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Nature Genetics
Q: Im looking for advice on how to deal with my almost-6-year-olds exceedingly snarky attitude. I know that eye-rolling, talking back, etc., are fairly age-appropriate, but, as our day-care provider put it, shes the sassiest little girl shes ever worked with in her decades as a preschool teacher. I was similar as a child, and my parents told me repeatedly that my attitude stunk and that I was unpleasant to be around. It wasnt until I was older and realized how many friendships had ended because of my attitude that I was able to make a change. What can I do for my daughter? I have no idea whether this have attitude, lose friends, learn from mistake process is inevitable. On the one hand, I want her to be a little sassy, unafraid to speak her mind and not polite to a fault. On the other hand, how do I get her to see that this level of attitude may alienate her? I dont want to change her. I just want her to understand the value of a filter to temper how she comes across.
A: There are a number of red flags in this question, and I want to address them so that we can clarify the real issue. I am not being critical of you; rather, I want to highlight a few concerns so that we can identify what you can change in your parenting life.
First, eye-rolling, talking back, etc., are not age-appropriate behaviors for your daughter. Although we sometimes see this in children of many ages, constant snark and sass are not appropriate. This is a sign of deeper frustration. I want to steer you away from the little girls are just sassy way of thinking. It is the equivalent of saying boys will be boys when little boys are violent, and I know we can look deeper here.
Second, sassiness and snark are not genetic. I know it is easy to see yourself in your child, but sassiness is not passed down through genes. Am I saying that I dont see generations of strong-willed women, one after another? Of course not. But this is more nurture than nature. If you look at temperament scales, outgoing parents can have outgoing children, and shy parents can have shy children. But sassiness? There is no sassiness temperament. Sassiness is a sign of something else.
[Our 6-year-old has a fun, comfortable life. Why isnt she grateful?]
Third, it can be fairly normal for children to be rude at home while acting like angels at school, but your daughter is being called the sassiest little girl in day care from a provider who has decades of experience. What is the day-care provider doing about this? Is everyone shrugging their shoulders like, Well, shes just completely obnoxious, and theres nothing we can do about it. I am concerned that there are lots of labels being put on your daughter but no help being offered.
Fourth, you are identifying with your daughter in a way that is preventing you from helping her. It seems clear from your note that you had a tough time when you were younger and paid for it. This suffering does not have to be your daughters fate, and you dont have to either go nuclear or just let her sort it out on her own. Shes almost 6 and needs some strong guidance, so lets get to it.
Regular and chronic sassiness and disrespect are a sign of deep discouragement and defensiveness in a child. Lets say youre married and dont feel like your spouse is listening to you and your opinions. You feel shut out, dismissed and rejected. Your impulses could go a couple of ways, depending on your alarm instincts. If youre like me, you are going to fight. You are going to confront, get mean and attack. Others retreat. They shut down, walk away and seek to avoid this pain. But the fighters? They will push, and then they will shut people out. So if your spouse asks you for your opinion and you have felt down and out for a long time, your heart will say: Oh, heck no. I dont trust this at all. And you very well may give an eye-roll and a smart comment. Your heart is saying: You have been too hurt by this dismissal. I am going to protect you, even if it hurts the situation.
Your daughter is defending herself against listening to people and taking instruction because her heart and mind have decided that is not safe. There is a little wall around your daughters heart, and every time she even perceives that she is being attacked or bullied, the wall springs up, protects her and becomes stronger.
She is not necessarily doing anything wrong. For very sensitive children, its a natural defense against vulnerability. They are taking in so much sensory information and experiencing so many emotions that their minds and hearts become overwhelmed and say, Thats enough, and the children shut down.
First bit of homework: Stop calling your daughter sassy. Rename this emotion discouragement, and you will instantly begin to have more empathy for her. Labeling her as sassy doesnt help her mature. It keeps her boxed in as a pain in the bottom, and you both dont need that. Also, dont take all this eye-rolling personally. Does this mean that you like it or dont care? Of course not. Just remember that she is reacting to emotions of alarm and protection. She is not consciously trying to hurt you.
Second bit of homework: You cannot demand respect or kindness from her. It will make her even more frustrated. The way into her heart is through small doses of connection in non-threatening ways. For instance, is there a project you can work on together where she can find her voice and have agency over something? Dedicate only a bit of time to this every day, because too much one-on-one time will discourage her.
