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9 Ways to Make Flex Work Work for You
Flex work arrangements are becoming increasingly common, as workplace tech evolves and allows remote employees to be productive and engaged members of a team.
But working from home can be easier said than done. It requires proper planning, organization and discipline -- especially considering all of the potential distractions, like pets, kids or household chores.
Sure, adjusting to flex work arrangements, like telecommuting or nontraditional hours, takes work from both employee who's working from home and the manager he or she reports in to. But if you're willing to put in the work, employee engagement and company culture don't have to suffer.
Here are nine strategies for making your flexible work arrangement work. And be sure to also check out or tips for Managing a Remote Work Force.
Get Help
It's nearly impossible to get anything done without childcare, even if you work a few hours a week. Be sure to hire a reliable, experienced, paid caregiver that you can count on. Based on budget and schedule needs, determine if you need a part-time nanny, daycare center or live-in au pair.
Carve out a Dedicated Office Space
Make sure your office is clean (no toys allowed!), has a desk, a comfortable office chair, file cabinets, organizers, and whatever else you need to make it a functional, stress-free environment. Making space in your home is crucial to your productivity and your ability to focus.
Set Office Hours
It can be very easy to get distracted by the kids, but if you keep a regular schedule even if your boss isn't keeping tabs is the best way to get work done. "Even though you're at home, you have to find a way to pretend that you are going to a space where kids are not there," according to Robi Ludwig, Psy.D, a contributor for Care.com.
Prioritize Work and Home Tasks Separately
With the never ending flow of dishes and laundry, plus everything else you need to get done in your personal life, it's hard not to be distracted when you're working. "Just because you can do it right now, doesn't mean you should do it right now," according to Paula Rizzo, founder of ListProducer.com.
Instead, Rizzo suggests making two lists of things that have to get done: one for home and one for work. List the tasks in order of importance and start to tackle what has to get done immediately. If you think of personal to-do's while you're working, just add it to the list and set aside time later to get it done.
Email, Call, and Skype
"Get in the mindset of over communicating, all the time," according to Allison O'Kelly, the founder and CEO of Mom Corps, a 100 percent virtual national flexible staffing firm. Constant communication is essential because it shows your boss and your clients that you're on top of your game. Respond to emails promptly and send your boss regular updates on the projects you're working on. If you have to run out for a few hours, be sure to tell your team that as well.
Get Out of the House
Even though you work remotely, scheduling in-office or virtual meetings are important to your success. "You are still a viable member of the team, so show your face," O'Kelly says. If you're an entrepreneur or freelancer, attend networking events, seminars, or workshops. And be sure to take short breaks to walk the dog or grab a cup of coffee.
Set Boundaries
You might have a more a flexible schedule, but that doesn't mean your family should expect you to drop everything to attend to their needs, which is why it's really important to set boundaries with them from the get-go. Make sure your family understands that they must respect your office hours so when the office door is shut, mommy is off-limits. "Encourage them to think of your job, though it takes place at home, just like they think of their office job -- mandatory and with a set schedule and routine," O'Kelly says.
And when you are with your children, set boundaries for yourself too by putting the smartphone away, Dr. Ludwig reminds.
Be Flexible and Realistic
Since work is always there, sometimes it might seem that you just can't break away. And there's bound to be a looming deadline or an overwhelming project nagging at you, which is why it's important to be realistic about what you can do in any given day, according to Rizzo. "Writing down attainable goals is very important because you don't want to have a to-do list that's a mile long and then you end up feeling like a failure at the end of the day because you couldn't get it done," she says. And always pencil in more time than you think you'll need. "You want to set yourself up for success."
Don't Feel Guilty
"There's always going to be a little bit of guilt because when you're a parent, there's a feeling that you should always be attending to your child's needs even if you do have a job," Dr. Ludwig says. So remind yourself the reasons you're working and how it is benefiting your family. "Your child will survive if you're attending to something other than him for a couple of hours throughout the day."
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Big Tech has gotten, is getting and will get its share of regulatory scrutiny. For Apple, there seems to be an increasing interest in its digital wallet, and how the firm is competing in the payments realm.
At the end of last week, as reported by CNBC, the EU's Commissioner for Competition Margrethe Vestager said at a press conference in Lisbon, Portugal that "we get many, many concerns when it comes to Apple Pay, for pure competition reasons."
The Commissioner also said, "People see that it becomes increasingly difficult to compete in the market for easy payments."
As noted, Apple Pay is available across all EU member states, and there are estimates that the vast majority of users are located outside the U.S. Smaller companies had reportedly been told to use Apple Pay rather than rival payment processors.
Scrutiny of the Apple payment offering would come alongside other anticompetitive investigations, with the European Commission looking into antitrust complaints by Spotify against Apple over music streaming services.
Vestager also expressed concerns about Google's recent acquisition of Fitbit for $2.1 billion, tied in part to continued competition issues over how the company lists shopping search results.
"In general, we have a concern if companies merge because of data," Vestager said.
Vestager hit Google with a EUR2.4 billion ($2.65 billion USD) fine two years ago for favoring its own price comparison shopping service over rivals.
Here In The States
A bit closer to home, a bipartisan effort by several U.S. senators earlier in the month debuted a bill aimed at fostering transparency of Big Tech platforms' algorithms.
As reported, the Filter Bubble Transparency Act would mandate that companies collecting data from at least 1 million users, and with top lines of more than $50 million, must inform their users of how they use algorithms across their platforms. The bill would also let users opt out of curated content.
The bill would also, as The Hill reported, make it illegal to operate large online platforms that deploy "secret" algorithms. The Federal Trade Commission would be able to enforce civil penalties against firms that violate the rules.
"This legislation is about transparency and consumer control," said Senator John Thune (R-SD). "For free markets to work as effectively and as efficiently as possible, consumers need as much information as possible, including a better understanding of how internet platforms use artificial intelligence and opaque algorithms to make inferences from the reams of personal data at their fingertips that can be used to affect behavior and influence outcomes."
Elsewhere, Facebook said last week that it will boost encryption capabilities on its Messenger communication platform. The movement would come despite requests from lawmakers and regulators not to do so, because criminal activity would ostensibly be harder to track. Facebook added that it is going to go over safety measures, and tell users how to avoid unwanted content, or how to report it.

