Tyrannosaurus rex was among the most fearsome carnivores to have ever lived, but this killer still had to endure an adolescent phase. Far from being awkward, however, these teenage titans managed to pack a tremendous punch prior to maturing into full-sized adults, as new research describes.

Unlike their lumbering yet undeniably powerful parents, teenage T. rex were fast and agile, equipped with teeth that were goodfor cutting, not crushing. These juveniles were able to hold their own in a perilous Cretaceous world, before entering into a growth spurt that brought them into adulthood and a new way of life.

Such are the findings of new research published in Scientific Reports, in which paleontologists analysed a pair of mid-sized T. rex skeletons found during the early 2000s. Known as Jane and Petey, these fossils were unearthed in Carter County, Montana by paleontologists from the Burpee Museum of Natural History in Rockford, Illinois.

Jane and Petey were roughly half the size of an adultT. rex, which could grow to 12 meters (40 feet) in length. Fully mature T. rexwith their 1.5-metre-long (5-foot) headswere basically gigantic chomping machines who used their powerful jaws to crush prey. Needless to say, this impressive bone-snapping ability, at an estimated 8,000 pounds of force, didnt appear until later in life. The new research is important because it shows how juvenile T. rexes survived before they developed this capacity.

Importantly, the new research could also settle a debate caused by the discovery of Jane, Petey, and other apparently mid-sized T. rex skeletons. Some paleontologists argued that these fossils didnt belong to T. rex, but rather a pygmy genus of tyrannosaurid, which they dubbed Nanotyrannus. The evidence presented in the new paper, led by Holly Woodward from the Department of Anatomy and Cell Biology at the Oklahoma State University Centre for Health Sciences, likely represents the death knell for the Nanotyrannus theory, which, to be fair, is a fringe theory to begin with.

The reason for this uncertainty and the ongoing debate, however, can be traced to the lack of juvenile dinosaur specimens.

Historically, many museums would collect the biggest, most impressive fossils of a dinosaur species for display and ignore the others, said Woodward in a press release. The problem is that those smaller fossils may be from younger animals. So, for a long while weve had large gaps in our understanding of how dinosaurs grew up, and T. rex is no exception.

Using a technique known as paleohistology, Woodward and her colleagues studied the microscopic structures embedded within the fossilized bones. Analysis of thin slices taken from the femur and tibia conveyed the specimens age, growth rate, and level of maturity.

To me, its always amazing to find that if you have something like a huge fossilized dinosaur bone, its fossilized on the microscopic level as well, said Woodward. And by comparing these fossilized microstructures to similar features found in modern bone, we know they provide clues to metabolism, growth rate, and age.

Results of the analysis showed that Jane and Petey were around 13 to 15 years old when they died, which means they had yet to experience their pre-adult growth spurt; T. rexes reached maturity at around 20 years of age, but they didnt live much beyond 30.

The new research also showed that T. rex exhibited rapid growth rates similar to modern birds and mammals, but their rate of growth was regulated by the availability of food. Variability in their growth, as evidenced by spacings the growth rings of their bones, suggests they grew quickly when food was in abundance and slowly when food was scarce.

This study helps us understand how T. rex went from a tiny baby to enormous adult, Steven Brusatte, a University of Edinburgh paleontologist not involved with the study, told Gizmodo in an email. Not only did they grow super fast, but they could change their growth rates depending on how much food and resources were available. This flexibility helped T. rex so utterly dominate its ecosystem.

And finally, the new research also shows that these pint-sized T. rexes were still a force to be reckoned with. They were sleek, slender, and fleet-footed and had wonderful knife-like teeth, said study co-author Scott Williams from the Museum of the Rockies in a press release. The new research suggests these animals probably dominated their ecosystems at all ages, he said.

Standing a bit taller than a large horse and measuring around 20 feet in length, teenage T. rexes mustve terrorised the Cretaceous landscape. It seems fitting that this iconic dinosaur, even before reaching full maturity, was already plenty deadly.

Read more from the original source:
Smaller But Still Deadly: New Insights Into The Life Of Teenage T. Rex - Gizmodo Australia

Researchers have given us a count of around 37.2 trillion cells in the human body. Each of these mammalian cells constitute a nucleus and a cell membrane.

And as revealed by cytologists, every cell is symmetrical to one another, and that there are 23 pairs of chromosomes found in most of humans. The reason behind this fascinating fact is due to the cell programming, in all probability.

As per this programming, each variety of cell strives to reach a particular, pre-determined target size; and in the process, it adjusts, readjusts itself from time to time assessing whether it has crossed or lagging behind that target. There are molecules that sense its own size and enable the human cell to maintain uniformity.

