As one of the top study abroad destinations in the world, the US has, for the first time, recorded a sharp decline in the number of international graduate student enrolment, as per data gathered from The Council of Graduate Schools.
The data reveals that the international graduate application rates had increased for the Fall 2020 session across different US universities. An overall growth of 3% had been detected between 2019 and 2020 Fall Session. However, between Fall 2020 and Fall 2021, a sharp decline of 39%.
The CGS data reveals that a 43% decline was seen for different Masters programme, while a 26% decline was seen for Doctoral level programmes. However, this rate of decline was witnessed in all different types of institutional types. First-time graduate student enrolment from markets such as India and China were significant, the data revealed.
CGS President Suzanne Ortega stated that the effects of COVID-19, especially the international travel restrictions and health concerns along with the lack of consistency and timely direction regarding the international graduate student visa policy by the Trump Administration, such sharp declines were expected.
Participating in the CGS report that included findings from the Fall 2020 admissions info, a total of 326 universities and colleges were involved, with 69% of the participants being public Universities while 65% of the participants being doctoral universities.
Considering the location wise decline in the number of first-time graduate enrolment, a 47% decline was witnessed in Asia, meanwhile, from Eastern and North African countries, a decline of 36% had been witnessed.
Also Read: Survey: Number of Foreign Scholars in the US Dropped by 9.6% in 2020
China and India, who previously have been the largest market shareholders in the first-time international graduate applications as well as overall enrolments, were among the countries with the sharpest decline in applications. China and India recorded a first-time graduate enrolment of 37% and 66% decline, respectively.
While a decline in the international first-time graduate enrolment was seen in far off countries, Canadaand Mexico were also among the countries that display a decline. First-time international graduate enrolment from Canada was recorded at -5%, meanwhile, a -6% international graduate first-time enrolment was seen from Mexico.
Additional surveys, i.e. the 2020 NAGAP/CGS Survey of Graduate Enrolment Management Professionals and the 2020 CGS International Graduate Admissions Supplemental Survey, were also fielded by The Council of Graduate Schools.
Also Read: Suffolk University's Initiatives to Accommodate International Students
It was revealed that over 80% of the participants highlighted an increase in the number of deferrals from new admitted international graduate students. Moreover, the institutions also revealed that an overall 5% increase in deferments have been witnessed over the past few years.
Similar to the overall international graduate first-time enrolment, the deferrals have been witnessed to be consistent across different degree levels, i.e. masters and doctoral programmes, with 12% and 10% deferrals across the programmes, respectively.
Ortega commented that while the declines are concerning, one of the bigger questions that must be answered is how the deferrals will affect the admission offers as well as the first-time enrolment for the Fall 2021 session, especially with continuing travel restrictions.


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- TitleCofounder and CEO
Reeves is cofounder and CEO of Gusto, a payroll and benefits platform that serves small businesses. In 2019, Reeves led Gusto through Series D funding, which saw it raise $200 million at a $3.8 billion valuation. During the pandemic, Gusto built new features to help small businesses apply for Paycheck Protection Program loans—a forgivable loan program that was the difference between survival and bankruptcy for many small businesses. To date, Gusto has enabled $2.5 billion in approved PPP funds for small businesses. Since Reeves cofounded Gusto in 2012, the firm has raised more than $500 million.

domain: finance


3 key challenges for Green Investment Banks
A recent OECD/New Climate Economy report on Green Investment Banks (GIBs) has found that 12 ‘GIB or GIB-like’ institutions now exist across the world, almost all of which have been created in the past 5 years. While the progress highlighted in the report is promising, my impression is that 3 key challenges remain for these institutions in promoting large-scale, low-carbon resilient development:
- Achieving transformational change from a relative niche
- Increasing the focus on financing adaptation
- Moving away from a reliance on public funds
Transformational change from a relative niche
The finance mobilized by GIBs to date is not enough to ensure the low-carbon vision for the future laid out by the Paris Agreement, nor ensure resilience in our global infrastructure over the coming century. The flagship UK GIB has committed GBP 3.4billion to the UK’s ‘green economy’ since its inception (approximately USD 4.2billion at today’s exchange rates), compared to roughly USD 56billion invested nationally in clean energy and energy efficiency from Germany’s mainstream national development bank, KfW, in 2015 alone.
The OECD/NCE report concludes with an analysis of the merits of creating Green Investment Banks versus mainstreaming green principles across the board in existing National and Multilateral Development Banks. This is essentially a trade-off between the independence and maneuverability of smaller dedicated institutions, and the potential for impact of larger, established entities. One way or another a step change is needed in the current impact of GIBs.
An increased focus on adaptation
Within the objectives of the GIBs studied in this report, most mention tackling harmful greenhouse gas emissions, particularly through clean energy investments. But very few (if any) focus on preparing our current and future infrastructure to withstand the threats of climate change. All 4 of the UK GIB’s ‘investment sectors’, for example, are targeted at emission-reducing schemes in the energy sector, with no mention of climate resilience.
The focus of GIBs on mitigation over adaptation reflects a broader consensus that low-carbon investments offer more viable economic opportunities than projects focused on adaptation. There is some truth to this. The markets for renewable energy and energy efficiency are now well established, and offer short term returns on investments, as well as broader cost-saving opportunities. On the other hand, the market for products and services that offer climate resilience is still emerging, and complicated by the difficulties of defining and measuring adaptation and the long-term rates of return associated with resilience investments.
However, the market for resilience has the potential to be far greater than the market for low-carbon, and given the increasing costs associated with climate impacts, GIBs will need to become much smarter about promoting resilience, to ensure the longevity of the predicted USD 90trillion in infrastructure investments set to be made over the next 15 years.
Transition away from a reliance on public backing
Regardless of the perceived risks associated with the privatisation of UK GIB, this must be the ultimate goal of all such institutions, once initial public support has allowed them to achieve competitive rates of return. Whilst public control of GIBs lends benefits in the shape of transparency, accountability, and the security of investments, the reliance on public capitalization stymies the level of total finance that can be raised. To meet the estimated USD 16.5trillion of investment in mitigation needed to ensure global warming is kept to 2 degrees, let alone challenges of climate-proofing global infrastructure, climate-smart investments must prove themselves to be on a par with conventional investments in terms of rates of return, and tap into the vast well private capital looking for viable investments.
Green Investment Banks have shown solid results in terms of mobilizing private investment for infrastructure, creating jobs, and reducing emissions of harmful greenhouse gases. We wait to see if this new finance can achieve transformational sustainable development.


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Monday, January 05, 2009
Newsbreak: MOF oppose, EPU insist with IJN privatisation to SD
The EPU meeting with IJN proceed as scheduled. Sime Darby was not present.
In the meeting, Director General of EPU, Datuk Dr Sulaiman Mahbob informed the meeting that Government insist IJN to be privatised to Sime Darby. Dr Sulaiman is the former Director of Institut Integriti Malaysia , Malaysia Institute of Economic Research (MIER), and Secretariat of National Economic Action Council (NEAC).
The initial information received from EPU source revealed the rationale was to improve doctors pay package and increase financial capacity for expansion. It is similar to Sime Darby's expressed justification for their proposed takeover of IJN.
The IJN side dispute the rationale of EPU with the doctors' near 'unanimous' press statement on December 19th, 2008 and IJN's financial reserve of RM400 million. They argued that IJN could raise more fund to finance expansion by leveraging on its reserve.
Sources said the representative from Ministry of Finance present strongly opposed to the privatisation and insisted IJN should remain a non-profit organisation. They explicitly expressed the Minister of Finance is opposed to the Sime Darby proposal.
Dr Sulaiman response was the Government insist the privatisation of IJN must go on, despite the public is overwhelmingly against the privatisation.
The same source believed the privatisation will proceed after the Kuala Terengganu by-election.
Why is EPU resonating Sime Darby's rationale? Does that explains Sime Darby's absence? EPU is speaking for them. EPU falls under the Prime Minister's Department. Is PM "taking instruction" from Sime Darby Chairman, Tun Musa Hitam? And, why the hurry?
Read back this blog's yesterday's posting here. Apanama reported Government approve Labu LCCT plan here.
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domain: news


text:
While I have talked about the Federal Trade Commission (FTC) and its guidelines on affiliate links and other ways you are at risk as a blogger, I haven’t addressed one of the worst ways an author can get busted by the FTC.
Don’t assume that most readers who use Kindle Unlimited (KU) are aware that an author make money for each page a reader views. It’s not a lot of money per page (estimated at around half a penny/page ($0.005), but some authors are making a lot of money, as in $10,000 – 25,000/month from KU. That’s a sizeable chunk of change, but I don’t see many authors letting potential readers know they are making money off page reads.
As I have said before, and will continue to say, authors and others need to inform people when they making money off a link, be it an affiliate link or a KU link. AND they need to give people a reasonable estimate of how much the links are generating in income.
Pingback: Some Terms You May Not Know | Ups and Downs of Family History V2.0

