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Jerome Charyn
Jerome Charyn (b. 1937) is a critically acclaimed author of nearly fifty books. Born in the Bronx, he attended Columbia College, where he fell in love with the works of Faulkner and Joyce. After graduating, he took a job as a playground director and wrote in his spare time, producing his first novel, a Lower East Side fairytale called Once Upon a Droshky, in 1964.
While stalled on a book he was writing about the dark ages, Charyn discovered a kind of dark ages flourishing in his own back yard. His older brother--a detective working homicide--took to driving him around New York City in his squad car, and Isaac Sidel was born. In 1974 Charyn published Blue Eyes, his first Isaac Sidel mystery. This first in the so-called Sidel quartet introduced the eccentric, near-mythic Sidel, and his bizarre cast of sidekicks. Although he completed the quartet with Secret Isaac (1978), he continued following the character through Citizen Sidel (1999), which ends with his antihero making a run at the White House. Charyn, who divides his time between New York and Paris, is also accomplished at table tennis, and once ranked amongst France's top ten percent of ping-pong players. You can find his website at this link.
"Charyn has trained his prose and makes it perform tricks. It's a New York prose, street smart, sly and full of lurches, like a series of subway stops on the way to hell." - New York Times
"These books contain the highest kind of novelist art . . . absolutely unique among contemporary writers." - Los Angeles Times
"Jerome Charyn is one of the most important writers in American literature." - Michael Chabon
"The joyous weirdness of Charyn's idiosyncratic New York City can't be described-it must be experienced." - Publishers Weekly
Tags: Jerome Charyn
Blue Eyes by Jerome Charyn
Marilyn The Wild by Jerome Charyn
The Education of Patrick Silver by Jerome Charyn
Secret Issac by Jerome Charyn
The Good Policeman by Jerome Charyn
Maria's Girls by Jerome Charyn
Montezuma's Man by Jerome Charyn
Little Angel Street by Jerome Charyn
El Bronx by Jerome Charyn
Citizen Sidel by Jerome Charyn
Elsinore by Jerome Charyn
At the Sudden Death Cafe by Jerome Charyn
Paradise Man by Jerome Charyn
The Bad Die Young by Jerome Charyn
The Lord of Sugar Hill by Jerome Charyn
Under the Eye of God by Jerome Charyn


Do want your child to be successful?
The simple answer is yes…of course!
Since 1993 I have had the pleasure of coaching and mentoring in many environments. I have spent time with skiers, hockey players, entrepreneurs and golfers.
Regardless of the chosen sport or activity, the people I have worked with who were/are the most successful have all had strong similarities. With that said, let me establish something right away…I measure success by where life has taken them not sport.
Success in sport is always short lived regardless of career length. Athletes will spend more years of their life being measured for their personal character than they will their athletic achievements. This needs to be emphasized young.
People who are successful in all aspects have a similar state of mind and character. Bottom line they were all coachable people. The list of things which make an athlete coachable is endless.
Important to note these are not sport skills as much as they are life skills. Empower your child with some solid skills early and they will be successful regardless of the career direction they pursue.
What should the focus be?
Always keep the focus on personal growth and success rather than athletic achievement. Show them it is more important to be liked for who they are than it is to be idolized for what they do. Bottom line, be good people who display a genuine interest and curiosity in others.
Lead by example and teach them to celebrate the achievements of those around them before patting themselves on the back. Good leaders are simply happy to be a part of success whether it is theirs or someone else's.
Empower them to be problem solvers and let them know they are capable of handling adversity. Never allow them to grumble about a player, coach or problem behind the issue. Teach them how to engage it face on and be open to working with those involved to come to up with a plan.
Our job as parents, coaches and mentors.
We have a responsibility as parents, teachers and coaches and it extends way beyond development of physical skills. We need to work together and spend more time modelling positive character traits and habits for our future leaders…sport or otherwise.


The University Center got a bit of a facelift with more plans in the works.
A Preview of the LSUS Basketball Season.
LSUS' Men and Women's soccer teams are excited about playing on their newly renovated field.


Looking more broadly, the figures are even lower. As of Sept. 1, only 1.26% of all trial adjustments were made permanent after three months, reported the Congressional Oversight Panel, which monitors the government's use of bailout funds.
Meanwhile, more and more people are falling into foreclosure. The combined percentage of loans in foreclosure or at least one payment past due was 14.4% in the third-quarter, according to the Mortgage Bankers Association. That's the highest the group has ever recorded.
Lenders say it's the fault of homeowners–that they don't provide documentation, or don't have jobs, or don't hold their mouths just right when they are licking the stamp to mail their trial payments. (Pardon me, my cynicism may be showing.) Borrowers report (to CNN, and on a smaller scale, to me) that they send the same documents over and over, but the lenders "lose" them.
While the Obama administration and the Treasury Department struggle to put enough pressure on banks and mortgage lenders to take the steps needed to prevent a total meltdown of our financial system AGAIN, I would just like to quietly remind them, and Congress, that giving bankruptcy judges the power to do just that might be a very good idea. Just a hint….


In Northwest Parking Garage we prepared, place and finished the first SOG area – 9,500 SF – 160 CY of Concrete.
We broke ground in the second Parking Garage job in Aventura.
60% of foundations were installed on Aventura Job placing 600+ CY of concrete.
A 60 LF retained concrete wall was installed on Beach Ball Project.


A redefinition, anti-wrinkle treatment that is specially made for firming normal and combination skins.
A face and neck cream based on anti-age technology ProGEN-in. An advanced cosmetic that provides a global firming effect and restores facial fullness. Indicated for normal to combination skins. It has a rich and supple texture.
Result: The Global Lift Contour cream promotes the restoration of the skin volume and strengthens the skin. Wrinkles are reduced and the skin is lifted. For a young and fresh look.
• After cleansing in the usual way, apply a small quantity of the product to the face and neck, allowing it to gently penetrate.
• Do not apply to the eye contour area.
I really like Skeyndor products and this cream is one of my favourites. I use it in the morning and use the Global Lift serum at night. Works well. The Global Lift eye cream is also very good.
This is a very nice light textured cream with a fine scent. It does not leave my skin shiny or greasy. Too early to see results yet.


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Bias : A CBS insider exposes how the media… | Folio | TinyCat |
Bias : A CBS insider exposes how the media distort the news
by Bernard Goldberg
Washington, DC : Lanham, MD : Regnery Pub. ; Distributed to the trade by National Book Network, c2002.
In his nearly thirty years at CBS News, Emmy Award winner Bernard Goldberg earned a reputation as one of the preeminent reporters in the television news business. When he looked at his own industry, however, he saw that the media far too often ignored their primary mission: to provide objective, disinterested reporting. Again and again he saw that the news slanted to the left. For years, Goldberg appealed to reporters, producers, and network executives for more balanced reporting, but no one listened. The liberal bias continued. Now, breaking ranks and naming names, he reveals a corporate news culture in which the closed-mindedness is breathtaking and in which entertainment wins over hard news every time.
LibraryThing member kkirkhoff
Bernard Goldberg spent twenty-eight years as a reporter for CBS. His book shows how the media unintentionally impose a liberal bias when reporting the news. He is quick to point out that for non-social issues like plane crashes or September 11 the media does a superb job. The bias comes out in their coverage of social issues. Several reasons support this feeling.
- A large majority of the press are Democrats compared with around 20% of the general population.
- When getting opinions on various news stories, they consult known liberal groups, but no conservative groups.
- They socialize and work with like-minded people, therefore, they view their stances as normal.
Their bias comes out in a distortion of facts, how people are portrayed in the news, and words used to describe ideas that do not match their own. Politicians are labelled "conservative" or "right-wing", but none are labelled "liberal" or "left-wing". Various conservative/Republican platform planks are schemes or something that has a negative connotation.
It was interesting how the media (60 Minutes in particular), who have no problem exposing corruption and questionable behavior, reacted with disdain, denial, and vindictiveness when Goldberg turns the tables. It was obvious to me that those who dish it out, can't take it.
The topics that he feels are subjected to this bias are the homeless, AIDS, men, terrorism, and race. This was very interesting because he would make a point and counter it with a "what if" scenario. For instance, Katie Couric jokingly asks if a jilted bride considered castration as a suitable remedy for the groom. Goldberg counters that with "what if" Matt Lauer were interviewing a groom in a similar situation. What if Lauer had mentioned cutting off the bride's breasts as a remedy? All Hell would break loose. Women's groups would be calling for his abusive-violence-against-women's head.
I would definitely recommend this book to anyone who rolls their eyes at the very thought of a media bias. It was eye-opening, and I'll never watch network news the same way again. Come to think of it, I never watch network news anyway. Oh well, no great loss.
By the way, Bernard Goldberg has never voted for a Republican, and voted for Bill Clinton twice.… (more)
LibraryThing member alexgieg
To have militant politics, militant judges and militant NGOs is bad enough, but to have militant journalists is simply ridiculous. Goldberg thus shows that liberals not only think wrong, they also do wrong, and worse, they do wrong where they shouldn't "do" anything at all. No wonder most americans distrust Big Media...
LibraryThing member ague
Interesting reading. I read it after Dan Rather had been dismissed from CBS news for poor journalism. The book was apparently written before then. It was very interesting that Bernard Goldberg came close to losing his pension because of criticizing CBS for having a liberal bias in the Wall Street Journal editorial pages. This brought him the wrath of Dan Rather. Goldberg may have had the last laugh as Dan Rather was eventually fired for using a forged document against President George W. Bush on the CBS news. The main point: our hard news should be fair, balanced, and unbiased.… (more)
LibraryThing member mramos
Bernard Goldberg is a liberal and an Emmy Award-winning broadcast journalist that worked for CBS for decades. This book is his expose of his fellow reporters' liberal bias that led to his own ostracism and rejection. Mr. Goldberg offers examples of how media interpretations of current events affect social climate of the country. This book is as timely as the Op-ed pieces Mr. Goldberg wrote when he was still on the CBS payroll. Everyone has a right to their opinion, but not when reporting the news. Our news is supposed to be objective. If they wish to give their own opinions, they should be commentators. I agree with the other reviews that state that this book is a solid indictment of the mainstream media's bias. We should demand that all news media returns to reporting facts and focus on being fair, balanced and objective.… (more)
LibraryThing member jpsnow
More than anything else, Goldberg fights back full-throttle at "The Dan." His case that the media has a liberal bias is clear, and he tempers it appropriately with discussion of the underlying dynamics and the (perhaps even scarier fact) that such bias is mostly unconscious.
LibraryThing member br77rino
For me, this was the first book to really lay out the bias in the news media. I consider it the godfather of the raft of such books that came out in the years immediately following it. It opened the floodgates and led the way to a conservative activism that in turn led to the tea parties.
LibraryThing member chichikov
A short account of Goldberg being blackballed from the MSM because he grew more conservative.
LibraryThing member JCO123
Nothing Rush hasn't pointed out already, but now it's an ''insider'' saying it, so people are listening.
JournalismObjectivity
Television broadcasting of newsUnited States
Similar in this library
Bad news : The decline of reporting, the business of news, and the danger to us all by Tom Fenton