However, there are certain cells in order to carry out some specific tasks, break out of this uniformity matrix.

Johns Hopkins University School of Medicine researchers conducted on genetically engineered mice, have suggested that the cilia count is dictated by a process observed in non-mammalian species. Known to have appeared first on single-celled organisms, cilia are small hair-like, finger-like primordial structures that serve as motors sensing the environment by shifting the cell or antennae.

What makes these cells noteworthy is that while other cells create 1 cilium per cell, these advanced cells go about creating hundreds of cilia.

In an attempt to answer the burning question, how the multi-cilliated cells are so drastically different from the rest of the body cells, Andrew Holland (PhD), professor of molecular biology and genetics (at the Johns Hopkins University School of Medicine), discovered that cilias base, centriole, where organelles are attached, gets formed prior to cell division; thereby leading to 2-parent centrioles in each cell.

Deuterosomes get created by multi-cilliated cells, which serve as a copy machine.

Keeping this theory in mind, Holland conducted experiments, which surprisingly ruled out deuterosomes pivotal function in determining cilias number. His experiments also disproved the idea that centrioles absence would impact the cilias number; and showed centrioles can be created spontaneously just like in small flatworm planaria which experiences the same de novo generation of centrioles.

Upon delving deeper, Holland observed that there is an area rich with fibrogranular material in the cell, where centrioles are flocking together. It is this protein concentrated region in the cell, brimming with required elements to create centrioles, which might be responsible for ultimately determining the number of cilia getting created, suspects Holland.

In his opinion, deuterosomes act to mitigate pressure from the parent centrioles. By being free from the activity of creating new centrioles, the parent centrioles thereby get to carry out other necessary activities.

All the experiments helmed by Dr Holland, have been chronicled in Nature Cell Biology, as Dec 2.

Unearthing the mechanisms or causes governing the cilia number, can shed light on treatment of respiratory infection, infertility, hydrocephaly-- all cilia-related ailments.

Get the best of News18 delivered to your inbox - subscribe to News18 Daybreak. Follow News18.com on Twitter, Instagram, Facebook, Telegram, TikTok and on YouTube, and stay in the know with what's happening in the world around you in real time.

Visit link:
This is How Cells in the Human Body Learn How to Count - News18

Cellular origin is well explained by the endosymbiotic theory, which famously states that higher organisms called eukaryotes have evolved from more primitive single-celled organisms called prokaryotes. This theory also explains that mitochondriaenergy-producing factories of the cellare actually derived from prokaryotic bacteria, as part of a process called endosymbiosis. Biologists believe that their common ancestry is why the structure of mitochondria is conserved in eukaryotes, meaning that it is very similar across different speciesfrom the simplest to most complex organisms. Now, it is known that as cells divide, so do mitochondria, but exactly how mitochondrial division takes place remains a mystery. Is it possible that mitochondria across different multicellular organismsowing to their shared ancestrydivide in an identical manner? Considering that mitochondria are involved in some of the most crucial processes in the cell, including the maintenance of cellular metabolism, finding the answer to exactly how they replicate could spur further advancements in cell biology research.

In a new study published in Communications Biology on December 20, 2019, a group of scientists at Tokyo University of Science, led by Prof Sachihiro Matsunaga, wanted to find answers related to the origin of mitochondrial division. For their research, Prof Matsunaga and his team chose to study a type of red algathe simplest form of a eukaryote, containing only one mitochondrion. Specifically, they wanted to observe whether the machinery involved in mitochondrial replication is conserved across different species and, if so, why. Talking about the motivation for this study, Prof Matsunaga says, Mitochondria are important to cellular processes, as they supply energy for vital activities. It is established that cell division is accompanied by mitochondrial division; however, many points regarding its molecular mechanism are unclear.

This exciting new research describes how mitochondrial replication is similar in the simplest to most complex organisms, shedding light on its origin. Credit: Tokyo University of Science

The scientists first focused on an enzyme called Aurora kinase, which is known to activate several proteins involved in cell division by phosphorylating them (a well-known process in which phosphate groups are added to proteins to regulate their functions). By using techniques such as immunoblotting and kinase assays, they showed that the Aurora kinase in red algae phosphorylates a protein called dynamin, which is involved in mitochondrial division. Excited about these findings, Prof Matsunaga and his team wanted to take their research to the next level by identifying the exact sites where Aurora kinase phosphorylates dynamin, and using mass spectrometric experiments, they succeeded in identifying four such sites. Prof Matsunaga says, When we looked for proteins phosphorylated by Aurora kinase, we were surprised to find dynamin, a protein that constricts mitochondria and promotes mitochondrial division.

