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HomeNews & Multimedia2018
Mega-Dams May Be History in the Brazilian Amazon!
What to Celebrate and What to Watch Out For
Christian Poirier
Last week, executives of Brazil's Ministry of Mines and Energy (MME) unexpectedly announced to the Brazilian newspaper O Globo that the country would cease building large dams on the Amazon's rivers. Like many of our allies, we celebrated this news and were especially heartened by the fact that the executives cited the need to "respect the social desire to restrict these projects." Acknowledging the complexity in both licensing and financing mega-dams in the era of controversial projects like Belo Monte, these officials indicated that Brazil would pursue new directions to meet its energy needs that emphasize clean renewable power and decentralization.
On face value, this news should be seen as a major victory of all those – including Amazon Watch and our indigenous and international NGO allies – who resisted and fought the disaster of Amazon dams, particularly those communities and organizations on the front lines. To halt a once-powerful dam-building juggernaut is a clear vindication of our decades-long struggle in defense of the Amazon's forests and all those who rely upon these irreplaceable ecosystems.
There are several factors that led to this apparent policy shift, including the privatization of the state energy company Electrobras and the obvious corruption involved in recent Amazon dam projects, which deeply undermined public support for new projects of this kind. Furthermore, when MME executive secretary Paulo Pedrosa grudgingly mentions "social desire," he is conceding that determined resistance to Brazil's dam-building program profoundly complicated his ministry's originally designs for the Amazon's rivers, which foresaw building dozens of large dams over the coming years. In a shocking departure from the MME's policy of obscuring the true impacts and implications of large dams, Pedrosa said: "We are not willing to make moves that mask their costs and their risks."
In 2010, Amazon Watch joined a coalition of allies – ranging from the grassroots to the global – to fight the Belo Monte dam and its proponents. Our combined efforts sought not only to stop one emblematic project, but also to challenge a destructive development model and encourage a paradigm shift toward truly clean, alternative solutions. While we were ultimately unsuccessful at halting this catastrophe from befalling the Xingu River and its peoples, our coalition's efforts took a profound political and financial toll upon the dam industry that ultimately contributed to the archiving of Belo Monte's mega-dam successor, known as São Luiz do Tapajós, in 2016. Last week's announcement seemingly extends this victory across the Brazilian Amazon while answering the public's call for accountability and viable energy alternatives.
However, it is important to temper this triumph with both historic and current context. It is wise to doubt the credibility of the Brazilian government in these matters, particularly as its actions frequently contradict its public statements. Last week, Brazil's national energy agency ANEEL accepted viability studies for the proposed Jatoba dam on the Tapajós River, an unquestionably large project with major implications for the region's ecosystems and the wellbeing of the Munduruku indigenous people.
Meanwhile, the government's ten-year energy plan cites the completion of studies for the São Luiz do Tapajós dam's energy transmission lines, implying that the project will again be on the country's development agenda in 2028. Indeed, the plan prolongs the government's abject failure to adequately recognize disputes around the social, environmental, and economic viability of large dams, including violations of the rights of indigenous peoples. Such mixed signals imply that all those working to defend the human rights and protect the Brazilian Amazon's rivers and forests must not drop their guard.
Last week's announcement should be celebrated as a tentative victory, albeit a fragile one that demands vigilance as Brazil continues to weather political and financial instability. With presidential elections scheduled for the end of the year, a new administration could honor or abandon the MME's proposals, the latter once again throwing the future stability of the Amazon into jeopardy. This victory will only become a reality when we insist it be upheld. We owe this to our on-the-ground partners for all they do on our behalf to defend this life-giving forest.
Pledge Solidarity with Brazil's Resistance!
Tapajós
Belo Monte Dam
Dirty Energy
Hydroelectric Dams
Australia and the Amazon: Two Terrible Tragedies With One Key Difference - Blog Post
BlackRock Responds to Demands for Stronger Climate Action with Bold New Commitments - Press Release
The Climate Movement Is Going After Wall Street - Press Release
Protecting the Amazon Is Going to Take All of Us! - Blog Post
Amazon Fires Wreak New Level of Havoc on Surroundings - Anadolu Agency
The New Hope: Indigenous and Youth Voices Rise for Climate Justice Despite Failure of COP25 - Blog Post
Protecting the Amazon Is Going to Take All of Us!
New Report at UN Climate Conference Exposes Plans to Drill for Oil in the Heart of the Amazon
You Rushed to Defend the Amazon at a Critical Tipping Point, but the Fight Is Not Over
Tell GeoPark to Stay Out of Achuar Territory!
Join the Call to Protect Earth Defenders!
Yes, I will donate to protect the Amazon!
"The work you do is vital, and I am happy to support it."
– Charlotte R. A.
Amazon Watch is a 501(c)(3) nonprofit organization founded in 1996 to protect the rainforest and advance the rights of indigenous peoples in the Amazon Basin. We partner with indigenous and environmental organizations in campaigns for human rights, corporate accountability and the preservation of the Amazon's ecological systems.
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This article reviews empirical research on applying the Attention, Relevance, Confidence, and Satisfaction (ARCS) model to real educational settings, including computer-based learning approaches. This review focuses on three aspects: (1) how the ARCS model was applied to what specific educational settings; (2) what research methods were used; and (3) what outcomes were reported in these studies. Our findings indicate that the ARCS model was applied to a variety of countries and educational settings. The course component(s) in which the ARCS model was incorporated included single course component (e.g. course email), multiple course components, and other programs (e.g. specific software or game). Quantitative methods were used more than qualitative and mixed methods in these reviewed studies. Four major research outcomes were found in regard to participants' affective domain, cognitive domain, learning behaviors, and psychological traits. We also summarized the studies in this review and provided future research directions. The latter includes applications of design-based research to educational problems that the ARCS model might address, especially in the context of computer-based learning.
Demographic data of MOOC learners: Can alternative survey deliveries improve current understandings?


Fire crews were out in the St Matthews area during Friday afternoon.
Lancashire Fire and Rescue Service sent a team of firefighters to a house in Bootle Street, off Ribbleton Lane.
The fire, at around 4pm on Friday (29 December), saw a pan of oil on the cooker hood overheat and ignite.
The spokesman for the fire service said they were called to more than 500 cooker fires across Lancashire in the last year, mainly due to people becoming distracted while cooking.


During summer vacation, I managed to lessen the dark spots on my face using 20% TCA Peel which I bought online.
Unfortunately I broke out real bad this July and August. Why? Hormonal imbalance and the #1 cause is Stress. There's a lot of schoolworks and papers. It's our senior year in college. You know how stressful it is.
After the injection, the cystic acnes were a little flat already. Im writing this 28 hours after the treatment and I can barely see most of them aside from the blood clots.
Hormonal imbalance is another cause so my dermatologist gave me Acneadvance Praventin. Im not sure how long will I take the pills. I took the first pill this night. We'll see how it goes. I'll review it soon.


