We want Youth Startup Weekend to be as impactful, educational and fun as possible! We believe that the first step to making that happen is to make sure you're extra prepared before you even come in.
You don't need to come with a business already created.
In fact, you're not allowed to! Come with an idea of a problem you'd like to solve, how you might solve it and the type of team you would need to do this! Our facilitator walks you through the ideation phase and pitching process, so no prep work is necessary!
We can't stress this one enough. We've seen teams form because they're best friends, but they aren't all interested in putting in the hard work or passionate about the business. Make sure that you form a team that seems to get along and each team member can contribute something unique.
They look like this ^. We have them formatted for you and ready to go, but these help mentors know what's going on. We'll show you how to use them at the event.
THIS IS THE MOST IMPORTANT PART, SO LISTEN CLOSE. This event is not about winning. It's about taking an idea and creating something from it. It's about doing that rapidly, managing your time well, and getting to know some awesome fellow entrepreneurs in the process. Come with that mindset and you'll move mountains.


Typically at Yum Cha there are three options to the tea: jasmine green tea, chrysanthemum herbal tea and Sow Mee tea 壽眉茶. Sow Mee tea is classed under the Chinese tea system as a white tea, alongside Pai Mu Tan and Silver Needle.
Depending on who you talk to, the rules on what makes a white tea can vary. But the general consensus is that it is a tea with the least amount of handling by people. Ideally the leaves and buds are just plucked and dried.
Of the three grades of white tea, Sow Mee is the tea of the common folk because it is cheap and can still be brewed into a strong dark liquor. Hence the name Sow Mee 壽眉: poetic licence to let buyers know that old folks love it.
Qigong 氣功 is on the most basic level focused breathing exercises designed to increase a person's inner energy. On the next level up, it is essentially for most people light aenorobic exercises that most people can do on a daily basis.
Done daily, both the drinking of tea like Sow Mee 壽眉茶 and qigong are more beneficial to the body than not doing them at all. Traditionally when a master was in repose, they were typically engaged in them and as such can be viewed as a form of wushu leisure.
Martial Qigong 武氣功 is the ancient discipline of using qigong as part of a master's martial art practice. A lot of it is hidden in secrecy, mystery and wuxia literature that makes the line between fact and fiction a little more than blurred.
But to dismiss it as outright mumbo-jumbo would be to miss the truth that some made up stuff is deliberately misleading to keep the "real secrets" hidden from prying eyes. The secret maybe something quite mundane and right in front of the observers' eyes, but may represent a strategic and tactical advantage to its bearer.
Sow Mee tea 壽眉茶 on one level has got nothing to do with Martial Qigong 武氣功. Then again, they share the same roots and there are Qigong exercises that involve little cups of tea being moved around the body.


My girlfriend and I are planning on getting married. However, she has racked up quite a bit of student loans(60K+). Currently, she has been on a repayment program (PAYE) with a 20 year loan forgiveness for 2 years. She makes around 30K a year and with the pay as you earn option her payments are kept low(~100/month).
If we get married, I suspect my income will be counted along side hers (combined total of 100-110K) for the loan forgiveness plans. Is that correct? Is there a way to avoid it?
This other question seems to indicate that if taxes are filled separately, then the spouses incomes are not claimed together. But the answer indicates that the policy may be dependent on the lender.
Under the PAYE income-driven repayment plan, the monthly payment is based on the borrower's Adjusted Gross Income (AGI) on his or her federal tax return. If you are filing married filing jointly (MFJ), the AGI will include both of your incomes, but if you file married filing separately (MFS), her AGI will not include your income.
The catch, of course, is that filing MFS will almost certainly result in a higher tax burden for the both of you than MFJ would.
If you file MFJ, it is possible that your combined income level will make you ineligible for the PAYE repayment plan, as the resulting monthly payment would be no less than the standard 10-year payment amount.
The idea of loan forgiveness is nice, but keep in mind that 20 years is a long time. During the whole time, you will need to worry about keeping your wife's income low (so you don't pay too much) and you need to file MFS, paying extra taxes each year.
An alternative for you is to simply decide that once you are married, you will pay off this student loan in full as quickly as you possibly can. With your combined income being well into the 6 figure range, you could conceivably pay off this loan in full in perhaps 3 years without much difficulty at all. You can file MFJ the entire time, saving money on taxes, and three years from now the debt will be out of your life and you'll have the full earning potential of both of you without worrying about whether or not it will mess up your student loan plan.
Not the answer you're looking for? Browse other questions tagged united-states student-loan repayment marriage or ask your own question.
If you're married, can you still file an income tax return as a single individual?
Can I file married filing separately if I already have a Roth IRA but no conributions?
How will getting married before the end of the year impact this year's taxes?


text:
By maja
Are you ready for the International Rome Marathon 2019
The 25th International Rome Marathon will be held this year on the first Sunday of April. On the 7th of April 2019 thousands of runners will gather in front of the Colosseum at the start line. What other place would have been better to start the race in the Eternal City than the Flavian Amphitheater?
The route of the race, as every year, will stretch around some of the most beautiful landmarks in Rome. At the very start the runners will pass by the ruins of the Roman Forum and Imperial Forums from where they will be able to notice the majestic Altare della Patria in Piazza Venezia. Then the route will follow the streets that will bring the runners to the Circus Maximus, the ancient stadium which capacity was around 120.000 spectators. The race will continue just behind the Caracalla Thermal baths and will continue down the Cristoforo Colombo street. The race will bend and will pass around St Paul's Basilica (St Paul's outside the walls). After a couple of kilometers the panorama will change and the athletes will run around the Pyramid (Piramide Cestia). This pyramid is not Egyptian, even if it was inspired by the Egyptian constructions, and it was used as the burial chamber of Gaius Cestius.
The Tiber Island (Isola Tiberina) will be soon spotted on the left hand side of the runners' route that will lead the marathon all the way along the river to the Vatican and the St Peter's Basilica.
After the Vatican, the second half of the marathon, will follow the route that reaches the Olympic Stadium and the Olympic Village, both built in the occasion of the Olympic games held in Rome in 1960. The race will continue again along the river Tiber and will reach the magnificent Piazza del Popolo with its impressive Porta del Popolo. Just few steps further the Spanish Steps square (Piazza di Spagna) will welcome the racers that will pass by the famous Bernini's fountain, La Barcaccia.
After passing by Piazza Navona, Largo Argentina (the archaeological site where Julius Caesar has been killed) the race will reach again Piazza Venezia. Here, the last efforts will be necessary, as just before the finish a short but pretty steep hill will be in sight. The road that will bring all the racers to the finish is in downhill, just around the Colosseum.
The runners of the Rome City Maraton will have a unique panorama for the race!
You can download the Marathon route here.
During the days before and after the International Rome Marathon, City Lights Tours will welcome all marathon runners, tourists, visitors and supporters with a 20% discount. At the checkout just insert RUNNERS to get your discount. You are not obliged to proof that you're running the marathon! You don't have to run! We will bring you for a nice strolls along the best places in the city!
For all the visitors in Rome, City Lights Tours will also arrange all your transfers, so you can save your energy for the race (or for a tour!).
Soon we will publish the discount code reserved for all visitors in Rome during the International Rome Marathon, stay tuned!
The (secret) Island of Montecristo
Italy's new rules for tourists (and locals!)
When in Rome, don't sit on the Spanish Steps!
#museums airport amalfi coast archaeology Art basilica carnival castelli romani exclusive food group tours guide guided tours italy marathon medieval Michelangelo museum naples roma rome Rome Tours Sicily Sistine Chapel sistine chapel guided tour skip the line special discount st peters basilica tour tours tours in rome transport travel Turin Vatican vatican city vatican city tour vatican guided tour vatican museums vatican museums tickets vatican tour vatican tours venice vip sistine chapel tour vip tour
Piazzas in Rome
transportation in rome
Walking in Rome
crome tours
discount on tours
rome city marathon
rome transport
visit rome
A ("new") Emperor Nero's house to be open to the public on the Palatine Hill
The best time to tour the Vatican, Sistine Chapel & Colosseum & Roman Forum; closures, holidays and crowded days in April 2019
All stories by:maja
With by Estrogeni SEO & Marketing Agency Roma
Indeed, bloggers do not only produce content to post on their blogs, but also build social relations with their readers and other bloggers.
We'll send you newsletters with news, tips & tricks. No spams here.