subset: commoncrawl


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#colfondo2/3inserito da Bele Casel @ Luca Ferraro
- feed di questo blog
- nella categoria "Prosecco Colfòndo"
- questo contenuto è disponibile anche in lingua inglese
By now, on twitter and elsewhere, we heard about all sorts of stuff: starting with #lambruschi1,2,3,4; then #barbera1 and the upcoming #aglianicodelvolture1 in just a few weeks.
It's just as easy as putting together 4 producers of Colfòndo, a few restaurant owners and some journalists in a ristorante owned by an enlightened family who plans to create a wine list with Proseccos sur lie only!
The slogan was "To see clearly, let's start from the bottom, fishing in the mud".
We started by reading a June 1974 article by Angelo Serafin, still extremely topical to this day, in which he wrote about the beloved Prosecco sure lie and its multifaceted and appreciated character.
The dialogue between producers is always interesting, with each one of us bringing his own idea to the table and all of us trying to figure out which way to go; together. Even when the discussion gets heated, it never degenerates into chaos.
Loris Follador, of Casa Coste Piane, an amazing individual and one of the first producers of Col fondo, told the story of how, during the years when wine guides started becoming popular, everyday wines like this took a serious drop, losing ground to more elaborated, overly structured and complicated wines with higher alcohol levels.
Lately there has been a desire by the consumer to rediscover more docile and healthier wines, wines that can be enjoyed without hangups for the whole meal. The dialogue evolved around organics, yeasts, pricing, crown caps and the future of Prosecco.
We tasted 5 types of Col Fòndo and we discussed how this typology allows the drinker to recognize the area of production and the handprint of the winemaker, something that, because of technology and excessive manipulation in autoclave, oft is often no longer possible.
It was an inspiring evening, full of great and constructive ideas.
My hope is that this might be the beginning of a long and prosperous journey for our beloved "old" Prosecco sur lie.
PS: please remember: Colfòndo is not charmat and not even champenoise.
Coming soon on this screen: #colfòndo1
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ONVIF Releases Profile T for Advanced Video Streaming
SAN RAMON, Calif. – October 25, 2018. ONVIF®, the leading global standardization initiative for IP-based physical security products, has announced the final release of Profile T, a new specification with advanced video streaming capabilities and an expanded feature set for metadata streaming and analytics. Profile T also offers support for H.265 video compression, which more efficiently handles image streams from high-definition cameras.
Is "Off the Record" Ever a Good Idea?
By Chelsie Woods The invitation to be interviewed by the media, whether it's with the local newspaper or an industry trade publication, is often considered an exciting opportunity. It's a chance to tell your story and to increase your company or brand's recognition by being interviewed as a subject matter expert. While a majority of interviewees find it's relatively easy to identify…


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We live under a cheerful delusion that sex might nowadays be easy - because we have been 'liberated' from the hang-ups and taboos of the olden days. Yet nothing could be further from the truth. Despite a veneer of openness, sex remains an extraordinarily complicated business, hard to discuss and surrounded by shame and unspoken desires.
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A bill introduced at the State Capitol Friday would give a mayor the right to fire the county's police chief.
Sen. Will Espero (D-Ewa Beach, Ewa by Gentry, Iroquois Point) introduced the bill. He says it isn't meant to slam anyone.
"Part of it is the mayor is the chief executive officer of the counties and the mayor works closely with the police chief on some matters," he said.
Espero said if passed, the bill would give the mayor the authority to remove, suspend or place the chief of police on leave for good and just cause.
Right now, the police commission has the authority to hire and fire the chief, which would not change.
"The police commissions, if you read the charters, they're not as strong as many of us want them to be and they're not involved in the day-to-day operations," Espero said.
If the bill is approved, it would apply to all of the chiefs across the state, including Honolulu's chief of police Louis Kealoha.
The bill comes two weeks after some state senators, including Espero, asked the commission to add a co-chief to the department to help Kealoha amid personal legal troubles.
Espero also recalls a situation that happened in 2012 dealing with Kauai's police chief.
Kauai County Mayor Bernard Carvalho ordered Chief Darryl Perry to take a leave of absence. The Kauai Police Commission took the mayor to court and asked the judge to determine who had that authority. The court ruled in favor of the mayor.
Espero also said if lawmakers don't want to give the power of firing the chief to the mayor, then they could consider amending the bill to give the city or county council that authority.
KHON2 contacted Honolulu Mayor Kirk Caldwell's office and the Honolulu Police Department, but neither wanted to comment on the bill. A spokesperson for the Honolulu Police Commission was unavailable.
In an earlier story, Kealoha told KHON2 his job performance hasn't been compromised.


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Mary mccormack will and grace
- Will & Grace casts American Horror Story actor as Will's suave new love interest
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Will & Grace casts American Horror Story actor as Will's suave new love interest
Eric McCormack Wants Justin Trudeau On 'Will And Grace' - EXTENDEDand with
Matt Bomer starred as Neal Caffrey across all six seasons of White Collar , before taking a turn as Donovan, a member of the afflicted who cosied up to Lady Gaga's character in the fifth season of American Horror Story. Commenting on the news, Bomer appeared to be just as excited as the rest of us, retweeting a story reporting his casting and adding the comment: "Dream come true!! Dream come true!! The same episode will also see the return of Minnie Driver as Karen's stepdaughter and nemesis, Lorraine Finster, as well as a cameo appearance from Olympic figure skater Adam Rippon. Along with Jack getting a new love interest, Debra Messing's character Grace will find love with Ross Gellar David Schwimmer himself , who's signed for a five-episode arc on the new season. Meanwhile, comedian and host Chelsea Handler has also jumped aboard the series to play a "high-powered lesbian" called Donna Zimmer who begins dating Grace's sister Janet once again played by Mary McCormack.
The two shows used to air one after the other on NBC's infamous Thursday night lineup. But he's not the only celebrity love interest coming to the show for season two. Handler will play a high-powered attorney and the love interest of Mary McCormack's character, Janet. The show will also be returning for a third season in Let us know. Virginia Streva PhillyVoice Staff.
This season will see the return of Alec Baldwin as he reprises his role as Karen's on-and-off lover, Malcolm Widmark. With Karen going through a divorce from her husband Stan, could Malcolm be playing for keeps? View this post on Instagram Things are gettin' steamy when Malcolm returns Thursday! The actor has recruited her real-life best friend Chelsea Handler to play her girlfriend. View this post on Instagram We're at sealfit training facility with actual navy seals.
McCormack was born in Plainfield, New Jersey.
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Mary Catherine McCormack (born February 8, ) is an American actress. She has had leading roles as Justine Appleton in the series Murder One (–97).
Mary McCormack | Will and Grace Wiki | FANDOM powered by Wikia
Daniel Pierce in the American crime drama Perception.


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05-Aug-2017 03:05
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In 2007, Domenica played at the house near the lake when Tony, Carmela, Bobby, and Janice celebrated Tony's birthday.I also want to make it clear that I have my own life and responsiblities and do not want a relationship or the commitments that come along with that at this time.