All modern equipment –be it a car you drive, the motorcycle, the lawnmower, industrial equipment, even a bicycle– are engineered for performance, efficiency, and economy. The most precise way to hold it together is with bolts and nuts. Each bolt is designed to hold its share of the load and to keep it in precise alignment. It means that you cannot go on guessing how much to tighten the bolt or nut without risking sheering off a bolt, stripping its thread, or under-tightening a nut at which point it will become loose even just during normal operation.
In the things like wheel nuts and axle nuts (where nut clamping power responsible on properly loading a bearing), under-tightening or over-tightening will cause you very expensive repairs in the future.
Never mind that a brake caliper bolts responsible for your safe stopping on the road. Proper tightening, clamping, torquing is not open for interpretations anymore. It is exact science, and you need to pay attention too. Lucky for you, you stumbled on our website. We do not only explain what are the different types of torque wrench available, we also provide you our top brand choices below to help you out in your buying decisions.
Believe us, other mechanics and gear heads will be envious if they found out you have this. The CDI Computorq 3 offers a body design that guarantees maximum durability and performance. It's an easy-to-use digital readout wrench that displays real time torque values in any of four torque units. Undoubtedly great for light industrial, automotive, motorcycle, watercraft, and aircraft applications. It likewise features a sleek new design and a 15 degree flex ratcheting head. There is a push button socket release head and a large, easy to read digital display. It takes lithium ion batteries for a long life and features an ergonomically designed molded non slip rubber grip.
What's more cool is that this computer wrench remembers the last unit and torque setting selected. An audible tone sounds when set torque value is reached or alarms when value is exceeded. This is a standard model electronic torque wrench. The torque is 10 to 100 foot pounds. Simply set the desired torque value and apply force until the green LED illuminates.
Capri Tools 31200 inch pound torque wrench has obviously ¼ inch drive. Although this wrench is an industrial-level torque wrench, it has a solid tool for easy and certain adjustments. Drive selection is straightforward, and a ball-bearing bit holder button (instead of a friction bearing) is a nice feature. It's high tooth count, which is handy when working in tight spaces, might find it handy to most auto mechanics. It's designed for regular, daily use and long-term durability (Approved for up to 10,000 clicks at max torque without re-calibration). It is also reversible (can tighten both clockwise and counter-clockwise).
For best fit application use it for 40 – 135 in.lbs range. Don't use it right at 150 in.lbs; the risk of overtightening something is great with the small tool.
The Gear Wrench company has a reputation of making great products, and this one is no exception. First of all, if you want a torque which meets all the required standards, then this one is a perfect fit as it meets all the ISO 6789 specifications and exceeds ASME B107.14M. Besides meeting all the required standards, it also has a durable build, and if you are one of those buyers who like being extremely precise, then it suits you, even more, better as it has an accuracy of plus or minus in the clockwise direction from 20% to 100%. To add on efficiency, the midpoint part of the handle is marked so the user can have an easier time. The ratcheting head can flex up to thirty degrees for improved access while fixing it. It uses a locking mechanism which slides up and down hence leading to a more firm lock in comparison to its predecessor which used a side to side lock leading to a loose clamp.
Just like the name suggests, Precision Instruments PREC3FR250F Silver 1/2" Drive is a high quality and relatively inexpensive. The torque wrench from Precision Instruments is a prime example of this. Where other wrenches must be calibrated, this one does not have to. The speed of wrenching is increased through the spring-loaded mechanism on the wrench. It is fairly long (22-1/8 inches). This means you can get more leverage out of this tool, which is one attractive feature according to several torque wrench reviews.
Setting the tool requires only fingertip force since the adjustment mechanism is not under load. There is no need to "work in" a C series torque wrench before starting using it.
BONUS: It is not necessary to adjust to the lowest torque setting after use. Split-Beam Click Wrenches overcome many of the problems associated with micrometer-style clock wrenches, especially in real life shop conditions. The wrench has few components as all critical parts welded together during manufacturing.
With dimensions of 42 by 2.5 by 2 inches, the CDI torque wrench is an ideal and must have tools for professionals. It weighs about 25 lbs and is quite long in comparison to most wrenches in the market hence giving it an advantage as it can easily torque heavier bolts. For instance, it has a torque range of 600-700 thus making it convenient. The handle is ergonomic and lightly knurled so the user can easily grip it while working and not have worries about it slipping. It also has quick release buttons which offer ideal socket maintenance and also removal and even though the company is yet to release specs on its accuracy most users have reported that it is quite precise.
Easy to change or customize it to your desired specifications.
If you are looking for a bicycle torque wrench, then the venzo happens to be one of the best ones in the market. The venzo bicycle torque wrench comes with a gauge for your bike's carbon parts as part of the package hence adds more convenience because finding a high-quality one compatible with such elements can prove to be a futile task. It has an accuracy of plus and minus four which is more than you would expect for its price and also which reduces calibration errors.
Unlike ordinary torque wrenches it has an Allen key which five millimeters longer is thus making it easy for the user to reach the bolts without straining too much. Besides making the calibration process accurate and the extra length of the Allen key, this torque wrench has a range of two to twenty four hence covers most parts of the installation. That not only makes thing more comfortable for the user but also minimizes the costs because now they can use one wrench for various installation eliminating the need of having to but other tools.
It also comes with one year of warranty which further assures you of its quality because not many torque wrench companies offer guarantees if they don't have confidence in their product.
The Wheeler 710909 digital firearms accurizing torque wrench packs a bunch of incredible features which is why it is a favorite to many professionals. Everything from its design to the technical features spells convenience and comfort. For instance, it has a large LCD digital display which makes it easy for the user to view the technical details such as the range hence promoting to even more accuracy. It has a comfortable and durable design, for instance, the wrench bits are made of S2 steel which is then hardened to 56-56 Rockwell C. This ensures that buyers do not have to worry about purchasing another one soon as the Wheeler digital F.A.T can stand the test of time. Besides resilience, accuracy is the last thing that buyers and current users have to worry about as it has an accuracy that is at +2 pounds which when combined with the audible and visual indicators allow the user to know when their desired torque is achieved and hence avoid making mistakes.
To add on that it has an extensive range of between 15 and 100 lbs. Which further minimizes the chances of inaccuracy ensuring that the results of whatever you are working ends up being nothing but perfect. It boasts a low battery indicator which alerts you of whenever you need to recharge.
It has various indicators such as low battery and audible indicator tone for further convenience.
It comes with an injection molded storage case which enables you to store it away safely whenever you are not using it.
With DYI automotive work on the rise and numerous industries using torque wrenches, it's important to take note of the 4 different basic sizes available for commercial applications. The different sizes roughly match the torque range that can be described in foot-pounds (ft-lb, lbs, lbf) and newton meters (n m, n-m) for metric fasteners and SAE fasteners. On smaller torque wrenches inch pounds (psi or lbf/in2) are used to describe the torque range.
Used for really small bolts and nuts and an appropriate range for automotive work is 50 to 250 psi which equals 4 to 21 ft-lbs.
The majority of light-trucks and automobiles use 3/8" bolts and can be torqued to spec using this size. Appropriate range for automotive work is 15 to 75 ft-lbs. For some reason if you can only get one size for now this drive won't work on everything, however, it's very versatile.
Larger bolts and nuts for applications like suspension, transmission, and engine mounts could require this drive torque to spec for different sized vehicles. The appropriate range for automotive work is 30 to 250 ft-lbs.
This is made for much larger applications like center lug wheels. This drive isn't typical of what a normal person would use, this is more suited for commercial sized trucks. You should select a range that is precise to your situation.
Why not get the biggest one they got with the most range and be done with it?
The answer to that question is, as your torque requirements increase so doesn't the size of your wrench. This makes it harder to get into smaller spaces where most of the automotive work takes place.
It's easy to picture tons of really tight bolts with torque specs in the triple-digits on a vehicle, the reality of the situation is that bolts and nuts are torqued to numbers lower and a smaller wrench is more versatile and is worth the trade-off of sacrificing some capability for the higher-end of the torque range. Remember that torque wrenches are more accurate in the middle of their torque range, so pick your range accordingly.
A quality tool should at least come with a 1-year warranty and the higher-end torque wrenches will come with specific warranties according to the manufacturer's warranty policies.
Most torque wrenches will have a varying accuracy, the nice ones have an accuracy of more than 5%. The more expensive torque wrenches will include a certificate of calibration with the accuracy and date. With that being said, torque wrenches should be brought in and serviced according to the manufacturer's recommendations.
Torque wrenches are calibrated instruments and need to be serviced according to the manufacture's recommendations to keep factory accuracy. If a torque wrench gets dropped and they do, you should do a quick calibration to validate the accuracy. You should always store your power tool according to the manufacturer's recommendations. The best torque wrench can make the difference in your repair work and if you take care of it, your torque wrench will always be ready when you need it to perform flawlessly.
Less expensive torque wrenches will be constructed with more plastic parts. Even though these wrenches work just fine, the wrenches made of metal parts will be more durable.
Ratcheting is very convenient especially when it's (bi-directional) clock-wise and counter clock-wise for fasteners with left-hand and right-hand threads.
Get a hard case, it's more durable versus soft cases that can allow your torque wrench to get roughed-up and knocked out of calibration. Most hard cases are plastic and they work really well to protect your torque wrench.
It doesn't matter if it's a digital readout or a mechanical twist handle, save yourself a lot of aggravation and get one that's easy to read.
Look for a torch wrench that has solid grip patterns etched on the handle. This will help when fluids leak onto the handle, the etched grooves are designed to disperse the fluid and leave your hand with a better grip to perform your work.
Using a torque wrench will be useless until you know the torque units and values you need to torque the nuts and bolts to. Here are the tables to take the guess work out of most commonly used fasteners. When it comes to intricately engineered and precisely designed parts, or components, you need to consult the repair manuals and assembly instructions.
For example, many engine manufacturers use single use bolts that are designed to Torqued-To-Yield (TTY). In that case, you torque with this wrench, then you turn the bolt X degrees more. Those are designed to utilize the clamping force of the bolt when it is overstretched. There are tools for that as well, and it will be covered on our Advanced guide.
You need to select the right torque wrench for the application. There are few things one needs to pay attention to, and it is very important to use the tool properly and handle it with care.
Choose a wrench that has your specified torque value from 20% to 90% of full scale. This will ensure the most precise torqueing in your application.
Impact of the tool on a hard surface can throw off its calibration. If the calibration is off, you will not get specified torque value that you need to achieve.
Most of the time ,it will tell to use a torque wrench only at the end of the final assembly. Unless you doing forensic disassembly, don't use it as the primary mean of removing nuts or bolts. When you use torque wrench for removing nuts or bolts, make sure it is rated for CCW, and torque value spec is 40% to 60% of the torque wrench full scale. Use appropriate tools for initial fastening as that could damage it and cause it to need recalibrating sooner.
The use of torque wrench in initial step could damage it and cause it to need re-calibrating sooner.
Fast or jerky movements can result to inconsistent and inaccurate torquing. It can also damage it.
When storing a click type torque wrench, set it to the manufacturer recommended setting. If the setting is not specified, set it to the lowest value on the scale.
Most torque wrenches are length specific so always grasp the wrench in the center of the handle. If two hands are needed, place one hand on top of the other. Sometimes, when the socket extension is used, support the torque wrench at the pivot point.
When a certain amount of time or number of cycles have been reached as specified by the manufacturer, or sooner if it have been mishandled or dropped.
Unless they are allowed by the manufacturer.
Preferably in a clean and dry protected area (preferably in the manufacturers case) and keep calibration certificate where you can access it for your reference.
For newbies out there who are new to using this tool, here's a great video on how to use a torque wrench properly.
When using this power tool, you need to make sure that the power torque setting of the tool is set to at least 30% down from the specified torque. Even certified torque settings on power tools are notoriously imprecise. On top of that, the power supplied by air or electricity can fluctuate due to the air pressure or voltage. Now you can use your torque wrench to set right torque values. Make sure you follow the manual instructions on how to use it.
Use the torque wrench in one smooth and confident motion.
Don't be insecure and double-click when you reach the proper value and you are using click type torque-wrench.


HTC will be shutting down its office in South Korea, reports The Next Web.
The reason for this is reportedly due to HTC's inability to compete with Korean companies like Samsung and even LG on their home ground, where sales of HTC devices are reportedly "sluggish". Apple is the only other non-native company that has done well in this market.
This does not bode well for HTC, who is also losing ground to Samsung in other market. HTC barely managed to scrape a profit in the second quarter. On the other hand, Samsung is growing from strengths and managed to achieve an impressive $5.9 billion in operating profits, overshadowed only by Apple in the mobile segment.
We'll see how HTC performed in the third quarter when they release their quarterly report. Hopefully, the One series of smartphones would have helped bolster the company's sales and profit figures.


