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Anatomy of a Sarin Bomb Explosion (Part II) – bellingcat

Introduction

Part I describes the basic behaviour and intended function of an air-delivered gravity bomb containing Sarin, designed along US/USSR cold war lines. When we left off in Part I, a well-crafted gravity bomb will have dispensed its Sarin broadly along this distribution:

Sarin, also commonly known by its old NATO nickname GB, is one of a family of chemical warfare agents known as nerve agents. It was invented by German scientists in 1938-1939 who were performing research on organophosphorous pesticides led by Dr. Gerhard Schrader. Sarin was named by the team of researchers who invented it. It is in a family of chemicals known as organophosphates. There are other chemicals within this family, including the chemical warfare agents Tabun, Soman, VX, and the pesticides Malathion, Parathion, and Amiton.

All of the nerve agents affect the human bodys nervous system. The human nervous system requires a delicate balance of chemicals to regulate itself. Nerve agents bind to a chemical known as acetylcholinesterase and, in doing so, disrupt the electrochemical reactions required for the body to operate properly. The binding of acetylcholinesterase leads to a build-up of acetylcholine, which then in turn leads to a syndrome called a cholinergic crisis. In effect, the nervous system starts to over-act and muscles and glands start to work over-time and cause serious problems. The signs and symptoms will vary in severity and timeline depending on the route of exposure and dose (i.e. the amount of Sarin absorbed). This will be discussed at length below.

There are several ways Sarin can enter the human body. These are called routes of exposure and are as follows:

Sarin acts very quickly through respiratory and ocular exposure, with onset of adverse effects within seconds to a few minutes depending on dose. Absorption through the skin is slower, i.e. minutes to hours, depending on dose. Rate of action for wound exposure is believed to be intermediate in speed between respiratory and dermal absorption. Gastrointestinal absorption is not well documented but is likely to be fast.

Sarin, as it is less persistent and evaporates at a faster rate relative to the other nerve agents, is foremost an inhalation hazard. Absorption through skin takes time, and even someone with liquid Sarin on their skin is extremely likely to suffer inhalation effects from the Sarin evaporating off of their clothing and skin, except in very cold weather. In moderate or warm temperature situations, the only realistic exposure scenarios for a liquid Sarin only, through skin absorption are for partially protected troops already wearing protective masks or donning them very quickly at the onset of a chemical attack. So, with unprotected target populations, the route of exposure of most significance is inhalation of aerosol and vapour.

The cholinergic crisis that Sarin (and its other cousins in the same family) provokes manifests itself in signs (things that are externally observable) and symptoms (subjective indications felt by the victim that are difficult or impossible to observe). This graphic, taken from the canonical Medical Aspects of Chemical Warfare (various editions accessible online) lists the major signs and symptoms:

Rhinorrhea is a fancy term for a profusely snotty nose. Miosis means pinpointing of the pupils. The rest is either self explanatory or you can look it up in a normal dictionary if unsure.

The order in which signs and symptoms appear and their severity will vary both with degree of exposure and route of exposure. For Sarin, this is principally inhalation. This graphic describes this exposure category in detail:

In the event of liquid absorption through skin, signs and symptoms progress differently. This is really more relevant for the more persistent, slower evaporating agents like Tabun and VX. In the case of Sarin exposure, an unprotected person with lots of Sarin liquid on them will get respiratory exposure from evaporation, and this is very likely to happen faster than dermal exposure. With Sarin, the likely exposure scenario is for someone who has protective equipment for their respiratory tract and eyes (e.g. a gas mask) but unprotected skin. For comparison purposes, this is the progression of signs/symptoms for dermal exposure:

When people die from nerve agent exposure, the mechanism of death is almost always a pulmonary death. Such respiratory failure, which denies the body oxygen happens through several mechanisms with nerve agent poisoning. Depending on route of exposure and dose, any or all of these will be the exact mechanism by which death occurs:

All of these conditions can cause cyanosis , a tell-tale blueish discolouring of skin due to oxygen deprivation.

Most studies of the toxicity of Sarin are derived from data involving animal research. Much of the information is now quite dated, having been developed in the 1950s and 1960s. These should all be taken with a reasonable margin for error. However, the following chart from the US Armys Field Manual 3-11-9 is as useful a summary as any Ive seen. Anyone interest in the footnotes can go to the Field manual and look them up, although some of the references are to studies and documents not readily available online. You might need a good research library.

These numbers probably mean little to most readers so I am going to unpack this at some length. Concentration is measured in milligrams per cubic meter. As there is almost nothing in toxicology thats instant, concentration is measured over a time domain. So for things like vapor exposure, the figures used are in milligrams per cubic meter per minute. For example 50 mg-min/m3 means 50 mgs of Sarin per 1 cubic meter of air for a period of 1 minute.

The key figure here is something called 50th percentile Lethal Concentration LCt50. This is the concentration that is reckoned to kill half of the exposed population, assuming a normal adult male (these studies were all based around Cold War soldiers) breathing at 15 liters of air per minute. This is the MV (respiratory minute volume) on the table. This is equivalent to a soldier engaged in moderate activity. (Someone asleep will be breathing slower, someone running full tilt is likely to be higher.) So, for Sarin, breathing 35 mg Sarin in aerosol or vapour, per cubic meter of air, continuously for 2 minutes, will kill about 50% of the exposed people. This is extremely lethal. By comparison, the similar figure for phosgene, the most lethal chemical weapon used in World War 1, is about 1500 mg-min/m3.

For severely debilitating effects, the figure for Sarin is 25 mg-min/m3, again over the course of 2 minutes, not much less than the lethal figure. It is likely that there would be some lethality at this level. For mild effects, the threshold is around 0.4 mg.

Sarin vapor and aerosol can enter through the skin. However, if you examine the table, these effects require a FAR HIGHER level of concentration and longer exposure. Lethal concentrations (LCt50) for this route of exposure are 6000 to 12000 mg-min/m3 for much longer durations of exposure (30 mins to 6 hours). This is an entirely difference exposure scenario. (The differences in the figures in the table are fordiffering airtemperatures.) So, yes, Sarin is lethal through a route of permeation through the skin, but only at levels that are literally hundreds of times higher than the levels that are dangerous for respiration. The figures for severe effects (4000-800) and minor effects (600-1200) are correspondingly lower, but still MUCH HIGHER than effective concentration levels for absorption via the respiratory route. It should be noted that a very dense aerosol may result in some condensation or deposit of liquid on skin, which behaves as described in the next paragraph.