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Alloantigen-enhanced accumulation of CCR5+ 'effector' regulatory T cells in the gravid uterus
Edited by Douglas T. Fearon, University of Cambridge, Cambridge, United Kingdom, and approved November 13, 2006 (received for review May 25, 2006)
Regulatory T cells play an essential role in preventing fetal rejection by the maternal immune system. Here we show that, based on the expression of CCR5, regulatory T cells can be divided into a highly suppressive CCR5+ and a far less suppressive CCR5− subpopulation, suggesting that the former represent the effector arm of regulatory T cells. Although regulatory T cells from CCR5−/− gene deletion mutants still suppress, they are less effective mediators of maternal–fetal tolerance. The accumulation of CCR5+ regulatory T cells at this site appears to be enhanced by alloantigen. This finding is in stark contrast to the systemic expansion of regulatory T cells during pregnancy, which appears to be alloantigen-independent. The fact that CCR5+ regulatory T cells preferentially accumulate in the gravid uterus and that expression of CCR5 on regulatory T cells can be induced by activation lead us to propose that CCR5 is responsible for the accumulation of those regulatory T cells that have been activated by paternal antigens.
Regulatory T cells (TR cells) play an important role in the maintenance of peripheral tolerance and the prevention of autoimmunity (1). Where TR cells exert their suppressive function and what attracts them to and retains them at their site of action is poorly understood. Inducible TR cells (Tr1-like cells) have a preference for skin homing (2), whereas naturally occurring Foxp3+ TR cells can be found in all lymphoid organs (3, 4). The CD103+ subpopulation of TR cells has been shown to home to the site of inflammation (5); however, the mechanism by which this occurs remains elusive.
Previously, we have demonstrated that naturally occurring TR cells mediate maternal tolerance to the fetus and can be found in the uterus during pregnancy (6). Although the uterine accumulation of macrophages (7), natural killer cells (8, 9), and eosinophils (10) has been extensively studied, there has been no insight on how TR cells find their way to the gravid uterus.
Upon activation, professional antigen-presenting cells express the chemokine CCL4, which leads to the recruitment and/or retention of TR cells (11). Although it remains unclear which chemokine receptor is responsible for the CCL4-mediated effects on TR cells, biochemical studies have shown CCL4 to bind to the chemokine receptor CCR5 (12). Expression of CCR5 on T cells has been associated with both proinflammatory and antiinflammatory T cell function in mouse and human. CCR5 is thought to be expressed on antigen-experienced, effector T cells that home toward sites of inflammation outside the secondary lymphoid organs (13–15). CCR5+ T cells have been shown to infiltrate inflamed sites such as the synovium of rheumatoid arthritis patients (16, 17) and the central nervous system of mice with experimental autoimmune encephalomyelitis (18). Expression of CCR5 in pancreatic islets correlates with increased severity of diabetes in mice (19), and CCR5 is thought to mediate T cell migration to the islets (20). Deficiency in CCR5 leads to a reduced T cell infiltration to sites of Trypanosoma cruzei (21), Toxoplasma gondii (22), and viral infections (23). CCR5 also mediates infiltration of allografts (24–27) by proinflammatory, IFNγ-producing T helper (TH) 1-biased cells (17, 26) and macrophage infiltration at sites of inflammation (28, 29).
However, under certain conditions, mice receiving allografts of CCR5-deficient cells displayed accelerated and more severe graft-versus-host disease (30, 31). This suggests an antiinflammatory role of CCR5+ cells. Support for this notion comes from the fact that mice lacking CCR5 show increased delayed-type hypersensitivity responses (32). Indeed, CCR5 have been shown to be up-regulated upon activation on TR cells (33). Thus, it appears that CCR5 is present on both antiinflammatory and proinflammatory T cells.
Here we show that expression of CCR5 defines the effector arm of TR cells carrying most of the suppressive activity. Lack of CCR5 on TR cells leads to an impairment of maternal–fetal tolerance despite their finding their way to the uterus. We present data suggesting that this is due to a lack of CCL4-mediated accumulation of those TR cells that have been activated by paternal alloantigen.
CCR5+ Effector TR Cells.
CCR5 appears to be the only cognate receptor for CCL4 (12). Given the previously shown role of CCL4 in the trafficking of TR cells (11), we examined their expression of CCR5. We purified the cells from nonimmunized mice kept under specific pathogen-free conditions; thus, the CD25+ subpopulation of CD4+ cells consists almost entirely of TR cells (34). Our analysis revealed that CCR5 is expressed on ≈20% of all CD4+CD25+ cells in the spleen (Fig. 1 a). Because virtually all CD4+CCR5+ cells were CD25+, the CCR5+ cells represent a subpopulation fully contained within the pool of CD25+ cells (Fig. 1 b). Similar results were obtained for cells from blood and lymph nodes (data not shown). Both the CCR5− and CCR5+ subpopulations of TR cells express Foxp3, although the latter do so at a slightly lower level (Fig. 1 c).
Expression of CCR5 has been mostly associated with proinflammatory effector memory T cells (13). Upon activation, naïve CD4+ T cells start to express CD25, a subpopulation of which also expresses CCR5. The conversion from CCR5− to CCR5+ TH cell is enhanced in the presence of proinflammatory cytokines, in particular IL-12 (35). Similarly, expression of CCR5 can be induced in CCR5−CD4+CD25+ TR cells by activation, in particular in the presence of IL-2 (33). However, unlike the CCR5+ cells present in the pool of CD4+CD25+ TR cells, the CCR5+ cells purified from activated TH cells [CD4+CD25− activated for 48 h with plate-bound anti-CD3 (2 μg/ml) in the presence of IL-12 (10 ng/ml) and then sorted into CCR5-enriched and CCR5-depleted populations] do not express Foxp3 (Fig. 1 d).
Given the distinct origin of these two CCR5+ cell populations, one would expect them to have a diametrically opposed effect on the proliferation of naïve T cells. To address this we performed coculturing experiments (Fig. 1 e). CD4+CD25− cells were activated by cross-linking with anti-CD3. Addition of CCR5+ cells (at a 1:10 ratio) purified from activated CD4+CD25− cells resulted in a 110% increase in proliferation of the target cells, confirming their proinflammatory effector cell status. In contrast, addition of the same number of CCR5+ cells purified from CD4+CD25+ TR cells resulted in a 62% inhibition of proliferation. These results confirmed that the two CCR5+ cell populations are functionally opposed.
Because CCR5+ proinflammatory T cells are effector cells we wondered whether the same applies to CCR5+ TR cells. Indeed, direct comparison of the CCR5+ and CCR5− subpopulations of TR cells revealed that the vast majority of the regulatory activity resides in the CCR5+ cells. In coculturing experiments using CD4+CD25− target cells, CCR5+ cells led to marked reduction (P = 0.02; t test) of the target cell proliferation at a 1:50 ratio (Fig. 1 f), even in the absence of antigen-presenting cells. The same number of CCR5− cells had no inhibitory effect. Only when we substantially increased the number of CCR5-depleted TR cells, we observed a slight increase in inhibition; however, this was not statistically significant. Notably, most "coculturing suppression experiments" described in the literature include irradiated antigen-presenting cells (36). These cells are likely to provide the costimulatory signals that facilitate the conversion of TR cells into effector cells. The presence of CCR5+ TR cells in naïve animals may be an indication of a baseline activation in response to self-antigens.
Accumulation of CCR5+ TR Cells in the Gravid Uterus.
Proinflammatory effector T cells home to sites of infection outside the secondary lymph organs (21). In analogy one might expect a similar directed accumulation of CCR5+ effector TR cells to the sites where their action is required. In the case of pregnancy, the site of implantation poses clearly a main target of effector TH cells (35). Similarly, we have shown that significant number of TR cells can be detected in the gravid uterus at the maternal–fetal interface (6). We therefore reexamined the accumulation of TR cells that migrate to the gravid uterus with respect to their expression of CCR5 (Fig. 2). We found that >70% of CD4+CD25+ cells in the gravid uterus and placenta expressed CCR5 (Fig. 2 e and f). In contrast, the frequency of CCR5+ cells in the spleen, blood, and other secondary lymphoid organs was significantly lower (P < 0.005; t tests for individual tissues) and in all cases <30% of all TR cells within the tissue (Fig. 2 a–d). Virtually all of these CD4+CD25+ cells were Foxp3+ (Fig. 2 g and h). Interestingly, the iliac and lumbar lymph nodes (Fig. 2 c), which drain the uterus, do not show the same elevation of CCR5 expression as the uterus itself.
Chemokine Expression in the Gravid Uterus.
CCR5 is a promiscuous chemokine receptor binding several chemokines. Its ligands CCL3 (37–39), CCL4 (8), and CCL5 (40) have been reported to be expressed by a variety of cells in the human endometrium. To assess their role in the accumulation of TR cells to the gravid uterus, we compared the levels of Foxp3 mRNA with those of CCL3, CCL4, and CCL5 in whole uterine tissue in the pregnant and nonpregnant state by quantitative RT-PCR (Fig. 3 a–d). The uterine levels of Foxp3 mRNA (Fig. 3 a) were significantly elevated in pregnant mice (P < 0.0001; t test). Similarly, CCL4 mRNA levels (Fig. 3 d) were significantly elevated in the gravid uteri (P < 0.0001; t test), whereas CCL3 and CCL5 mRNA levels (Fig. 3 b and c) did not show any statistically significant change (P = 0.85 and P = 0.28 respectively; t test). These results show a strong correlation between uterine CCL4 expression and the number of TR cells present in the tissue.
CCL4 Preferentially Attracts CCR5+ TR Cells.
The fact that naïve TR cells can be distinguished from activated, effector TR cells based on the expression of CCR5 suggests a difference in their migratory behavior. To study this difference in an unbiased fashion, we examined the migration of total splenocytes toward a range of CCL4 concentrations (0–500 ng/ml) in transwell migration assays (Fig. 3 e and f). The number of CD4+CCR5+ cells in the input and migrated cell populations was determined by FACS. We found that the vast majority of cells that migrated toward CCL4 expressed CCR5. Only 1.8% of CD4+ cells (Fig. 3 e, black) in the input population expressed CCR5. In contrast, 61.8% of CD4+ cells (Fig. 3 e, red) that had migrated toward CCL4 were CCR5+. The migration index (T m × C m/C i, where T m is the number of migrated cells, C m is the number of migrated cells expressing the cognate marker, and C i is the number of input cells expressing the marker) is an accurate indicator of both the potency and specificity of a chemokine. CD4+CCR5+ cells exhibited a migration index of 64 for migrations to 500 ng/ml CCL4 (Fig. 3 f). These results demonstrate that, at least in vitro, CCL4 preferentially accumulates CCR5+ effector TR cells.
The Role of CCR5 on TR Cells in Pregnancy.
CCR5−/− gene deletion mutant mice as such have an unremarkable phenotype (25) and display a normal pregnancy outcome in allogeneic matings. Both proinflammatory and antiinflammatory effects are reported when using T cells from these mice, depending on the experimental model used (30, 41). These observations may be due to the fact that both proinflammatory effector TH cells and effector TR cells express CCR5. Thus, any impairment of TR cells caused by the lack of CCR5 (30) might be compensated by an opposing effect caused by lack of CCR5 on activated TH cells (41), resulting in an immunological stalemate. Indeed, both CCR5-deficient TR (33) and TH (25, 33) cells are impaired in their migration toward CCL4. This could explain why successful allogeneic pregnancies are possible in these mice, because the lack of CCR5 will affect both aggressors and regulators.
Thus, it is necessary to examine the mutant cells in the context of a wild-type immune system to reveal the effect of CCR5 deficiency on TR cells in pregnancy. We adoptively transferred wild-type CD25-depleted splenocytes reconstituted with CD25+ cells prepared from either CCR5-deficient or wild-type mice at a 15:1 ratio into F5×Rag1−/− female recipients (semilymphopenic, lacking CD4+ T cells). Both donor mice and recipient mice were of the same genetic background (H-2b). The mice were then allogeneically mated (BALB/c males, H-2d). The homeostatic expansion after transfer of 1.5 × 107 cells into lymphopenic animals is minimal (42) and further minimized by using semilymphopenic recipients. Intact and resorbing fetuses were scored blindly at mid-gestation (Fig. 4 a). C57BL/6 control females had an average litter size of 8 (n = 8) and 1% resorbing fetuses. F5×Rag1−/− recipients that had received CD25-depleted cells reconstituted with wild-type CD25+ cells had an average litter size of 7 (n = 8) and 2% resorbing fetuses. Neither the average litter size (number of intact fetuses, P = 0.33; t test), nor the number of resorbing fetuses (P = 0.72; nonparametric test) between the control and the experimental group that had received CD25+ cells from wild-type mice shows a statistically significant difference. In contrast, F5×Rag1−/− recipients, which had received CD25-depleted cells reconstituted with CCR5-deficient CD25+ cells, had an average litter size of 6.8 (n = 8) and 17% resorbing fetuses. The percentage of resorbing fetuses was significantly higher than that observed in both the control (P = 0.01; nonparametric test) and the experimental group that received wild-type CD25+ T cells (P = 0.02; nonparametric test). These data demonstrate an impairment of CCR5-deficient TR cells in the sustenance of maternal–fetal tolerance, albeit not a complete loss of function. The inability of CCR5-deficient TR cells to fully protect against fetal loss could be due to impaired function and/or accumulation of these cells. In the case of proinflammatory effector T cells, CCR5 alters the length of their interaction with antigen-presenting cells, leading to enhanced T cell activation (43). To assess whether CCR5 is required for the suppressive activity of TR cells, we performed coculturing experiments with CD25+ cells prepared from either wild-type mice or CCR5−/− gene deletion mutants. We found that CD25+ cells prepared from CCR5-deficient mice clearly suppressed the proliferation of CD4+CD25− target cells in vitro (P = 0.009; nonparametric test). However, they were slightly less (P = 0.04; nonparametric test) suppressive than wild-type TR cells (Fig. 4 b).
CCR5-Mediated Accumulation of TR Cells.
To test whether CCR5 deficiency leads to an impairment in the accumulation of TR cells in the gravid uterus, we compared uterine Foxp3 mRNA levels in wild-type and CCR5−/− gene deletion mutant mice at embryonic day 10.5 (E10.5) (Fig. 4 c). We detected equivalent levels of Foxp3 in both lines of mice (P = 1; nonparametric test) revealing that CCR5-deficient TR cells still find their way to the gravid uterus. This suggests that the recruitment of TR cells to the gravid uterus itself can be achieved independent of CCR5. However, this does not rule out a role for CCR5 in the preferential accumulation of activated effector TR cells, competing against nonactivated TR cells for the same niche. To test this hypothesis we performed in vivo competition experiments between wild-type TR cells, CCR5-deficient TR cells, and TR cells expressing CCR5 ectopically.
TR cells prepared from either wild-type mice or CCR5 gene deletion mutant mice were transduced with a retroviral vector carrying a constitutively expressed GFP gene. This allowed us to follow these cells after adoptive transfer into wild-type females. The recipients were allogeneically mated. At E10.5 we determined the number of GFP-tagged TR cells in the uterus (Fig. 5 a) and spleen (Fig. 5 b).
In the uterus we found only half as many CCR5-deficient TR cells as we did find wild-type TR cells (P = 0.048; t test). In contrast, there was no significant difference (P = 0.80; t test) in the number of GFP-tagged CCR5-deficient and wild-type cells in the spleen of the recipients. This indicates that CCR5 is not only a marker for TR cells that accumulate in the uterus, but is functionally involved in the accumulation itself. The TR cells used in the experiment were prepared from the spleens of nonpregnant mice, and only ≈20% of them expressed CCR5. In addition, paternal alloantigen and fetal antigens might lead to activation and thus CCR5 expression on some of the cells. However, it is clear that only a subpopulation of cells will express CCR5. One would predict that constitutive expression of CCR5 in the TR cells transferred would lead to a further increase in their uterine accumulation, because in this scenario all transferred cells have the potential to accumulate. Indeed, we found that TR cells transduced with a retroviral vector carrying a constitutively expressed CCR5 gene accumulated with almost twice the efficiency (P = 0.01; t test) in the uterus (Fig. 5 a). Interestingly, we found significantly fewer (0.64×) of these cells in the spleen (P = 0.012; t test) (Fig. 5 b). These results show that expression of CCR5 on TR cells has a direct effect on their selective accumulation in the gravid uterus.
Antigen-Induced Accumulation of TR Cells.
Not all TR cells will have antigen specificities suitable to the recognition of paternal/fetal antigens, and only the antigen-activated TR cells, which will express CCR5, will have to be retained. Obviously, in the case of the CCR5-deficient mice this selective retention would be irrelevant because the antipaternal/fetal proinflammatory TH cells would be likewise impaired by the CCR5 deficiency. If maternal–fetal tolerance requires the selective accumulation of alloantigen-specific effector TR cells one would expect fewer CCR5+ T cells in the uterus of syngeneic pregnancies. Because there is no paternal alloantigen, activation of TR cells is restricted to fetal antigens (e.g., male antigens, carcinoembryonic antigens, etc.) (44), resulting in fewer activated CCR5+ cells. As demonstrated above this would lead to a reduction in the number of CCR5+ cells accumulating in the uterus. To test this hypothesis, we compared the relative abundance of CCR5+ TR cells among total uterine cells recruited to the uterus of syngeneic versus allogeneic pregnancies at E10.5 (Fig. 5 c). We found that the number of CD4+CD25+CCR5+ cells in the uteri of allogeneic pregnancies was significantly (P = 0.0096; t test) higher (0.041% of all uterine cells) than that in the uteri of syngeneic pregnancies (0.03% of all uterine cells). In contrast, there was no significant difference (P = 0.16; t test) in the spleens (Fig. 5 d) of the animals compared. Therefore, the selective accumulation of CCR5+ TR cells in the gravid uterus is affected by antigen.
We conclude not only that TR cells migrate to the uterus, but that the antigen-activated CCR5+ effector TR population accumulates in this tissue. Given the concurrent expression of CCL4, this may be based on a CCL4-mediated mechanism and could be due to either preferential recruitment of CCR5+ cells or preferential retention of CCR5+ effector TR cells that have been recruited by a CCR5-independent mechanism.
The effector arm of proinflammatory T cells is characterized by three main criteria (13–15, 26): (i) effector function manifested in the increased production of proinflammatory cytokines such as IFNγ, (ii) migration to inflamed tissue, and (iii) the expression of CCR5. Similarly, individual effector features have been ascribed to TR cells. Activation of TR cells has been shown to result in increased suppressive potential (45) and to lead to up-regulation of CCR5 (33). Furthermore, the CD103+ subpopulation of TR cells is thought to migrate into inflamed sites where it appears to exert its suppressive function (5). Here we show that the CCR5+ subpopulation of TR cells carries most of the suppressive capacity within the pool of TR cells. This effector function can be shown for both CCR5+ cells isolated from nonimmunized mice and those induced by de novo activation of CCR5− TR cells. We therefore propose that these CCR5+ cells constitute the effector arm of TR cells.
CCR5+ cells can be found at the site of antigenic insult such as infection (22) and organ transplants (46). Furthermore, they have been found at sites of organ-specific autoimmunity (16, 47) and in the proximity of tumors (48). In most cases this is thought to be an influx of proinflammatory effector T cells. However, at least in some cases, CCR5+ TR cells have been shown to contribute to this population (33). We propose that the equilibrium of these two effector cell populations with diametrically opposed functions can determine the outcome of immune responses. We show that during pregnancy CCR5+ TR cells accumulate in the uterus, interference with which causes a significant increase in fetal resorptions. A similar increase in fetal loss can be induced by injection of "TH1-educated" CCR5+ proinflammatory effector TH cells, which also home into the uterus (35). In normal pregnancy, dominance of the effector TR cells leads to tolerance (6). If, however, this dominance of effector TR cells is broken, be it experimentally by interference with effector TR cell recruitment, by injection of proinflammatory effector TH cells (35), or naturally by a uterine infection (44, 49), the balance can quickly tip toward an aggressive immune response. In the case of pregnancy this rapidly inducible flexibility might be of advantage. Uterine infections are likely to spread to the fetus. In this scenario it is better for the maternal immune system to sacrifice a fetus that is likely to be damaged rather than risk both the mother's life and that of her unborn offspring (44).
CCR5 has multiple ligands, among them CCL4 (12), which is involved in the modulation of the recruitment/retention of TR cells to activated antigen-presenting cells (11). We build on this finding by demonstrating that in transwell migration assays CCL4 predominantly acts on CCR5+ effector TR cells rather than on the TR cell population as a whole. This makes CCL4 a likely candidate for the recruitment of effector T cells to the uterus. Indeed, we observed a strong correlation between the expression of CCL4 and the accumulation of TR cells, but not with that of the other CCR5 ligands CCL3 and CCL5. Yet, the lack of a detectable difference in uterine Foxp3 mRNA levels between wild-type and CCR5 gene deletion mutant mice shows that CCR5-deficient TR cells still find their way to the uterus. Although we cannot formally exclude compensatory mechanisms in the gene deletion mutants, we think it is more likely that there are CCR5/CCL4-independent mechanisms of TR cell recruitment. This, however, does not rule out a function for CCR5 in the accumulation of effector TR cells.
A hint comes from the fact that in the case of allogeneic pregnancies more CCR5+ cells accumulate in the uterus than in syngeneic pregnancies. The only difference between the two scenarios is the presence or absence of paternal alloantigen. We have previously demonstrated that the expansion of TR cells during pregnancy is independent of paternal alloantigen (6), yet we find this alloantigen-dependent difference in the number of CCR5+ cells in the uterus. Given that activation of TR cells can induce CCR5 expression, it is not too far-fetched to speculate that the CCR5+ cells found in the uterus are likely to be antigen-experienced or even alloantigen-induced effector TR cells. The fact that, in contrast to wild-type TR cells, CCR5-deficient TR cells are not able to completely prevent fetal loss highlights that the accumulation of CCR5+ effector TR cells is of biological importance. Pregnancy is clearly not the only scenario in which the antigen-specificity of the recruited TR cell appears to be essential. In a TetTNFα/CD80 inducible diabetes model those TR cells that can prevent the onset of disease preferentially accumulate in the pancreatic lymph nodes and islets (50). The accumulation of antigen-specific TR cells appears not to be restricted to self-antigens, because it also can be observed in chronic Leishmania major infections (51). Recently, Yurchenko et al. (52) examined the migration of TR cells to sites of L. major infection and demonstrated that CCR5 has an important role in the homing and presence of TR cells at their site of action, interference with which dramatically affects the outcome of the infection. In another study, tracking of CCR5+ TR cells revealed their long-term accumulation in graft-versus-host disease target organs, whereas CCR5-deficient TR cells were impaired in this accumulation, leading to decreased survival of the graft recipients (33). These findings are in agreement with our interpretation that CCR5+ TR cells are antigen-specific effector TR cells.
Furthermore, we were able to demonstrate that CCR5-deficient TR cells are handicapped in their accumulation in the gravid uterus when adoptively transferred into a wild-type animal. In contrast, TR cells constitutively expressing a CCR5 transgene appear to have a competitive advantage. In summary (Fig. 5 e), we propose that CCR5 is responsible for an enhanced recruitment and/or retention of those TR cells that have already been activated by antigen in the periphery. In addition, TR cells that have migrated into the uterus in a CCR5-independent manner might become activated and possibly expand within the uterus itself. These cells are likely to be retained, in preference over those that have not been activated and thus do not express CCR5.
Materials and Methods
Experimental animals, FACS analysis, quantitative real-time RT-PCR, and adoptive transfers are described in detail in supporting information (SI) Materials and Methods .
Preparation of Uterine Tissue.
Uteri (implanted and nonimplanted segments) were separated from surrounding tissue (including fetuses/placenta), immersed in liquid nitrogen, pulverized, and resuspended in RNA lysis buffer. Total RNA was prepared by using the RNeasy kit (Qiagen, Crawley, U.K.) including on-column DNase digestion, as per the manufacturer's instructions. For FACS analysis uterine tissue was collagenase A (Roche Diagnostics, Burgess Hill, U.K.) digested for 15 min.
Cell Purifications and Proliferation Assays.
Lymphocytes were isolated from single-cell suspensions by using Lympholyte M or Mammal (Cedarlane, Ontario, Canada). CD4+ cells were isolated by depletion with anti-CD11b, anti-CD11c, anti-GR1, anti-CD19, and anti-CD8 antibodies (Becton Dickinson, Oxford, U.K.). CCR5 and CD25 subpopulations were isolated by positive selection by using an autoMACS (Miltenyi Biotec, Bisley, U.K.). For each step, the purity was >99.5% except for CCR5+, where experimental limitations allowed only 40% purity. To avoid cell density-dependent effects, the total cell number was kept constant. Cell counts were verified by FACS using CaliBRITE beads (Becton Dickinson). Effector cell suppression assays were performed by using CFSE-labeled target cells. A total of 2 × 104 CFSE+CD4+CD25− target cells were plated on U-bottom 96-well plates (Corning, Schipol-Rijk, The Netherlands) with 2 μg/ml plate-bound anti-CD3 (Becton Dickinson). To these either 2 × 104 freshly isolated CCR5-enriched cells or CCR5-depleted CD4+CD25+ cells or CD4+CD25+ CCR5-enriched cells isolated from CD4+CD25− cells that had been activated for 24 h with 2 μg/ml anti-CD3 and 10 ng/ml IL-12 (R & D Systems, Abingdon, U.K.) were added. After 72 h, the cells were analyzed by FACS by using CaliBRITE beads for volume-independent quantification. In some cases, [3H]thymidine incorporation was used (6).
Migration Assays.
Transwell migration assays were performed as described previously (11). CCL4 was used at 0–500 ng/ml. Migrated and input cells were analyzed by FACS.
Retroviral Transfection and Analysis of Transduced TR Cells.
The MLV-based retroviral plasmid m6pgfp carrying GFP and either CCR5 m6pgfp[CCR5] or blasticidine-S-deaminase m6pgfp[Blast] (control) were cotransfected with pCl-Eco packaging plasmid into 293TEBNA cell line by using CaPO4 precipitation. After 42 h, the supernatant was collected and used immediately. Freshly purified CD25+ T cells were activated by using plate-bound anti-CD3ε and murine IL-2 (20 ng/ml). After 36 h of activation, TR cells were transduced by using a 1:3 dilution of viral supernatant supplemented with 8 μg/ml polybrene, followed by centrifugation for 2 h at 450 × g and incubation at 37°C for 4 h. Transduced cells were cultured 36 h in medium containing murine IL-2 (10 ng/ml). Matching transduction efficiencies were confirmed by FACS. Female mice received 7.5 × 105 transduced cells i.v. and were allogeneically mated 48 h after transfer. Uterine and splenic lymphocytes were analyzed at E10.5 by FACS.
We thank F. Randow (Laboratory of Molecular Biology, Medical Research Council) for critical reading of the manuscript and provision of the m6p retroviral vector system and Theresa Langford and her team for expert animal handling. This work was supported by grants from the Arthritis Research Campaign (B0750) and the Carlsberg Foundation.
- †To whom correspondence should be addressed. E-mail: betz{at}mrc-lmb.cam.ac.uk
Author contributions: M.K. and A.G.B. designed research; M.K., K.G.A., and K.A.W. performed research; M.K. and A.G.B. analyzed data; and M.K. and A.G.B. wrote the paper.
↵*Present address: The Babraham Institute, Babraham Research Campus, Cambridge CB2 4AT, United Kingdom.
The authors declare no conflict of interest.
This article is a PNAS direct submission.
This article contains supporting information online at www.pnas.org/cgi/content/full/0604268104/DC1.
- Abbreviations:
- TR cell,
- regulatory T cell;
- T helper;
- En,
- embryonic day n.
- © 2006 by The National Academy of Sciences of the USA
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- Piccirillo CA


