Noam Dar's journey to become PWE Champion has been a seemingly endless one. He's seen some of his best friends and some of the most dangerous men in British Wrestling take the title before him. Most recently his best pal Grado holding the gold for over a year before before Iestyn Rees usurped him in controversial circumstances; Cashing in the Money In The Bank contract he won that night to catch Grado off guard and end his reign. Rees winning the title brought Noam's almost reluctant pursuit of Grado to an end. Giving him a more natural enemy in the form of the big man from Gloucester, but a more natural enemy doesn't make for an easier opponent.
Whilst Noam has seen his many PWE Title challenges fail, including being involved in the final to crown the companies first ever champion, losing out in the end to Andy Wild, all of those experiences have been part of steep learning curve for the Jewdi Master. Involved in wrestling from a very young age, he's almost a veteran at the tender age of 22. His vast experience and unquestionable natural ability has led to recognition from WWE and he will be one of the participants in WWE's Cruiserweight Classic tournament. He'd certainly like to head into the biggest challenge of his career in high spirits, and locking Iestyn Rees in the X-Wing and becoming the PWE Champion would be the perfect send off the Ayrshire native and the culmination of a journey in PWE that has been bumpier than he'd have wanted, but ultimately was always leading to him becoming the companies champion.
He faces a dangerous opponent in Rees, who benefited from some help from Polo Promotions to successfully defend his title against Joe Coffey at "Are You Ready!" but the match itself was certainly Iestyn's strongest showing in PWE to date and a sign that the longer he holds the belt, the more he improves as champion. A win over Dar would also serve to strengthen the hometown crowd's disdain for their champion. Having already seen him take the belt from another Ayrshire native, Stevenston's own Grado, there's potential for riots if he becomes the latest to deny Noam Dar a prize that many think is rightfully his.
While they enter the 5th Anniversary Weekender locked in a feud, Noam Dar and Iestyn Rees do have a mutual worry. Whoever emerges from their match as champion has their next challenger to think about and with Drew Galloway holding two victories over Rees in PWE, there's a good chance another hometown favourite will be entering the title picture sooner rather than later. For now Rees just has to contend with the two time Elite Rumble winner Noam Dar. A globetrotting, wrist-kissing, knee shattering wrestling maestro who may or may not be best pals with Vince McMahon. As imposing as Iestyn Rees is, he'll struggle to stop destiny and it feels like Noam's destiny to walk out of the 5th Anniversary Weekender as PWE's figurehead going forward.


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Undergraduate and Graduate Education
Quantum Information Science and Engineering Network (QISE-NET)
Certificates Program in Quantum Engineering and Technology
This is the golden age of innovation
by t-9eaysh | Nov 7, 2019 | Uncategorized
By Paul Dabbar, Under Secretary for Science at the U.S. Department of Energy.
The Arrow of Time is a theory from physicist Arthur Eddington describing how time moves forward and what will change. And we can say with confidence that humanity and America are at a special point in time, due to where we are on the prospects for innovation across a wide set of areas.
One critical area of innovation is in quantum information technologies. Late last month, Google announced it achieved Quantum Supremacy in computing. A team led by John Martinis from Google and the University of California, Santa Barbara, used a 53 qubit quantum computer to solve a mathematical problem in just three minutes that would take the fastest current computer 10,000 years to calculate. This small, profound step is the tip of the spear for a new technology.
This discovery is a critical turning point for quantum computing. It calls for us to continue our efforts in research & development across the federal science and technology enterprise. It calls for us to continue and expand our international collaborations in this field as well. Investment by the federal government, academia and industry into cutting edge innovation, in concert with the entrepreneurial culture of researchers and business, makes for a potent combination.
Quantum computers are still an early-stage technology, but they promise to someday allow us to perform some calculations exponentially faster than today's most advanced supercomputers. Although we're still a long way off from quantum computers being broadly and routinely available, quantum computers will one day revolutionize how we overcome the challenges we face today.
Just as the invention of the transistor led us to personal computers, this development starts us on the road for amazing jumps in technological innovation. The Department of Energy (DOE) is already looking to build quantum networks in Chicago in support of the National Quantum Initiative signed into law last year by President Trump.
New retraining certificates, curriculum to build the quantum workforce
Creating and observing current vortices in 2D materials
Prem Kumar named editor-in-chief of Optica
Building a Quantum Computer From Off-the-Shelf Parts
Scientific process inspires UChicago art/science lab
Affiliation, if applicable

redpajama_set_name: RedPajamaCommonCrawl


text:
A Geochelone a hüllők (Reptilia) osztályába és a teknősök (Testudines) rendjébe és a Szárazföldi teknősfélék (Testudinidae) családjába tartozó nem.

Rendszerezés
A nembe az alábbi 2 élő és 1 régen kihalt faj tartozik:

 indiai csillagteknős (Geochelone elegans)
 burmai csillagteknős (Geochelone platynota)
 máltai óriásteknős (Geochelone robusta) kihalt a késő pleisztocén korban

Sok korábban idesorolt fajt leválasztottak és különböző egyéb nemekbe soroltak át.

A két fajt hosszú kutatás után 2007-ben helyezték vissza az Astrochelys nembe, ahová korábban tartoztak. Sokáig ebbe a nembe sorolták mindkét fajt.
 angonoka teknős vagy ekevasteknős (Astrochelys yniphora vagy Geochelone yniphora)
 sugarasteknős (Astrochelys radiata vagy Geochelone radiata)

Áthelyezve az Aldabrachelys nembe - 4 faj

 Aldabrai óriásteknős (Aldabrachelys dussumieri), korábban (Geochelone gigantea) – Aldabra korallzátonya
 Seychelle-szigeteki óriásteknős (Aldabrachelys hololissa) – Seychelle gránitszigetei
 Arnold-óriásteknős (Aldabrachelys arnoldi) – Seychelle gránitszigetei
 Daudini-óriásteknős (Aldabrachelys daudinii) – kihalt, Seychelle-szigetek

Áthelyezve a Centrochelys nembe - 1 faj

 sarkantyús teknős (Centrochelys sulcata), korábban (Geochelone sulcata)

Áthelyezve a Chelonoidis nembe - 4 faj

 fekete teknős vagy szenesteknős (Chelonoidis carbonarius), korábban (Geochelone carbonaria)
 argentin teknős (Chelonoidis chilensis), korábban (Geochelone chilensis)
 táblás erdeiteknős (Chelonoidis denticulatus), korábban (Geochelone denticulata)
 galápagosi óriásteknős vagy más néven elefántteknős (Chelonoidis nigra) - fajkomplex 1 vagy 13 faj

Áthelyezve a Stigmochelys nembe - 1 faj
 leopárdteknős (Stigmochelys pardalis), korábban (Geochelone pardalis)

Források
 ITIS szerinti rendszerbesorolása
 Biolib szerinti rendszerbesorolása
 Tekifarm.extra.hu magyar nevek listája

Hüllőnemek

redpajama_set_name: RedPajamaWikipedia


Physical Data: yellow mixture, prepared in situ.
1-Ethoxyvinyllithium; Lithium Bis(1-ethoxyvinyl)cuprate; Lithium (Z)-Bis(2-ethoxyvinyl)cuprate; Lithium Divinylcuprate.
3. Chavdarian, C. G.; Heathcock, C. H. JACS 1975, 97, 3822.
4. Fujii, N.; Habashita, H.; Shigemori, N.; Otaka, A.; Ibuka, T.; Tanaka, M.; Yamamoto, Y. TL 1991, 32, 4969.
5. Baldwin, J. E.; Höfle, G. A.; Lever, O. W., Jr. JACS 1974, 96, 7125.
6. Gschwend, H. W.; Rodriguez, H. R. OR 1979, 26, 1.
7. Lever, O. W., Jr. T 1976, 32, 1943.
8. Santiago, B.; Soderquist, J. A. JOC 1992, 57, 5844.
9. Bélanger, A.; Philibert, D.; Teutsch, G. Steroids 1981, 37, 361.