redpajama_set_name: RedPajamaCommonCrawl


Occasionally we let a gem-of-a-game slip through the cracks. And once we realize our oversight, we'll make it a point to feature the game even if it's not brand-new, and particularly during times like this when new releases are slow. One such title is On The Run, an absurdly fun little game hosted and contracted by Miniclip Games, developed by Officine Pixel. This Shockwave game is a third-person car racer, or rather chaser, as you spend the entire game being pursued by a mysterious, clandestine group of baddies called the "Corporation" that's trying to hunt you down and run you off the road.
You sport a little yellow coupe, while the bad guys have a fleet of cars, SUV's and vans, all of which stop at nothing to wreck your car and stop you from escaping. What are you escaping from? Why are you "on the run" in the first place? It's never really explained, and it doesn't need to be. The fun of this game isn't the story, it isn't the characters...it's the gameplay, plain and simple. You'll be surprised that despite all the flashy racing games available today, you can have such a blast trying to outrun and outwit your pursuers in a little Web game made a couple years ago.
You control the car using the [arrow] keys and [space] to hit the e-brake. Once the starting light turns green, you're let loose in a Euro-style city with no map, no Crazy Taxi-style arrow pointing you in the right direction. The city is unfamiliar and yours to explore, although you won't have much time to enjoy the scenery as you push the pedal to the metal, gunning it through intersections, tunnels, ramps and even down narrow alleys. You have only two things to worry about: your car's health and gas, both of which are measurable by meters at the top of the screen. Run out of gas and it's game over. Wreck your car and obviously it's game over.
You can replenish these meters with gas and repair power-up orbs, both which seem plentiful at first, but get tougher to find as you zoom farther along. Besides trying to find your way out of the city to the goal, you'll constantly have Corporation bad guys chasing you from behind, trying to ram you from the side, and even coming at you head-on as you turn corners. The intuitive strategy is to dodge them, although if you take advantage of the game's decent AI, you can trick enemy cars into crashing by hitting the brake at just the right moments, or pulling a 90-degree-turn out of the blue.
Analysis: On The Run is one of those diamonds-in-the-rough; a simple, small game that doesn't feature mind-blowing graphics or cutting-edge physics, it's just ridiculously fun to play. Your initial run may take anywhere from 15 to 45 minutes to beat the game, depending on how many times you fail. Once you've memorized the route, the game can be beat in under 10 minutes, but even that doesn't water-down the replay value. There are always alternate routes you can take and new ways to lose the bad guys. The driving mechanic is quite gratifying, featuring simple-yet-responsive steering and accurate inertia physics. (Just the traction component alone is awesome.) Collision physics can sometimes get iffy; especially when you get boxed in (your health will often drain super-quickly without an ability to escape). But if you've ever wanted to take a few minutes out of your day and pretend you're the star of an action movie during the famous car-chase scene, you'll love what this game has to offer.
Note: For those on Intel-based Macs, you will need Shockwave Player 10 and run your browser in Rosetta emulation mode to play this game.
This game is a real classic. Anyone who hasn't played it should definitely do so. Consider it a part of your 'casual game history' education.
Who actually uses the brakes in this game?
I only have one real gripe in this game, and it's that you can easily get wedged between an enemy car and something else, and have it drain you from full health to zero in ~1 second, and it can happen out of the blue (so you can be quite far along and doing well, and suddenly die with no warning).
I made it to the second train crossing, but it gave me a cutscene of the train passing through, and then said I was "captured"? What am I supposed to do?
> Note: For those on Intel-based Macs, you will need Shockwave Player 10 and run your browser in Rosetta emulation mode to play this game.
Well, I tried that too. But neither Shockwave Player 11 (in native mode) nor Shockwave Player 10 (in Rosetta) works. Either way, I get an error that "This application requires an Xtra (Havok Physics Scene) that either does not exist or failed to initialize properly".
I'm using Safari 3.1.1 on Mac OS X 10.5.3.
Peter - the Havok extra is included in Shockwave Player 10, so is it possible that your Rosetta emulation mode browser actually has the version 11 player?
Try uninstalling Player 11, then reinstalling player 10. That worked for me (Safari 3.1.1 and Mac OS X 10.5.3).
Ah, I found the problem. I'd installed Shockwave Player 11 first, and Shockwave Player 10's installer didn't completely delete it, so Safari kept using 11. So make sure you delete 11 before installing 10.
There's a bug in the Euro-style town: You can drive through the cul-de-sac and end up in empty space.
There are actually several reasons to use the brake. One of them being stopping short of an ambush, of which there are several.
Small tip....when you reach the overpass, don't actually drive up on it until you see something cool happen.
You need to drive as quickly as possible over the train tracks. If you don't get through before the bars come down, you're "captured."
It's not perfect. Sometimes it glitches. Once I even lost all of the enemy cars and did wheelies around the place.
This game ROCKS. It was the first racing game I ever liked or completed, and the beginning of my flash game addiction in early college.
Good choice for a review!
this really reminds me of that old game "streets of simcity"
this game has a POINT!?!?!?!?!
i guess it's time to try again!
because this is shockwave and making all online games "flash games" doesnt sound right.
I absolutely LOVE this game!!!! I'm like Vinny; I had no clue that this game actually HAD a point. But now that I KNOW what the point actually is, it's sooo much funner!!
What a conidence! i wanted to find this game yesterday! for all the people who haven't finished, the exit is: driving into an outside sewer, going LEFT, and passing the cross road. watch the enemys run into the bars and fly up!
This reminds me of "Need for madness" - demolition derby + racing game, in my opinion, "Need for Madness" is better, you aren't defenseless anymore, you can crash their car with yours.
I especially love how the authors "economized" by forcing you to retrace your tracks and integrated it smoothly into the gameplay via railway ramp - it makes the game longer, and it creates a nice twist by making you work against yourself although you are not even aware of it at the time (because you've picked up all the easy-to-get powerups, they will now be missing when you need them the most).
This looks like it'd be a fun game if it didn't glitch constantly. Three games in a row I got the 'no-wheel-traction' glitch. Every other time, I ended with the instant death wedge that ribs was talking about.
What a terrible, buggy, laggy, horrible game. Seriously, there's something badly badly wrong with it.
Finally this game is featured on jayisgames!!!! I've been playing it 3 years ago but the website was taken down and now I found it again!!
kinda glitchy...but nontheless fun...there is actually a way to get the baddies off your back..what i did was i went to the stone paved road area and i turned back and i somehow made the crash and i went back to the stone area..and they couldnt find me..
so in other words, they cant see you if u hide..
after i made it to the 2nd train crossing and made it through, the baddies made it through as well..and in the ending movie, they did catch me..
Finished in 4 minutes 11 seconds!
Sadly, I always get to the part where some large, somewhat colourful vehicle blocks my path and then I'm always trapped with no choice but to die.
Can anyone give a full route to how to escape? I always get stuck when i cross the bridge and go into that little village place with small streets and stuff. From then no, choice but too die. Anyone help?
Hi all...here's a short walkthrough. Feel free to explore new routes to do this, but here's the requirements for a win.
1. From the stoplight, proceed straight up the hill, avoid the SUV that comes from the left at the top.
2. Make a LEFT turn at the top of the hill and then proceed straight, passing the car lot, and the billboard. Go downhill.
3. Keep going, passing the office building and on around. You'll see on overpass. Get up on it.
4. Go through the alcove and continue through the twisty litte town road. You'll come out to a court yard.
5. Make a right-hand u-turn to exit the courtyard via another road. You'll then need to make a quick left. Go through the tunnel.
7. Make a left turn just before the railroad. Avoid the SUV that's waiting at the mouth of the tunnel. Proceed through this tunnel and collect the orb at the end of it. Proceed straight and then take your first left. You'll see the stoplight again.
8. Repeat steps 1 through 6 to get back to the railroad. Drive across the railroad and avoid the oncoming SUV ahead. Now, you'll see a garbage truck pull out, make a right turn there and go through the gate.
9. Make a gentle left to go past the building. Collect all of the orbs around this parking lot. Now drive over the dirt mound and drop into the sewer.
10. Drive as fast as possible through the sewer, narrowly avoiding the columns and the pipes that are sticking out of the sides. About 1/3 of the way through, you'll have an SUV oncoming to avoid. When you get to the end of the sewer, go up the ramp, and the make a right turn to exit the courtyard. Drive as fast as possible over the railroad and you'll just barely make it through before the gate closes, trapping your pursuers.
am i just stupid because ive been playing this game for 3 yrs now, and just now realized it had a point too.
i cant get past the 1st railway tracks, it stops everytime i go near it...help!
Oh gosh i remember playing this in elementary school . Good times.
On the Run is one of my favorite game. When ever i am playing this i will forget my timings. It is very good time pass game. I love this game thoroughly.


The Taco Solar Circulators with integral variable speed solar control integrates the advanced features of the external speed and solar controls with the dependability and ease of access of Taco's 00 cartridge circulators.
Taco Pumps for Solar Heating Systems are extremely easy to install and maintain, since all the wiring is done directly to the circulator and the LED status panel allows you to conveniently monitor and regulate the pump's functionality. The concept behind this unit is that if an appropriate delta T is maintained through the collector, then higher source temperatures can become available over longer periods of time, regardless of weather conditions. The Taco 006-VTF4 continuously optimizes the flow through the collector in order to result in a maximum energy gain. This all-in-one solar circulator can be quickly installed in several solar applications, just with the flip of a dip switch!


text:
Irak na Letnich Igrzyskach paraolimpijskich w Pekinie reprezentowało 20 zawodników.

Medale

Srebro
 Mohsin Rasool - podnoszenie ciężarów, kategoria poniżej 65 kg

Brąz
 Thaer al-Ali - podnoszenie ciężarów, kategoria poniżej 82,5 kg

Linki zewnętrzne
 Strona IPC

Państwa uczestniczące w Letnich Igrzyskach Paraolimpijskich 2008
Sport w Iraku

redpajama_set_name: RedPajamaWikipedia


text:
import windows
from . import winstructs

def bitness():
    """Return 32 or 64"""
    import platform
    bits = platform.architecture()[0]
    return int(bits[:2])

# Use windows.current_process.bitness ? need to fix problem of this imported before the creation of windows.current_process
if bitness() == 32:
    winstructs.CONTEXT = winstructs.CONTEXT32
    winstructs.PCONTEXT = winstructs.PCONTEXT32
    winstructs.LPCONTEXT = winstructs.LPCONTEXT32

    winstructs.EXCEPTION_POINTERS = winstructs.EXCEPTION_POINTERS32
    winstructs.PEXCEPTION_POINTERS = winstructs.PEXCEPTION_POINTERS32

    winstructs.SYSTEM_MODULE = winstructs.SYSTEM_MODULE32
    winstructs.SYSTEM_MODULE_INFORMATION = winstructs.SYSTEM_MODULE_INFORMATION32
else:
    winstructs.CONTEXT = winstructs.CONTEXT64
    winstructs.PCONTEXT = winstructs.PCONTEXT64
    winstructs.LPCONTEXT = winstructs.LPCONTEXT64

    winstructs.EXCEPTION_POINTERS = winstructs.EXCEPTION_POINTERS64
    winstructs.PEXCEPTION_POINTERS = winstructs.PEXCEPTION_POINTERS64

    winstructs.SYSTEM_MODULE = winstructs.SYSTEM_MODULE64
    winstructs.SYSTEM_MODULE_INFORMATION = winstructs.SYSTEM_MODULE_INFORMATION64

from . import winfuncs

redpajama_set_name: RedPajamaGithub


text:
Q: how to change values in buttons done in a loop Tkinter how to change values in buttons done in a loop?
I mean a different text, a command for each of the resulting buttons.
the program counts files in a given folder, then this value is passed to the loop that displays the appropriate number of buttons.
here is the sample text:
files = os.listdir(".")
files_len = len(files) - 1
print(files_len)

def add():
    return

for i in range(files_len):
        b = Button(win, text="", command=add).grid()

A: You don't really need to change the Button's text, because you can just put the filename in when they're created (since you can determine this while doing so).
To change other aspects of an existing Button widget, like its command callback function, you can use the universal config() method on one after it's created. See Basic Widget Methods.
With code below, doing something like that would require a call similar to this: buttons[i].config(command=new_callback).
To avoid having to change the callback function after a Button is created, you might be able to define its callback function inside the same loop that creates the widget itself.
However it's also possible to define a single generic callback function outside the creation loop that's passed an argument that tells it which Button is causing it to be called — which is what the code below (now) does.
from pathlib import Path
import tkinter as tk

win = tk.Tk()

dirpath = Path("./datafiles")  # Change as needed.
buttons = []

def callback(index):
    text = buttons[index].cget("text")
    print(f"buttons[{index}] with text {text!r} clicked")

for entry in dirpath.iterdir():
    if entry.is_file():
        button = tk.Button(win, text=entry.stem,
                           command=lambda index=len(buttons): callback(index))
        button.grid()
        buttons.append(button)

win.mainloop()