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Most people know what to do to maintain good oral health, but do you know the warning signs of all the dental conditions that could affect you? Having a dead tooth is one of the conditions that you need to educate yourself about so that you can get professional help immediately. In this article, Dr. Fardi Farhat, a dentist in Sterling Heights, MI, explains the causes, signs, prevention, and treatment options for a dead tooth.
Why a Tooth May Die
A tooth is described as non-vital or dead if there is no blood flowing to it. Two significant factors can lead a tooth to die, namely;
Tooth Decay
When you suffer from tooth decay, you develop cavities. Any untreated cavities can worsen and reach the pulp inside your tooth. The pulp may fight off the resultant infection for a while, but it may eventually become overwhelmed, and the pressure inside the tooth will rise. At this point, the blood vessels supplying the tooth will then become blocked, and your tooth will die.
Tooth Trauma
One or more of your teeth can still die even if you maintain the highest level of oral hygiene. This is because physical trauma, such as during a fall, can cause blood vessels connected to a tooth or teeth to burst, leading to the death of the affected teeth.
Signs That You Have a Dead Tooth
Dr. Fardi Farhat explains that while not all dead teeth will show visible signs that a layperson can identify, there are things you can watch out for. Here are some of those signs.
See a dentist in Sterling Heights, MI if you experience any type of tooth pain regardless of the magnitude of that pain because you could be having a dead tooth. In some people, a dead tooth can cause excruciating pain while the pain may be mild in other people.
A Bad Smell or Taste
Tooth infections can trigger a bad smell or bad taste in your mouth. Sterling Heights dentists caution that people who experience this bad taste or smell in the mouth could be having a dead tooth since the infection causing the smell or taste could have caused an abscess to form in that dead tooth.
Swelling is a common sign of inflammation, and this swelling can soon block blood from flowing to your tooth if the swelling isn't contained alongside the underlying cause of the swelling. A dead tooth can also cause swelling, mainly when the infection in the tooth spreads to the surrounding areas.
Altered Tooth Color
Dr. Farhat explains that when a tooth is no longer vital, it begins to darken. However, not all dead teeth will show this sign immediately, so see a professional when you notice the other signs discussed earlier.
Treatment Options for a Dead Tooth
Root Canal
If the dentist in Sterling Heights, MI diagnoses you with a dead tooth, you may have to undergo a root canal. During this treatment, the dentist at Dental One Care will remove all the infected pulp and clean out the tooth before filling the dead tooth permanently. This will prevent you from losing that tooth completely.
Tooth Extraction
In some cases, it may not be possible to save the dead tooth by performing a root canal. In such situations, your Sterling Heights dentist may extract the dead tooth and discuss tooth replacement options, such as implants and dental bridges. One of the adverse consequences of a delay to replace a missing tooth is bone resorption (loss of bone density and height due to lack of stimulation for the jawbone in that area).
How to Prevent Tooth Death
Wear a Mouth Guard
While it is hard to predict and forestall many accidents that lead to tooth death, some categories of people can wear mouth guards to protect their teeth from trauma. These include individuals who play contact sports. A custom-made mouthguard will offer more protection than a mass-produced one since customized mouth guards fit better.
Maintain Oral Hygiene
Dr. Fardi Farhat recommends that one of the best ways to prevent your teeth from dying is by sticking to an oral hygiene regime of brushing two times each day and flossing once a day. Use fluoride toothpaste when brushing so that you safeguard your teeth against the action of oral bacteria. Many people find that they have dead teeth resulting from tooth decay, so don't slack off on oral hygiene.
See Your Dentist Regularly
It is also advisable to see a Sterling Heights dentist every six months for professional cleanings and an annual dental checkup. These visits to Dental One Care will address any dental issues early before those conditions kill your teeth.
While taking the preventive steps above may not guarantee that you will not have a dead tooth, taking the suggested preventive steps will ward off most of the avoidable causes of dead teeth. Dental One Care is here to partner with you on this journey of retaining your beautiful smile. When the worst gets to the worst and a dead tooth has to be extracted, we shall recommend the most suitable replacement options.