redpajama_set_name: RedPajamaCommonCrawl


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HomeLagos: Burden of a former federal capital
Lagos: Burden of a former federal capital
Benjamin Okorie
shared this article with you from Inoreader
Via The Nation Nigeria
In 1992, Lagos lost its status as the federal capital. Its loss is Abuja's gain. Despite cries for it to be granted a special status, Lagos, more or less, has been abandoned, writes EMMANUEL OLADESU
Lagos, the former Federal Capital Territory and the fifth largest economy in Africa, is in pains. When will it get special status?
The city provokes an ambivalent emotion. On one hand, it is a prosperous city; a city of peculiar hope and promise. On the other hand, it is a city of stress, distress and disappointment. Lagos, it can be argued, is a reference point in 'the good, the bad, and the ugly.' However, in reality, it is perceived by many as the city of first choice and pride of Nigeria.
Since the federal capital was relocated to Abuja in 1992, the Federal Government has not looked back. Put succinctly, Lagos, more or less, has been abandoned.
A city encircled by the sea, seventy-five per cent of Lagos is water. Therefore, flooding is a natural occurrence, despite the government's effort.
There is much pressure on the social amenities provided by the state government. This is due to the sheer population explosion. The over-population had initially destroyed the implementation of the original Master Plan of the city as the federal capital of Nigeria.
As the commercial nerve centre, host to headquarters of major multinationals and embassies, and the major seaport, Lagos is critical to Nigeria's economy. The economic worth of Lagos is underscored by its contribution to the total Value Added Tax (VAT), which is put at more than 50 per cent.
Even, foreign officials acknowledge the importance of Lagos to the country. World Bank officials, who visited the late President Umaru Yar'Adua in Abuja, were taken aback when no representative of Lagos State government was in the team that accompanied him. Taking a cue from that omission, the former President later gave the then Governor Babatunde Fashola (SAN) a special seat in his Economic Team.
As far back as 2001, the World Bank had rated Lagos as the regional economic capital of West Africa. Also, the Vision 2020 and the National Financial Sector Strategy document have emphasised that Lagos was crucial to any economic calculation and reform that may be contemplated by the Federal Government.
It is indisputable that Lagos contributes 31.98 per cent to the nation's Gross Domestic Product (GDP). It is the nation's lead contributor in the non-oil sector, with the 19 per cent attainment, which is equivalent to the contribution of 13 Nigerian states.
A member of the National Assembly, Opeyemi Bamidele, said: "The city of Lagos alone accounts for over 70 per cent of national industrial investment, 65 per cent of total cargo freight, over 50 per cent of Nigeria's communication subscribers and over 70.16 per cent of international and 58.30 per cent of domestic aviation traffic.
"With three lighter terminals and two ports, Lagos generates 50 per cent of Nigeria's port revenue and the Murtala Muhammed Airport, located in the heart of Lagos, is the major hub for aviation within West Africa, as well as between the regions and Europe."
Historically, Lagos had served as the seat of government from the colonial days. It is a huge city, with a sprawling population thirsty for sophisticated infrastructure. It is a city of economic potentialities. Covering an area of 3,600 square kilometres, it is endowed with rich natural resources, including natural gas and oil. In the Lagos hinterland of Epe, Apa-Kingdom in Badagry, Eti-Osa, Ikeja and Ikorodu are found crude oil and bitumen, silica sands, clays and woods. Some of them have not been tapped.
Lagos shoulders enormous national and regional responsibilities. There is no family in the country that is not represented in Lagos. The search for employment has led to migration to the city by Nigerians in search of real or imagined greener pastures. The population grows in geometric proportion. The bustling nature of the populous city is discernable in the morning through the traffic snarl. The sheer movement of people creates a pilgrimage scenario. Thousands of vehicles enter the city from sunrise. Few of them would leave before sunset.
Lagos has suffered systematic political marginalisation, subjugation, deprivation and oppression. The hand of previous federal administrations were heavy on the city-state. The metro-line project conceived by former Governor Lateef Jakande was cancelled by military rulers. The Independent Power Project (IPP) initiated by former Governor Bola Tinubu was frustrated by the Obasanjo administration, claiming that power was in the Exclusive List.
Oil-producing states are entitled to 13 per cent derivation, but Lagos, the major VAT haven, is entitled to nothing. In the distribution of local councils, Lagos was also short-changed. While old Kano State, from which Jigawa was carved out, could boast of 74 local governments, Lagos only has 20 councils. When Asiwaju Tinubu created an additional 37 local council development areas, it drew the ire of the power-loaded Federal Government. The allocations to the pre-existing 20 councils were withheld.
Today, the city groans over the collapse of federal roads. The Federal Government is a distant government. Thus, to Lagosians, the state government is to blame for all bad federal roads.
The 'Lagos Question' resonates. The solution, many believe, is a special status or special economic assistance to the Centre of Excellence.
Many Nigerians thought that Lagos would achieve the dream under the Buhari administration. Their hopes were rekindled when Senator Oluremi Tinubu (Lagos Central) sponsored "A Bill for an Act to make provision for federal grants to Lagos State in recognition of its strategic socio-economic significance and other connected purposes" in the Senate. However, the hope was dimmed, as a majority of the senators shot the bill down at its Second Reading.
Does Lagos, the economic capital, deserve much strategic care like Abuja, the political capital?
Since the relocation of the seat of power from Lagos to Abuja, the city has been denied the status of a former national political and administrative headquarters. Nigeria has refused to follow the paths of other countries, such as the United States and Brazil, which accorded their former capitals special status when they moved them to new cities.
It appears there was no concrete agreement on the role of the Federal Government in maintaining Lagos and Abuja as "dual cities," unlike the experience of Germany, Brazil, Malaysia, Australia and Tanzania, where capitals were relocated.
Bonn was the capital of Germany between 1945 and 1994 before it was moved to Berlin. The agreement on the movement was signed. According to the document, the German Government has responsibilities for the maintenance of the old capital.
Rio de Janeiro was the capital of Brazil before it was moved to Brazilia. The relocation did not lead to its neglect. The federal roads, buildings and other infrastructures in the old and new capitals are still been maintained simultaneously.
The former capital of Malaysia is Kaura-Lampur. Now, the new capital is Putrajaya, reputed as a leading computerised city in the world. While Putrajaya is the administrative capital, Kuala-Lampur is the legislative capital hosting the country's National Assembly.
In Australia, Sydney was the capital before it was moved to Campera. However, most government activities still take place in the old capital. These include international conferences, conventions and other important meetings.
The old capital of Tanzania is Dar-es-Salam before it was moved to Dodoma. The city has not lost influence, despite the relocation.
Due to the neglect of Lagos, there is much discomfort. The Trunk A roads, drainages and canals which the Federal Government should construct and maintain have been abandoned. Until now, Lagos/Ibadan Expressway was an eyesore. Lagos/Ore and Lagos/Abeokuta roads are still death traps.
Lagosians have had a bitter experience during the raining season. Waters come from the drainages of local government and state roads do not find space in bigger drainages on federal roads, thereby compounding flooding. Lagos government had invested huge resources on infrastructural development, including the construction of drainages, roads, urban beautification and renewal, and restoration of parks to prevent flooding, erosion and other environmental hazards. But, the increasing population has made all these interventions inadequate. That is why Lagosians are demanding for more ecological funds to assist the state to deal with the environmental hazards.
It is evident that, despite its N30 billion monthly Internally Generated Revenue (IGR), Lagos still needs federal help. The pressure on its social amenities makes any robust investment in social infrastructure like a drop in the ocean. Schools are congested. Health centres appear grossly inadequate. Thousands are jobless and homeless, making violent crimes an option for frustrated, idle hands. The state government, which has been elevated by circumstances into a mini-Federal Government, carries the burden.
Senator Oluremi Tinubu's bill was meant to address some of these problems in the national interest. Noting that Lagos is under strains, the federal legislator once said: "It is obvious that Lagos State has been left to deal with these pressures on its own at a huge cost."
Those who support the bill were of the opinion that appropriating an amount not less than one per cent of the total revenue accruing to the Federal Government to Lagos as a first-line charge from the Federation Account would be a right step in the right direction. If the Federal Government can grant the request for special economic assistance, the grants will be utilised in meeting the infrastructural needs of millions of Nigerians who have made Lagos their home. The allocation would also be invested in improving on the intra-city railway infrastructure to decongest the roads and to make the socio-economic environment-friendly.
But, the "Bill for an Act to make provision for federal grants to Lagos State in recognition of its strategic socio-economic significance and other connected purposes" was rejected by the majority of the legislators.
Those who opposed the bill said it was untimely. Others said they would only support the bill if Calabar and Abuja would receive the same consideration.
Ordinarily, there is no politician and businessman of note who does not have anything to do with the megacity. Across the 57 councils and five political divisions of Ikeja, Lagos, Epe, Ikorodu and Badagry, there is a thin line of difference between the indigenes and non-indigenes. Unlike in other states, the doors of political and elective offices, and the civil service are not shut against non-indigenes, who now appear to be in the majority in the urban areas. There is no discrimination in Lagos by the sons of the soil.
In the 70s, former military Head of State Gen. Yakubu Gowon had set up the Federal Government/Lagos Committee to recommend certain special considerations for the city. The committee was headed by former Federal Commissioner for Finance, the late Alhaji Shehu Shagari, who later became the President of Nigeria. But, the recommendations did not see the light of the day.
Gowon's successor, the late Gen. Murtala Muhammed, whose administration approved the relocation of the capital from Lagos to Abuja, following the late Justice Akinola Aguda Panel Report, promised that the city would not be abandoned because of its position as the economic nerve centre. The decision was captured by the minutes of the defunct Supreme Military Council (SMC).
When former military President Ibrahim Babangida moved the Presidency to Abuja, a prominent women leader, the late Alhaja Abibat Mogaji, reminded him during the commissioning of the Third Mainland Bridge, to redeem his promise to Lagos. "As you relocate to Abuja, keep your promise to Lagos," she told the Gen. Babangida.
When the late Head of State, Gen. Sani Abacha, initiated the creation of zonal centres of excellence, he accorded Lagos a priority, along with Port-Harcourt, Kaduna, Kano and Enugu. However, it did not become a reality.
When Alhaji Femi Obasanjo left office, prominent Lagos leaders, including Alhaji Femi Okunnu (SAN) and the Eleko of Lagos, Oba Rilwanu Akiolu, took on the battle of reclaiming Lagos lands and other property illegally acquired by the Federal Government. Not all the property have ben reclaimed.
Does Lagos also deserve compensation for hosting the major seaport at Apapa? The Federal Government makes billions of naira daily from port activities. It is even doubtful if the port authorities and multi-nationals transacting businesses there maintain a commensurate corporate responsibility to the state.
The question is: when will Lagos get special status?
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by Ben Okorie's Blog, 2019 Blogger


