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Genetics key to livestock disease relief – Iowa Farmer Today – Iowa Farmer Today

Ask people in the research business if they have a wish list, and many will answer in the affirmative.

There are always different things you want to see done, says Jim Reecy, an animal scientist and director of the Office of Biotechnology at Iowa State University.

Much of Reecys work involves genetically changing traits in cattle to better predict performance.

For example, researchers are working to find cattle that offer genetic resistance to respiratory ailments such as bovine respiratory disease (BRD). This trait would be similar to others producers have selected for years, such as birth and weaning weights.

There is a large consortium of universities working on this, and its very exciting, Reecy says. It would work just like any other EPD (expected progeny difference) that producers are already using to select genetics.

Heat tolerance is another trait being looked at under the microscope. Reecy says projects at the University of Missouri and the University of Florida could greatly influence genetic selection.

The project at Missouri is looking at hair coat shedding, and the other in Florida is looking at internal body temperatures, he says. This research would allow producers to select cattle that handle heat better.

At Iowa State, researchers are looking at what traits allow certain cattle to better respond to vaccinations used for respiratory disease.

Something like this will allow producers to cull off cattle that do not respond as well to vaccinations, Reecy says.

The top item on his wish list would be the elimination of communicable diseases like BVD (bovine virus diarrhea).

Something like this would be similar to the gene editing that led to de-horning, Reecy says. Something like that would change the industry.

Much of the work in the hog industry also involves genetics, says Dave Pyburn, a veterinarian and senior vice president for science and technology with the National Pork Board.

The most promising research, he says, comes from the University of Missouri where scientists have isolated the point where the PRRS virus enters a cell.

They have been able to remove that attachment point from the cell, Pyburn says. They also looked at pigs who were not affected. So, through natural selection or gene editing, we could get to the point where we have pigs that are resistant to PRRS.

This disease cost the industry $664 million last year, so this is very significant.

Pyburn says the technology could be available in five to 10 years.

Other areas receiving attention from researchers include biosecurity, animal welfare and pork quality.

We need to take our biosecurity research to the next level, Pyburn says. There are things we need to better understand, such as filtration systems in buildings. The key is to try and prevent the disease, and subsequently reducing the need for antibiotics.

He says animal welfare issues include different euthanasia methods and pain management.

More research is needed on teeth and tail clipping, as well as castration, Pyburn says. We need to look at analgesics that can be passed through the mammary glands to the baby pigs. So far, weve had to use too much analgesic to be effective, but I think we will figure it out.

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Genetics key to livestock disease relief - Iowa Farmer Today - Iowa Farmer Today

DMIT, a trending scientific procedure to test one’s inborn intelligence – Business Standard

ANI | New Delhi [India] June 17, 2017 Last Updated at 16:42 IST

Choosing oneself to become just a successful engineer or a doctor in future is passe. With the growing competition and the growth in career options, Kids and their parents are becoming more confused towards identifying their actual passion and talent. Just as the 10th and 12th board results are out, parents are now worried about what goals have their kids made up in their mind to peruse in future. There are dozens of questions revolving in their head making them befuddled with thoughts like, does my kid fits for his goals or his talent lay in some other streams?

Consulting a career counsellor for all such question is not a new thing. Many people also consult their astrologer for the same, but very few understand the science involved in it. To give it a more structured understanding, a new method called Dermatoglyphic Multiple Intelligence Test (DMIT) is being used to evaluate one's inborn intelligences through simple biometrics, where fingerprints will let you know what career plans your talent indicates.

Vineet Jain, Reiki Master, says, "Science says fingerprints start developing in foetus from 14-24 weeks with the brain pattern growing simultaneously and are interconnected. DMIT is a scientific study of fingerprint patterns that helps in understanding an individual's potential and personality. D.M.I Assessment technique has been developed by scientists and research experts from World-renowned universities and is based on knowledge from Genetics, Embryology, Dermatoglyphics, Psychology and Neuroscience."

After a simple method of collecting fingerprints of all the fingers of a child, the results of ridges are then manually counted and a detailed analysis is done with the help of software. According to dermatoglyphic experts, thumb print tells about action and execution; index finger logic and creativity; middle finger limb motor ability and art appreciation; ring power of voice recognition; little finger text image discerning. Based on assessment report of 27-35 pages, parents then explained all the answers which include positives and limitations, perspective and reflex sensitivity, innate personalities and characteristics like IQ, EQ, preferred learning style and career options.

The method costs between Rs. 2500 to Rs.10,000 and is not only beneficial for children and their parents, but also for young adults who have just entered their career and want to see their growth parameter and the areas they need to work on. This process is also beneficial for entrepreneurs and businessmen for their successful expansion.

(This story has not been edited by Business Standard staff and is auto-generated from a syndicated feed.)

Choosing oneself to become just a successful engineer or a doctor in future is passe. With the growing competition and the growth in career options, Kids and their parents are becoming more confused towards identifying their actual passion and talent. Just as the 10th and 12th board results are out, parents are now worried about what goals have their kids made up in their mind to peruse in future. There are dozens of questions revolving in their head making them befuddled with thoughts like, does my kid fits for his goals or his talent lay in some other streams?

Consulting a career counsellor for all such question is not a new thing. Many people also consult their astrologer for the same, but very few understand the science involved in it. To give it a more structured understanding, a new method called Dermatoglyphic Multiple Intelligence Test (DMIT) is being used to evaluate one's inborn intelligences through simple biometrics, where fingerprints will let you know what career plans your talent indicates.

Vineet Jain, Reiki Master, says, "Science says fingerprints start developing in foetus from 14-24 weeks with the brain pattern growing simultaneously and are interconnected. DMIT is a scientific study of fingerprint patterns that helps in understanding an individual's potential and personality. D.M.I Assessment technique has been developed by scientists and research experts from World-renowned universities and is based on knowledge from Genetics, Embryology, Dermatoglyphics, Psychology and Neuroscience."

After a simple method of collecting fingerprints of all the fingers of a child, the results of ridges are then manually counted and a detailed analysis is done with the help of software. According to dermatoglyphic experts, thumb print tells about action and execution; index finger logic and creativity; middle finger limb motor ability and art appreciation; ring power of voice recognition; little finger text image discerning. Based on assessment report of 27-35 pages, parents then explained all the answers which include positives and limitations, perspective and reflex sensitivity, innate personalities and characteristics like IQ, EQ, preferred learning style and career options.

The method costs between Rs. 2500 to Rs.10,000 and is not only beneficial for children and their parents, but also for young adults who have just entered their career and want to see their growth parameter and the areas they need to work on. This process is also beneficial for entrepreneurs and businessmen for their successful expansion.

(This story has not been edited by Business Standard staff and is auto-generated from a syndicated feed.)

ANI

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DMIT, a trending scientific procedure to test one's inborn intelligence - Business Standard

How research helped me get over my fear of having an IVF baby … – Stuff.co.nz

AMY KLEIN

Last updated14:37, June 16 2017

123RF

Articles, blogs and "mummy boards" do little to ease a woman's fears about going down the IVF route.

OPINION: When I first visited a fertility doctor because of pregnancy problems, I had no idea that the in vitro fertilisation, or IVF, he was suggesting to help me was actually the "test-tube baby" technique that I'd heard about, an approach that had sounded scary, like something out of science fiction.

After I educated myself and started treatment, the concerns continued: Would the hormone-stimulating drugs have adverse effects on me? What would the drugs do to the fetus?

And more important, would conceiving a child outside the womb (not actually in a test tube but in an embryology lab) have any long-term effects? Most important, would my child - if I would be lucky enough to give birth to one - be as physically and mentally healthy as naturally conceived children?