When she is sassy, relabel it as frustration right then and there. When she rolls her eyes, say, I see how frustrated you are with this decision. The more we can put names to her feelings, the more we can move her from sassy, snarky and bad to frustrated, discouraged and sad. These words will help you communicate with her about her true feelings.
Place some boundaries on her behavior. For instance, let her know that if she has a play date and acts this way, her friend will leave immediately. Make good on this the first time it happens. She will throw a tantrum of epic proportions, but as long as you dont punish her and put your relationship on the line, she will adapt. Dont draw boundaries everywhere (you will never stop fighting), but choose your lines thoughtfully and stick with your rule.
Finally, take a listening stance whenever possible. When she says something rude, say: Sounds like you really dont like that idea. I wonder what you are really thinking. Then pause. See what happens.
I will warn you that if your daughter has been acting this way for a long time, things wont work themselves out overnight. Children who push boundaries can be frustrating, so do what you need to do to keep your feelings in check as you do this heavy emotional lifting. But this can get better! Good luck.
Send questions about parenting to meghan@mlparentcoach.com.
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Don't blame genetics for daughter's sassy demeanor. It's more nurture than nature. - Washington Post
Submitted by The Whale Museum
Learn about South resident killer whale genetics at a free lecture at 6:30 p.m., Thursday, Sept. 14 at The Whale Museum.
Dr. Lance Barrett-Lennard, head of the Cetacean Research Program at the Vancouver Aquarium, will discuss genetic comparisons of orca populations in the North East Pacific. This presentation is part of the museums Summer Lecture Series.
Barrett-Lennards research shows that at least nine genetically discrete overlapping populations of killer whales inhabit the northeastern Pacific Ocean. It also shows that resident killer whales avoid inbreeding through an elaborate clan-based mating system. His findings are the reason the Southern resident killer whales are listed as an endangered population through the Committee on the Status of Endangered Wildlife in Canada. More recently, he co-chaired a panel that produced a comprehensive recovery strategy for resident killer whales.
Barrett-Lennard has performed studies on behavioral and population biology of killer whales in British Columbia, Washington, Alaska since 1984, as well as species in Norway, Spain and the sub-Antarctic. He uses DNA analysis to better understand population divisions, dispersal patterns and mating systems. In addition to killer whales, Lance is involved in research on baleen whales, dolphins, sea otters, and belugas.
The Summer Lecture Series are given by local or visiting experts in their field, who share their recent research projects, stories and experiences. Each lecture is free and held at The Whale Museum. Donations are appreciated.
For more information, call 360-378-4710 ext.30 or visit http://www.whalemuseum.org.
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Top researcher gives free lecture on orca genetics - Journal of the San Juan Islands
Myriad Genetics, Inc.MYGN introduced riskScore under its myRisk Hereditary Cancer testing portfolio. The launch is aimed at solidifying the company's footprint in the rapidly growing hereditary cancer testing market. Based in Salt Lake City, UT, this leading molecular diagnostics and personalized medicines providerintends to make riskScore a precision medical tool for patients who use myRisk to get their tests done.
Notably, riskScore helps determine a woman's risk of developing breast cancer by combining genetic markers throughout the genome with the patient's family and clinical history.
Per management, this highly advanced prediction tool will also aid 90% of the patients with negative results for heredity cancer genes to derive proper conclusions.
In June, the company had presented encouraging data from a 2,000-patient clinical study with myRisk Hereditary Cancer testsat the American Society of Clinical Oncology (ASCO). The results highlighted the importance of the multi-gene panel testing for advancement of the hereditary cancer-risk evaluation platform. Per management, around 50% of the identified mutations were found in patients who did not comply with the testing guidelines. The study also found 34% of identified mutations in unexpected genes.
Myriad Genetics has been riding high on strength in the Heriditary Cancer testing space. In the last reported quarter, the company saw 6% year-over-year rise in Heriditary Cancer testing volumes, marking the third consecutive quarter of sequential growth.
Per a report by DPI Research on Medium, the breast cancer screening market in the United States is expected to reach a value of roughly $5.8 billion by 2022. Moreover, per an article by BrestCancer.Org, approximately 252,710 new cases of invasive breast cancer in women are likely to be diagnosed in the United States in 2017. They also project 63,410 new cases of non-invasive (in situ) breast cancer this year as well.