This list contains information on famous rock stars with the most kids, loosely ranked by fame and popularity. Several famous guitarists, vocalists, and all around rock Gods have four or more children. Some famous rockers have had all their kids with the same partner while other celebrity rock musicians have had children with multiple partners. A few famous rock stars have even adopted children.
Who will you find on this list of famous rock stars with the most kids? Ozzy Osbourne is near the top. The Black Sabbath front-man has six children with two different women. His kids Kelly and Jack – along with his wife Sharon Osbourne – appeared on the reality show The Osbournes from 2002-2005. Rolling Stones vocalist Mick Jagger has eight children with five different women.
While many rock stars have reputations of being unfaithful, Jon Bon Jovi has had all four of his children with his wife, Dorothea Hurley. Other famous rock and rollers with a lot of kids include Rod Stewart, Brian Wilson, and Ray Charles who had 12 children with 10 women.


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Unified Communications: Uniting Communication Across Different Networks
REDMOND, Wash. — Oct. 1, 2009 — Microsoft today announced two new offerings for Microsoft Office Communications Server, which delivers streamlined communication for users to find and communicate with the right person, at the right time, from the applications they know and use most.
Eric Swift, general manager of the Unified Communications Group at Microsoft
First, Microsoft is releasing the Microsoft Office Communications Server 2007 R2 XMPP Gateway at no additional licensing cost; it allows basic presence sharing and instant messaging (IM) with Extensible Messaging and Presence Protocol networks Cisco Jabber and Google Talk. For Office Communications Server customers, this means Cisco Jabber and Google Talk users can now be part of Office Communications Server IM contacts. Starting today, the Microsoft Office Communications Server 2007 R2 XMPP Gateway can be downloaded here, while a video that explains how the Gateway works can be viewed here.
Second, Microsoft is changing its public instant messaging connectivity (PIC) license requirements for Office Communications Server connectivity to the Windows Live and AOL public IM networks. Now, customers with Office Communications Server 2007 R2 Standard CAL (or equivalent Software Assurance rights) will no longer require an additional license to connect with the millions of people who use Windows Live and AOL for instant messaging and presence. This change took place in July for Windows Live, and is scheduled for AOL in October 2009.
Eric Swift, general manager of Microsoft Unified Communications Group, talked with PressPass about today's news and Microsoft's commitment to increase interoperability of its unified communications and collaboration solutions with products from other vendors. He also discussed the latest significant developments in unified communications (UC), a valuable tool for business that brings together e-mail, calendaring, voice mail, instant messaging, Voice over Internet Protocol (VoIP), and conferencing for secured connectivity and communication with colleagues and customers.
PressPass: Why are these new developments important to unified communications?
Swift: People shouldn't have to log into multiple IM networks and manage several different contact lists to reach the people they need to work with, and vice versa. With these advances in interoperability, we're taking a step closer to creating ubiquitous IM and presence connectivity that narrows the remaining gaps in communicating and connecting with people across different networks. Providing a single identity allows Office Communications Server users to see their colleagues' availability and make contact with these other communities, which is an essential requirement for business.
PressPass: In what other ways have you increased interoperability on the Microsoft unified communications platform?
Swift: Last December we introduced the expansion of the Exchange ActiveSync IP licensing program, and for the first time publicly posted the technical documentation for protocols built on Exchange ActiveSync.
Last May, we also announced we're working with HP to provide endpoint interoperability between HP Halo Telepresence Solutions and Microsoft Office Communications Server unified conferencing. In the future, Office Communicator users will be able to join Halo Telepresence sessions right from their computer. In addition, we have video integration with Tandberg and Polycom for teleconferencing and telepresence.
We also have 73 vendors signed up for the Microsoft Unified Communications Open Interoperability Program, qualifying their enterprise telephony infrastructure, including IP-PBX, PBX and PSTN Gateways and Carrier SIP Trunking services, with the Direct SIP interoperability available with Office Communications Server.
PressPass: Why is Microsoft working with competitors to advance interoperability in unified communications?
Swift: Now more than ever, customers want software vendors to do a better job of making their products work together, so we're responding to meet that demand. We also have a strong commitment to interoperability with other vendors because of our shared vision to make business communications a simple, person-centric experience that is not closed within a specific network or technology. For example, this vision can be seen in the work done by IBM in its recent update to the company's Sametime Gateway, to allow Sametime users to exchange presence information and instant messages with Office Communications Server users. Microsoft is also working with Cisco to connect to Cisco's Unified Communications Manager via Direct SIP connectivity with Office Communications Server 2007 R2.
PressPass: What does the future look like for interoperability in unified communications?
Swift: I'm excited about the progress we're making in presence interoperability with PBX systems and other server-based applications. Customers tell us they want an easy way to show the presence, or real-time availability status, of all users, including those who use traditional phones for voice calls. If someone is on a call, their presence information should show that. However, across the industry today, we don't have a simple way to get this information from the PBX. So, we intend to make presence inquiries and updating possible through the universally adopted Session Initiation Protocol, which will provide PBX systems with the ability to access and set presence in future versions of Office Communications Server. The SIP/SIMPLE (Session Initiation Protocol for Instant Messaging and Presence Leveraging Extensions) standards also provide a presence interface that is ideal for a wide variety of business applications.
We also provide a versatile set of Application Programming Interfaces (APIs) that let developers take advantage of the power of software-based communications in their products. Over the past 12 months, more than 150 independent software vendors (ISVs) have started building products on the Microsoft unified communications platform. We expect this deep integration of communications functionality in software will completely change how people and businesses communicate in the coming years.
Finally, we'll continue to listen to customers, partners and competitors to find out what their priorities are in interoperability. Because there are always new interoperability scenarios and standards in development, our job is to make sure our product innovations are in step with these priorities and technologies so people have the best experience possible in unified communications.