Articles and blogs fed into my worries - not to mention the online "mummy boards" at pregnancy and fertility websites where women trade rumours, innuendoes and fears, often based on nothing more than a friend's experience.

READ MORE: *Pregnant women may be having stranger's child in Dutch IVF clinic sperm mix-up *Woman whose IVF was paid for by George Michael wishes she got to thank him *Two babies within ten months after thinking it was impossible to have kids

Since the first test-tube baby, Louise Brown, was born in England in 1978, about 6.5 million children have been born worldwide with the help of assisted reproductive technologies (ART) such as IVF. So there is now enough information to address my concerns. Overall, those findings leave me pretty confident that the risks are pretty small and well worth taking if, like me, you want to have a baby but can't.

Although taking fertility medications drove me crazy - some hormones gave me nightmares, others kept me up at night, and the main ones made my mind race loopily - looking at studies allowed me to conclude that IVF probably has no long-term bad effects.

For instance, a 2013 study of 21,646 women in Australia concluded that "there is no evidence of an increased risk of ovarian cancer following IVF in women who give birth".

Another study of 9825 American women found no link between gonadotropins - the drugs I was taking to increase my egg production - and ovarian cancer for women who gave birth. There was one worrisome point: Both studies found an increased cancer risk for women with "resistant infertility" - eg.those who did not give birth - although the researchers did not know why.

A recent study in the journal JAMA of about 25,000 women who had fertility treatments between 1980 and 1995 found that those who had gone through IVF had no greater risk of getting breast cancer in the subsequent 21 years than those who used other techniques.

Whew. I went through nine rounds of IVF before I got pregnant, which means I took a lot of ovary-stimulating drugs, so these studies are reassuring.

"Numerous studies and opinions from [the American Society for Reproductive Medicine] confirm low risk for ovarian and breast cancer from the use of fertility drugs, regardless of the number of IVF cycles performed," said Jeffrey Braverman, founder and medical director at Braverman IVF & Reproductive Immunology in New York.

So how about risks to the baby? Would he or she be affected by her medically assisted conception?

Two studies have raised concerns.

A 2016 study in JAMA Pediatrics found increased risk for birth defects in babies conceived through ART. The study, which involved more than 4 million infants, found that "singleton infants conceived using ART were 40 per cent more likely to have a nonchromosomal birth defect (such as cleft lip and/or palate or a congenital heart defect) compared with all other singleton births."

The researchers acknowledged that the study "did not account for some factors related to infertility that might explain the observed increases in risk for birth defects." In other words, IVF may not have caused the defects. They recommended further research.

A comprehensive review of a group of other studies suggested that the risk for developmental disabilities was greater with ART - which, in addition to IVF, includes egg freezing and surrogacy - than with natural childbirth. The review examined studies of IVF and autism, cerebral palsy, intellectual disability, attention-deficit/hyperactivity disorder and sensory impairment, among others, and found conflicting information, no correlation or that the disabilities could have been caused by other factors such as preterm birth.

And a study published in March found an increased risk of neoplasms - tumours that can be benign or malignant - in children born through ART.

But I focused on a study that followed children conceived with ART into their teenage years. It offers a much more reassuring view. The study, published in January, compared 253 16- and 17-year-olds who were conceived with fertility treatments to a cohort of teenagers conceived naturally and found that "no differences were detected in general and mental health of ART adolescents or cognitive ability, compared with the reference group".

The researchers, who said this was the first long-term study of such children, concluded that their "preliminary results provide reassurance that in the long run, health and functioning of ART-conceived adolescents is not compromised".

One of the researchers on the study, Mark Weiser, a psychiatry professor at Tel Aviv University's Sackler School of Medicine, said in an interview that the findings should be a relief to parents who used IVF and other assisted reproductive technology.

"We show there is nothing wrong with these kids" when compared with children born naturally. "This is a very positive message to parents who are not able to get pregnant on their own. If you look down the line, the kids are perfectly normal."

As for me: After an uneventful pregnancy, my daughter was born full term nearly two years ago at a healthy six pounds, six ounces, with all her fingers and toes and brown hair that would soon turn to curls. She is a delightful, chatty, feisty toddler. Every parent worries about their child, and I know that I will be no different. But for now it seems clear to me that the risks of having used IVF were minimal - and the reward huge.

-The Washington Post

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How research helped me get over my fear of having an IVF baby ... - Stuff.co.nz

Global Immunology Drugs Market to 2022 – Increasing …

Global Immunology Drugs Market to 2022 - Increasing Prevalence, Repositioning Opportunities and Strong Uptake of Interleukin Receptor Inhibitors to Drive Growth

Summary

Immunology is a therapy area characterized by disorders of the immune system, specifically an aberrant autoimmune response against healthy tissues in the body, leading to chronic or acute inflammation. Depending on the specific site affected, this can lead to various types of chronic pain and mobility loss, and have a negative impact on quality of life.

A number of therapies have been approved for immunological disorders, including the largely genericized disease-modifying anti-rheumatic drug (DMARD) class of small molecule drugs. However, as these therapies often fail to elicit an adequate long-term response, a large second-line therapy segment has emerged in these markets, beginning with the approval of Remicade (infliximab) and Enbrel (etanercept) in 1998. There is currently no cure for immunological disorders due to the highly complex nature of the immune system and the fact that many components of the pathophysiological states of these diseases have roles in the healthy immune system.

Autoimmune disorders are currently incurable, and treatment is aimed at managing the disease, in order to reduce the severity of its symptoms and lower the risk of associated co-morbidities. Cytokines and their receptors, such as Tumor Necrosis Factor- and Interleukin-6 are the most effective and most common therapies used in immunology. This class of compounds has been the most commercially successful in the past decade, particularly in the RA market, with many clinical trials underway across various immunological indications. The market for immunological disorders is largely accounted for by premium products, with only a relatively small revenue share accounted for by generics and biosimilars.

Inflectra, a biosimilar of Remicade was recently approved by the FDA in 2016. However, the gradual uptake of biosimilars such as Inflectra is not expected to act as a strong growth driver for the biosimilar segment within the forecast period. This therefore means existing products such as Remicade are expected to maintain high revenues during the forecast period

Although there is a high degree of failure and uncertainty in R&D of immunological drugs, there are 2,054 drugs in active development in the immunology pipeline. In the long-term, this is expected to drive growth in this market in spite of the anticipated approval of biosimilars for key blockbuster drugs and resultant erosion of revenues. Cytokines and their receptors account for the largest single segment of each of the pipelines which make up the largest individual class.

The report focuses on four key indications within immunology: Rheumatoid arthritis, Systemic lupus erythematosus (SLE), Psoriasis and Inflammatory bowel disease (The two major types of Inflammatory bowel disease covered in this report are Ulcerative colitis and Crohns disease). With no curative therapies available, symptomatic medications prescribed off-label are an important part of the treatment paradigm, especially in SLE, increasing the need for extensive R&D within this area.

Scope

- Global revenues for the immunology market are forecast to grow at a compound annual growth rate of 3.63%, from $57.7 billion in 2015 to $74.1 billion in 2022. - Which drugs will achieve blockbuster status and how will the key player companies perform during the forecast period? - The immunological disorders pipeline is large and diverse, and contains 2,054 products. How does the composition of the pipeline compare with that of the existing market? - What molecular targets and molecule types are most commonly being trialed in pipeline products in the key indications? - Which products will contribute to market growth most significantly, and which will achieve blockbuster status? - Will the current market leaders retain their dominance over the forecast period, and how is their revenue share of the immunology market set to change?