We believe an ageing population, rising awareness and expenditure in healthcare will continue to drive growth in the breast cancer screening market. However, this market is dominated by many well established players, Quest Diagnostics DGX being the most prominent one. In this space, Quest Diagnostics' Quest Vantage services help in the discovery of genetic variants related to the hereditary risk of 15 types of cancer, including breast, colorectal, pancreatic and renal.
Moreover, Myriad Genetics has been gaining investor confidence on consistently positive results. Over the past three months, the company's share price has outperformed the broader industry . The stock has gained 41%, higher than the broader industry's 12.6%. The company has also outperformed the 0.7% gain of the S&P 500 market over the same time frame.
Zacks Rank & Key Picks
Myriad Genetics carries a Zacks Rank #3 (Hold). A couple of better-ranked medical stocks are Edwards Lifesciences Corporation EW and Lantheus Holdings, Inc. LNTH . Edwards Lifesciences sports a Zacks Rank #1 (Strong Buy), while Lantheus Holdings carries a Zacks Rank #2 (Buy). You can see the complete list of today's Zacks #1 Rank stocks here.
Edwards Lifesciences has a long-term expected earnings growth rate of 15.2%. The stock has rallied roughly 23.6% over the last six months.
Lantheus Holdings has a long-term expected earnings growth rate of 12.5%. The stock has gained 30.2% over the last six months.
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Myriad Genetics Boosts myRisk Hereditary Cancer Test Suite - Nasdaq
Newswise Again and again, its the rare among humans that help the rest of us. The exploration of human genetics is revealing new targets to combat heart disease among atypical variants. Mutations in genes that play a role in heart health are the inspiration for a cluster of new heart drugs. One of the best examples is the discovery of mutations in the PCSK9 gene. People with a variant of this enzyme have lower LDL levels (the bad cholesterol), which protects them against heart disease. The discovery led to the development of a new class of heart medications called PCSK9 inhibitors, which markedly reduce LDLs in people with out-of-control levels. At the annual meeting of the American College of Cardiology this past spring, researchers announced that these inhibitors reduced the combined risk of having a heart attack or stroke or dying from cardiovascular disease in high-risk patients by 15 percent.
Other investigators are extending the hunt for how these mutations affect risk to tackle other aspects of heart disease. For instance, people whose LDL levels are under control but have elevated triglycerides are still at risk for continued plaque buildup in their arteries. Individuals with mutations in genes that play a role in breaking down excess triglycerides in the blood are pointing geneticists to other ways to protect at-risk people. In fact, a recent New York Times article describes a trio of papers about these rare mutations in people with extremely low triglyceride levels. These studies followed a previous discovery that mutations in the APOC3 gene naturally cause extra-low triglyceride levels. Normally, the APOC3 gene instructs cells to make a molecule that inhibits the breakdown of triglycerides.
Daniel Rader, MD, chair of Genetics, and other Penn Medicine researchers, were coauthors on these recent human-genetic studies, as well as others earlier this year. All of the APOC3 variants are associated with low triglycerides, independent of LDL cholesterol levels. The findings represent a potential new and separate line of attack for lowering risk of heart disease.
If we could harness the protective aspects of these APOC3 variants to develop therapies that act similarly and lower triglycerides and heart disease risk, these could theoretically work alongside existing LDL-lowering drugs, Rader said.
He adds that its hard to say how many people have normal LDL but high triglycerides, but its clearly in the millions, not a small number. There are currently no proven therapies to further reduce risk in these individuals.
Studies of large groups of people with one disabled APOC3 gene have led to its characterization as a highly validated therapeutic target for reducing the risk of heart disease. In other words, these studies have shown that diminished function of APOC3 is consistently associated with lower triglyceride levels and reduced risk of heart disease in large populations across the world.
One new therapy targeting APOC3 is showing promise: an antisense oligonucleotide, which is essentially a small stretch of DNA that binds to the APOC3 RNAs to block the protein from being made. This antisense drugs, which is administered subcutaneously, has shown substantial reductions in triglyceride levels in humans, further proving that disabling the APOC3 protein works the way the researchers had hoped.