With nearly 18,000 acres of open space, miles of trails, scenic views and a host of recreational opportunities, Westchester County Parks offer ideal settings for year-round camping adventures. Whether you're a seasoned camper or just getting started, we have accommodations and facilities to suit your camping needs, from full service cabins with all the amenities to tent camping and lean-tos to test your self-reliance. There are even recreational vehicle sites available with full electric and water hookups.
Campers will find a wide range of things to see and do, and places to visit during their stay in county parks. You can hike, bike, fish, study nature and the outdoors or discover our local history. There are six public golf courses where you can practice your putt, an authentic early 1900s working farm, an arboretum, and the famous Playland Park, where you can thrill to exciting rides, entertainment and non-stop family fun.
For reservations, call the parks directly. Camping permit holders must be 21 years of age or older.
Situated on a peninsula overlooking the scenic Hudson River, this 500-acre park offers cabins and sites for tents and recreational vehicles. Recreational options include a beach, hiking trails, picnic areas, ball fields, boat launch and fishing. In addition, the Croton Point Nature Center offers weekly events and programs throughout the year. During the summer months, the park hosts several major special events, fairs, festivals and concerts. Learn more about Croton Point Park and camping amenities and fees.
Croton Point Park was listed among the top 15 camping spots in New York, read more.
The 1,082 acre Mountain Lakes Park is Westchester's northernmost county park. It is characterized by a rugged landscape and native hardwood forest with miles of trails. The park boasts five lakes and a spectacular overlook that make for breathtaking hiking destinations. Learn more about the park and camping fees.
This 4,315-acre park is the largest in the Westchester County Parks system. Amenities include wooded areas, open spaces, miles of marked hiking and equestrian trails, picnic areas, fishing in the Cross River and cross-country skiing and sledding in winter. The on-site Trailside Nature Museum houses wildlife exhibits and offers weekly interpretive nature programs all year long. Camping facilities include open-faced lean-tos and tent sites. Learn more about Ward Pound Ridge and camping fees.
Located at the scenic Blue Mountain Reservation in Peekskill, this 1,538-acre park in the northwest section of Westchester County features miles of trails for mountain biking, strolling and nature study, and offers challenging hikes to the tops of two large peaks, Mt. Spitzenberg and Blue Mountain. The rustic Trail Lodge offers dormitory-style accommodations that sleep up to 30 people. It features a kitchen and a dining hall with a large fireplace and shower facilities. It is heated and available throughout the year for rental by groups. For information and to reserve, call (914) 231-4575 or (914) 862-5275.
Permits for using shelters, cabins, RV's and tent sites are available to adults 21 years old or over.
All firewood brought into appropriate, fire-approved facilities must be packaged and kiln dried with identification on the package. No other firewood will be allowed.
Any cancellation made at least 30 days prior to reservation arrival date will result in a refund minus a $25 cancellation fee.
Any cancellation made less than 30 days, but at least seven days prior to reservation arrival date will be entitled to a credit for a future stay, minus a $25 cancellation fee.
Any cancellation made less than seven days prior to reservation arrival date shall receive no refund or credit.
Failure to arrive by noon of the day following your scheduled date of arrival will result in cancellation of reservation, with no refund or credit for "No Show".
Camping is an outdoor experience, therefore, we do not give refunds or credits for weather or natural conditions.


A study by MIT and the Santa Fe Institute published in the journal Nature Energy on August 15 finds that electric car range anxiety is overstated in most cases. The study analyzed the driving habits of drivers on a second-by-second basis. It concluded that 87% of vehicles on the road today could be replaced by a low-cost electric car even if there is no possibility of recharging it during the day.
The finding confirms what we already know — the typical driver seldom drives more than 45 miles a day on a regular basis. That means even an electric car with limited range like an original Nissan LEAF has more than enough range to satisfy the needs of the majority of Americans.
Jessika Trancik, a researcher with MIT's "Institute for Data, Systems and Society" and senior author of the study says the research combined hourly temperature data in different US regions, survey data about trip lengths, empirical data on the fuel economy of different cars, and GPS-derived data on the speeds of vehicles and how they vary on a second-by-second basis. It assumed a modestly priced electric vehicle such as a 2013 Nissan Leaf and daily overnight charging.
The study also gives a boost to developing carsharing models. Even though a car may be adequate for the majority of daily needs, drivers still want a car that can take them over the river and through the woods to grandmother's house occasionally, or camping, or for anything other than getting back and forth to work. A second car in the household could be used for that, but many believe in the future we may simply rent another vehicle to fulfill those occasional needs.
Expanding the network of fast-charging stations so people could recharge their cars while away from home would also reduce range anxiety significantly. The Obama administration is a strong advocate for expanding the public charging infrastructure.
Transitioning to electric vehicles would significantly reduce emissions in the US, which is a large part of the governmental push. "If that 90 percent adoption potential was reached, then one could replace about 60 percent of gasoline consumption. That would only reduce emissions about 30 percent, which is still a very significant number," Trancik said.
Of course, longer range means bigger batteries and bigger batteries mean higher cost. Higher cost means fewer potential buyers. It's a vicious circle, one that will only be broken in time as more and more electric cars take to the highways. The changeover to zero-emissions transportation is a process and it will take decades if not generations to complete.


My wife Cindy and I with a custom grouping of our birds. We can create a custom base to fit your niche. First we create an original wooden bird carving and have a mold made to reproduce them in Limited Editions . We have been creating wading bird wood carvings , statues and sculptures since the 1990's .We maintain the highest quality by doing the work in house we have no employees .We are a true Mom and Pop business . Cindy does most of the assembly and base coat painting and I do finish carved and painted details and mounting on unique wooden bases. All products that go into our sculptures are Made in America .The resins we use are good indoors or out. We stand behind our work and aim for 100% satisfaction. Each bird comes with a hang on card that tells about our work. Shop in confidence and we will create you an heirloom for you to pass on for generations.
The Great Blue Heron is a large wading bird that is common near large bodies of water.The blue heron can be found over most of North America . An all white heron population can be found in the Florida Everglades . They were once thought to be a separate species known as the Great White Heron but DNA research has determined that they are merely a unique color morph of the Great Blue Heron .
Yellow -crowned Night Heron (Nyctanassa violacea)Limited Edition of 500 This bird sculpture is 12 inches tall on a 1 of a kind base of twisted driftwood that blends into a black wooden base . This is my favorite piece of driftwood. This piece as you see it is $400.00 It is available on a flat driftwood base for only $220.00 Call- 941-286-3299 to order.
Louisiana tricolored ( Egretta tricolor)heron Limited Edition of 1000 24 inches tall on driftwood base with reed grasses. I often see these on my way to Sanibel Island and that is how I was inspired to do this sculpture. I have named him Sanibel Jack in honor of a good friend who lives on Sanibel.$260.00 Call- 941-286-3299 to order.
Roseate spoonbill sculpture 27 inches tall , I start a piece like this by gathering all my reference material to decide on a pose. I then select my wood design and draw my pattern then cut out the basic shape.Then I carve shape and sand until there is nothing left to do but paint . Then I put my base color on and add several thin coats of paint to give a translucent light feel to the feathers that closely mimic a live bird. (Ajaia ajaja) - Roseate Spoonbill statue by Rod Becklund ($350.00) Call- 941-286-3299 to order.
Sandhill Crane (Grus canadensis)32 inches tall on driftwood base with reeds . The Sandhill Crane is a migratory bird and is often seen at golf courses. Sandhill Cranes mate for life and the Chinese hold them in high regard as a symbol of fidelity and loyalty . His name is Terrence the Sandhill. This is a signed and numbered limited edition of 500 $400.00 Call- 941-286-3299 to place your order.
A link to Rod Becklund's facebook art page with more art.


UMD researchers have identified genetic mechanisms to control cancer-like growths in the plant Arabidopsis, commonly known as mouse-ear cress. The cancer-like tumors as a result of a mutated gene in the plant cause the formation of abnormal flowers and sterility, and the cell cycle complexes disrupted in the mutant plant work similarly in animal and human cells to regulate cell division and organ growth. Using the latest CRISPR gene editing technology, researchers are now able to correct the cancer-like behavior in the plant and have elucidated the underlying mechanisms relevant plants, animals, and humans. With this ability and a clearer understanding of the mechanisms that contribute to uncontrolled cell growth, a path can be laid to the control of plant, animal, and human cancers connected to these genes.
Mouse-ear cress is a small flowering plant closely related to mustard and cabbage plants, and it is often used as a model system given its genetic similarities across plants, animals, and humans and how easy it is to propagate. Dr. Zhongchi Liu, Affiliate Professor with the Department of Plant Science and Landscape Architecture and Professor in the Department of Cell Biology and Molecular Genetics, works with mouse-ear cress often in her research. She named the TSO1 gene she discovered in mouse-ear cress after the Chinese word for "ugly" because of the large cancer-like blobs found in the mutated plant where flowers should be.
The TSO1 gene (aka the ugly gene) is a regulatory gene whose gene product is a member of a cell cycle complex known as the DREAM complex. This complex is conserved and similar to regulatory complexes in animals and humans known to balance cell proliferation and differentiation, determining what cell should be what cell type and how much of it is needed. When these things get out of control, tumors and cancers form. "There are always multiple genes at work that control and produce one phenotype or physical trait, whether that trait is a beautiful and healthy flower or a cancer-like 'ugly' blob," says Liu.
This work is published in The Proceedings of the National Academies of Science here.