Reasons to buy

- Understand the current clinical and commercial landscape by considering disease pathogenesis, diagnosis, prognosis, and the treatment options available at each stage of diagnosis - Visualize the composition of the immunology market across each indication, in terms of dominant molecule types and targets, highlighting the key commercial assets and players - Analyze the immunological disorders pipeline and stratify by stage of development, molecule type and molecular target, with a granular breakdown across key indications - Understand the growth in patient epidemiology and market revenues for the immunology market, globally and across the key players and product types - Stratify the market in terms of the split between generic and premium products, and assess the role of these product types in the treatment of the various immunological disorders. - Identify commercial opportunities in the immunology deals landscape by analyzing trends in licensing and co-development deals

1 Table of Contents 1 Table of Contents 4 1.1 List of Tables 6 1.2 List of Figures 6 2 Introduction 9 2.1 Therapy Area Introduction 9 2.1.1 Rheumatoid Arthritis 9 2.1.2 Systemic Lupus Erythematosus 10 2.1.3 Psoriasis 11 2.1.4 Inflammatory Bowel Disease 12 2.2 Symptoms 13 2.3 Etiology and Pathophysiology 15 2.3.1 Pathophysiology 17 2.4 Epidemiology 21 2.4.1 Rheumatoid Arthritis 22 2.4.2 Systemic Lupus Erythematosus 23 2.4.3 Psoriasis 23 2.4.4 Inflammatory Bowel Disease 24 2.5 Co-morbidities and Complications 25 2.6 Treatment 26 2.6.1 Rheumatoid Arthritis 27 2.6.2 Systemic Lupus Erythematosus 30 2.6.3 Psoriasis 31 2.6.4 Inflammatory Bowel Disease 32 3 Key Marketed Products 34 3.1 Overview 34 3.2 Humira (adalimumab) 34 3.3 Enbrel (etanercept) 36 3.4 Remicade (infliximab) 38 3.5 Rituxan (rituximab) 40 3.6 Stelara (ustekinumab) 42 3.7 Simponi (golimumab) 43 3.8 Prograf (tacrolimus) 45 3.9 Cimzia (certolizumab pegol) 46 3.10 Entyvio (vedolizumab) 47 3.11 Cosentyx (Secukinumab) 49 4 Pipeline Landscape Assessment 51 4.1 Overview 51 4.2 Pipeline Development Landscape 51 4.3 Molecular Targets in the Pipeline 54 4.4 Clinical Trials 56 4.4.1 Failure Rate by Stage of Development, Indication, Molecule Type and Molecular Target 56 4.4.2 Clinical Trial Duration by Stage of Development, Indication, Molecule Type and Molecular Target 60 4.4.3 Clinical Trial Size 65 4.4.4 Aggregate Clinical Program Size 69 4.4.5 Assessment of Key Pipeline Products 72 4.5 Conclusion 80 5 Multi-scenario Market Forecast to 2022 81 5.1 Overall Market Size 81 5.2 Generic Penetration 83 5.3 Revenue Forecast by Molecular Target 84 5.3.1 Tumor Necrosis Factor-Alpha 84 5.3.2 Interleukin Receptor 86 5.3.3 B and T Lymphocyte Antigens 86 5.3.4 Janus Kinases 87 6 Company Analysis and Positioning 89 6.1 Revenue and Market Share Analysis by Company 90 6.1.1 AbbVie Will the Patent Expiration of Humira Cause a Loss in Market Size? 94 6.1.2 Pfizer Xeljanz to Overcome Enbrel Revenue Loss 95 6.1.3 Johnson & Johnson Steady Market Leader over Forecast Period 96 6.1.4 Amgen Will the Patent Expiration of Enbrel Have an Effect on Overall Immunology Revenue? 97 6.1.5 Roche Moderate Revenue Loss Expected due to Biosimilar Competition 98 6.1.6 Eli Lilly Approval of RA Drug to Drive Revenue 99 6.1.7 Bristol-Myers Squibb Will Biosimilar Competition Affect Orencia Revenue? 100 6.1.8 Celgene Otezla and Ozanimod Hydrochloride to Become Blockbuster Drugs 101 6.2 Company Landscape 103 6.3 Marketed and Pipeline Portfolio Analysis 103 7 Strategic Consolidations 106 7.1 Licensing Deals 106 7.1.1 Deals by Region, Year and Value 106 7.1.2 Deals by Stage of Development and Value 108 7.1.3 Deals by Molecule Type, Mechanism of Action and Value 109 7.1.4 Licensing Deals Valued over $100m 111 7.2 Co-development Deals 115 7.2.1 Deals by Region, Year and Value 116 7.2.2 Deals by Stage of Development and Value 117 7.2.3 Deals by Molecule Type, Mechanism of Action and Value 118 7.2.4 Co-development Deals Valued over $100m 120 8 Appendix 124 8.1 References 124 8.2 Table of All Clinical Stage Pipeline Products 132 8.3 Abbreviations 136 8.4 Disease List 137 8.5 Methodology 138 8.5.1 Coverage 138 8.5.2 Secondary Research 138 8.5.3 Market Size and Revenue Forecasts 138 8.5.4 Pipeline Analysis 139 8.5.5 Competitive Landscape 139 8.6 Contact Us 139 8.7 Disclaimer 140

1.1 List of Tables Table 1: Immunology Therapeutics Market, Symptoms of RA, SLE, Psoriasis and IBD 14 Table 2: Immunology Therapeutics Market, Etiology of RA, SLE, Psoriasis and IBD 16 Table 3: Immunology, Global, Epidemiology of Inflammatory Immunological Disorders, 2017 22 Table 4: Immunology Therapeutics Market, Global, Approved Indications for Humira, 2017 35 Table 5: Immunology Therapeutics Market, Global, Approved Indications for Enbrel, 2017 37 Table 6: Immunology Therapeutics Market, Global, Approved Indications for Remicade, 2017 39 Table 7: Immunology Therapeutics Market, Global, Approved Indications for Rituxan, 2017 41 Table 8: Immunology Therapeutics Market, Global, Approved Indications for Stelara, 2017 43 Table 9: Immunology Therapeutics Market, Global, Approved Indications for Simponi, 2017 44 Table 10: Immunology Therapeutics Market, Global, Approved Indications for Prograf, 2017 45 Table 11: Immunology Therapeutics Market, Global, Approved Indications for Cimzia, 2017 46 Table 12: Immunology Therapeutics Market, Global, Approved Indications for Entyvio, 2017 48 Table 13: Immunology Therapeutics Market, Global, Approved Indications for Cosentyx, 2017 50 Table 14: Immunology, Global, Annual Revenue Forecast for Key Products ($m), 20152022 82 Table 15: Immunology, Global, Usage of Generics Across Key Indications, 2017 84 Table 16: Immunology Therapeutics Market, Global, Forecast Revenues by Company, 20152022 91 Table 17: Immunology Therapeutics Market, Global, Licensing Deals Valued over $100m, 20062016 111 Table 18: Immunology Therapeutics Market, Global, Co-development Deals Valued over $100m, 20062017 120