Therapeutic antibodies engineered molecules that bind to specific proteins on cell surfaces are an established way to inhibit or inactivate circulating proteins to treat disease, and Rader notes that creating antibodies to the AP0C3 protein may be another useful strategy. The recently approved antibody to the PCSK9 protein is one example of this approach in action for lowering LDL and reducing heart disease.
In the newest human genetics study from the Rader lab, the team studied people with one disabled copy of the APOC3 gene (found by searching the over 50,000 participants in the Penn Medicine Biobank) and mice expressing the same human variant and showed that both had markedly reduced levels of APOC3 protein and triglycerides in their blood. From this, they showed that an antibody targeting the APOC3 protein could accelerate the breakdown of triglyceride-rich lipoproteins in the mice, mimicking the effects of this natural mutation.
The APOC3 protein antibody was developed by the biotech firm Argenx in collaboration with Staten Biotechnology. Rader says this approach is currently being developed by Staten and could be in clinical trials within the next two years.
This new translational genetics study, Rader said, adds one more check in the win column for the value of studying rare human genetic variants to inform our understanding of common conditions.
SEE ORIGINAL STUDY
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Human Genetics Studies Reveal New Targets to Reduce Heart Disease - Newswise (press release)
BOTHELL, Wash.--(BUSINESS WIRE)--Seattle Genetics, Inc. (NASDAQ:SGEN) announced today that management will present at the Morgan Stanley Global Healthcare Conference on Tuesday, September 12, 2017 at 2:05 p.m. EDT. The presentation will be webcast live and available for replay from the Investors section of the Seattle Genetics website at http://www.seattlegenetics.com.
About Seattle Genetics
Seattle Genetics is an innovative biotechnology company that develops and commercializes novel antibody-based therapies for the treatment of cancer. The companys industry-leading antibody-drug conjugate (ADC) technology harnesses the targeting ability of antibodies to deliver cell-killing agents directly to cancer cells. ADCETRIS (brentuximab vedotin), the companys lead product, in collaboration with Takeda Pharmaceutical Company Limited, is the first in a new class of ADCs and is commercially available globally in 67 countries for relapsed classical Hodgkin lymphoma (HL) and relapsed systemic anaplastic large cell lymphoma (sALCL). Seattle Genetics is also advancing enfortumab vedotin, an ADC in a planned pivotal trial for metastatic urothelial cancer, in collaboration with Astellas and tisotumab vedotin, an ADC in a phase 1/2 trial for solid tumors, in collaboration with Genmab. Headquartered in Bothell, Washington and with European and international operations in Zug, Switzerland, Seattle Genetics has a robust pipeline of innovative therapies for blood-related cancers and solid tumors designed to address significant unmet medical needs and improve treatment outcomes for patients. The company has collaborations for its proprietary ADC technology with a number of companies including AbbVie, Astellas, Bayer, Celldex, Genentech, GlaxoSmithKline and Pfizer. More information can be found at http://www.seattlegenetics.com.
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Seattle Genetics to Present at Morgan Stanley Global Healthcare Conference - Business Wire (press release)
The sequencing of the canine genome along with next generation sequencing technologies like whole exome sequencing have facilitated quicker, easier and more efficient identification of genes and mutations that can cause diseases in dogs. In a study published in Skeletal Muscle researchers have used these technologies to study a form of Limb-girdle muscular dystrophy (muscle wasting and weakness in shoulder and hip muscles) in Boston terriers. Here to tell us about the research and what this means for the breed is lead author of the study Melissa L. Cox.
Melissa L. Cox 5 Sep 2017
Dogs live with humans, and have access to medical care nearly as sophisticated as ours. We are also close in other ways: sharing approximately 85% of our genome that is our complete sets of genes any naturally occurring gene mutation that may cause a disease in dogs is likely to cause a similar condition in humans, and vice versa. Dogs can serve as models of human disease; for example, treatments such as gene therapy can be tried in dogs before going into clinical trials in humans, which can benefit both species.
The sequencing of the canine genome greatly increased the speed and efficiency with which genes that cause disease can be detected. It has also facilitated research into the origin of dogs and the search for genes that underlie specific traits in dogs, such as height and skull shape, and many hereditary diseases. Next generation sequencing (NGS), including whole exome sequencing (WES) technologies which allow geneticists to determine the precise order of nucleotides within DNA and RNA molecules much more quickly and cheaply than before and the establishment of publically available databases has also allowed for easier identification of genes and mutations that may cause disease.