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Q: Ionic with angular-google-maps directive I have been trying to get angular-google-maps up and running and for the life of me i cannot firgure out why it is not working...
first i install the
cordova plugin add cordova-plugin-geolocation

here is the index html
<head>
<meta charset="utf-8">
<meta name="viewport" content="initial-scale=1, maximum-scale=1, user-scalable=no, width=device-width">
<title></title>

<link href="lib/ionic/css/ionic.css" rel="stylesheet">
<link href="css/style.css" rel="stylesheet">

<!-- IF using Sass (run gulp sass first), then uncomment below and remove the CSS includes above
<link href="css/ionic.app.css" rel="stylesheet">
-->

<!-- google maps javascript -->
<script src='//maps.googleapis.com/maps/api/js?sensor=false'></script>
<script src="lib/lodash/dist/lodash.min.js"></script>
<script src="lib/angular-google-maps/dist/angular-google-maps.min.js"></script>

<!-- ionic/angularjs js -->
<script src="lib/ionic/js/ionic.bundle.js"></script>

<!-- cordova script (this will be a 404 during development) -->
<script src="cordova.js"></script>

<!-- your app's js -->
<script src="js/app.js"></script>
<script src="js/controllers.js"></script>
<script src="js/services.js"></script>

</head>

my map.html
<ion-view view-title="Map">
  <ion-content ng-controller="MapCtrl">
    <ui-gmap-google-map center='map.center' zoom='map.zoom'></ui-gmap-google-map>
  </ion-content>
</ion-view>

and finally my module and controller
var myApp = angular.module('myApp', ['ionic','uiGmapgoogle-maps']);

myApp.controller('MapCtrl', function($scope) {

   $scope.map = { center: { latitude: 45, longitude: -73 }, zoom: 8 };

});

when this is run a get a blank screen on both chrome browser and on android phone.. any ideas what i may be doing wrong?? thanks for looking
so after moving google dependencies below ionic.bundle the map now loads... however i cannot set height to 100% using
.angular-google-map-container {
    height: 100%;
}

any ideas??

A: Try this.
 <map center="{{latitud}}, {{longitud}}" zoom="12" id="map_views" data-tap-disabled="true"></map>

A: <script src="lib/angular-google-maps/dist/angular-google-maps.min.js"></script>

shall be loaded AFTER ionic as ionic bundle includes angular Framework

redpajama_set_name: RedPajamaStackExchange


text:
Webb named preseason All-American
Alex Webb playing catcher in a Jacksonville State matchup against Auburn University at Jim Case Stadium in April 2019. (Courtesy of JSU)
Kyle Davie, Correspondent
The hype has already begun for the Jacksonville State Gamecocks 2020 baseball season as their senior catcher, Alex Webb, was named to the Collegiate Baseball Preseason All-American team by Diamond Sports. Although the season has yet to start the accolades are already pouring in.
Webb has been making a name for himself over the past year and the awards have become the new normal thanks to his stellar play. Last season, Webb's first season with the Gamecocks, Webb was named to the Ohio Valley Conference First Team as well as named the most valuable player in the OVC Tournament.
Webb was consistently dominant all season long and was a major factor in the Gamecocks sweep of the OVC regular season title. His team-leading batting average of .346 helped power the Gamecocks into first place in the conference and a 22-9 conference record. Then, his heroics over the course of three games in the conference tournament helped the Gamecocks win their fifth OVC Tournament Championship. Webb batted .429 with 5 RBIs in route to MVP honors.
Awards like this are nothing new for Webb, he has been bringing them home since high school and seems to embrace the opportunity to lead his team to victory. While in high school at Columbia Central, Webb was ranked the top catcher in all of Tennessee by Perfect Game USA. He claimed all-district honors three consecutive years, all-state honors in back-to-back years, and topped it all off with a team leading 13 home runs and a District MVP award his senior year.
The praise and glory did not come without patience and hard work as Webb played sparingly, yet still produced, his redshirt freshman year at the University of Alabama. After sitting out 2016 as a redshirt, Webb started 14 games and played in 31 games for Alabama in 2017. Even with lesser play time Webb took advantage of his opportunities and batted .328 during his time with the Crimson Tide.
Following that season, in his lone season away from Division I baseball, Webb was terrific at Chipola Junior College in Mariana, Florida. Webb was responsible for 27 runs scored, 46 hits, and 36 RBIs, with a .272 batting average and even shined on defense, catching nine base stealers. That production led to a national title for the Indians of CJC and a return to D1 baseball for Webb.
Coming off a season in which JSU won their first ever Division I Regional game the expectations and hopes are high for the Gamecocks and star players like Webb. Next month, February 14 at Rudy Abbott Field at Jim Case Stadium, will start the journey to what is hopefully another award filled, history making season as the Gamecocks will host the University of Missouri.
The Gamecocks will need Alex Webb at his best if they want to repeat the success of last season, but judging by his consistent development and knack for producing when it matters most, that won't be too much to ask of the reigning conference MVP.
Be the first to comment on "Webb named preseason All-American"

redpajama_set_name: RedPajamaCommonCrawl


Christian Legagneur hates his job, but he hides it well. He might be a beloved gameshow host, but his contestants, elderly singles all dressed up in pathetic finery with gauche pink hearts pinned to their fronts, disgust him. Watching a rerun, he points a finger towards one old lady and comments how she was drenched in a nauseating perfume. The writer Roland Wolf sits in silence and watches. He's here to conduct interviews for Christian's biography. But like Christian, he hides his true feelings well. When he shows up at Christian's country estate for a prolonged stay to collect information, he brings only a few things: a couple changes of clothing, a tape recorder, and a loaded pistol. Something sinister lurks beneath Legagneur's charming veneer. But then, the same thing could be said for Roland. A dangerous mouse-and-cat game, Claude Chabrol's Masks (1987) takes delight in obfuscating its characters' intentions.
Many are the secrets hidden in Christian's (Philippe Noiret) mansion: why does the mute chauffeur stare so intently at Roland (Robin Renucci) in the rear-view mirror while driving him to the estate; why does Legagneur suffer a perpetually grinning middle-aged fortune teller to live in one of his rooms; who is this sickly godchild Catherine (Anne Brochet) with such startlingly pale, startling round eyes?
This last mystery proves the most bizarre. Legagneur dominates poor Catherine, policing her day-to-day activities, confiscating her checkbook, and forcing strange medicinal pills on her all hours of the day. Her past and reasons for being in Legagneur's care reveal themselves only gradually, unlike her tepid romance with Roland which begins like a gunshot when she storms his room on his first night in the mansion and kisses him. Notice how Chabrol juxtaposes their outfits at the start: Catherine wears such tight-fitting, full-body outfits that it's amazing she can breathe; Roland wears ill-fitted, oversized suits. Roland represents the freedom she has been so long denied. As the film progresses and the mysteries deepen, Roland will evolve from investigator to lover to protector, freeing her of more than just her mental hang-ups.
Chabrol has always been the most difficult member of the French New Wave to write about and Masks does little to change this. More than any of his Cahiers contemporaries, he wore his cinematic influences on his sleeve: the emotional detachment and subject matter of Alfred Hitchcock; the continental, bourgeoise refinement of Ernst Lubitsch; the geometric cinematography (and morality) of Fritz Lang. Yet his work repeatedly denies broad characterization. We can say with general certainty that Jean-Luc Godard was preoccupied with ideology; Éric Rohmer with people; François Truffaut with the cinema itself. But Chabrol?
At times seeming more similar to the classic Hollywood craftsmen like Michael Curtiz than the classic Hollywood auteurs, he juggled multitudinous genres with equal skill and ease. But time and again he returned to the murder mystery genre. Well, "murder mystery" perhaps isn't the right term: Chabrol loved movies about murder, particularly their aftermath and their impact on bystanders. Masks (1987) is one such film. The only murder takes place long before it begins and an attempted second gets stopped at the last moment. But the pieces of the mystery all fall into the right places too predictably: the only decent third-act revelation involves Roland's true intentions—intentions which we have already figured out. Much like with Hitchcock, by the end everything is cleanly resolved with the bad guys getting caught and the passionate lovers triumphing. But unlike Hitchcock, Chabrol seems neither interested in surprising his audience nor in subverting the expectations of the genre. The only surprising thing about Masks is how unsurprising it is.


text:
* Fix issue #16 - does not work well with Material UI theme.
* Fix issue #17 - Atom v1.12 incompatibilities.

## 0.1.0
* @hasCharles add always hide/show settings.

## 0.0.11
* @aki77 speeds up start-up time

## 0.0.10
* Fix issue #7 - Uncaught TypeError.
* Clean up stlyes to look better with more themes.
* Learn how to scroll up/down with arrow keys.