domain: economics


text:
Aug 15, 2013
Kim Kardashian has secluded herself from the rest of the world since the birth of her baby with Kanye West, North West. Kim, who is usually very active and friendly in the media (unlike her boo thing) hasn't been spotted out since June.
TMZ, of course, has the first photos of 'Ye, Kim and baby out and about. The three, plus a nanny, visited the doctor's office. And surprisingly enough,...
Team Hennessy owned a "Very Special" JL nights birthday celebration with Common, LA Dodger's Matt Kemp, Marcedes Lewis of the Jacksonville Jaguars, and NBA player Kenyon Martin the other night. Check out some photos from the event above.
Kid Ink's new "Show Me" single is rapidly climbing both the Billboard and radio charts, and an official visual featuring and directed by Chris Brown will be dropping next week.
Check out the gallery above for an exclusive first look at the making of the video (courtesy of Born Original), and cop the single on iTunes. It'll be included on Ink's major label debut My Own Lane, which is scheduled to...
Jay-Z's highly anticipated album, Magna Carta Holy Grail, was supposed to drop at midnight for Samsung users, although a fair share of technical glitches delayed the album's release through the app, which left many users extremely frustrated.
Nonetheless, the album's out there now, and last night in celebration of Magna Carta, Samsung and Hov held an album release party.
Jay Z and Dame Dash, former Rocafella partners, reunited last night in NYC when they attended a mutual friend's birthday party.
At the event for a music industry executive's birthday, the two smiled for a photo together. In a recent interview Jay had revealed he couldn't remember that last time he'd seen Dame Dash, although he said he still had love for him.
Hopefully it's not years and years...
HotNewHipHop was on hand for Sabi's recent video shoot for the song "Cali Love" with Tyga, which is an ode to West Coast classics.
Appropriately, the visual was shot in California at a house in El Segundo. The video is directed by Michael Mihail, and you can expect to see a crazy house party going down complete with a pinata, confetti, and of course, drinks. In this particular scene, the duo...
Check out some concert and backstage photos of Waka Flocka during his Triple F Life Tour. Photos by: Mike DeLeon
May 17, 2014
When hip hop 'It' couple Jay Z and Beyonce recently showed up courtside at the Brooklyn Nets vs. Miami Heat game amidst major controversies. the buzz of the pairs appearance was carried around swiftly.
Major celebrities attending basketball games is nothing new and has come to be expected. Always known to have the best seats in the arena these celebrities are at times just as much of a spectacle...
Jul 20, 2013
For a lot of us, summer is already half-way over. So, in the spirit of this short but sweet season, we wanted to share a photo collection of some of our favorite artists with their hot girlfriends, wives, baby mamas and much more!
Enjoy this list of photos and share with us how you're gonna do it up this summer.
Big Sean's new album Hall Of Fame officially dropped today, but Sean Don's been celebrating it. Last week in Ohio at Villa Big Sean held a block party in celebration of the album, and HotNewHipHop was on hand at the event.
We also helped out a few lucky Big Sean fans by hooking them up with the VIP treatment, which included cutting the line and taking a photo with the rapper.
LeBron James and long-time girlfriend Savannah Brinson were married this weekend at Del Grand Mar Hotel over a three-day event. They kept the guest list at a modest number, inviting only 200 people, but the people on the list were anything but. Chris Paul, Carmelo Anthony, Dwyane Wade and Gabrielle Union were in attendance as well as Jay Z and Beyonce, who performed. Ne-Yo also sang at the...
Throughout the years we have seen an assortment of Jordan Fusions rise and fall. Remember the Jordan Dub Zero? How about the CMFT 13s? Forgettable as past fusions have been, there have been some success stories. The Jordan Spizike for instance, combining elements of the Jordan III, IV, VI, IX and XX, continues to have new colorways release every year, many of which end up selling out....
May 30, 2013
Cassie used to model and act before she got into singing, but today we find her returning to her modeling roots for the latest issue of Esquire Magazine.
Cassie shot a bunch of photos with Esquire for their June/July issue, check them out in the gallery above.
She also told a few "funny jokes" for Esquire which you can watch here.
As reported by MissInfo, Kanye West took a minute to celebrate his birthday with friends before a performance at the Governors Ball in New York City last night. Those in attendance at the private birthday dinner at Miss Lilly’s included Nas, Jay-Z, Beyoncé, Jonathan Cheban, Scott Disick, David Blaine, actor and comedian Aziz Ansari and Kanye’s former A&R...
Ace Hood has linked up with Lil Wayne and friends to shoot a visual for his single featuring Weezy, "We Outchea."
Ivan Berrios comes through with photos from the set, peep them in the gallery above.
Ace Hood's album, Trials & Tribulations, is set to drop on July 16th.

domain: celebrity


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November 28, 2018, 6:00 PM @ Rio Rancho City Hall, Governing Body Chambers
Regular Governing Body meetings take place on the second and fourth Wednesday of each month at 6 p.m. Meetings are streamed on the City's website and broadcasted on the city's government cable channel 56, RioVision (available to Rio Rancho Cable One subscribers).
November 29, 2018, 6:30 PM @ Sandia Vista Elementary School
Starting in October, a town hall meeting will be held in each of the six City Council Districts. The meetings will be co-hosted by Mayor Gregg Hull and the respective City Councilor for that district. The joint town hall meetings are intended to create venues where citizens can share information and collaborate with the Mayor and their City Councilor in a positive manner. Residents are encouraged to attend and ask questions or voice concerns about an issue unique to a specific City Council District.


For a while there, I was starting to believe that catching a break was a fairy tale we are fed by the media in our daily soap operas, but they do happen; I caught an epic break by getting a job and an apartment, all in the same month. My buddy and roommate has been a pessimist for a long time now, but he isn’t the reason why I felt that way, or, at least, not the only reason.
But my buddy did provide me with an insight. Well, it was actually there in plain sight. The way you look at the world actually has an impact on your world itself. Perception is everything. It’s as simple as this: If you don’t look for a break, you can’t catch one. If you don’t believe that anything good can happen to you, if your outlook on your future is utterly bleak, well, then you are doomed to a life of despair. I’m not superstitious, but it was like a curse. I couldn’t get anything done, because I believed it was pointless. I was content with the fact that my life wasn’t going anywhere. I was Ok with wasting my days away with playing videogames and drinking alcohol until I passed out. I couldn’t pinpoint the time when my attitude turned, it probably happened in steps, gradually. I did very much notice a difference when I started blogging for real. I tried blogging once before, when I was stinking drunk, I only wrote two posts on that blog and gave up after I found I had no audience at all, but that wasn’t on WordPress, where I have a wonderful community. I digress.
Blogging did two things for me. Well, maybe it’s just one thing. I choose to present it as two items, after all, perception, and in extension presentation, is everything:
· I was exposed to new thoughts and perspectives
· Writing about myself forced me to think about myself
I read a lot of blogs. Most of those blogs are very much like journals, people write about their problems, worries and fears for everyone to read; also their opinions, but they are intimately linked to the problems, worries and fears. I try to present people with solutions, or at least sympathy. Why do I do it? Well, because I do sympathize. The anonymity on the Internet gives me the luxury of not having to care, so when I do care, I can do it completely and honestly. Being exposed to those stories, of course, also gives me the urge to share my own feelings and faults, not only in the comment section for everyone who happens to stumble on the post I happened to read, but on my own blog for everyone who cares to find directly. You can see now where this all could be presented as one single item. It’s not even a dualism, but more of an action – counteraction relationship, like Newton’s third law of motion. I digress.
So, in danger of sounding like one big softy and hippy, both of which I may even be, I will say this: Share and Care, it will improve you and your environment, but be honest about it. When someone’s being a total dick to you, stand up for yourself or walk away, but don’t let them tear you down. Easier said than done, I know. But you’ll catch a break, when you’re looking for it.


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Q4 FY13 dollar revenues for Mindtree were in-line with estimates (US$113mn v/s expectation of US$112.6mn).
Q4 FY13 dollar revenues for Mindtree were in-line with estimates (US$113mn v/s expectation of US$112.6mn). The strong growth was on the back ramp-ups of deals won in the recent past with volumes growing 3.7% qoq (4.2% offshore and 1.1% onsite). Due to higher number of billing days, the realised productivity was down 1.4% sequentially. In rupee terms, revenues grew ~4% qoq to Rs6.1bn.
The key business segments of IT services and Product engineering services grew well posting a 3.1% qoq and 2.3% sequential growth respectively in dollar terms. Amongst the verticals, the growth was led by Manufacturing and retail (+8.3 qoq), others (+5.3% qoq) and Travel, media and services (+2.8% qoq). Within services, IMS continued to drive the growth (+8.3% qoq) followed by maintenance (+2.8% qoq). Discretionary service of package implementation also grew well at 15.4% qoq albeit on a lower base. Growth amongst geographies was driven only by RoW (~66% of incremental revenues) which grew 19.8% qoq. From the clients’ perspective, US$20mn+ clients grew sequentially by one to 5 clients. Top 6-10 and the non-top 10 clients drove the performance growing 5% and 5.5% respectively.
The OPM performance for Mindtree was also in-line with estimates coming in at 19% (141bps sequential correction). Hiring was strong during the quarter with gross addition of ~1000 employees resulting in increased employee expenses (+160bps qoq as proportion of revenues) and lower utilisation (down 2.2% qoq). A leverage on the SG&A costs (+14bps qoq), on the other hand, supported the OPM. Higher than expected OI and in-line operating profits resulted in higher than estimated net profit of Rs789mn (versus expectation of Rs736mn). Net employee additions (+6% qoq) were strong as company hired 550 freshers in Q4 FY13. The reported attrition inched further down to 13.4% (15.1% in Q3 FY13).
Management’s qualitative guidance and commentary remained positive with an expectation of a better growth in FY14 than FY13. Improvement in outlook for PE services, decent deal wins in IT services space (driven by IMS) and overall improvement in spending behaviour of its client portfolio were the key reasons for the constructive commentary. An even distribution of growth versus (back-end loaded in FY13) and decent hiring (to hire 1700 in FY14) also add credibility to the guidance of a better FY14. On the margin front, sizeable headroom in margin levers (esp. utilization) should also help maintain the OPM if not improve. We keep our estimates largely unchanged (11%/6% dollar revenue/rupee earning CAGR over FY13-15E). Maintain BUY with 9-month TP of Rs950.
|(Rs mn)||Q4 FY13||Q3 FY13||% qoq||Q4 FY12||% yoy|
|OPM (%)||19||20.4||(141) bps||18.7||25 bps|
|Effective tax rate (%)||21.7||21.8||-||16.5||-|
|Adj. PAT margin (%)||12.9||16.7||(286) bps||13.1||(22) bps|
|Y/e 31 Mar (Rs m)||FY12||FY13||FY14E||FY15E|
|Revenues (Rs m)||19,152||23,618||26,109||28,743|
|yoy growth (%)||26.9||23.3||10.5||10.1|
|Reported PAT (Rs m)||2,185||3,389||3,855||3,828|
|yoy growth (%)||115.1||55.1||13.8||(0.7)|
OPEN A DEMAT ACCOUNT & Get