A: Try this. By making a list.
files = os.listdir(".")
files_len = len(files) - 1
print(files_len)

def add():
    return
b=[]
for i in range(files_len):
        b[i] = Button(win, text="", command=add).grid(row=i)

redpajama_set_name: RedPajamaStackExchange


This is our flagship travel product. Cover and benefits can be tailored to your client's needs. Premiums are fixed at the outset based on an estimated travel for the cover period. Spouses/Partners and Dependent Children are automatically included when accompanying Insured Persons on business trips. Cover can be extended to include the pleasure trips of named persons (and their family).


text:
Impact of external sources of infection on the dynamics of bovine tuberculosis in modelled badger populations
Joanne L Hardstaff1,
Mark T Bulling1,4,
Glenn Marion2,
Michael R Hutchings3 &
Piran C L White1
The persistence of bovine TB (bTB) in various countries throughout the world is enhanced by the existence of wildlife hosts for the infection. In Britain and Ireland, the principal wildlife host for bTB is the badger (Meles meles). The objective of our study was to examine the dynamics of bTB in badgers in relation to both badger-derived infection from within the population and externally-derived, trickle-type, infection, such as could occur from other species or environmental sources, using a spatial stochastic simulation model.
The presence of external sources of infection can increase mean prevalence and reduce the threshold group size for disease persistence. Above the threshold equilibrium group size of 6–8 individuals predicted by the model for bTB persistence in badgers based on internal infection alone, external sources of infection have relatively little impact on the persistence or level of disease. However, within a critical range of group sizes just below this threshold level, external infection becomes much more important in determining disease dynamics. Within this critical range, external infection increases the ratio of intra- to inter-group infections due to the greater probability of external infections entering fully-susceptible groups. The effect is to enable bTB persistence and increase bTB prevalence in badger populations which would not be able to maintain bTB based on internal infection alone.
External sources of bTB infection can contribute to the persistence of bTB in badger populations. In high-density badger populations, internal badger-derived infections occur at a sufficient rate that the additional effect of external sources in exacerbating disease is minimal. However, in lower-density populations, external sources of infection are much more important in enhancing bTB prevalence and persistence. In such circumstances, it is particularly important that control strategies to reduce bTB in badgers include efforts to minimise such external sources of infection.
A common factor complicating the control of livestock diseases is that many such diseases are capable of infecting multiple wildlife hosts [1–3]. One of the most persistent diseases with a wide host range is bovine tuberculosis (bTB), which is caused by the bacterium Mycobacterium bovis and is a major concern to the livestock industry in many countries, including the UK [4]. The existence of wildlife hosts has reduced the success of bTB control programmes in certain countries. In Europe, bTB occurs in a wide range of species [3, 5]. Commonly affected wildlife species are wild boar (Sus scrofa), red deer (Cervus elaphus), fallow deer (Dama dama), roe deer (Capreolus capreolus), badgers (Meles meles) and red foxes (Vulpes vulpes) [5].
In Britain and Ireland, badgers are particularly important in enabling the persistence of bTB in cattle [6]. Badger populations are structured socially and spatially in a territorial system, but the size of groups varies considerably, largely as a consequence of habitat quality [7, 8]. Group sizes in Britain tend to be higher than in continental Europe, particularly in local areas with a history of persistent bTB in cattle. For example, group sizes in south-west Britain, a region of high bTB prevalence, range between 3–10 individuals [9], with exceptional group sizes up to 27 individuals [10]. These compare with group sizes of 2–7 in Poland and Spain [11, 12] and 6–8 in Portugal [13]. Studies using epidemiological models suggest a threshold group size of around 6–8 individuals is required to enable bTB to persist in badger populations in Britain in the absence of external infection [14–16]. However, bTB can persist where badger group sizes are below such levels, as is the case in Ireland where the mean badger group size has been estimated to be 3.9 (3.41-4.45) badgers per sett [17] with a different study observing a range of 1–14 badgers per sett [18]. The persistence of disease at lower population levels may be enabled by variations in the social structure of the badger host population in different situations [19]. However, it may also be enabled by the existence of infection within a wider host community, including livestock, which through either direct or environmental transmission of the infection to badgers may effectively lower the threshold population density required for disease persistence. Such external sources of infection, originating from outside the focal host species, are thought to be one of the mechanisms underlying the persistence of canine distemper in Yellowstone National Park [20] and enables the disease to be transmitted among neighbouring populations, such as from grasshopper mice (Onychomys leucogaster) to prairie dog (Cynomys ludovicianus) populations [21]. It is also thought that external, but as yet unexplained, sources of infection are responsible for the high levels of bTB in the New Zealand feral pig population [22]. Understanding the impact of sources external to the badger population on the dynamics and persistence of bTB is therefore important for the development of more effective and targeted bTB control strategies.
In this paper, we use a spatial, stochastic simulation model to examine the relative effect of badger group size, internal (badger intra- and inter-group) infection rates, and infection from external sources (i.e. non-badger) on the prevalence and persistence of bTB within badger populations across a wide range of equilibrium group sizes found in Europe. We use two different modelling scenarios. Scenario 1 considers solely badger-derived infection and scenario 2 considers both badger-derived and trickle-type infection from external sources of infection.
This section summarises the full sensitivity analysis, which is presented in the Additional file 1. Colonisation and dispersal were the most importance influences on mean group size in the absence of external infection, accounting for 21% and 15% respectively of variations in group size at an equilibrium group size of 8. Colonisation and dispersal by females had a slightly greater impact than colonisation and dispersal by males, especially for smaller group sizes, probably because of the more direct impact that females have on the group's reproductive potential. As equilibrium group size increases, a group is more likely to contain more than a critical number of females, and hence the relative importance of the female parameters in influencing group size and prevalence declines. As rates of external infection increase, colonisation becomes less important in influencing group size. For example, the influence of adult female colonisation on variation in group size for an equilibrium group size of 4 decreased from 49% to 30% as the rate of external infection increased from 0.0001 to 0.01. However, as rates of external infection increased, disease-related parameters such as intra-group transmission and the rate at which badgers changed between infectious and latent states, assumed greater importance in affecting group size. For example, the influence of the transfer of females from a latent to infectious state at an equilibrium group size of 4 increased from 0.06% at an external infection probability of 0.0001 to 30% at an external infection probability of 0.01.
Intra-group transmission was the dominant disease-related parameter overall in terms of its effect on prevalence, accounting for between 30% and 78% of the variation in prevalence for equilibrium group sizes of 4, 8 and 12 at all external infection probabilities. Its influence was greatest for the higher group sizes (8 and 12). The importance of intra-group infection reflects the spatio-temporally persistent nature of bTB in badger populations, and is representative of a disease that is generally maintained through interactions within rather than between groups. At lower group sizes, at or just below the threshold population density for disease persistence, the parameters of infection itself, such as disease-induced mortality and the rates of transfer between different infectious states, became more important in influencing prevalence. In the absence of disease, the badger population persisted at all group sizes, although the inclusion of disease at the smallest equilibrium group size of 2 did contribute to the extinction of the badger population in up to 8% of scenario simulations at this group size. Populations did not go extinct at any higher group sizes under either scenario.
Badger-derived infection only (scenario 1)
With infection derived solely from within the badger population, higher prevalences were obtained with higher equilibrium group sizes (Figure 1a), and increased non-linearly with an increase in equilibrium group size, after equilibrium group sizes reached 6. There was a clear threshold group size of around 6–8 individuals required for the disease to persist in the population (Figure 1b). At an equilibrium group size of 8 individuals, the disease persisted in all simulation runs (Figure 1b) at a mean prevalence of 5%, and for an equilibrium group size of 12, the mean prevalence was 36%.
Relationships of (a) mean prevalence and (b) percentage of model runs in which disease has persisted as a function of equilibrium group size. The thick line shows badger-derived infection only and the thin black lines show combined badger-derived and external sources of infection (scenario 2) with probabilities of 0.0001 (thin dotted line), 0.001 (thin dashed line) and 0.01 (thin solid line). Vertical bars denote 95% confidence intervals.
When disease became established in the population, at an equilibrium group size of 6 or above, intra-group transmission events dominated the dynamics of disease (Figure 2). The relative importance of intra-group to inter-group transmission events declined slowly as group size increased.
The ratio of intra to inter-group infection rates for different sources of infection where disease persisted. The graph shows badger-derived infection (scenario 1; solid bars) compared with badger-derived and externally-derived infection (scenario 2; dotted bars). For scenario 2, the low density-dotted bars represent an externally-derived transmission probability of 0.0001, the medium density-dotted bars represent a probability of 0.001 and the high density-dotted bars represent a probability of 0.01. 95% confidence intervals are also shown. For a group size of 4, infection did not persist unless the probability of externally-derived infection was at least 0.001.
Badger-derived and external infections combined (scenario 2)
The lowest probability of external infection (0.0001) had a negligible effect on the mean prevalence of the disease compared with badger-derived infection alone (Figure 1a). A marked increase in mean prevalence was only obtained with the highest probability of external infection (0.01). For an equilibrium group size of 8, the mean prevalence was 19% at an external infection probability of 0.01, compared with between 2% and 4% for lower external infection probabilities of 0.001 and 0.0001. However, external infection at all levels had a much greater impact on disease persistence. Even the lowest probability of external infection (0.0001) enabled the disease to persist much more readily in populations with a mean group size below the badger-only infection threshold density (Figure 1b). With higher probabilities of external infection (0.001 and 0.01), this effect became more pronounced. The relative impact of external infection in increasing disease persistence and prevalence was greatest at or around, and particularly just below, the equilibrium group size. At an equilibrium group size of 4 individuals, disease persisted in only 15% of simulations when infection was solely badger-derived. However, when badger-derived infection was supplemented by external infection, disease persisted in 75% of simulations at the lowest external infection probability (0.0001), and persisted in all simulations at the intermediate (0.001) and highest probabilities (0.01) of external infection (Figure 1b).
When disease became established in the population as a consequence of both badger-derived and external infection, the relative pattern of intra- and inter-group transmission was similar to that obtained with badger-derived infection alone, with the relative importance of intra-group to inter-group transmission events declining as group size increased beyond the threshold group size of 6. However, with the two highest probabilities of external infection (0.001 and 0.01), the relationship was shifted to the left (Figure 2) with a significant number of intra-group transmission events now occurring at equilibrium group size of 4.
Our results are consistent with those from other computer models that support the existence of a threshold group size for the persistence of bTB in badger populations at around 6–8 adults per group [14–16]. The general increases in prevalence with group size, albeit it in a non-linear pattern, also support the broader literature on the dynamics of disease in a range social host species [23]. However, recent empirical work has found a negative relationship between bTB prevalence and badger abundance, with prevalence highest in smaller social groups and at lower population densities [24]. The most plausible hypothesis to explain this finding is that badger contact behaviour changes according to group size, and greater mobility of badgers between groups at lower population densities may result in a higher proportion of contacts leading to disease transmission [24]. However, there are no behavioural data available from free-living badger populations at low densities to test this hypothesis or to re-parameterise the model. In the absence of such data, the model assumed that individual badgers at all densities exhibited the behaviour patterns recorded in a moderate-density population [25], and this assumption probably explains the predicted increases in prevalence with group size in the model. A relatively higher frequency of contacts between badgers at lower densities would have the effect of lowering the threshold for disease persistence in much the same way as increased external transmission does, and thus the predictions of the model for lower social group sizes should be treated with caution, and considered as lower bounds in terms of disease persistence and prevalence.