1.2 List of Figures Figure 1: Immunology, Global, Epidemiology Patterns for Rheumatoid Arthritis (000), 20162023 22 Figure 2: Immunology, Global, Epidemiology Patterns for Systemic Lupus Erythematosus (000), 20162023 23 Figure 3: Immunology, Global, Epidemiology Patterns for Psoriasis (000), 20162023 24 Figure 4: Immunology, Global, Epidemiology Patterns for Inflammatory Bowel Disease (000), 20162023 25 Figure 5: Immunology, Global, Key Marketed Products and Approved Indications, 2016 34 Figure 6: Immunology Therapeutics Market, Global, Annual Revenues for Humira ($bn), 20062022 36 Figure 7: Immunology Therapeutics Market, Global, Annual Revenues for Enbrel ($bn), 20062022 38 Figure 8: Immunology Therapeutics Market, Global, Annual Revenues for Remicade ($bn), 20062022 40 Figure 9: Immunology Therapeutics Market, Global, Annual Revenues for Enbrel ($bn), 20062022 42 Figure 10: Immunology Therapeutics Market, Global, Annual Revenues for Stelara ($bn), 20062022 43 Figure 11: Immunology Therapeutics Market, Global, Annual Revenues for Simponi ($bn), 20062022 44 Figure 12: Immunology Therapeutics Market, Global, Annual Revenues for Prograf ($bn), 20062022 46 Figure 13: Immunology Therapeutics Market, Global, Annual Revenues for Cimzia ($bn), 20062022 47 Figure 14: Immunology Therapeutics Market, Global, Annual Revenues for Entyvio ($bn), 20062022 49 Figure 15: Immunology Therapeutics Market, Global, Annual Revenues for Cosentyx ($bn), 20062022 50 Figure 16: Antibacterial Drug Market, Global, Overall Pharmaceutical Industry Pipeline by Therapy Area, 2017 51 Figure 17: Immunology Therapeutics Market, Global, Pipeline for Immunology by Stage of Development, Molecule Type and Program Type, 2017 52 Figure 18: Immunology Therapeutics Market, Global, Pipeline for Key Immunology Indications by Stage of Development, 2017 53 Figure 19: Immunology Therapeutics Market, Global, Pipeline for Key Immunology Indications by Molecule Type, 2017 54 Figure 20: Immunology Therapeutics Market, Pipeline by Mechanism of Action (%), 2017 55 Figure 21: Immunology Therapeutics Market, Global, Pipeline for Key Immunology Indications by Molecular Target, 2017 56 Figure 22: Immunology Therapeutics Market, Global, Clinical Trial Attrition Rates by Stage of Development (%), 20062017 57 Figure 23: Immunology Therapeutics Market, Global, Clinical Trial Attrition Rates by Stage of Development and Indication (%), 20062017 58 Figure 24: Immunology Therapeutics Market, Global, Clinical Trial Attrition Rates by Stage of Development and Molecule Type (%), 20062017 59 Figure 25: Immunology Therapeutics Market, Global, Clinical Trial Attrition Rates by Stage of Development and Molecular Target (%), 20062017 60 Figure 26: Immunology Therapeutics Market, Global, Clinical Trial Duration by Stage of Development (months), 20062017 61 Figure 27: Immunology Therapeutics Market, Global, Clinical Trial Duration by Stage of Development and Indication (months), 20062017 62 Figure 28: Immunology Therapeutics Market, Global, Clinical Trial Duration by Stage of Development and Molecule Type (months), 20062017 63 Figure 29: Immunology Therapeutics Market, Global, Clinical Trial Duration by Stage of Development and Molecular Target (months), 20062017 64 Figure 30: Immunology Therapeutics Market, Global, Clinical Trial Size by Stage of Development (patients), 20062017 65 Figure 31: Immunology Therapeutics Market, Global, Clinical Trial Size by Stage of Development and Indication (participants), 20062017 66 Figure 32: Immunology Therapeutics Market, Global, Clinical Trial Size by Stage of Development and Molecule Type (participants), 20062017 67 Figure 33: Immunology Therapeutics Market, Global, Clinical Trial Size by Stage of Development and Molecular Target (participants), 20062017 68 Figure 34: Immunology Therapeutics Market, Global, Clinical Program Size by Stage of Development (months), 20062017 69 Figure 35: Immunology Therapeutics Market, Global, Clinical Program Size by Stage of Development and Indication (participants), 20062017 70 Figure 36: Immunology Therapeutics Market, Global, Clinical Program Size by Stage of Development and Molecule Type (participants), 20062017 71 Figure 37: Immunology Therapeutics Market, Global, Clinical Program Size by Stage of Development and Molecular Target (participants), 20062017 72 Figure 38: Immunology Therapeutics Market, Global, Revenue Forecast for sarilumab ($bn), 20162022 74 Figure 39: Immunology Therapeutics Market, Global, Revenue Forecast for sirukumab ($m), 20152022 75 Figure 40: Immunology, Global, Annual Revenue Forecast for baricitinib ($bn), 20152022 77 Figure 41: Immunology, Global, Annual Revenue Forecast for upadacitinib ($m), 20152022 78 Figure 42: Immunology, Global, Annual Revenue Forecast for ozanimod ($bn), 20192022 79 Figure 43: Immunology, Global, Market Size ($m), 20152022 81 Figure 44: Immunology, Global, Annual Revenue Forecast for Key Products ($m), 20152022 83 Figure 45: Immunology, Global, Annual Revenue Forecast for Tumor Necrosis Factor-Alpha Inhibitors ($bn), 20152022 85 Figure 46: Immunology, Global, Annual Revenue Forecast for Interleukin Inhibitors ($bn), 20152022 86 Figure 47: Immunology, Global, Annual Revenue Forecast for B and T Lymphocyte Antigens ($bn), 20152022 87 Figure 48: Immunology, Global, Annual Revenue Forecast for Janus Kinases ($bn), 20152022 88 Figure 49: Immunology Therapeutics Market, Global, Cluster by Growth and Market Share, 20152022 89 Figure 50: Immunology Therapeutics Market, Global, Forecast Market Share by Company (%), 20152022 92 Figure 51: Immunology, Global, Companies by Compound Annual Growth Rate (%), 20142022 93 Figure 52: Immunology, Global, Revenues by Product Type, 20152022 94 Figure 53: Immunology, Global, AbbVie Annual Revenue Forecast ($bn), 20152022 95 Figure 54: Immunology, Global, Pfizer Annual Revenue Forecast ($bn), 20152022 96 Figure 55: Immunology, Global, Johnson & Johnson Annual Revenue Forecast ($bn), 20152022 97 Figure 56: Immunology, Global, Amgen Annual Revenue Forecast ($bn), 20152022 98 Figure 57: Immunology, Global, Roche Annual Revenue Forecast ($bn), 20152022 99 Figure 58: Immunology, Global, Eli Lilly Annual Revenue Forecast ($bn), 20152022 100 Figure 59: Immunology, Global, Bristol-Myers Squib Annual Revenue Forecast ($bn), 20152022 101 Figure 60: Immunology, Global, Celgene Annual Revenue Forecast ($bn), 20152022 102 Figure 61: Immunology, Global, Companies by Type, 2017 103 Figure 62: Immunology, Global, High-Activity and Late-Stage Pipeline Developers by Level of immunology specialization, 2017 104 Figure 63: Immunology, Global, Proportion of Company Revenue Attributed to immunology, 20152022 105 Figure 64: Immunology, Global, Licensing Deals, 20062017 107 Figure 65: Immunology, Global, Licensing Deals by Indication and Value, 20062017 108 Figure 66: Immunology, Global, Licensing Deals, 20062017 109 Figure 67: Immunology, Global, Licensing Deals by Molecule Type and Mechanism of Action, 20062017 110 Figure 68: Immunology, Global, Co-development Deals, 20062017 116 Figure 69: Immunology, Global, Co-development Deals by Indication and Value, 20062017 117 Figure 70: Immunology, Global, Co-development Deals, 20062017 118 Figure 71: Immunology, Global, Co-development Deals by Molecule Type and Mechanism of Action, 20062017 119 Figure 72: Immunology, Global, Table of all Clinical Stage Pipeline Products, Part I, 2017 132 Figure 73: Immunology, Global, Table of all Clinical Stage Pipeline Products, Part II, 2017 133 Figure 74: Immunology, Global, Table of all Clinical Stage Pipeline Products, Part III, 2017 134 Figure 75: Immunology, Global, Table of all Clinical Stage Pipeline Products, Part IV, 2017 135

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Global Immunology Drugs Market to 2022 - Increasing ...