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2021 Cultural Parade | Saturday, June 12th @12PM
JUNETEENTHKC
JKC SWAG
COVID-19 PLAN
The Real History
"Strange Fruit"
Original poem by Abel Meeropol
Under the pseudonym (Lewis Allen)
A poem written in response to lynching's in US southern states.
Southern trees bear a strange fruit,
Blood on the leaves and blood at the root,
Black body swinging in the Southern breeze,
Strange fruit hanging from the poplar trees.
Pastoral scene of the gallant South,
The bulging eyes and the twisted mouth,
Scent of magnolia sweet and fresh,
And the sudden smell of burning flesh!
Here is a fruit for the crows to pluck,
For the rain to gather, for the wind to suck,
For the sun to rot, for a tree to drop,
Here is a strange and bitter crop.
Poet and spoken word artist Glenn North reading his poem "Lynch Family Blues", inspired by Joseph Hirsch's Lynch Family.
Visit The Billie Holiday at Sugar Hill Exhibition in Kansas City at The American Jazz Museum
May 8 - August 1, 2021
Meeropol wrote Strange Fruit after seeing Lawrence Beitler's distressing photograph of the August 7,1930 lynching of Thomas Shipp and Abram Smith in Marion, Indiana in the New York Times.
"Strange Fruit" is a song written and composed by Abel Meeropol and recorded by Billie Holiday in 1939. The lyrics were drawn from a poem by Meeropol that was published in 1937.
The song protests the lynching of Black Americans. Its lyrics compare the victims to the fruit of trees. Such lynchings had reached a peak in the Midwest and Southern United States at the turn of the 20th century. The great majority of victims were Black.
The song has been called "a declaration" and "the beginning of the civil rights movement."
One of Billie Holiday's (Eleanora Fagan (April 7, 1915 – July 17, 1959) most iconic songs, "Strange Fruit," is a haunting protest against the inhumanity of racism. Many people know that the man who wrote the song was inspired by a photograph of a lynching. They might not realize that he is also tied to another watershed moment in America's history.
When Holiday decided to sing the song, it reached millions of people. While the lyrics never mention lynching, the metaphor is painfully clear. Soon after publication, Meeropol set the song to music. It was performed at union meetings and even at Madison Square Garden by the jazz singer Laura Duncan.
It was there that Robert Gordon, the new floor manager at the jazz club Café Society first heard Strange Fruit in 1938. He mentioned it to Barney Josephson, the club's founder, and Meeropol was invited to play it for Holiday.
Rosenberg's Meeropol and his wife adopted the two boys from Julius and Ethel Rosenberg, who were sentenced to death for conspiring to give atomic secrets to the Soviet Union. The Rosenbergs were also Communists. Julius and Ethel Rosenberg were taken to prison after being found guilty of nuclear espionage. They were subsequently executed. The couple's trial and execution made national headlines. News accounts described it as "the first husband and wife to die in the electric chair."
New York lawmakers did not like "Strange Fruit." In 1940, Meeropol was called to testify before a committee investigating communism in public schools. They wanted to know whether the American Communist Party had paid him to write the song. They had not — but, like many New York teachers in his day, Meeropol was a Communist.
Abel Meeropol died in 1986. His sons, Robert and Michael, both became college professors.
The Black Archives of Mid-America in Kansas City is proud to be part of the Community Remembrance Project. EJI collaborates with communities to memorialize documented victims of racial violence and foster meaningful dialogue about race and justice. Schedule Your Visit
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News has a way of helping readers separate fact from fiction. But what happens when news is fiction?
Some fake stories of 2016 reaffirmed people's biases: "FBI agent suspected in Hillary email leak found dead in apparent murder-suicide," while others were outright outrageous: "Woman Arrested For Defecating On Boss' Desk After Winning The Lottery." In a time of "alternative facts" consumers must be on the lookout.
Some in Donald Trump's inner circle have likened the new president to Andrew Jackson. A couple weeks ago, Trump even had a portrait of Jackson – America's first populist leader – hung in the Oval Office as a source of inspiration.
Whether Trump's social and political leanings are anything like Old Hickory's is a point of debate. But their paths to the White House do share an important feature: Both were accompanied by a resurgence of fake news.
What's behind the rise of 'fake news'?
The concept of "fake news" has evolved quickly.
First it was false or misleading stories spread on social media in the run-up to the presidential election. There was a lot of talk about fake news swaying the election results, and while bogus news stories were shared widely, researchers at Stanford University and New York University concluded in January they didn't have outsize influence on the election results.
How did fake news get to such an important place in the body politic?
It's a perfect model for how to sell a false story.
Exaggerate wildly. Manipulate statistics egregiously. Double down on lies. Apply grotesque, racist stereotypes. When people who know the facts tell you you're wrong, accuse them of being part of a globalist conspiracy. Bonus points if you can get an alternative-universe lawmaker or two, like Idaho's Heather Scott, to spread your tale.
Judging by online comments, there's a lot of confusion about the different parts of a news report – is it a story, an editorial, or a column? When people got their news exclusively from the printed newspaper it was much easier to differentiate. An editorial appeared on the Opinion page. A local news columnist's work looked different from a regular news article, usually because it included the columnist's photo. Those visual cues aren't as apparent online.
Our newspaper's critics are split: Are we The Socialist-Review or are we The Spokesman-Republican?
Fresh young reporters at The Spokesman-Review quickly learn that they have been pronouncing the name of their paper wrong. "It's the Socialist-Review," a neighbor will correct them, with a grin. The second thing that they'll learn, possibly from neighbors on the opposite side of the street, is that their paper might as well be called The Spokesman-Republican, since it marches in lockstep with the GOP. In most cases, this tells you more about the political leanings of your neighbors than it does about the paper. A look into the political history of The Spokesman-Review shows that the reality is more complicated.


When young medusa Ria inadvertently turns an entire village to stone, she and her older sister flee to Nelroote, an underground settlement populated by other non-humans also marginalised by society. There she becomes their gatekeeper, hoping to seek redemption and love…until her friendship with a man from above threatens to dismantle the city she swore to protect.
Nuraliah Norasid holds a PhD in English Literature and Creative Writing from Nanyang Technological University. She works as a research associate at the Centre for Research on Islamic and Malay Affairs (RIMA), where she studies marginalities and the confluence of religious ideas and secular society. Her writing has been published in QLRS, Karyawan Magazine, AMPlified and Perempuan: Muslim Women Speak Out. The Gatekeeper is her first novel.


Kerala which is situated on the southwest coast of India, now referred to as 'Gods Own Country', has coconuts growing in abundance and as a result, coconut has become a significant aspect within Keralan cooking. Coconut milk, cream and kernel (grated or sliced) are commonly used within dishes for flavouring and thickening, in turn reducing the amount of oil/ghee that is required when cooking. Spices are a fundamental element within the cuisine of Kerala and enable each dish to encompass its own distinctive flavour. Those spices most commonly used are black pepper, cardamom, chillies, cloves, coriander, ginger, tamarind and turmeric, all of which are cultivated in profuse amounts within Kerala.
South Indian cuisine offers a variety of healthy, vegan friendly and gluten free option.
Taste of Kerala Kitchen is a style of restaurant that offers some of the finest South Indian cuisine within New York. It is our humble attempt to introduce a variety of authentic dishes especially light and simple authentic curries from the land which has adopted the slogan "Gods Own Country"


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Q: How to preserve metric values over training sessions in Keras? I have a fit() function that uses the ModelCheckpoint() callback to save the model if it better than any previous model, using save_weights_only=False, so it saves the entire model. This should allow me to resume training at a later date by using load_model().
Unfortunately, somewhere in the save()/load_model() roundtrip, the metric values are not preserved -- for example, val_loss is set to inf. This means that when training resumes, after the first epoch ModelCheckpoint() will always save the model, which will almost always be worse than the previous champion from the earlier session.
I have determined that I can set ModelCheckpoint()'s current best value before resuming training, as follows:
myCheckpoint = ModelCheckpoint(...)
myCheckpoint.best = bestValueSoFar

Obviously, I could monitor the values I need, write them out to a file, and read them in again when I resume, but given that I am a Keras newbie, I am wondering if I have missed something obvious.