The addition of external trickle-type infection in the model decreased the threshold group size for bTB persistence [26], allowing for persistence in smaller group sizes, and raised the prevalence in larger group sizes. It enabled an increase in prevalence to occur in already infected populations that consisted of larger group sizes. The driver for this was an increase in intra-group transmission rates. However, this effect was not consistent across all group sizes, and relatively greater impacts were achieved at lower group sizes, particularly just below the threshold level. At these lower group sizes, there is a more heterogeneous distribution of infection across groups, and hence it is more likely that external infection will result in disease being introduced into fully susceptible groups that do not have contiguous borders with infected groups. Following introduction of disease into susceptible groups, the relatively higher rates of intra-group transmission lead to higher levels of disease. These results suggest that only relatively minor changes in intra-group contact behaviour at lower densities may be sufficient to have a significant impact on the persistence of bTB in lower-density populations. With high levels of external infection, bTB is thus able to persist in smaller badger social groups commonly found within Europe [27], as well as in Ireland [18]. In these situations, badger populations are likely to be fragmented, and external infections may provide a means for infection to reach those groups which would otherwise have been relatively isolated from dispersing individuals from other sub-populations.
External infections of badger populations may arise from livestock, other wildlife or environmental sources. For example, deer can shed M. bovis in faecal matter and nasal mucous [28] which can contaminate the environment, and cattle can shed M. bovis through nasal mucous [29] that can contaminate water sources [30]. In larger badger group sizes, for example above 10–12, as are found in parts of south-west England where bTB is believed to be endemic in the badger population [31], external infection is not required for disease persistence. Nevertheless, even in these situations, significant external infection can cause increases in prevalence when there is endemic disease. Where these external sources of infection include maintenance hosts, disease control strategies should include management of these other potential sources of disease. However, effective control of bTB in the badger population may also help to reduce the significance of these external sources, especially if the other species are acting solely as spillover hosts [32]. With larger group sizes, even occasional infectious disease contact can cause low levels of disease to persist, thereby complicating control measures.
Studies on bTB in other wildlife in south-west England have found several other wildlife species to be infected with bTB, for example various rodent species, foxes, red deer, roe deer, fallow deer and muntjac (Muntiacus reevesi) [33]. However, only some of the affected species excrete bTB and are therefore capable of contributing to a pool of external infection. Of the affected species, only fallow deer and muntjac, at densities of over 56 per km2 and 47 per km2 respectively, are likely to act as maintenance hosts [32]. Spillover host status may be provided by roe deer, red deer, muntjac and fallow deer at lower densities [32, 34]. However, the capacity of these species to maintain the disease as part of a multi-species host community has yet to be explored, and it may provide further opportunities for external infection to the badger population, as well being able to act as a spillover for bTB from badgers. Moreover, the presence of multispecies hosts of disease increases the possibility of contact across a wider variety of habitats due to a range of differences between species including foraging and dispersal distances. For example, the foraging distance of a badger may only reach 250 m whereas the foraging distance of a roe deer doe may be more than 1800 m [35, 36].
It is likely that a low level of seeding from external sources, for example external seeding from infected livestock and/or from infected environmental sources such as water, food and soil [37] occurs in many areas where bTB persists in wildlife populations around the world. In Northern Michigan, a survey of wildlife for M.bovis infection discovered infected opossums (Didelphis virginianus) and a grey fox (Urocyon cinereoargenteus) which had been located on bTB-depopulated cattle farms [38]. M. bovis has been recovered from soil samples [39], badger setts and badger latrines [40] in areas with infected badgers, and has shown to be able to survive for long periods of time within soil [41] and on the forest floor in areas of high possum (Trichosurus vulpecula) density [42]. Our analysis of external infection of bTB in badgers has shown that low levels of external infection alone are relatively unimportant compared with disease processes internal to the host population in determining the persistence of bTB in badgers above the threshold group size. However, at lower group sizes, as occur throughout many areas where bTB persists in cattle, external sources of infection are likely to assume a much greater significance. This may account for bTB infection in badgers in Switzerland, France and Spain [27, 43]. For example, bTB persists in badger populations in Ireland despite an average group size of 3.9 badgers [17]. All else being equal, a greater level of external infection would be required to maintain bTB in badgers in Ireland, because of the smaller badger group sizes, than is the case in Britain, where group sizes are frequently well above the threshold level predicted by the model. However, our results suggest that the Irish situation is also more sensitive to the effects of external infection than that in Britain, since the group size in Ireland is within a critical range just below the threshold for disease persistence, where the potential role of any external sources is magnified. In Ireland, bTB persistence is therefore likely to be a consequence of a combination of badger-derived infection, infection from livestock and from other environmental sources [44, 45], as well as possible differences in badger behaviour at lower densities [24]. In many parts of Britain, especially where badger densities are higher, bTB is likely to be maintained simply through badger-derived infection.
The control of bTB has been based historically on the testing and slaughter of infected cattle, or taken a dual approach, combining a test-and-slaughter policy with wildlife culling [46, 47]. Culling of badgers may result in more dispersal of individuals, with the potential to lead to a perturbation effect (higher bTB as a consequence of disruption to the badger social system due to badger culling [48, 49]). However, the extent of the any perturbation effect is likely to depend on both the extent of behavioural change in the badger population relative to the previous situation, as well as on the relative dependence of the disease system on badger-derived infection compared with cattle-derived infection. Perturbation is more likely to occur where bTB persistence is predominantly badger-derived, and where the effects of culling are to cause significant changes in behavioural patterns.
Our work suggests that the effectiveness of bTB control through badger culling is therefore dependent on the interplay between badger population density and group size (which determine social behaviour and the likely extent of any perturbation effect), and the presence and significance of external sources of infection. As badger populations are decreased by culling, especially where initially high-density populations are reduced significantly, disease may transiently increase due to a perturbation effect. Where a disease problem is still present in the cattle, disease may continue to persist, or even resurge, due to the role of cattle-derived infection in the system [50, 51], and this may be exacerbated by longer-term changes in the behaviour of the badger population. Any culling-based strategy to reduce bTB in badgers therefore needs to aim to reduce badger populations to not only below the level at which perturbation effects on disease are most pronounced, but also below the critical range where the disease in badgers can be maintained by trickle-type infection from other sources in the ecosystem.
Our analysis has shown that additional sources of infection, such as other infected bTB-excreting wildlife, environmental contamination, and cattle failing to test positive and being removed from a farm due to imperfect test sensitivity [52] will reduce the effectiveness of disease management. In our model, external trickle-type infection only occurred during the summer season. Whilst the overall amount of external infection in the system is unknown, it may also occur at other times of the year, especially where badgers enter farm buildings frequently [53]. The addition of external infection at other times of the year would further enhance its role in enabling bTB persistence in badger populations at sub-threshold densities. This highlights the need for integrated strategies for bTB management, addressing both the livestock-wildlife host system and other environmental sources of infection, to reduce the risk of bTB in badger populations.
Model structure and parameters
We used a spatial simulation model following the structure of that in White and Harris [15]. This model shares the same general form as the badger-bTB model produced by the Food and Environment Research Agency [14, 16, 54] and used by the Department of Environment, Food and Rural Affairs (Defra) to inform the management of bTB in badgers in England. The models have produced similar predictions regarding the ecology and management of bTB in badger populations, including the identification of a threshold badger group size of around 6–8 individuals for disease persistence.
The White and Harris model was adapted to allow continued infection from external sources and enable different forms of disease control (Figure 3). Space in the model was represented by a grid of square cells (12 x 12), with each cell representing a badger territory. Within a territory, the numbers of individuals in each age (cub, yearling, adult), sex (male, female) and disease state (susceptible, latent, infectious) category were tracked through time. The model was stochastic, with progression of disease between susceptible, latent and infectious states based on probabilities derived from the literature (Table 1). For each potential transition between disease states, a random number between 0 and 1 was generated and the transition occurred if that number was less than or equal to the specific probability. Transmission of infection could occur within territories (intra-group transmission) or between neighbouring territories (inter-group transmission), where a neighbour was a contiguous territory either directly to the north, east, south or west of the focus territory. Data for intra- and inter-group infections were derived from studies using proximity data loggers and thus do not represent records of actual transmission events. As a consequence, transmission via these routes may be overestimated in the model, although there are no data on transmission events within free-living badger populations that can be used to quantify the extent of any overestimation. The structure of the model allowed inter-group transmission only with immediate neighbours or via dispersal, although inter-group contacts with non-neighbours were occasionally recorded via the field data. However, since inter-group contacts are rare and were not identified as important within the sensitivity analysis, this impact of this minor difference on the results of the model is likely to have been minimal.
Structure of the model showing disease dynamics. The dotted line indicates the separation between adjacent cells of the model which represent the boundary between two adjacent badger territories to demonstrate movement of individuals of different infectious states between groups. The additional compartments of birth, natural death and mortality from bTB are also included below the line to show how individuals enter and leave the population, and these processes are common to all cells in the model. The short hashed lines represent disease transmission events, thick continuous lines represent state transitions colonisation or dispersal events and thin continuous lines represent demographic processes.
Table 1 The parameters originally used in the model
Data from the simulations were obtained from the central 10 x 10 territories only, in order to avoid biases due to edge effects. Time in the simulation progressed in discrete iterations corresponding to the four seasons in a year of equal duration i.e. three months. A second layer to the simulation represented the habitat quality of each territory in the form of a carrying capacity, with the link between this and badger group size being established through density-dependent cub mortality [15]. The balance between fecundity and cub mortality was calibrated in an initial series of runs under a range of habitat qualities (equilibrium group sizes 2 to 12, representing the full range of group sizes recorded in Europe), to establish the parameter values that maintained the required equilibrium group sizes. Assumptions within the model were as follows: only adult females can breed; breeding is unaffected by disease status; dispersal is by adults and to contiguous territories only; all cubs are born susceptible to disease; there is no vertical or pseudo-vertical disease transmission; and there is homogeneous mixing within social groups. The impact of culling was not explored in these scenarios.
We used boosted regression trees to determine which parameters had the greatest influence on badger group size and disease prevalence for group sizes 4, 8 and 12. These analyses were carried out using the 'R' statistical and programming environment (R 2.7.0, R Development Core Team 2010).
Modelling the different scenarios
Initially, we ran the model across a range of equilibrium group sizes (2 to 12 individuals per group in increments of 2), with the initial equilibrium group size being identical across the grid at the start of each simulation. The model was run for 50 years (200 seasons) to allow the populations to stabilise according to the pre-determined equilibrium group size [15]. Then, we introduced infection in different ways as described below and allowed 25 years for the disease dynamics to stabilise. Data were then recorded for the following 50 years. Each model configuration was run 50 times. We recorded the following data every 'summer' season: group size; number of empty/filled territories (grid cells); number of intra-group infections; number of inter-group infections; number of external infections; and number of infectious groups.