## 0.0.9
* Hide cheatsheet on 'escape' when it is focused.

## 0.0.8
* Fix issue #6 - Error: unrecognized expression: [data-keybinding-group=unset!]

## 0.0.7
* @izuzak fixes atom engine semver

## 0.0.6
* Fix issue #4, toggle keymap not working.
* Fix all deprecation warnings.

## 0.0.5
* Fix a deprecation warning in deprecation cop.

## 0.0.4
* Fix issue #3, filter editor using deprecated class.
* Add support for cross platform bindings.

redpajama_set_name: RedPajamaGithub


text:
WhatsApp to starting banning older mobile phones from New Year's Eve
Check your model to find out what date the service will stop working
Trinity Shaw
Neil Shaw
Popular chat platform WhatsApp has warned users a ban on a number of phone models will soon come into affect.
And this date is now looming as the company has revealed the phones which will no longer be able to support the service..
WhatsApp has warned users that older models of phones will no longer support the app and has recommended that people upgrade their handset.
Earlier this month WhatsApp used their support page to announce that their app would be banned on many phones including but not limited to all Windows style models. The change is to be introduced as early as December 31, 2019.
Second storm heading for UK after battering from Atiyah
One dead, more badly injured after volcano erupts in New Zealand
The phones that will feel the impact of these blocks will include any iPhones that run on a version of iOS older than 7, and any Android devices currently running on version 2.3.7.
The restriction will be fully functional by February 1, 2020, and all users are advised to check the list to make sure they don't lose access to the service.
If WhatsApp is your social media of choice you will need to upgrade your phone by the these dates to guarantee a fully functional experience.
The full list of dates that phones become cut off by the site:
• Nokia Symbian S60 after June 30, 2017
• BlackBerry OS and BlackBerry 10 after December 31, 2017
• Nokia S40 after December 31, 2018
• All Windows Phone operating systems after December 31, 2019
• Android versions 2.3.7 and older after February 1, 2020
• iPhone iOS 7 and older after February 1, 2020
Leader of Italy's right-wing party bans Nutella
Poundland sharing very rude and cheeky posts for Christmas
A spokesman for WhatsApp said: "As we look ahead to our next seven years, we want to focus our efforts on the mobile platforms the vast majority of people use"
"While these mobile devices have been an important part of our story, they don't offer the kind of capabilities we need to expand our app's features in the future. This was a tough decision for us to make, but the right one in order to give people better ways to keep in touch with friends, family, and loved ones using WhatsApp."
"If you use one of these affected mobile devices, we recommend upgrading to a newer Android, iPhone, or Windows Phone to continue using WhatsApp."
The Facebook owned firm has seen rumors in the tech community of another massive change to the layout of the app, a WhatsApp dark mode.How the change will look is becoming clearer as more and more screenshots appear online.
Queen's cousin will have to use public transport after driving ban
Save almost £700 in a year by starting with just 1p
According to the team at WABetainfo the change could improve battery life on most phones.
This big update would provide an option to change the theme of your screen when power is running low in order to conserve the energy of your device and use it for extended periods of time.
There is currently no official release date for the change, or even confirmation of if it will happen.
tendendo


#// Figure out how to do the pull.
#// when replaceing an old dist with a new dist.
#x-CEB-x    @echo +++ client.mak: checking out the client with "$(CVS_BRANCH)"
Environment variable MOZ_SRC isn't set.
Environment variable MOZ_TOOLS isn't set.