A: I ended up quickly writing my own callback that keeps track of the best training values so I can reload them. It looks like this:
# State monitor callback. Tracks how well we are doing and writes
# some state to a json file. This lets us resume training seamlessly.
#
# ModelState.state is:
#
# { "epoch_count": nnnn,
#   "best_values": { dictionary with keys for each log value },
#   "best_epoch": { dictionary with keys for each log value }
# }

class ModelState(callbacks.Callback):

    def __init__(self, state_path):

        self.state_path = state_path

        if os.path.isfile(state_path):
            print('Loading existing .json state')
            with open(state_path, 'r') as f:
                self.state = json.load(f)
        else:
            self.state = { 'epoch_count': 0,
                           'best_values': {},
                           'best_epoch': {}
                         }

    def on_train_begin(self, logs={}):

        print('Training commences...')

    def on_epoch_end(self, batch, logs={}):

        # Currently, for everything we track, lower is better

        for k in logs:
            if k not in self.state['best_values'] or logs[k] < self.state['best_values'][k]:
                self.state['best_values'][k] = float(logs[k])
                self.state['best_epoch'][k] = self.state['epoch_count']

        with open(self.state_path, 'w') as f:
            json.dump(self.state, f, indent=4)
        print('Completed epoch', self.state['epoch_count'])

        self.state['epoch_count'] += 1

Then, in the fit() function, something like this:
# Set up the model state, reading in prior results info if available

model_state = ModelState(path_to_state_file)

# Checkpoint the model if we get a better result

model_checkpoint = callbacks.ModelCheckpoint(path_to_model_file,
                                             monitor='val_loss',
                                             save_best_only=True,
                                             verbose=1,
                                             mode='min',
                                             save_weights_only=False)

# If we have trained previously, set up the model checkpoint so it won't save
# until it finds something better. Otherwise, it would always save the results
# of the first epoch.

if 'best_values' in model_state.state:
    model_checkpoint.best = model_state.state['best_values']['val_loss']

callback_list = [model_checkpoint,
                model_state]

# Offset epoch counts if we are resuming training. If you don't do
# this, only epochs-initial_epochs epochs will be done.

initial_epoch = model_state.state['epoch_count']
epochs += initial_epoch

# .fit() or .fit_generator, etc. goes here.

A: I don't think, that you have to store the metric values by yourself. There has been a feature-request at the keras project about something very similiar, but it has been closed. Maybe you could try to use the solution which has been presented over there. In the philosophy of keras it is not very useful to store the metrics, as you are just saving the model which means: the architecture and the weights of each layer; not the history or anything else.
The easiest way would be to create a kind of metafile which contains the metric-values of a model and the name of the model itself. Then you could load the metafile, get the best metric values and get the name of the model which yield them, to load the model again, to resume the training.