text:
|Torn World Forums
|World Building Blog Fest
|Page 1 of 1|
|Author:||wyld_dandelyon [ Mon Jan 28, 2013 9:15 pm ]|
|Post subject:||World Building Blog Fest|
So, Ellen, what's this about a World Building Blog Fest?
|Author:||ellenmillion [ Tue Jan 29, 2013 4:41 pm ]|
|Post subject:||Re: World Building Blog Fest|
I ran across it in Layla's journal and signed up on a lark.
It's basically a bloghop, where many blogs touch on the same topics for a period of time, and you can go read other posts in the series. Torn World's first installment is here, on the topic of Geography and Climate: http://torn-world.livejournal.com/134270.html
The second installment is History and Politics, and is posted here: http://torn-world.livejournal.com/134506.html
Tomorrow's installment is on Magic and Religion, though I will be concentrating on time crystals, Others and boundaries.
Day four is Food, Drink, Holidays, & Culture, and Day five will be an excerpt with an example of the worldbuilding.
|Page 1 of 1||All times are UTC - 9 hours|
|Powered by phpBB® Forum Software © phpBB Group

domain: geography


text:
The social security and supplemental social security disability about your eligibility for disability benefits . My social security set yourself free open a my social security account today and rest easy knowing that youre in control disability and survivors benefits. Do it yourself social security disability benefits delivers the formula for winning a social security disability ssd ssi claim without an attorney. If you are disabled and no longer able to work you may be eligible to receive social security disability benefits those who have a disability illness or have . Ssdi refers to the social security disability insurance the social security disability benefits ill get if i win my do it yourself legal help
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domain: law