TRNT1 (CCA-adding transfer RNA nucleotidyl transferase) enzyme deficiency is a new metabolic disease caused by defective post-transcriptional modification of mitochondrial and cytosolic transfer RNAs (tRNAs).
We investigated four patients from two families with infantile-onset cyclical, aseptic febrile episodes with vomiting and diarrhoea, global electrolyte imbalance during these episodes, sideroblastic anaemia, B lymphocyte immunodeficiency, retinitis pigmentosa, hepatosplenomegaly, exocrine pancreatic insufficiency and renal tubulopathy. Other clinical features found in children include sensorineural deafness, cerebellar atrophy, brittle hair, partial villous atrophy and nephrocalcinosis.
Whole exome sequencing and bioinformatic filtering were utilised to identify recessive compound heterozygous TRNT1 mutations (missense mutation c.668T>C, p.Ile223Thr and a novel splice mutation c.342+5G>T) segregating with disease in the first family. The second family was found to have a homozygous TRNT1 mutation (c.569G>T), p.Arg190Ile, (previously published).
We found normal mitochondrial translation products using passage matched controls and functional perturbation of 3' CCA addition to mitochondrial tRNAs (tRNACys, tRNALeuUUR and tRNAHis) in fibroblasts from two patients, demonstrating a pathomechanism affecting the CCA addition to mt-tRNAs. Acute management of these patients included transfusion for anaemia, fluid and electrolyte replacement and immunoglobulin therapy. We also describe three-year follow-up findings after treatment by bone marrow transplantation in one patient, with resolution of fever and reversal of the abnormal metabolic profile.
Our report highlights that TRNT1 mutations cause a spectrum of disease ranging from a childhood-onset complex disease with manifestations in most organs to an adult-onset isolated retinitis pigmentosa presentation. Systematic review of all TRNT1 cases and mutations reported to date revealed a distinctive phenotypic spectrum and metabolic and other investigative findings, which will facilitate rapid clinical recognition of future cases.
The field of monogenic mitochondrial disease has increased exponentially since the advent of next generation sequencing. Commencing with 'targeted gene panels' sequencing nuclear genes encompassing the mitochondrial proteome, moving rapidly to whole exome sequencing (WES) and more recently whole genome sequencing, it has enabled the diagnosis of many mitochondrial disease patients worldwide. New syndromes have been revealed [1, 2] and older syndromes such as Sengers syndrome have acquired genetic redefinition . One of the processes that has been particularly associated with disease is mitochondrial translation. A number of new genetic disorders have recently been found in this pathway [4–7] with the majority of the newly reported cases being tRNA aminoacyl synthetase deficiencies. Furthermore the genetic disorders of mitochondrial protein synthesis have been flagged as an exciting area for clinicians as there appear to be tissue specific diseases making it possible to draw genotype-phenotype correlations .
In this study we explore a syndrome resulting from the deficiency of TRNT1 (CCA-adding tRNA nucleotidyl transferase enzyme), which performs an essential post-transcriptional modification by adding on the cytosine-cytosine-adenine (CCA) trinucleotide sequence to the 3′ end of all newly produced tRNAs. This TRNT1-dependent tRNA modification is essential for both cytosolic and mitochondrial tRNAs (mt-tRNAs) to participate in protein biosynthesis. The CCA trinucleotide sequence is required to accurately attach amino acids, to position the tRNA on the ribosome and also to conclude protein translation .
Recently, two different TRNT1 related disease entities have been reported; a haematological description of a congenital sideroblastic anaemia associated with immunodeficiency, fevers, and developmental delay (SIFD) in childhood [10–12] and an adult presentation of retinitis pigmentosa with a focus on ophthalmological features . In this report we describe four cases including a new family with two severely affected children whose presentation encompassed both sets of clinical features, and in whom we have identified a novel TRNT1 mutation. We explored the functional significance of the TRNT1 mutations in these children and found clear evidence of impaired post-transcriptional modification of mt-tRNAs. We systematically review all the features reported in the cases published thus far and study the complete clinical phenotype, including a metabolic description that will enable physicians to diagnose this disease clinically and perform targeted genetic investigations.
We report one new family and also add a metabolic context to the phenotype of one previously reported family [10, 11]. Both families attended the metabolic clinic at our institution for diagnosis and treatment.
P1 was born to unrelated white European parents after a normal pregnancy. She presented at 2 weeks of age with a febrile illness associated with poor feeding and diarrhoea. No infective cause was found and she recovered from this episode. However over the next 3 years she had multiple recurring acute systemic illnesses. These episodes were characterised by fever, diarrhoea and vomiting, metabolic acidosis, electrolyte imbalance (episodic hyponatraemia, hypokalaemia, hypocalcaemia, hypomagnesaemia and hypophosphataemia), elevated hepatic transaminases and raised inflammatory markers.
She was investigated for an immune deficiency and was found to have severe hypogammaglobulinaemia with B cell maturation arrest requiring three-weekly sandoglobulin supplementation. She was also found to have a transfusion dependent sideroblastic anaemia with variable neutropaenia and thrombocytopaenia. Immunological investigations revealed low IgG, IgA and IgM (Table 1) while blood films showed anisocytosis, neutropaenia, pencil cells and elliptocytes. Bone marrow examination showed that most erythroblasts had abnormal siderosis with around 2/3 being ring or crescent forms. Megakaryopoiesis was abundant but with dysplastic nuclear morphology.
Moderate exocrine pancreatic insufficiency (stool elastase 182 μg/g, normal >200); later undetectable.
Duodenal biopsy: partial villous atrophy. Liver iron:143 μg/100 ml dry weight.
She had recurrent episodes of encephalopathy associated with nystagmus and photophobia which appeared to improve markedly with benzodiazepine therapy. Development was globally delayed and she had retinal dystrophy. Brain MRI was initially normal but subsequently progressive cerebellar atrophy was observed. In addition, in the last stages of her disease, brain MRI showed widespread abnormalities with multiple lesions resembling infection. She developed recurrent bacterial infections and gastrointestinal involvement with chronic gastritis, partial villous atrophy, hepatosplenomegaly and pancreatic insufficiency (undetectable stool elastase).
Biochemical investigations revealed mildly elevated blood lactate at 2.5 mmol/L (reference range <2) and muscle mitochondrial respiratory chain complex IV activity at the lower end of the reference range (ratio to citrate synthase 0.015, reference range 0.014–0.034). Muscle histology was normal. In particular, neither ragged-red nor cytochrome oxidase-negative fibres were observed. She died at 3 years and 3 months following a progressive encephalopathy.
P2 is the younger male sibling of P1 and is the older sibling of non-identical twins (Fig. 1a). He was admitted at 3 weeks of age with poor feeding, loose stools and pallor, and again at 4 weeks with poor feeding, fever and anaemia (haemoglobin 66 g/L). Although his blood film showed occasional nucleated red cells with possible sideroblastic granules, bone marrow examination at one month showed dyserythropoeisis but no ringed sideroblasts. He had central hypotonia, retinal pigmentation, hepatosplenomegaly and exocrine pancreatic insufficiency. Immunological investigations revealed initially low B cells which normalised and low IgG, IgA and IgM (Table 1). He had recurrent seizures and his MRI brain at 10 months demonstrated multiple focal lesions in the cerebral hemispheres and cerebellum (Fig. 2). He died at 10 months of age because of intractable status epilepticus.
P3 and P4, previously reported as cases 1 and 2  were born to first cousin Pakistani parents (Fig. 1d). They had five children including a stillborn baby at 32 weeks' gestation and two other daughters who are well except for radioulnar fusion due to Cenani-Lenz syndrome caused by a homozygous LRP4 mutation . P3 was first diagnosed with sideroblastic anaemia at 8 months. She developed recurrent episodes of fever from 1 year and global developmental delay, retinitis pigmentosa and bilateral sensorineural deafness. She had low B cells with hypogammaglobulinaemia and features of sideroblastic anaemia on bone marrow examination. She required numerous blood transfusions to maintain her Hb above 70 g/L. During the febrile episodes she developed hyponatraemia, hypokalaemia, hypocalcaemia, hypomagnesaemia and hypophosphatemia and generalised aminoaciduria. Plasma amino acid analysis revealed elevated proline 347 μmol/L (85–290), alanine 749 μmol/L (150–450) and glutamine 1014 μmol/L (480–800). Urine organic acids showed strongly raised 3-hydroxybutyrate and acetoacetate. Urate was mildly raised and red cell nucleotide profile showed the presence of some abnormal nucleotides. At four years, she was found to have a urate renal calculus which resulted in right sided hydronephrosis. Porphyria screen and sequencing of exons 9 and 11 of the mevalonate kinase gene (performed because of the recurrent fevers) were normal. Muscle biopsy demonstrated markedly reduced complex IV activity expressed as a ratio to citrate synthase at 0.007 (0.014–0.034) (Table 1). She died after multiorgan failure and presumed cephalosporin-induced toxic epidermal necrolysis at 14 years.
Her younger brother P4 had global developmental delay and hypotonia with a microcytic anaemia. He presented at two months with high fever, vomiting and diarrhoea. Anaemia (haemoglobin 71 g/L) and panhypogammaglobulinaemia were noted (Table 1). His blood film showed slightly immature neutrophils with toxic granulation and marked red cell abnormalities including poikilocytosis, microcytosis, elliptocytosis, hypochromic red cells and polychromasia, similar to the findings in his sister P3. He had fever recurring every 7–10 days, which was associated with vomiting and diarrhoea. Urine organic acids revealed mildly raised pyruvate. Pearson syndrome was excluded in both P3 and P4 by screening for mitochondrial DNA deletions. P4 underwent bone marrow transplantation (BMT) after which his fevers resolved, his growth improved and he made some developmental progress. He remains systemically well 3 years post BMT. At 10.5 years of age he has started to walk independently and is making progress with speech, but continues to have moderate hearing loss and retinopathy.
Genetic investigations were performed with ethical approval from the National Research Ethics Committee London Bloomsbury, UK and informed consent was obtained from parents for investigations and publication of findings. Whole exome sequencing (WES) was performed in P1 and P2 using the Agilent SureSelect capture kit and Illumina's HiSeq 2000 high throughput sequencing. Raw fastq files were aligned to the hg19 reference genome using novoalign version 2.08.03. We processed 2600 in-house control samples together with these samples to create gVCF files using the Haplotype Caller module of the Genome Analysis Tool Kit (GATK) version 3.1.1. These individual gVCF files were pooled into combined gVCF of 100 samples, and used for variant calling (Genotype gVCF module of GATK 3.1.1). Variant quality scores were re-calibrated according to GATK recommendations for indels and SNPs. Rare variants (defined as an allele frequency <0.5 % in our in-house control samples) which were splicing, nonsynonymous, frameshift or presumed loss-of-function and present in both P3 and P4 were prioritised. In view of non-consanguinity, compound heterozygous inheritance was assumed.
Whole genome-wide SNP genotyping was performed in P3 and P4, their parents and one unaffected sibling using the Illumina HumanCytoSNP-12 microarray. LOD scores were calculated as published before . All processing was carried out in accordance with the Infinium HD Ultra Assay protocol (Rev B, 2010, Illumina Inc, San Diego, USA). Data were initially analysed assuming an autosomal recessive model using the Illumina Genome Studio software which generates genotypes, copy number and loss of heterozygosity data (cnvPartition v3.1.6, Illumina). Quality control checks were performed to assess data quality. Samples were assessed for their call rate which should be >98 and >99 % average across the batch. The B-allele frequency plots and copy number analysis results were checked to identify potentially contaminated samples.
All exons and exon-intron boundaries of candidate genes located within homozygous intervals in P3 and P4 were amplified (GoTaq PCR Kit Promega) according to the manufacturer's protocol and Sanger sequenced. The TRNT1 mutations identified by WES in P1 and P2 were also confirmed by Sanger sequencing, using primer sequences for TRNT1 exons 3 and 6 (exon 3: Forward ATAGCAGGAGGAGCAGTGAG and reverse GACTGCAGGGTTTATGACGG and exon 6 forward CAGATTTTGCTTGTGATATGCCA and reverse ACCCCATAACCCAAACTTTGTC) All PCR products were sequenced using the Big Dye Terminator Reaction Kit on a 2400GeneAmp® 9700 sequencer. Sequencing data were analysed using the Sequencher v. 5.2.4 software.
Western blot was performed as described previously  using OXPHOS antibody cocktail (Abcam) in P1 and P2 compared to controls. Fibroblast cells were not available for P3 and P4.
Patient and control fibroblasts were plated on 6-well plates. At 80 % confluence, they were washed twice with methionine and cysteine-free DMEM (1 mL/well of a 6 well plate). Labelling medium (600 μL) was added to each well and incubated for 20 min at 37 °C, before adding emetine (SIGMA, 25 mg/ml in PBS) to a final concentration of 100 μg/mL with a further incubation at 37 °C for 30 min. 100 μCi L-[35S]-methionine (Perkin Elmer - NEG009L005MC) was then added to each well to a final concentration of 166.6 μCi/mL per well and incubated for 30 min at 37 °C. The cells were washed with PBS and trypsinised, protein was isolated and concentration determined using BCA assay, and western blot was performed. The gel was stained with SimplyBlue SafeStain (Thermo Fisher Scientific), dried at 80 °C under vacuum for 1 h and exposed to a phosphorimage screen for 72 h.
Circularisation reverse transcription PCR (cRT–PCR) and sequencing were used to determine both 5' and 3' ends of mt-tRNA as described previously . Briefly, 2.5 μg of total RNA was circularized with T4 RNA ligase (New England Biolabs) in the presence of DNase I (Roche) followed by phenol–chloroform extraction and ethanol precipitation. Reverse transcription was carried out using Omniscript Reverse Transcriptase (Qiagen) with a gene-specific reverse primer (tRNA_His_R1).
Newly synthesized cDNA was used as a template for a PCR reaction, primed with R1 primer and a forward primer, F1. The region amplified contained the junction of the 5' and 3' extremities. Products were cloned using TOPO TA Cloning Kit (Life Technologies) and sequenced. The following primers were used in the analysis: tRNA_His_Reverse: CAATCTGATGTTTTGGTTAAACTATA, tRNA_His_Forward: AATCTGACAACAGAGGCTTACGACCC, tRNA_SerAGY_Reverse: CATGAGTTAGCAGTTCTTGTGAGC TT, tRNA_SerAGY_Forward: CCCCATGTCTAACAACATGGCTTTC, tRNA_Cys_Reverse: TGCAATTCAATATGAAAATCACCTCG and tRNA_Cys_Forward: TTCGAAGAAGCAGCTTCAAACCTGCC. The following TOPO clones were sequenced: (a) mt-tRNAHis C1 29 clones, P1 32 clones, P2 29 clones (b) mt-tRNACys 16 clones for C1, P1 and P2 (c) mt-tRNASerAGY C1 13 clones, P1 16 clones, P2 15 clones.
Northern blot analysis was performed as described previously . Briefly, total RNA was isolated from primary skin fibroblasts using TRIzol® LS Reagent (Life Technologies) according to the manufacturer's instructions. RNA was resolved by Urea-PAGE on a 10 % gel, transferred to a nylon membrane, UV-crosslinked to the membrane and hybridised with radioactively labelled T7-transcribed RNA probes.
The molecular graphics program MOE (Molecular Operating Environment, 2012) running on an Ubuntu Linux workstation was used to visualize, mutate and analyse the crystal structure of full-length human mitochondrial CCA-adding enzyme  solved at a resolution of 1.9A.
A PubMed search was performed using the terms'TRNT1', 'SIFD' and 'sideroblastic anaemia'. Since the gene TRNT1 was only associated with human disease in 2014 we searched for publications from 2014 to date. Only papers reporting cases with confirmed TRNT1 mutations were included.
Only four genes (CEL, SLC12A1, SRRM, TRNT1) containing compound heterozygous mutations shared between the affected siblings P1 and P2, were found after bioinformatic filtering (Fig. 1b). Of these, TRNT1 appeared the most likely causative gene given the clinical history. We identified a novel splice mutation c.342+5G>T together with a known pathogenic missense mutation, c.668T>C p.Ile223Thr. Parents were each heterozygous for one mutation, confirming segregation with disease in this family (Fig. 1c).
Homozygosity mapping was performed prior to the advent of WES in P3, P4, parents and an unaffected sibling. The mapping revealed 7 significant homozygous regions shared between the two affected siblings spanning a total of 56.8 megabases, including four regions with a LOD score of 1.93 (Fig. 1e) containing 716 genes including 11 genes with a Maestro (predicted mitochondrial localisation) score >10 (TRNT1, GRPEL1, LONP1, NDUFA11, CLPP, TIMM44, NDUFA7, ATP6V1E1, SLC25A1, TXNRD2 and CHCHD10). The TRNT1 mutation illustrated in Fig. 1f (c.569G>T, p. Arg190Ile) in this family has previously been published by another group  who were also investigating this family, unbeknown to us.
Immunoblotting showed no decrease in the steady-state levels of either mtDNA or nuclear encoded OXPHOS subunits in the patients (P1 and P2) when compared with controls.