redpajama_set_name: RedPajamaStackExchange


Neutropenia is a decrease in circulating neutrophils in the nonmarginal pool, which constitutes 4-5% of total body neutrophil stores.  Most of the neutrophils are contained in the bone marrow, either as mitotically active (one third) or postmitotic mature cells (two thirds).  Granulocytopenia is defined as a reduced number of blood granulocytes, namely neutrophils, eosinophils, and basophils. However, the term granulocytopenia is often used synonymously with neutropenia and, in that sense, is again confined to the neutrophil lineage alone.
The risk of serious infection increases as the absolute neutrophil count (ANC) falls to the severely neutropenic range (< 500/µL). The duration and severity of neutropenia directly correlate with the total incidence of all infections and of those infections that are life threatening. Tuberculosis (see the image below) is one type of infection that may cause neutropenia.
Anteroposterior chest radiograph in a young ED patient presenting with cough and malaise. The radiograph shows a classic posterior segment right upper lobe density consistent with active tuberculosis. This woman was admitted to isolation and started empirically on a 4-drug regimen in the ED. Tuberculosis was confirmed on sputum testing. Image courtesy of Remote Medicine, remotemedicine.org.
Concurrent anemia, thrombocytopenia, and/or an abnormal result on a peripheral blood smear from a patient with neutropenia suggest an underlying hematologic disorder. In this setting, immediately perform a bone marrow aspiration and obtain a biopsy from the posterior iliac crest. Cytogenetic analysis and cell-flow analysis of the aspirate may be indicated.
Neutropenia is a decrease in circulating neutrophils in the nonmarginal pool, which constitutes 4-5% of total body neutrophil stores.  Most of the neutrophils are contained in the bone marrow, either as mitotically active (one third) or postmitotic mature cells (two thirds). [2, 12] Granulocytopenia is defined as a reduced number of blood granulocytes, namely neutrophils, eosinophils, and basophils. However, the term granulocytopenia is often used synonymously with neutropenia and, in that sense, is again confined to the neutrophil lineage alone.
Neutropenia is defined in terms of the absolute neutrophil count (ANC). The ANC is calculated by multiplying the total white blood cell (WBC) count by the percentage of neutrophils (segmented neutrophils or granulocytes) plus the band forms of neutrophils in the complete blood count (CBC) differential. See the Absolute Neutrophil Count calculator.
Note that many modern automated instruments actually calculate and provide the ANC number in their reports. These instruments do not analyze separately bands from segmented neutrophils, and so the combined number is termed the absolute neutrophil count (ANC), representing both bands and more mature segmented neutrophils. If a band number is reported separately, usually by smear review, then one can divide the ANC into bands and segmented neutrophils by subtracting the absolute band number from the total ANC.
The lower limit of the reference value for ANC in adults varies in different laboratories from 1.5-1.8 109/L or 1500-1800/µL (mm3). For practical purposes, a value lower than 1500 cells/µL is generally used to define neutropenia. Age, race, genetic background, environment, and other factors can influence the neutrophil count. For example, blacks may have a lower but normal ANC value of 1000 cells/µL, with a normal total WBC count.
Neutropenia is classified as mild, moderate, or severe, based on the ANC. Mild neutropenia is present when the ANC is 1000-1500 cells/µL, moderate neutropenia is present with an ANC of 500-1000/µL, and severe neutropenia refers to an ANC lower than 500 cells/µL. The risk of bacterial infection is related to both the severity and duration of the neutropenia.
The term agranulocytosis is used to describe a more severe subset of neutropenia. Agranulocytosis refers to a virtual absence of neutrophils in peripheral blood. It is usually applied to cases in which the ANC is lower than 100/μL. [12, 13, 14, 15] The reduced number of neutrophils makes patients extremely vulnerable to infection. [12, 16] Cardinal symptoms include fever, sepsis, and other manifestations of infection. Causes can include drugs, chemicals, infective agents, ionizing radiation, immune mechanisms, primary bone marrow failure syndromes, and heritable genetic aberrations.
Some cases, such those from benign familial neutropenia, are characterized by only mild neutropenia and are of no obvious significance for health.  This article is limited to discussing neutropenia (ANC < 1500/µL) and agranulocytosis (ANC < 100/µL). It does not address the transient neutropenia associated with cancer chemotherapy, nor does it consider agranulocytosis occurring as part of primary marrow-failure syndromes (eg, aplastic anemia, pancytopenia, acute leukemia, myelodysplastic syndromes).
For more information, see the Medscape article Pediatric Autoimmune and Chronic Benign Neutropenia.
Mature neutrophils are produced by precursors in the bone marrow. The total body neutrophil content can be divided conceptually into the following three compartments: the bone marrow, the blood, and the tissues. In the marrow, the neutrophils exist in two divisions: the proliferative, or mitotic, compartment (myeloblasts, promyelocytes, myelocytes) and the maturation-storage compartment (metamyelocytes, bands, mature neutrophils, polymorphonuclear leukocytes ["polys"]).
Neutrophils leave the marrow storage compartment and enter the blood without reentry into the marrow. In the blood, two compartments are also present, the marginal compartment and the circulating compartment. Some neutrophils do not circulate freely (marginal compartment), but are adherent to the vascular surface, and these constitute approximately half of the total neutrophils in the blood compartment.
Neutrophils leave the blood pool in a random manner after 6-8 hours and enter the tissues, where they are destined for cellular action or death. Thus, if the process producing neutropenia is unknown, measurements of the blood neutrophil number, ANC, must often be supplemented by bone marrow examination to determine whether adequate production of neutrophils or increased destruction of neutrophils exists.
Sites and mechanisms that cause neutropenia can be restricted to any of the three compartments or their subcomponents: bone marrow (mitotic or mature storage pools); blood (circulating and marginal pools); or tissues (sequestration). For example, benign congenital neutropenias are associated with a decrease in only the pool of circulating neutrophils; affected individuals have entirely normal marrow pools, marginal blood pools, and tissue neutrophils.
Disorders of the pluripotent myeloid stem cells and committed myeloid progenitor cells, which cause decreased neutrophil production, include some congenital forms of neutropenia, aplastic anemia, acute leukemia, and myelodysplastic syndromes. Other examples include bone marrow tumor infiltration, radiation, infection (especially viral), and bone marrow fibrosis. Cancer chemotherapy, other drugs, and toxins may damage hematopoietic precursors by directly affecting bone marrow.
The clinical sequelae of neutropenia usually manifests as infections, most commonly of the mucous membranes. Skin is the second most common infection site, manifesting as ulcers, abscesses, rashes, and delays in wound healing. The genitalia and perirectum are also affected. However, the usual clinical signs of infection, including local warmth and swelling, may be absent, as these require the presence of significant numbers of neutrophils. Fever, however, is often present, and its presence requires urgent attention in the setting of severe neutropenia.
The risk of serious infection increases as the ANC falls to the severely neutropenic range (< 500/µL). The duration and severity of neutropenia directly correlate with the total incidence of all infections and those infections that are life threatening. When the ANC is persistently lower than 100 cells/µL for longer than 3-4 weeks, the incidence of infection approaches 100%. In prolonged severe neutropenia, life-threatening gastrointestinal and pulmonary infections occur, as does sepsis. However, patients with neutropenia are not at increased risk for parasitic and viral infections, as these are defended by innate and lymphocyte-mediated immune mechanisms.
Bacterial organisms most often cause fever and infection in neutropenic patients. Fungal organisms are also significant pathogens in the setting of neutropenia. Historically, gram-negative aerobic bacteria (eg, Escherichia coli, Klebsiella species, Pseudomonas aeruginosa) have been most common in these patients. However, gram-positive cocci, especially Staphylococcus species and Streptococcus viridans, have emerged as the most common pathogens in fever and sepsis because of the increasing use of indwelling right atrial catheters.
After neutropenic patients receive treatment with broad-spectrum antibiotics for several days, superinfection with fungi is common. Candida species are the most frequently encountered organisms in this setting.
The list for all the potential causes of neutropenia is not short. The etiology of neutropenia can conceptually be viewed in two broad ways, by mechanism or etiologic category.
The mechanisms that cause neutropenia are varied and not completely understood. In many cases, neutropenia occurs after prolonged exposure to a drug or other substance, resulting in decreased neutrophil production by hypoplastic bone marrow. This suggests a direct stem cell toxic effect. In other cases, repeated but intermittent drug or other exposure is needed. This suggests an immune mechanism, although this idea has not been proven. In many clinical situations, the exact exposure and its duration in relation to the onset of neutropenia are not known.
In view of this incomplete understanding of the mechanisms for neutropenia, classification by broad etiologic category is simpler to retain. In this schema, the etiology of neutropenia can be classified as either congenital (hereditary) or acquired. Though this categorization may have limited clinical diagnostic utility, it can be useful to clearly separate hereditary causes of neutropenia from the panoply of acquired causes. In the setting of hereditary neutropenias, these disorders can be further described as associated with isolated neutropenia or with other defects, whether immune or phenotypic.
Many hereditary disorders are due to mutations in the gene encoding neutrophil elastase, ELA2. Several alleles are involved. The most common mutations are intronic substitutions that inactivate a splice site in intron 4. Genes other than ELA2 are also involved. The Table below lists some of the genetic conditions involved; these are uncommon conditions.
AML = acute myeloid leukemia; G-CSF = granulocyte colony-stimulating factor; MDS = myelodysplastic syndrome.
Causes of acquired neutropenia are complex, but most are related to three major categories: infection, drugs (both direct toxic or immune mediated), and autoimmune. Chronic benign neutropenia, or chronic idiopathic neutropenia, appears to be an overlap disorder with hereditary and acquired forms, and is sometimes indistinguishable. Some neutropenic patients give a clear history and familial pattern, whereas others have no familial history, few blood test determinations, and an unknown duration of neutropenia. This group of patients could have hereditary or acquired neutropenia.  A brief summary of both congenital and acquired neutropenic disorders follows.
Neutropenia with abnormal immunoglobulins is observed in individuals with X-linked agammaglobulinemia, isolated immunoglobulin A (IgA) deficiency, X-linked hyperimmunoglobulin M (XHIGM) syndrome, and dysgammaglobulinemia type I.  In XHIGM, which is due to mutations in the CD40 ligand, patients can actually have normal or elevated levels of IgM but markedly decreased serum IgG levels. In all these disorders, the infection risk is high, and the treatment is intravenous immunoglobulin (IVIG).
Patients with reticular dysgenesis demonstrate severe neutropenia, no cell-mediated immunity, agammaglobulinemia, and lymphopenia.  Life-threatening infections occur that are refractory to granulocyte colony-stimulating factor (G-CSF). [22, 23, 24] Bone marrow transplantation is the treatment of choice.
Severe congenital neutropenia (SCN), or Kostmann syndrome, is most often caused by a recessive inheritance and found in remote, isolated populations with a high degree of consanguinity.  Autosomal dominant and sporadic cases have also been reported, most often due to mutations in the G-CSF receptor. No uniform genetic defect exists in this syndrome. Mutations in ELA2, which are causative for cyclic neutropenia (see below) are not sufficient to explain the phenotype of Kostmann-like SCN.
Patients present by age 3 months with recurrent bacterial infections. The mouth and perirectum are the most common sites of infection. This type of neutropenia is severe, and the treatment is G-CSF. Risk of conversion to myelodysplastic syndrome (MDS)/acute myelogenous leukemia (AML) with monosomy 7 after G-CSF treatments is associated with additional acquired mutations. Most of these cases are caused by a mutation in the G-CSF receptor. Patients whose condition responds clinically to G-CSF are treated for life.
Some patients with other forms of SCN appear to have mutations in GFI1, a zinc-finger transcriptional repressor gene involved in hematopoietic stem cell function and lineage commitment decisions.
Cyclic neutropenia (CN) is characterized by periodic bouts of neutropenia associated with infection, followed by peripheral neutrophil count recovery. Its periodicity is about 21 days (range, 12-35 d). Granulocyte precursors disappear from the marrow before each neutrophil nadir in the cycle because of accelerated apoptosis of myeloid progenitor cells.  Some cases may be genetically determined with an autosomal recessive inheritance. Other cases may be due to an autosomal dominant inheritance. In some sporadic cases of CN, patients have mutations in ELA2.
People with CN typically present as infants or children, but acquired forms of CN in adulthood exist. The prognosis is good, with a benign course; however, 10% of patients will experience life-threatening infections. The treatment for cyclic neutropenia is daily G-CSF.
Affected individuals with chronic benign neutropenia have an overall low risk of infection.
Familial chronic benign neutropenia is a disorder with an autosomal dominant pattern of inheritance observed in western Europeans, Africans, and Jewish Yemenites. Patients are typically asymptomatic, and the infections are mild. No specific therapy is required.
In nonfamilial chronic benign neutropenias, mild infections with a benign course typify this disorder. The ANC, however, does respond to stress, such as infection, corticosteroids, and catecholamines.
Idiopathic chronic severe neutropenia is a diagnosis of exclusion. Affected patients exhibit infections and severe neutropenia.
Shwachman syndrome (Shwachman-Diamond) has an autosomal recessive inheritance pattern. The neutropenia is moderate to severe, with a mortality rate of 15-25%, and the syndrome presents in infancy, with recurrent infections, diarrhea, and difficulty in feeding. Dwarfism, chondrodysplasia, and pancreatic exocrine insufficiency can occur.
Shwachman-Diamond syndrome and X-linked dyskeratosis congenita (DC), cartilage-hair hypoplasia (CHH), and Diamond-Blackfan anemia (DBA) all appear to share common gene defects involved in ribosome synthesis. Most cases of Shwachman-Diamond syndrome are caused by mutations in the SBDS gene.  The precise function of this gene is still being elucidated; however, it is involved in ribosome synthesis and RNA processing reactions. The treatment is G-CSF.
In CHH, the inheritance pattern is autosomal recessive on chromosome 9, and it is observed in Amish and Finnish families. CHH is caused by mutations in the RMRP gene, which encodes the RNA component of the ribonuclease mitochondrial RNA processing (RNase MRP) complex. The neutropenia is moderate to severe. CHH presents with cell-mediated immunity defects, macrocytic anemia, gastrointestinal disease, and dwarfism. It also shows a predisposition to cancer, especially lymphoma. The treatment is bone marrow transplantation.
Dyskeratosis congenita (Zinsser-Cole-Engman syndrome) presents with mental retardation, pancytopenia, and defective cell-mediated immunity. Dyskeratosis congenita is more common in men than in women and is hematologically similar to Fanconi anemia. Dyskeratosis congenita is usually X-linked recessive, although autosomal dominant and autosomal recessive forms of this disorder exist.
The X-linked recessive form of the disorder has been linked to mutations in DKC1, which encodes dyskerin, a nucleolar protein associated with ribonucleoprotein particles. The autosomal dominant form is associated with mutations in another gene, TERC, which is part of telomerase. Telomerase has both a protein and RNA component, and TERC codes the RNA component. Patients with this disorder have shorter telomeres than normal. The treatment is G-CSF, granulocyte-macrophage colony-stimulating factor (GM-CSF), and bone marrow transplantation.
Barth syndrome is an X-linked recessive disorder presenting with cardiomyopathy in infancy, skeletal myopathy, recurrent infections, dwarfism, and moderate to severe neutropenia.
Chediak-Higashi syndrome is an autosomal recessive disorder with recurrent infections, mental slowing, photophobia, nystagmus, oculocutaneous albinism, neuropathy, bleeding disorders, gingivitis, and lysosomal granules in various cells. The neutropenia is moderate to severe, and the treatment is bone marrow transplantation.
Myelokathexis presents in infancy with moderate neutropenia and is associated with recurrent infections. The condition is due to accelerated apoptosis and decreased expression of bcl-x in neutrophil precursors. An abnormal nuclear appearance is observed, with hypersegmentation with nuclear strands, pyknosis, and cytoplasmic vacuolization. The treatment is G-CSF and GM-CSF.
Lazy leukocyte syndrome is a severe neutropenia with associated abnormal neutrophil motility. The etiology is unknown, and the treatment is supportive in nature.
These are chronic neutropenias with variable ANCs. They include glycogen storage disease type 1b and various acidemias, such as isovaleric, propionic, and methylmalonic. In glycogen storage disease type 1b, the treatment is G-CSF and GM-CSF.
A drug may act as a hapten and induce antibody formation. This mechanism operates in cases due to gold, aminopyrine, and antithyroid drugs. The antibodies destroy the granulocytes and may not require the continued presence of the drug for their action. Alternatively, the drug may form immune complexes that attach to the neutrophils. This mechanism operates with quinidine.
In isoimmune neonatal neutropenia, the mother produces IgG antineutrophil antibodies to fetal neutrophil antigens that are recognized as nonself. This occurs in 3% of live births. The disorder manifests as neonatal fever, urinary tract infection, cellulitis, pneumonia, and sepsis. The duration of the neutropenia is typically 7 weeks.
Chronic autoimmune neutropenia is observed in adults and has no age predilection. As many as 36% of patients will exhibit serum antineutrophil antibodies, and the clinical course is usually less severe. Patients can have this disorder in association with systemic lupus erythematosus, rheumatoid arthritis, Wegener granulomatosis, and chronic hepatitis.
If chronic autoimmune neutropenia is associated with these diseases, corticosteroids are indicated as treatment. In neonates and children, this disorder is associated with a lower risk of infection and milder infections involving the middle ear, gastrointestinal tract, and skin.
T-gamma lymphocytosis, or lymphoproliferative disorder, is a clonal disease of CD3+ T lymphocytes or CD3- natural killer (NK) cells that infiltrate the bone marrow and tissues. Also known as leukemia of large granular lymphocytes (LGL-leukemia), T-gamma lymphocytosis can be associated with rheumatoid arthritis and is associated with high-titer antineutrophil antibodies. The neutropenia is persistent and severe. The treatment is often supportive in nature, but it is also directed at eliminating the clonal population.
Bilateral interstitial infiltrates in a 31-year-old patient with influenza pneumonia.
Lateral chest radiograph in a 31-year-old patient with influenza pneumonia. Image courtesy of Remote Medicine, remotemedicine.org.
The most commonly involved organisms are from endogenous flora. Staphylococcus aureus organisms are found in cases of skin infections. Gram-negative organisms are observed in infections of the urinary and gastrointestinal tracts, particularly Escherichia coli and Pseudomonas species. Candida albicans infections may also occur. Mixed flora may be found in the oral cavity.
Viral infections often lead to mild or moderate neutropenia. Agranulocytosis is uncommon but may occur. The most common organisms are Epstein-Barr virus, hepatitis B virus, yellow fever virus, cytomegalovirus, and influenza. Many overwhelming infections, both viral and bacterial, may cause severe neutropenia.
Nutritional deficiencies that can cause neutropenia include vitamin B-12, folate, and copper deficiency.
Numerous drugs have been associated with neutropenia. The highest risk categories are antithyroid medications, macrolides, and procainamides. As stated above, many drugs act by an immune-mediated mechanism. However, some drugs appear to have direct toxic effects on marrow stem cells or neutrophil precursors in the mitotic compartment. For example, drugs such as the antipsychotics and antidepressants and chloramphenicol may act as direct toxins in some individuals, based on metabolism and sensitivity in this manner. Other drugs may have a combination of immune and nonimmune mechanisms or may have unknown mechanisms of action.
Analgesics and anti-inflammatory agents include aminopyrine, dipyrone, indomethacin, ibuprofen, acetylsalicylic acid, diflunisal, sulindac, tolmetin, benoxaprofen, barbiturates, mesalazine, and quinine.
Antipsychotics, antidepressants, and neuropharmacologic agents include phenothiazines (chlorpromazine, methylpromazine, mepazine, promazine, thioridazine, prochlorperazine, trifluoperazine, trimeprazine), clozapine, risperidone, imipramine, desipramine, diazepam, chlordiazepoxide, amoxapine, meprobamate, thiothixene, and haloperidol.
Anticonvulsants include valproic acid, phenytoin, trimethadione, mephenytoin (Mesantoin), ethosuximide, and carbamazepine.
Antithyroid drugs include thiouracil, propylthiouracil, methimazole, carbimazole, potassium perchlorate, and thiocyanate.
Cardiovascular drugs include procainamide, captopril, aprindine, propranolol, hydralazine, methyldopa, quinidine, diazoxide, nifedipine, propafenone, ticlopidine, and vesnarinone.
Antihistamines include cimetidine, ranitidine, tripelennamine (Pyribenzamine), methaphenilene, thenalidine, brompheniramine, and mianserin.
Diuretics include acetazolamide, bumetanide, chlorothiazide, hydrochlorothiazide, chlorthalidone, methazolamide, and spironolactone.
Hypoglycemic agents include chlorpropamide and tolbutamide.
Antimalarial drugs include amodiaquine, dapsone, hydroxychloroquine, pyrimethamine, and quinine.
Miscellaneous drugs include allopurinol, colchicine, aminoglutethimide, famotidine, bezafibrate, flutamide, tamoxifen, penicillamine, retinoic acid, metoclopramide, phenindione, dinitrophenol, ethacrynic acid, dichlorodiphenyltrichloroethane (DDT), cinchophen, antimony, pyrithyldione, rauwolfia, ethanol, chlorpropamide, tolbutamide, thiazides, spironolactone, methazolamide, acetazolamide, IVIG, and levodopa.
Heavy metals include gold, arsenic, and mercury.
Exposure to drugs or chemicals is the most common cause of agranulocytosis: about one half of patients have a history of medication or chemical exposure. Any chemical or drug that can depress the bone marrow and cause hypoplasia or aplasia is capable of causing agranulocytosis. Some drugs do this to everyone if they are administered in large enough doses. Other agents seem to cause idiosyncratic reactions that affect only certain susceptible individuals.
Some agents (eg, valproic acid, carbamazepine, and beta-lactam antibiotics) act by direct inhibition of myelopoiesis. In bone marrow cultures, these agents inhibit granulocyte colony formation in a dose-related fashion. Direct damage to the bone-marrow microenvironment or myeloid precursors plays a role in most other cases.
Immunologic neutropenias may occur after bone marrow transplantation and blood product transfusions.
Felty syndrome is a syndrome of rheumatoid arthritis, splenomegaly, and neutropenia. Splenectomy shows an initial response, but neutropenia may recur in 10-20% of patients. Treatment is directed toward rheumatoid arthritis.
In complement activation–mediated neutropenia, hemodialysis, cardiopulmonary bypass, and extracorporeal membrane oxygenation (ECMO) expose blood to artificial membranes and can cause complement activation with subsequent neutropenia.
In splenic sequestration, the degree of neutropenia resulting from this process is proportional to the severity of the splenomegaly and the bone marrow's ability to compensate for the reduction in circulating bands and neutrophils.
Go to Pediatric Autoimmune and Chronic Benign Neutropenia for complete information on this topic.
The incidence of drug-induced neutropenia is one case per million persons per year.The exact frequency of agranulocytosis is unknown; the estimated frequency is 1.0-3.4 cases per million population per year.
Age can influence the neutrophil count. Elderly individuals have a higher incidence rate of neutropenia than younger individuals.
Agranulocytosis occurs in all age groups. The congenital forms are most common in childhood; acquired agranulocytosis is most common in the elderly population.  Go to Pediatric Autoimmune and Chronic Benign Neutropenia for complete information on this topic.
Neutropenia occurs more commonly in females than in males. Agranulocytosis occurs slightly more frequently in women than in men, possibly because of their increased rate of medication usage. Whether this higher frequency is related to the increased incidence of autoimmune disease in women is unknown.
Race and genetic background can influence ANC. Blacks, Ethiopians, Yemenite Jews, and certain populations in the world could have lower ANCs due to lower WBC counts. Data from US National Health and Nutritional examination 1999 to 2004 survey found the prevalence of neutropenia to be 4.5% among black participants, 0.79% in white individuals, and 0.38% in Mexican-Americans.  Blacks have a lower neutrophil count either due to defective granulocyte release from normal bone marrow, or they may have a compromised bone marrow reserve.
Agranulocytosis has no racial predilection.
The prognosis of a patient with neutropenia depends on the primary etiology, duration, and severity of the neutropenia. Improved broad-spectrum antibiotic agents, combined with improved supportive care, have improved the prognosis for most patients with severe neutropenia. Ultimately, patient survival depends on the recovery of adequate neutrophil numbers.
Morbidity in those with neutropenia usually involves infections during severe, prolonged episodes of neutropenia. The infections may be superficial, involving mainly the oral mucosa, gums, skin, and sinuses, or they may be systemic, with life-threatening septicemia.
If agranulocytosis is untreated, the risk of dying is high. Death results from uncontrolled sepsis. If the condition can be reversed with treatment, the risk of dying is low. Antibiotic and antifungal medications can cure the infection if the ANC rises. Agranulocytosis secondary to viral infections is usually self-limited, and patients with such conditions have a good prognosis.
Drug-induced agranulocytosis carries a mortality rate of 6-10%. If treated promptly and vigorously, patients with drug-induced agranulocytosis have a good prognosis.
Patients with neutropenia should be instructed to avoid exposure to people with respiratory tract infections.  They should avoid overcrowded areas, and if their ANC is less than 1000/µL, they should wear a facemask in public places.
Patients should be instructed to avoid any drug that was previously implicated in causing them neutropenia. They should be educated about the importance of frequent CBC testing in the initial period when a new drug with a high propensity to cause neutropenia is introduced. The exact frequency of testing depends on the specific drug and the time course of neutropenia association. At the first sign of a drop in the ANC, the drug should be discontinued.
The Centers for Disease Control and Prevention offers patient education information on neutropenia and infection risk for cancer patients receiving chemotherapy and preventing infections during cancer therapy. In the workplace, people must be educated to follow regulations from the Occupational Safety and Health Administration (OSHA) that cover safety precautions when they deal with toxic substances.
For patient education information, see the Blood and Lymphatic System Center and Immune System Center, as well as Anemia, Sepsis (Blood Infection), Leukemia, and Lymphoma.
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The margins of this massive spleen were palpated easily preoperatively. Medially, the 3.18-kg (7-lb) spleen crosses the midline. Inferiorly, it extends into the pelvis.
Doppler sonogram at the splenic hilum reveals hepatofugal venous flow in a patient with portal hypertension.