Understanding human behviour through the power of data – The Drum

Just a few years ago, the world was abuzz with the potential that beacon technology offered to reshape the retail industry. Now, several years on, there are even more technologies that offer similar promise. Beacons represent an important source of data regarding in-store customer movement, but the emergence of other sophisticated data collection technologies has added to the potential for understanding human behavior in the real world. To that end, what companies really need now is a solution that allows them to understand the fragmented data sets and their sources -- whether its beacons, sensors, or GPS -- and get a better sense of the bigger picture.

People spend an average of 5 hours a day on their phones. That sounds like a lot, but what happens in those other 19 hours? People have lives outside of their phones. The problem for marketers, then, is how to access that information to better understand how people behave in the real world, and then integrate that with what they already know about their online persona. At the moment, there are bits and pieces of data everywhere -- some proximity data here, some geodata there -- but otherwise, there are so many fragmented data sources that each tell a tiny piece of the story of a consumers offline activity. Moreover, the initial promise that beacons held to completely revitalize brick-and-mortar businesses and drastically increase in-store attribution has taken longer to materialize than expected.

Beacons were implemented so that retailers and other businesses could tell where a customer was at any given point, and allow businesses to send out targeted messages to phones that have activated a beacon. Businesses were quick to adopt this new technology, including Macys, Lord & Taylors, Major League Baseball, and American Airlines. However, there are still blank spots on the canvas. The real world is fluid, made up of many different behaviors and movements -- there is no one magic solution.

The information gleaned from one data source alone is not enough to get a complete view into peoples behavior or motivations. That said, proximity and location data have tremendous potential for filling in the blank spots on the canvas when used strategically. For the proximity industry alone, weve seen companies double down on their investments, validating the demand for technologies that provide a clearer understanding of how people behave in the real world.

Having a strong understanding of the various technologies on the market has also helped us determine that the efficacy of this data and technology depends on what goals companies wish to achieve. Deterministic methodologies used by beacon and Wifi technology can pinpoint almost exactly where someone was at any given point -- where they were in a store, for example, or even what floor they were on. Probabilistic technologies, such as GPS and geodata, on the other hand, provide massive scale as well as an overarching idea of people's movements in less densely-populated spaces.

In order for companies to understand a consumers offline behavior as accurately as they understand their online activity, they first need to stitch these different data sources together as they apply to their specific goals. That being said, there are over 400 proximity service providers (PSPs) alone, and thousands of GPS sources and geo-enabled apps -- just getting access to the data requires forming partnerships with each of those entities individually.

The Real World Graph

Unacast built the Real World Graph to provide a solution to that problem. Unacast has created a platform of proximity and location providers to paint a clear picture of how people move in the real world. Just as Google has indexed online behavior and Facebook has created the Social Graph, The Real World Graph provides a place where multiple data sets and technologies are collected and harmonized, all while ensuring individual privacy is respected. Our meticulous methodologies filter for quality to provide transparency, and highlight strategic data that can be used to marry online profiles with real world behaviors. Different data sources tell different stories, and The Real World Graph goes beyond the boundaries of industry to bring those stories together.

The mission at Unacast is to provide the technology and tools that will help data-driven industries understand the physical world the same way we understand the online world. Not only is this vital for the evolution of retail, advertising and other consumer-centric industries, but it can also significantly affect the evolution of e-commerce, financial technology, real estate, and health technology, among other industries.

Data from sensors, beacons, proximity data, GPS, NFC all tell an individual piece of a users behavior in the real world. But combined, the different data sources can tell the most in-depth, accurate story about what people are doing in the real world, and thats what matters most.

Thomas Walle, CEO & Co-founder, Unacast.

Email: hello@unacast.com

Web:unacast.com

Twitter:@unacast

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Understanding human behviour through the power of data - The Drum

Right to life forfeited by those who commit murder – News Letter Journal

Dear Editor,

While I was not particularly interested in learning all the details of how a firing squad works, I most certainly did appreciate the young mans letter in last weeks paper supporting the death penalty for willful murder and other base crimes.

Various religious leaders may pontificate that all life is sacred. And sociologists, psychologists, and the supposed wise men of the world think that their studies, investigations, and theories of human behavior can negate the need or justification for the death penalty. But these are all conclusions derived merely by human reasoning which, apart from the guidance of Gods written Word, is inevitably perverted by our corrupted and sinful natures to excuse sin and tolerate injustice. It is simply not right to bury the dead, but allow his or her killer to live.

The notion that all life is sacred may sound very pious and holy, but it is an idea that is simply not found in the Scriptures. All innocent life is sacred, yes! But criminal, degenerate life is not. When someone has so little respect for the life of his fellow human beings that he kills them, he has forfeited any right he had to his own life and society has every right and duty to take it from him.

The Bible says plainly: Whoever sheds mans blood, his blood will be shed by man, for God made man in the image of God. (Gen. 9:6) In applying this verse, one Bible commentator has written: How carefully God protects the rights of men! He has attached a penalty to willful murder. If one murderer were permitted to go unpunished, he would by his evil influence and cruel violence subvert others. God must punish murderers. He gives life, and He will take life if that life becomes a terror and a menace. (SDA Bible Commentary, Vol. 7-A, p. 1091) And the principle that human governments have the right to use capital punishment to maintain order in society and to execute justice on behalf of the victim is substantiated by countless examples in sacred history. Ceasar (human government) does not bear the sword in vain. (See Romans 13:4)

In all the moral issues of life, the word of our infinite Creator God must stand sovereign and supreme. Our only duty as His sinful, erring, and fallible creatures is to submit unquestioning to His infallible judgments, decisions, and requirements.

Leonard Lang

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Right to life forfeited by those who commit murder - News Letter Journal

Why Do Men Have Nipples? – ScienceAlert

It's a question that's been bothering humans for centuries, even before the theory of evolution was first conceived. Why do men and other male mammals have nipples if they don't feed their young? What's the point?

"I have received more than a dozen requests to explain how evolution could possibly produce such a useless structure," evolutionary biologist Stephen Jay Gould wrote in a journal column back in 1993.

After all, the vast majority of men never lactate, although there are a few exceptions which typically involve some hormonal problem. But when we think about traits from an evolutionary perspective, we often think in terms of 'What is this thing good for?'

It turns out that the case of male nipples somewhat contradicts that very question.

The short answer is that it's not necessarily a feature produced by evolution - instead, it's more like a feature that evolution didn't bother to get rid of, or possibly even couldn't.

"In my view of life ... male nipples are an expectation based on pathways of sexual differentiation in mammalian embryology," wrote Gould.

What he was referring to is the fact that all mammal embryos - male and female - start out looking exactly the same, with potential to develop into either sex.

But if the embryo has an XY chromosome set, after the first few weeks a gene called SRY kicks in, triggering the genetic switch that sends the embryo down the male development path.

But here's the thing - mammary glands start developing super-early, even before SRY can do its job. And so the precursors to breast tissue, nipples and all, are preserved even once an embryo becomes biologically male.

And it's not like having nipples is a costly feature to have. So even if evolution could rewire the developmental process to get rid of them for men, it's more likely that it just shrugged and let them be.

It's also a reminder that evolution is kinda messy. According to evolutionary biologist Rob Brooks from the University of New South Wales in Australia, several genes can be involved in the making of a trait, leaving it around even if it's not being selected for.