Percutaneous liquid exposure takes time, as was noted above. Time of exposure is a bit different here, and is less significant than the amount absorbed through the skin. A large gob of Sarin landing mostly on outer clothing and almost instantly removed by decontamination may result in less net absorption of Sarin into the body than a small droplet on the back of the neck that goes unnoticed until symptoms appear.

LD50 for Sarin is calculated at 1700 mg for a 70 kg male. This means that, for a normal 70kg human male, 1700 mg of Sarin absorbed into the human body would kill about half of the people with that level of poisoning. Statistically, some would die with less, and some could survive with a much higher exposure. ED50 is the level of exposure for serious, disabling effects. For Sarin it is 1000 mg for the same assumptions. Note that at this level of dose, some are likely to die. This is an awful lot of Sarin when compared to the amounts that are needed to kill or seriously incapacitate people through inhalation.

The behaviour of Sarin on skin is important. Several things happen when Sarin is on human skin:

For those who are curious, heres what some of the other columns mean:

Now that we understand the practical toxicology here, it is easy to analyze exposure scenarios in the field. It is clear from the toxicological data that Sarin is far more efficient as a killer in an aerosol or vapour form, easily by several orders of magnitude. A weapon system that dispenses its contents in the form of liquid would largely be a waste of expensive Sarin. So, we are now understandably back to the concept of a weapon system that is designed and tested to optimize the quantity of aerosol.

In our suspected scenario in April 2017, there is a well-substantiated allegation that an air-dropped Sarin bomb was dropped. It appears to have functioned as designed and created an aerosol that drifted downwind, as the victims were a distance away from the bomb. Any person close enough to have been splashed with some liquid was probably close enough to the bomb to die very quickly. In any case, the impact point appears to be in the middle of a road.

So, for a person to be seriously ill or to die, there is a need to create an aerosol of a concentration of 25 to 50 mg-min/m3. So, people exposed to an aerosol of this density will get sick and easily could die. People exposed to an aerosol of only 2 or 5 mg-min/m3 may easily get very ill, particularly if they are in it for minutes. But think it through. A cubic meter is a lot of air. And thats a very small amount of Sarin. How much Sarin is actually going to get deposited on their skin, hair, and clothing. A few milligrams, maximum.

Next, these people either escape or are carried away a significant distance and then receive emergency treatment. There are firm reports of responders going to rescue people becoming victims. However there are videos taken in locations some distance away from the impact site. People wearing little or no protective gear are seen handling the victims. Why are they not being seriously affected by Sarin? The simple answer is that these victims were affected by aerosol and/or vapour. Very little material actually got deposited on them. Even if it did, it would have been in the order of a few milligrams. And it takes 1700 milligrams over a period of time to kill someone by simple absorption. Responders arent falling over because, simply, the math doesnt work and Sarin isnt a magical substance.

Why then do emergency responders in more developed/better equipped situations train to wear full protective equipment? For several reasons. Emergency responders wear equipment that is prescribed through obeisance to occupational health and safety regulations, not a what can I get away with and not die ethos. Second, in the early stages of an incident, the chemical agent that was used may not be known. Even if you knew it was a nerve agent, you arent likely to know it was Sarin and not one of its more persistent cousins. VX, for example, is a different game altogether being primarily a contact/liquid hazard and requiring more skin protection when dealing with victims.

The bottom line is that Sarin evaporates quickly, not much is needed to do harm to people, and people who are exposed only to aerosol and vapour are a minimal contact or respiratory hazard to others. Even given this, some responders reported illness. So, the Responders didnt die on film so it wasnt Sarin is an incorrect line to take here and displays a basic ignorance of the facts.

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Anatomy of a Sarin Bomb Explosion (Part II) - bellingcat

‘Grey’s Anatomy’ Stars TR Knight, Kate Walsh Reunite: Photo! – Us Weekly

Paging Grey's Anatomy fans! T.R. Knight and Kate Walsh reunited in NYC Thursday, April 20, and took a photo to mark the occasion.

Knight, 44, attended Walsh's performance in the Roundabout Theatre Company production of If I Forget with comic actress Bridget Everett.

"O, my beautiful friends! @bridgeteverett and I got to see @katewalsh in IF I FORGET last night in NYC! She was brilliant, as was the production! So lucky I got to see it. I love these humans," the Catch star captioned an Instagram pic of the trio.

Walsh, 49, reposted the pic. "[Love] my @t.r.knight & @bridgeteverett & so grateful they came to see my show...also: no filter in the world can make me look less tired," she wrote. (Walsh stars in the recent Netflix hit 13 Reasons Why.)

The former costars played Dr. George O'Malley and Dr. Addison Montgomery on the Shonda Rhimescreated medical drama, which debuted in 2005. Knight's beloved character died in the season 6 premiere, while Walsh reprised her role in its spinoff, Private Practice, from 2007 to 2013.

Walsh opened up about her time at Grey Sloan Memorial Hospital in an exclusive interview with Us Weekly in December 2015. "I loved how smart [Addison] was and capable and how fallible she was. It made it a really fun character to play and Shonda's really good at that at creating very multifaceted characters," she said at the time. "She and I loved working together. We had a great experience and that's always a positive. Doing something else for her works for me!"

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'Grey's Anatomy' Stars TR Knight, Kate Walsh Reunite: Photo! - Us Weekly

How Virtual Anatomy Will Change Med School – Fortune

Last week I spent a day at the venerable Cleveland Clinicthe citys best-known celebrity, perhaps, next to this guy . The hospital (and really, its a hospital system with outposts in several cities in the U.S. and abroad) has always been on the spear point of progressbut that has been particularly true over the past 13 years, under the guidance of CEO Toby Cosgrove .

As I wrote in my editors letter for Fortune s souped-up Future Issue (on newsstands very soon), I visited Ohios second-largest city to check out a cool piece of technology that the Clinicand its Cleveland cousin, Case Western Reserve Universityare using to teach meds students anatomy: and teach it in a whole new, dynamic, and interactive way.

Case Westerns Dr. Mark Griswold , a professor of radiology who is an expert in magnetic resonance imaging, has worked with colleagues to build a virtual anatomy tool on the Microsoft HoloLens augmented reality platform. Put on the HoloLens visor, plug in the human circulation program (one of various anatomy modules that Griswolds team has built), and youll find yourself staring at a life-size, 3D human figure, with every vein and artery in perfect bodily placement and scale.