LGMDs are a varied group of Mendelian disorders characterized by muscle wasting and weakness in the muscles of the shoulders and hips
Our group made use of these technologies to study a form of Limb-girdle muscular dystrophy (LGMD) in Boston terrier dogs. LGMDs are a varied group of Mendelian disorders diseases caused by single genes that are inherited according to Mendels laws characterized by muscle wasting and weakness in the muscles of the shoulders and hips. Four affected dogs from three unrelated families were identified by their primary veterinarians, and referred for specialized investigation.
Clinical examination and pathology results confirmed that all affected dogs were suffering from LGMD, and immunohistopathological assays, which use antibodies that bind to certain tissues to reveal their presence, suggested a sarcoglycanopathy that is a disease resulting from mutations in one of four genes that code for a certain type of protein, called a sarcoglycan. Sarcoglycanopathies are autosomal recessive, and have severe symptoms similar to Duchenne muscular dystrophy.
The group originally looked at four Boston terriers affected by LGMD from three unrelated families.
There are six sarcoglycan proteins, four of which (, , , ) are involved in structural and signal functions in muscle. The absence of the sarcoglycans from the muscle of affected dogs made the genes that code for these proteins our candidate genes, and whole exome sequencing allowed us to investigate them simultaneously.
DNA was available from two of the four dogs, and from several relatives of one of the dogs. Whole exome sequencing was performed on a total of 5 dogs, including the two dogs that had the disease and an obligate carrier a dog that didnt have the disease but which had to carry the gene mutation based on analysis of the family history. In one affected dog (Case 3), we found that two nucleotides the buildings blocks of DNA were deleted in one of the sarcoglycan genes. The dogs obligate carrier parent and one other relative each also had one copy of the deletion.
The other affected dog (Case 1) did not share this mutation, which was very surprising to us, given that they were the same breed. Breed structures limit genetic diversity, because dogs are only bred to other dogs of the same breed. This increases the chance that any two dogs will be related, and that they will carry a mutation that is identical by descent, that is, inherited from a shared ancestor. For this reason, most dogs in a breed with the same disease will share the same gene mutation.
This is also a good reminder to the animal breeding and veterinary community that even within one breed, a disease may be caused by more than one mutation
Further analysis showed that Case 1 had a different deletion in the same gene as Case 3. We hypothesize that the dogs have very similar phenotypes because the same portion of the protein coded by the gene is eliminated in the two different mutations.
We screened 200 more Boston terriers from North America and Europe, as well as a large variety of other breeds, and these mutations were not found outside of these two cases and family members. This is good news for the breed, as it appears that these are private mutations, found only in these two families. Although we have developed genetic tests for these two mutations, it will not be necessary for breeders of Boston terriers to add LGMD testing to their routine genetic screening at this time.
This is also a good reminder to the animal breeding and veterinary community that even within one breed, a disease may be caused by more than one mutation. For this reason, it is best practice for testing laboratories to indicate which specific mutation(s) have been tested when writing reports.
The two mutations were found in the sarcoglycan gene SGCD, which has been classified as Limb-girdle muscular dystrophy 2F (LGMD2F) (the number 2 denotes that it is an autosomal recessive gene, while F is the gene name). LGMD2F is the least common form of sarcoglycanopathy in humans, so our report of the first large animal model of sarcoglycanopathy may also be of interest to human medicine.
The work also demonstrates the utility of whole exome sequencing to identify mutations in an extremely small number of affected animals. This allows mutations to be identified more quickly than in the past, as it is not necessary to gather samples from large family groups. The early establishment of a genetic testing program to distinguish between normal and unaffected carrier animals can therefore prevent a disease from unintentionally spreading through a breed population.
Excerpt from:
Investigating the genetics behind muscular dystrophy in dogs - BMC Blogs Network (blog)
Commercial bull breeders are increasingly having to venture into the five figure range to fill their orders. Image: Angus Australia
Agents and vendors smile with relief when commercial cattle producers turn up at a sale looking for more than a couple of bulls.
Some buyers roll up every year looking for lines while others are not so regular with their buying patterns dictated by seasons, the number females that need to be joined and the ages in the bull paddock.
Confident commercial bull buyers, cashed up by the good cattle prices, appear to be setting their sights higher and forcing seedstock producers to bid higher for the top end genetics.