Having gained a little more insight into how mitochondria divide in red algae, the scientists then wondered if the process could be similar in more evolved eukaryotes, such as humans. Prof Matsunaga and his team then used a human version of Aurora kinase to see if it phosphorylates human dynaminand just as they predicted, it did. This led them to conclude that the process by which mitochondria replicate is very similar in different eukaryotic organisms. Prof Matsunaga elaborates on the findings by saying, Using biochemical in vitro assays, we showed that Aurora kinase phosphorylates dynamin in human cells. In other words, it was found that the mechanism by which Aurora kinase phosphorylates dynamin in the mitochondrion is preserved from primitive algae to humans.

Scientists have long pondered over the idea of mitochondrial division being conserved in eukaryotes. This study is the first to show not only the role of a new enzyme in mitochondrial replication but also that this process is similar in both algae and humans, hinting towards the fact that their common ancestry might have something to do with this. Prof Matsunaga concludes by talking about the potential implications of this study, Since the mitochondrial fission system found in primitive algae may be preserved in all living organisms including humans, the development of this method can make it easier to manipulate cellular activities of various organisms, as and when required.

As it turns out, we have much more in common with other species than we thought, and part of the evidence lies in our mitochondria!

Reference: Cyanidioschyzon merolae aurora kinase phosphorylates evolutionarily conserved sites on its target to regulate mitochondrial division by Shoichi Kato, Erika Okamura, Tomoko M. Matsunaga, Minami Nakayama, Yuki Kawanishi, Takako Ichinose, Atsuko H. Iwane, Takuya Sakamoto, Yuuta Imoto, Mio Ohnuma, Yuko Nomura, Hirofumi Nakagami, Haruko Kuroiwa, Tsuneyoshi Kuroiwa and Sachihiro Matsunaga, 20 December 2019, Communications Biology.DOI: 10.1038/s42003-019-0714-x

Read more here:
Breakthrough in Understanding Evolution Mitochondrial Division Conserved Across Species - SciTechDaily

How are cell towers similar to DDT, an insecticide infamous for its environmental impacts? Its a good question. On Dec. 8, about 90 local residents asked this question and many more at an event to explore the health and environmental impacts of wireless technology. As new cell towers are being proposed in the area, interest was high, with standing-room only in the Point Reyes Community Presbyterian Church.

The event was sponsored by the West Marin Alliance for Human and Environmental Health, the Point Reyes Coalition for SafeTech and the Ecological Options Network. I spoke alongside Dr. Madga Havas from Canada and Ellie Marks of the California Brain Tumor Association.

I am a physician who has studied and developed policies for environmental toxins for over 25 years. When I learned of a proposal to place a cell tower on my daughters school 10 years ago, I dove into the research. What I learned is that wireless technology and infrastructure is a broad environmental and human toxin. We use and are increasingly surrounded by these devices: cell phones, laptops, smart watches, smart meters and internet routers. Unfortunately, we are told these devices are safe, that we do not really know if there is harm or that the research is inconclusive. Myself and over 250 expert scientists who have looked at this issue conclude the opposite.

To start with, the standard set by the Federal Communications Commission is based only on a single impact: heating of the tissues. This is like a cooking standard, and it ignores other biological effects. Nature and human biology are much more complex than technology. Humans evolved over millions of years in an environment with extremely low electromagnetic radiation. Our bodies use very tiny electrical signals that communicate within a labyrinth of molecules which are critical to the proper development of a fetus and to the healthy functioning of an adult.

In medical school, I learned about only a fraction of the thousands of dizzying interactions within and between cells that regulate reproduction, energy metabolism, the immune system, the gut, the brain and the nervous system. I learned that biology is both intricate and fragile, like a symphonic orchestra in which every instrument must be played perfectly. In studying toxic exposures, I learned that there can be different mechanisms at work that cause harm to our cells and biology.

One of these mechanisms is oxidation, which, like rust, causes aging and the breakdown of DNA, proteins, lipids and other critical molecules. The insecticide DDT causes oxidation, and antioxidants we consume counter this effect. The effect of oxidation on cells has been well studied; scientific literature connects oxidative cellular harm to inflammation and human disease. This mechanism does not involve heat injury.

When non-ionizing electromagnetic radiation is emitted from wireless devices, it passes through us and is variably absorbed in our bodies. The radiation is absorbed by water and blocked by metal. Of 100 peer-reviewed articles on radio frequency radiation and oxidation, 93 studies found a positive result, or resulting damage to DNA, lipids and proteins. This is not a thermal effect; it is a biological effect.