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Quality One Australia and Asia Services
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5 Days in 5 Months Business Process Improvement teaches a disciplined method of process engagement and facilitation in business through a simple yet rigorous approach to knowing your business and creating documentation that supports focus and action to keep up to date with market changes, improvements and volatility.
This course has Work Based Learning Requirements in order to achieve the highest results. Work Based Learning Requirements are designed to allow participants to apply knowledge and theory direct to their business while conducting formal training sessions. The application of Work Based Learning Requirements defines the measurable immediate return on investment and immediate integration to Business as Usual that the unique approach of this course offers. Participants will be expected to submit Work Based Learning Requirements for assessment in order to achieve results. Work Based Learning Requirements must also represent the AS-IS state of the business.
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After the completion of the course, participants will be able to:
This course is delivered over 5 months 1 day per month. The next course will run on the 30th May, 30th June, 18th July, 5th September and 29th September 2014. This allows for participants to absorb and implement course material in a work environment as part of their business process improvement and gain feedback in the training setting.
Duration: 5 Days
Format: Public Courses or On site at your facility
Pricing Public: $3500+GST per participant (subject to schedule)
Pricing Onsite: $2500+GST per day plus materials, set up and extraneous expenses. Consulting and Coaching price negotiable.
Click here to enquire and email your 5 Days in 5 Months to Business Process Improvement Training Enquiry
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William Jackson and Aida Correa
Strategies Beyond SEO and Google
Video presentation provided by
William Jackson of My Quest To Teach
WordPress TV
WordCamp Presentations in 2018
Speaking at WordCamp Philly in
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conference with wonderful speakers
and equally wonderful sponsors and
via William Jackson: Strategies Beyond SEO and Google to Build Your Brand and Market Your Social Media Awesomeness
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Speaking at WordCamp DC in Washington, DC
The first WordCamp in Washington, DC was such
an honor to be able to speak at this historic event.
Looking forward to WordCamp DC in 2019
via William Jackson: How to be Dope and Lit on Social Media – Be an Online Community Activist
WordCamp Presentations in 2017
Speaking at WordCamp Wilmington in
Wilmington, NC
WordCampILM was a wonderful experience.
Meeting many engaging and talented people
with a passion for the open source and technology
via William Jackson: How To Be Dope And Relevant On Social Media