You can walk around this anatomically correct scaffold, spying organs and tissues from any angle, and poke your head in to see the interior of, say, a heart. Within, youll see that organs distinct chambersand within those, the discrete valves.

What is most striking is that this body seems to take up real physical space. (Dr. Griswold points out that nearly everyone who has sampled the program walks around the Da Vincian figures outstretched skeletal hands so as not to bump into them.) Everyone who dons the goggles sees the same images, making medical instruction easierand the fact that you experience the real world along with the virtual one makes conversation and consultation easier, too. (Seeing this demo with Dr. Cosgrove, a former heart surgeon who pioneered techniques for valve repair that are widely used to this day, was an extra treat.)

In AR anatomy, the real merges fluidly with the imagined; the laws of the physical world bend just enough to allow for a four-dimensional understanding (3D plus a magnified view of the interior), but not so much that it makes you queasy.

The idea is to teach students anatomy in a way that they absorb the knowledge more readily, more intuitivelyand more quickly. Seeing and touching intertwined veins and arteries as they navigate through the human form gives you an understanding of circulation that is difficult (or maybe impossible) to get by studying even the most finely etched schematic in a textbook.

And the better and faster they learn the human roadmap, the sooner these budding surgeons can start driving on their ownwhich is to say, repairing living bodies.

Have a great weekend. And if you like getting our Fortune Brainstorm Health Daily newsletter, please share with a friend. Were not just sending out a newsletter every day, were building a community. Thank you all for being a part of it.

This essay appears in today's edition of the Fortune Brainstorm Health Daily. Get it delivered straight to your inbox.

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How Virtual Anatomy Will Change Med School - Fortune

Anatomy of a Song: Willow Parker, ‘Wild’ – Bend Bulletin

Artist: Willow Parker

Featured song: Wild

Singer-songwriter Willow Parker grew up in Bend and started performing at local open mic nights about five years ago. Shes still a frequent open mic performer, and can be regularly heard at the Astro Lounges open mic nights on Mondays and M&J Taverns Wednesday open mic. This song, Wild, is one of her originals.

Q: Whats the story behind this song how was it written, recorded, etc.?

A: (The process) varies from song to song. Sometimes Ill come up with themes first, sometimes I really like poetry, so sometimes Ill have the lyrics first. Most of my originals are written in standard tuning, and I was getting a little bored, so I decided to branch out a little bit. The first one I did was open E (tuning). I loved it, I did a few riffs, I thought I was gonna write maybe a couple different songs with it, but they ended up flowing all together, and so the music part came first and then I put lyrics to it.

Q: Whats the story inside this song whats it about?

A: Well, its pretty self-explanatory when you hear it. Basically (its) just about a relationship, love and lust and feeling confident in a relationship with affirmation and attention.

Brian McElhiney, The Bulletin

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Anatomy of a Song: Willow Parker, 'Wild' - Bend Bulletin

Aspen Princess: Anatomy of a meltdown – Aspen Times

I honestly don't even know where to begin.

Do I start with how I was robbed on the street in Miami and my purse was stolen with my laptop in it so I am now typing this column on my old computer, the one with a little plastic nub where the letter "R" key fell off so I get a blister on the tip of my finger?

Or a compelling opener might be an excerpt from a dinner conversation at the Naples Beach Hotel where everyone in my crazy extended family was comparing what dosage Zoloft they're on.

Do I write about what it was like to travel with a toddler who was getting over the flu, and how, even though he was cleared to travel by his pediatrician, puked all over me, himself, his car seat, and his grandparents the night before we left? Or how I got, like, four minutes of sleep before my 5 a.m. wake-up call because I was up all night worrying, wondering if I should travel with him?

Maybe I could explain how, even on a good day, traveling with a 400-pound diaper bag o' tricks that bottomless pit of diapers, wipes, sippy cups, food pouches, teething wafers, books, toys, snacks and whatever other crap modern life has done to make our lives so much more pushed me to the brink? Or I could talk about when he'd drop something on the floor of the plane for the 500th time and I had to become a contortionist just so I could reach the one thing that would keep us both sane all while feeling like I was going to bust an organ.

I also could write about the award-winning tantrum the babe had the night of our arrival when he threw his head back so violently while sitting in my lap that the back of his noggin left a nice welt on my cheekbone.

That's when I lost it.

Yes, after 15 months of baby bliss I had my first official, bona fide meltdown. Talk about a slap in the face my sweet little angel had basically cold-cocked me.

I could write about what it's like to drive in a car in a new city with my parents, who absolutely refuse to trust GPS unless it's the one in their own car, as if their GPS was an old friend they could rely on and any other GPS was not to be trusted.

I explained to them, for the 50th time, that our iPhones can do the same thing as the GPS in their beloved Mazda CX-5. Soon everyone in the car had their iPhones programmed with the address so each time there was a direction we'd hear it multiple times, like an echo. "In half a mile, merge left onto Interstate 75 East In half a mile In half a mile "

Still, my mother insisted the GPS was wrong. "She's confused," she'd chime in from the back seat. "She doesn't understand." I have no idea why she thought she knew better, considering she'd never been to Naples in her entire life.

I tried to explain that "she" is actually a computer and in fact does know exactly where we're going and how to get there and how long it will take. But Lindarose wasn't buying it. Every time the GPS dictated a direction she'd say, "OK, honey," in this really patronizing tone dripping in sarcasm as if the GPS was a little old lady suffering from dementia and we were all just humoring her.

It didn't help matters when we rushed out to buy diapers and I plugged in the wrong street address on the way back and we ended up on Mahogany Lane (which is in the only trailer park in all of Naples) instead of Mahogany Run Lane, which is in the fancy-pants golf resort where we were staying.

I could write about what it's like to travel with my parents, who are not only retired from working, but also anything that takes any work in general, like all the rigmarole involved with caring for a toddler. That meant I was the one loading and unloading the baby and the 500 pounds of other crap that this tiny little person somehow requires. It seemed like I was always red-faced and sweating, my clothes wrinkled and disheveled, on the brink of pulling my frizzy humidity hair out and leaving it in heaps on the pavement like dryer lint screaming, "Help me!"

I could talk about how it's taken me this long to realize that I don't need high heels or nice outfits because I am so catatonic by the time I finally get my little monster to bed that I no longer care if I have drool and crusted baby food all over my shirt sleeves and would rather stick a needle in my eye than put on uncomfortable shoes or a shirt that requires a bra.

