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The Johns Hopkins University Applied Physics Laboratory (APL) in Laurel, Maryland, USA, has established a center of excellence to guide major advances in additive manufacturing (AM). The center will initially focus on significant technical challenges that are currently preventing more widespread adoption of additive manufacturing technologies in the Defense Department and also on topics of interest to the intelligence community. Other future initiatives will include printed microelectronics and bioprinting. ‘For many years, we have been at the forefront of advanced manufacturing technology,’ said Jim Schatz, who leads APL’s research and exploratory development department. ‘The investments we are making in additive manufacturing will place us among the leaders in this area nationally, and allow us to rapidly develop and deliver game-changing capabilities to our government sponsors.’ The lab plans to invest in additional powder bed fusion and hybrid additive-subtractive systems. The center will engage in the following activities: This story uses material from Johns Hopkins University Applied Physics Laboratory, with editorial changes made by Materials Today. The views expressed in this article do not necessarily represent those of Elsevier.


Treeshrews or tree shrews or banxrings – technically called scandentians – are long-tailed, long-nosed, omnivorous mammals that inhabit the forests of southern and southeastern Asia. They superficially recall squirrels, are typically regarded as such by many people who inhabit the places where they occur, and were described as squirrels when first encountered by Europeans during the late 1700s. Mammalogist Louise Emmons has even said that the name ‘squirrelshrews’ might have been a better one than ‘treeshrews’ (Emmons 2000). Until recently, very little was known of treeshrew biology, ecology or behaviour. This situation has improved considerably since about 2000. We know that treeshrews are skittish, highly alert animals, that they exhibit hardly any sexual dimorphism, and that females practise ‘absentee care’: they spend hardly any time with their babies, visiting the nursery nests only on alternate days. They only give birth to one or two babies, and these have giant stomachs (to deal with intermittent milk meals) and are also able to thermoregulate in the absence of a parent. Treeshrews are also now known to be highly vocal. Conspicuous acoustic differences exist between species, often between populations that look alike but are suspected to represent distinct phylogenetic units (or… species) (Esser et al. 2008). Arboreal and scansorial treeshrews have hands and feet well adapted for grasping. For this reason, they’ve been used as model organisms in discussions of early primate evolution, though experts have disagreed as to whether treeshrews or opossums make the better proto-primate models (Lemelin 1999, Sargis 2002, 2004, Schmitt & Lemelin 2002). Whatever, grasping like that seen in the living arboreal Pentail treeshrew Ptilocercus lowii was very probably ancestral for the clade that includes primates, treeshrews and their kin: the euarchontans. Despite the common name, not all of the 20 or so living treeshrew species are tree-dwellers. Many are terrestrial, despite a postcranial anatomy which evidences a climbing ancestry. Indeed, the group as a whole encompasses more diversity than typically imagined. An amazing 120 species and subspecies have been named since 1820. While these aren’t all recognised as valid today, you can still appreciate how much the many treeshrew taxa differ thanks to the various illustrations used here: there’s substantial variation in body shape, skull form, snout length, pelage and ecology. Treeshrews: where in the placental family tree? Traditionally, treeshrews were regarded as members of Insectivora, this being due both to their highly superficial similarity to shrews, and to the idea that Insectivora should serve as a catch-all group for a poorly defined, amorphous group of placentals that lack the specialisations of other lineages. During the 1920s, Wilfred Le Gros Clark and Albertina Carlsson made it obvious that treeshrews share anatomical characters with Primates (Huxley had also noted this connection in 1872), and this eventually led to the proposal that they should be removed from Insectivora and placed within that group (Simpson 1945, Sargis 2004). However, treeshrews are so different from classic primates – and so obviously outside the clade that includes all ‘true’ primates fossil and living – that the idea of distinct, ordinal status became