For scenario 1 (solely badger-derived infection), bTB was introduced in the form of a single infected badger in a single group, selected at random. For scenario 2 (badger-derived infection, supplemented by trickle-type infection from an external source), bTB was introduced as in scenario 1, but then supplemented by trickle-type infection across the whole grid on an annual basis (once each year during the summer). Summer was chosen as it represents the season with the greatest risk of transmission from external sources, due to cattle returning to pasture in late spring and summer, combined with increases in badger territory sizes and foraging activity in summer [8]. The simulations were run with the probability of external transmission set at 0.0001, 0.001 and 0.01 per season for each susceptible individual.
Analysis of results
We calculated the means, standard deviations and 95% confidence intervals for prevalence, intra-group infection rate, inter-group infection rate, the number of external infectious contacts, the number of empty territories and the number of infected groups based on the final 50 years of the simulations. Outputs from simulations using lower equilibrium group sizes (2–6) were non-parametrically distributed, although the larger equilibrium group sizes yielded parametric data.
Cleaveland S, Laurenson MK, Taylor LH: Diseases of humans and their domestic mammals: pathogen characteristics, host range and the risk of emergence. Phil Trans R Soc Lond B. 2001, 356: 991-999. 10.1098/rstb.2001.0889.
Daszak P, Tabour GM, Epstein J, Plowright R: Conservation medicine and a new agenda for emerging diseases. Annals New York Acad Sci. 2004, 1026: 1-11. 10.1196/annals.1307.001.
Gortazar C, Ferroglio E, Hofle U, Frolich K, Vicente J: Diseases shared between wildlife and livestock: a European perspective. Eur J Wildl Res. 2007, 53: 241-256. 10.1007/s10344-007-0098-y.
Delahay RJ, Cheeseman CL, Clifton-Hadley RS: Wildlife disease reservoirs: the epidemiology of Mycobacterium bovis infection in the European badger (Meles meles) and other British mammals. Tuberculosis. 2001, 81: 43-49. 10.1054/tube.2000.0266.
European Food Safety Authority: The community summary report on trends and sources of zoonoses and zoonotic agents in the European Union in 2007. The EFSA Journal. 2009, http://www.efsa.europa.eu/de/scdocs/doc/223r.pdf.
Krebs JR, Anderson RM, Clutton-Brock T, Donnelly CA, Frost S, Morrison WI, Woodroffe R, Young D: Badgers and bovine TB: Conflicts between conservation and health. Science. 1998, 279: 817-818. 10.1126/science.279.5352.817.
Da Silva J, Woodroffe R, Macdonald DW: Habitat, food availability and group territoriality in the European badger, Meles meles. Oecologia. 1993, 95: 558-564.
Palphramand KL, Newton-Cross G, White PCL: Spatial organization and behavior of badgers (Meles meles) in a moderate-density population. Behav Ecol Sociobiol. 2007, 61: 401-413.
Delahay RJ, Langton S, Smith GC, Cheeseman CL: The spatio-temporal distribution of Mycobacterium bovis (bovine tuberculosis) infection in a high-density badger population. J Anim Ecol. 2000, 69: 428-441. 10.1046/j.1365-2656.2000.00406.x.
Rogers LM, Cheeseman CL, Mallinson PJ, Clifton-Hadley R: The demography of a high-density badger (Meles meles) population in the southwest of England. J Zool. 1997, 242: 705-728. 10.1111/j.1469-7998.1997.tb05821.x.
Revilla E, Palomares F: Spatial organization, group living and ecological correlates in low-density populations of Eurasian badgers, Meles meles. J Anim Ecol. 2002, 71: 497-512. 10.1046/j.1365-2656.2002.00617.x.
Kowalczyk R, Zalewski A, Jedrzejewska B, Jedrzejewski W: Spatial organization and demography of badgers (Meles meles) in Bialowieza Primeval Forest, Poland, and the influence of earthworms on badger densities in Europe. Can J Zool. 2003, 81: 74-87. 10.1139/z02-233.
Rosalino LM, Macdonald DW, Santos-Reis M: Spatial structure and land-cover use in a low-density Mediterranean population of Eurasian badgers. Can J Zool. 2004, 82: 1493-1502. 10.1139/z04-130.
Smith GC, Richards MS, Clifton-Hadley RS, Cheeseman CL: Modelling bovine tuberculosis in badgers in England: Preliminary results. Mammalia. 1995, 59: 639-650.
White PCL, Harris S: Bovine tuberculosis in badger (Meles meles) populations in south-west England: the use of a spatial stochastic simulation model to understand the dynamics of the disease. Phil Trans R Soc Lond B. 1995, 349: 391-413. 10.1098/rstb.1995.0126.
Smith GC, Cheeseman CL, Clifton-Hadley RS: Modelling the control of bovine tuberculosis in badgers in England: culling and the release of lactating females. J Appl Ecol. 1997, 34: 1375-1386. 10.2307/2405255.
Sleeman DP, Davenport J, More SJ, Clegg TA, Collins JD, Martin SW, Williams DH, Griffin JM, O'Boyle I: How many Eurasian badgers Meles meles L. are there in the Republic of Ireland. Eur J Wildl Res. 2009, 55: 333-334. 10.1007/s10344-008-0244-1.
Olea-Popelka FJ, Griffin JM, Collins JD, McGrath G, Martin SW: Bovine tuberculosis in badgers in four areas in Ireland: does tuberculosis cluster?. Prev Vet Med. 2003, 59: 103-111. 10.1016/S0167-5877(03)00055-2.
Hutchings MR, White PCL: Mustelid scent-marking in managed ecosystems: implications for population management. Mammal Rev. 2000, 30: 157-169. 10.1046/j.1365-2907.2000.00065.x.
Almberg ES, Cross PC, Smith DW: Persistence of canine distemper virus in the Greater Yellowstone Ecosystem's carnivore community. Ecol Appl. 2010, 20: 2058-2074. 10.1890/09-1225.1.
Salkeld DJ, Salathe M, Stapp P, Holland-Jones J: Plague outbreaks in prairie dog populations explained by percolation thresholds of alternate host abundance. PNAS. 2010, 107: 14247-14250. 10.1073/pnas.1002826107.
Nugent G: Maintenance, spillover and spillback transmission of bovine tuberculosis in multi-host complexes: A New Zealand case study. Vet Microbiol. 2011, 151: 34-42. 10.1016/j.vetmic.2011.02.023.
Côté IM, Poulin R: Parasitism and group size in social animals – a meta-analysis. Behav Ecol. 1995, 6: 159-165. 10.1093/beheco/6.2.159.
Woodroffe R, Donnelly CA, Wei G, Cox DR, Bourne FJ, Burke T, Butlin RK, Cheeseman CL, Gettinby G, Gilks P, Hedges S, Jenkins HE, Johnston WT, McInerney JP, Morrison WI, Pope LC: Social group size affects Mycobacterium bovis infection in European badgers (Meles meles). J Anim Ecol. 2009, 78: 818-827. 10.1111/j.1365-2656.2009.01545.x.
Böhm M, Hutchings MR, White PCL: Contact networks in a wildlife-livestock host community: identifying high-risk individuals in the transmission of bovine TB among badgers and cattle. PLoS One. 2009, 4 (4): e5016-10.1371/journal.pone.0005016.
Cohen T, Colijn C, Finklea B, Murray M: Exogenous re-infection and the dynamics of tuberculosis epidemics: local effects in a network model of transmission. J R Soc Interface. 2007, 4: 523-531. 10.1098/rsif.2006.0193.
Martin-Atance P, Leon-Vizcaino L, Palomares F, Revilla E, Gonzalez-Candela M, Calzada J, Cubero-Pablo MJ, Delibes M: Antibodies to Mycobacterium bovis in wild carnivores from Donana national park (Spain). J Wildl Dis. 2006, 42: 704-708.
Lugton IW, Wilson PR, Morris RS, Nugent G: Epidemiology and pathogenesis of Mycobacterium bovis infection of red deer (Cervus elaphus) in New Zealand. New Zeal Vet J. 1998, 46: 147-156. 10.1080/00480169.1998.36079.
McCorry T, Whelan AO, Welsh MD, McNair J, Walton E, Bryson DG, Hewinson RG, Vordermeier HM, Pollock JM: Shedding of Mycobacterium bovis in the nasal mucus of cattle infected experimentally with tuberculosis by the intranasal and intratracheal routes. Vet Rec. 2005, 157: 613-618.
Michel AL, De Klerk L, Van Pittius NC, Warren RM, Van Helden PD: Bovine tuberculosis in African buffaloes: observations regarding Mycobacterium bovis shedding into water and exposure to environmental mycobacteria. BMC Vet Res. 2007, 3: 23-30. 10.1186/1746-6148-3-23.
Cheeseman CL, Wilesmith JW, Stuart FA: Tuberculosis: the disease and its epidemiology in the badger, a review. Epidemiol Inf. 1989, 103: 113-125. 10.1017/S0950268800030417.
Ward AI, Smith GC: Predicting the status of wild deer as hosts of Mycobacterium bovis infection in Britain. Eur J Wildl Res. 2012, 58: 127-135. 10.1007/s10344-011-0553-7.
Delahay RJ, Smith GC, Barlow AM, Walker N, Harris A, Clifton-Hadley RS, Cheeseman CL: Bovine tuberculosis infection in wild mammals in the South-West region of England: A survey of prevalence and a semi-quantitative assessment of the relative risks to cattle. Vet J. 2007, 173: 287-301. 10.1016/j.tvjl.2005.11.011.
Ward AI, Smith GC, Etherington TR, Delahay RJ: Estimating the risk of cattle exposure to tuberculosis posed by wild deer relative to badgers in England and Wales. J Wildl Dis. 2009, 45: 1104-1120.
Garnett BT, Delahay RJ, Roper TJ: Ranging behaviour of European badgers (Meles meles) in relation to bovine tuberculosis (Mycobacterium bovis) infection. Appl Anim Behav Sci. 2005, 94: 331-340. 10.1016/j.applanim.2005.02.013.
Chapman N, Claydon K, Claydon M, Forde PG, Harris S: Sympatric populations of muntjac (Muntiacus reevesi) and Roe deer (Capreolus capreolus): a comparative analysis of their ranging behaviour, social aggregation and activity. J Zool. 1993, 229: 623-640. 10.1111/j.1469-7998.1993.tb02660.x.
Palmer MV, Whipple DL: Survival of Mycobacterium bovis on feedstuffs commonly used as supplemental feed for white-tailed deer (Odocoileus virginianus). J Wildl Dis. 2006, 42: 853-858.
Witmer G, Fine AE, Gionfriddo J, Pipas M, Shively K, Piccolo K, Burke P: Epizootiologic survey of Mycobacterium bovis in wildlife and farm environments in Northern Michigan. J Wildl Dis. 2010, 46: 368-378.
Sweeney FP, Courtenay O, Hibberd V, Reilly LA, Wellington EMH: Immunomagnetic recovery of Mycobacterium bovis from naturally infected environmental samples. Lett Appl Microbiol. 2006, 43: 364-369. 10.1111/j.1472-765X.2006.01983.x.
Sweeney FP, Courtenay O, Hibberd V, Hewinson RG, Reilly LA, Gaze WH, Wellington EMH: Environmental monitoring of Mycobacterium bovis in badger faeces and badger sett soil by real-time PCR, as confirmed by immunofluorescence, immunocapture and cultivation. Appl Env Microbiol. 2007, 73: 7471-7473. 10.1128/AEM.00978-07.
Young JS, Gormley E, Wellington EMH: Molecular detection of Mycobacterium bovis and Mycobacterium bovis BCG (Pasteur) in soil. Applied and Environmental Mircrobiology. 2005, 71: 1946-1952. 10.1128/AEM.71.4.1946-1952.2005.
Jackson R, De Lisle GW, Morris RS: A study of the environmental survival of Mycobacterium bovis on a farm in New Zealand. New Zeal Vet J. 1995, 43: 346-352. 10.1080/00480169./1995.35918.
Zanella G, Durand B, Hars J, Moutou F, Garin-Bastuli B, Duvauchelle A, Ferme M, Karoui C, Boschiroli ML: Premier foyer de tuberculose a M. bovis dans une population de cerfs et de sangliers sauvages en France. Bull Epidemiol. 2008, 29: 1-5.
Young JS, Gormley E, Wellington EMH: Molecular detection of Mycobacterium bovis and Mycobacterium bovis BGC (Pasteur) in soil. Appl Environ Microbiol. 2005, 71: 1936-1952.
Sweeney FP, Courtenay O, Ul-Hassan A, Hibberd V, Reilly LA, Wellington EMH: Immunomagnetic recovery of Mycobacterium bovis from naturally infected environmental sample. Lett Appl Microbiol. 2006, 43: 364-369. 10.1111/j.1472-765X.2006.01983.x.
Donnelly CA, Woodroffe R, Cox DR, Bourne FJ, Cheeseman CL, Clifton-Hadley RS, Wei G, Gettinby G, Gilks P, Jenkins H, Johnston WT, Le Fevre AM, McInerney JP, Morrison WI: Positive and negative effects of widespread badger culling on tuberculosis in cattle. Nature. 2006, 439: 843-846. 10.1038/nature04454.
Mairtin DO, Williams DH, Griffin JM, Dolan LA, Eves JA: The effect of a badger removal programme on the incidence of tuberculosis in an Irish cattle population. Prev Vet Med. 1998, 34: 47-56. 10.1016/S0167-5877(97)00067-6.
Donnelly CA, Woodroffe R, Cox DR, Bourne FJ, Gettinby G, Le Fevre AM, McInerney JP, Morrison WI: Impact of localised badger culling on tuberculosis incidence in British cattle. Nature. 2003, 426: 834-837. 10.1038/nature02192.
Jenkins HE, Woodroffe R, Donnelly CA, Cox DR, Johnston WT, Bourne FJ, Cheeseman CL, Clifton-Hadley RS, Gettinby G, Gilks P, Hewinson RG, McInerney JP, Morrison WI: Effects of culling on spatial associations of Mycobacterium bovis infections in badgers and cattle. J Appl Ecol. 2007, 44: 897-908. 10.1111/j.1365-2664.2007.01372.x.
White PCL, Benhin J: Factors influencing the incidence and scale of bovine tuberculosis in cattle in Southwest England. Prev Vet Med. 2004, 63: 1-7. 10.1016/j.prevetmed.2004.02.003.
Woodroffe R, Donnelly CA, Jenkins HE, Johnston WT, Cox DR, Bourne FJ, Cheeseman CL, Delahay RJ, Clifton-Hadley RS, Gettinby G, Gilks P, Hewinson RG, McInerney JP, Morrison WI: Culling and cattle controls influence tuberculosis risk for badgers. Proc Natl Acad Sci. 2006, 103: 14713-14717. 10.1073/pnas.0606251103.
Clegg TA, More SJ, Higgins IM, Good M, Blake M, Williams DH: Potential infection-control benefit for Ireland from pre-movement testing of cattle for tuberculosis. Prev Vet Med. 2008, 84: 91-11.
Tolhurst BA, Delahay RJ, Walker NJ, Ward AI, Roper TJ: Behaviour of badgers (Meles meles) in farm buildings: Opportunities for the transmission of Mycobacterium bovis to cattle?. Appl Anim Behav Sci. 2009, 117: 103-113. 10.1016/j.applanim.2008.10.009.
Wilkinson D, Smith GC, Delahay RJ, Cheeseman CL: A model of bovine tuberculosis in the badger Meles meles: an evaluation of different vaccination strategies. J Appl Ecol. 2009, 41: 492-501.
Woodroffe R, Macdonald DW, da Silva J: Dispersal and philopatry in the European badger, Meles meles. J Zool. 1995, 237: 227-239. 10.1111/j.1469-7998.1995.tb02760.x.
Cresswell WJ, Harris S, Cheeseman CL, Mallinson PJ: To breed or not to breed: an analysis of the social and density-dependent constraints on the fecundity of female badgers (Meles meles). Phil Trans R Soc Lond B. 1992, 338: 393-407. 10.1098/rstb.1992.0157.
Wilkinson D, Smith GC, Delahay RJ, Rogers LM, Cheeseman CL, Clifton-Hadley RS: The effects of bovine tuberculosis (Mycobacterium bovis) on mortality in a badger (Meles meles) population in England. J Zool. 2000, 250: 389-395. 10.1111/j.1469-7998.2000.tb00782.x.
This work was supported by the EU (project number 212414). SAC and BioSS receive support from the Scottish Government.
Environment Department, University of York, York, YO10 5DD, UK
Joanne L Hardstaff, Mark T Bulling & Piran C L White
Biomathematics and Statistics Scotland, James Clerk Maxwell Building, Kings Buildings, Edinburgh, EH9 3HH, UK
Glenn Marion
Disease Systems, Scottish Agricultural College, West Mains Road, Edinburgh, EH9 3JG, UK
Michael R Hutchings
Biological Sciences, University of Derby, Kedleston Road, Derby, DE22 1 GB, UK
Mark T Bulling
Joanne L Hardstaff
Piran C L White
Correspondence to Piran C L White.
PCLW, MRH, GM and JH conceived and designed the study. JH and MTB conducted the modelling and the sensitivity analysis. All authors participated in drafting the manuscript. All authors have read and approved the final manuscript.
Additional file 1 : Sensitivity analysis of model.(DOC 258 KB)
Hardstaff, J.L., Bulling, M.T., Marion, G. et al. Impact of external sources of infection on the dynamics of bovine tuberculosis in modelled badger populations. BMC Vet Res 8, 92 (2012). https://doi.org/10.1186/1746-6148-8-92
Host community
Perturbation


