The kitchen and dining area at 32 Dunns Tce, Scarborough.“The minute you open the front door your eyes are taken straight across the kitchen, lounge and dining area, and you notice this huge expanse of height, due to the cantilevered ceiling. “It allows so much light into the space and it gives a dramatic sense of space and design.”More from newsLand grab sees 12 Sandstone Lakes homesites sell in a week21 Jun 2020Tropical haven walking distance from the surf9 Oct 2019The layout of the home means all the living areas and the master bedroom are on the ground floor. A media room is tucked away at the front of the home and the open-plan living, dining and kitchen area flows out to the back patio. The home at 32 Dunns Tce, Scarborough.THIS contemporary executive home is new to the market in Scarborough. The property at 32 Dunns Tce is within strolling distance of Queens Beach. It is the work of small residential developer SixBuilt. Rachel Eglington from SixBuilt said when it came to the design for the house, they opted for an open-plan layout with plenty of natural light, multiple living areas and four bedrooms. “We wanted to create a modern building with a few edgy elements to give the area an alternate option to the current house designs available,” she said. The floorplan of 32 Dunns Tce, Scarborough. The front balcony at 32 Dunns Tce, Scarborough.“The home would suit a family with teenagers or slightly older children, executives and older couples that want a single floor style of living, with extra bedrooms upstairs for visitors, children or grandchildren.” The property is being marketed by Stephan Siegfried and Johanne Fenton of One Agency Redcliffe for $869,000. One of the bedrooms at 32 Dunns Tce, Scarborough.The kitchen has an island bench, stone countertops, stainless-steel appliances and pendant lighting. The master bedroom has a walk-in robe, ensuite and patio access. Upstairs, the three remaining bedrooms have built-in robes and two have access to the balcony. “The whole house has great use of natural light and well-designed spaces, and is in an excellent location — it’s close to the beach, shops, restaurants and fabulous proximity to schools,” Ms Eglington said.
Latvian telco Lattelecom could cease to carry Modern Times Group-owned channel TV3 at the end of this month unless an increasingly bitter dispute over carriage fees between the pair is resolved.Lattelecom has said it may pull the channel unless MTG modifies its terms. It has accused the Scandinavian programming group of dramatically increasing its price, forcing Lattelecom to pay over €1 million a year for the channel.The telco has accused MTG of “aggressive commercial practices” and abuse of its dominant position in the country’s TV market, in which MTG holds a share of about 35%.MTG in turn has counter-argued that Lattelecom’s basic package costs €9.32, while MTG is asking for less than €0.18 for carriage of the channel.Lattelecom, which is owned by the Latvian state and TeliaSonera, has appealed to the country’s competition regulator for redress.
Lee Jae-yong, the vice-chairman and effective head of Samsung Electronics, was arrested this morning in connection with the corruption scandal that felled South Korean president Park Geun-hye.According to local news agency Yonhap News, the Seoul Central District Court issued a warrant after prosecutors levelled additional charges against Lee, including hiding criminal proceeds and violating a law on transferring assets abroad, in a second attempt to secure his arrest. An initial request a few weeks ago had been turned down.Prosecutors allege that Lee bribed Choi Soon-sil, an associate of the president, to secure government backing for a merger between two of the consumer electronics giant’s affiliate companies.Lee has effectively been head of the company since his father Lee Kun Hee was hospitalised in 2014.Samsung strategy chief Choi Gee-sung, seen as a mentor to Lee since his father’s incapacitation, is now expected to take a leading role while the investigation continues.The court rejected a separate request for a warrant against Samsung president Park Sang-jin.Park was impeached by the Korean national assembly at the end of last year. The country’s constitutional court is currently considering whether to confirm her removal.The arrest could have an onward impact on Samsung’s organisation. In addition to the controversial merger – seen as a move to consolidate the control of the Lee family – there is speculation that moves to split the company into a holding unit and an operating unit could be put on hold.