I could write about the Airbnb my brother and I rented in Miami that was supposed to be all hip and eclectic, when in reality it was a dump in a neighborhood where we were robbed on the street in broad daylight.

Or I could write about how one of my favorite things about being a mother is sharing my baby with my family. How despite it all, it's one the most joyful experience of my life. I could talk about how my brother is the most loving uncle my baby boy could ever ask for. Or how my cousin Leslee showered the babe with an ocean love that came pouring out of her oversized heart.

I also might mention how the baby was oblivious to it all, happy to play in the sand and kick his feet in the sea and to grace us all with the song of his laughter.

The Princess is getting a serious blister on her "R" finger. Email your love to alisonmargo@gmail.com.

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Aspen Princess: Anatomy of a meltdown - Aspen Times

OPINION: How Marines can better predict human behavior – Marine Corps Times

The term human terrain is often used within the military. Individual Marines are encouraged to understand more about a local population they interact with, either on a deployment or while on liberty.

At the Marine Corps' Combat Hunter course, we specifically dive into this topic to help Marines better understand, to identify, and most importantly to predict human behavior.

For several hundreds of years scientists have studied our behavior as a species. Unilaterally, they conclude that we are predictable as creatures of habit that set patterns and are driven, at times, by uncontrollable responses in the brain.

Combat Hunter highlights these patterns to help recognize and explain why we act or react in a specific predictive pattern. Behavior that is consistent becomes predictable, which directly relates to military operations overseas or while on leave and liberty at home.

Imagine a popular singer visits your local diner and the fuss that creates. People are swarming and asking for autographs and selfies. We call this a Proxemic pull: We are pulled into situations we are interested in or feel safe around.

Conversely, if a crowd of Marines having a smoke see the first sergeant walking toward them, they scatter quickly. This is a Proxemic push: We push away from encounters we dont like or when we sense danger.

A crowd of people conducting normal business in a market overseas will show the same pushes and pulls that can be recognized and observed. When these occur, they have meaning and are not just random.

Thats where the so what? comes in. Why did the locals grab their kids and bolt? What caused the men to congregate only around a car that just pulled up? How come yesterday the locals were smiling and shaking our hands, yet today they keep their distance and are quickly closing up the market?

Every one of us knows we like our space. We dont like strangers getting too close to us, so we move out of the way or cross the street to get away from them. Remember the last time you were in an elevator: Where did the next person stand when they entered? Typically they take a position furthest from another person, and so on as others enter the elevator.

This is another example of proximity or how we use the space around us. It is predictable, and a Marine can observe when a meeting takes place between more than one person: Do they know each other or not? Is one acting submissive or dominant over the other? Are they interested or uninterested? Are they acting comfortable or uncomfortable? This behavior can be seen in a crowd or in an individual and give a read to the others intent.

Anybody can practice this by taking the time to observe people around them in their daily life. The next time you are in a mall, for example, take a seat in the food court or a bench and just watch people. Pick out who is together, who are just dating, the loners, who seems to be in a hurry, how most patrons dress, who is acting a bit odd, and determine why they stand out to you. By practicing this, you will be surprised how quickly you build file folders, or memories, of specific behavior. When you notice it again during one of your future travels, you will key in on it instantly.

People across the globe are wired the same on the inside-the culture may be different, but understanding what to expect behaviorally from people will help you to predict what they will do.

Human behavior is consistent and predictable.Understanding and studying this behavior will equip a Marine with a better understanding of the human terrain they are faced with no matter where they are deployed.

Gus Mingus is a retired Force Recon Marine and infantry officer who currently teaches profiling as an instructor at Combat Hunter, Advanced Infantry Training Battalion, School of Infantry-East, Camp Geiger, North Carolina. Opinions expressed in this commentary are his own.

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OPINION: How Marines can better predict human behavior - Marine Corps Times

Cattle producers offered intro to genetic technology – Tri-State Neighbor

Cattle produers can learn about using genetic technology to improve cattle herds at a program offered in Rapid City by the King Ranch Institute for Ranch Management in May.

Sessions on Application of Advanced Genetic Technology in Beef Cattle will be offered May 11-12 at the Rushmore Inn and Suites in Rapid City. South Dakota State University West River Ag Center is co-hosting the lectureships. The cost is $300, which covers materials and meals.

"We hear many of our producers are beginning or wanting to use genetic technology to improve their herds. Some question if they are using it correctly; some feel it is information overload," said Kristi Cammack, director of the West River Ag Center.

Keeping up with genetic selection and evaluation innovations can be challenging. Early adopters who have been trying the technology as well as those who are interested but don't know where to start can learn from the classes.

The sessions are meant to strengthen the understanding of the genetic principles and help attendees build on the information. Faculty contracted by the King Institute will share how to apply advanced genetic technologies in the real world of seedstock and commercial cattle production.

Instructors will be Bob Weaber, Ph.D., extension specialist in animal sciences and industry from Kansas State University and Matt Spangler, Ph.D., beef genetics extension specialist in the animal science department at the University of Nebraska-Lincoln. Along with the basics, they will look at the application of advanced genetic tools including genomically enhanced expected progeny differences and marker assisted management in genetic advancement.

Cammack expects that the sessions will appeal to both commercial and seed stock producers from across the state, region and throughout the country.

Information will focus on developing breeding objectives for the herd and determining the economics relative for each operation as that may vary within a region. Owners want to know what will work for them at their location, taking into consideration different feedstuffs and different markets.

The tools have advanced so they are producer friendly. Cammack said the speakers will share knowledge that producers can apply and use in their operation, including an applied understanding of how to use genomic selection tools.

Cattle producers will get a lot out of the 1 -day program, she said. Producers will participate in interactive sire selection scenarios where they will break out into groups and practice how to pick sires.

"We hope the result is that cattle producers will learn to use advanced genetics. Applying these tools, in the correct way, will pay off with improved genetics. Producers will find it advancing herd genetics really pays it forward," Cammack said.

Contact Cammack at 605-394-2236, or email Kristi.Cammack@sdstate.edu. To see the agenda and make a reservation, go to the King Ranch Institute website.

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Cattle producers offered intro to genetic technology - Tri-State Neighbor

NewLink Genetics: Initiating Coverage With Buy Rating And First … – Seeking Alpha

NewLink Genetics (NASDAQ:NLNK) is Ames, Iowa, based emerging biotechnology company in the field of immuno-oncology. The company's common stock sank last year after the failure of two Phase 3 trials of its HyperAcute cellular immunotherapy in metastatic pancreatic cancer. Afterwards, the stock more than doubled from its 2016 lows in anticipation of data from its IDO inhibitor pipeline and has pulled back from the recent highs, thus providing an attractive long entry point.