text:
Home » Remembering Our Military Members This Christmas
I spent more than three decades serving men and women in the U.S. Armed Services as an Army chaplain. It's an incredibly unique role in the military—being a spiritual guide to those who might face trauma, death, and devastation in their day-to-day "job" as selfless protectors of the freedom of our nation. I witnessed time and time again how, when Christmas comes around, the trials of Military life can be particularly profound.
This isn't an entirely unique circumstance. Many families face amplified feelings of loss and separation amid family-oriented holidays. However, holiday separations are a consistent aspect of the military journey. For example, about one-third of the active-duty military members are either stationed or deployed outside the United States. That means that this Christmas, thousands of daughters and sons, fathers and mothers, aunts and uncles, brothers and sisters, who are serving in the military will miss the chance to sit at a dinner table with their parents, kids, and other family members. While these men and women are so resilient, I don't want to miss the fact that being away during these special moments is one of the many sacrifices made.
In a way, 2020 has given us all a taste of the challenges military families face. The fear that a parent might die, the separation from extended family—it's been a painful reality for so many Americans. For everyone, really, so much of what we thought we could rely on turned out to be shallow in our most significant time of need. How do military families cope? How might we all manage?
We've completed research at the American Bible Society, which shows that those who turn to the Bible in times of trauma can cope better than those who do not. We now know that frequency of Bible reading makes a real difference. In other words, those individuals in perpetual engagement with the Bible can cope and recover more successfully from trauma. They also tend to be more satisfied in life overall—not to mention more empathetic and caring towards others. Additionally, in the research we completed that looked at how individuals' sense of overall wellbeing changed amid the pandemic (January 2020 versus June 2020), those respondents who read the Bible remained steadier in maintaining community and feeling satisfied and secure.
It's why the American Bible Society has been providing Bibles to the U.S. Military for over 200 years. In 2020 and beyond, we will continue to expand on the Bible-based resources we provide to troops, chaplains, Veterans, and their families. In partnership with our Trauma Healing Institute, we're creating resources for all of these groups, explicitly tailored to their unique experiences.
While I know the holiday season can feel taxing, complicated, and even just plain sad for many of us, I hope each individual could see that they are not alone. Christmas's original and longstanding gift was the Immanuel, meaning "God with us." Second of all, there is a community of thousands of others who are going through similar circumstances. I know many of us have felt the loss of the community of Bible study groups and in-person church gatherings, but utilizing available resources can help you navigate these difficult circumstances. The Bible is so full of joy, but it is also full of stories of people who faced great hardships and full of tools for navigating grief and loneliness. I invite troops, Veterans, and those with loved ones in the military to visit our Armed Services Ministry website to find a program or other resources that are right for you.
If you're reading this as an active duty member of the military, I encourage you to connect with your chaplain, who wants the best for you and has access to resources designed specifically for you.
To the rest of us— I get asked often by civilians what they can do to support our military that will really make an impact. You can pray— for hope, healing, and restoration to any areas where there's been loss or hardship for military members and their families. You can also invest in organizations working to provide biblical resources and establish best-practices for faith-based trauma healing. As we enter this time of joyful celebration, let's do it arm-in-arm with the wonderful men and women who protect our freedom to do so.
A special thank you to retired Army Colonel Gordon Groseclose for his service and report. Groseclose served as U.S. Army Chaplain for 32 years before partnering with the American Bible Society's Armed Services Ministry to develop Scripture resources for military members, Veterans, and their families.
Trending In Culture, News Stories on Religion and Faith, The Latest on Christian Service
Smart Tips for Getting the Best Out of Online Shopping in 2021
Facing Depression, Anxiety, Other Mental Health Struggles
Exclusive: Alveda King, Other Top Faith Leaders Say 'Look to God' for Peace, Healing, and Hope in This Time of Crisis


text:
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Memo To Self: A rambling miscellany! Now with Pictures!
A day out at the dam.
Cooking with DinnerDad. Serious face!
A beautiful gift from her Aunt Strawberrypot.
And just for a laugh, we went to the Pregnancy, Babies and Children Expo on Friday, and Lolly managed to snag a formula balloon - lol Here she is with it. I did give her a breastfeed while it was hovering overhead, does that cancel it out? I should also say that this slogan "the perfect mix of science and love" SHITS ME TO TEARS!!!!!
Hehehe that balloon is just evil!! ;) I love Ikea but the thought of going there with Imogen gives me the heebie jeebies!
Love the pics, especially the first one at the lake. We love Ikea too, especially 'cause no one cares when the kids sit on all the lounges and lie on all the beds.
wow that felt glower crown is awesome!!!


Construct a Reduced Conflict Intersection at the south junction of Hwy 1 and Hwy 53. Most of the work will take place within the median with minor changes to Hwy 1 and County Road 122.
Construct four, 2½-mile-long, center passing lanes.
Please click here for the Highway 53 Intersection and Passing Lane Improvements Environmental Assessment Worksheet.
A public open house was held for this project December 6, 2018 at the Cook Community Center.
Hwy 53 at the south junction with Hwy 1 near Cook in St. Louis County and at various locations along Hwy 53 between Cook and International Falls in St. Louis and Koochiching Counties.


The University of Denver is a 4-year research institution, founded in 1864. DU, which is 4.5 miles from the center of the city, is located in Denver, CO. It is the oldest the 11th biggest institution in the state of Colorado. DU offers subjects including sociology and biomedical engineering. Students are offered nine certificates, 71 degrees at the bachelors level, 73 degrees at the masters level, and 23 doctoral level degrees by it. 11,842 students pursued degrees from the 113 programs at this university in 2010. This mid-sized university is accredited by the North Central Association of Colleges and Schools, The Higher Learning Commission. This university is one of 7 research universities in Colorado.
9,337 students applied to this university in 2010. DU admitted around 72% of applicants or 6,723 students. About 56% of the admitted students are women.
In 2010, this university enrolled 11,842 students.
This university has 1,244 instructors. Close to half of the faculty are full-time and around half of the faculty are part-time. Nearly half of the instructors are female.


text:
L.A.M.B. Fall 2011 Ready-to-Wear
L.A.M.B. closed out New York fashion week (only a small Finnish label followed it), and tonight's show suggested that there was some poetic justice in that: Gwen Stefani's collection cycled its way back through not only the trends of the season, but of past seasons, too. The show was divided into six groups, each with its own look, its own soundtrack, and its own models (often, a little oddly, grouped by race). The "Soldier Girls" wore military looks. The Rasta "Ragga Muffins," Navajo print. Some "London Girls" had menswear-inspired suiting, and Malcolm McLaren-style "Buffalo Girls" were outfitted with outdoorsy blanket plaids. The "Mod Girls" wore leopard, stripes, and dots, and the "Glamour Girls" who closed—all Stefani-blonde—had seventies jumpsuits and halters in basic black.
It's a worthy validation of the concept that fashion should be fun to suggest, as L.A.M.B. does, that there's no need to lock yourself into one specific look. Try boho one day, Charlie Girl the next. For any and all, L.A.M.B. is there. But it's not much fun to wear things that are poorly made. The platform of one model's shoe went flying off mid-walk; she, flying to the ground. It didn't inspire confidence. It did prove to be a girl-power moment, though. She was a Buffalo Girl by look, but she bravely Solidered on.


Kyoto Japan Perfecta FE SAE 5W-30 is a high performance fuel conserving semi synthetic oil for gasoline- and diesel engines in passenger cars en light vans with or without turbocharger. This product is unsuitable for diesel engines equipped with a Diesel Particle Filter (DPF).
Longer oil drain interval possible.


Sixers Fans Want To Ban Kendall Jenner & Here's Why!
The diehards are petitioning to keep her away from their arena.
Philadelphia 76ers fans are crying foul on Kendall Jenner. They're blaming the model for their team's embarrassing loss Friday to the struggling Cavs. They think she's such bad luck; they've signed a petition to block her from coming to anymore games. Read on for more details.
Kendall was sitting courtside when the 76ers got beat 121-112. She was watching her beau Ben Simmons, who plays for Philly.
About 3000 people have signed the petition that says, "we as fans cannot sit idly by and let Kendall Jenner ruin what could be a truly special season by her attendance at Sixers games. We must take action." The outrage comes after their team lost their first home game of the season. The defeat was also the Cavs' first win on the road.
Kendall and the basketball star have been linked together for months.
Ironically, the winning team also starred a player linked to a Kardashian. Khloe's boyfriend and father to daughter True, Tristan Thompson plays for the Cavaliers. Of course, their relationship has been strained since he cheated on Khloe days before she gave birth.
What do you think about the fans trying to ban Kendall from games? Let us know in the comments.


Looking into buying an EMV software for wrtiting emv chips and reading it as well. copying it from one chip to the next and also editing the chip. if you are able to write a software like this u must be use to msr 206 writing and functioning for magnetic strips.