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This is the key advantage of dxf file meaning: they are supported by nearly any CAD program on this planet. The introduction of DFX recordsdata allowed different companies to work collectively on a design utilizing the same file. Before that, corporations alongside the design course of that had been utilizing completely different items of software program struggled to work together cohesively. It's not uncommon for different corporations to use completely different software program primarily based on want and finances, but it's distinctive for all those companies to be able to work together on one file. This allowed engineers to have the ability to work with architects, and not just alongside them.
For instance, let's say you will have designed a construction with Hot Rolled steel section units referred to as "Column"and " Girder", in addition to a Wood part set called "Joist". When you sort in a member layer title equivalent to "STEEL" then all members, regardless of dimension, will seem on a layer named "STEEL". This can be a Yes/No choice. For those who choose "Yes", the program will take members and assign them to a layer which uses their form label because the layer identify.
I suspected I could write a script that may parse the DXF and get the coordinates. He went to work getting me the DXF file while I gave myself a crash course on the DXF format. The DXF format was created by Autodesk for exchanging AutoCAD information. What I knew going in, and what made me confident I could write the script I needed, was that it's a plain textual content format, something I deal with on a regular basis. Autodesk has published many reference manuals on the format and has a pleasant webified manual for one of the older versions. In a nutshell, the DXF format is a sequence of sections, every of which comprises a number of key/value pairs on successive lines.
Is there an easy approach to export a flat panel shaped half made by utilizing reduce extrudes, so that it's going to open in autocad as a polyline? Also, these tops some times have routs in – for instance a gap minimize for heat venting, or rebated thinner to accomodate something beneath. Is it doable to represent this in a 2D dxf file? Or ought to we be taking a look at getting the factory some extra sophisticated software program that can routinely interpret a 3D part?