Dozens of studies have linked wireless radiation to sperm, ovarian and embryo harm, and to miscarriage. Neurologic injury is also a worry because studies show damage to nerve cells, the alteration of neurotransmitter levels, the opening of the blood-brain barrier (with large epidemiologic studies indicating memory impairment), behavioral changes and an increase in brain cancer.

Addiction to and the overuse of wireless devices is especially problematic for children. Six studies have demonstrated brain shrinkagein white and grey matterin those addicted to electronic devices. A new article in the Journal of the American Medical Association Pediatrics showed evidence of microstructural brain changes and brain shrinkage in children age 3 to 5 years who use an electronic device more than one hour a day.

Studies on cell towers show an increase in cancer in those living within 1,500 feet of towers; other studies show an alteration in stress hormones and blood abnormalities. A significant percentage of people also report non-specific or vague health symptoms, including headaches, fatigue, dizziness, nausea and insomnia when living close to cell towers. Electro-sensitivity is a real disease and more peoplefrom 3 to 18 percentare reporting vague symptoms when they use wireless devices.

Wireless radiation can also affect the health, behavior and migration of animals. Bees appear particularly sensitive, and plants and trees are also adversely affected. Precaution on all fronts is needed with the placement of cell towers, as the radiation they emit is constant. Once a large cell tower is in place, 5G small cells will follow. Cell towers become a permanent Trojan horse.

Cindy Russell, a plastic surgeon practicing in Mountain View, is the executive director of Physicians for Safe Technology. For more information, visit MDSafeTech.org.

Read the original post:
The health impacts of cell towers - Point Reyes Light

Biological Imaging Reagents Market: Introduction

Transparency Market Research has published a new report on the biological imaging reagents market for the forecast period of20192027. According to the report, the globalbiological imaging reagents marketwas valued at ~US$ 13.5 Bnin2018and is projected to expand at a CAGR of8.5%from2019to2027.

Global Biological Imaging Reagents Market:Overview

Biological imaging reagents are substances used in research and diagnosis purposes in imaging modalities, to enhance THE visualization of internal organs and in vivo live cell imaging.

These reagents are used in different imaging modalities such as X-ray, MRI, and ultrasound for THE diagnosis of different diseases, as well as in drug discovery.

Growth of the global biological imaging reagents market can be attributed to the rise in the demand for diagnostic imaging procedures across the globe.

Asia Pacific is a highly lucrative market for biological imaging reagents, due to the improving healthcare infrastructure and increase in the geriatric population.

North America dominated the global biological imaging reagents market in2018,and the trend is projected to continue during the forecast period, due to the higher prevalence of diseases and high number of imaging procedures.

Request a Sample of Biological Imaging Reagents Market Report

https://www.transparencymarketresearch.com/sample/sample.php?flag=S&rep_id=48474

High Prevalence and Increase in Incidence Rate of Chronic Diseases to Drive Market

The prevalence of chronic diseases has increased in the past few years across the globe. These diseases include cardiovascular diseases, cancer, diabetes, and neurological disorders.

These diseases need diagnostic imaging tests. Life science reagents such as biological imaging reagents are an integral part of a large number of diagnostic imaging tests. Hence, the high prevalence of these chronic diseases and increasing research activities to discover treatments for these diseases are propelling the global biological imaging reagents market. According to WHO, cardiovascular diseases account for around17.9 milliondeaths globally every year, which constitutes an estimated31%of all deaths.

Rise in the number of diagnostic imaging procedures and increase in research activities for new drug development are the other factors driving the global market.

Moreover, the launch of new imaging reagents and approval of products for specific indications in the past few years contributed to the growth of the global biological imaging reagents market.

Nuclear Reagents to be Lucrative Option

Based on class, the global biological imaging reagents market has been classified into contrast reagents, optical reagents, and nuclear reagents.

The optical reagents segment dominated the global biological imaging reagents market in2018. However, the contrast reagents segment is anticipated to dominate the global market from2019to2027.

Nuclear reagents are expected to be a highly lucrative segment during the forecast period, owing to the better visualization effects of imaging achieved by these reagents and rise in the demand for radiopharmaceutical agents in imaging modalities

Request for a Discount on Biological Imaging Reagents Market Report -.

https://www.transparencymarketresearch.com/sample/sample.php?flag=D&rep_id=48474

Optical Imaging Dominated Global Market

In terms of modality, the global biological imaging reagents market has been categorized into MRI, ultrasound, X-ray & CT, nuclear, optical imaging, and others. The nuclear segment has been bifurcated into PET and SPECT.