A simply recipe for breakfast migas made with tortilla chips, onions, jalapeños, and scrambled eggs! Perfect for a hearty breakfast, brunch, or brinner!
Elevating your scrambled egg game to level 1000.
All the best things we love about Mexican food coming together in the form of a scramble and all in one bowl.
Let's really think about this: refried black beans, sliced avocados, onions, jalapeños, zesty salsa, CHEESE, tortilla chips, and the ever so controversial, CILANTRO!
And when all these flavors get together in a bowl or in the curvature of a warm flour or corn tortilla and get topped with spicy salsa it's hard to not dream about this meal long after it's gone. If you serve this for a brunch meal to a group of friends, it's easy to see why people are going to want to have brunch with you more often.
Migas are a crowd pleasing kinda meal.
I can't even begin to tell you the number of times these breakfast migas have been lunch or dinner on weekdays when i'm single. It's the quickest thing to throw together and it's hearty and filling <— pretty much all the marks I want to hit with a meal.
Let me also point out that these are more 'street-style' breakfast migas as they use store-bought tortilla chips. Traditional migas from more authentic Tex-mex joints usually use corn tortillas that are cut into wedges or strips and are fried in oil before adding the eggs and scrambling. When i'm starving and 0.2 seconds away from shoving the entire contents of my pantry in my mouth – these are my go to migas!
They also happen to be perfect when you've got a bag full of half pieces of tortilla chips that are no good for dipping in salsa. To be clear, i'm talking about the pieces that are about ½ or ¼ of the original chip size. Not the crumbs, you don't wanna use those. Smaller pieces shouldn't even exist and around here, they usually get left in the bag, clipped, and forgotten in the back of the pantry until the cleaning rampage hits and then things get tossed. But migas are the perfect way to use up those smaller pieces.
SCORE. I hate wasting food!
What we're doing here is sautéing the onions and jalapeños for a few minutes to sweat them down. Then we'll add scrambled eggs and push them around the pan until they're half firm.
Toss in broken tortilla chips and stir until they're mixed in with the scramble. Add the cheese on top, put a lid on it, and allow the cheese to melt and become perfectly stringy. I like to have someone heating the tortillas and black beans at this time. Slice up the avocados and get that salsa out. Keep the coffee flowing too!
And if you're Anees this will MOST DEFINITELY need to be served in warm tortillas and topped with salsa. Me? I could go either way. Sometimes I'll make myself a bowl of migas and other times a taco. There's really no wrong way to serve these. I've had 'em at a local joint where they cooked up broccoli and zucchini in a warm ranchero sauce and added that to the bowl with the eggs on top and MAN!
Since we're still on our 10 day west coast trip, I'll tell you that these migas were a lifesaver the last few days before we left. Too often I found myself enjoying a bowlful of this stuff.
Guys, this is such a magical meal. It's breakfast, it's lunch, it's dinner, and it's EVERYTHING in between. So skip the frozen pizza, grab a few eggs, and let's get crackin'.
Migas make me [extra] clever.
Heat the oil in a large skillet over medium high heat. Add the onions and jalapeños and sauté for 2-3 minutes or until they begin to sweat and the onions turn translucent.
Lower the heat to low and slowly pour in the eggs, pushing the eggs around the pan every 5-7 seconds until they're half set. Add the tortilla chips and continue to stir until the chips mingle with the eggs and star to set. Top with cheese. Put a lid on it and allow the cheese to melt for 1-2 minutes. Top with cilantro and season with a pinch of salt and pepper.
Serve the migas inside tortillas with black beans, salsa, additional cheese, sliced avocados, and anything else you like!
Marzia the migas look amazing! I really can't wait to try them this weekend.
Can I please ask you where you bought the speckled bowl from? It's gorgeous, and I've been looking for once like this. Thanks!


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The Marxists of the Rhode Island Departments of "Commerce" & "Health" send out letter to RI businesses, guess what's missing? Any mention of death or serious harm from COVID, Delta, and Omicron. More fear mongering from fascist Democrats. |
The Marxists of the Rhode Island Departments of "Commerce" & "Health" send out letter to RI businesses, guess what's missing? Any mention of death or serious harm from COVID, Delta, and Omicron. More fear mongering from fascist Democrats.
Here is the latest propaganda from the RI Democrat Marxists:
Dear Business Owners and Managers,
Thank you for everything you have done [been forced] to help slow the spread of COVID-19 [which clearly hasn't worked seeing we are one of the worst states in the country in this regard]. We know the pandemic has been extremely challenging for businesses across the state. Your partnership has been crucial in promoting the safety and well-being of your employees and customers and in keeping our economy going.
The COVID-19 response remains a high priority as the changing virus remains a threat to Rhode Islanders and our neighbors across the country. Rhode Island has been experiencing high COVID-19 community transmission since August 2021 and we have seen the transmission rate increase during the month of December. With the identification of expected [better yet, hoped for] new variants, people spending more time indoors, and the high rate of community transmission, hospitalizations in Rhode Island are predicted to increase in the coming weeks and into early 2022. Although the dominant strain of COVID-19 is the Delta variant, a new variant, [flu-like lethal, immunity giving] Omicron, has been identified in Rhode Island and is expected [hoped for so fascist democrats can take more of your freedoms away] to cause a significant number of COVID-19 infections in Rhode Island within the coming weeks and months [which always happens to every virus, so the perfect excuse to acclimate you to the Democrats' "New Normal"]. In addition, Rhode Island and other states have experienced early influenza outbreaks [Fascist BONUS!] with a strain of flu known to be associated with more hospitalizations and deaths in people age 65 or older. This is why it is important to implement strategies to keep your staff and customers safe and your business thriving [customers heading to other, less fascist states].
We know you may have questions about implementing mitigation measures and ensuring a successful holiday season for your business. The Rhode Island Department of Health (RIDOH) and our State partners remain committed to supporting your business's short-term and long-term needs. [OR ELSE!]
In September, a letter was sent to businesses across Rhode Island, which included information about four key prevention strategies [reminders we rule over you and your business] that would help ensure that Rhode Island reopened safely: masking, vaccination, testing, and ventilation. We know these mitigation strategies work [a lie]. Studies show that wearing a high-quality mask can decrease transmission by 70% or 80% [no balanced proof given, ever]. RIDOH has updated some of the resources that are available for you and that can help you make decisions about how to keep your staff and your customers safe. Click below to view the complete guide which lists/shows you the most current RIDOH resources for business owners.
Rhode Island Department of Health in cooperation with Rhode Island Commerce
* All text in italics above was added by the editors of the Rhody Report


In reality, it often means that a less experienced appraiser, often from as far away as 100 miles, receives work that formerly went to local appraisers with significant experience and extensive familiarity with a market. Thus, rather than being an improvement, this AMC list/rotation mechanism can result in inaccurate values that perpetuate the mortgage/foreclosure crisis & poor housing market.
Be sure that you request us if your lender asks you for YOUR choice of appraisal firms.More than likely we are already on their approved list, and if not we will quickly provide your lender with the necessary documentation to become approved.
The key to a smooth lender/appraisal relationship is to approach it as a team effort. Communication, openness, dedication, loyalty and compassion on the part of the lender can go a long way toward insuring that the appraiser is a true team player.
IF YOUR APPRAISAL VENDOR IS NOT ON TOP OF THEIR GAME, FIRE THEM AND HIRE SOMEONE WHO IS.
When appraisal management companies (AMCs) entered the mortgage loan process (after sweeping government regulations took effect in May of 2009), the mechanism for appraiser selection changed significantly. Appraisers now receive work by being put on the AMC's list, and then the appraisal assignments are distributed randomly on a rotational basis (or an appraisal is sent to numerous appraisers and whoever hits the accept key the fastest gets the assignment). In theory, this would be one step in preventing any pressure on appraisers to hit a value.


Unlocked and fully user-configurable are the keywords for Eurocom's Sky X9E Extreme Edition desktop replacement laptop.
This machine isn't called Extreme Edition for nothing. The Nepean, Ont.-based tech firm Eurocom made sure there a lot of goodies baked into its Sky X9E.
Open up the rig (no special tools needed), and inside you'll a BIOS unlocked, 6th generation Intel Core i7 6700K processor, an Intel Z170 chipset and the powerful Nvidia GeForce GTX980 graphics card.
Eurocom unleashes the Sky X9E Extreme Edition laptop. This desktop replacement laptop from Canadian computer maker Eurocom, is not called Extreme Edition for nothing.
The 17" Sky X9E is powered by an unlocked Intel Core i7 6700K processor and Nvidia's powerful GeForce GTX 980 (desktop edition) graphics card. The Sky X9E has 64GB of RAM, and offers 1TB of storage which is upgradable to 5TB. It is completely user-upgradable and fully customizable to suit every need from awesome gaming machine to high-performance computing workstation.


Revolutionary slide-a-part straw that gives you complete inside access for quick, easy, and thorough cleaning.
100K in Funding! Thank You!!
Additional content © Jeremy Smith from the Rain Straw: The Reusable Slide-Apart Straw for Easy Cleaning project.


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Otto Johann Drescher (5 October 1895 – 13 August 1944) was a German general in the Wehrmacht of Nazi Germany during World War II. He was a recipient of the Knight's Cross of the Iron Cross. Drescher died on 13 August 1944 in Memel (Klaipėda).

Awards and decorations

 Knight's Cross of the Iron Cross on 6 April 1944 as generalleutnant and commander of 267th Infantry Division

References

Citations

Bibliography

1895 births
1944 deaths
Lieutenant generals of the German Army (Wehrmacht)
Austro-Hungarian military personnel of World War I
Recipients of the clasp to the Iron Cross, 1st class
Recipients of the Gold German Cross
Recipients of the Knight's Cross of the Iron Cross
German Army personnel killed in World War II
People from Svitavy District


Green cover with gold lettering. Cover shows wear and fading. Contents clean. Author also wrote Credo, Lost Forever, God-man, The arena and the throne, and others. Contains surveys of famous revivals in history, individual experiences, Evangelist and revival agencies such as moody and sankey, women evangelist. Has a section on The Holy Ghost: His work beyond the limits of Christendom. Rare.