Related StoriesNeural pathways explain the relationship between imagination and willingness to helpRush University Medical Center offers new FDA-approved treatment for brain aneurysmsAn active brain and body associated with reduced risk of dementiaIn their most recent inquiry, Tanzi, neuroscientist Ana Griciuc, PhD, and their colleagues set out to discover how CD33 and TREM2 interact, and what role that “crosstalk” might play in neuroinflammation and the origin of AD. To do that, they posed a question: What happens when these critically important genes are silenced–individually and simultaneously?To find answers, Tanzi and his team studied laboratory mice specially bred to have brain changes and behavior consistent with AD. The team began by observing and testing a strain of AD mice that had their CD33 genes turned off. They discovered that these mice had reduced levels of amyloid plaque in their brains and performed better than other AD mice on tests of learning and memory, such as finding their way in a maze. However, when mice had both CD33 and TREM2 silenced, the brain and behavior benefits disappeared–which also happened when only a single TREM2 gene was quieted. “That tells us that TREM2 is working downstream of CD33 to control neuroinflammation,” says Tanzi. That theory was bolstered by sequencing of microglia RNA, which indicated that both CD33 and TREM2 regulate neuroinflammation by increasing or decreasing activity of an immune cell called IL-1 beta and the cell receptor IL-1RN.”We are increasingly realizing that to help Alzheimer’s patients, it is most critical to stop the massive brain nerve cell death that is caused by neuroinflammation,” says Tanzi. “We now see that the CD33 and TREM2 genes are the best drug targets for achieving this goal.” Source:Massachusetts General HospitalJournal reference:Griciuc, A. et al. (2019) TREM2 Acts Downstream of CD33 in Modulating Microglial Pathology in Alzheimer’s Disease. Neuron. doi.org/10.1016/j.neuron.2019.06.010. Reviewed by Kate Anderton, B.Sc. (Editor)Jul 11 2019A new study by scientists at Massachusetts General Hospital (MGH) offers clues about how to prevent inflammation of brain tissue, which promotes Alzheimer’s disease (AD). The findings of this study online now and appearing in the September 4, 2019 print issue of the journal Neuron, could contribute to the development of new therapies for AD.It’s known that the brains of people with AD fill with deposits of damaged nerve cells and other proteins, known as amyloid plaques, as well as tangled formations of proteins called tau. “But if you just have plaques and tangles alone, you probably won’t develop Alzheimer’s disease for a long time, if at all,” says neuroscientist Rudolph E. Tanzi, PhD, director of the Genetics and Aging Research Unit at MGH, and senior author of the Neuron study. Rather, explains Tanzi, it’s the inflammation that occurs in response to plaques and tangles, or neuroinflammation, that is the primary killer of neurons, which leads to cognitive decline.Tanzi’s lab discovered the first gene associated with neuroinflammation in AD, known as CD33, in 2008. CD33 carries the genetic code for receptors found on microglia cells, which normally act as one of the brain’s housekeepers, clearing away neurological debris, including plaques and tangles. In 2013, Tanzi and colleagues published their discovery that CD33 influences the activity of microglia: When the gene is highly expressed, microglia turn from housekeepers to neuron killers, sparking neuroinflammation.Meanwhile, other investigators identified another gene, TREM2, which has the opposite effect of CD33: It shuts down microglia’s capacity to promote neuroinflammation. In other words, says Tanzi, CD33 is the “on” switch for neuroinflammation, while TREM2 acts like an “off” switch. The Holy Grail in this field has been to discover how to turn off neuroinflammation in microglia.”Rudolph E. Tanzi, PhD, director of the Genetics and Aging Research Unit at MGH
Explore further Provided by Washington University in St. Louis Like our eyes, microscopes are limited in what they can see because of their resolution, or their ability to see detail. The detail, or information, from the object is there, but some of it gets lost as the light reflecting off of the object moves through the air. It takes a village—How researchers built their own microscope to decipher ‘superbugs’ Ulugbek Kamilov, an engineer in the School of Engineering & Applied Science at Washington University in St. Louis, plans to use a three-year, $265,293 grant from the National Science Foundation to capture the information that normally gets lost and add it to the information researchers typically receive from microscopes. Ultimately, this work, along with that of his collaborator, Lei Tian at Boston University, may lead to a more precise microscope that can see objects as miniscule as 100 nanometers, such as viruses. Currently, microscopes have a resolution limit of about 500 nanometers, which allows them to see bacteria. A human hair, for instance, is 100,000 nanometers wide.”The whole premise of this is built on one single fact—the way light interacts with any matter is linear,” said Kamilov, assistant professor of electrical & systems engineering and computer science & engineering. “But the reality is that the interaction is actually not linear.”For example, if you shine a flashlight through your hand, you can’t see the source of the light because it’s bending, and that is nonlinearity. With a single cell, the bending is so light that it is nearly transparent, which is linear.When light interacts with a cell or an object, the light going out of the cell loses the information it gathers from that interaction. But because of that interaction, there