The optical imaging segment dominated the global biological imaging reagents market in2018, owing to advanced technologies in optical imaging and large number of research activities on this method.

In-vivo to be Promising Application

Based on application, the global biological imaging reagents market has been bifurcated into in vitro and in vivo.

The in vitro segment has been classified into proteomics, genomics, and cell biology.

In vivo is likely to be a highly promising segment in the next few years, owing to an increase in vivo research activities by CROs for drug discovery, and growth of the biopharmaceutical industry.

About Us

Transparency Market Research is a next-generation market intelligence provider, offering fact-based solutions to business leaders, consultants, and strategy professionals.

Our reports are single-point solutions for businesses to grow, evolve, and mature. Our real-time data collection methods along with ability to track more than one million high growth niche products are aligned with your aims. The detailed and proprietary statistical models used by our analysts offer insights for making right decision in the shortest span of time. For organizations that require specific but comprehensive information we offer customized solutions through adhoc reports. These requests are delivered with the perfect combination of right sense of fact-oriented problem solving methodologies and leveraging existing data repositories.

TMR believes that unison of solutions for clients-specific problems with right methodology of research is the key to help enterprises reach right decision.

ContactTransparency Market ResearchState Tower,90 State Street,Suite 700,Albany NY 12207United StatesTel:+1-518-618-1030USA Canada Toll Free:866-552-3453Email:[emailprotected]Website:http://www.transparencymarketresearch.com

This post was originally published on Market Research Sheets

Read this article:
Biological Imaging Reagents Market is Projected To Surge At a CAGR of 8.5% from 2019 to 2027 - Market Research Sheets

Physician Eric Rubin, M90, GBS90, has a lot going on. He directs a prolific lab doing groundbreaking work on tuberculosis at the Harvard T.H. Chan School of Public Health. He sees patients as an infectious disease specialist. And in September, he started another role: editor-in-chief of the New England Journal of Medicine, the oldest and most widely read general medical journal in the world.

Wearing that many hats isnt a problem, he said, because all those things are fun.

It's like when youre a kid and you want to be a policeman or a fireman, he said, and I can be a policeman and a fireman. Its like I never grew up.

Rubin was raised in Brockton, Massachusetts, and studied biochemistry at Harvard before earning his M.D. and Ph.D. at Tufts School of Medicine and Graduate School of Biomedical Sciences. He talked with Tufts Now about his time at Tufts, the upside of acknowledging your mistakes, and the editorial challenge of conflicts of interest.

Tufts Now: When you graduated from Harvard, you went right into the M.D./Ph.D. Medical Scientist Training Program at Tufts. Did you always know you wanted to do research?

Eric Rubin: I always wanted to be a doctor, but I hadnt really considered research until college, when I worked in a lab and I really liked it. I thought doing research as well as medicine would be great, but I didnt actually apply to M.D./Ph.D. programs, because applying seemed like a lot of work. But Tufts was just starting its M.D./Ph.D. program. After I got into the Tufts School of Medicine, the new director of the M.D./Ph.D. program called me up and asked me to join the first class. I said, Is there an essay involved? And he said, No. I said, Yes.

The microbiology department where I did my Ph.D. was one of the best places to do a Ph.D. in the world, and remains that way. Theres just a terrific, nurturing environment for graduate students. Great, great facultymany of whom are still thereand new ones theyve added have maintained the ethos of that place. It really made an impression on me and helped shape my career.

Youve been an author on more than 150 research papers. Whats one that stands out in your mind?

At Tufts, I decided to work on a problem that had been very difficultfiguring out how botulism works. Botulism is caused by a toxin. At the time, we had no idea what that toxin did. So I started working with it and quickly identified a function for the proteins that people hadnt found.

I wrote it up as a paper and submitted it to Nature. It got very good reviews and came back with a few suggestions. Then I realized that something was wrong. In fact, the activity that I was measuring wasnt due to the toxin that causes botulism, it was due to contaminants. They have nothing to do with botulism, but they have really interesting and novel mechanisms of action. And thats what I spent the rest of my Ph.D. career on.

Is there a moral to that story?

The bottom line is that youre best off doing things carefully and rigorously, even if you end up disproving your favorite hypothesis. In this case, the more exciting paper would have been to attribute what we found to the toxin that causes botulismthat would have gotten us into Nature.