It wasnt so long ago commercial buyers could fill their orders in the $5000 to $7000 range but these days many need to venture into the five figure range to fill their orders.
If thats what we have to pay we have to pay it, one commercial bull buyer told Beef Central.
With some big catalogues of bulls coming forward in the next few weeks, especially in the north, Beef Central has looked for examples of commercial producers buying bulls in todays market.
Last weeks Rennylea Angus sale at Culcairn NSW needed more than a couple of multi-bull buyers to clear 148 bulls for an average $9682.
While studs dominated Rennyleas top end (Hugh Munro from Booroomooka took the top two bulls at $38,000 and $36,000 following Booroomookas $2.19 million sale two weeks earlier) commercial producers competed vigorously.
One commercial buyer was David McKillop who manages Yamalla at Greenthorpe in the New South Wales central west for Malcolm Sinclair. This long time Rennylea client took five bulls out of the catalogue at an average $9600 with a top of $11,000.
These bulls arrived at their new home after the district received 50 to 70mm of welcome August rain after a dry June-July. However, a couple of screaming late winter frosts have dented pasture progress.
Yamalla has been buying Rennylea bulls for seven years and are happy with what theyve done in the straight bred Angus herd of 530 cows that will calve down this year.
We look for low birth weight, high growth, eye muscle area and fat depth and weve found that fertility follows, Mr McKillop said. Last year 87pc of the heifers and 98pc of the mature females scanned pregnant.
We dont buy heifer bulls as such, we want good genetic gain in our replacement heifers.
Their pattern has been to sell surplus females to restockers through AuctionsPlus but last year increased demand from beef grinders to supply the Angus brand burger market pushed many of the older cows went that way.
Steers are taken through to a 450kg liveweight average and sold direct to feedlots.
We see the price we have to pay these days for our bulls (close to $10,000) as an indication of where the market is. said Mr McKillop.
Initially, it was pretty easy to improve the herds genetics (from a low base) but these days it is harder and harder to get that important genetic gain he said.
Yamalla also runs a flock of 3000 Merino and first cross ewes joined to Dorset rams for prime lamb production.
Don McCrae of Goondiwindi Qld and Walcha NSW took home seven bulls from Rennylea paying a top $16,500 and an average $13,143. This will bring to 54 the number of bulls introduced to his Bullseye Angus herd over the past five years, most from Rennylea and a few from Te Mania.
Over the past few years Bullseye has registered over 1000 Angus Commercial Register (ACR) non seedstock females to keep an eye on the high performers. McCrae stresses he is not a seedstock producer but purely a commercial producer aiming to generate a superior product.
At the ANC Charolais sale at Gulugaba Qld on August 25, 125 bulls averaged $6148. Demand came from northern breeders looking for a Charolais infusion into their Brahman based northern herds.
While the top priced ANC bull at $37,000 went to a stud (Bauhinia Park) commercial producers then took over.
The Slack-Smith family paid to $17,000 and an average $10,500 for six bulls for their Richmond and Julia Creek based Brahman herds while the Scotts Rosetta Station near Collinsville Qld paid an average of $6136 for 22 bulls to join bull battery servicing 15,000 Brahman influenced cows.
As the bull sales move north the range of bos Indicus genetics increases, vendors and agents will be looking for bulk buyers to put a floor on the market. And the going price could be close to the $10,000 mark or even more for the better bulls.
Read the rest here:
Weekly genetics review: What are commercial producers paying for bulls? - Beef Central
What happened
Shares of Myriad Genetics (NASDAQ:MYGN), a leading developer of molecular diagnostic tests, surged by 26% during the month of August, according to data from S&P Global Market Intelligence. Why the sudden surge? The bulk of the gains look traceable to the company's fourth-quarter and full-year earnings release on Aug. 8, as well as positive insurance coverage decisions made on a key diagnostic product mid-month.
The rally really began for Myriad Genetics following the release of its fourth-quarter report. During Q4, Myriad wound up generating $200.5 million in sales, an 8% year-over-year improvement, largely helped by growth in its GeneSight test.Despite the jump in sales, its adjusted profit fell by 17% to $0.30 per share. Nevertheless, Myriad wound up topping Wall Street's sales and profit projections for the fourth quarter. This beat, coupled with growth from newer diagnostic products, which have helped offset competitive weaknesses in its hereditary cancer testing franchise (e.g., BRCA gene tests), clearly have investors upbeat about Myriad's prospects.