increasingly popular from the 1960s onwards (Van Valen 1965, McKenna 1966, Szalay 1968). Today they are universally identified as the isolated group Scandentia*. Bony features used to unite Scandentia mostly concern details of braincase vasculature but fusion of the scaphoid and lunate in the wrist also appears distinctive (Silcox et al. 2005). * Not to be confused with the fossil lizard Scandensia. Treeshrews might not be part of Primates, but they do share anatomical characters (in the skeleton and in numerous organ systems) with primates as well as with the so-called flying lemurs (Dermoptera). The idea that they’re part of the placental group Euarchonta is therefore universally accepted… more or less (read on). Some molecular studies suggest an especially close relationship between treeshrews and flying lemurs (Murphy et al. 2001, Olson et al. 2005, Springer et al. 2007, Prasad et al. 2008, Asher et al. 2009). This hypothesis has become quite popular and the clade that contains the two has been termed Sundatheria (Olson et al. 2005) or Paraprimates (Springer et al. 2007). ‘Sundatheria’ refers to the idea that these mammals are strongly associated with Sundaland, the biogeographical region that incorporates Borneo, Sumatra, peninsula Malaysia and the adjacent continental shelf region that would have been exposed during times of low sea level. Other studies do not support this proposal, however, and instead find treeshrews to be closest to Primates (Wible & Covert 1987, Kay et al. 1992), or find dermopterans to be the closest kin of primates (Janeka et al. 2007). A real surprise is provided by Meredith et al.’s (2011) conclusion – based on a molecular supermatrix – that treeshrews are not part of Euarchonta at all but are instead the sister-group to Glires. I’m very sceptical of this proposal. It’s not impossible but it contradicts so many other studies that emphasise the primate-like anatomy and genetics of these animals. Treeshrew diversity. About 20 extant treeshrew species are currently recognised, classified in five genera. Four of these (Anathana, Dendrogale, Tupaia and Urogale) are included together within Tupaiidae. Tupaia contains the greatest number of species (c 15) though there have been suggestions from both molecular and morphological data that Tupaia is not monophyletic, some species being closer to Urogale and perhaps Anathana than to the remainder of Tupaia (Olson et al. 2004, 2005, Roberts et al. 2011). Some authors suggest lumping Urogale and Anathana into Tupaia; others suggest the recognition of Lyonogale for species currently included within Tupaia… The final taxon – the Pen-tailed treeshrew or Pentail treeshrew Ptilocercus lowii – differs enough from the others in anatomy, ecology and behaviour that it’s typically considered worthy of its own ‘family’, Ptilocercidae. Ptilocercus is nectarivorous (regularly consuming a substantial portion of nectar that has fermented to alcohol) and has a tail that combines an essentially naked shaft and a bushy tip. A tail of this sort is elsewhere only seen in gliders. Ptilocercus has especially prominent, silvery eyeshine and is thought to have excellent night vision (Emmons 2000). Its eyeshine can in fact be seen from tens of metres away – Emmons (2000) said that, once she knew what to look for, these apparently rare animals proved rather numerous. Treeshrews as a whole have excellent visual acuity. Ptilocercus is universally regarded as being more similar to the ancestral scandentian in ecology and morphology than tupaiids (Olson et al. 2004). The fossil treeshrews. All known fossil members of this group come from southern Asia: a number of Paleogene placentals from Europe, Asia and North America (including Tupaiodon, Adapisoriculus, Litolestes and Anagale) have been suggested at times to have scandentian affinities but all are now placed elsewhere in placental phylogeny. They’re variously erinaceomorphs, possible lipotyphlans or members of Glires. More confidently identified fossil members of Scandentia are known from the Middle Eocene onwards if Eodendrogale (known only from teeth) is correctly identified. These teeth are very similar to those of the living smooth-tailed tree shrews (Dendrogale). Other fossil scandentians from the Miocene and Pliocene are also highly similar to living taxa. They include extinct species of Tupaia from China and Thailand as well as the wholly extinct Prodendrogale and Palaeotupaia (Ni & Qiu 2012). The pattern of treeshrew evolution. Roberts et al. (2011) argued on the basis of molecular phylogeny that treeshrew diversification began as early as the Paleocene but that the majority of