text:
Pancreatic β-cell dysfunction is a diagnostic criterion of Type 2 diabetes and includes defects in glucose transport and insulin secretion. In healthy individuals, β-cells maintain plasma glucose concentrations within a narrow range in concert with insulin action among multiple tissues. Postprandial elevations in blood glucose facilitate glucose uptake into β-cells by diffusion through glucose transporters residing at the plasma membrane. Glucose transport is essential for glycolysis and glucose-stimulated insulin secretion. In human Type 2 diabetes and in the mouse model of obesity-associated diabetes, a marked deficiency of β-cell glucose transporters and glucose uptake occurs with the loss of glucose-stimulated insulin secretion. Recent studies have shown that the preservation of glucose transport in β-cells maintains normal insulin secretion and blocks the development of obesity-associated diabetes. To further elucidate the underlying mechanisms, we have constructed a computational model of human β-cell glucose transport in health and in Type 2 diabetes, and present a systems analysis based on experimental results from human and animal studies. Our findings identify a metabolic threshold or “tipping point” whereby diminished glucose transport across the plasma membrane of β-cells limits intracellular glucose-6-phosphate production by glucokinase. This metabolic threshold is crossed in Type 2 diabetes and results in β-cell dysfunction including the loss of glucose stimulated insulin secretion. Our model further discriminates among molecular control points in this pathway wherein maximal therapeutic intervention is achieved.
Citation: Luni C, Marth JD, Doyle FJ III (2012) Computational Modeling of Glucose Transport in Pancreatic β-Cells Identifies Metabolic Thresholds and Therapeutic Targets in Diabetes. PLoS ONE 7(12): e53130. https://doi.org/10.1371/journal.pone.0053130
Editor: Filippo Castiglione, National Research Council of Italy (CNR), Italy
Received: August 22, 2012; Accepted: November 23, 2012; Published: December 27, 2012
Copyright: © 2012 Luni et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Funding: This research was funded by the Institute for Collaborative Biotechnologies through grant W911NF-09-0001 from the US Army Research Office (CL, FJD), and by US National Institutes of Health (NIH) grant DK048247 and GM100192 (JDM). The content of the information does not necessarily reflect the position or the policy of the Government, and no official endorsement should be inferred. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing interests: The authors have declared that no competing interests exist.
Glucose transport across the plasma membrane is an essential process among cells and organisms , , . Glucose is a major source of metabolic energy, yet deviations of glucose concentration from a narrow range in the blood of mammals can be life threatening. A chronic elevation of blood glucose concentration is linked to the pathology of diabetes. Normally, pancreatic β-cells sense a postprandial rise in blood glucose and secrete insulin into circulation by a process termed glucose-stimulated insulin secretion (GSIS). The resulting activation of insulin receptors among peripheral tissues increases glucose uptake in normalizing blood glucose levels . In this way, the pancreatic β-cell acts in concert with peripheral insulin action to regulate glucose homeostasis in the organism. The ability of the β-cell to transport glucose across the plasma membrane and thereby sense changes in blood glucose concentration is an essential component of normal β-cell function and the maintenance of glucose homeostasis.
In Type 2 diabetes (T2D), β-cells appear defective in sensing glucose, and this has recently been linked with diminished expression of both GLUT-1 and GLUT-2 glucose transporters , . Deficiency of glucose transporter expression and glucose uptake among normal β-cells causes β-cell dysfunction with loss of the GSIS response . A similar study in mice administered a high-fat diet indicated that diminished β-cell Glut-2 expression contributed to disease pathogenesis, while preservation of β-cell glucose transport and GSIS prevented β-cell failure and the onset of obesity-associated diabetes . Those studies further reported a conserved sequence of molecular events in human and mouse β-cells initiated by elevated levels of free fatty acids, transmitted by nuclear exclusion and down-modulation of HNF1A and FOXA2 transcription factors, and affected by GNT-4A glycosyltransferase deficiency. These events were found to diminish expression of GLUT-1 and GLUT-2 with markedly reduced glucose transport and loss of GSIS, and revealed that an acquired deficiency of β-cell glucose transport promotes the pathogenesis of diabetes.
Glucokinase (GK) activity is normally the limiting factor in β-cell glucose utilization . Upon entering the β-cell, glucose is rapidly phosphorylated by GK forming glucose-6-phosphate (G6P). This ensures that glucose cannot exit the β-cell through the same diffusive glucose transporters GLUT-1 and GLUT-2, and instead can enter glycolysis. Intracellular concentrations of G6P normally increase in response to elevated blood glucose. This promotes glycolysis and subsequent events including the GSIS response. The inheritance of partial defects in GK activity by gene mutation impedes the formation of G6P and disables the GSIS response, as observed in the human disease known as Mature Onset Diabetes of the Young, MODY2 .
In understanding how the acquisition of deficient β-cell glucose transport may contribute to the pathogenesis of Type 2 diabetes, we have developed a mathematical model of glucose transport that integrates experimental findings that include human data from β-cells of normal and T2D donors , with supporting data from rodent studies. This model includes the GLUT-1 and GLUT-2 glucose transporters of human β-cells as well as components of a molecular pathway that controls their expression . Our findings indicate a physiological and metabolic threshold exists below which glucose entry, and not GK activity, is rate limiting in G6P production. Among β-cells isolated from animal models of diabetes and human T2D donors, we show that β-cell glucose transport is below this threshold while healthy humans and rodents maintain glucose transport well above the threshold. We further identify molecular nodes within this pathogenic pathway where therapeutic intervention would be most effective.
Initial Steps in GSIS
Glucose transport into the β-cell occurs by facilitated diffusion through plasma membrane-resident GLUT-1 and GLUT-2. While Glut-2 is the main transporter in mouse β-cells and is essential for GSIS, in human β-cells both GLUT-1 and GLUT-2 are present and it appears that either can support GSIS , , , , , . Both transporters exhibit Michaelis-Menten kinetics with different values for glucose indicating the concentration of glucose when the rate is half of the maximum velocity. This is approximately 3 mM for GLUT-1 and 17 mM for GLUT-2 . Despite these differences, expression of either transporter alone can promote sufficient glucose entry for phosphorylation by GK and the GSIS response , , . The GK rate is described by Hill kinetics with a of 8 mM  and an exponent of 1.7 . The parameter in the Michaelis-Menten and Hill kinetics is dependent on the level of expression of the glucose transporters and GK. We therefore expressed of GLUT-1 and GLUT-2 as:(1)where is the parameter value for normal β-cells, and represents the fraction of plasma membrane-resident glucose transporter expression compared to normal. Thus, is equal to unity in normal cells, and less than unity in β-cells from T2D donors in which the glucose transporters are diminished. We assumed identical GK activities in β-cells from T2D donors and normal human β-cells. The complete system of equations for this element of the model is reported in (Text S1).
We simulated the first stages of glucose uptake and utilization in normal β-cells and from two T2D donors whose average plasma membrane-resident GLUT-1 and GLUT-2 are markedly reduced to 14% and 5% of normal, respectively . This simulation included a postprandial glucose excursion from 2.8 mM to 16.8 mM (Figure 1), which corresponds to the concentration range used in previous experiments . The net glucose uptake by the cell is given by the difference between the inward and the outward flow of unphosphorylated glucose through GLUT-1 and GLUT-2. The qualitative behavior of the two glucose transporters is similar: when plasma glucose is increased to 16.8 mM, glucose enters the β-cell at a high rate because the extra-cellular glucose concentration is greatly above equilibrium considering the intracellular concentration. The glucose uptake rate is progressively compensated by the export rate until a steady-state is reached at a higher glucose concentration. The result is a rise in net glucose transport through each transporter until this new steady-state is established. Due to the lower of GLUT-1, GLUT-2 accounts for most of the glucose uptake when both transporters are present. The kinetics (i.e., time-dependent behavior) of glucose transport through the two transporters is also different. In addition, because of the lower value of GLUT-1, the relative difference between the steady-states at high and low blood glucose is smaller for this transporter (Figure 1).
A change in plasma glucose concentration from 2.8 mM to 16.8 mM was applied as an input to the model. Net GLUT1-dependent glucose uptake was calculated as the difference between inwards and outwards rates, and . Net GLUT2-dependent uptake was calculated analogously. Phosphorylated glucose concentration includes also the concentration of its derivates in the pathway that are not explicitly modeled. Black lines refer to the behavior of healthy β-cells, gray lines represent behavior of β-cells from T2D donors.
The diminished β-cell surface expression of GLUT-1 and GLUT-2 in T2D can strongly affect glycolysis, even in the presence of normal GK activity. Since intracellular glucose concentration is much lower than normal, the GK rate and G6P accumulation are also strongly reduced (Figure 1).
Once inside the β-cell, intracellular glucose is subject to two competitive mechanisms: outward diffusion through glucose transporters and phosphorylation by GK. The GK rate has been calculated to be a slow enzymatic step that normally is rate-limiting for insulin secretion . For a range of intracellular glucose concentrations, we compared the GK rate of G6P production with the outward diffusion rates of glucose through GLUT-1 and GLUT-2 in a healthy β-cell (Figure 2A). The results confirm that the glucose phosphorylation rate by GK is much slower than the outward glucose transport through both GLUT-1 and GLUT-2 under normal conditions. This means that after glucose enters the cell most of it diffuses out because GK phosphorylation is relatively slow. Thus GK is the glucose sensor and rate-limiting factor in G6P formation among healthy β-cells. However, when β-cell surface expression of GLUT-2 is approximately 20% of normal ( in equation (1)), its outwards transport rate is comparable to the GK rate (Figure 2A). Thus, in a β-cell expressing 20% of normal GLUT-2, and in the absence of GLUT-1, there is a transition in the controlling mechanism forming G6P. Below this threshold of GLUT-2 expression, glucose transport becomes the rate-limiting factor.
(A) GLUT-1 and GLUT-2 outwards rates ( and , respectively), and GK kinetics as a function of intra-cellular glucose concentration for normal () glucose transporters’ expression and reduced GLUT-2 expression (). (B) Steady-state GK rate calculated at 16.8 mM extra-cellular glucose concentration as a function of concerted GLUT-1 and GLUT-2 deficiency. ε1 and ε2 are the fractions of GLUT-1 and GLUT-2, respectively, compared to normal. The solid line indicates the threshold between transport- and phosphorylation-limited G6P formation (derived in (A)), whereas asterisks indicate the positions of T2D patients β-cells. Inset represents an enlargement of the lower left region.
We evaluated the steady-state G6P production rate at reduced levels of glucose transporter expression when extra-cellular glucose concentration is elevated to 16.8 mM, in order to determine when the GK rate falls below the calculated threshold. We used the model to simulate the concerted reductions of GLUT-1 and GLUT-2 at the β-cell plasma membrane. The results are shown in Figure 2B, where a healthy β-cell is represented at the top right corner, with a GK rate of 0.12 nmol/min/105 cells. The T2D patients previously studied  are represented in the lower left region. In β-cells expressing 20% GLUT-2 and no GLUT-1, the threshold condition identified in Figure 2A, intracellular glucose concentration is about 6.5 mM and GK rate is 0.07 nmol/min/105 cells. This intracellular glucose concentration is 50% of normal and consequently the GK rate is approximately 60% of normal. This further specifies the critical threshold or tipping point when transition occurs from GK-controlled to glucose transport-controlled G6P formation. In Figure 2B, we highlighted all the possible combinations of GLUT-1 and GLUT-2 expression that produce the same critical GK rate. Strikingly, data points from the T2D patients are located below this threshold. These findings further agree with experimental data  and indicate that glucose transport by GLUT-1 can compensate for the absence of membrane GLUT-2 leaving GK as a glycolytic pacemaker when GLUT-1 is expressed at normal levels (Figure 2B).
Regulation of GLUT-1 and GLUT-2 Expression
The model above describes glucose entry into the human pancreatic β-cell and its accumulation following phosphorylation by GK. Considering that diabetes can be induced in animal models by β-cell glucose transporter deficiency, we integrated the previous human model (modules VI in Figure 3) with factors involved in the transcriptional and post-translational regulation of GLUT-1 and GLUT-2 (Figure 3). Experimental data obtained from human β-cell studies of normal donors, T2D donors, and palmitic acid-treated normal β-cells, supported model development  (Methods). Results from rodent studies were also integrated where indicated. As experimental data were obtained from a pool of cells, the single-cell model we developed is representative of average β-cell behavior, neglecting the intrinsic heterogeneity of the cell population. Stochastic noise is also averaged in the experimental cell population, further justifying our deterministic modeling approach.
The six subsystems discussed in the text are highlighted and denoted by roman numbers. Thick blue arrows indicate activation of transcription by promoter binding and histone hyperacetylation, thin blue arrows activation only by promoter binding; red bars indicate an inhibitory effect on nuclear residency of transcription factors. Ø symbol indicates degradation, hexagons the glycosylated forms of the proteins. Green arrows show the path of glucose entrance into the cell, its phosphorylation, and the ultimate activation of insulin secretion.
The full model includes the regulation of GLUT1 and GLUT2 genes by the transcription factors HNF1A and FOXA2. Specifically, we described the production and degradation of HNF1A and FOXA2 at the RNA and protein level, and the translocation of the two proteins to the nucleus where they transactivate their target genes (modules I and II in Figure 3) , . Besides GLUT1 and GLUT2, HNF1A and FOXA2 also regulate MGAT4A, another gene particularly relevant for β-cell glucose entry, as discussed below. The transcription of these three genes, GLUT1, GLUT2 and MGAT4A, includes two layers of regulation: first, HNF1A induces histone hyperacetylation at target gene promoter nucleosomes , , , ; and second, HNF1A and FOXA2 bind to target gene promoter sequences and promote transcription , ,  (modules III and IV).
GLUT-1 and GLUT-2 are regulated also at the post-translational level, by protein glycosylation. In particular, glucose transporter residency at the β-cell plasma membrane requires a specific N-glycan structure produced on both transporters by the Golgi-resident GNT-4A glycosyltransferase enzyme, the product of MGAT4A gene, , ,  (module V). This post-translational modification promotes GLUT-1 and GLUT-2 interaction with one or more lectins at the plasma membrane and maintains their residency at the membrane by a mechanism competing with normal endocytic internalization and degradation rates. Thus, despite cycles of production and degradation, GLUT-1 and GLUT-2 glycoproteins are steadily present at the β-cell plasma membrane in healthy individuals . The model includes these post-translational regulation steps, as schematically shown in Figure 3, where GLUT-1 and GLUT-2 are simply identified as ‘glycosylated’ or ‘unglycosylated’, according to the presence or absence of the GNT-4A-dependent N-glycan modification, although N-glycosylation comprises multiple different N-glycan structures on the glucose transporters. We assumed the same kinetic rates for GLUT-1 and GLUT-2 interactions with MGAT4A and lectins. Thus, in the model, differences in the concentration of the two transporters at the membrane are the result of differences in transcription.
Within the network considered, our previous experimental work showed that both β-cells from T2D donors and β-cells from healthy donors treated with palmitic acid exhibit reduced glucose transporter expression, diminished glucose uptake and impaired G6P production, compared to normal β-cells . Underlying this functional impairment there are multiple network disruptions including decreased HNF1A and FOXA2 nuclear localization, reduced transcription of the MGAT4A, GLUT1 and GLUT2 genes, and decreased abundance of plasma membrane-resident glucose transporters . We verified that the model was able to capture all these experimental observations by simply perturbing the network at the level of HNF1A and FOXA2 translocation to the nucleus (Figure 3, red arrows). Introducing an inhibitory factor acting on these translocations produces, by itself, all the other observed alterations as well as the impairment of glucose transport.
The complete model structure, parameter values and comparisons between model results and human experimental data are provided in the (Text S2), and are summarized in the Methods section. We also verified the model with glucose uptake measurements from normal β-cells co-cultured with LacNAc and (LacNAc)3 glycans  (Figure 4). These glycans compete with the GNT-4A-glycosylated glucose transporters for binding to β-cell lectins that promote cell surface residency, thereby resulting in reduced expression of GLUT-1 (75% of normal with LacNAc and 57% with (LacNAc)3) and GLUT-2 (80% and 48%, respectively).
Comparison between experimental data (white) (Ohtsubo et al., 2011) and model results (black) of glucose uptake at 10 mM extracellular glucose concentration, for β-cells from healthy and T2D patients, and for cells from healthy donors treated with LacNAc and (LacNAc)3, as indicated. Error bars represent standard deviation of the data. The percentage of GLUT-1 and GLUT-2 expression compared to healthy β-cells is also indicated in each case.
In healthy human β-cells, GLUT-1 is the predominantly expressed transporter; however, GLUT-2 is also expressed at lower level , , . From these and other observations, we assumed that, in healthy human β-cells, ∼80% of plasma membrane glucose transporters are GLUT-1 and ∼20% are GLUT-2. Nevertheless, the higher value of for GLUT-2 means that a single molecule of GLUT-2 transports more glucose than a single molecule of GLUT-1. Therefore, GLUT-2 accounts for the majority of glucose transport even if it is expressed at much lower levels than GLUT-1. Simulating glucose transporter expression in a β-cell from a T2D donor, by inhibiting HNF1A and FOXA2 translocation to the nucleus, without further modifications, we calculated that in disease conditions 92% of the glucose transporters present at the β-cell surface are GLUT-1 and 8% are GLUT-2. Thus, also in human T2D β-cells, GLUT-1 remains the most abundant transporter at plasma membrane.
Control Point Identification
The full mathematical model provides a link between glucose transporter expression and specific intracellular biological components affecting their residency at the cell membrane. Thus, points of this regulatory network that are more sensitive targets of therapeutic intervention can be investigated to identify best strategies for restoring normal glucose transport and β-cell function.
We used the T2D β-cell model of reduced glucose transport due to the effect of nuclear exclusion of HNF1A and FOXA2 (red arrows in Figure 3). We measured the effect on the GK rate when perturbing different points in the network by a local sensitivity analysis. A high sensitivity to perturbation suggests a more effective point for potential therapeutic intervention because larger increases in glucose transport leading to GSIS are produced. Perturbations were applied to the RNA content of HNF1A, FOXA2, MGAT4A, GLUT1 and GLUT2, singularly. Propagation of these changes to the GK rate of G6P formation was calculated at 2.8 and 16.8 mM blood glucose concentrations. The results are shown in terms of normalized sensitivity coefficients, as defined in Methods section, to produce a fair comparison between the effects of different perturbations (Figure 5).
Steady-state sensitivity of GK rate in T2D cells with respect to elevation in the RNA abundance of the genes indicated, at two plasma glucose concentrations, as shown in the legend. The sensitivity coefficients are normalized with respect to the GK rate and abundance of the RNAs among β-cells.
The model indicates highest sensitivity to the perturbation of MGAT4A RNA, in comparison with perturbation of RNAs encoding the other proteins. This finding remains valid at different extracellular glucose concentrations, but is more critical at higher glucose concentrations when the effect of these perturbations is emphasized. The sensitivity of the GK rate to HNF1A and FOXA2 is mediated by the role they play as transcriptional activators of MGAT4A, GLUT1, and GLUT2. Because HNF1A also affects histone acetylation, the impact of an intervention on HNF1A RNA expression is much more pronounced than an intervention involving FOXA2 RNA expression. A change in GLUT2 RNA has a higher impact on GK rate than the same percentage change in GLUT1 RNA because, even if much less abundant, GLUT-2 has a higher and accounts for most of glucose uptake.
Deficient pancreatic β-cell glucose transport has been found to be a key pathogenic feature of a pathway to diabetes that incorporates multiple factors linked in a sequence of molecular events . We have developed a computational model for β-cell glucose transport and the alterations that occur in health and diabetes from the published findings of multiple laboratories. Our simulations closely approximated the experimental data and provide insights including the presence of a metabolic threshold or “tipping point” in β-cell glucose uptake and utilization. While GK is normally rate limiting in G6P production and β-cell glucose utilization, our model indicates that glucose transport across the plasma membrane becomes rate limiting among models of obesity-associated diabetes in rodents and human β-cells from donors with T2D. The consequence of disrupting β-cell glucose transport across the plasma membrane appears most severe during increased concentrations of glucose typical of postprandial blood glucose excursions that normally lead to the GSIS response. In modeling multiple approaches to increase glucose transporter expression to prevent disease onset, we have detected different sensitivities to intervention. The most effective therapeutic perturbation indicated by the model and supported by experimental data is not achieved by a direct increase in glucose transporter expression per se, but instead by conservation of the GNT-4A glycosyltransferase enzyme that supports β-cell glucose transporter residency at the plasma membrane.
The switch in control of G6P formation from GK activity to glucose transport in diabetes results from diminished expression of both GLUT-1 and GLUT-2 glucose transporters at the β-cell plasma membrane. Human β-cells express both GLUT-1 and GLUT-2, however, GLUT-2 appears to be responsible for the majority of glucose transport. Diminished glucose transporter expression reaches a critical threshold at various combinations of GLUT-1 and GLUT-2 deficiencies. When less than 20% of normal GLUT-2 expression occurs in absence of GLUT-1, for example, glucose transport becomes rate limiting in the formation of G6P, which correlates to approximately 60% of the normal GK rate. Although the precise “tipping point” varies with the relative levels of GLUT-1 and GLUT-2, our modeling indicates that this threshold is greatly exceeded in β-cells isolated from animal models of obesity-associated diabetes and human T2D donors. Median decrements of β-cell surface glucose transporter expression in T2D reached more than 85% for each transporter. Substantial decrements of GLUT-2 expression appear required to abolish GSIS, while normal expression of GLUT-1 can compensate for the absence of GLUT-2 and restore GSIS. This is consistent with the deficiency of both GLUTs along with GSIS in T2D β-cells and recent findings that unaltered expression of either GLUT-1 or GLUT-2 is sufficient to maintain GSIS in normal β-cells .
The computational model that we constructed revealed markedly different sensitivities to molecular perturbations among different pathway components. Preservation of the β1-4GlcNAc glycan linkage produced by the GNT-4A glycosyltransferase is predicted to be most effective at maintaining glucose transporter expression at the β-cell surface and maintaining normal glucose transport with GSIS activity. This feature of the model is consistent with experimental data showing that increased Glut2 gene expression in mouse β-cells cannot similarly maintain normal glucose transporter expression and inhibits all disease signs in obese mice . The reason appears to reflect the diminished half-lives at the β-cell surface of misglycosylated GLUT-1 and GLUT-2 in the absence of sufficient GNT-4A activity. This misglycosylation results in the absence of the glycan ligand of cell surface resident lectins, including one or more of the galectins . Even with low levels of GLUT RNA expression, sufficient MGAT4A-encoded GNT-4A activity and normal GLUT glycosylation can maintain β-cell surface GLUT expression sufficiently to support GSIS. The sensitivities of the model to FOXA2 and HNF1A are also different. Higher sensitivity of HNF1A is predicted due to its additional role in modulating chromatin histone acetylation. The increase of FFA and, specifically, palmitic acid was also included in the model, but was limited to its inhibitory effect on HNF1A and FOXA2 translocation to the nucleus. Thus, the model would capture a beneficial effect of FFA reduction on glucose uptake. However, down-modulation of FFA receptor binding and signaling was not incorporated into our model. It has been reported that FFA receptors are essential to normal β-cell function . An efficacious inhibitor of FFA receptor signaling may disrupt the normal functions of multiple cell types. In contrast, chronic elevations of FFAs may become pathogenic , perhaps by membrane fusion in receptor independent processes among cell organelles including mitochondria, leading to increased oxidative stress with changes to intracellular transcriptional networks.
From computational modeling of the initial steps in pancreatic β-cell glycolysis, beginning with glucose transport and G6P formation, we have achieved an integration of experimental and computational data that encompasses a recently discovered pathogenic pathway to T2D that proceeds through attenuation of pancreatic β-cell GNT-4A activity and glucose transport . This model closely simulates outcomes of rigorous experimentation in rodents and human β-cells, and further indicates the presence of a metabolic threshold wherein the pacemaker of β-cell glycolysis switches from GK activity to glucose transport. Beyond this tipping point, β-cells are defective in glucose sensing and are unable to produce G6P by mechanisms that support normal functions including GSIS. Our model is further consistent with studies of human β-cells from T2D donors, in which this metabolic threshold is crossed and GSIS is defective. With inherent metabolic flexibility, β-cells can subsequently respond by increasing their oxidation of fatty acids as a substitute source of cellular energy. However, this flexibility cannot restore normal insulin secretion processes linked to glucose sensing, thereby inducing a pathogenic pathway leading to diabetes.
The mathematical model was developed as a system of ordinary differential equations. Most of the biochemical kinetic rates were expressed by mass action laws. Exceptions are the GLUT-1 and GLUT-2 transport described by Michaelis-Menten kinetics, and the GK rate and glucose transporters interaction with lectins described by Hill kinetics. Further details and MATLAB programs are provided in (Text S1, S2 and S3).
Relative sensitivity coefficients, , were calculated approximating by finite differences the expression , where represents GK rate at steady-state for a given extra-cellular glucose concentration, and the concentration of RNA perturbed, for corresponding to HNF1A, FOXA2, MGAT4A, GLUT1, and GLUT2.
Detailed description of the reduced mathematical model.
Detailed description of the full model.
Conceived and designed the experiments: CL JDM. Performed the experiments: CL. Analyzed the data: CL JDM FJD. Wrote the paper: CL JDM FJD.
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domain: medical