1.what is the different of virgin hair,rimy hair,non remyy hair ?
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5.do you have wigs ?which style wig do you have in stock ?


text:
Generation of power must be on commercial considerations: Suresh Prabhu
Union Power Minister Suresh Prabhu spoke to Principal Correspondent Sayantan Chakravarty on the grid failure, the crumbling system and long - term solutions.
SAYANTAN CHAKRAVARTY
Union Power Minister Suresh Prabhu spoke to Principal Correspondent Sayantan Chakravarty on the grid failure, the crumbling system and long-term solutions. Excerpts:
Q. What do you think caused the unprecedented blackout across seven states and a Union territory?
A. Preliminary probe by the Power Grid Corporation suggests that there was a large-scale 'grid indiscipline'.
Q. Can you elaborate?
A. When a particular sector trips, the others become overloaded. The Power Grid Corporation, which runs the Regional Load Despatch Centre to maintain a balance in the grid, asks some plants to cut generation so that the other sectors don't become overloaded. Repeated instructions, it appears, went unheeded.
Q. What is the estimate of the revenue loss to the Government as a result of the grid failure?
A. We generated 15,500 MW less power as a result of the failure, which is equivalent to about a day's production in the affected region. The loss worked out to about Rs 125 crore.
Q. What corrective action will you take?
A. The punishment will be harsh keeping in view the high revenue loss to the Government, besides the nearly Rs 500 crore estimated loss to the industry. I shall make both the report and the action public.
Q. Isn't the grid collapse a symptom of a bigger malaise in the system?
A. Any major grid collapse is caused by a number of factors that contribute to the failure of a system.
Q. Like what?
A. In the past 10-15 years problems like wide frequency fluctuations caused by overdrawing of power by the state electricity boards (SEB) has adversely affected the system. There is also over generation by power plants.
Q. There must be other deep-rooted problems.
A. Yes. Look at the losses. Because the difference between our gross cost per unit (Rs 2.80) and the average per unit tariff (Rs 2.07) is 73 paise, the annual loss is to the tune of Rs 50,000 crore. Losses from theft make for another Rs 20,000 crore.
Q. How long do you think will the situation persist?
A. We need to bring down our transmission and distribution losses on a war-footing. This is possible if we immediately invest Rs 40,000 crore every year in improving transmission and distribution. There is no further scope for academic debates and seminars on this.
Q. Are politicians responsible for the present state of affairs?
A. We have a vote bank to cater to, so we become emotional. Unfortunately, the motion of turbines does not understand emotion. Generation of power must be on commercial considerations.


text:
Ereignisse

Politik und Weltgeschehen
 27. Juli: Ziyadat Allah III. ermordet seinen Vater Abu l-Abbas Abdallah II., der sich selbst erst im Vorjahr an die Macht geputscht hat, und macht sich zum Emir der Aghlabiden in Ifrīqiya. Er lässt sofort alle Brüder und Onkel hinrichten, um potentielle Konkurrenten auszuschalten. Während Ziyadat Allah so die eigene Macht sichert, verliert die Dynastie durch diese Vorgänge das letzte Ansehen bei der Bevölkerung. Die konkurrierenden Kutāma unter Abū ʿAbdallāh asch-Schīʿī gewinnen so weiter an Macht und können die Stadt Sétif erobern.
 Wikingerzeit: Die Wikinger (Loire-Normannen) plündern Tours.
 Erste urkundliche Erwähnung von Pleskau

Religion
 August: Nach dem Tod von Benedikt IV. wird Leo V. zum Papst gewählt.
 September: Nach nur 30 Tagen im Amt wird Papst Leo V. durch eine Revolte gestürzt. Christophorus lässt ihn in den Kerker werfen und sich zum Gegenpapst wählen und weihen.

Geboren

Geburtsdatum gesichert

 7. Dezember: Abd ar-Rahman as-Sufi, persischer Astronom († 986)

Genaues Geburtsdatum unbekannt

 Kūya, japanischer Mönch und Wanderprediger († 972)

Geboren um 903

 Eadgifu, angelsächsische Prinzessin und Königin des Westfrankenreichs († nach 951)

Gestorben

Todesdatum gesichert
 13. Januar: Franco, Bischof von Lüttich
 26. März: Sugawara no Michizane, japanischer Gelehrter, Poet und Politiker der Heian-Zeit (* 845)
 27. Juli: Abu l-Abbas Abdallah II., Emir der Aghlabiden in Ifriqiya

Genaues Todesdatum unbekannt
 August: Benedikt IV., Papst
 Adalhard, Sohn des Markgrafen Heinrich I. von Babenberg
 Moses Bar-Kepha, Theologe der syrisch-orthodoxen Kirche (* um 833)
 Oda, Gemahlin des Arnulf von Kärnten (* um 873/874)

Weblinks


Scientists have proposed that the most recently discovered ancient human relatives — the Denisovans — somehow managed to cross one of the world's most prominent marine barriers in Indonesia, and later interbred with modern humans moving through the area on the way to Australia and New Guinea.
Three years ago the genetic analysis of a little finger bone from Denisova cave in the Altai Mountains in northern Asia led to a complete genome sequence of a new line of the human family tree — the Denisovans. Since then, genetic evidence pointing to their hybridisation with modern human populations has been detected, but only in Indigenous populations in Australia, New Guinea and surrounding areas.
In contrast, Denisovan DNA appears to be absent or at very low levels in current populations on mainland Asia, even though this is where the fossil was found.
Published today in a Science opinion article, scientists Professor Alan Cooper of the University of Adelaide in Australia and Professor Chris Stringer of the Natural History Museum in the UK say that this pattern can be explained if the Denisovans had succeeded in crossing the famous Wallace's Line, one of the world's biggest biogeographic barriers which is formed by a powerful marine current along the east coast of Borneo. Wallace's Line marks the division between European and Asian mammals to the west from marsupial-dominated Australasia to the east.
"The recent discovery of another enigmatic ancient human species Homo floresiensis, the so-called Hobbits, in Flores, Indonesia, confirms that the diversity of archaic human relatives in this area was much higher than we'd thought," says Professor Stringer, Research Leader in Human Origins, Natural History Museum, in London. "The morphology of the Hobbits shows they are different from the Denisovans, meaning we now have at least two, and potentially more, unexpected groups in the area.
"The key questions now are where and when the ancestors of current humans, who were on their way to colonise New Guinea and Australia around 50,000 years ago, met and interacted with the Denisovans," says Professor Cooper.


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text:
//
//  ShareMenuView.h
//  ShareViewController
//
//  Created by zc on 16/4/28.
//  Copyright © 2016年 56dian. All rights reserved.
//

#import <UIKit/UIKit.h>
#import "ShareMenuModel.h"
#import "ShareMacro.h"

@interface ShareMenuView : UIView

@property (nonatomic,strong) NSArray <ShareMenuModel *> * menus;

@property (nonatomic,copy) void (^(DimissBlock))();

@property (nonatomic,copy) void (^(DidSelectedMenu))(ShareMenuModel *model);

+(instancetype)shareMenuView;

- (void)showInView:(UIView *)view;

- (void)dismiss;

/** 每行得最大列数 */
@property (nonatomic,assign) NSInteger colums;

@end

redpajama_set_name: RedPajamaGithub


Tort law is civil law regarding when one person violates another. This violation against another can be physical, pain and suffering, or property damage. These laws decide if an individual is legally the cause of your accusations. It also ensures that the plaintiff receives monetary compensation for punitive damages from an individual who's made life difficult.
Like most common law, tort liability and Tort laws and aren't criminal laws. However, a tort against another can be a criminal offense. While criminal cases are used to discipline someone who carries out a criminal offense or through negligence, tort cases are used to discipline someone that's made an offense toward another.
It's important that you know the basics of tort law if you want to bring a civil claim against someone else.
There are several elements that you need to make up a tort case between two people.
In order to win a tort case, you have to prove that the other person (also known as tortfeasor) owed you a duty of care.
This duty involves taking all precautions to protect you from any type of harm. That harm isn't limited to physical injuries or illnesses.
That could mean a manufacturer owes you a safe product when you purchase their products. They owe you that duty of care.
Next, you have to prove that this individual breached their owed duty of care toward you.
So, say the product you bought that was built by this manufacturer (the defendant) went haywire and caused a personal injury (the plaintiff). By selling the product, they should have ensured that the product had no issues.
Now the causation of the incident needs to be proved. This means what caused the violation or harm toward you is proved.
The product you purchased from this manufacturer caused you an injury because it was improperly made. You need to prove that this specific product created your injuries or violation.
In other words, you wouldn't have had the injury without using this product.
Lastly, in a tort case, you need to prove in court that you did, indeed, receive injuries.
This product caused you to cut off a chunk of your finger. Medical records from your ER visit and further visits you've had can help you prove that you received an injury from the faulty product.
This is basically evidence that proves the injury of the plaintiff. Without some type of injury or violation, you wouldn't be filing a civil case against the manufacturer or receive punitive damages.
Tort law is a broad term for the civil laws from torts (or offenses against someone). There are numerous types and subtypes of torts, but we're going to learn about the four major torts.
An intentional tort is, simply put, when the tortfeasor was out to hurt you or damage your property. They had clear intentions to violate or harm you. Most intentional torts are criminal offenses.
Your lawyer must show evidence that proves that the individual had intentions to hurt you. Sometimes, all your lawyer will have to prove is that the person should have known that the actions of their consequences would end up harming you in some way.
Negligent torts are when someone violates or harms you without intention. However, their actions are negligent or reckless, which ended up with you to pay for their choices.
Negligent tort is the most common form of tort and slips and falls are the most common type of negligent torts.
Strict liability torts are when violation or damage is caused but it wasn't due to any negligence nor was harm intended. But even without intention or negligence, there were harmful consequences.
Our example on the manufacturer sending out a faulty product fits into the strict liability category. The manufacturer didn't want their product to cut off your finger and it wasn't due to careless behavior.
It has to be proved that the manufacturer knew about the product defect before it was sent out to stores and customers.
To be able to bring a strict liability tort case, it first has to be proved that this company manufactured the product you purchased. Then, it has to be proved that the product was defective when you bought it.
Federal tort laws are laws that allow you to file a tort case against the U.S. government. Now, it hasn't always been as easy to bring these types of cases to civil court.
The Federal Tort Claims Act (FTCA) grants you permission to sue the federal government. When someone that's working for and acting for the federal government violates or harms you, you can take this to court to receive deserved compensation.
In order to start a civil lawsuit against a federal employee or agency, you must first file an administrative claim with that specific federal agency within two years of the incident. You receive a response to your claim within six months.
If you don't like the response, you have six months to file a tort lawsuit against the government.
Unfortunately, there are some bad eggs out there. Whether someone intentionally set out to harm you or it was due to their reckless behavior, you deserve compensation for the damage done.
It's these situations that brought tort laws in place. And it's these situations that deserve to be brought to civil court.