The mitochondrial translation rate in the TRNT1 deficient patients (P1 and P2) was within the range detected in passage matched healthy and non-mitochondrial disease controls (Fig. 3a). We sought to determine if the identified TRNT1 mutations result in diminished CCA addition to mitochondrial tRNAs (mt-tRNAs). To this end we performed high resolution northern blotting of total RNA isolated from P1 and P2 primary fibroblasts. This analysis suggested partial lack of CCA in mt-tRNACys (P1: 5 %, P2: 5 %, C1: <1 %, C2: <1 %) and mt-tRNALeuUUR(P1: 2 %, P2: 2 %, C1: <1 %), when compared to controls. However, we detected no obvious differences in CCA addition for other mt-tRNAs tested, including mt-tRNAIle , -His, -Arg, -Pro, -Phe, -Ser(AGY) (Fig. 3b). In order to uncover more subtle differences in maturation of the 3' end of mt-tRNA, potentially beyond Northern blotting detection limits, we analysed the ends of mt-tRNA after circularisation, reverse transcription, PCR amplification and cloning (cRT–PCR). The cRT-PCR analysis of mttRNASerAGY and mt-tRNACys was consistent with the high resolution northern blotting analysis where we found a proportion of incorrectly processed mt-tRNACys (Fig. 3). Also in agreement with northern blots, we did not find any defects in maturation of mt-tRNASerAGY in this additional cRT-PCR. In addition this method also detected a proportion of incorrectly processed mt-tRNAHis (Fig. 3c). Taken together these data indicate that TRNT1 mutations lead to defective CCA addition to mt-tRNAs.
Together with the patients in this report, we analysed clinical features in 18 subjects reported to date. There appears to be a spectrum of disease ranging from a neonatal-onset disease to an adult presentation. The earliest presentation was within 3 h of birth with pallor and splenomegaly. Of the 18 cases described to date, including the 4 patients in this report, more than half (10/18, 55 %) presented in the first 2 months of life (range 1 day-19 years). The most striking initial feature (9/18, 50 %) was a systemic 'inflammatory' illness where an infective aetiology was not identified. The febrile illness was accompanied by gastrointestinal upset such as poor feeding, diarrhoea (8/18, 44 %) and vomiting (7/18, 39 %). In one adult case  a febrile illness was recorded in childhood, which was thought to be due to juvenile rheumatoid arthritis, and in one paediatric case  lactic acidosis and vomiting was noted but fever was not reported. The inflammatory episodes appeared to wax and wane cyclically. Other first presentations included anaemia and delayed development. The adult cases presented between the ages of 18 and 21 years with impaired vision. Table 2 demonstrates key clinical features and laboratory findings in all patients.
Sideroblastic anaemia (13/18, 72 %) is a very significant feature of the clinical syndrome. In the majority of cases it was observed during investigation of unexplained febrile illness. Interestingly the three adult cases had an asymptomatic microcytosis with a haemoglobin often in the lower end of the reference range (~130 g/L), contrasting with the paediatric cases who had severe anaemia (Hb range 48–82 g/L). One child appeared to have a predominantly neurological phenotype with no febrile episodes or sideroblastic anaemia . Overall 16 (89 %) cases had evidence of anaemia (mild in the adult cases) with microcytosis (median Hb 72 g/L, median MCV 63.4 fl). The majority of cases (12/18, 67 %) also had B cell lymphopaenia with or without an accompanying hypogammaglobulinaemia. Only two cases had a low total white cell count.
Of the four cases followed at our institution, one had retinal dystrophy and two other cases developed pigmentary retinopathy. Overall six cases (33 %) had pigmentary retinopathy, of which three were adults. In the adult patients this was the only discernible symptomatic feature. Although largely asymptomatic in childhood, one adult patient reported a history of night blindness as a child.
Most patients (14/18, 78 %) had developmental delay, which was global except in one case reported to have isolated motor delay. Sensorineural deafness was reported in 7/18 (39 %) cases. Seven patients developed seizures, six patients had ataxia and five patients were hypotonic. Two of our cases (P1 and P2) developed episodes of encephalopathy. Only one patient was reported to have ptosis and ophthalmoplegia. Four patients had cerebral atrophy, two were noted to have brainstem changes, one had thalamic changes and two had cerebellar changes (atrophy in one, cerebellar hypoperfusion in the other) on neuroimaging. Two of our cases (P1 and P2) also had multiple cerebral and cerebellar focal lesions which resembled infection (Fig. 2).
Six patients (33 %) had splenomegaly. Five patients had nephrocalcinosis (28 %) and four (22 %) had hepatomegaly. One of the cases followed at our institution (P3) developed a urate renal calculus.
In addition to some patients developing cyclical vomiting and diarrhoea accompanying the febrile illness, three cases had pancreatic insufficiency and two had partial villous atrophy on duodenal biopsy.
Only one case was reported to have (dilated) cardiomyopathy.
Brittle hair was noted in five cases.
Median age of death was 37.5 months (range 10 months - 14 years). The three adult patients were alive and systemically well at 18, 19 and 21 years. Two patients  underwent myeloablative allogenic bone marrow transplant (BMT). Both were alive 3 years post BMT with no recurrence of periodic fever.
Analysis of findings in all cases revealed that an elevated lactate was recorded in six cases, associated with metabolic acidosis in five cases, elevated plasma alanine in three cases and evidence of renal tubulopathy in four cases.
We performed detailed metabolic investigations in the patients seen at our institution (Table 1). Blood lactate was mildly elevated in all four subjects (P1-P4) in the current study, ranging from 2.4–3.1 mmol/L (reference range <2). Plasma alanine was elevated in three subjects (patient range 458–875; reference range 150–450 μmol/L) and proline was elevated in two subjects (patient range 304–452; reference range 85–290 μmol/L). Plasma threonine was high in all patients (patient range 256–556; reference range 70–220 μmol/L) and plasma glycine was raised in three cases (patient range 332–504; reference range 100–330 μmol/L). Branched chain amino acids and ornithine were elevated in P3 and P4. Interestingly P4 had a normal amino acid profile post bone marrow transplant.
Electrolyte abnormalities in P1 and P3 observed during acute inflammatory episodes included hyponatraemia, hypokalaemia, hypocalcaemia, hypomagnesaemia and hypophosphataemia. Renal tubular dysfunction was documented in 3 patients (P1, P2 and P3; not done in P4), with high urinary N-acetyl-beta-D-glucosaminidase (NAG):creatinine and retinol binding protein (RBP):creatinine ratios. In P1 elevated hepatic transaminases were a persistent feature.
Muscle respiratory chain enzymes (RCEs) were measured in two of the four patients (P1 and P3) described here in detail. P3 had definitively low complex IV of 0.007, 30 % of control mean (reference range 0.014-0.034) whereas P1 had a value at the lower end of the reference range (0.015), which was disproportionately low compared to complexes I-III (Table 1). In one patient (N) reported previously complex IV was affected in muscle (0.25, control range 0.58–2.5) and liver (0.25, control range 0.6–2.5) while complex II + III 0.06 (0.5–1.9) and complex I + III 0.15 (0.58–2.5) were also low in muscle .
All TRNT1 mutations published to date are shown in Fig. 4a and all reported missense mutations are modelled in silico in Fig. 4b. The homozygous p.Arg190Ile substitution harboured by P3 and P4 is predicted to cause a severe conformational protein change when the hydrogen bond network formed by arginine is broken by isoleucine, leaving the protein either unfolded, or folded but dysfunctional (Fig. 3c).
One of the mutations found in P1 and P2 (c.688C>T, p.Ile223Thr) was also found in SIFD patients from eight apparently unrelated pedigrees of white Caucasian, Afro-Caribbean and Hispanic origins reported previously . This suggests that this may be a mutational hotspot. In silico modelling of p.Ile223Thr showed that isoleucine is a buried amino acid and, since the substituted threonine can also be buried satisfying its H-bond, it confers a mild phenotype.
The adult patients had either a mononucleotide deletion or insertion of an adenine at the same position (c.1246) on one allele. These changes were located in the last exon and predicted to result in a truncated protein. Interestingly the deletion at c.1246 was also found in a paediatric SIFD patient . The other allele in the adult patients contained either a deletion or splicing mutation; the authors predicted that the deletion caused a minor change to the protein conformation and that the splicing was altered in a subset of transcripts .
We report a new family with TRNT1 mutations, including a novel pathogenic splicing mutation, and show that TRNT1 mutations cause a complex multisystem disease leading to manifestations in most organs. In this report we used a systematic review of all previously reported cases to characterise the phenotypic presentation of TRNT1 deficiency, a new disorder of mitochondrial and cytoplasmic translation. Our in vitro studies provide evidence of mitochondrial pathogenicity in this disease, indicating clear functional impairment of the addition of CCA to mt-tRNAs in patient fibroblasts, leading to defective mt-tRNA post transcriptional modification.
From the descriptions thus far, there are two ends of the disease spectrum: a paediatric disorder which starts early in life with unexplained cyclical febrile episodes accompanied by gastrointestinal upset and features of sideroblastic anaemia, and an adult disease with retinitis pigmentosa and asymptomatic microcytosis [10–13]. In addition to being almost the only sign of adult disease, retinitis pigmentosa was also found in three paediatric patients, suggesting that this may be a key feature of the disease which is under-reported, since it may be undetected if patients are not specifically screened by an experienced ophthalmologist. Also splenomegaly, nephrocalcinosis and hepatomegaly were reported in six, five and four cases respectively.
We highlight oxidative phosphorylation (OXPHOS) impairment in TRNT1 deficiency, with evidence of mitochondrial complex IV being definitively low in two patients and at the lower end of the reference range in one patient. It is not possible to know how many patients would display OXPHOS abnormalities in this disease if muscle respiratory chain enzyme analyses were performed in all patients. Given the pivotal role of TRNT1 in mitochondrial translation, multiple RCE abnormalities would be expected. The observation of mtDNA translation defects with biochemical evidence of isolated complex IV deficiency is similar to other mitochondrial translation disorders (e.g., RARS2 and YARS2 deficiency) where biochemical findings ranged from normal to multiple RCE defects or isolated complex IV deficiency [20, 21]. The multi-organ involvement in these patients is perhaps unsurprising given the ubiquitous nature of the TRNT1 enzyme and its key role in protein synthesis both in cytoplasm and mitochondria. One of the limitations of this study is that we have not studied the effect of the TRNT1 mutations on cytoplasmic tRNAs. As a dually localised enzyme, TRNT1 is responsible for the maturation of both nuclear and mitochondrially encoded tRNAs. Whilst an affect on cytosolic tRNA maturation cannot therefore be ruled out, we chose to focus on defects of the mitochondrial translation system, in view of the clinical presentation of a mitochondrial disease in our patients along with others previously reported . Primarily mitochondrial disease presentations have been previously reported for other dually localised enzymes such as PUS1, MTO1 and TRIT1 [22–24], perhaps indicating a greater susceptibility of the mitochondrial translation apparatus to such perturbations than its comparatively more robust cytosolic counterpart.
Variable changes were observed in the plasma amino acid profiles of these four children with TRNT1 deficiency. It is difficult to ascertain the relevance of these findings in a small group of patients. One possible explanation is that impaired muscle metabolism leads to decreased break down of branched chain amino acids. On the other hand the abnormalities could be related to TRNT1 deficiency and resulting backlog from disordered cellular protein translation and further studies will be needed to establish this.
Often patients with inherited metabolic disease decompensate with febrile illness and metabolic physicians are involved in the care of these patients during these acute phases. In all four patients presented here, febrile illness was a component of the disease rather than a precipitant and mevalonate kinase deficiency (which is characterised by recurrent episodes of fever in infancy) was excluded. TRNT1 deficiency produces a complex multisystem disease which can be confused with overwhelming sepsis given the febrile episodes with raised inflammatory markers. Whereas sepsis obviously must be excluded in the first instance, clues at this stage are the presence of microcytic anaemia with anisocytosis and B cell lymphopaenia, typically with hypogammaglobulinaemia.
The paediatric TRNT1 disease (SIFD) enters into the differential diagnosis of genetic sideroblastic anaemia, inherited immunodeficiencies and also of autoimmune inflammatory disease. Other genetic sideroblastic anaemias which present similarly and may need exclusion include Pearson syndrome (caused by mtDNA deletions) with sideroblastic anaemia, exocrine pancreatic failure and pancytopaenia ; and YARS2 and PUS1 deficiency which cause myopathy, lactic acidosis and sideroblastic anaemia (MLASA) syndrome [26–28]. YARS2 is specifically a mitochondrial aminoacyl tRNA synthetase whereas PUS1 has a dual subcellular location. Of the cytoplasmic translation defects, LARS mutations have been noted to present with a multi-system disease consisting of acute liver failure, anaemia, renal tubulopathy, developmental delay, seizures, failure to thrive and deterioration of liver function with illness . Cyclical fever and B cell immunopathy are not features of these diseases, and so they can be distinguished clinically from TRNT1 deficiency.
The mainstay of the acute management of these patients consists of treatment of the episodes of inflammation with rehydration and electrolyte supplementation and transfusion for anaemia. So far two patients have received BMT and the results appear encouraging, although more long-term data are needed. It is not known whether BMT early in the disease course might prevent the neurodevelopmental features of this disorder. Ideally randomised double-blinded placebo-controlled clinical trial evidence is necessary to draw meaningful conclusions but this is not always possible in ultra-rare diseases .
TRNT1 null mutations are probably embryonically lethal given that siRNA knockdown of the gene led to cytotoxicity and apoptosis . Although TRNT1 functions both in the cytoplasm and the mitochondrion, the presence of syndromic manifestations typical of a mitochondrial disease suggests that post-transcriptional modification of mt-tRNAs, specifically CCA addition, is critical to disease pathogenesis. We examined the impact of the patient mutations on tRNA modification in primary patient fibroblast cell cultures and found mt-tRNAs partially lack 3' CCA in mt-tRNACys, mt-tRNALeuUUR and mt-tRNAHis. While being beyond the scope of the current study, it would be interesting to study all mt-tRNAs using cRT-PCR in patients with different TRNT1 mutations since our finding contrasts with the findings of a previous study which suggested that only mt-tRNASer(AGY) was reduced, with more profound decrease of CCA-tailed mt-tRNASer(AGY) in a patient with the more severe clinical phenotype . We did not find a reduction in mt-tRNASer(AGY) on Northern blot or cRT-PCR. The reasons for these differences are not clear at present but one possible explanation is that these functional differences and patient survival are related to the severity of the genetic mutation. For example it could be hypothesised that the long survival of patient 8 reported by Wiseman et al.  who was homozygous for p.Ile223Thr, is explained by the amino acid change where in silico analysis revealed a mild conformational change in the protein. In severely affected compound heterozygote patients with p.Ile223Thr in one allele, the splicing mutation found in the opposing allele may explain the severe phenotype.
In summary we investigated patients with a complex, childhood-onset, multisystem disorder who fall into the SIFD spectrum of TRNT1 disease. In addition adult onset retinitis pigmentosa has been reported in TRNT1 deficiency. We demonstrate that deficiency of TRNT1 had an impact on mt-tRNA post-transcriptional modification in affected patient cells. Systematic review of all cases reported to date allowed us to amalgamate knowledge of the clinical phenotype. This will aid clinical recognition of further cases. Early bone marrow transplantation should be considered in these cases to halt the episodic febrile and metabolic decompensations, thereby improving quality of life.
We thank Kerra Pearce for her assistance with homozygosity mapping.
This work was funded by research grants from MDUK and the Lily Foundation, and a Wellcome Trust clinical research fellowship (grant number 097978/Z/11/Z) to YW. MM, SP and CP are funded by the Medical Research Council, UK as part of the core funding for the Mitochondrial Biology Unit (MC_U105697135). PM is supported by by Great Ormond Street Hospital Children's Charity Research Leadership Grant V2516. SR is supported by Great Ormond Street Hospital Children's Charity Research Leadership Grant V1260.
All available data, including PCR primer sequences, have been included in this manuscript.
YW contributed to study design, acquisition, analysis and interpretation of data, and wrote the manuscript. RS, EF, SP, CAP, VP, JS, RK, WKC, EF and PBM contributed to acquisition of data, analysis of data and critical revision of the manuscript. PTC and MM contributed to study conception and design, acquisition, analysis and interpretation of data and critical revision of manuscript. JWT contributed to supervision of study design, interpretation of data and critical revision of the manuscript. SR conceived and designed the study, supervised acquisition, analysis and interpretation of data, and co-wrote the manuscript. All authors read and approved the final manuscript.
Parental consent was obtained for publication of findings.
Ethical approval was obtained from the National Research Ethics Committee London Bloomsbury, UK and informed consent was obtained from parents for investigations.