"Even for periods of time, something can be selected neither for nor against, and what you would expect under those circumstances is that the presence or absence of our traits will drift," Brooks told ScienceAlert.

So the answer seems pretty simple in the end. But exploring the question about male nipples also gives us a nice lesson about adaptive thinking in evolution.

People sometimes get carried away and try to find an evolutionary explanation for every trait they see. After all, when you understand the basic premise of evolution, it becomes a pretty compelling narrative.

"It's really tempting to [view traits as adaptive] because once you understand the adaptive logic, then you start - like with all confirmation bias - to see the signature of adaptation everywhere," says Brooks.

But just because a story is compelling, doesn't mean it's accurate. Sure, you could come up with some elaborate story on how male nipples must be attractive for females somehow, but it's much more plausible to consider the simple developmental wiring problem we explained above.

Gould himself was famously critical of "just-so stories" about natural selection, but bear in mind that they can be an excellent starting point for further experiments.

"Science is there to test the ideas, so adaptive storytelling is hugely important, because it's the source of our hypotheses," Brooks told ScienceAlert.

"If you don't come up with an adaptive story, then there's nothing to test."

Of course, in the case of male nipples, we don't need an adaptive story. Just treat them as accessories, guys.

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Why Do Men Have Nipples? - ScienceAlert

Newly identified method of gene regulation challenges accepted … – Phys.Org

June 15, 2017

Researchers at the Stanford University School of Medicine have discovered an unexpected layer of the regulation of gene expression. The finding will likely disrupt scientists' understanding of how cells regulate their genes to develop, communicate and carry out specific tasks throughout the body.

The researchers found that cellular workhorses called ribosomes, which are responsible for transforming genes encoded in RNA into proteins, display a never-before-imagined variety in their composition that significantly affects their function. In particular, the protein components of a ribosome serve to tune the tiny machine so that it specializes in the translation of genes in related cellular pathways. One type of ribosome, for example, prefers to translate genes involved in cellular differentiation, while another specializes in genes that carry out essential metabolic duties.

The discovery is shocking because researchers have believed for decades that ribosomes functioned like tiny automatons, showing no preference as they translated any and all nearby RNA molecules into proteins. Now it appears that broad variation in protein production could be sparked not by changes in the expression levels of thousands of individual genes, but instead by small tweaks to ribosomal proteins.

'Broad implications'

"This discovery was completely unexpected," said Maria Barna, PhD, assistant professor of developmental biology and of genetics. "These findings will likely change the dogma for how the genetic code is translated. Until now, each of the 1 to10 million ribosomes within a cell has been thought to be identical and interchangeable. Now we're uncovering a new layer of control to gene expression that will have broad implications for basic science and human disease."

Barna is the senior author of the study, which will be published online June 15 in Molecular Cell. Postdoctoral scholars Zhen Shi, PhD, and Kotaro Fujii, PhD, share lead authorship. Barna is a New York Stem Cell Robertson Investigator and is also a member of Stanford's Bio-X and Child Health Research Institute.

The work builds upon a previous study from Barna's laboratory that was published June 1 in Cell. The lead author of that study was postdoctoral scholar Deniz Simsek, PhD. It showed that ribosomes also differ in the types of proteins they accumulate on their outer shells. It also identified more than 400 ribosome-associated proteins, called RAPs, and showed that they can affect ribosomal function.

Every biology student learns the basics of how the genetic code is used to govern cellular life. In broad strokes, the DNA in the nucleus carries the building instructions for about 20,000 genes. Genes are chosen for expression by proteins that land on the DNA and "transcribe" the DNA sequence into short pieces of mobile, or messenger, RNA that can leave the nucleus. Once in the cell's cytoplasm, the RNA binds to ribosomes to be translated into strings of amino acids known as proteins.

Every living cell has up to 10 million ribosomes floating in its cellular soup. These tiny engines are themselves complex structures that contain up to 80 individual core proteins and four RNA molecules. Each ribosome has two main subunits: one that binds to and "reads" the RNA molecule to be translated, and another that assembles the protein based on the RNA blueprint. As shown for the first time in the Cell study, ribosomes also collect associated proteins called RAPs that decorate their outer shell like Christmas tree ornaments.

'Hints of a more complex scenario'

"Until recently, ribosomes have been thought to take an important but backstage role in the cell, just taking in and blindly translating the genetic code," said Barna. "But in the past couple of years there have been some intriguing hints of a more complex scenario. Some human genetic diseases caused by mutations in ribosomal proteins affect only specific organs or tissues, for example. This has been very perplexing. We wanted to revisit the textbook notion that all ribosomes are the same."

In 2011, members of Barna's lab showed that one core ribosomal protein called RPL38/eL38 is necessary for the appropriate patterning of the mammalian body plan during development; mice with a mutation in this protein developed skeletal defects such as extra ribs, facial clefts and abnormally short, malformed tails.

Shi and Fujii used a quantitative proteomics technology called selected reaction monitoring to precisely calculate the quantities, or stoichiometry, of each of several ribosomal proteins isolated from ribosomes within mouse embryonic stem cells. Their calculations showed that not all the ribosomal proteins were always present in the same amount. In other words, the ribosomes differed from one another in their compositions.

"We realized for the first time that, in terms of the exact stoichiometry of these proteins, there are significant differences among individual ribosomes," said Barna. "But what does this mean when it comes to thinking about fundamental aspects of a cell, how it functions?"

To find out, the researchers tagged the different ribosomal proteins and used them to isolate RNA molecules in the act of being translated by the ribosome. The results were unlike what they could have ever imagined.

"We found that, if you compare two populations of ribosomes, they exhibit a preference for translating certain types of genes," said Shi. "One prefers to translate genes associated with cell metabolism; another is more likely to be translating genes that make proteins necessary for embryonic development. We found entire biological pathways represented by the translational preferences of specific ribosomes. It's like the ribosomes have some kind of ingrained knowledge as to what genes they prefer to translate into proteins."

The findings dovetail with those of the Cell paper. That paper "showed that there is more to ribosomes than the 80 core proteins," said Simsek. "We identified hundreds of RAPs as components of the cell cycle, energy metabolism, and cell signaling. We believe these RAPs may allow the ribosomes to participate more dynamically in these intricate cellular functions."

"Barna and her team have taken a big step toward understanding how ribosomes control protein synthesis by looking at unperturbed stem cells form mammals," said Jamie Cate, PhD, professor of molecular and cell biology and of chemistry at the University of California-Berkeley. "They found 'built-in' regulators of translation for a subset of important mRNAs and are sure to find more in other cells. It is an important advance in the field." Cate was not involved in the research.

Freeing cells from micromanaging gene expression

The fact that ribosomes can differ among their core protein components as well as among their associated proteins, the RAPs, and that these differences can significantly affect ribosomal function, highlights a way that a cell could transform its protein landscape by simply modifying ribosomes so that they prefer to translate one type of genesay, those involved in metabolismover others. This possibility would free the cell from having to micromanage the expression levels of hundreds or thousands of genes involved in individual pathways. In this scenario, many more messenger RNAs could be available than get translated into proteins, simply based on what the majority of ribosomes prefer, and this preference could be tuned by a change in expression of just a few ribosomal proteins.

Barna and her colleagues are now planning to test whether the prevalence of certain types of ribosomes shift during major cellular changes, such as when a cell enters the cell cycle after resting, or when a stem cell begins to differentiate into a more specialized type of cell. They'd also like to learn more about how the ribosomes are able to discriminate between classes of genes.

Although the findings of the two papers introduce a new concept of genetic regulation within the cell, they make a kind of sense, the researchers said.