But in fact, I think we learned a lot more, and learned about a class of proteins that turned out to be very important in cell biology, particularly in cancer cell biology. So it took us in a direction we hadnt expected to go. But if we hadnt been careful, we wouldnt have noticed what the problem was.

Youve been an editor at the New England Journal of Medicine since 2012, and youve had editorial roles at other journals since 2002. Whats fun about being an editor?

Seeing a lot of really interesting science, and being involved in helping to shape how that gets communicatedI think thats exciting. At the New England Journal of Medicine, we make decisions collectively and meet all the time. And that means you hear about everything.

You hear all the best stories in medicine being presented by an expert in the topic. Its amazing and so, so interesting. Learning about whats going on in science and medicine has been great, and being able to work with incredibly smart people has also been fantastic.

Youve said that conflicts of interests are among the most contentious issues that the journal deals with. What do you think can be done better?

We rely on our authors and reviewers and editorialists to be honest in their reporting and I think in the overwhelming majority of cases they are. When occasionally they arent, or they forget the conflicts that they have, sometimes people catch them on it. But we dont have detectives going out there to check that what people said is true. We say, this is our policy we expect our authors etc., to live up to that and then put the burden on them. And I think its fair and I think that almost entirely works.

Then come the policy questions. How much of a conflict is a conflict? Right now, we have some very, very strict rules for our own editors. We dont let them have any financial conflicts whatsoever. For our editorialists, we allow them to have rather minimal conflicts, although they help define what those are.

And for our authors, we essentially allow them to have conflicts as long as they disclose them. And I think thats important. But what exactly should the limits be? If youre going to write an editorial, which makes recommendations based on an original article that we published, how much can you be involved in that field? And I think thats something that we have to continuously reevaluate.

The best experts oftentimes are conflicted. And so were constantly having to choose between people who might be the best authors and might make the most informed recommendations, and people who may be less informed but are unconflicted. So that means we have to draw a line somewhere and we will continue to think about where those lines should be.

Julie Flaherty can be reached at julie.flaherty@tufts.edu.

Original post:
At the Helm of the World's Most Influential Medical Journal - Tufts Now

BILLERICA, Mass., Dec. 30, 2019 /PRNewswire/ -- Bruker Corporation (Nasdaq: BRKR) announced today it will participate in the 38th annual J.P. Morgan Healthcare Conference in San Francisco. Frank Laukien, Chairman, President & CEO and Gerald Herman, CFO will present on behalf of the company on Monday, January 13th, 2020 at 11:30 AM Pacific Time.

A live audio webcast of the presentation will be available on the Investor Relations section of the Company's website at https://ir.bruker.com . A replay of the presentation will be posted in the "Events & Presentations" section of the Bruker Corporation Investor Relations website after the event and will be available for 30 days following the presentation.

About Bruker Corporation (Nasdaq: BRKR)

Bruker is enabling scientists to make breakthrough discoveries and develop new applications that improve the quality of human life. Bruker's high-performance scientific instruments and high-value analytical and diagnostic solutions enable scientists to explore life and materials at molecular, cellular and microscopic levels. In close cooperation with our customers, Bruker is enabling innovation, improved productivity and customer success in life science molecular research, in applied and pharma applications, in microscopy and nanoanalysis, and in industrial applications, as well as in cell biology, preclinical imaging, clinical phenomics and proteomics research and clinical microbiology. For more information, please visit: http://www.bruker.com.

Contact: Miroslava MinkovaDirector, Investor Relations & Corporate DevelopmentBruker CorporationT: +1 (978) 663 3660, ext. 1479E: Investor.Relations@bruker.com

View original content to download multimedia:http://www.prnewswire.com/news-releases/bruker-corporation-to-present-at-the-38th-annual-jp-morgan-healthcare-conference-300979682.html

SOURCE Bruker Corporation

Read this article:
Bruker Corporation to Present at the 38th Annual JP Morgan Healthcare Conference - BioSpace

By Jonny Lupsha, News Writer

According to the results of the recently published study, more than 180,000 women were observed over the course of 10 years. During this time, any weight loss of greater than 2 kg that wasnt put back on in full was considered sustained weight loss. Compared with women with stable weight (plus or minus 2 kg), women with sustained weight loss had a lower risk of breast cancer, the paper said. This risk reduction was linear and specific to women not using postmenopausal hormones. Linking lifestyle choices to cancer rates has been a challenging process for doctors, but theyre starting to get results.

Due to the countless variations in our individual diets and our individual bodies, studies correlating the two have been difficult to conductalthough researchers have tried.