|Publication number||US4779592 A|
|Application number||US 07/128,216|
|Publication date||Oct 25, 1988|
|Filing date||Dec 3, 1987|
|Priority date||Dec 5, 1986|
|Also published as||DE3778848D1, EP0271030A2, EP0271030A3, EP0271030B1|
|Publication number||07128216, 128216, US 4779592 A, US 4779592A, US-A-4779592, US4779592 A, US4779592A|
|Inventors||Kanji Takeuchi, Yosuke Setaka|
|Original Assignee||Nippondenso Co., Ltd.|
|Export Citation||BiBTeX, EndNote, RefMan|
|Patent Citations (16), Referenced by (14), Classifications (21), Legal Events (6)|
|External Links: USPTO, USPTO Assignment, Espacenet|
The present invention relates generally to an apparatus for controlling the intake air amount of an internal combustion engine, and more particularly to a stepping motor applicable particularly, but not exclusively, to systems for driving an air intake device such as throttle valve to introduce air into an internal combustion engine.
Generally, in internal combustion engines for motor vehicles, a throttle valve is provided in an air intake passage and operatively coupled to an accelerating pedal of the motor vehicle and the engine output is controllable by the opening and closing operation of the throttle valve made in connection with vehicle driver's depressing operation of the accelerating pedal. As a system for preventing a vehicle slip possible when the vehicle is runing on a low running resistance surface such as a frozen road surface is known a so-called traction control system, in which wheel slipping is detected on the basis of signals from wheel speed sensors attached to driven and non-driven wheels of the vehicle and, in response to the detection, the throttle valve is controlled to be operated to the closing direction. This may repress the engine output to enhance the gripping force of the wheel, resulting in prevention of the wheel slipping.
The traction control system generally requires a means for driving the throttle valve independently of the accelerating pedal as described in Japanese Patent Provisional Publication No. 57-116140, for example, where the throttle valve is operatively coupled to a drive motor which is in turn controlled in accordance with the depressing amount of the accelerating pedal, the degree of the wheel slipping and so on. While successfully performing the optimal control of the throttle valve and making easy the constant-speed control of the vehicle, such an apparatus would suffer a problem that the throttle valve is fully opened when the control unit malfunctions. One possible solution would be to use a system as disclosed in European Patent Provisional Publication No. 0089492, in which two throttle valves are provided in a series in an air intake passage, the first valve being driven by the accelerating pedal and the second valve being driven by a drive motor. Normally, the second throttle valve is fully opened and the first throttle valve is operated in accordance with operation of the accelerating pedal. In response to the requirement of the traction control, the second throttle valve is controlled to be closed so that the engine output is reduced irrespective of operation of the first throttle valve to allow the prevention of vehicle slipping. Although satisfactory for improving the reliability of the throttle valve control, this system results in a bulky throttle valve arrangement and difficulty is encountered to mount it on the motor vehicle.
It is therefore an object of the present invention to provide new and improved stepping motor and intake air quantity control apparatus with the stepping motor for use in a motor vehicle.
A feature of an intake air quantity control apparatus according to the present invention is that intake air quantity control is performed through a stepping motor which is coupled to a throttle valve provided in an air intake passage of an engine of the vehicle and further to an accelerating pedal of the vehicle so that the throttle valve is operated in accordance with depression of the accelerating pedal and which is further controllable in response to a control signal from a traction control unit. The stepping motor comprises an inner rotor and an outer rotor which are resiliently coupled to each other, the inner rotor being connected to the throttle valve and the outer rotor being mechanically coupled to the accelerating pedal. Therefore, in response to depression of the accelerating pedal, the throttle valve can be operated through the outer rotor and the inner rotor. On the other hand, the outer rotor is arranged not to be rotated in response to excitation of a stator of the stepping motor and the inner rotor is arranged to be rotatable due to the exctation thereof. Thus, in response to a control signal from an electronic control unit, only the inner rotor can be rotated independently of operation of the accelerating pedal so as to control the opening degree of the throttle valve, resulting in allowing the traction control. Here, the reacted rotation of the outer rotor due to the rotation of the inner rotor does not occur because the outer rotor is mechanically stopped due to the coupling to the accelerating pedal. In addition, the air intake quantity control apparatus has a fail-safe function against the abnormality of the traction control unit. That is, the rotation of the inner rotor with respect to the outer rotor is restricted by a stopper means so as to prevent the throttle valve from excessively opened due to the abnormality of the traction control unit. The stopper means a stopper pin planted on the outer rotor and a stopper member attached to the inner rotor which are arranged to come into contact with each other when the inner rotor has been rotated by an amount corresponding to the depressing amount of the accelerating pedal in the throttle valve opening direction. Thus, the rotatable amount of the inner rotor depends upon the depressing amount of the accelerating pedal so that the opening amount of the throttle valve is restricted below the the opening amount corresponding to the pedal depressing amount.
In accordance with the present invention, there is provided a stepping motor comprising: a cylindrical stator having a plurality of magnetic poles and a plurality of windings respectively wound around the magnetic poles, the plurality of magnetic poles being arranged to extend to the axis of the cylindrical stator; a first rotor disposed coaxially with the stator and rotatable with respect to the stator by means of a rotational torque generated in response to excitation of the windings of the stator; and a second cylindrical rotor disposed between the stator and the first rotor and arranged so as not to generate a rotational torque with respect to the stator in response to excitation of the windings and so as to allow transmission of magnetic fluxes from the stator to the first rotor.
In accordance with the present invention, there is further provided an intake air quantity control apparatus for use in a motor vehicle for controlling an intake air quantity introduced into an engine of the motor vehicle by controlling the opening degree of a throttle valve provided in an air intake passage of the engine, comprising a stepping motor connected to the throttle valve and operatively coupled through a link device to an accelerating pedal of the motor vehicle so that the stepping motor drives the throttle valve by an amount corresponding to the operating amount of the accelerating pedal, the stepping motor being further controllable in response to a control signal from a control unit of the motor vehicle and comprising: a cylindrical stator having a plurality of magnetic poles and a plurality of windings respectively wound around the magnetic poles, the plurality of magnetic poles being arranged to extend to the axis of the cylindrical stator and the plurality of windings being excited due to the control signal; a first rotor disposed coaxially with the stator and rotatable with respect to the stator by means of a rotational torque generated in response to excitation of the windings of the stator; and a second cylindrical rotor disposed between the stator and the first rotor and arranged so as not to generate a rotational torque with respect to the stator in response to excitation of the windings and so as to allow transmission of magnetic fluxes from the stator to the first rotor; wherein the second rotor is connected through the link device to the accelerating pedal and the first rotor is resiliently coupled to the second rotor and coupled to the throttle valve.
Preferably, the second rotor of the stepping motor has magnetic portions and non-magnetic portions which are alternatively arranged in the circumferential direction to form a cylindrical configuration, and the number of the magnetic portions is a multiple of the number of the magnetic poles and the first rotor has a plurality of circumferential spaced teeth whose number is not the magnefication of the number of the magnetic poles thereof.
The object and features of the present invention will become more readily apparent from the following detailed description of the preferred embodiments taken in conjunction with the accompanying drawings in which:
FIG. 1 is a schematical perspective view of an intake air quantity control apparatus according to an embodiment of the present invention which is incorporated into a motor vehicle;
FIG. 2 is a cross-sectional view of a stepping motor used in the intake air quantity control apparatus of FIG. 1; and
FIG. 3 is a cross-sectional view taken along a line I--I of FIG. 2.
Referring now to FIG. 1, there is illustrated an air intake control system according to an embodiment of the present invention which is connected to a throttle valve 7 provided in an air intake passage 1 which is in turn coupled to an internal combustion engine (not shown) of a motor vehicle. In FIG. 1, the throttle valve 7 is fixedly secured by a screw 3 to a shaft 5, one end of which is pivotally supported by a wall 1a of the air intake passage 1 so that the throttle valve 7 is rotatable about the axis of the shaft 5. The other end of the shaft 5 is integrally connected to an output shaft 11 (FIG. 2) of a stepping motor 9 which may be of the permanent-magnet type and which electromagnetically rotates stepwise. The stepping motor 9, as illustrated in FIGS. 2 and 3, comprises a stator 15, an inner rotor (first rotor) 17 and an outer rotor (second rotor) 19, the stator 15 being fixedly disposed in a cylindrical yoke 13 and the inner and outer rotors 17 and 19 being cylindrically shaped and coaxially arranged so that the outer rotor 19 is interposed between the stator 15 and the inner rotor 17 in spaced relation thereto. The outer rotor 19 is, at one end, connected to a disc member 21 so that the axis of the outer rotor 19 passes through the center of the disc member 21. To the disc member 21 is attached a lever 21a which is in turn coupled through a link device 23 to an accelerating pedal 25 of the motor vehicle and also connected to a return spring 27, the other end of which is connected to a stationary portion. Therefore, when the disc member 21 is rotated in the direction indicated by an arrow A in response to a depression of the accelerating pedal 25, the spring 27 biases the disc member 21 in the opposite direction indicated by an arrow B. On the other hand, the output shaft 11 is inserted into a hole of the inner rotor 17, which is defined in the axial direction thereof, and secured to the inner wall thereof. The other end of the output shaft 11 is connected to a disc member 30 which is positioned in parallel to and outwardly of the disc member 21 connected to the outer rotor 19. To a peripheral portion of the disc member 30 is attached a stopper member 31 which is arranged to allow coming into contact with a stopper pin 29 planted on a surface of the disc member 21. A different peripheral portion of the disc member 30 is coupled through a spring 33 to a portion of the disc member 21 so that the inner rotor 17 and the outer rotor 19 are rotated in the same direction, that is, when the outer rotor 19 is rotated in the throttle valve opening direction indicated by the arrow A, the inner rotor 17 follows in the A-direction.
The stator 15 comprises a laminated core and has stator windings 36 to form magnetic poles 37, i.e., four phases and eight poles. The inner rotor 17 is composed of a laminated core having circumferentially equally spaced teeth 38 whose number is 50. The output shaft 11, i.e., the inner rotor 17, is rotatably supported through bearings 16 and coupled to the shaft 5 of the throttle valve 7. The outer rotor 19, also rotatably supported through the bearings 16, comprises magnetic portions 45, made of a magnetic material such as iron, and non-magnetic portions 47, made of a non-magnetic material such as aluminum and resin, which are arranged alternatively to form a cylindrical configuration as shown in FIGS. 2 and 3. The number of each of the magnetic materials 45 and non-magnetic materials 47 is 48 which is the magnification, or a multiple, of the number of the magnetic poles 37. Therefore, even in the case of switching operation of excitation of the windings 36, the permeance of the outer rotor is not changed and this results in no generation of a torque between the stator 15 and the outer rotor 19. On the other hand, since the number of the magnetic portions 45 of the outer rotor 19 is 48 and the number of the teeth 38 of the inner rotor 17 is 50, the phase difference is 1/4 pitch whereby the inner rotor 17 exerts a rotational torque with respect to the stator 15 when excitation of the windings 36 are effected to provide rotational magnetic fields. More specifically, the center lines of the magnetic pole 37a, magnetic material 45a and tooth 38a are coincident with each other. On the other hand, although the center lines of the adjacent magnetic pole 37b and magnetic material 45 are coincident with each other, the center line of the tooth 38b is shifted counterclockwise by 45°-(360°/50)×6=1.8° with respect thereto. Therefore, when excitation is performed in terms of the magnetic pole 37a, the inner rotor 17 and the outer rotor 19 are positioned as shown in FIG. 2 and, when the excitation is switched to the magnetic pole 37b, only the inner rotor 17 is rotated clockwise by 1.8° to take the position at which the permeance is the maximum. The inner rotor 17 is further rotated in response to successive exciting of magnetic poles 37c and 37d.
A description will be made hereinbelow in terms of operation of the throttle valve 7 in connection with the stepping motor 9. In response to depression of the accelerating pedal 25, the disc member 21 is rotated in the direction indicated by the arrow A so that the outer rotor 19 is rotated and the inner rotor 17 is also rotated due to the provision of the spring 33 whereby the throttle valve 7 is opened in accordance with the rotation of the shaft 5 connected to the output shaft 11 of the stepping motor 9, enhancing the quantity of intake air into the engine. 0n the other hand, in response to release of the accelerating pedal 25, the disc member 21 is rotated in the direction indicated by the arrow B by means of the return spring 27 and the inner rotor 17 is similarly rotated by means of the spring 33 to close the throttle valve 7. That is, normally, the throttle valve 7 is controlled directly in accordance with the operation of the accelerating pedal 25. On the other hand, under the traction control performed on the basis of signals from a wheel sensor and so on, the magnetic poles 37 successively generate rotational magnetic fields in response to switching of the excitation. Since the number of the magnetic portions 45 of the outer rotor 19 is set to a multiple of the number of the magnetic poles 37, even if the magnetic poles 37 are successively excited, the pereance between the magnetic poles 37 and the outer rotor 19 is not varied, resulting in no generation of a torque between the stator 15 and the outer rotor 19. The fluxes from the magnetic poles 37 reach the inner rotor 17 after passed through the outer rotor 19. Since the pitches of the magnetic portions 45 and teeth 38 are slightly different to cause the phase differene of 1/4 pitch between the successive magnetic poles 37, the permeance between the inner rotor 17 and the outer rotor 19 is varied in response to switching of the exciting and the outer rotor is mechanically stopped by means of the equilibrium between the the depressing force of the accelerating pedal 25 and the biasing force of the return spring 27, resulting in rotation of the inner rotor 17 with respect to the outer rotor 19. Thus, even if the the throttle valve 7 is opened by a given degree in response to depression of the accelerating pedal 25, a rotational torque is applied to the inner rotor 17 which is in turn rotated against the spring 33 to close the throttle valve 7. This results in reduction of the engine output and increase in the gripping force of the wheel. The rotation of the inner rotor 17 with respect to the outer rotor 19 is restricted by means of the stopper pin 29 and the stopper member 31. That is, even in case that the windings 36 are energized to open the throttle valve 7 due to the abnormality of the control unit for the traction control, the inner rotor 17 and the outer rotor 17 are apt to be rotated in the opposite directions due to reaction therebetween and the stopper member 31 comes into contact with the stopper pin 29 to stop the rotation of the inner rotor 17. In this state, since the opening degree of the throttle valve 7 is restricted to be below the opening degree corresponding to the depression of the accelerating pedal 25, the excessive intake of air into the engine can be prevented.
It should be understood that the foregoing relates to only embodiments of the present invention, and that it is intended to cover all changes and modifications of the embodiments of the invention herein used for the purposes of the disclosure, which do not constitute departures from the spirit and scope of the invention. For example, although the above description is made in terms of a four-phase eight-pole VR type stepping motor, the invention is not limited thereto but applicable to stepping motors of different types. Furthermore, although in the above description the outer rotor and inner rotor are connected to each other by means of a spring, it is also appropriate that they are magnetically coupled to each other by always energizing one or more of the stator windings.
|Cited Patent||Filing date||Publication date||Applicant||Title|
|US859368 *||Nov 16, 1904||Jul 9, 1907||Gen Electric||Dynamo-electric machine.|
|US2864017 *||Nov 28, 1955||Dec 9, 1958||Dimitroff Waltscheff Dimo||Inducto-motive power apparatus with a plurality of rotors|
|US3221191 *||Sep 12, 1962||Nov 30, 1965||Daco Instr Company Inc||Angular displacement solenoid|
|US3944865 *||May 23, 1974||Mar 16, 1976||Reyrolle Parsons Limited||Homopolar dynamo-electric machines|
|US4367805 *||Nov 3, 1980||Jan 11, 1983||Nippondenso Co., Ltd.||Governing control apparatus for automobiles|
|US4375047 *||Jul 23, 1981||Feb 22, 1983||General Signal Corporation||Torque compensated electrical motor|
|US4523565 *||Mar 30, 1984||Jun 18, 1985||Aisin Seiki Kabushiki Kaisha||Control system and method for a fuel delivery system|
|US4532447 *||Nov 18, 1982||Jul 30, 1985||Pierre Cibie||Rotary electric machine forming more especially a speed variator or a torque converter|
|US4586471 *||Dec 4, 1984||May 6, 1986||Isuzu Motors, Ltd.||Fuel control mechanism for internal combustion engine|
|US4681374 *||Oct 23, 1985||Jul 21, 1987||Toyota Jidosha Kabushiki Kaisha||Wheel slip control system|
|US4714864 *||May 23, 1986||Dec 22, 1987||Nippondenso Co., Ltd.||Throttle control device for vehicles|
|US4724811 *||Apr 3, 1987||Feb 16, 1988||Robert Bosch Gmbh||Throttle valve adjuster|
|EP0089492A1 *||Feb 17, 1983||Sep 28, 1983||Audi Ag||Internal-combustion engine|
|JPS49117859A *||Title not available|
|JPS57116140A *||Title not available|
|JPS59122742A *||Title not available|
|Citing Patent||Filing date||Publication date||Applicant||Title|
|US4898138 *||Oct 24, 1988||Feb 6, 1990||Mazda Motor Corporation||Engine control apparatus|
|US4944269 *||Sep 18, 1989||Jul 31, 1990||Siemens-Bendix Automotive Electronics L.P.||Accelerating pedal for electronic throttle actuation system|
|US4947815 *||Sep 4, 1987||Aug 14, 1990||Robert Bosch Gmbh||System for regulated dosing of combustion air into internal combustion engine|
|US5035218 *||Jun 7, 1990||Jul 30, 1991||Nippondenso Co., Ltd.||Throttle valve control apparatus for vehicles|
|US5060613 *||Mar 2, 1990||Oct 29, 1991||Robert Bosch Gmbh||System for transferring a control position of a set-point value transducer|
|US5107811 *||Aug 17, 1990||Apr 28, 1992||Robert Bosch Gmbh||Apparatus having a control motor for intervention into a force transmission device|
|US5113824 *||May 30, 1991||May 19, 1992||Robert Bosch Gmbh||Adjusting device|
|US5161633 *||May 1, 1990||Nov 10, 1992||Fiat Auto S.P.A.||Vehicle speed control system|
|US5311849 *||Jul 14, 1992||May 17, 1994||Gas Research Institute||Carburetor assembly for an internal combustion gas engine|
|US5605129 *||Nov 29, 1994||Feb 25, 1997||Onan Corporation||Electrically controlled actuator apparatus and method|
|US6116215 *||Jul 16, 1998||Sep 12, 2000||The Barber-Colman Company||Integrated throttle valve and actuator|
|US6465974 *||Dec 21, 2000||Oct 15, 2002||Mitsubishi Denki Kabushiki Kaisha||Air intake amount control apparatus for an engine|
|USRE34302 *||Sep 10, 1991||Jul 6, 1993||Siemens Automotive L.P.||Accelerating pedal for electronic throttle actuation system|
|USRE34574 *||Sep 10, 1991||Apr 5, 1994||Siemens Automotive L.P.||Accelerator control apparatus|
|U.S. Classification||123/399, 180/197|
|International Classification||H02K37/24, F02D41/20, F02D41/00, B60K28/16, H02K37/14, H02P8/14, F02D9/02, H02K37/04, F02D11/10|
|Cooperative Classification||F05C2201/021, F02D11/10, F02D2011/103, B60K28/16, H02K37/04, H02K37/24|
|European Classification||H02K37/04, F02D11/10, H02K37/24, B60K28/16|
|Dec 3, 1987||AS||Assignment|
Owner name: NIPPONDENSO CO., LTD., 1-1, SHOWA-CHO, KARIYA-SHI,
Free format text: ASSIGNMENT OF ASSIGNORS INTEREST.;ASSIGNORS:TAKEUCHI, KANJI;SETAKA, YOSUKE;REEL/FRAME:004805/0036
Effective date: 19871120
Owner name: NIPPONDENSO CO., LTD.,JAPAN
Free format text: ASSIGNMENT OF ASSIGNORS INTEREST;ASSIGNORS:TAKEUCHI, KANJI;SETAKA, YOSUKE;REEL/FRAME:004805/0036
Effective date: 19871120
|Apr 9, 1992||FPAY||Fee payment|
Year of fee payment: 4
|Apr 16, 1996||FPAY||Fee payment|
Year of fee payment: 8
|May 16, 2000||REMI||Maintenance fee reminder mailed|
|Oct 22, 2000||LAPS||Lapse for failure to pay maintenance fees|
|Dec 26, 2000||FP||Expired due to failure to pay maintenance fee|
Effective date: 20001025