Over the past decade, the importance of indoor air quality has become more publicized. On average, people spend 90% of their time indoors. Healthy indoor air is imperative to the overall well-being of building occupants. The air you breathe at work and at home can have a significant impact upon your health.
Facility managers are now being tasked with achieving healthy indoor air quality in the workplace. Research has demonstrated that exposure to VOCs exacerbates allergy and asthma symptoms and can cause dizziness, fatigue, nausea, and impaired thinking. Asthma and allergies have become a top reason for employee absenteeism. There are numerous studies that have concluded that poor indoor air quality can be directly linked to decreased worker productivity and increased absenteeism.
Therefore, it has become the responsibility of facility managers to find ways to improve air quality and create a healthier work environment. There are several effective ways to make indoor air quality a routine part of your facility's cleaning program.
To achieve measurable results, a two-fold approach to tackling indoor air quality will be most effective. First, it is important to overhaul the standard processes for purchasing and using cleaning supplies and to use products and techniques that reduce the number of VOCs introduced into your air. Secondly, it is also imperative to focus on improving the air by using air purifiers and optimizing your facility's ventilation.
Most commercially available cleaning products contain dozens of harsh chemicals that pose several serious health risks. Facility managers are faced with the challenge of keeping the facility clean without relying on commercial cleansers. Thankfully, numerous products have recently been introduced to the market that contain natural ingredients and that can still provide similar results to commercial cleansers without the harsh chemical ingredients. By changing products and techniques used to clean a facility, the overall quality of the air can be drastically improved.
Secondly, facilities managers need to work on improving a building's ventilation and on purifying the air. Maintaining your current HVAC system will help keep a constant flow of fresh air circulating throughout the facility. Standalone air purification systems have also become an extremely effective solution. Alternatively, simply placing a HEPA air filter in existing HVAC systems drags down the efficiency of that very same system.
Commercial-grade air purifiers use sophisticated technology and HEPA filtration to rid indoor spaces of up to 99.97% of airborne contaminants, including VOCs, germs, allergens, and odors. These units can be placed in problem areas to address specific air quality issues, such as public restrooms. This provides a more complete solution to odors in those spaces and can serve as a gateway to air purification being introduced into other areas.
Help protect your workspace indoor air quality by directing the Facilities Manager to these helpful tips.
© 2019 Prism Analytical Technologies. All Rights Reserved.