They took a bunch of different countries and asked the question, If you look at the overall diet of everyone in the country and you say on a population basis, whats the relationship between fat consumption in the diet and breast cancer?' said Dr. David Sadava, Adjunct Professor of Cancer Cell Biology at the City of Hope Medical Center. You get a graph thats quite famous in the annals of cancer research.

Heres a percent of calories as fat, and it ranged from 10 percent, that is a pretty low-fat diet, in Thailand, to about 45 percent in the United Kingdom, Dr. Sadava said. It goes up and you say, Whoa, that means more fat means more breast cancer. But wait a minute, are the people who consumed the high-fat diet the same ones who got breast cancer?

According to Dr. Sadava, a study of 337,000 women found that that wasnt the case at all. When you look at a case-control study of relative risk versus the percent of fat in a diet, so it ranges from 20 percent to 45 percent of fat in the diet, you find the relative risk on an individual basis is the same, he said.

Of course, a high-fat diet is still harmful for the body, but it doesnt always correlate with the types of cancer one would expect. Obesity, as it turns out, is a far better metric.

Obesity is determined by ones body mass index (BMI), which in turn is calculated by the relation of height to weight in an adult. The ranges on the BMI scale tell an individual if theyre underweight, normal, overweight, obese, or severely obese.

People over a certain body mass index are at risk to getting cancer as well as many other things, Dr. Sadava said. It could be a descriptive risk factorin other words, it could be a risk factor that makes these people more prone to getting cancer for other causes. Or it could be a causative risk factor, which means the fat thats accumulating may actually cause the cancer.

Most evidence suggests that the stored fat in those with high BMIs is a causative risk factor, although as always, scientists are hesitant to definitively link one thing to another, since correlation does not imply causation. Regardless of whether fat is a descriptive or causative risk factor, this months published article in The Journal of the National Cancer Institute says a lot for weight loss as breast cancer prevention.

Dr. David Sadava is Adjunct Professor of Cancer Cell Biology at the City of Hope Medical Center in Duarte, CA. Professor Sadava graduated from Carleton University as the science medalist with a B.S. with first-class honors in biology and chemistry. A Woodrow Wilson Fellow, he earned a Ph.D. in Biology from the University of California, San Diego.

See the article here:
Weight Loss in Women over Age 50 Works as Breast Cancer Preventative - The Great Courses Daily News

Owing to the presence of a limited key players, theglobaloptical microscopes marketis likely to be extremely competitive. The players are competing on the basis of cost, quality, and features of the microscopes for example, associated software, magnification power, product performance, and price of the product. There has been an uptake in the investment in research and development in several sectors for example, healthcare, pharmaceuticals, and electronics. This lead the competition to intensify in forthcoming years.

Some of the key players in the global optical microscopes market are Leica Microsystems, Carl Zeiss, Nikon Instruments, Meiji Techno, and Olympus. Besides, there are some more important organizations such as ACCU-SCOPE, 3B Scientific, Ample Scientific, Aven, AmScope, BARSKA, Bruker, BestScope, Bulbtronics, Cole-Parmer, Thermo Fisher Scientific, Celestron, Euromex, Ken-A-Vision, Huvitz, Parco Scientific, Motic, Swift Opticals, Magnus Analytics, and Thomas Scientific.

Request PDF Sample of Optical Microscopes Market Report @https://www.transparencymarketresearch.com/sample/sample.php?flag=S&rep_id=42638

According to Transparency market Research (TMR), the global optical microscopes market is anticipated to expand at a steady CAGR of 6% within the forecast period from 2016 to 2025. In 2015, the market was valued around worth of US$1.5 bn. This figure is expected to grow in coming years. Based on end-use industry the optical microscopes market is segmented into diagnostics labs, pharmaceuticals and biotechnology firms, clinics and hospitals, academic and research institutes, and so on. Among these, pharmaceuticals and biotechnology firms segment is prognosticated to lead the market with highest number of share in the market, in 2016. Regionally, the global market is dominated by Asia Pacific and North America regions, owing to the presence of most of the biotechnology and pharmaceutical firms established in these regions.

Advancement in Nanotechnology to Fuel Optical Microscopes Market

Some of the factors, for example, rise in investment in research and development, progress in nanotechnology, improvement in the field of optical microscopy, and advancement in software technology are anticipated to drive demand in optical microscopes within the upcoming years. Blood cells discovery in human body provides good scope for studies in cell biology. Additionally, discovery of genes responsible of body development is expected to surge the market in forecast period. These improvements are expected to impel interest for optical microscopes. Confinements of optical microscopy in the field of research when contrasted with small scale vendors and electron microscopes offering cost-effective products are the primary limitations for the optical microscopes market.