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Dhiraagu fixed broadband customers are facing service interruption due to a technical issue.
The telecom company said their customers may face interruptions on broadband services due to an unexpected technical issue. Apoligising for the inconvenience caused, the company said they are working to rectify the issue at the earliest.
Dhiraagu is the leading and largest provider of telecommunications and digital services in the Maldives. The company caters to over 75% of households across the country.


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Streamberry is a completely free cam to cam chat site.
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She's always looking for hot new topics, destinations, and brands to bring to Urbanette readers.e Harmony is more than just another 30s dating service.But when I phoned a dating agency eight months ago, everything had taken on a new sense of urgency. 'Haven't you found yourself a husband yet, Bridgey? But don't look desperate — men hate that.' I went speed-dating, online-dating, wine-tasting dating, quiz-dating and dinner-dating.I realised that since turning 35 three years ago, I hadn't met anyone I liked romantically, who was also single, straight and interested in me. ' one married ex-boyfriend wrote on my Facebook page. I joined running clubs, did acting classes and dance classes, went on skiing holidays and singles holidays and badgered my friends to set me up with their friends.No, men will run a mile.' She paused, then added: 'Sorry, dear.' I've never been someone who absolutely has to be in a relationship.Whenever I was between boyfriends in the past, I would just enjoy life until another man came along — through work, mutual friends or our eyes meeting across a crowded room.Thousands of couples have shared their story with us. 'Men want someone who is fertile but who doesn't want children just yet,' she continued.
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A cake shop where east meets west.
Ever wanted to put your life on pause? Located within the Portico Langsuan, this dark toned little dessert and coffee bar is designed for exactly those moments. It's a small space with indie music playin' and black tissue napkins to match the minimalist décor, but what really marks it out from the competition is not so much the colour scheme as the dessert list: a fusion of east with west. Take
'Twisted Far East' (B175), which is P2P's most popular signature dessert. Comprised of soybean, brown sugar, ginger jelly and a scoop of ice cream, the aim is to mimic the taste of a traditional Thai dessert that uses the same ingredients, and it's largely successful. For people who like their desserts super sweet the 'Baklava GaGa' (B155) is also worth considering. It's essentially Turkish Baklava: fruits & nuts wrapped by crispy pastry, the difference here being the modern presentation, scoop of vanilla ice cream and orange mandarin sauce.
For those of you who are impatient or just plain short on time, they also serve brownies and parfaits that you don't have to wait around for. Monthly specials mix things up (scan their Facebook fan page for updates) and, if none of the sweet stuff appeals, there are even wines. Lovers of a good cup of joe are also in the right place, as the blends here are from Vittoria, an esteemed brand from Australia. A single espresso costs B75, a double B95. It's notgroundbreaking, but Pause 2 Play strikes us as being a stylish alternative for sweet tooths who have tired of the same old slices. Try pausing the next time you're going past.
Pause 2 Play
Unit 207 The Portico, Lang Suan Road, Lumpini | 081-842-9424 | facebook.com/pause2play