Nathan Rabin is the longtime head writer for The A.V. Club, the entertainment section of The Onion and the author of The Big Rewind.
What does it mean to be a great American? Ask five of your countrymen, and you'll get five different answers.
For me, it means having some of the qualities that make our nation worth celebrating — like resilience, determination and optimism.
Country legend Johnny Cash, bon vivant George Plimpton and consummate entertainer Sammy Davis Jr. don't have much in common. But their lives have much to tell us about what it means to be a great American.
Johnny Cash: The Biography, by Michael Streissguth, paperback, 368 pages
F. Scott Fitzgerald famously said, "There are no second acts in American life." Clearly, someone forgot to tell the subject of Michael Streissguth's Johnny Cash: The Biography. Cash transformed pop music with early songs about trains, prisons and Jesus. By the late 1960s, however, Cash was written off as a self-destructive has-been lost in a downward spiral of booze and pills.
His 1968 live album from Folsom Prison changed all that. Suddenly Cash was vital and dangerous and relevant all over again. But a second act wasn't good enough. Cash insisted on a third when he teamed up with outlaw producer Rick Rubin in the 1990s for a series of albums that brought together punk, rock, metal, blues and country in a state of harmonious musical democracy.
Yes I Can: The Story of Sammy Davis, Jr., by Sammy Davis Jr., Farrar Straus & Giroux, paperback, 611 pages, $35
Like Cash, Sammy Davis Jr. grew up poor and hungry. He was barely 30 when he put out Yes, I Can, his massive memoir. Yet no one could accuse him of lacking material. He had been a child vaudevillian, a controversy magnet and a recording and movie star.
Given the brutal racism he suffered, both as a household name and as an anonymous soldier, it would be easy for Davis to give in to hopelessness. But Davis never let our nation's ugly history of Jim Crow and slavery keep him down. Yes I Can teaches us to see green lights where others see only roadblocks. It's fitting that our first black president only had to tweak the title of Davis' memoir slightly to create a campaign slogan that appealed to the better angels in each of us.
George, Being George: George Plimpton's Life as Told, Admired, Deplored, and Envied by 200 Friends, Relatives, Lovers, Acquaintances, Rivals — and a Few Unappreciative Observers. by Nelson W. Aldrich, hardcover, 432 pages
If Cash and Davis Jr. grew up with nothing, George Plimpton grew up a pampered child of privilege. Yet he didn't let his family's enormous wealth keep him from making friends throughout the social strata. After reading George, Being George, Nelson W. Aldrich's wonderful oral history of George Plimpton, I didn't just want to befriend its subject: I wanted to slip inside his skin, if only for a day. For Plimpton was blessed with a special form of grace. People fascinated him and were fascinated by him.
During his charmed life, Plimpton did everything. He wrote. He edited. He acted. He endorsed video games. He even trained with the Detroit Lions. Like Forrest Gump, he had a way of stumbling into the forefront of history. Plimpton clowned around with Muhammad Ali, helped take down Sirhan Sirhan and tried to bribe Lisa Simpson into throwing a spelling bee. Through it all, he maintained a very American sense of curiosity, optimism and innocence we can all learn from.
Johnny Cash, Sammy Davis Jr. and George Plimpton each give us a model for making the most of the opportunities afforded us — and show us that nothing is impossible, so long as you're willing to laugh at yourself and at a world that is as comic as it is tragic.
Three Books ... is produced and edited by Ellen Silva and Bridget Bentz.