are fluctuations in the vicinity of that cell that work with such matter and get retransformed and remitted. Those fluctuations are encoded into the nonlinearity of the interaction, but today’s microscopes are unable see this, Kamilov said.”We want to take into account this nonlinear interaction of light, objects and premises, and if we do it correctly, we can extract that information, which normally disappears in a current microscope and is treated as ‘noise,'” Kamilov said. “We want to decode the information from the noise and add it back into the resolution, and that should give us features that are smaller than the resolution limit.”Kamilov said there are two types of noise: imperfections and mathematical noise that is the result of science’s current limitations. It is the mathematical noise that he wants to capture.”In reality, that noise is information, and we want to use that information to break the barrier to see beyond the resolution limit,” he said.Kamilov’s collaborator, Tian, assistant professor of electrical & computer engineering, received a $250,707 grant from the NSF to build a new microscope that will use Kamilov’s computational results, algorithms and software and could be used in medical imaging, biological and material imaging, brain mapping and drug discovery. Together, the set of studies totals $516,000.Kamilov also plans to use machine learning to learn the features of the objects they are looking at with the microscope.”We want to look at the distinguishing features of cells so that when we combine them with the nonlinear measurements and fuse that information, we will be able to get higher resolution images,” he said. “We hope to get up to five times improvement.”Kamilov uses high-powered graphical processing units (GPUs) in his lab, which significantly speed the processing time. What took two days of processing on a regular computer takes just milliseconds on a GPU, he said.”This project is very timely, because we have the mathematical sophistication of signal processing, the computational tools and machine learning,” he said. “All of those things have improved together. It would have been very difficult to do this project 10 years ago.” Citation: Engineer to combine math, machine learning and signal processing to lay groundwork for high-resolution microscope (2018, June 26) retrieved 18 July 2019 from https://phys.org/news/2018-06-combine-math-machine-groundwork-high-resolution.html Engineers at Washington University in St. Louis are investigating new techniques that could lead to better, more precise microscopes. Credit: Washington University in St. Louis This document is subject to copyright. Apart from any fair dealing for the purpose of private study or research, no part may be reproduced without the written permission. The content is provided for information purposes only.
Why Do Some Animals Eat Their Own Poop? While we were migrating around the globe, inventing agriculture and visiting the moon, chimpanzees — our closest living relatives — stayed in the trees, where they ate fruit and hunted monkeys. Modern chimps have been around for longer than modern humans have (less than 1 million years compared to 300,000 for Homo sapiens, according to the most recent estimates), but we’ve been on separate evolutionary paths for 6 million or 7 million years. If we think of chimps as our cousins, our last common ancestor is like a great, great grandmother with only two living descendants. But why did one of her evolutionary offspring go on to accomplish so much more than the other? [Chimps vs. Humans: How Are We Different?] AdvertisementIs Pumpkin (Everything) Good for You?This time of year, it seems like pumpkin-flavored options are available for pretty much everything. But is all this pumpkin healthy?Volume 0%Press shift question mark to access a list of keyboard shortcutsKeyboard Shortcutsplay/pauseincrease volumedecrease volumeseek forwardsseek backwardstoggle captionstoggle fullscreenmute/unmuteseek to %SPACE↑↓→←cfm0-9关闭选项Automated Captions – en-US facebook twitter 发邮件 reddit 链接https://www.livescience.com/32503-why-havent-all-primates-evolved-into-humans.html?jwsource=cl已复制直播00:0001:3201:32 Originally published on Live Science. Lucy belongs to one of the best known early human species, Australopithecus afarensis, which lived about 3.85 million to 2.95 million years ago. Credit: Copyright Field Museum; photographer John Weinstein “The reason other primates aren’t evolving into humans is that they’re doing just fine,” Briana Pobiner, a paleoanthropologist at the Smithsonian Institute in Washington, D.C., told Live Science. All primates alive today, including mountain gorillas in Uganda, howler monkeys in the Americas, and lemurs in Madagascar, have proven that they can thrive in their natural habitats. “Evolution isn’t a progression,” said Lynne Isbell, a professor of anthropology at the University of California, Davis. “It’s about how well organisms fit into their current environments.” In the eyes of scientists who study evolution, humans aren’t “more evolved” than other primates, and we certainly haven’t won the so-called evolutionary game. While extreme adaptability lets humans manipulate very different environments to meet our needs, that ability isn’t enough to put humans at the top of the evolutionary ladder. Take, for instance, ants. “Ants are as or more successful than we are,” Isbell told Live Science. “There are so many more ants in the world than humans, and they’re well-adapted to where they’re living.” While ants haven’t developed writing (though they did invent agriculture long before we existed), they’re enormously successful insects. They just aren’t obviously excellent at all of the things humans tend to care about, which happens to be the