lineages evolved within the last 20 million years. Seeing as there are many species on islands, it’s likely that ancient landbridges and changing sea levels were important in influencing treeshrew distribution across their southeast Asian range. In fact, the history of the group must have been complicated, involving numerous different dispersal and vicariance-driven events. Some species are widespread and occur on landmasses that have been separated for some considerable time (e.g., T. minor: it occurs on Sumatra, Borneo, Thailand and Malaysia), others are island endemics (e.g., T. nicobarica, T. moellendorffi). I might come back to treeshrew distribution and biogeography at a future date as there’s a lot to be said. This article is but a brief introduction to this group. With this in place, it will prove easier to future to provide more detailed discussions of various of the treeshrew lineages and species. For previous Tet Zoo articles on euarchontans, see... Asher, R. J., Bennett, N. & Lehmann, T. 2009. The new framework for understanding placental mammal evolution. BioEssays 31, 853-864. Esser, D., Schehka, S. & Zimmermann, E. 2008. Species-specificity in communication calls of tree shrews (Tupaia: Scandentia). Journal of Mammalogy 89, 1456-1463. Janeka, J. E., Miller, W., Pringle, T. H., Wiens, F., Zitzmann, A., Helgen, K. M., Springer, M. S. & Murphy, W. J. 2007. Molecular and genomic data identify the closest living relative of Primates. Science 318, 792-794. Kay, R. F., Thewissen, J. G. M. & Yoder, A. D. 1992. Cranial anatomy of Ignacius graybullianus and the affinities of the Plesiadapiformes. American Journal of Physical Anthropology 89, 477-498. Lemelin, P. 1999. Morphological correlates of substrate use in didelphid marsupials: implications for primate origins. Journal of Zoology 247, 165-175. McKenna, M. C. 1966. Paleontology and the origin of Primates. Folia Primatologica 4, 1-25. Meredith, R. W., Janeka, J. E., Gatesy, J., Ryder, O. A., Fisher, C. A., Teeling, E. C., Goodbla, A., Eizirik, E., Simão, T. L., Stadler, T., Rabosky, D. L., Honeycutt, R. L., Flynn, J. J., Ingram, C. M., Steiner, C., Williams, T. L., Robinson, T. J., Burk-Herrick, A., Westerman, M., Ayoub, N. A., Springer, M. S. & Murphy, W. J. 2011. Impacts of the Cretaceous Terrestrial Revolution and KPg extinction on mammal diversification. Science 334, 521-524. Murphy, W. J., Eizirik, E., O’Brien, S. J., Madsen, O., Scally, M., Douady, C. J., Teeling, E. C., Ryder, O. A., Stanhope, M. J., de Jong, W. W. & Springer, M. S. 2001. Resolution of the early placental mammal radiation using Bayesian phylogenetics. Science 294, 2348-2351. Olson, L. E., Sargis, E. J. & Martin, R. D. 2004. Phylogenetic relationships among treeshrews (Scandentia): a review and critique of the morphological evidence. Journal of Mammalian Evolution 11, 49-71. Olson, L. E., Sargis, E. J. & Martin, R. D. 2005. Intraordinal phylogenetics of treeshrews (Mammalia: Scandentia) based on evidence from the mitochondrial 12S rRNA gene. Molecular Phylogenetics and Evolution 35, 656-673. Prasad, A. B. Allard, M. W., NISC Comparative Sequencing Program & Green, E. D. 2008. Confirming the phylogeny of mammals by use of large comparative sequence data sets. Molecular Biology and Evolution 25, 1795-1808. Roberts, T. E., Lanier, H. C., Sargis, E. J. & Olson, L. E. 2011. Molecular phylogeny of treeshrews (Mammalia: Scandentia) and the timescale of diversification in Southeast Asia. Molecular Phylogenetics and Evolution 60, 358-372. Sargis, E. J. 2004. New views on tree shrews: the role of tupaiids in primate supraordinal relationships. Evolutionary Anthropology 13, 56-66. Schmitt, D. & Lemelin, P. 2002. Origins of primate locomotion: gait mechanics of the Woolly opossum. American Journal of Physical Anthropology 118, 231-238. Silcox, M. T., Bloch, J. I., Sargis, E. J. & Boyer, D. M. 2005. Euarchonta (Dermoptera, Scandentia, Primates). In Rose, K. D. & Archibald, J. D. (eds) The Rise of Placental Mammals: Origins and Relationships of the Major Extant Clades. The Johns Hopkins University Press, Baltimore and London, pp. 127-144. Simpson, G. G. 1945. The principles of classification and a classification of mammals. Bulletin of the American Museum of Natural History 85, 1-350. Springer, M. S., Murphy, W. J., Eizirik, E., Madsen, O., Scally, M., Douady, C. J., Teeling, E. C., Stanhope, M. J., de Jong, W. W. & O’Brien, S. J. 2007. A molecular classification for the living orders of placental mammals of the phylogenetic placement of primates. In Ravosa, M. J. & Dagosto, M. (eds) Primate Origins: Adaptations and Evolution. Springer, New York, pp. 1-28.