"About 60 percent of a cell's energy is spent making and maintaining ribosomes," said Barna. "The idea that they play no role in the regulation of genetic expression is, in retrospect, a bit silly."

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Again we're shocked to discover that the higher energy environment our solar system experiences, the greater the tightening and finite organizing we see at the cellular level. What will we find only to lose it as our system passes out of higher energy is astonishing. Looking thru this lens of higher energy in past cycles reforms myths into potential truths.

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Newly identified method of gene regulation challenges accepted ... - Phys.Org

The anatomy of Beavers’ win streaks – Mail Tribune

By Bob LundebergMid-Valley Media Group

The two longest winning streaks in Division I baseball this year belong to Oregon State.

The top-seeded Beavers (54-4), who open the College World Series at noon Saturday against Cal State Fullerton (39-22), will take the field at TD Ameritrade Park in Omaha, Nebraska as winners of 21 consecutive games. OSU closed the regular season with 16 straight victories and has outscored opponents 44-9 during its five NCAA tournament games.

Earlier this year, the Beavers won a program-record 23 in a row from Feb. 25 to April 9, including a 12-0 start in Pac-12 play.

The two streaks have accounted for 44 of the teams 54 victories, another single-season school record. With a winning percentage of .931, OSU is on pace to break Arizona States 45-year-old all-time mark of .914 (the Sun Devils finished 64-6 in 1972).

Below is a breakdown of the Beavers winning streaks.

Streak 1, Feb. 25-April 9

Length: 23 games

Runs scored: 136 (5.9 per game)

Runs allowed: 49 (2.1 per game)

One-run games: 6

Shutouts: 6

A loss to Ohio State, which finished 148th in the NCAA RPI, dropped Oregon State to 5-1 early in the season.

The Beavers began the longest winning streak in school history with a 5-2 neutral-site victory over Nebraska, which later came to Oregon for the Corvallis Regional. OSU then got revenge against the Buckeyes to wrap up play in Surprise, Arizona before sweeping consecutive home series with UC Davis and Ball State.

Entering Pac-12 play 14-1 overall, the Beavers outscored Arizona State 16-1 during the three-game set to seize an immediate stranglehold on the conference standings. Starting pitchers Luke Heimlich (eight two-hit innings), Bryce Fehmel (eight innings, one run, four hits) and Jake Thompson (seven two-hit innings) were close to untouchable in the desert.

OSU picked up its first of six walk-off wins at Goss Stadium on March 24, knocking off Arizona 4-3 on a KJ Harrison single that plated Adley Rutschman. The Beavers trailed 3-1 entering the eighth.

One night later, OSU again overcame a deficit and walked off again when Preston Jones scored all the way from second on a wild pitch for a 5-4 win. A comfortable 11-7 decision in the series finale pushed the team to 20-1 overall and 6-0 in Pac-12 play.

The Beavers kept the streak alive with another come-from-behind effort, scoring three times in the ninth to steal a 4-3 victory at Saint Marys on March 28. Nick Madrigal collected the game-winning hit, a two-out, two-RBI single with the bases loaded.

Following another road sweep in which the Beavers outscored Stanford 25-8, OSU pulled out a 4-3 road decision at Portland for its 20th win in a row. Rutschmans two-run single in the sixth put the Beavers in front for good.

A home sweep of Utah including two more walk-offs left OSU 28-1 overall (12-0 Pac-12). Steven Kwan hit a game-winning single in the opener while a Rutschman sacrifice fly brought home Jack Anderson for a 5-4, 16-inning victory in Game 2.

The streak finally came to an end April 13, a 3-2 loss at Washington. But the Beavers fought back to win the final two games of the series.

Streak 2, April 30-current

Length: 21 games

Runs scored: 158 (7.5 per game)

Runs allowed: 41 (2.0 per game)

One-run games: 5

Shutouts: 6

After starting the year 28-1, the Beavers went just 5-3 during a two-week span from April 13-29. The rocky patch included a 7-5, 10-inning home loss to USC, which finished in the Pac-12 basement with Arizona State.

Oregon State came back to rout the Trojans 10-1 in the series finale, igniting a winning streak that has yet to end.

A midweek home victory over Oregon followed by a three-game sweep of California put the Beavers on the brink of the Pac-12 championship. After cruising past the Ducks in Game 1 of the Civil War conference series, Mitchell Verburg struck out Ryne Nelson with the bases loaded in the bottom of the ninth to seal a 5-4 victory and the outright Pac-12 title.

Verburgs heroics also delivered career win No. 1,000 for coach Pat Casey.

The Beavers blanked Oregon 1-0 to sweep the series and cruised by Portland two days later before coming out flat against Washington State May 19. Trailing 3-2 entering the ninth, Steven Kwan and Jack Anderson drew consecutive base-loaded walks off Cougars closer Scott Sunitsch for a true walk-off.

OSU went on to outscore Washington State 19-3 in the final two games of the series, finishing with the best record in conference history at 27-3.

The streak nearly ended again May 26 against Abilene Christian, the Beavers final regular-season opponent. Knotted at 4 in the bottom of the 11th, Anderson knocked in Andy Atwood with a single for the teams sixth walk-off of the year. Reliever Mitch Hickey proposed to his girlfriend on the Goss Stadium turf immediately following the game.

The Beavers entered the NCAA tournament with a 49-4 record and breezed through the Corvallis Regional, outscoring Holy Cross and Yale by a combined margin of 27-3. Two comfortable wins over Vanderbilt in the Corvallis Super Regional pushed the winning streak to 21 as OSU prepares for its CWS opener.

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The anatomy of Beavers' win streaks - Mail Tribune

London fire: Anatomy of a high-rise horror – The Sydney Morning Herald

London:It began with a sudden, frantic knocking on a door, late at night.

On the fourth floor of Grenfell Tower, a block of flats in west London, pregnant Maryam Adam, 41, had been deep in sleep when the loud banging woke her. The clock told her it was just after a quarter to one in the morning.

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Fears the toll will rise with 12 confirmed dead and 78 taken to hospital after the massive blaze at the 24-storey Grenfell Tower in London.

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WARNING, DISTRESSING IMAGES: Two people died at the scene and five later died in hospital after an explosion near a kindergarten in east China's Jiangsu Province.

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A blimp at the US Open golf tournament in Wisconsin caught fire and crashed on Thursday.

Fears the toll will rise with 12 confirmed dead and 78 taken to hospital after the massive blaze at the 24-storey Grenfell Tower in London.

She went to the door. It was her neighbour, identified by one newspaper on Thursday as a 44-year old taxi driver from Ethiopia.

"He was shouting that his flat was on fire," Adam said.

She looked across the central corridor in the core of the 24-storey tower. A big bag of clothes sat outside the man's flat.

His door was open and through it she saw a "small" fire in his kitchen, she said later.

Another woman on the same floor, Aalya Moses, had a similar experience.

"There was no alarm, no sprinkler, just my neighbour who told everyone on my floor and the surrounding floors," she said. "If he hadn't told me I wouldn't have known."

Adam echoed the sentiment. "If he had not knocked, I don't know what would have happened."

They left the building, spooked. It was about 10 minutesto one in the morning on Wednesday, June 14.

Within an hour, the place would be an inferno.

This is a story that has many revisions to come.There will be surprise reunions and inevitable funerals. There will be police reports, fire reports and an inquest into the deaths: 17 at Thursday's count, a number that will rise over days and possibly weeks.

And there will be an official public inquiry into what happened and what can be learnt, what must be learntfrom a tragedy that, it appears, could have been and was foreseen, and could have been but wasn't prevented.

It was a pleasant night after a warm day. Many in Grenfell Tower had left their windows open to capture a light, cool night breeze.