What's not to like about Google?
It's simple, you always get some kind of answer and almost everyone uses it. Usually, you get an answer on the 1st page.
But, what if you don't get an answer that helps you right away?
If you're like me, you have to start searching again and again – which can be very frustrating.
That's why I wish Google would check out Clusty. It's not as big as Google or as deep. But, it's interesting – because it 'clusters' answers, providing another 'filter' to make your search easier.
On Google, if you enter your name, you'll get a list of the most visited sites that include it.
On Clusty, your might find choices that might differentiate your professional skills, golf tournaments you have played in or articles you have written.
Clustering might provide an edge in behavioral targeting, the much touted 'next generation' of internet advertising which attempts to link a consumer's 'behavior' (such as the pages they visit in searching for a new Audi) to more effective and targeted ad displays.
A more differentiated search is a powerful tool. Google might want to try a Beta version.


text:
Home › Featured › 6 Must-See Filming Locations
A favourite of filmmakers, New York City is always ready for its close-up. Pay homage to the Big Apple's quintessential movie moments with this list of 15 must-see, must-Instagram filming locations.
Taxi Driver, Midnight Cowboy, Date Night, Captain America, Big, Shaft (the original!), A Chorus Line, Vanilla Sky, Birdman. The list of movies shot in the neon-lit heart of New York City is endless.
Times Square is at its brightest and most boisterous at night, but don't go there hungry. En route, stop at West 51st Street and Broadway for a bite at Ellen's Stardust Diner—featured in New Year's Eve—where the showtunes-singing wait staff are part of the experience.
Insta-worthy: For a panoramic view of the world's most-visited tourist attraction, jostle for a spot on the stepped red roof of the TKTS discount booth just below 47th Street.
Fans of The Godfather will recognize this famed theatre as the spot Michael Corleone and Kay Adams learn about the assassination attempt on Don Corleone. Billed as the "Showplace of the Nation" when it opened in 1932, Radio City Music Hall continues to host hundreds of concerts and events each year. Don't have a ticket? Get an insider's view of the venue and meet one of the world-famous Rockettes during the guided one-hour Stage Door Tour ($27 USD).
Insta-worthy: The marquee shoots best at night from the intersection of 6th Avenue and West 50th Street.
The most iconic skyscraper in New York City (thanks, King Kong!), the Empire State Building has played a starring role in Elf and Sleepless in Seattle—though, sadly, the latter film's emotional climax was filmed on a replica set. Head out early in the morning to avoid long lineups for tickets, security and the elevator leading up to the famous open-air Observation Deck on the 86th floor (standard passes start at $34 USD).
Insta-worthy: The only problem with the 360-degree view from the Empire State Building is that it doesn't include the Empire State Building! For that, you'll need to visit Top of the Rock Observation Deck at Rockefeller Center 16 blocks north. You can save money and skip lines by purchasing a New York CityPASS ($158 CDN) get access to both experiences.
Although you saw it destroyed by a flying saucer in Men in Black, the real-life Unisphere stands tall in Flushing Meadows-Corona Park in Queens. The 12-storey stainless-steel globe was commissioned for the 1964 New York World's Fair to celebrate the dawn of the space age and "Peace Through Understanding," and shines like new thanks to recent restoration efforts.
Baseball fans will want to visit nearby Citi Field, home of the New York Mets, while little ones will enjoy the Queens Zoo.
Insta-worthy: If you're visiting in the summer, a selfie with the reflecting pool and fountains is a must. In the off-season, when the pool is empty, stand underneath the globe for a unique angle.
Grand Central Terminal
A transportation hub for travellers and commuters since 1913, Grand Central Terminal has been the big screen backdrop for everything from chases (North by Northwest) and gun battles (Carlito's Way) to alien invasions (The Avengers) and flash mobs (Friends with Benefits). To learn more about this Beaux Arts beauty, download the Grand Central Tour app ($5) for an official self-guided audio tour, then stop by the Magnolia Bakery location in the Lower Concourse for one of their deeply delicious cupcakes.
Insta-worthy: Watch the ebb and flow of the bustling main concourse from the east or west balconies or aim high for a photo of the arched windows and constellation-themed ceiling mural.
Conceived by John D. Rockefeller during the Depression as a "city within a city," Rockefeller Center encompasses six square blocks of Midtown Manhattan. Several of the complex's most popular attractions have made film appearances, including The Rainbow Room (Sleepless in Seattle), Top of the Rock (The Adjustment Bureau) and The Rink at Rockefeller Plaza (Elf, Home Alone 2: Lost in New York).
After a day of sightseeing, relax with a cocktail at the stately Lotte Palace New York on Madison Avenue—its Tavern On 51 bar offers a cool Old New York vibe. The mansion-turned-hotel appears in the rom-coms 27 Dresses and Just My Luck.
5 Things in New York City You ...
Yankees Win Opener against the Mets, as Masahiro Tanaka Scores a Painful Run
5 Summer Vacations within a Day's Drive of Los Angeles
You should Know these 7 things to See and do in Samoa
5 Literary Landmarks around World
N.B.A. Finals 2018 Live: Warriors Sweep Cavs for Third Title in Four Years
5 Things in New York City You Must Visit


text:
Proton for PSA, Lotus for Geely?
By HO WAH FOON
Saturday, 18 Feb 2017
FILE PHOTO - A worker checks new Proton cars at a yard near Kuala Lumpur January 12, 2009. REUTERS/Zainal Abd Halim/File Photo GLOBAL BUSINESS WEEK AHEAD PACKAGE - SEARCH BUSINESS WEEK AHEAD 13 FEB FOR ALL IMAGES
DRB-Hicom Bhd is most likely to sell a controlling stake in Proton Holdings Bhd to French auto giant PSA Group, which produces Peugeot cars, according to sources.
"PSA is ready to invest a lot of money in Proton and build a new plant in Tanjung Malim, Perak. It has presented the best proposal to rescue and expand Proton's operation in Asean," the source says.
But Chinese car manufacturer Geely Automobile Holdings Ltd, the other contender to buy a 51% stake in Proton, may be offered a proposal to take over Lotus from Proton.
In earlier negotiations with DRB-Hicom , Geely had expressed more interest in acquiring Lotus, which produces sports cars, rather than the whole of Proton.
"Proton is of no use to Geely. It wants Proton because of the auto technology in Lotus. And for PSA, which is strong in sport-utility vehicles (SUVs), it is not keen on Lotus," says the source.
Indeed, China's government has been encouraging its auto companies to acquire technology that it lacks. The auto sector has been identified as a weak segment within its manufacturing sector.
Invitation by DRB-Hicom for bids to be Proton's strategic partner closed two days ago. Only PSA and Geely have submitted their proposals, according to press reports.
Proton started the exercise to get a foreign strategic partner more than six months ago after the government gave it financial assistance of RM1.5bil to pay off the vendors of the troubled national car manufacturer.
One of the conditions of the financial assistance was that Proton, wholly owned by DRB-Hicom, needed to secure a foreign strategic partner as soon as possible.
DRB-Hicom recently stated that it would conclude a decision on a technical partner for Proton within the first half of this year. Key considerations include strategy and operation of the potential partner.
According to the source, the French company has proposed to move Proton's Shah Alam plant to its under-utilised plant in Proton City in Tanjung Malim.
In addition, PSA will build another new plant in the Perak township to raise the production of vehicles to achieve economies of scale and be competitive.
"PSA is a latecomer in this region. Now it sees the opportunity to penetrate the Asean market of 600 million people by using Malaysia as a base to export its vehicles tax-free to any of the 10 Asean members," says the source.
Among PSA's proposals that look attractive to Malaysia is a plan to raise the production capacity of Proton cars to one to two million units from 150,000 currently.
PSA also intends to produce SUVs for the Asean market.
If PSA's grand plan comes to fruition, then Tanjung Malim may be turned into Malaysia's auto hub.
Besides centralising Proton's operations, the PSA plan could create 10,000 jobs for the local community, says the source.
It will also help lift Proton out of its prolonged financial troubles, as the government is not prepared to pump in more money into the bleeding company, which was set up in 1983 by former prime minister Tun Dr Mahathir Mohamad as part of the strategy to industrialise Malaysia.
Perusahaan Otomobil Nasional Bhd (Proton) was incorporated on May 7, 1983 to manufacture, assemble and sell motor vehicles and related auto products. It produced Malaysia's first commercial car, the Proton Saga, in July 1985.
Used to being the market leader in the local auto sector, Proton's market share fell to 12.5% last year from 15.3% in 2015.
Its total sales fell 29% year-on-year to 72,300 units due to deteriorating market conditions, said Hong Leong Investment Bank Research in a recent report.
On the bids for Proton, StarBiz recently reported that Geely was the frontrunner in securing the valuable strategic partnerhip with Proton. Other media followed suit.
Last year, a senior official of DRB-Hicom was seen in China to conduct negotiations with Geely on the possibility of its entry into Proton. He asked not to be named.
Keen on the Asean market, Geely produces a variety of vehicle types, including SUVs and sedans.
It owns the Volvo brand, which it acquired in a US$1.8bil deal in 2010.
Tags / Keywords: Business , proton
Next In Business News
Kanger inks construction deals
Medical glove exports face more delays amid shipping container shortage
Batu Kawan raises stake in CCM to 92%, to proceed with delisting plan�
SKP suspends Johor Baru operations due to Covid-19�
KNM plans new RM54.9mil private placement exercise �
Notion VTec says 87 Covid-19 cases found
Samaiden bags RM25.8mil biomass power plant project�
South Korea, Thailand lead Asia losses as US aid delivery in question
PBOC: China will support economic recovery
Trending in Business