What better way to see the incredible sights of Central Florida than from the calm of a hot air balloon at sunrise? Look down on the magical land of Disney World and drift over swamps that haven't been touched for thousands of years as you ride at treetop height or thousands of feet in the air.
Orlando is one of the USA's most visited cities and attracts millions of visitors every year from around the world. Most people know the name because the area plays host to more than a dozen theme parks, and an enormous number of film studios (from which it earned the nickname "Hollywood East"). Add the second largest university campus in the country, one of the largest single-storey malls in America, and half a dozen premier sports teams, and it's easy to understand the attraction!
But Orlando is more than just the city. It's surrounded by stunning scenery, with world-famous orange groves, swamps that have lain untouched for thousands of years, and hundreds of natural lakes spotted throughout the wetlands.
Get away from the hustle and bustle with this amazing hot air ballooning experience and see Orlando in a new light. Fly without engine noise as a new day dawns over Central Florida, as the sun slowly rises to illuminate the clear, still waters of the hundreds of lakes, spreading the warmth and light that grows the famous Florida oranges enjoyed the world over.
Arriving about an hour before sunrise, we'll take you out to the launch site and brief you on flight procedures to make sure you're completely safe. Then we'll inflate the balloon and it's time to take to the air. Maybe you'll even ride in our latest addition - the country's biggest balloon! Over 11 storeys tall and holding over a million cubic feet of hot air, this monster is five times the size of a standard balloon!
Climb into the basket and get ready for a magical experience as you rise gracefully from the ground, taking to the skies in complete safety and tranquility. Our course and height will depend on prevailing conditions, so you may fly at treetop height or rise way above the clouds, to several thousand feet.
You'll see the theme parks, the city, the wetlands and swamps, the innumerable lakes, those orange groves and plenty more as our pilot points out each spectacular sight.
After an hour, your FAA-certified, full-time professional pilot will bring you in for an exciting (and completely safe) landing on terra firma. And what better way to finish than with a traditional champagne toast to celebrate your exciting adventure?
Children fly for $109 (please call us to purchase).
It doesn't matter whether you've been ballooning before or if this is your first time off the ground - this experience is guaranteed to create memories you'll talk about for the rest of your life. Definitely one for the bucket list!
Women are not permitted to fly during pregnancy, for insurance reasons.
Our meeting point is at the Orlando Balloon Rides Welcome Center, located at the intersection of Interstate 4 and Highway 27 (just past the McDonalds and Wendy's restaurants).
A typical flight lasts around 1 hour, depending on weather conditions. The entire experience can last 3-4 hours, depending on prevailing weather and landing site availability.
Most balloons carry 4 or 5 passengers, though our biggest carries 24!
This is an outdoor soft adventure experience. Please dress sensibly. We recommend comfortable layers of outdoor clothing to match the season (the temperature isn't much different in the air), a hat, and sturdy shoes for morning dew. No open footwear or high heels are permitted.
Floating at treetop level or thousands of feet in the air as you marvel at the sights of Central Florida - everything from the magic of Disney World to orange groves and spectacular natural scenery!