(NewLink Genetics, common stock price chart. Source: Bloomberg)

Product Pipeline:

(NewLink Genetics, IDO inhibitor immuno-oncology product pipeline)

The company's immuno-oncology pipeline is focused on the inhibition of IDO (indoleamine-2, 3-dioxygenase) pathway which is believed to be an immune checkpoint similar to PD-1 and CTLA-4 pathways. It is one of the handful of companies which are developing IDO inhibitors (and the one of two public ones). The IDO pathway regulates the immune response by suppressing T cell activation, which enables the tumor cells to evade the host immune response. IDO inhibitors are believed to be the next potential blockbuster class of checkpoint inhibitors. Incyte (NASDAQ:INCY)'s direct IDO enzyme inhibitor epacadostat is being tested in various solid tumors in partnership with Merck's (NYSE:MRK) Keytruda. Peak sales estimates for epacadostat are as high as $9 billion in various solid tumor indications.

(Mechanisms of actions of Indoximod and GDC-0919)

Indoximod: It acts on the T cells by mimicking tryptophan and, thus, signals the activation of T cells. It, thus, acts as an indirect inhibitor of IDO pathway. Indoximod attracted widespread investor attention after its recent data release in the treatment of advanced melanoma at the recently concluded AACR meeting. In an ongoing Phase 1b/2 trial in 60 patients enrolled so far, Indoximod and Keytruda combination resulted in 59% overall response rate (ORR) and 74% disease control rate (DCR). The cohort also included ocular melanoma patients (which have poor treatment response) and when these were excluded, ORR was 59% and DCR was 80%. The results were spectacular considering that Keytruda alone has shown ORR of only 33% in this patient population. A combination of Bristol-Myers Squibb's (NYSE:BMY) Opdivo and Yervoy (anti-CTLA-4) resulted in 58% ORR in advanced melanoma but had higher incidence of Grade 3 and 4 treatment-related adverse events (58% in the combination vs. 21% in Opdivo alone).

In a smaller Phase 1 study of 19 patients with advanced melanoma, Incyte's epacadostat and Keytruda combination resulted in 58% ORR, 26% complete remission rate (CR) and 74% DCR. The CR was lower in the above mentioned Phase 1b/2 trial of Indoximod+Keytruda (10%). However, Indoximod+Keytruda have shown efficacy and safety in the largest patient population of advanced melanoma treated with anti-PD1+anti-IDO combination so far, and till Incyte and Merck show efficacy and safety in a similar sized patient population, we like Indoximod in this indication so far.

In a Phase 1/2 trial, Indoximod+gemcitabine+abraxane resulted in impressive 45% ORR in metastatic pancreatic cancer (compared with 34% for Folfirinox regime and 9.4% for gemcitabine).

Indoximod is also being tested in various other cancers, and data from these indications is expected to be released over next 12 months. NewLink Genetics hold all worldwide commercialization rights to Indoximod. It will pay royalty payments on net sales of Indoximod (single-digit percentage) to Lankenau Institute of Medical Research, Augusta University, and Iowa State Department of Economic Development (ISDED). Various patents for Indoximod extend till 2027.

GDC-0919: It is a direct IDO enzyme inhibitor. Roche/Genentech (OTCQX:RHHBY) has licensed its worldwide commercial rights, thus showing confidence in its potential. In exchange, NewLink Genetics received $150 million of upfront payment and may receive up to $1 billion in future milestone payments and double-digit percentage of net sales as royalty payments.

A combination of GDC-0919 and Roche's anti-PDL1 Tecentriq is being tested in an ongoing Phase 1b, open-label study in various solid tumors like melanoma, NSCLC, head & neck squamous cell cancer, gastric cancer, ovarian cancer, Merkel cell cancer, cervical cancer, endometrial cancer, renal cell cancer, triple-negative breast cancer, and urothelial/bladder cancer. About 305 patients are planned to be enrolled. The estimated completion date of the trial is December 2018, but interim data is expected in mid-2017.

Various patents for GDC-0919 extend till 2032.

NLG802: NewLink Genetics is also developing NLG802, a prodrug of Indoximod to increase bioavailability and exposure. An IND was filed in 2017, and Phase 1 trial is expected to start this year.

Potential competition:

Other companies developing IDO inhibitors include Incyte, iTeos Therapeutics, and Redx Pharma.

HyperAcute Cellular Immunotherapy Program:

Despite failing in metastatic pancreatic cancer, a tough to treat cancer, this program is not dead yet. A combination of Tergenpumatucel with Indoximod and docetaxel is being tested in a Phase 1b trial in advanced non-small cell lung cancer (NSCLC). Dorgenmeltucel-C is being tested in combination with checkpoint inhibitors in a Phase 2 trial in advanced melanoma. Results from these trials are expected in 2018. Various patents for this program extend till 2029.

Vaccine program:

The company's Ebola Zaire vaccine has Breakthrough therapy designation from FDA. Interim data from a Phase 3 trial showed the vaccine's efficacy in preventing Ebola infection. Merck has licensed worldwide commercial rights to the rVSVG-ZEBOV GP vaccine (Ebola). NewLink Genetics received upfront $30 million and $20 million in milestone payments so far. It may also receive royalty payments on net sales of the vaccine.

Leadership:

CEO, chief scientific officer, and chairman of the board, Charles J. Link Jr. MD: He co-founded NewLink Genetics in 1999 and was a practicing oncologist for 18 years. He also served as the director of the Human Gene Therapy Research Institute at the Iowa Methodist Medical Center.

Co-founder and chief medical officer, Nicholas Vahanian, MD: He has led the algenpantucel-L (HyperAcute Cellular) program and worked at the National Cancer Institute and National Center for Human Genome Research Institute (both at the NIH).

Lead Director, Thomas Raffin, MD: He was the faculty member at the Stanford University School of Medicine for 30 years where he was the Colleen and Robert Haas Professor Emeritus of Medicine and Biomedical Ethics.

Director of the board, Paul R. Edick: He was the CEO of Durata Therapeutics, GANIC Pharmaceuticals, and MedPointe Healthcare.

Director of the board, Paolo Pucci: He is the current CEO of ArQule, Inc. He also worked as the senior VP of Bayer-Schering Global Oncology/Specialized Therapeutics Business Unit at Bayer AG.