The building benefited from new insulation, installed in a renovation that finished in 2016: a sleek aluminium composite cladding covering old, stained concrete.

That cladding was starting to catch fire.

Mahal Egal was another who got out from the fourth floor with his two small children, warned by a neighbour, among the first to evacuate.

He said the neighbour told him his fridge had exploded.

Leaving was against the building's fire safety advice. If residents knew there was a fire outside their flat, they were supposed to shut their door and wait for rescue.

Such buildings are designed to isolate fires. And with residents safe inside their flats, firefighters have more chance of running an orderly evacuation if it becomes necessary.

Indeed, this was reportedly the early advice that firefighters and 000 emergency operators were giving before an evacuation was ordered some time later. If this turns out to be the case, it could have been a fatal mistake firefighters and fire safety experts later said this fire spread faster than any high-rise blaze they had seen before.

Even as Egal left his flat, the first of many fire engines were arriving.

"At first it seemed controllable," he said, watching the fire from the outside. "At this point the fire was no higher than an average tree.

"But really quickly the fire started to rise, as the cladding caught fire."

There was already smoke inside the building, in the single central stairwell, he said.

He thought of his extended family and friends still inside the building, and he worried, and he watched the fire grow out of control, leaping eagerly up the building.

Within minutes it had climbed a dozen floors.

Witness Tanya Thompson said she saw it go "up like a firewall, straight up the side of the building" in about ten minutes. Another, Omar, said it was "like a piece of paper like dominos, fire and then fire and then fire. It was so quick and shocking."

Mickey (Michael) Paramasivan, 37, was woken on the seventh floor by the smell of burning plastic. He tucked his six-year-old daughter Thea into her dressing gown and they ran downstairs.

By the time they were outside "we looked up at the tower and it was like a horror movie", he said.

Mouna Elogbani was on the 11th floor with her husband and three children a friend called and warned her to get out. When they first opened the door to escape "flames burst into the house", she said. They managed to get out down the stairs.

On the 17th floor a man who identified himself on radio as "Methrob" was woken by fire sirens, grabbed his aunty and they started to make their way down.

"By the time that we got downstairs, the fire had gone all the way up and was just about reaching our windows," he said. "The whole side of the building was on fire. The cladding went up like a matchstick."

There are many more stories of narrow escapes. Other stories do not end well.

Jessica Urbano, 12, borrowed someone's phone as she hid in a stairwell with a group of friends making their way down from the 20th floor. She rang her mum.

"Jessica had been asleep in our flat when something woke her - I don't know if it was the smoke or a fire alarm - so she rang me at 1.39am as I was on my way home from work," Jessica's mum, Adriana, told the London Telegraph. "She said,''Mum where are you? Mummy come and get me'." Mrs Urbano urged Jessica to run down the stairs of the tower block and try to find a fire fighter to lead her to safety.

"I told her to get out of there as quickly as she could. I said 'run as fast as you can', but then the line cut out".

On Thursday Jessica was listed among the missing.

On the 14th floor, at 1.38am, ZainabDean phoned her brother Francis.

"She said there was a fire in the building," Francis said later. "She was very nervous and scared. She is a nervous person anyway. She said the fire service arrived and had told everyone to keep calm and to stay where she was."

Twenty minutes later, he got to the building and tried to get in to rescue his sister, but police stopped him.

After an hour, he was desperate with worry.

"I could see the building was going up in flames. I said Zainab you have to get out of the building it's not looking good. She said she didn't want to go down the stairs because there was too much smoke.

"But she tried anyway and then [her three-year-old son]Jeremiah collapsed in her arms."

Their last contact was at 3am.

"On the phone I just keep telling her they were coming to get her."

He handed his phone to a fireman. The fireman handed it back, saying "tell her you love her".

"I knew then to fear the worst. The phone went dead and I couldn't talk to her."

One firefighter was heard telling his crew "we're going in and we're going up".

"My firefighters battled through intense heat to reach some of the highest floors," said London Fire Brigade Commissioner Dany Cotton.

"I was looking at a building that was engulfed in fire where I knew members of the public were still trapped yet I was committing hundreds of firefighters into a building that to a lot of people looked terribly unsafe.

"My firefighters were desperate to get in there and desperate to rescue people, and we committed crew after crew into a very dangerous, very hot and very difficult situation because we had a passion to do as much as we could to rescue the people in there."

The firefighters were told to write their names and numbers on their helmets before they went in.

"It was like a war zone in there," said one. They rescued at least 65 people.

Another said they were "knee deep in debris and bodies" once they climbed past the 11th floor but they kept going up as high as they could, as far as their legs and oxygen canisters would taken them, touching and feeling their way along corridors and stairs, "sweeping and stamping" to check for obstacles or collapsed flooring.

Outside, the fire hoses simply couldn't reach the upper floors.

By the time the fire reached the top floors, the internal stairwell was ink-black with smoke and those remaining felt there was no escape.

Nura Jemal, mother of three on the 22nd floor, told a friend on the telephone "I'm so sorry, goodbye. Please forgive us. We are not going to make it."

The first victim of the fire to be name was Mohammed al-Haj Ali, 23, a Syrian refugee who came to the UK in 2014 and was studying civil engineering.

He had been in a flat on the 14th floor with his brother Omar.

"We smelled the smoke, opened the door, saw smoke," Omar said. "The smoke came inside. I've seen the fire around me."

They left the apartment together and headed for the stairs.

"I couldn't see anything, even my fingers," Omar said. "I thought I was going to die on those stairs. I was breathing smoke, lots of smoke."

Then, when he was almost out, "I looked behind me and I didn't see my brother."

"I called him [on the phone] and said 'where are you'? He said 'I'm in the flat'. I said 'why didn't you come?' He said 'no one brought me outside'."

There they stayed, Omar outside and Mohammed in. They spoke to the end.

"I was speaking to my brother [on the phone]he said 'I'm dying'. He said 'I cannot breathe'."

Among the lost are a 57-year-old man who told his wife and son to leave him behind, and has not been seen since, and Tony Disson, 66, whose phone fell silent at 4am after speaking to a friend and saying "tell my sons I love them".

Ali Jafari, 82, was escaping with his wife and daughter in the lift but got out at the 10th floor, unable to breathe, and did not get back in before the doors closed.

A mother lost her grip on her 12-year-old daughter's hand as they stumbled down the pitch-black stairwell. She spent Thursday travelling from hospital to hospital searching for her child.

Rania Ibrahim posted frightened videos on Snapchat and Facebook while trapped on the 23rd floor, the hallway outside impassable with smoke. Her last message was "guys, I can't get out".

But there were more survivors, too, emerging from the blaze in the arms of firefighters.

Natasha Elcock, trapped on the 12th floor with her six-year-old daughter, flooded the bathroom and kept her flat damp. After 90 minutes the fire crew told them to get out but they couldn't the door of the flat was too hot to open.

"The door was buckling and the windows bubbling and cracking, it was terrifying," she said.

Fire crews rescued her at 3am. She stepped over a body on the way out.

Schools inspector Marcio Gomes, 38, was told to stay put but by 4.30am the fire had engulfed the whole building, and fire crews were unable to make it up to them.

He wrapped his family up in wet towels and said, "There's no turning back, we have to go," he told the Sun.

"As soon as we opened the door all the smoke came in. We had no choice because the fire started coming in through the windows. We had to go down the stairs.

"You couldn't see anything. We didn't see people, we just felt people. We were just climbing over bodies."

He stayed on the line to the fire operator all the way down.

"They said 'keep going down, keep using your voice'."

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London fire: Anatomy of a high-rise horror - The Sydney Morning Herald