Image source: Getty Images.
The other catalyst driving big gains in August was favorable insurer coverage decisions for EndoPredict, a next-generation prognostic test that helps physicians determine a best course of care for patients with breast cancer. Myriad wound up announcing that Palmetto GBA, the Medicare contractor that oversees the MoIDx (Molecular Diagnostics) program, and Anthem, the second-largest insurer nationally, have decided to cover EndoPredict.Following the implementation of these decisions, Myriad will be able to cover more than 90% of breast cancer patients, which is pretty impressive considering EndoPredict was launched less than six months ago.
In a world of personalized medicine, Myriad Genetics continues to lead the charge. Unfortunately, this is also an increasingly crowded space that tends to rely on healthy reimbursements from Medicare and Medicaid. With the Trump administration looking to cut long-term payouts to both programs, it leaves Myriad's future somewhat cloudy.
By a similar token, the company has also seen price erosion from competition in its hereditary cancer segment, from which it derives about three-quarters of its sales. However, growth from new products, compounded with volume growth in hereditary cancer testing, even at a lower margin, could still fuel substantial sales and profit improvements in the coming years.
So, what's an investor to do? I'd suggest that modest optimism seems fair at these levels. It's probably going to take a few more years before sales in Myriad's core operating segment level off, but at the same time it should be able to continue to grow its newly launched diagnostic products. Once the company has a more balanced revenue stream, it should be able to throttle back a bit on its operating expenses and allow its operating margin to soar. Patient investors with at least a five-year time horizon should do just fine.
Sean Williams has no position in any of the stocks mentioned. The Motley Fool has no position in any of the stocks mentioned. The Motley Fool has a disclosure policy.
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The 2 Major Catalysts Behind Myriad Genetics, Inc.'s 26% Gain in August - Motley Fool
NewLink Genetics Corporation (NASDAQ:NLNK) plunged -4.06% with the closing price of $7.79. The overall volume in the last trading session was 1.15 million shares.
Company Growth Evolution:
ROI deals with the invested cash in the company and the return the investor realize on that money based on the net profit of the business. Investors who are keeping close eye on the stock of NewLink Genetics Corporation (NASDAQ:NLNK) established that the company was able to keep return on investment at in the trailing twelve month while Reuters data showed that industrys average stands at 4.85 and sectors optimum level is 15.02.
NewLink Genetics Corporation (NLNK) have shown a high EPS growth of 0.30% in the last 5 years and has earnings decline of -108.00% yoy. Analysts have a mean recommendation of 2.20 on this stock (A rating of less than 2 means buy, hold within the 3 range, sell within the 4 range, and strong sell within the 5 range). The stock appeared $25.17 above its 52-week highs and is up 16.97% for the last five trades. MA ended last trade at $7.79 a share and the price is up more than -24.22% so far this year. The company maintains price to book ratio of 0.00 vs. an industry average at 0.59. Its sales stood at 80.40% a year on average in the period of last five years. A P/B ratio of less than 1.0 can indicate that a stock is undervalued, while a ratio of greater than 1.0 may indicate that a stock is overvalued.
Oasis Petroleum Inc. (NYSE:OAS)ended its day at $7.39 with the rising stream of 1.23% and its total traded volume was 6.39 million shares less than the average volume.
Returns and Valuations for Oasis Petroleum Inc. (NYSE:OAS)
Oasis Petroleum Inc. (NYSE:OAS), maintained return on investment for the last twelve months at -, higher than what Reuters data shows regarding industrys average. The average of this ratio is 4.85 for the industry and sectors best figure appears 15.02. Oasis Petroleum Inc. (NYSE:OAS), at its latest closing price of $7.39, it has a price-to-book ratio of 0.00, compared to an industry average at 0.59. A lower P/B ratio could mean that the stock is undervalued. This ratio also gives some idea of whether youre paying too much for what would be left if the company went bankrupt immediately.
Oasis Petroleum Inc. (NYSE:OAS), stock is trading $17.08 above the 52-week high and has displayed a high EPS growth of -28.70% in last 5 years. The 1 year EPS growth rate is -328.10% . Its share price has decline -24.28% in three months and is up 2.07% for the last five trades. The average analysts gave this company a mean recommendation of 2.10.
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