Keywords: Out-of-Vocabulary (OOV) words, Rare words, Machine Translation (MT), Generalized-Example-based Machine Translation (G-EBMT).
Keywords: Number of Clusters, Spectral Clustering, Templates, Machine Translation (MT), Generalized-Example-based Machine Translation (G-EBMT).
Keywords: Active Learning, Pool-based, Machine Translation (MT), Example-based Machine Translation (EBMT).
Keywords: Bilingual Spectral Clustering, Machine Translation (MT), Generalized-Example-based Machine Translation (G-EBMT).


text:
Le Dragon du Wawel (en polonais : Smok Wawelski) est un célèbre dragon dans la culture polonaise et l'histoire de la ville de Cracovie.

Légende
Selon la légende, cet animal fabuleux vivait dans une grotte située à l'intérieur de la falaise sur laquelle s'élève la colline du Wawel surplombant la Vistule.

Sur cette falaise se dresse un château ainsi que la cathédrale du Wawel devant laquelle se dresse une statue du dragon ainsi qu'une plaque commémorative en l'honneur du légendaire prince Krakus qui vainquit l'animal et fonda la ville de Cracovie sur l'antre du dragon qui avait été tué. Ce prince légendaire donna son patronyme à la cité.

Selon la légende, chaque jour, le terrible dragon battait le chemin à travers la campagne environnante, tuant les habitants, pillant leurs maisons et dévorant leur bétail. Dans certaines  versions de cette histoire, le dragon appréciait particulièrement de dévorer les jeunes filles, et ne pouvait être apaisé que si les gens du coin lui laissaient une jeune fille en face de sa grotte une fois par mois.

Le roi Krakus voulait en finir avec ce dragon, il demanda l'aide aux plus braves des chevaliers de son royaume de venir s'affronter à l'animal. Tous y laissèrent leur vie à cause du souffle de feu sortant de la gueule de la bête. Dans les versions impliquant le sacrifice des jeunes filles, toutes les filles de la ville furent finalement sacrifiées, sauf une, la fille du roi, Wanda. En désespoir de cause, le roi a promis la main de sa belle demoiselle en mariage à qui pourrait vaincre le dragon. Les plus valeureux des guerriers se battirent contre l'animal mais aucun ne réussit à vaincre le dragon. Un jour, un pauvre apprenti cordonnier, nommé Dratewka, releva le défi. Il fourra un agneau avec du soufre et le mit à l'extérieur de la grotte du dragon. Ce dernier sortit et dévora rapidement l'animal. Peu de temps après il eut énormément soif. Il se dirigea vers la Vistule et but tout son saoul et même davantage tellement le soufre l'avait assoiffé. Mais il but sans cesse sans que pour autant son estomac se calme de la douleur qui le tenaillait. Il continua à boire et son ventre gonfla énormément à mesure qu'il vidait les eaux de la Vistule. Il finit par exploser. Le petit cordonnier Dratewka épousa la fille du roi comme promis et ils vécurent heureux.

La grotte du dragon du Wawel, appelée en polonais Smocza Jama, est aujourd'hui un point d'intérêt touristique traditionnel. Depuis 1970, s'élève à l'entrée de la grotte, une statue du dragon, réalisée par Bronisław Chromy.

Notes et références

Dragon légendaire
Culture à Cracovie


text:
Categories Actor
Often asked: Which James Bond Actor Won An Oscar For His Role In The Untouchables?
1 What James Bond actor just died?
2 What movie did Sean Connery get an Oscar for?
3 How did Sean Connery pass?
4 What famous person died today 2020?
5 Who died in 2020?
6 Which actor has won the most Oscars?
7 Why did Sean Connery stop playing James Bond?
8 Who is the best Bond actor?
9 How much is Sean Connery worth now?
10 How much is Jason Connery worth?
11 Is James Bond British?
12 Did Sean Connery have dementia?
What James Bond actor just died?
Sean Connery, the irascible Scot from the slums of Edinburgh who found international fame as Hollywood's original James Bond, dismayed his fans by walking away from the Bond franchise and went on to have a long and fruitful career as a respected actor and an always bankable star, has died in Nassau, the Bahamas.
What movie did Sean Connery get an Oscar for?
His acting career spanned seven decades and he won an Oscar in 1988 for his role in The Untouchables. Sir Sean's other films included The Hunt for Red October, Highlander, Indiana Jones and the Last Crusade and The Rock.
How did Sean Connery pass?
Sean Connery died in his sleep from heart failure due to pneumonia and old age, according to his death certificate obtained by TMZ.
What famous person died today 2020?
A number of such celebrities passed away in 2020 including Kobe Bryant, Chadwick Boseman and Naya Rivera. Bryant passed away in a helicopter crash on January 26 in Calabasas, California, alongside his 13-year-old daughter, Gianna, and seven others. He was 41.
You might be interested: FAQ: Who Is The Highest Paid Actor Per Movie?
Who died in 2020?
In July, Glee stars and fans alike shared heartfelt tributes to Naya Rivera. More recently, Supreme Court Justice Ruth Bader Ginsburg died at age 87, beloved Black Panther star Chadwick Boseman died at age 43, and Jeopardy! host Alex Trebek died at age 80. 4 дня назад
Which actor has won the most Oscars?
The most successful figure to date in the history of the Academy Awards is Katharine Hepburn, who won four Oscars throughout her acting career. The Academy Awards began in 1929 as a way of celebrating excellence within cinema, and winning an Oscar has long been considered prestigious among stars in the movie industry.
Why did Sean Connery stop playing James Bond?
While Roger Moore succeeded Connery as Bond in the official film series and would enjoy his own lengthy tenure in the role, Connery chose roles that deliberately distanced himself from the character that made him a star, publicly expressing his contempt for his continuing association with the role in the immediate
Who is the best Bond actor?
Sean Connery, the Scottish actor best known for playing James Bond, died Oct. 31. He was 90-years-old. Connery appeared in seven Bond films from 1962 to 1983, tying Roger Moore (who died in 2017) for the most appearances as the renowned secret agent.
How much is Sean Connery worth now?
How much was Sean Connery worth?
Profession: Professional Actor
Country: Scotland, United Kingdom
How much is Jason Connery worth?
So, do you know how rich Jason Connery is, as of mid- 2019? The total sum of Jason's wealth has been estimated by sources at $2 million, which should increase, assuming that he successfully continues his career.
You might be interested: Readers ask: Who Won The Oscar For Best Actor In 2016?
Is James Bond British?
James Bond is a British literary and film character. He is often depicted as a peerless spy, notorious womanizer, and masculine icon. He is also designated as agent 007 (always articulated as "double-oh-seven") in the British Secret Intelligence Service, or MI6.
Did Sean Connery have dementia?
"It was no life for him," the French-Moroccan artist told the Mail, revealing that the actor, who died on Saturday in his sleep, had been struggling with dementia. "It took its toll on him. He was not able to express himself (at the end)." Roquebrune, 91, explained that Connery died in his sleep.
Question: Actor Who Played The Rifleman?
FAQ: Who Was The Actor Who Died Today?
Question: How Do I Become An Actor On Disney Channel?