Enquiry for Discount on Optical Microscopes Market Report @https://www.transparencymarketresearch.com/sample/sample.php?flag=D&rep_id=42638

Rising Educational Institutes to Augment Demand for Low-Cost Optical Microscopes

With training organizations multiplying, the market for optical microscopes has an uplifting outlook in the past few years. A few worldwide activities carried out by the United Nations, for example, Global Education First Initiative prevailing in not just allotting funds for basic and secondary education in several nations, but also initiated techniques to enhance the nature of training being provided. As a result of this, there has been a growth in number of educational centers in the previous couple of years. The rise in number of education centers all over the world is supporting the uptake in the demand for low-cost optical microscopes market.

This post was originally published on Industry Mirror

Go here to read the rest:
Optical Microscopes Market is Expected to Expand at an Impressive Rate by 2025 - Industry Mirror

DUBLIN--(BUSINESS WIRE)--The "Understanding Pathophysiology. Edition No. 7" book has been added to ResearchAndMarkets.com's offering.

Make difficult pathophysiology concepts come to life! Filled with vibrant illustrations, simplified language, and detailed online content Understanding Pathophysiology, 7th Edition delivers the most accurate information on treatments, manifestations, and mechanisms of disease across the lifespan. This new edition is fully revised and includes coverage of rare diseases and epigenetics to you with a thorough understanding of conditions affecting the human body. Plus, with over 30 new 3D animations on the companion Evolve site, quick check boxes at the end of each chapter, and disease progression algorithms, this text helps you engage with the fundamental knowledge you need to succeed in nursing school and in practice.

Key Topics Covered:

PART ONE: BASIC CONCEPTS OF PATHOPHYSIOLOGY

Unit 1: The Cell

1. Cellular Biology

2. Genes and Genetic Diseases

3. Epigenetics and Disease

4. Altered Cellular and Tissue Biology

5. Fluids and Electrolytes, Acids and Bases

Unit 2: Mechanisms of Self-Defense

6. Innate Immunity: Inflammation and Wound Healing

7. Adaptive Immunity

8. Alterations in Immunity NEW

9. Infection and Defects in Mechanisms of Defense

10. Stress and Disease

Unit 3: Cellular Proliferation: Cancer

11. Biology of Cancer

12. Cancer Epidemiology

13. Cancer in Children and Adolescents

PART TWO: BODY SYSTEMS AND DISEASES

Unit 4: The Neurologic System

14. Structure and Function of the Neurologic System

15. Pain, Temperature, Sleep, and Sensory Function

16. Alterations in Cognitive Systems, Cerebral Hemodynamics, and Motor Function

17. Disorders of the Central and Peripheral Nervous Systems and Neuromuscular Junction

18. Alterations of Neurologic Function in Children

Unit 5: The Endocrine System

19. Mechanisms of Hormonal Regulation

20. Alterations of Hormonal Regulation

21. Obesity and Disorders of Nutrition NEW

Unit 6: The Hematologic System

22. Structure and Function of the Hematologic System

23. Alterations of Hematologic Function

24. Alterations of Hematologic Function in Children

Unit 7: The Cardiovascular and Lymphatic Systems

25. Structure and Function of the Cardiovascular and Lymphatic Systems

26. Alterations of Cardiovascular Function

27. Alterations of Cardiovascular Function in Children

Unit 8: The Pulmonary System

28. Structure and Function of the Pulmonary System

29. Alterations of Pulmonary Function

30. Alterations of Pulmonary Function in Children

Unit 9: The Renal and Urologic Systems

31. Structure and Function of the Renal and Urologic Systems

32. Alterations of Renal and Urinary Tract Function

33. Alterations of Renal and Urinary Tract Function in Children

Unit 10: The Reproductive Systems

34. Structure and Function of the Reproductive Systems

35. Alterations of the Female Reproductive System

36. Alterations of the Male Reproductive System

Unit 11: The Digestive System

37. Structure and Function of the Digestive System

38. Alterations of Digestive Function

39. Alterations of Digestive Function in Children

Unit 12: The Musculoskeletal and Integumentary Systems

40. Structure and Function of the Musculoskeletal System

41. Alterations of Musculoskeletal Function

42. Alterations of Musculoskeletal Function in Children

43. Structure, Function, and Disorders of the Integument

44. Alterations of the Integument in Children

Glossary Index

Author

For more information about this book visit https://www.researchandmarkets.com/r/73mf81

Follow this link:
Understanding Pathophysiology - 7th Edition - ResearchAndMarkets.com - Business Wire