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Fruit fly windpipes are much more like human blood vessels than the entryway to human lungs. To create that intricate network, fly embryonic cells must sprout “fingers” and crawl into place. Now researchers at The Johns Hopkins University have discovered that a protein called Mipp1 is key to cells’ ability to grow these fingers. A summary of the research, which has implications for understanding normal and abnormal development of human and other animal tissues, was published online on Nov. 25 in the journal Cell Reports. “Fruit flies don’t have blood to bring oxygen to their cells,” said Deborah Andrew, Ph.D., professor of cell biology at the Johns Hopkins University School of Medicine. “Instead, the tubes of the windpipe, or trachea, branch out repeatedly, getting thinner and thinner — like the tiny capillary blood vessels throughout our bodies — so that oxygen can diffuse directly from the trachea to nearby tissue.” Fruit flies are a research animal favorite among biologists because their genes and chemistry are relatively easy to manipulate, and because they can be easily and quickly bred. And since evolution highly conserves key biological events, what is learned in flies can shed light on the development of many species, including humans, Andrew notes. Andrew said two major ducts of the embryonic fruit fly trachea run parallel to each other along the length of the embryo. From these wide “dorsal trunks,” several thinner branches split off and grow toward the top of the embryo until they meet and merge in the middle, forming a contiguous network. Before and after elongating, the dorsal branches are just six interconnected cells. They start off stacked three high and wrapped around the thin tube connected to the dorsal trunk. In order to elongate the tube, the cells at the top grow fingerlike structures called filopodia that reach out and pull the cells away from the dorsal trunk. At the same time, the cells rearrange themselves to form a structure six cells high. “A few years ago, we discovered that in developing fly embryos, the protein Mipp1 is controlled by the master regulator gene that orchestrates all of tracheal development,” said Yim Ling Cheng, Ph.D., a cell biology postdoctoral fellow at the Johns Hopkins University School of Medicine and the primary author of the paper. At that point, the researchers knew that Mipp1 was an enzyme responsible for turning the molecule IP6 into IP3 ¬— two different chemical messengers — by breaking off three phosphate groups. They wanted to know why Mipp1 was in the trachea. By tracking its location in the trachea, they found that, at first, the protein is located throughout the developing tissue. But it soon becomes concentrated in the top pair of cells in the three-cell-high dorsal branches that are about to elongate. Those are the cells that grow filopodia, and when there was too much Mipp1, the research team saw too many filopodia. Too little Mipp1 resulted in too few filopodia and branches that were slow to elongate. Wondering if Mipp1’s presence in the top cells was the cause or a result of the cells’ position, the researchers genetically manipulated the flies so that the dorsal branch cells would turn on the Mipp1 gene at random. They expected Mipp1 to then be found in the six positions of the branch at random, but instead they found that in the top two cells, it was present more than three times as frequently as in other cells. That suggests, said Andrew, that Mipp1 makes cells more likely to climb to the top, where they are needed to elongate the branches. The team learned from further experiments that Mipp1 decorates the outside edge — not the interiors — of the top cells in the tracheal branches, where it converts IP6 into IP3, but they wonder how exactly that influences finger growth. They hope to find out in their ongoing experiments.