text:
- HHS has released a report this week illustrating health insurance marketplace consumers actively shopped around for plans last year, with 31% of returning enrollees from 2014 changing plans for 2015.
- The findings show consumers who changed to a plan at the same level of coverage saved nearly $400 annually after tax credits, compared to what they would have paid if they had remained in the same plan. Consumers who also changed to a new issuer at the same level of coverage saved even more, at more than $490 after tax credits.
- HHS estimates during the coming open enrollment, consumers who change to the lowest premium plan at the same level can expect to save an average of $610 annually before tax credits.
As we approach an enrollment period with premiums going up an average of 7.5%, the administration's message is most consumers will still actually have options that can save them money.
The agency says for 2016, more than eight in 10 current ACA plan enrollees will be able to find a plan at the same level with lower premiums before tax credits--if they shop.
“Our message to returning Marketplace customers is simple: Shopping may save you money,” HHS Secretary Sylvia M. Burwell said in a prepared statement.
Among the report's findings:
- Plan-switching among marketplace consumers is high compared to historical estimates of plan switching among consumers of employer sponsored plans, the Federal Employee Health Benefits Program and Medicare Drug Plans.
- Markeplace consumers more commonly switched issuers in 2015 than metal level (bronze, silver, etc.)
- Silver plans reign in popularity. Enrollment is higher for this level than any other, and most 2014 silver plan enrollees (91%) remained in silver plans for 2015.