things humans excel at. “We have this idea of the fittest being the strongest or the fastest, but all you really have to do to win the evolutionary game is survive and reproduce,” Pobiner said. Our ancestors’ divergence from ancestral chimps is a good example. While we don’t have a complete fossil record for humans or chimps, scientists have combined fossil evidence with genetic and behavioral clues gleaned from living primates to learn about the now-extinct species whose descendants would become humans and chimps. “We don’t have its remains, and I’m not sure if we’d be able to place it with certainty in the human lineage it if we did,” Isbell said. Scientists think this creature looked more like a chimpanzee than a human, and it probably spent most of its time in the canopy of forests dense enough that it could travel from tree to tree without touching the ground, Isbell said. Scientists think ancestral humans began distinguishing themselves from ancestral chimps when they started spending more time on the ground. Perhaps our ancestors were looking for food as they explored new habitats, Isbell said. “Our earliest ancestors that diverged from our common ancestor with chimpanzees would have been adept at both climbing in trees and walking on the ground,” Isbell said. It was more recently — maybe 3 million years ago — that these ancestors’ legs began to grow longer and their big toes turned forward, allowing them to become mostly full-time walkers. Why Humans Outlive Apes “Some difference in habitat selection probably would’ve been the the first notable behavioral change,” Isbell said. “To get bipedalism going, our ancestors would have gone into habitats that didn’t have closed canopies. They would have had to travel more on the ground in places where trees were more spread out.” The rest is human evolutionary history. As for the chimps, just because they stayed in the trees doesn’t mean they stopped evolving. A genetic analysis published in 2010 suggests that their ancestors split from ancestral bonobos 930,000 years ago, and that the ancestors of three living subspecies diverged 460,000 years ago. Central and eastern chimps became distinct only 93,000 years ago. “They’re clearly doing a good job at being chimps,” Pobiner said. “They’re still around, and as long as we don’t destroy their habitat, they probably will be” for many years to come. Could Evolution Ever Bring Back the Dinosaurs?
Published on A view of Visakhapatnam Railway Station. File Photo COMMENT February 28, 2019 railway SHARE Andhra Pradesh Modi to visit Vizag today The announcement of new railway zone for Andhra Pradesh by the NDA government has triggered a huge political row in the State, with the ruling Telugu Desam Party describing it as “a political ploy intended more to suit the political interests of the BJP in Odisha rather than bringing any benefit to the people of Andhra Pradesh” and the BJP leaders hotly contesting the charge.Just two days ahead of Prime Minister Narendra Modi’s visit to Visakhapatnam on Friday, Union Railway Minister Piyush Goyal made a brief statement in New Delhi late Wednesday night that the government intended to create a new railway zone, with Visakhapatnam as the headquarters.Odisha angleThe Waltair railway division will be divided to facilitate the formation of the new zone with Visakhapatnam as its headquarters. A new division will be formed at Rayagada in Odisha and some of the stations now under Waltair will be merged with that division and some of the stations in AP will be merged with the Vijayawada division.The TDP condemned the proposal outright, opposing the division of the Waltair railway division which is now under the East Coast Railway based in Bhubaneswar. Chief Minister N Chandrababu Naidu said, “The BJP has played a trick on the people of Andhra Pradesh, making the announcement two days ahead of the PM’s visit to Vizag, making it seem as though it had done a great favour to the people of AP, but actually benefiting the people of Odisha, where the BJP is trying to make inroads.”“But by the kind of artificial division of the Waltiar division the NDA government is proposing, the bulk of the revenue of the existing Waltair division will go to Odisha and the proposed new zone in AP will be left only with passenger revenue. The cream will go to Odisha and AP will be left only with the bun. It is a cheap trick played by the Modi government which is being too clever by half. People will see through the game,” Naidu said.Naidu also expressed surprise that the local BJP leaders were going gaga over “this mockery of a zone” and the YSR Congress leaders are also welcoming it. “It is one more proof that the two parties are in league and they are out to betray the people of the State,” he alleged.The TDP, the left and the Congressmen are planning to hold protest demonstrations against Prime Minister Modi in Vizag on Friday.BJP defenceTaking exception to the CM’s comments but not directly naming him, senior BJP leader and Visakhapatnam member of Parliament K Haribabu said, “We can never satisfy the doubting Thomases. They will always raise some doubt or the other. We made a promise in the BJP manifesto that a new railway zone would be formed with Vizag as headquarters. We have fulfilled the promise.”D Purandeswari, former minister in the UPA government and now in the BJP, and the sister-in-law of Naidu, also took exception to the CM’s statement.The YSR Congress leaders in general welcomed the proposal, even though there were a few dissenting voices within that party also, and the Congress leaders and Communist leaders also opposed the division of the Waltair division. These leaders termed it yet another “betrayal of the people of AP” by the Modi government. COMMENTS SHARE SHARE EMAIL