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Working with human breast cancer cells and mice, scientists at The Johns Hopkins University say new experiments explain how certain cancer stem cells thrive in low oxygen conditions. Proliferation of such cells, which tend to resist chemotherapy and help tumors spread, are considered a major roadblock to successful cancer treatment. The new research, suggesting that low-oxygen conditions spur growth through the same chain of biochemical events in both embryonic stem cells and breast cancer stem cells, could offer a path through that roadblock, the investigators say. “There are still many questions left to answer but we now know that oxygen poor environments, like those often found in advanced human breast cancers serve as nurseries for the birth of cancer stem cells,” said Gregg Semenza, M.D., Ph.D., the C. Michael Armstrong Professor of Medicine and a member of the Johns Hopkins Kimmel Cancer Center. “That gives us a few more possible targets for drugs that diminish their threat in human cancer.” A summary of the findings was published online March 21 in the Proceedings of the National Academy of Sciences. Semenza said scientists have long known that low oxygen environments affect tumor growth, but, in the case of advanced tumors, there was a paradox. “Aggressive cancers contain regions where the cancer cells are starved for oxygen and die off, yet patients with these tumors generally have the worst outcome. Our new findings tell us that low oxygen conditions actually encourage certain cancer stem cells to multiply through the same mechanism used by embryonic stem cells.” All stem cells are immature cells known for their ability to multiply indefinitely and give rise to progenitor cells that mature into specific cell types that populate the body’s tissues during embryonic development. They also replenish tissues throughout the life of an organism. But stem cells found in tumors use those same attributes and twist them to maintain and enhance the survival of cancers. According to Semenza, “Chemotherapy may kill more than 99 percent of the cancer cells in a tumor but fail to kill a small population of cancer stem cells that are responsible for subsequent cancer relapse and metastasis.” “The search has been intense to find these cells’ Achilles’ heel. If we could get cancer stem cells to abandon their stem cell state, they would no longer have the power to keep repopulating tumors,” said Semenza, who also directs the Vascular Biology Research Program at the Institute for Cell Engineering. Aiding their new research, Semenza said, was the knowledge that whereas the air we breathe is 21 percent oxygen, oxygen levels average around 9 percent in healthy human breast tissue but only 1.4 percent in breast tumors. Recent studies showed that low oxygen conditions increase levels of a family of proteins known as HIFs, or hypoxia-inducible factors, that turn on hundreds of genes, including one called NANOG that instructs cells to become stem cells. Studies of embryonic stem cells revealed that NANOG protein levels can be lowered by a chemical process known as methylation, which involves putting a methyl group chemical tag on a protein’s messenger RNA (mRNA) precursor. Semenza said methylation leads to the destruction of NANOG’s mRNA so that no protein is made, which in turn causes the embryonic stem cells to abandon their stem cell state and mature into different cell types. To see whether cancer stem cell renewal involves a chain of events similar to that used by embryonic stem cells, and whether the process was affected by oxygen levels, Semenza and graduate student Chuanzhao Zhang focused their studies on two human breast cancer cell lines that responded to low oxygen by ramping up production of the protein ALKBH5, which removes methyl groups from mRNAs. (Breast cancer is categorized and treated based on the presence or absence of three hormone receptors displayed on the outer membranes of cells. One human cell line they studied displays the receptors for estrogen and progesterone, and one, known as triple negative, displays none.) Zeroing in on NANOG, the scientists found that low oxygen conditions increased NANOG’s mRNA levels through the action of HIF proteins, which turned on the gene for ALKBH5, which decreased the methylation and subsequent destruction of NANOG’s mRNA. When they prevented the cells from making ALKBH5, NANOG levels and the number of cancer stem cells decreased. When the researchers manipulated the cell’s genetics to increase levels of ALKBH5 without exposing them to low oxygen, they found this also decreased methylation of NANOG mRNA and increased the numbers of breast cancer stem cells. Finally, using live mice, the scientists injected 1,000 triple-negative breast cancer cells into their mammary fat pads, where the mouse version of breast cancer forms. Unaltered cells created tumors in all seven mice injected with such cells, but when cells missing ALKBH5 were used, they caused tumors in only 43 percent (six out of 14) of mice. “That confirmed for us that ALKBH5 helps preserve cancer stem cells and their tumor-forming abilities,” Semenza said. Semenza said his team will continue its mouse studies to see if metastasis — the spread of cancer from the original tumor — is affected by the low oxygen/ALKBH5/NANOG relationship too. The researchers also want to see what other proteins and mRNAs are involved in the relationship, and why some cancer cell lines they tested did not show the same increased ALKBH5 levels in response to low oxygen levels.


