterological Association (Research Scholar Fellowship)National Science Foundation (U.S.). Graduate Research Fellowship (1122374

Non-equilibrium dynamics and floral trait interactions shape extant angiosperm diversity.

Why are some traits and trait combinations exceptionally common across the tree of life, whereas others are vanishingly rare? The distribution of trait diversity across a clade at any time depends on the ancestral state of the clade, the rate at which new phenotypes evolve, the differences in speciation and extinction rates across lineages, and whether an equilibrium has been reached. Here we examine the role of transition rates, differential diversification (speciation minus extinction) and non-equilibrium dynamics on the evolutionary history of angiosperms, a clade well known for the abundance of some trait combinations and the rarity of others. Our analysis reveals that three character states (corolla present, bilateral symmetry, reduced stamen number) act synergistically as a key innovation, doubling diversification rates for lineages in which this combination occurs. However, this combination is currently less common than predicted at equilibrium because the individual characters evolve infrequently. Simulations suggest that angiosperms will remain far from the equilibrium frequencies of character states well into the future. Such non-equilibrium dynamics may be common when major innovations evolve rarely, allowing lineages with ancestral forms to persist, and even outnumber those with diversification-enhancing states, for tens of millions of years

Increased brain white matter axial diffusivity associated with fatigue, pain and hyperalgesia in Gulf War illness

Background Gulf War exposures in 1990 and 1991 have caused 25% to 30% of deployed personnel to develop a syndrome of chronic fatigue, pain, hyperalgesia, cognitive and affective dysfunction. Methods Gulf War veterans (n = 31) and sedentary veteran and civilian controls (n = 20) completed fMRI scans for diffusion tensor imaging. A combination of dolorimetry, subjective reports of pain and fatigue were correlated to white matter diffusivity properties to identify tracts associated with symptom constructs. Results Gulf War Illness subjects had significantly correlated fatigue, pain, hyperalgesia, and increased axial diffusivity in the right inferior fronto-occipital fasciculus. ROC generated thresholds and subsequent binary regression analysis predicted CMI classification based upon axial diffusivity in the right inferior fronto-occipital fasciculus. These correlates were absent for controls in dichotomous regression analysis. Conclusion The right inferior fronto-occipital fasciculus may be a potential biomarker for Gulf War Illness. This tract links cortical regions involved in fatigue, pain, emotional and reward processing, and the right ventral attention network in cognition. The axonal neuropathological mechanism(s) explaining increased axial diffusivity may account for the most prominent symptoms of Gulf War Illness

Histone H3K36 methylation regulates pre-mRNA splicing in Saccharomyces cerevisiae

Co-transcriptional splicing takes place in the context of a highly dynamic chromatin architecture, yet the role of chromatin restructuring in coordinating transcription with RNA splicing has not been fully resolved. To further define the contribution of histone modifications to pre-mRNA splicing in Saccharomyces cerevisiae, we probed a library of histone point mutants using a reporter to monitor pre-mRNA splicing. We found that mutation of H3 lysine 36 (H3K36) – a residue methylated by Set2 during transcription elongation – exhibited phenotypes similar to those of pre-mRNA splicing mutants. We identified genetic interactions between genes encoding RNA splicing factors and genes encoding the H3K36 methyltransferase Set2 and the demethylase Jhd1 as well as point mutations of H3K36 that block methylation. Consistent with the genetic interactions, deletion of SET2, mutations modifying the catalytic activity of Set2 or H3K36 point mutations significantly altered expression of our reporter and reduced splicing of endogenous introns. These effects were dependent on the association of Set2 with RNA polymerase II and H3K36 dimethylation. Additionally, we found that deletion of SET2 reduces the association of the U2 and U5 snRNPs with chromatin. Thus, our study provides the first evidence that H3K36 methylation plays a role in co-transcriptional RNA splicing in yeast