text:
Ostřice řídkoklasá (Carex remota, syn.: Vignea remota) je druh jednoděložné rostliny z čeledi šáchorovité (Cyperaceae). Někdy je udávána také pod jménem tuřice řídkoklasá.

Popis
Jedná se o rostlinu dosahující výšky nejčastěji 20–50 cm. Je vytrvalá a trsnatá. Listy jsou střídavé, přisedlé, s listovými pochvami. Pochvy dolních lodyžních listů jsou hnědé a nerozpadavé. Lodyha je trojhranná, dosti chabá a často poléhavá, v horní části drsná. Čepele listů jsou asi 1,5–2 mm široké, ploché nebo žlábkovité. Ostřice řídkoklasá patří mezi stejnoklasé ostřice, všechny klásky vypadají víceméně stejně a většinou obsahují samčí a samičí květy, dolní klásek však někdy bývá celý samičí. V dolní části klásku jsou samičí květy, v horní samčí. Klásky jsou uspořádány do rozvolněného, cca 15–20 cm dlouhého lichoklasu (klasu klásků). Zvláště nejspodnější klásek bývá o 2–5 cm oddálen od následujícího. Každý klásek je podepřen nápadně dlouhým listenem, u nejdolejšího klásku délka listenu často přesahuje celé květenství. Okvětí chybí. V samčích květech jsou zpravidla 3 tyčinky. Čnělky jsou většinou 2. Plodem je mošnička, která je vejčitě kopinatá, cca 2,5–3,5 mm dlouhá, žlutohnědá, vynikle žilkovaná a vně vypouklá, na vrcholu je krátký drsný dvouklaný zobánek. Každá mošnička je podepřená plevou, která je bělavá až bělavě hnědá se zeleným kýlem. Kvete nejčastěji v květnu až v červnu. Počet chromozómů: 2n=62.

Rozšíření
Ostřice řídkoklasá roste skoro v celé Evropě, v některých částech jižní Evropy však jen málo, chybí v severní Skandinávii a v severním Rusku. Dále roste na Kavkaze a ostrůvkovitě jinde v Asii na východ až po Japonsko. V Evropě roste subsp. remota, v Himálaji subsp. alta a v JV Asii subsp. rochebruni. Mapka rozšíření viz zde: .

Rozšíření v Česku
V ČR je to hojný druh rozšířený od nížin do podhůří. Roste hlavně ve vlhkých lesích, především v luzích a prameništních olšinách a na lesních prameništích.

Reference

Literatura
 Grulich V. et Řepka V (2002): Carex L. In: Klíč ke Květeně České republiky, Kubát K. et al. (eds.), Academia, Praha
 Nová Květena ČSSR, vol. 2, Dostál J. (1989), Academia, Praha

Externí odkazy

  – flóra Pákistánu
  – mapky rozšíření
 Carex interactive identification key

Šáchorovité
Flóra Česka
Flóra Indického subkontinentu
Flóra jihovýchodní Evropy
Flóra jihozápadní Asie
Flóra jihozápadní Evropy
Flóra Kavkazu
Flóra severní Afriky
Flóra severní Evropy
Flóra střední Evropy
Flóra východní Evropy

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