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Now, that chemical biologist and his colleagues at the Johns Hopkins University School of Medicine report that tests of triptolide in human cells and mice are vastly improved by the chemical attachment of glucose to the triptolide molecule. The chemical add-on makes the molecule more soluble and essentially turns it into a "cruise missile" that preferentially seeks out cancer cells, the research says. The change might also decrease side effects in patients and make the drug easier to administer. A summary of the research is published in the journal Angewandte Chemie and was published online on Aug. 30. "We have a long way to go before we can test this derivative of triptolide in humans, and we think that additional adjustments could improve it even more," says Jun O. Liu, Ph.D., professor of pharmacology and molecular sciences at the Johns Hopkins University School of Medicine and a member of the Johns Hopkins Kimmel Cancer Center, "but it already has the key characteristics we've been looking for: It is quite water soluble, and it prefers cancer cells over healthy cells." Liu, a native of a small town north of Shanghai in China, explains that the thunder god vine has been used in traditional Chinese medicine for more than 400 years, mostly to calm an overactive immune system, which can cause diseases like rheumatoid arthritis and multiple sclerosis. His laboratory specializes in figuring out how natural compounds with known healing properties exert their effects on human cells. Five years ago, he and his colleagues discovered that triptolide halts cell growth by interfering with the protein XPB, part of the large protein machine transcription factor IIH, which, in turn, is needed by enzyme complex RNA polymerase II to make mRNA. Because triptolide halts cell growth, it works well to fight the multiplication of cancer cells, Liu says, both in lab-grown cells and in laboratory animals with cancer. Unfortunately, it—and many of its derivatives—has failed to work well in patients because it doesn't dissolve well in water or blood, and has too many side effects due to its indiscriminate killing of healthy cells as well as tumor cells. Liu's latest research sought to "train" triptolide to target cancer cells by exploiting the knowledge that most cancer cells make extra copies of proteins, called glucose transporters. Those transporters form tunnels through a cell's membrane to import enough glucose to fuel rapid growth. By attaching glucose to triptolide, the researchers hoped to trick the cancer cells into importing the cell-killing poison, as had been done successfully with other anticancer drugs. "We were looking for something that could be administered intravenously, remain stable in the blood and then become active as soon as it was imported into cancer cells," says Liu. To begin, the chemists designed and synthesized five derivatives of triptolide, dubbed glutriptolides. Each derivative had glucose attached to the same spot on the triptolide molecule but had different "linkers" connecting them. An initial experiment showed that none of the glutriptolides were good at blocking the activity of purified transcription factor IIH. Liu explains that what might seem like bad news was actually a positive result, since it suggested that the drugs would only be active once they entered cells and had their glucose attachments removed. When the five glutriptolides were tested on human embryonic kidney cells, glutriptolide 2 slowed down cell growth better than the rest and is the only derivative they continued to study. In later test tube and cell experiments, the researchers confirmed that glutriptolide 2 works just like triptolide—by interfering with XPB—though it does so only in higher concentrations. They also showed that a cancer cell line (DLD1-Mut) known to produce lots of glucose transporter 1 was more sensitive to glutriptolide 2's effects than a similar cell line (DLD1-WT) without extra copies of the transporter. When the researchers assessed triptolide's effects on a variety of healthy cells and cancer cells in parallel with glutriptolide 2, they found that triptolide tended to equally slow the growth of healthy cells and cancer cells, while glutriptolide 2 was eight times more effective against cancer cells, on average. Liu says this result suggests that the new compound—if tested in humans—may be more selective against cancer cells and could therefore have fewer side effects. Finally, due to the differences in the compounds' general toxicity, tests showed that mice could tolerate a dose of 0.2 milligram/kilogram of triptolide and 1 milligram/kilogram of glutriptolide 2. At those doses, glutriptolide 2 eradicated tumors more quickly in mice with prostate cancer and prevented tumor cells from reappearing for a full three weeks after treatment had stopped. "We were totally surprised to see that sustained antitumor activity," says Liu. "It's something we want to study further." The group plans to test additional modifications to the biochemical links that connect glucose to triptolide to see if it can further decrease the compound's toxicity to healthy cells and increase its effectiveness against cancerous ones. The work was accomplished through a close international collaboration among three research groups led by Liu, Martin Pomper of the Johns Hopkins University School of Medicine and Biao Yu of the Chinese Academy of Sciences. Other authors of the report include Qing-Li He, Il Minn, Sarah Head and Emmanuel Datan of the Johns Hopkins University School of Medicine, and Qiaoling Wang and Peng Xu of the Shanghai Institute of Organic Chemistry at the Chinese Academy of Sciences. This work was supported by a Synergy Award from the Johns Hopkins University School of Medicine and the Johns Hopkins Institute for Clinical and Translational Research, which is funded in part by the National Center for Advancing Translational Sciences (UL1 TR 001079). A nondisclosure agreement for the invention/technology described in this publication has been executed between The Johns Hopkins University and Rapafusyn Pharmaceuticals Inc. Dr. Liu is a co-founder of and a Scientific Advisory Board Member for Rapafusyn Pharmaceuticals Inc. This arrangement has been reviewed and approved by The Johns Hopkins University in accordance with its conflict of interest policies. More information: Qing-Li He et al, Targeted Delivery and Sustained Antitumor Activity of Triptolide through Glucose Conjugation, Angewandte Chemie International Edition (2016). DOI: 10.1002/anie.201606121

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