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Regulation of the Porphyromonas gingivalis fimA(Fimbrillin) Gene
Hua Xie, Whasun O. Chung, Yoonsuk Park, Richard J. Lamont
Hua Xie
School of Dentistry, Meharry Medical College, Nashville, Tennessee, 1 and
Whasun O. Chung
Department of Oral Biology, University of Washington, Seattle, Washington 2
Yoonsuk Park
Richard J. Lamont
DOI: 10.1128/IAI.68.12.6574-6579.2000
In common with many bacterial virulence genes, the fimbrillin (fimA) gene of Porphyromonas gingivalis is modulated in response to environmental fluctuation. Thetrans-acting components that comprise the regulatory system for transcriptional activity of the fimA gene inP. gingivalis were investigated. Three major proteins were found to bind to the upstream region of the fimApromoter. One of these proteins was fimbrillin itself, and the other two were a major arginine protease (Rgp) and lysine protease (Kgp). Production of these proteins was necessary for maximal fimA transcription. An exogenousfimA promoter-lacZ reporter was inactive when introduced into a strain of P. gingivalis carrying a mutation in the indigenous fimA gene. Furthermore,fimA mRNA levels were significantly decreased inrgp and kgp mutant strains. These data indicate that P. gingivalis has evolved multiple levels of control of fimbrial gene expression to enhance its survival in hostile environments.
Periodontal diseases are a group of chronic inflammatory infections that affect millions of people worldwide and cause destruction of the periodontal tissues, eventually leading to exfoliation of the teeth. Periodontal diseases ensue following the establishment of a mixed microbial subgingival biofilm, and foremost among these pathogenic agents is the gram-negative anaerobe Porphyromonas gingivalis (25). A number of virulence factors contribute to the pathogenicity ofP. gingivalis. These include proteolytic enzymes that degrade host tissue and inactivate immune effector molecules; hemagglutinins that target the cells towards hemin, a requisite iron source; and fimbriae that are required for attachment to oral surfaces such as epithelial cells and to antecedent plaque bacteria and for invasion of epithelial cells (4, 9, 11, 28). As the oral cavity is a continuously changing environment, successful colonizers such as P. gingivalis have the ability to sense and respond to environmental conditions. Regulation of proteases, hemagglutinins, superoxide dismutase, and fimbriae has been documented, primarily at the transcriptional level, although it has also been reported at the posttranscriptional level (2, 9, 11,26). However, although regulation of virulence genes is known to occur, the nature of the regulatory proteins and pathways inP. gingivalis has not been defined.
To gain an understanding of the regulatory networks in P. gingivalis, we are studying the expression of fimbrillin, the monomeric subunit of the P. gingivalis major fimbriae. Previous work has shown that expression of the gene encoding fimbrillin (fimA) and subsequent fimbria-dependent phenotypic activity are tightly regulated by environmental cues (30). Expression of the fimA gene is maximal at a relatively lower temperature and higher hemin concentration compared to normal growth conditions. In contrast, serum and salivary molecules inhibitfimA promoter activity. More-detailed site-specific mutagenesis experiments suggested that the fimA upstream region has a ς70-recognized RNA polymerase binding site along with an upstream element and a site determining positive regulation (31). Thus, we have proposed thattrans-acting element(s) are involved in positive regulation of expression of the fimA gene in P. gingivalis by interacting with the fimA promoter region. The objective of this study was, therefore, to identify the proteins involved in regulation of the fimA gene. The results indicate that fimA expression is regulated by fimbrillin itself and by two major proteases of P. gingivalis.
Bacterial stains, vectors, and growth conditions.Bacterial strains and plasmids used in this study are listed in Table1. P. gingivalis strains were grown in Trypticase soy broth (Becton Dickinson) or on 1.5% Trypticase soy broth agar plates, supplemented with yeast extract (1 mg/ml; Difco), hemin (5 μg/ml), and menadione (1 μg/ml), at 37°C in an anaerobic chamber (85% N2, 10% H2, 5% CO2). Antibiotics—erythromycin (20 μg/ml) and gentamicin (100 μg/ml)—were used where appropriate. Escherichia coliDH5α was used as the host strain for recombinant plasmids and grown in L broth with antibiotics—ampicillin (100 μg/ml), kanamycin (50 μg/ml), trimethoprim (200 μg/ml), and tetracycline (10 μg/ml) when necessary.
Bacterial strains and plasmids used and constructed in this study
Purification of sequence-specific DNA binding proteins.To purify P. gingivalis proteins binding to the regulatory sequences upstream from the fimA promoter, we utilized biomagnetic beads (Dynal, Oslo, Norway) according to the manufacturer's instructions. Briefly, the P. gingivalis 33277 fimA promoter region with a deletion of the RNA polymerase −35 binding site (31) was amplified by PCR. The template was plasmid MP58, which carries the mutatedfimA promoter (31). The primers used were 5′-GGAATTCCGACGCTATATGCAAGACAA-3′ and 5′-TGTAACGGGTTCTGCCTCGT-3′, which was biotinylated at the 5′ end to facilitate binding to streptavidin-coated magnetic (M-280) beads. PCR mixtures contained 10 pmol of template DNA, 30 pmol of each primer, 1.5 mM of MgCl2, a 10 mM concentration of each deoxynucleoside triphosphate (dNTP) and 5 U of Taq DNA polymerase (Gibco-BRL). The amplification was performed in a thermal cycler (Techne) at 94°C for 45 s, 42°C for 1 min, and 72°C for 1 min for a total 30 cycles, followed by 10 min of elongation at 72°C. The PCR product was 166 bp (designated F166) and was immobilized on magnetic beads through a streptavidin-biotin interaction. A cell extract of P. gingivalis was prepared from the cells grown at 37°C to late log phase and disrupted by sonication. The extract was partially purified on a DEAE-cellulose column (Pharmacia Biotech) prior to reaction with F166-coated beads. The reaction mixture was separated in a magnetic field and washed, and specific DNA binding proteins were eluted with 1 M NaCl. Finally, the DNA binding proteins were resuspended in 10 mM Tris buffer by passing through CentriSpin-20 (Princeton Separations, Inc), and visualized by sodium dodecyl sulfate–10% polyacrylamide gel electrophoresis (SDS-PAGE) on 10% gels (7) stained with Coomassie blue. As a control, beads were coated with fimA promoter region from which the regulatory sequences were deleted. Template plasmid pMP591 was amplified by PCR with primers MP150 (31), 5′-GCTATGGTGTTGTTGGGTTGCATATTCA-3′, and biotin- 5′-TGTAACGGGTTCTGCCTCGT-3′. The PCR product was 103 bp (designated F103) and contains deletions from position −240 to −90, position −85 to −71, and position −64 to −48.
Recombinant protein, antisera, and immunoblotting.Recombinant fimbrillin (rFim) was produced by PCR amplification of thefimA coding sequences from P. gingivalis33277 chromosomal DNA (6) and cloning into the pET30 expression system (Novagen). Following induction in E. coli, rFim was purified by chromatography over a Ni2+ metal chelation resin and elution with imidazole. Upstream vector-derived sequences were then removed by cleavage with enterokinase. rFim is full-length mature fimbrillin without the leader amino acid sequence. Monospecific rabbit antibodies to rFim were produced by Covance Inc., Princeton, N.J. For blotting, proteins were separated by SDS-PAGE and transferred onto a nitrocellulose membrane. Antibodies to rFim orP. gingivalis cells (1:10,000) were used as the probe with peroxidase-conjugated secondary antibodies (1:3,000). Antigen-antibody binding was developed with 0.05% diaminobenzidine tetrahydrochloride.
Mobility shift DNA-binding assay.Mobility shift DNA-binding assays were conducted by using the Bandshift kit (Pharmacia Biotech), as previously described (31). The F166 PCR product containing the fimA upstream region was used as probe. Briefly, the DNA fragment was labeled with [α-32P]dATP (3,000 μCi/mmol; NEN) using the Klenow fragment. For the protein-DNA reaction, 1 μg of32P-labeled DNA and 1 μg of protein were mixed and incubated at room temperature for 20 min. The mixture was then loaded onto a 5% nondenaturing polyacrylamide gel and electrophoresed in 0.5 Tris-borate-EDTA buffer at 10 V/cm. Finally, the gel was dried and exposed to X-ray film at −70°C.
Construction of fimA mutant strains.Site-specific mutations in the fimA upstream region were generated by a unique-site elimination mutagenesis kit (Pharmacia Biotech) as described in detail previously (31). Three mutant alleles of the fimA promoter were created and fused with a lacZ gene. One mutation (MPF35) was located in the −35 RNA polymerase binding site (−46 to −44), with a 3-bp substitution (TTG to CAA), and the second (MP150) carried a deletion from position −240 to −90, a region in which we have detected positive regulatory sequences (31). The third (MPS10) was a 3-bp substitution (TAA to GCC) at position −11 to −9, a region that is not involved in promotion of fimA transcription. The mutant alleles were then conjugated into P. gingivalis33277 and integrated to the chromosomal DNA by a single crossover (Fig.1). The authenticity of the mutated sequence was verified by DNA sequencing and PCR analysis with specific pairs of primers for each mutation (31).
Introduction of the mutated fimA promoter into P. gingivalis chromosomal DNA. Two genomic configurations can occur after a single crossover between plasmid MPF35 MPF150, or MPS10 and chromosomal DNA. In configuration 1, the crossover occurs upstream of the mutation. In configuration 2, the recombination occurs downstream of the mutation. Pmut. and Pwild represent the mutated and wild-type fimA promoter, respectively;ermF is an erythromycin resistance gene. Configuration 2 was selected by examination by PCR with primer pairs designed for Pmut. andfimA and for Pwild and lacZ.
RT-PCR.The level of fimA mRNA expression was tested in the rgpA and kgp null mutants YPP1 and YPP2 (23). The oligonucleotides for the fimA gene were as follows: fimA1, 5′-AATCGTGCTTTTGGAGTTGG-3′; fimA2, 5′-ACCAACGAGAACCCACTCAG-3′. Reverse transcription was performed in the presence of 2 μg of total RNA, 50 ng of reverse primer, 50 U of reverse transcriptase (RT) (Ambion), 13 U of RNase inhibitor, a 10 mM concentration of each dNTP, and 1× RT buffer. The reaction was carried out at 72°C for 2 min and then at 48°C for 1 h. Controls without RT were included in all experiments. The resulting cDNA was amplified, with each 100 μl of PCR mixture containing 1× PCR buffer, 3 μl of cDNA, 1.5 mM MgCl2, a 10 mM concentration of each dNTP, 100 ng of each primer, and 2.5 U of Taq DNA polymerase. The amplification conditions were denaturation at 96°C for 30 s, annealing at 45°C for 30 s, and elongation at 72°C for 2 min. The expected size of the fimA PCR product was 1 kbp. As a control, an unrelated gene (an open reading frame demonstrating homology to theluxS gene) was also amplified.
Protein sequencing.The DNA binding proteins eluted from magnetic beads were separated by SDS–10% PAGE. Following visualization with Coomassie blue, proteins were excised from the gel. Tryptic digestion followed by high-pressure liquid chromatography separation and Edman degradation were performed at the Biotechnology Center at the Fred Hutchinson Cancer Research Center, Seattle, Wash.
β-Galactosidase assays.Expression of the lacZgene under control of the fimA promoter was measured by the standard spectrophotometric β-galactosidase assay witho-nitrophenyl-β-d-galactopyranoside as the substrate, as described by Miller (17). P. gingivalis strains were recovered from late log phase and tested at an optical density at 600 nm of 0.4 to 0.6.
Interaction between P. gingivalis proteins and thefimA promoter.It is well documented that regulatory proteins can bind to specific sites in the upstream regions of genes, and this, in turn, influences the function of RNA polymerase (3). To search for regulatory proteins involved infimA expression, we used a magnetic bead-bound DNA fragment of the fimA upstream region (F166) as bait for potential DNA-binding proteins from a cell extract of P. gingivalis 33277. After elution from the fimA promoter and visualization by SDS-PAGE, three major fimA binding proteins were observed, with molecular masses of approximately 60, 50, and 43 kDa (Fig. 2, lane 1). None of these proteins were recovered after incubation of the cell extract with magnetic beads conjugated with F103, the fimAupstream region from which the regulatory sequences were deleted (Fig.2, lane 2). Furthermore, extract from the fimA null mutant, YPF1, did not bind to F166 (Fig. 2, lane 3). Western blot analysis with anti-FimA antibody indicated that the 43-kDa band was fimbrillin (Fig. 2, lane 4). Antibodies to P. gingivalis cells revealed additional fainter bands in the 45- to 49-kDa region (Fig. 2, lane 5).
Proteins binding to the fimA upstream region. Proteins were eluted from magnetic beads conjugated with F166 (lanes 1, 3, 4, and 5) or with F103 (lane 2) and separated by SDS-PAGE. Coomassie-stained proteins from strains 33277 are shown in lanes 1 and 2. Lane 3 contains a Coomassie stain of strain YPF1 (FimA deficient). Lanes 4 and 5 are immunoblots of 33277 eluted proteins, developed with antifimbrillin or anti-P. gingivalis antibodies, respectively. Sizes are indicated.
The identity of the major binding proteins was further investigated by amino acid sequencing. Three trypsin-digested peptide fragments from the 43-kDa band matched the fimbrillin amino acid sequence (Fig.3A). Furthermore, a peptide derived from the 60-kDa peptide demonstrated 100% homology to the arginine-specific cysteine protease, Rgp (Fig. 3C). Thus, this molecule could be either RgpB or a posttranslational processed fragment of RgpA (4). Four of the peptides from the 50-kDa protein were 100% homologous to the lysine-specific cysteine protease, Kgp (Fig. 3B).