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The new bank for rural poor: The post office
March 12, 2013 Editor 0
Post offices in Nigeria are becoming surrogate bank branches for the unbanked rural poor, under a government project launched last month.
Opening new bank branches in remote areas to reach the financially excluded is often prohibitively expensive, because the rural poor wouldn't use a branch enough to cover its costs.
That's why India and Nigeria have banks that are collaborating with post offices to turn them into banking outlets. This transformation will not be too far of a stretch considering just how many financial services many public post offices already provide in these regions: small savings accounts, life insurance, mutual funds, e-money orders and foreign exchange. Collaborating directly with banks would let post offices add small credit, remittances and various insurance policies, too. Very small-scale lending, for instance, does not require extensive knowledge and could be learned by the existing post office staff. Small savings deposits that already exist can be a useful start-up resource for lending. And India Post, for example, already has more than a century of experience operating Postal Life Insurance, which could be extended to include an array of valuable insurance policies for the rural poor.
The post office-to-bank transformation is one variation of "agent banking," the supply of financial services to customers by a third party in support of a bank or other licensed provider. Already, supermarkets, convenience stores, pharmaceutical retailers and lottery outlets have been turned into banking outlets.
90 percent of India's post offices are located in rural areas, compared to just 37 percent of its commercial banks. Because of this, discussions about an India Post Bank have been carrying on for a long time now, though plans have yet to materialize.
For Borno State in Nigeria, utilizing post offices to bring financing to the 87 percent of the population that lives in rural areas seems to banking industry leaders like a no-brainer. "In 2010, the average distance for a Nigerian to a bank was more than 10 kilometers," the Center for Financial Inclusion's Jeffrey Riecke wrote last month. "In addition to extending financial services to those without access, agent banking would help financial institutions regain customers that they might have lost over the year through the closings of unprofitable bank branches."
It is clear that post offices in remote locations provide a physical advantage over commercial banks, but will the money it takes to train postal workers, secure necessary licenses, implement technology, and raise salaries to match those of bank staff make this option any more sustainable than extending traditional banks into rural areas?
Those working on the Borno project seem to think so.
"If we succeed with the project in Borno, it will be extended to other states of the federation," Enterprise Bank CEO Ahmed Kuru said last month. "And we are convinced that we will succeed."There are more than twice as many post offices as banks in rural India, making post offices the more accessible network for the unbanked. Photo: irish (flickr)Related articles:Resources:
Related Posts
- Turning the post office into a force for financial inclusion
- Why financial inclusion matters
- Financial Liberalization and Foreign Bank Entry on the Domestic Banking Performance in MENA Countries
- World Bank Group's ICT Strategy – Using ICT for Greater Development Impact
- Why financial inclusion for youth will raise all economic boats
- Three ways digital cash helps the poor
Categories: Development, Feature Articles
Tags: bank, financial inclusion, nigeria, post office, rural poor
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text: Related Program: The Exchange What Are Your Questions For U.S. Rep. Chris Pappas? By The Exchange • Sep 3, 2019 Related Program: The Exchange ShareTweetEmail Credit Allegra Boverman for NHPR The Exchange will be talking with U.S. Rep. Chris Pappas on Thursday, Sept. 5. Submit your questions below for the first-term congressman. Pappas, a Democrat, represents New Hampshire's 1st District and serves on the Veterans' Affairs and Transportation and Infrastructure Committees. _ Tags: Chris PappasNew Hampshire Congressional Delegation1st Congressional DistrictNH PoliticsShareTweetEmailView the discussion thread. Related Content Pappas To Run For Reelection, Says Dem Presidential Nominee Must Appeal To 'The Middle' By The Exchange • May 31, 2019 Allegra Boverman for NHPR Over his first five months on the job, Congressman Chris Pappas has experienced the country's longest government shutdown and a spiraling controversy around President Trump. "This president operates like no other president in history," Pappas said this week on The Exchange. "He flouts the law, flouts the conventions of our democracy. And I think it's really important that he doesn't set a precedent for future presidents to be able to conduct themselves in a similar fashion." Democrat Dan Feltes Announces Run For Governor By Associated Press • Sep 3, 2019 Allegra Boverman for NHPR New Hampshire Senate Majority Leader Dan Feltes is seeking the Democratic nomination for governor. Feltes, in his third term, announced his candidacy Tuesday in a web video, saying he'll work hard, leave no one behind and get things done.


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Kate Weigel
Kate is an artist, educator and builder originally from Maine. She is currently the AmeriCorps Permaculture Initiative Assistant at USU Moab Extension for 2020. She has a BFA in Studio Art with a concentration in Sculpture from New York University. Kate is a former Global Academic Fellow in Visual Art at NYU Abu Dhabi and also the former co-founder of the Columbus Learning Cooperative, an alternative to school based on self-directed learning for kids and teens. In 2011, Kate participated in Bike and Build (ME2SB11), biking from Maine to Santa Barbara to raise money and awareness for affordable housing causes while building houses along the way. Since then, she has been active in affordable housing, completing an AmeriCorps term with Habitat for Humanity in Columbus, OH and later moving to Moab in 2019 to participate in an internship with Community Rebuilds. Her passions also include rock climbing, scenic carpentry, social justice and backpacking.


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Recycled Rides is a nationwide community service program that focuses on vehicle and parts recycling. Members of NABC repair and donate recycled vehicles to families and service organizations. Recycled Rides recruits collision repairers, insurers, paint suppliers, parts vendors and others to refurbish the vehicles.
The JM&A Group, an extended warranty provider, donated a one-year extended warranty on Hodges' vehicle. GEICO, Hall | MileOne Autogroup, Enterprise Rent-A-Car and local participating vendors donated gifts, gas cards, groceries and more.
Following the presentation of the car title, Hodges, who is also a minister, belted out a hymn of praise, thanking everyone who helped put her life back on track. Accompanying Hodges at the event were her daughter Precious, 16, and her adult son Elijah.
"I am most excited about driving to the grocery store and not having to haul bags of groceries on the bus," Hodges said. "This will open up a whole new world for my family and me.
"I can take people to church, get to my doctor appointments, see my grandchildren and volunteer with the United Way. Now I can visit my father in New Jersey, who I haven't been able to see in years."
With solid transportation, Hodges is moving toward self-sufficiency. Her next move is to develop a steady income. A talented seamstress and designer, Hodges hopes to one day open her own business, which she has already dubbed the Glory Boutique.
Lance Carson, Hall's director of collision centers and parts operations, said it felt amazing to help.
"It is definitely not work, because we get so much out of it. Hall is proud to be part of this group effort that will impact the life of someone like Anjenette," he said.
He said it was the sixth time the dealership has partnered with GEICO to refurbish and gift an automobile.
According to GEICO spokeswoman Toiya Adair Sosa, the whole experience was humbling.
"It is not often you can give back by changing the trajectory of someone's future," she said.


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Went to Walmart and got a $1 small dog chain. Cut 2 holes in the cuttlebone and used zip ties to hold the cuttlebone to the dog chain on both ends (dog chain for weight to keep it on the bottom).
Just an idea.