Director of the board, Lota S. Zoth: She worked as the senior VP and CFO of MedImmune.

Financials and valuation:

NewLink Genetics is expected to have $131.5 million in cash reserves at the end of 2016. The operating cash burn was $65.9 million in 2016. The management expects to end 2017 with cash reserves of $75 million. We don't see any risk of equity dilution in 2017. The company has long-term debt of about $0.5 million and $6 million of royalty obligation to ISDED.

The size of melanoma market is $2.06 billion globally in the US and is expected to grow to $4.7 billion globally by 2020. About 76,000 new cases of melanoma are seen every year in the US and another 80,000 cases per year are seen in the EU. About 10% of these are diagnosed at advanced stage, thus providing our target market for Indoximod+Keytruda combination in advanced melanoma = 7,600 cases/year in the US and 8,000 cases/year in the EU. A combination of Opdivo and Yervoy is priced at average wholesale price = $256,000 in the US. Opdivo alone is priced at AWP of $150,000 in the US. We expect Indoximod to be priced in a similar range, thus providing us AWP = $106,000 in the US. At average sales price = 74% of AWP (average per Pharmagellan guide), we input ASP = $78,440 in the US. ASP of drugs in the EU and Japan is about 50% of that in the US. We input ASP = $39,220 in the EU. We input probability of reaching the market = 65% for the combination at this stage (average for drugs who passed Phase 2). The biggest competition for the combination in the melanoma market is Keytruda+epacadostat and Opdivo+Yervoy combinations. We input peak 20% market penetration in this indication for Indoximod+Keytruda combination in this combination in a base conservative scenario. Using these inputs, we modeled peak $106 million risk-adjusted revenue in this indication in the US+EU in 2024. Peak estimates for Opdivo+Yervoy combination in advanced melanoma is $350 million.

Peak sales estimate for epacadostat in various cancers is expected to be as high as $9 billion. Peak sales estimate for Tecentriq in various cancers is $3.5 billion in 2020. We are optimistic that GDC-0919 can achieve $1 billion in worldwide sales at the peak in combination with Tecentriq in various cancer mentioned above. Using probability of reaching the market = 60% at this stage and 20% of revenue as royalty payments for NewLink Genetics, we modeled peak $120 million risk-adjusted royalty revenue from GDC-0919 in 2024.

We also added NPV of potential $1 billion milestone payment from Genentech (equally distributed from 2017 to 2024, risk-adjusted at 60% probability and discounted at 15% for NPV of $336.5 million).

Using rNPV method (20% cost of capital), we calculated fair value of equity = $850.3 million after adjusting for non-operating assets, operating loss carry-forwards, and liabilities (using diluted share count) or $23.80 per share.

We are initiating coverage on NewLink Genetics common stock with Buy rating and first price target = $24.

We have not yet modeled revenue from Indoximod in other non-melanoma indications mentioned above, revenue from HyperAcute cellular immunotherapy pipeline, and Ebola vaccine program, which could add to further upside. We will adjust our model for these indications as we get more data.

Bristol-Myers acquired Flexus Therapeutics, another company developing IDO inhibitor pipeline (in preclinical stage) for $1.25 billion in 2015. In 2016, Merck acquired IOmet Pharma for its preclinical stage IDO inhibitor pipeline for $400 million.

OrbiMed Advisors, one of the largest healthcare institutional investors in the world, is the second largest investor in NewLink Genetics, and owns $33 million worth of stock (6.8% of the outstanding shares).

Several sell-side analysts reiterated Buy ratings on the stock recently, including Cantor Fitzgerald (PT = $20, April 4), and Stifel (PT = $26, April 4). SunTrust Robinson Humphrey considers NewLink Genetics as a takeover target and has price target of $30 on the stock.

Upcoming catalysts:

Risks in the investment:

It is possible that the ongoing clinical trials may fail, regulatory agencies might not approve the products, unexpected side effects might be seen in the future, clinicians might not widely prescribe the products, or insurers might not reimburse them. Competing products from other companies might gain significant market share in the planned clinical indications. The company may also need to raise additional capital in future.

Author's note: To get more investment ideas like this as soon as they are published, click on my profile and hit the big orange "Follow" button and choose the real-time alerts option.

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Disclosure: This article represents my own opinion and is not a substitute for professional investment advice. It does not represent solicitation to buy or sell any security. Investors should do their own research and consult their financial adviser before making any investment.

Disclosure: I am/we are long NLNK, INCY, BMY.

I wrote this article myself, and it expresses my own opinions. I am not receiving compensation for it (other than from Seeking Alpha). I have no business relationship with any company whose stock is mentioned in this article.

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Regulators holding fistful of livestock genetics magic at the gate – Agri-Pulse

WASHINGTON, April 19, 2017- A mounting wave of new genetics technology is on its way, promising improved health and growth to farm animals, along with improved management tools and profits to livestock owners.

Still, use of this new channel of technological wonders, called gene or genome editing (see text box) apparently awaits the Trump administrations decisions about what kind of regulations theyll impose.

Bubbling up from technology companies and universities, and research collaborators in both, are gene editing techniques to breed cattle and swine immunity to foot-and-mouth disease, cattle that produce antibodies for fighting cancer in people, poultry resistant to highly pathological bird flu and, for example, improved heat-tolerance into cattle breeds that built their genomes in cool, northern-European climates.

The world market for shares of promising genome editing products in human and animal physiology, immune responses and other medical and agricultural applications is likely to grow to $8.1 billion by 2025, according to a projections by Grand View Research of California.

In the agricultural arena, for example, already at least two developers, Acceligen (the agricultural genetics subsidiary of Recombinetics) and a collaborative of university and Genus researchers, can offer genome editing technology to ensure strong resistance to PRRSV (the disastrous porcine reproductive and respiratory syndrome virus).

But thats just one item on Acceligens gene-editing menu of marvels. For the dairy sector, it has the right stuff for hornless (polled) cattle. It is a trait dairy farmers have long been able to select for Holsteins, which would relieve cattle from the stressful removal of horns or horn buds plus save dairy farm labor. However, unfortunately, choosing the trait has meant sacrificing other desired traits for health, milk production and more.

So, says Tad Sonstegard, Acceligens chief scientific officer: How do you get polled cattle without having to physically dehorn the animal or backcross in polled genetics, slowing your genetic improvement program? That is where our technology comes in.