(A) Sequences of the digested peptides from the 43-kDa protein in Fig. 2. The fimbrillin (FimA) sequence is given in boldface letters. (B) Sequences of the peptides from the 50-kDa protein in Fig.2. The lysine-specific cysteine proteinase (Kgp) sequence is given in boldface letters. (C) Sequence of the peptide from the 60-kDa protein in Fig. 2. The Gingipain R2 (RgpB) sequence is given in boldface letters. Numbers represent amino acid residues from sequences deposited in GenBank (accession numbers: FimA, BAA86887; Kgp, AAC26523; RgpB,A55426).
Mobility shift.To test the ability of FimA to bind directly to the fimA promoter region, a bandshift experiment was performed (Fig. 4). Proteins eluted from the magnetic beads interacted with the fimA promoter, resulting in the formation of DNA-protein complex that halted movement of the DNA fragment (F166) (Fig. 4, lane 4). Mobility shift occurred in the presence of unrelated DNA (Fig. 4, lane 5), but was competitively inhibited by excess unlabeled F166 (Fig. 4, lane 3). The bandshift profile indicated more than one mobility change, which was probably due to instability of the multiple protein-DNA complex during the experimental process. Purified fimbrillin alone failed to associate with the fimA promoter (Fig. 4, lane 2), suggesting that fimbrillin may not bind to its own promoter directly but may associate with the promoter through other regulatory proteins. Proteases could function in this capacity; however, this appears unlikely, as in the absence of FimA the proteases could not be recovered from F166 (Fig. 2). Minor binding proteins visualized by Western blotting with whole P. gingivalisantibodies (Fig. 2) are also potential candidates, and work is under way to resolve this issue.
Mobility shift DNA binding assay. Lane 1,fimA upstream fragment (F166) only; lane 2,fimA promoter fragment and 1 μg of purified fimbrillin; lane 3, fimA promoter, the 33277 proteins eluted from magnetic beads, and 250 pmol of unlabeled F166; lane 4,fimA promoter and the 33277 eluted proteins from magnetic beads; lane 5, fimA promoter, the 33277 eluted proteins from magnetic beads, and 3 μg of calf thymus DNA.
Effect of fimA mutations on fimA promoter activity.Based on the evidence provided by the binding assays, we predicted that fimbrillin serves as a regulatory protein in its own expression. To further test this hypothesis, we generated P. gingivalis strains containing a fimApromoter-lacZ reporter chromosomal fusion along with a mutation in the indigenous fimA promoter. Thus, these strains contain two fimA promoters, with one driving thefimA structural gene and the other promoting transcription of the lacZ gene. Insertion of thefimA::lacZ construct does not alter expression of fimA mRNA or levels of FimA protein (31). The resulting strains, MPF35A and MP150A, contain mutations at the −35 region (3-bp substitution) and the upstream regulatory sequence (150-bp deletion), respectively. These strains allow us to examine the influence of loss of production of FimA protein on fimA promoter activity (as reported by lacZactivity). RT-PCR confirmed both that fimA mRNA is either not produced (MPF35A) or significantly reduced (MP150A) and that there was no transcriptional read-through from theermF gene (not shown). As shown in Table2, lacZ activity decreased by around 40% in strain MP150A and to background levels in MPF35A. As an additional control, a mutation was introduced into a region upstream of the fimA structural gene and distal to the −10 site (MPS10A). This mutation does not affect promoter activity (31), and the resulting strain possessed wild-type levels offimA mRNA and did not have reduced β-galactosidase activity (Table 2).
Effect of fimA promoter mutations (fimA MP) on the expression offimA::lacZ fusion genes
Transcription of fimA in rgp andkgp mutants.As the data indicated that the major cysteine proteases of P. gingivalis are also involved in regulation of fimA expression, loss of protease expression should cause downregulation of fimA. Thus, we examined fimA mRNA levels in P. gingivalis strains YPP1 (which contains an insertional inactivation of the rgpA gene) and YPP2 (which contains an insertional inactivation of the kgp gene) (23) by RT-PCR (Fig. 5). Expression offimA mRNA was significantly reduced in these mutants compared to wild type. In contrast there were no differences in expression of a luxS-like gene that was identified by a homology search of the P. gingivalis genome database (http://www.tigr.org).
RT-PCR of fimA mRNA in YPP1 and YPP2 protease-deficient mutants. Lanes 1, 5, and 9, YPP1; lanes 2, 6, and 10, YPP2; lanes 3, 7, and 11, 33277; lanes 4 and 8, negative controls without RT. Lanes 1 to 4, cDNA amplified for 30 cycles withfimA primers; lanes 5 to 8, amplified for 40 cycles withfimA primers; lanes 9 to 11, amplified for 35 cycles with control primers for a luxS-like gene.
It is becoming increasingly apparent that fine control over the expression of bacterial virulence determinants is required for successful bacterial colonization and disease progression. Such control can be the outcome of complex and regulatory networks that sense the prevailing environmental conditions and transduce information to modulate gene expression (16). P. gingivalisis well adapted to life in the subgingival environment and regulates gene expression in response to orally relevant parameters (2, 9, 11, 26). However, the signal transduction pathways and regulatory mechanisms in this strict anaerobe are not well understood. Evidence provided here suggests that several well-known proteins of P. gingivalis are members of afimA regulatory system. These include fimbrillin itself, along with an arginine-specific cysteine protease (Rgp) and a lysine-specific cysteine protease (Kgp). These proteins could bind to, and cause a mobility shift of, the fimA upstream region. Site-specific mutagenesis also showed that the wild-typefimA promoter was maximally activated only when thefimA structural gene was fully expressed. Indeed, a 3-bp replacement in the −35 region of fimA alone was sufficient to repress transcription from the intact fimA promoter in a reconstituted lacZ gene fusion system. Furthermore, transcriptional activity of fimA was significantly reduced in mutants lacking expression of either RgpA or Kgp. Thus, the presence of all three of these proteins appears to be necessary for maximal expression of fimA. Whether these proteins assemble prior to or after DNA association remains to be determined, and it is possible that the observed participation of the proteolytic enzymes is a consequence of their preexisting association with prefimbrillin in a processing capacity. In either event a role for additional direct DNA-binding proteins is suggested. Work is currently under way to identify these molecules.
The phenomenon of autoregulation is well established for several bacterial genes. Liberek and Georgopoulos (12) reported that in E. coli, the heat shock genes, dnak,dnaJ, and grpE, were negatively autoregulated, and mutations in any one of these genes could lead to their own constitutive expression. In some studies the mechanisms of gene autoregulation were revealed. The simplest autoregulation pathway involves the gene products serving as activators or repressors by binding to the promoter region of the same gene (5). An alternative pathway involves autoregulation at the translational level, whereby the protein can bind to its own mRNA (15). Autoregulation at a posttranscriptional level is unlikely inP. gingivalis, since an operon fusion was used in our experimental system. Autoregulation affords bacteria an additional level of genetic control and thus facilitates fine-tuning of protein expression. In the case of P. gingivalis fimbrillin, this may be important in optimizing protein levels during the transition from colonization to initiation of disease. Fimbriae are essential mediators of adherence and invasion and are thus necessary for colonization of the organism (1, 8, 9, 10, 29). However, fimbriae are also potent inducers of immune cell function (19,20) and hence may be detrimental to the organism when it engages in a more intimate interaction with periodontal tissues. The ability to amplify down- and upregulation signals may thus provide P. gingivalis with a selective advantage in mixed microbial oral biofilms.
P. gingivalis is an asaccharolytic organism and utilizes a number of proteolytic enzymes to provide peptides for growth. These proteinases also have a variety of effects with relevance to pathogenicity, including tissue destruction and inactivation of effector molecules of the immune system (4, 28). Previous studies have also reported a role for proteases in the fimbriation ofP. gingivalis. Mutants that are defective in Rgp production possess very few fimbriae on their cell surfaces (18). These observations have been explained on the basis of posttranslational processing, since proteases can cleave the N-terminal amino acid (leader peptide) of FimA protein in vitro (21). However, reports vary on whether fimbriation is affected in singlergpA or kgp mutants, or whether a doublergpAB mutation is required to reduce fimbrillin production. For example, Nakayama et al. (18) showed that anrgpA-rgpB double mutant possessed very few fimbriae on the cell surface, whereas fimbriation was normal in an rgpAsingle mutant. In contrast, Tokuda et al. (27) demonstrated that an rgpA single mutant did not express detectable levels of the FimA protein as determined by Western blotting, nor were fimbriae visible following electron microscopy of the cells. Moreover, the rgpA single mutant in the latter study had reduced expression of fimA mRNA. Our observations are more consistent with those of Tokuda et al. (27) and demonstrate that individual proteases can play a direct role in fimbrillin production at the transcriptional level. Linkage of fimbrillin expression to proteolytic activity may allow coordination of activity of a number of the molecules that drive the pathophysiology of the organism.
The fimbriae of P. gingivalis contribute significantly to virulence. Indeed, fimbria-deficient mutant cells are less pathogenic in animal models (14) and are unable to form biofilms (Y. Park, J. W. Costerton, G. S. Cook, D. R. Demuth, and R. J. Lamont, Abstr. 77th Meet. Int. Assoc. Dent. Res., abstr. 2514, 1999). P. gingivalis fimbriae do not exhibit homology to other gram-negative fimbriae, either in terms of sequence or chromosomal arrangement, and may represent a unique class of fimbrial structure (6). An understanding of the mechanism of transcriptional control of fimbria production should provide important insights into the basis of the pathogenicity of this important periodontal pathogen.
The support of the NIDCR (DE00401, DE11111, and DE12505) is gratefully acknowledged.
Editor: V. J. DiRita
Received 25 May 2000.
Returned for modification 1 August 2000.
Accepted 7 September 2000.
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Infection and Immunity Dec 2000, 68 (12) 6574-6579; DOI: 10.1128/IAI.68.12.6574-6579.2000
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The five risks the economy faces this year, according to the RBI
By Jomy Pullokaran Jun 7, 2018 6:36:56 AM IST (Updated)
The RBI on Wednesday has highlighted five risks to Indian economy in its monetary policy, which can derail country's high growth.
In its second bi-monthly monetary policy of 2018-19, the Reserve Bank of India (RBI) on Wednesday raised the repo rate by 25 basis points to 6.25% and reverse repo to 6% from 5.75%.
The resolution of the Monetary Policy Committee (MPC) to hike key rates for the first time in over four years, comes due to inflation concerns, and risks associated with the Indian economy.
The central bank has highlighted five risks to India's economy in its monetary policy, which can derail the country's high growth.
As usual, the main culprit remains crude oil prices. The MPC said there has been a 12% increase in the price of Indian crude basket, which was sharper, earlier than expected and seems to be durable.
"Crude oil prices have been volatile recently and this imparts considerable uncertainty to the inflation outlook – both on the upside and the downside," the MPC said.
The five risks the economy faces this year, according to the RBI:
First, global financial market developments have emerged as another important source of uncertainty.
Second, the significant rise in households' inflation expectations as gathered in the May 2018 round of the RBI's survey could feed into wages and input costs in the coming months. However, the pass-through to output prices remains muted presently.
Third, the staggered impact of house rent allowance (HRA) revisions by various state governments may push headline inflation up. While the statistical impact of HRA revisions will be looked through, there is a need to watch out for any second round impact on inflation.
Fourth, the impact of the revision in the Minimum Support Price (MSP) formula for kharif crops is not possible to assess at this stage in the absence of adequate details.
Fifth, as forecast by the India Meteorological Department (IMD), if the monsoon is normal and well-distributed temporally and spatially, it may help keep food inflation benign.
These five risks made the MPC to hike key rates today to achieve the medium-term target for headline inflation of 4% on a durable basis.
Read our full coverage of the RBI Monetary Policy here
First Published: Jun 6, 2018 4:48 PM IST
Bi-monthly Monetary Policyinterest ratesRBIRBI Monetary PolicyUrjit Patel