text:
About Mountain View Mirror
Career Headshots
Contact The Mountain View Mirror Editorial Staff
Mountain View Mirror Advertising
Mountain View Mirror Newspaper
The Mountain View Mirror Flickr Project
Mountain View Mirror
Real Stories, Real People, Real Life.
Events & Lifestyle
American Image
Stand Back! I'm Going to Try Science
The Mirror ACTS!
Parent-2-Parent
Careers & College
Career Center News
Everything is Art
Shelfies
From the Pearl Harbor Bombing to the Nuclear Age in Asia
ricardi|March 16, 2018
How did World War II create a nuclear age in our world?
The war for the United States began with the Japanese bombing of Pearl Harbor on December 7, 1941 but it ended with the United States being the first and only nation to drop 2 atomic nuclear bombs on major cites. The American fight against the Japanese during the early 1940s brought the dawn of the "nuclear age".
President Roosevelt had the US Pacific Fleet move to Pearl Harbor in 1939 and Japan wanted to expand in the Pacific. Military leaders and politicians saw a war going on between Japan and the United States and decided to attack first. Japan bombed Pearl Harbor on December 7, 1941.
2,403 people were killed and 1,178 people were injured from the bombing.
The United States tried to avoid World War II as it was going on, but the attack on Pearl Harbor forced the US to join World War II. Although World War I was the first war that involved aircraft, it was during World War II where aircraft took a major role. There were three major types of planes, fighter planes, bombers, and transport. Fighter planes were made for air to air combat. Bombers where designed to carry and drop bombs on enemy targets. The transport planes were made to carry troops and supplies to take around the world. Transport planes where important during the war, many of them where civilians planes used by the air force for the war.
Throughout the war new technology emerged but none proved more powerful than the atomic bomb.
What was the "Manhattan Project? How did the atomic bomb come to be? The Manhattan Project was research and development project during World War II for a nuclear bomb. The project began in 1939 and ended in December 31, 1946. By July 1945 a prototype was ready for testing and on the July 6, 1945 the first atomic bomb was dropped for testing in a desert.
President Truman's decision led to thousands of deaths. Although it was a harsh decision it wasn't an easy one. There were many different factors when Truman was making this decision.
Truman was "eager" to drop the bomb, he writes, and was unwilling to explore alternatives for three reasons.
First, Truman wanted to avoid a land invasion of Japan, which would have killed thousands of Americans.
Second, he was determined to impose unconditional surrender on the Japanese because anything short of that would have made him appear weak. He also worried that a failure to achieve unconditional surrender might fortify those in Japan who wanted to continue fighting.
Finally, Truman hoped to end the Pacific War before the Soviet Union entered the fray against the Japanese, a development that might permit Stalin to obtain territory in Asia or demand a role in America's postwar occupation of Japan. Consequently, Truman was in a hurry to use the bomb.
-Tsuyoshi Hasegawa's "Racing the Enemy: Stalin, Truman, and the Surrender of Japan," a landmark book that brilliantly examines a crucial moment in 20th-century history.
https://www.csmonitor.com/2005/0802/p17s01-bogn.html
2 separate atomic bombs were dropped on two Japanese cities named Hiroshima and Nagasaki. The bomb dropped on Hiroshima, on August 6, 1945, caused severe destruction and immediately killed 150,000 people. The bomb exploded with an energy of 15 kilotons. The second bomb dropped, Nagasaki, killed 75,000 people. The two bombs ended the war.
What happened in Japan during the years following World War II? Do they have nuclear technology today? When did they get access to it? After world war 2 the allied powers of Great Britain, the Soviet Union, the Republic of China, and the United States discussed how to disarm Japan, deal with its colonies, stabilize the Japanese economy, and prevent the re-militarization of the state in the future. Japan currently does not have any nuclear bombs. They are banned from having a military and nuclear technology. The demilitarization of Japan and the protection of the United States' nuclear umbrella led to a strong policy of non-weaponization of nuclear technology. here
How did countries such as Pakistan and India who were once under the control of the British empire during World War II become nuclear powers today?
As World War II was coming to an end many countries started becoming independent and forming governments. It was expected that after the war the British colonies would soon disintegrate. The Pakistan Movement was led by Muhammad Ali Jinnah and resulted in Pakistan becoming a Muslim state. Pakistan gained its independence on August 14, 1947. India's independence came right after that on August 15, 1947. on June 15, 1947 the British House of Commons passed the Indian Independence act, or Mountbatten Act. This act divided India into two dominions. India and Pakistan was granted independence. Muslims ignored attempts to include them in an Indian government lead by Hindus. Riots broke out between the Muslims and Hindus in multiple Indian cities. In August 1946, four days of fighting left more than 5,000 dead and more than 15,000 hurt in Calcutta. Partition is when a country is divided in two and then would form two separate governments and the British were finally convinced that the only way to solve this bloodshed would be to do that.
When did Asia enter into the nuclear age?
Russia. After Soviet leaders learned that United States and Germany had embarked on efforts to build an atomic bomb they decided to also start creating the atomic bomb. In February 1943, the Soviets began their own program led by nuclear physicist Igor Kurchatov and political director Lavrentiy Beria. The Soviet atomic program was tiny compared to the Manhattan project with approximately 20 physicists and a small number of staff. On August 29, 1949 the Soviets successfully tested their first nuclear device, called RDS-1 or First lightning.
China started developing nuclear weapons in the late 1950s with help from the Soviets. In the 1960s China made remarkable progress and a 32 month period China successfully dropped its first atomic bomb on October 1964.
India's nuclear weapons program started at the Bhabha Atomic Research Center. India's first nuclear test named Smiling Buddha was dropped on May 18, 1974.
Pakistan. In the mid 1970s Pakistan gained access to uranium and were on the path to atomic weapons. Shortly after India had tested their atomic bomb Pakistan conducted their first test in May, 1998.
Iran In 2015 a deal was made called Iran's nuclear deal. The agreement was that Iran would stop trying to make nukes and the US and allies would go lightly on the sanctions. But now the deal is over and President trump says the US is going to put harsh sanctions on Iran and its big export oil. That means higher gas prices in the US.
Israel- in 2016 an email was leaked saying there were "200" nuclear weapons in Israel. Although that number is most likely a exaggeration Israel has nuclear weapons. They joined the nuclear club in the 1950s.
Korea conducted their first atomic bomb test on October 9, 2006. On October 3, 2006 it was announced that a nuclear test would be happening.
The nuclear age has its pros and cons. Being able to use the nukes as a threat can help stabilize other nations. But are the pros really greater than the cons? If a nuke was to be used millions of people would die and for what? What about the effects it would cause to the environment? Having nuclear weapons is a great and reliable source for power and status but it also has serious effects that come with it. Why do innocent civilians need to die if war has broke out? Why should people live in fear that a bomb could hit them and kill them at any time? In my opinion the nuclear age was a good thing to help with other nations and keep them in check and also make a stand if other nations make threats. But in the end is it worth all the damage that it could do?
RePost & Share
Atomic bombings of Hiroshima and Nagasaki
A House Divided Shall Not Stand
The State of Covid in America
Coptic Heritage; Preserving Religious Freedom in Egypt
Hispanic Heritage in America; History, Culture and Politics
Understanding the Election
Can We Trust the President with Covid-19?
Hurricane Delta; A sign of the Times
It's Not About You
Women and Violence in Burial Rites
Story of Fat Angie
© 2021 • FLEX WordPress Theme by SNO • Log in • Register


Related by locale to a popular family retriever, labradorite is named after the Labrador Peninsula in Canada where its was first discovered in 1770. A sodium rich plagioclase feldspar, labradorite also occurs in Australia, Madagascar, Russia, Mexico, China, the Scandinavian Peninsula and the United States.
Available in brilliant pastels and deep gold colors, this variety of feldspar produces some stunning gem-quality stones perfect for summer wardrobes. Transparent labradorite should be fine, clear and relatively free from inclusions, displaying shades that vary from an almost lime-yellow color to bright canary yellows and golden tones.
While it appears in orange, yellow, colorless and red, the dark smoke gray material that shows a play of color or "shiller" is the variety most frequently used in bead necklaces, brooches, rings and ornamental objects. Valued for its lustrous metallic reflections that are said to resemble a Brazilian butterfly's wing, this play of color or shiller is aptly called "labradorescence" in gemological circles and appears as stunning rainbow colored reflections when light strikes the gem in a particular direction.
Mainly caused by the interference of light from lattice distortions, this affect often appears in violet, blue, green, yellow and even orange-reddish tints, although specimens displaying the complete color spectrum are those most highly valued, such as the particularly brightly colored variety found in Finland, which is also know as spectrolite. As the background color is arguably uninteresting, when selecting dark smoke gray labradorite observe the strength and intensity of the labradorescence when the gemstone is viewed from different angles. This may result in different colors being visible or even a range of colors all visible at the same time.
Calling it "firestone" because of its captivating play of color, the Native Indians of Labrador attributed mystical qualities to labradorite, using the powdered gem as a magical potion to cure their ailments. Interestingly, some modern mystics believe that labradorite is a gem that assists the practice of magic, unleashes the power of imagination and helps to release personal limitations.
Labradorite has many healing properties, it is said to detoxify the body and assists in anti-aging. Astrologically, labradorite is associated with the signs of Sagittarius, Scorpio, and Leo. Associated with the Winter season, and the January Moon (Wolf Moon). This gem also has Feng Shui properties. It enhances positive attitudes and clears the mind of negativity.


When we get an error while synchronizing a user in CA Provisioning Manager, we do not see the error details in the error message on the Provisioning Manager. The error does not even show up on the etatranslog. We are not able to see any errors on the Provisioning Manager side. None of the errors are being logged in Provisioning Server etatrans logs either. We need the logs to work correctly.
This could be caused from disk space on the logging server is full. When attempting to generate the error message from provisioning server the data is stored in temp files. If these temp files can't be created then it will result in a blank screen. Please verify your disk space. If the disk is full, clear/backup data and reattempt. You should notice logging has picked up again.


Future pharmacy techs in New York should explore their options for training and certification to maximise their probability of success for employment. Vocational training may help you learn the skills you may need in less time with a much smaller investment. It is common for banks and customers to treat any business with caution that has an element of 'high-risk' in it.
Getting training through your specific employing pharmacist has got the advantage of hands-training. You use a primary care doctor you trust with your medical concerns, right. Efficacy with the drug was determined by the number of patients the need to seek bone radiation.
The restrictions were placed from the governments along with the other health care related agencies. They are paid in salary as opposed to hourly wages. In most states physician assistants can prescribe medication also.
While there is a small chance you can get laid off (as an example, when the chain supermarket closes some stores) you should not have much problem finding another job. Factors staying taught in universities regularly variations, which is a fact. Veri - Sign and Scan - Alert Hacker Safe will be the two names you have to be looking out for as well as these names will proclaim why these websites feel at ease for paying online.
'	Sri Venkateshwara College of Pharmacy - Hyderabad. I feel this aspect is probably the toughest part in the residency curriculum. Several brands of natural cleaners might be found at most large stores, including Bio - Kleen and Seventh Generation.