With its new gene editing for hornless cattle, we could make (the genetics for) that animal tomorrow in a laboratory . . . and move it into an animal once we validated that it has been properly edited, Sonstegard explains. His company secured a USDA grant to edit the cattle genome for the polled trait, qualifying for the funds because the trait is associated with both animal welfare and safety for people handling cattle. Acceligen then hired scientists at the University of California, Davis, to produce the technology.

Amid the stream of such animal gene editing magic, the Food and Drug Administration posted its intent in January to regulate genome editing as it has transgenic processes, generally called genetic engineering. It is part of a move that the FDA, USDA and the Environmental Protection Agency took at the end of the Obama administration to modernize the regulatory system for biotechnology products, as then-President Obama had suggested in a 2015 memorandum. FDAs proposed guidance would specifically apply regulatory authority over animals intentionally altered through use of genome editing techniques.

Sonstegard says that, even though the agency has no regulation on use of gene editing products currently, its proposed guidance leaves commercial use of gene editing of farm animals in limbo until FDA moves to waive regulation, or require pre-market or post-market regulation.

That may not be helpful for industry, he says, because we made animals (genetic changes) two to three years ago in some cases. So at a minimum, the regulation is three years behind the technology. And, he says, I just dont know if . . . they (FDA) have reached the place where that approach is equal to their proposed regulation. And, he worries, If its too expensive and it takes too long, it wont fit into the (livestock) system.

Meanwhile, Kellye Eversole, a veteran biotechnology policy consultant in Bethesda, Md., doesnt agree that commercial production of gene-edited animals must wait for FDA to act. The agency doesnt regulate genome editing now, and it would be a change in FDA principles if they did look at what technology was used. Instead, theyve always been very product oriented. That is, she says, the results of gene editing arent different than what is done every day in conventional breeding practices . . . modifications that go on all the time within an organisms genetic makeup.

Regulators would be unable to differentiate with certainty the products of gene editing from other conventionally bred specimens because gene editing involves no introductions of foreign genetic matter, according to Eversole and Sonstegard.

Brad Shurdut, an Intrexon vice president for regulatory and government affairs, emphasizes that a product-based approach is needed by FDA. Intrexon is known for developing a host of transgenic products, including male mosquitos that cause female mosquitos offspring to die before adulthood. A subsidiary, AquaBounty, is developing a fast-growing freshwater salmon calledAquAdvantage. Intrexon is also editing the genomes of tilapia, for example, to produce large, higher-quality fillets, so genome editing looms large, for that company, too.

FDAs regulations must ensure that products are safe and effective, Shurdut says. But also, it is important to us and to agriculture that we have a transparent, predictable regulatory system so we can understand . . . the regulatory pathway. Obviously that has impact on our ability to bring innovation forward.

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Re Cases Y, Z, AA, AB & AC (Human Fertilisation and Embryology Act 2008) [2017] EWHC 784 (Fam) – Family Law Week

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Case summary coming soon

Case numbers omitted Neutral Citation Number: [2017] EWHC 784 (Fam) IN THE HIGH COURT OF JUSTICEFAMILY DIVISION

Royal Courts of Justice Strand, London, WC2A 2LL

Date: 12 April 2017

Before :

SIR JAMES MUNBY PRESIDENT OF THE FAMILY DIVISION

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In the Matter of the Human Fertilisation and Embryology Act 2008 (Cases Y, Z, AA, AB and AC)

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Ms Deirdre Fottrell QC (instructed by Goodman Ray Solicitors LLP) for the applicants

Hearing date: 21 March 2017

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Judgment This judgment was handed down in open court

Sir James Munby, President of the Family Division : 1.Since I handed down judgment in In re A and others (Legal Parenthood: Written Consents) [2015] EWHC 2602 (Fam), [2016] 1 WLR 1325, I have had to consider a number of cases raising issues very similar to those which confront me here. The most recent judgments were Re the Human Fertilisation and Embryology Act 2008 (Cases P, Q, R, S, T, U, W and X) [2016] EWHC 2273 (Fam) and Re the Human Fertilisation and Embryology Act 2008 (Case K) [2016] EWHC 2356 (Fam). They were the sixteenth to twenty-fourth of these cases in which I have given a final judgment. This judgment relates to another five cases, Cases Y, Z, AA, AB and AC. That amounts to 29 cases in all. There are at least another five cases in the pipeline, Cases AD, AE, AF, AG and AH.

2.For the purposes of this judgment I shall take as read the analysis in In re A and the summary of the background to all this litigation which appears in Re the Human Fertilisation and Embryology Act 2008 (Case O) [2016] EWHC 2273 (Fam).

The facts3.For reasons which will by now be familiar, I propose to be extremely sparing in what I say of the facts and the evidence in these cases.

4.All relate to treatment provided by Care Fertility Group Manchester, except Case X which relates to treatment provided by Care Fertility Group Manchester. Each of the clinics is and was regulated by the Human Fertilisation and Embryology Authority. I shall refer to the applicant in each case as X, the respondent as Y and the child as C. In each case X seeks a declaration pursuant to section 55A of the Family Law Act 1986 that he or she is, in accordance with sections 36 and 37 or, as the case may be, sections 43 and 44 of the Human Fertilisation and Embryology Act 2008, the legal parent of C. In each case Y is wholeheartedly supportive of X's application. In each case the clinic, the HFEA, the Secretary of State for Health and the Attorney General have all been notified of the proceedings. None has sought to be joined, although representatives of Care Fertility Group attended the hearing. In each case, given the nature of the issues (see below) I decided that there was no need for C to have a guardian appointed.

5.I heard the cases sequentially, in the order Case Y, Case AA, Case AC, Case AB and Case Z, on 21 March 2017. In each case X was represented by Ms Deirdre Fottrell QC. At the end of each of the hearings I indicated that I was making the orders sought. I now (xx April 2017) hand down judgment explaining my reasons.

6.Although I am acutely conscious of the stress, worry and anxiety burdening all the parents in these cases, and of the powerful human emotions that are inevitably engaged, each of these cases is, in terms of the applicable legal analysis, straight-forward and simple. They raise no new points. In each case the evidence, which there is no need for me to rehearse in detail, is compelling. In each case the answer is clear.