text:
Stacking The Shelves is a weekly meme hosted by Marlene of Reading Reality. It’s all about sharing the books you are adding to your shelves, may it be physical or virtual. This means you can include books you buy in a physical store or online, books you borrow from friends or the library, books for review from authors, Netgalley, Edelweiss or publishers, as well as gifts or books you won. If you click on the covers, it will take you to Goodreads.
Last week I added 8 books/audiobooks to my shelves (my smallest haul in a very long time), and this week I added 19 books and 2 audiobooks (back at it). I still have 22 books and 5 audiobooks pending between Netgalley and Edelweiss, so I won’t run out of things to read or listen to.
Netgalley: 13 Books, 3 Audiobooks
Edelweiss: 3 Books
Blog Tours: 1 book
Library, Amazon: 1 Audiobook, 2 Books
So, this week, I added 21 books/audiobooks 🤔🙄. I am on track to read or listen to 10 novels/audiobooks this week, so my TBR mountain grows quite a bit this week. 🏔📚
What did you add to your shelves this week? Do any of these books appeal to you?

domain: literature


text:
The Father 4/11/21
Reportedly French writer/director Florian Zeller had Anthony Hopkins directly in mind as Zeller was writing the screenplay-- so much so that he stated that if Hopkins did not accept the role, Zeller would have made the film in the French language.
The movie uses as a basis several actual facts: Mankiewicz did get to know Marion Davies, then William Randolph Hearst through the writer Charles Lederer who was Davies nephew; Mank may have been a house guest at Hearsts San Simeon (although Hearsts rule of no one having more than one cocktail like...
Zappa was a life-long compulsive recorder and editor, frequently compiling recordings consisting of sessions or concerts recorded sometimes years apart.
The Report 12/15/19
The film might be of interest to those who work in D.C., or to folks who study its machinations.
At Eternity's Gate 3/05/19
One wonders if Dafoe exhibits more resemblance to Van Gogh from his right side, since in the film they incorrectly chose the left ear for excision, whereas in real life it was the right.
Green Book 1/28/19
If the films title and subject matter were any indication that the focus was on Don Shirley, his beliefs, and his quest to endure a music tour of the South, then it came as a surprise that the thrust of the story put most of the emphasis on Tony Lip: his background, his actions, his philosophy, his ...
Phantom Thread 2/13/18
The film was anticipated to be masterful, the presumption magnified by Daniel Day-Lewis' announcement that he was retiring from film making due to the rigors of performance in this project.
The Shape of Water 1/27/18
But the sole popularity of the film will depend upon it's emotional appeal to those captured by the poignant story of a poor mute girl who finds love and fulfillment with a humanoid amphibian; the Cinderella meets The Creature from the Black Lagoon aspect.

domain: entertainment