Castle Acre Priory is one of the many Norfolk castle ruins which remain very much intact today. It oozes historical importance for both Norfolk and for England, and as you wander around the well kept grounds, you get a very good idea of what it must have been like to live and work here.
It is one of the largest and most impressive monastic sites in England, being the home of the first cluniac monks in England, hence the importance of this particular ruin. It's also one of the best preserved priories in the UK.
Founded in 1089, the priory was originally situated within the castle, (the castle ruins at Castle Acre are also well worth a visit whilst you're here) but it proved to be too inconvenient so was moved to its present site about a year after the castle was built.
The Nave of the church is the oldest part of this priory ruin, but like many of the priories in Norfolk such as Binham Priory, it was dissolved in 1537 under Henry VIII. Castle Acre Priory was eventually passed to the Coke family of Holkham Hall, and the Priory and the Castle are still owned by the present Earl of Leicester, although the site is managed by English Heritage.
These are fabulous ancient priory ruins with the west front almost complete. There's a lot to see here, the beautiful west end church gable, the buildings around the cloisters, as well as the prior's lodging, which is the most solid building within the priory walls.
There's a car park within the priory surrounds, as well as a small shop which is where you will need to pay your entrance fee. The shop however, does have an excellent little exhibition about life in the abbey, and a wonderful model of how the priory would have been when fully intact.
The priory is set on the banks of the River Nar, a wonderful clear chalk stream trout river where you will often see trout swimming along. Refreshingly cool in the summer months too to dip your toes into!
There are various walks you can take around the Priory.
One is a long circular walk around Castle Acre, over to West Acre and back again.
It's all a wonderful haven for taking photos!
Why not get your money's worth by making a day of it. Castle Acre is an extremely pretty village with a pub and tea rooms. You can visit the Castle, or walk along the Nar Valley Trail.
You could even take a picnic and eat at one of the picnic tables in the well kept surrounds of the priory where you can enjoy peace and tranquillity amongst the very beautiful Norfolk countryside.
This is one of the best monastic ruins you'll visit in Norfolk, and in England. One of the other excellent castle ruins near Kings Lynn is Castle Rising Castle. This is yet another very well preserved example within a very pretty traditional Norfolk village.
Nearby is the impressive Tudor stately home of Oxburgh Hall, well worth the visit.


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