7.Just as in each of the other cases I have had to consider, so in each of these cases, having regard to the evidence before me, I find as a fact that:

i)The treatment which led to the birth of C was embarked upon and carried through jointly and with full knowledge by both the woman (that is, Y) and her partner (X).

ii)From the outset of that treatment, it was the intention of both X and Y that X would be a legal parent of C. Each was aware that this was a matter which, legally, required the signing by each of them of consent forms. Each of them believed that they had signed the relevant forms as legally required and, more generally, had done whatever was needed to ensure that they would both be parents.

iii)From the moment when the pregnancy was confirmed, both X and Y believed that X was the other parent of the child. That remained their belief when C was born.

iv)X and Y, believing that they were entitled to, and acting in complete good faith, registered the birth of their child, as they believed C to be, showing both of them on the birth certificate as C's parents, as they believed themselves to be.

v)The first they knew that anything was or might be 'wrong' was when, some while later, they were contacted by the clinic.

8.I add that there can be no suggestion that any consent given was not fully informed consent. Nor is there any suggestion of any failure or omission by the clinic in relation to the provision of information or counselling.

The facts: the individual cases9.In each of Cases Y, AA, AC and AB the applicant is a woman. In Case Z the applicant is a man. None of them was either in a civil partnership with or married to the respondent mother.

10.Case Y: Adopting the terminology I have used in previous cases, the problem in this case is very shortly stated. The Form PP was correctly completed. There is no Form WP in the clinic's records. X and Y do not assert any positive memory of a Form WP. Ms Fottrell invites me to proceed on the basis that there is a Form IC, signed by both X and Y, in a form which, on the basis of my judgments in previous cases, suffices to entitle X to the declaration she seeks. The relevant declaration, signed by X, reads as follows:

"I am the partner of [Y]. I acknowledge that she and I are being treated together In consenting to the course of treatment outlined above, I understand that I will become the legal parent of any resulting child(ren) subject to the completion of the appropriate HFEA consent forms [see page 1, section 4 of this consent]."

That cross-reference is to Forms WP and PP. But for the inclusion of the words "subject to the completion of the appropriate HFEA consent forms", there could be no question of this not being a Form IC sufficient to entitle X to the declaration she seeks. The only question is whether those words are fatal to the efficacy of the document for this purpose. In my judgment they are not. The document has to be read as a whole and, read as a whole, it is clear that both parties were signing a document which contemplated that X would be a parent. If X was not to be a parent, why sign the declaration at all? X is entitled to the declaration she seeks: see In re A, para 63(iii).

11.Case AA: Again, the problem is very shortly stated. The Form WP was properly completed. The Form PP contains two errors: first, Y's name, rather than X's, appears in section 1, and X's name, rather than Y's, appears in section 2; secondly, the declaration in section 5 has been signed by Y and not by X. However, and importantly, the consent box in section 3 has been ticked and the second page, which contains section 3, has been signed at the foot by X. Both errors are obvious. The first error, the transposition of the names, can be corrected by way of rectification: see In re A, para 47, Re the Human Fertilisation and Embryology Act 2008 (Case G) [2016] EWHC 729 (Fam) and Re the Human Fertilisation and Embryology Act 2008 (Cases P, Q, R, S, T, U, W and X) [2016] EWHC 2273 (Fam), paras 17 (Case S) and 18 (Case T). The second error is irrelevant: see Re the Human Fertilisation and Embryology Act 2008 (Cases P, Q, R, S, T, U, W and X) [2016] EWHC 2273 (Fam), paras 13 (Case Q) and 15 (Case R). X's signature at the foot of the second page is sufficient to satisfy the statutory requirement: see Re the Human Fertilisation and Embryology Act 2008 (Cases P, Q, R, S, T, U, W and X) [2016] EWHC 2273 (Fam), paras 13 (Case Q) and 15 (Case R). In these circumstances X is entitled to a decree of rectification and the declaration she seeks.

12.Case AC: Again, the problem is very shortly stated. The Form WP was properly completed. In the Form PP, Y's name, rather than X's, appears in section 1, and X's name, rather than Y's, appears in section 2. However, the consent box in section 3 has been ticked, the second page, which contains section 3, has been signed at the foot by X, as has the declaration in section 5. The error is obvious. The transposition of the names can be corrected by way of rectification: see the authorities referred to in paragraph 11 above. X is entitled to a decree of rectification and the declaration she seeks.

13.Moreover, there is again a quite separate ground on which X is entitled to the relief she seeks. Both Y and X signed a Form IC which, in all material respects, was in the same form as the Form IC considered in paragraph 10 above. In the circumstances, X is, in principle, entitled to the declaration she seeks on this ground also.

14.Case AB: Again, the problem is shortly stated. The Form PP was properly completed. In the Form WP, which was otherwise properly completed, the consent box in section 3 on the second page was not ticked. The omission of the ? in the consent box is not fatal to the validity either of a Form PP or, as here, of a Form WP: see Re the Human Fertilisation and Embryology Act 2008 (Case J) [2016] EWHC 1330 (Fam), para 15, followed by Peter Jackson J in D v D (Fertility Treatment: Paperwork Error) [2016] EWHC 2112 (Fam), and Re the Human Fertilisation and Embryology Act 2008 (Cases P, Q, R, S, T, U, W and X) [2016] EWHC 2273 (Fam), paras 11 (Case P) and 17 (Case S). X is entitled to the declaration she seeks.

15.Again, there is a quite separate ground on which X is entitled to the relief she seeks. Both Y and X signed a Form IC which, in all material respects, was in the same form as the Forms IC considered in paragraphs 10 and 13 above. In the circumstances, X is, in principle, entitled to the declaration she seeks on this ground also.

16.Case Z: Again, the problem is shortly stated. The Form WP was properly completed. In the Form PP, which was otherwise properly completed, the consent box in section 3 on the second page was not ticked. The omission of the ? in the consent box is not fatal to the validity either of a Form WP or, as here, of a Form PP: see the authorities referred to in paragraph 14 above. X is entitled to the declaration he seeks.

17.Again, there is again a quite separate ground on which X is entitled to the relief he seeks. Both Y and X signed a Form IC, indeed a number of Forms IC, which, in all material respects, were in the same form as the Forms IC considered in paragraphs 10, 13 and 15 above. X is, in principle, entitled to the declaration he seeks on this ground also.

Outcome18.It was for these reasons that at the conclusion of the hearing of each case I made a declaration in the terms sought by X.

Costs19.In each case the clinic has very properly agreed to pay the applicant's reasonable costs.

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Re Cases Y, Z, AA, AB & AC (Human Fertilisation and Embryology Act 2008) [2017] EWHC 784 (Fam) - Family Law Week