NEW YORK (CNNMoney.com) -- Shares of department store operator JC Penney eased Monday after the company adopted a plan to combat an activist shareholder.
Shares of Plano, Texas-based Penney (JCP, Fortune 500) slipped more than 2% to $33.11 in late trading after falling as low as $32.47 earlier in the session.
Pershing Square, a large hedge fund run by activist investor Bill Ackman, disclosed in regulatory filings last week that it owns 16.5% of Penney's common stock. In a separate filing, Vornado Realty Trust, a Maryland real estate investment trust, said it holds a 9.9% stake in the retailer's common stock.
The adoption of the plan,also known as a poison pill, came "in light of recent rapid accumulations of a significant percentage of the company's outstanding common stock," Penney said in a regulatory filing.
The plan kicks in if any person or group buys more than 10% of the company's common stock, or tries to expand existing stakes beyond 10%, according to the filing. It has a life span of one year.
Despite the dip on Monday, shares of Penney have been on a tear since falling to a low of $19.50 in late August. The stock is up nearly 24% so far this year.
The disclosures raised speculation that Ackman, who was involved in a drawn-out proxy battle with Target (TGT, Fortune 500) last year and forced the sale of fast-food giant Wendy's, will shake things up at Penney.
Analysts at Barclay's Capital said last week that they remain optimistic about Penney's sales growth, but downgraded the stock to "equal weight" from "overweight" on unspecified distractions ahead of the key holiday shopping period.
"As we are heading into the important holiday selling season, where the company earns almost two-thirds of its annual profits, we are concerned that management may be distracted and miss an opportunity for sales and profit gains," Barclays analysts wrote.
Same-store sales, an important gauge of a retailer's health, increased 5.1% for the five-week period ended Oct. 2, the company said, topping its own expectations.
Morningstar analysts said in a research report that they do not expect Pershing Square to make a significant impact on J.C. Penney's operations, though they acknowledged that "financial engineering" remains a possibility.
"We do think Pershing will shake things up," the Morningstar analysts said. "At a minimum, we believe real estate will be one of the ways Pershing will attempt to increase the value of its stake."


Free watches for swift owners ??
Discussion in 'Swift Motorhomes' started by adventure, Jan 10, 2008.
Quote "If any of our Swift customers would like a Swift branded watch as a gift please send me your name and address. Let me have your vehicle details so that I can send you the right brand.
where did this quote come from ?
That quote came from swiftgroup on the darkside.
as swiftgroup are now 'funners' do you thing it applies to us as well now????????????
Dunno I asked for one!!!!
I have just had to close the "sale" on the watches as we have run out. Sorry - if I get hold of some more, I will let you know. This forum will get the first ones.
I'll second that! Mind you quoting Swift managed to get my Autocruise fixed - eventually - so that must be a plus!!!!


Take Route 40 east towards Pennsylvania and look for signs after you cross the Pennsylvania State Line.
Take Route 70 east to the West Alexander Exit (Exit 1) in PA. Turn right at the end of the off ramp and go into town. At the first stop sign, make a left and follow the signs to Route 40. At the Route 40 intersection, turn left and follow signs to the fair.
Take Route 40 west towards West Virginia and look for signs when you get to West Alexander.
Take Route 70 west to the West Alexander Exit (Exit 1). Turn right at the end of the off ramp and go into town. At the first stop sign, make a left and follow the signs to Route 40. At the Route 40 intersection, turn left and follow signs to the fair.


The Safesuite Series of Controllers ushers in a new area in Security design and deployment. Combining Access Control, Burglar Alarm, Keypad Arming Stations and Monitoring functionality into an unprecedented Controller and complete security solution…. The SS2014 PoE Keypad!
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Packed with features such as built-in Access Control, PoE Plus, Email notification, SMS notification, the SS2014 now defines the new standard in the Security industry.
For retrofitting existing buildings that already have proprietary wiring in place, the New SS2014 PoE Keypad includes a backward compatibility channel to utilize the old wiring when LAN/WAN might not exist.
Complete with remote access via web or App this New Keypad/Access Control/Alarm Panel truly does have it all.
Axiom SafeSuite has been specifically designed for complete integration with the AxiomV Enterprise Security Management System to allow for flexible offsite notification and onsite interaction with the building's security and elevator controls.


I was searching for a Property and found this listing (MLS® #1908174). Please send me more information regarding 635 Mccown Dr., Conway, SC, 29526. Thank you!
I'd like to request a showing of 635 Mccown Dr., Conway, SC, 29526 (MLS® #1908174). Thank you!